Medical Surgical Nursing I & II Deepak Sethi, Kirti Rani
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fm1Medical Surgical Nursing I and IIfm2
fm3Medical Surgical Nursing I and II
Deepak Sethi MSc (Nursing) Associate Professor Saraswati Nursing Institute Kurali, Punjab, India Capt Kirti Rani BSc (Nursing) Military Nursing Services (MNS) Command Hospital (WC) Chandimandir Cantonment Panchkula, Haryana, India
fm4
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Medical Surgical Nursing I and II
First Edition: 2016
9789385891250
Printed at
fm5Dedicated to
My Parents
Mr Sushil Kumar Sethi
and
Mrs Shashi Sethifm6
fm7Preface
The complexity of the patients, increasing care demands, and increasing regulatory demands push a medical-surgical nurse into new ways of thinking. In the future, the medical-surgical nurses' role will continue to expand. Their practice demands skill and expertise in a wide variety of disease states, medications, and communication techniques, as well as the ability to work with numerous members of the health care team. While some have interpreted this recommendation as addressing the advanced practice nurses, the intent of the recommendation was broader, including the practice of the registered nurses.
When considering the practice of the medical-surgical nurses, there is much that can be done in considering the full extent of practice. Often the clinical decision-making and work in care coordination by the medical-surgical nurses is not fully recognized. These nurses have long been involved in seeing the whole picture for the patients, looking beyond the patients' immediate state to the steps post hospitalization. The medical-surgical nurses have the opportunity to connect with the patients, the families, physicians, nursing staff, and the rest of the health care team. This provides an opportunity to make connections and carefully plan for the patients' care as they recover from their acute state to the time of rehabilitation, whether in a facility or as they return home. In the accountable care environment, the role of the medical-surgical nurses will be the key in providing quality care and preventing readmissions. The practice of the medical-surgical nurses is considered to be primarily in the acute care setting.
The increasing complexity of patients at home stretches the boundaries of the medical-surgical nurses' practice. The nurses in the long-term acute care describe their practice as that of the medical-surgical nurses. Other changes within health care may continue to stretch the practice settings and opportunities for the medical-surgical nurses.
This book focuses on the immediate and first-aid nursing care of patients. It includes additional chapters on medical-surgical nursing, interstitial lung disease, lung transplantation, etc. Significant modifications have been made in this book, almost in all the chapters, especially in Cardiovascular Disorders, Respiratory Disorders and Immunological Disorders. With these changes, I hope it will meet most of the requirements of both the students as well as the medical-surgical nursing faculty.
Deepak Sethifm8
fm9Acknowledgments
First and foremost, I would like to thank my wife Kirti for standing beside me throughout my career and writing this book. She has been my inspiration and motivation for continuing to improve my knowledge and move my career forward. She is my rock as she has helped me in difficult times. Thus, I dedicate this book to her.
I also thank my wonderful child Kawyaa for always making me smile and for understanding me on those weekend mornings while writing this book instead of playing games with her. I hope one day she will read this book and understand why I spent so much time in front of my computer. I would like to thank my parents and grandparents for allowing me to follow my ambitions throughout my career. I would like to express my gratitude to all those who saw me through this book, and to all those who provided support, talked things over, read, wrote, offered comments, allowed me to quote their remarks and assisted in the editing, proofreading and designing work. Thanks to all my friends for sharing my happiness when starting this project and following with encouragement when it seemed too difficult to be completed. I would have probably given up without their support.
I would like to thank Dr (Mrs) Raman Kalia (Principal, Saraswati Nursing Institute, Kurali, Punjab, India) for her critical evaluation and valuable comments for improving and giving a professional shape to this book.
Speaking of encouragement, I must mention that Mrs Manjeet Kaur (RN, Australia) and Mr Bharat Pareek (Vice Principal, Saraswati Nursing Institute) are responsible for giving me constant support and encouragement.
I would like to thank Ms Manpreet Kaur (Lecturer, Saraswati Nursing Institute) for helping me in editing one of the chapters of this book (Chapter on Oncological Conditions).
I convey my sincere thanks to Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India for their efforts and suggestions, especially Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Group President), Ms Chetna Vohra (Associate Director), and Ms Payal Bharti (Project Manager) for helping me through my idea.
fm11INC Syllabus
Basic BSc Nursing Year II
MEDICAL SURGICAL NURSING I
(ADULT INCLUDING GERIATRICS)
Course Description: The purpose of this course is to acquire knowledge and develop proficiency, caring for patients with medical surgical disorders in varieties of health care settings home.
 
COURSE CONTENTS
 
UNIT I: INTRODUCTION
  • Introduction to medical surgical nursing: Evolution and trends of medical and surgical nursing
  • Review of concepts of health and illness, disease: concepts, causations, classification, diseases (ICD-10 or later version), acute illness, stages of illness
  • Review of concepts of comprehensive nursing care in medical surgical conditions based on the nursing process
  • Role of a nurse, patient and family in care of adult patients
  • Role and responsibilities of a nurse in medical surgical settings:
    • Outpatient department
    • Inpatient unit
    • Intensive care unit
    • Home and community settings
  • Introduction to medical surgical asepsis:
    • Inflammation and infection
    • Immunity
    • Wound-healing
  • Care of surgical patient (preoperative)
    • Intraoperative
    • Postoperative.
 
UNIT II: COMMON SIGNS AND SYMPTOMS AND MANAGEMENT
  • Fluid and electrolyte imbalance
  • Vomiting
  • Dyspnea and cough, respiratory
  • Fever
  • fm12Shock
  • Unconsciousness, syncope
  • Pain
  • Incontinence
  • Edema
  • Age-related problems—geriatric.
 
UNIT III: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH RESPIRATORY PROBLEMS
  • Review of anatomy and physiology of respiratory system
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical surgical, dietetics and nursing management of adults, including elderly with:
    • Upper respiratory tract infections
    • Bronchitis
    • Asthma
    • Emphysema
    • Empyema
    • Atelectasis
    • Chronic Obstructive Pulmonary Diseases (COPD)
    • Bronchiectasis
    • Pneumonia pulmonary tuberculosis
    • Lung abscess
    • Pleural effusion
    • Cysts and tumors
    • Chest injuries
    • Respiratory arrest and insufficiency
    • Pulmonary embolism
    • Special therapies, alternative therapies
    • Nursing procedures
    • Drugs used in treatment of respiratory disorders.
 
UNIT IV: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH DISORDERS OF DIGESTIVE SYSTEM
  • Review of anatomy and physiology of digestive system
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical, surgical, dietetics and nursing management
  • Disorders of:
    • Oral cavity: Lips, gums, tongue, salivary glands and teeth
    • Esophagus: Inflammation, stricture, obstruction, bleeding and tumors
    • fm13Stomach and duodenum: Hiatus hernia, gastritis, peptic and duodenal ulcer bleeding, tumours, pyloric stenosis
    • Small intestinal disorders: Inflammation and infection, enteritis, malabsorption, obstruction, tumour and perforation
    • Large intestinal disorders: Colitis, inflammation and infection, obstruction and tumor and lymph hernias
    • Appendix: Inflammation, mass, abscess, rupture
    • Anal and rectum: Hemorrhoids, fissures, fistulas
    • Peritonitis/acute abdomen
    • Pancreas: Inflammation, cyst, abscess and tumors
    • Liver: Inflammation, cyst, abscess, cirrhosis, portal hypertension, hepatic failure, tumors
    • Gallbladder, inflammation, obstruction, stones and tumors
    • Special therapies, alternative therapies
    • Nursing procedures, drugs used in treatment of disorders of digestive system.
 
UNIT V: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH BLOOD AND CARDIOVASCULAR PROBLEMS
  • Review of anatomy and physiology of blood and cardiovascular system
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical, surgical dietetics and nursing management of:
  • Vascular system of:
    • Hypertension, hypotension
    • Artherosclerosis
    • Raynaud's disease
    • Aneurism and Peripheral vascular disorders.
Heart
  • Coronary artery diseases:
    • Ischemic heart disease
    • Coronary atherosclerosis
    • Angina pectoris
    • Myocardial infarction.
  • Valvular disorders of the heart:
    • Congenital and acquired
    • Rheumatic heart diseases
  • Endocarditis, pericarditis, myocarditis
  • Cardiomyopathies
  • Cardiac dysrhythmias, heart block
  • Congestive cardiac failure edema, cardiogenic shock, cardiac tamponade
  • fm14Cardiac emergencies and arrest
  • Cardiopulmonary Resuscitation (CPR)
  • Blood:
    • Anemias
    • Polycythemia
    • Bleeding disorder; clotting factor defects and platelet defects
    • Thalassemia
    • Leukopenias and agranulocytosis
    • Lymphomas
    • Myelomas
  • Special therapies:
    • Blood transfusion safety checks, procedure and requirements, management of adverse transfusion reaction, records for blood transfusion
    • Management and counseling of blood donors, phlebotomy procedure, and post-donation management. Blood bank functioning and hospital transfusion committee. Biosafety and waste management in relation to blood transfusion
    • Role of a nurse in organ donation, retrieval and banking
    • Alternative therapies, nursing procedures, drugs used in treatment of blood and cardiovascular disorders.
 
UNIT VI: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH DISORDERS OF GENITOURINARY PROBLEMS
  • Review of anatomy and physiology of genitorurinary system
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, clinical manifestations diagnosis, treatment modalities and medical, surgical, dietetics and nursing management of:
    • Nephritis
    • Nephrotic syndrome
    • Nephrosis
    • Renal calculus
    • Tumors
    • Acute renal failure
    • Chronic renal failure
    • End-stage renal disease
    • Dialysis, renal transplant
    • Congenital disorders, urinary infections
    • Benign prostate hypertrophy
    • Disorders of ureter, urinary bladder and urethra—inflammation infection, stricture obstruction, tumor, prostate
  • Special therapies, alternative therapies
  • Nursing procedures, drugs used in the treatment of genitourinary disorders.
fm15
 
UNIT VII: NURSING MANAGEMENT OF DISORDERS OF MALES (ADULTS INCLUDING ELDERLY) REPRODUCTIVE SYSTEM
  • Review of anatomy and physiology of male reproductive system
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, clinical manifestation diagnosis, treatment modalities and medical, surgical dietetics and nursing management of disorders of male reproductive system
    • Congenital malformation, cryptorchidism
    • Hypospadiasis, epispadiasis
    • Infections
    • Testis and adjacent structures
    • Penis
    • Prostate: Inflammation, infection, hypertrophy, tumor
    • Sexual dysfunction
    • Infertility
    • Contraception
    • Breast, gynecomastia, tumor
    • Climacteric changes
  • Special therapies, alternative therapies
  • Nursing procedures, drugs used in treatment of disorders of male reproductive system.
 
UNIT VIII: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH DISORDERS OF ENDOCRINE SYSTEM
  • Review of anatomy and physiology of endocrine system
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, diagnosis, treatment modalities and medical, surgical, dietetics and nursing management of:
    • Disorders of thyroid and parathyroid
    • Diabetes mellitus
    • Diabetes insipidus
    • Adrenal tumor
    • Pituitary disorders
  • Special therapies, alternative therapies
  • Nursing procedures, drugs used in treatment of disorders of endocrine system.
 
UNIT IX: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH DISORDERS OF INTEGUMENTARY SYSTEM
  • Review of anatomy and physiology of skin and its appendages
  • Nursing assessment
  • History and physical assessment
  • fm16Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical, surgical, dietetics and nursing management of disorders of skin and its appendages:
    • Lesions and abrasions
    • Infection and infestations, dermatitis
    • Dermatomes, infectious and noninfectious ‘inflammatory dermatoses’
    • Acne vulgaris
    • Allergies and eczema
    • Psoriasis
    • Malignant melanoma
    • Alopecia
  • Special therapies, alternative therapies
  • Nursing procedures, drugs used in treatment of disorders of integumentary system.
 
UNIT X: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH MUSCULOSKELETAL PROBLEMS
  • Review of anatomy and physiology of musculoskeletal system
  • Nursing assessment
  • History and physical assessment
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical, surgical, dietetics and nursing management of disorders of:
    • Muscles, Ligaments and Joints: Inflammation, infection, trauma
    • Bones: Inflammation, infection dislocation, fracture, tumor and trauma
    • Osteomalacia and osteoporosis
    • Arthritis
    • Congenital deformities
    • Spinal column: Defects and deformities, tumor, prolapsed intervertebral discs, Pott's spine
    • Paget's disease
  • Amputation
  • Prosthesis
  • Transplant and replacement surgeries
  • Rehabilitation
  • Special therapies, alternative therapies
  • Nursing procedures
  • Drugs used in treatment of disorders of musculoskeletal system.
 
UNIT XI: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH IMMUNOLOGICAL PROBLEMS
  • Review of immune system
  • Nursing assessment: History and physical assessment
  • fm17Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical, surgical, dietetics and nursing management of:
    • Immunodeficiency disorder
    • Primary immunodeficiency
      • Phagocyte dysfunction
      • B-cell and T-cell deficiencies
  • Secondary immunodeficiency syndrome (AIDS)
  • Incidence of HIV and AIDS
  • Epidemiology
  • Transmission–Prevention of transmission
  • Standard safety precautions
  • Role of nurse, Counseling
  • Health education and home care consideration
  • National AIDS Control Program—NACO, various national and international agencies
  • Infection control program
  • Rehabilitation
  • Special therapies, alternative therapies
  • Nursing procedures, drugs used in treatment of disorders of immunological system.
 
UNIT XII: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH COMMUNICABLE DISEASE
  • Overview of infectious disease, the infectious process
  • Nursing assessment: History and physical assessment
  • Epidemiology, infections, process, clinical manifestations, diagnosis, treatment, prevention and dietetics. Control and eradication of common communication diseases:
    • Tuberculosis
    • Diarrheal
    • Hepatitis A, E
    • Herpes
    • Chickenpox
    • Smallpox
    • Typhoid
    • Meningitis
    • Gas gangrene
    • Leprosy
    • Dengue
    • Plague
    • Malaria
    • Diphtheria
    • Pertussis
    • Poliomyelitis
    • fm18Measles
    • Mumps
    • Influenza
    • Tetanus
    • Yellow fever
    • Filariasis
    • HIV, AIDS
  • Reproductive tract infections
  • Special infection control isolation, quarantine, immunization, infectious disease hospitals
  • Special therapies, alternative therapies
  • Nursing procedures, drugs used in treatment of communicable diseases.
 
UNIT XIII: PREOPERATIVE NURSING
  • Organization and physical set-up of the operation theatre (OT):
    • Classifications
    • OT design
    • Staffing
    • Members of the OT team
    • Duties and responsibilities of a nurse in an OT
  • Principles of health and operating room attire
    • Instruments
    • Sutures and suture materials
    • Equipment
    • OT tables and sets for common surgical procedures
    • Positions and draping for common surgical procedures
    • Scrubbing procedures
    • Gowning and gloving
    • Preparation of OT sets
    • Monitoring the patient during surgical procedures
  • Maintenance of therapeutic environment in OT
  • Standard safety measures:
    • Infection control: Fumigation, disinfection and sterilization
    • Biomedical waste
    • Prevention of accidents and hazards in OT
  • Anesthesia:
    • Types
    • Methods of administration
    • Effects and Stages
    • Equipment
    • Drugs
  • Cardiopulmonary Resuscitation (CPR)
  • Pain management techniques
  • Legal aspects.
fm19Basic BSc Nursing Year III
MEDICAL SURGICAL NURSING II
(ADULT INCLUDING GERIATRICS)
Course description: The purpose of this course is to acquire knowledge and develop proficiency in caring for patients with medical and surgical disorder in varieties of health care settings and at home.
 
COURSE CONTENTS
 
UNIT I: NURSING MANAGEMENT OF PATIENTS WITH DISORDER OF EAR, NOSE AND THROAT
  • Review of anatomy and physiology of the ear, nose and throat
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical and surgical nursing management of ear, nose and throat disorders:
    • External ear: Deformities, otalgia, foreign bodies, and tumors
    • Middle ear: Impacted wax, tympanic membrane perforation, otitis media, otosclerosis, mastoiditis, tumors
    • Inner ear: Meniere's disease, labyrinthitis, ototoxicity, tumors
    • Upper airway infections: Common cold, sinusitis, ethinitis, rhinitis, pharyngitis, tonsillitis and adenoiditis, peritonsilar abscess, laryngitis
  • Upper respiratory airway, epistaxis
  • Nasal obstruction, laryngeal obstruction, cancer of the larynx
  • Cancer of the oral cavity
  • Speech defects and speech therapy
  • Deafness: Prevention, control and rehabilitation
  • Hearing aids, implanted hearing devices:
    • Special therapies
    • Nursing procedures
    • Drugs used in treatment of disorders of ear, nose and throat, role of a nurse communicating with hearing impaired and muteness.
 
UNIT II: NURSING MANAGEMENT OF PATIENTS WITH DISORDERS OF EYE
  • Review of anatomy and physiology of the eye
  • Nursing assessment: History and physical assessment
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities, and medical and surgical nursing management of eye disorder
    • Refractive errors
    • Eyelids: Infections, tumors and deformities
    • Conjunctiva: Inflammation and infection, bleeding
    • fm20Cornea: Inflammation and infection
    • Lens, cataract
    • Glaucoma
    • Disorder of the uveal tract
    • Ocular tumors, disorders of posterior chamber and retina, retinal and vitreous problems
    • Retinal detachment
    • Ocular emergencies and their prevention
    • Blindness
    • National Programme for Control of Blindness
    • Eye banking
    • Eye prostheses and rehabilitation
  • Role of a nurse: Communication with a visually impaired patient, eye camps
  • Special therapies
  • Nursing procedures
  • Drugs used in the treatment of disorders of eye.
 
UNIT III: NURSING MANAGEMENT OF PATIENTS WITH NEUROLOGICAL DISORDERS
  • Review of anatomy and physiology of the neurological system
  • Nursing assessment: History and physical and neurological assessment and Glasgow coma scale
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities, and medical and surgical neurological disorders
    • Congenital malformations
    • Headache
    • Head injuries
    • Spinal injuries
    • Paraplegia
    • Hemiplegia
    • Quadriplegia
    • Spinal cord compression: Herniation of intervertebral disc
    • Tumors of brain and spinal cord
    • Intracranial and cerebral aneurysms abscess, neurocysticercosis
    • Movement disorders
    • Chorea
    • Seizures
    • Epilepsies
    • Cerebrovascular accidents (CVA)
    • Cranial, spinal neuropathies: Bell's palsy, trigeminal neuralgia
    • Peripheral neuropathies: Barré syndrome
    • fm21Myasthenia gravis
    • Multiple sclerosis
    • Degenerative:
      • Delirium
      • Dementia
      • Alzheimer's disease
      • Parkinson's disease
  • Management of unconscious patients and patients with stroke
  • Role of a nurse in communicating with a patient having neurological deficit
  • Rehabilitation of patients with neurological deficit
  • Role of a nurse in long-stay facility (institutions) and at home
  • Special therapies
  • Nursing procedures
  • Drugs used in the treatment of neurological disorders.
 
UNIT IV: NURSING MANAGEMENT OF PATIENTS WITH DISORDERS OF FEMALE REPRODUCTIVE SYSTEM
  • Review of anatomy and physiology of the female reproductive system
  • Nursing assessment: History and physical assessment
  • Breast self-examination
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities, and medical and surgical nursing management of disorder of female reproductive system
    • Congenital abnormalities of female reproductive system
    • Sexuality and Reproductive Health
    • Sexual Health Assessment
    • Menstrual disorders: Dysmenorrheal, Amenorrhea,
    • Pelvic Inflammatory Disease
    • Ovarian and fallopian tube disorder, infections, cysts, tumors
    • Uterine and cervical disorders: Endometriosis, polyps, Fibroids, Cervical and uterine tumors
    • Uterine displacement
    • Cystocele/Urethrocele rectocele
    • Vaginal disorders: Infections and discharges, fistulas
    • Diseases of breast: Deformities, infections, cysts and tumors
    • Menopause and Hormonal Replacement Therapy
    • Infertility
    • Contraception: Types methods, risk and effectiveness
    • Spacing methods
    • Barrier methods, Interauterine devices, hormonal, postconnectional methods, etc.
    • Terminal methods
    • Sterilization
    • fm22Emergency contraception methods
    • Abortion: Natural, medical and surgical abortion; MTP Act
    • Toxic shock syndrome
    • Injuries and trauma, sexual violence
  • Special therapies
  • Nursing procedures
  • Drugs used in the treatment of gynecological disorders
  • National Family Welfare Programme.
 
UNIT V: NURSING MANAGEMENT OF PATIENTS WITH BURNS, RECONSTRUCTIVE AND COSMETIC SURGERY
  • Review of anatomy and physiology of the skin and connective tissues and various deformities
  • Nursing assessment: History and physical assessment and assessment of burns and fluid and electrolyte loss
  • Etiology, classification, pathophysiology, clinical manifestations, diagnosis, treatment modalities, and medical and surgical nursing management of burns and reconstructive and cosmetic surgery
  • Types of Reconstructive and Cosmetic surgery; for burns, congenital deformities, injuries and cosmetic purposes
  • Role of nurse
  • Legal aspects
  • Rehabilitation
  • Special therapies
  • Psychosocial aspects
  • Nursing procedures
  • Drugs used in the treatment of burns, reconstructive and cosmetic surgery.
 
UNIT VI: NURSING MANAGEMENT OF PATIENTS WITH ONCOLOGICAL CONDITIONS
  • Structure and characteristics of normal and cancer cells
  • Nursing assessment: History and Physical Assessment
  • Prevention Screening, Early detection, Warning signs of cancer
  • Epidemiology, Etiology, Classification
  • Pathophysiology, Staging, clinical manifestations, diagnosis, treatment modalities and management of oncological conditions.
  • Common malignancies of various body systems; Oral, larynx, lung, Stomach and Colon, Liver, Leukemias and lymphomas, Breast, Cervix, Ovary, Uterus, Sarcoma, Brain, Renal, Bladder, Prostate, etc.
  • Oncological emergencies
  • Modalities of treatment:
    • fm23Immunotherapy
    • Chemotherapy
    • Radiotherapy
    • Surgical interventions
    • Stem cell
    • Bone marrow transplant
    • Gene therapy
    • Other forms of treatment
  • Psychosocial aspect of cancer
  • Rehabilitation
  • Palliative care; symptom and pain management, nutritional support
  • Home care
  • Hospice care
  • Stomal therapy
  • Special therapies
  • Psychosocial aspects
  • Nursing procedures
 
UNIT VII: NURSING MANAGEMENT OF PATIENTS IN EMERGENCY AND DISASTER SITUATIONS
  • Concept and principles of Disaster Nursing
  • Causes and Types of Disaster: Natural and Man-made
    • Earthquakes, Floods, Epidemics, Cyclones
    • Fire, Explosion, Accidents
    • Violence, Terrorism: biochemical War
  • Policies related to emergency/disaster management; International, national state, institutional
  • Disaster preparedness:
  • Team, Guidelines, protocols, Equipments Resources
  • Coordination and involvement of Community, various government departments, nongovernment organizations and International agencies
  • Role of a nurse: Working
  • Legal Aspect of Disaster Nursing
  • Impact on Health and aftereffects; Posttraumatic Stress Disorder
  • Rehabilitation; physical psychosocial, Financial, Relocation
  • Emergency Nursing
  • Concept, priorities, principles and Scope of emergency nursing
  • Organization of emergency services; physical setup, staffing, equipment and supplies, protocols, concepts of triage and role of a triage nurse
  • Coordination and involvement of different departments and facilities
  • Nursing assessment: History and Physical assessment
  • fm24Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical and surgical nursing management of patient with medical and surgical Emergency
  • Principles of emergency management
  • Common Emergencies
  • Respiratory Emergencies
  • Cardiac Emergencies
  • Shock and Hemorrhage
  • Pain
  • Polytrauma, road accidents, crush injuries, wounds
  • Bites
  • Poisoning: Food, Gas, Drugs, and chemical poisoning
  • Seizures
  • Thermal Emergencies: Heat stroke and Cold injuries
  • Pediatric Emergencies
  • Psychiatric Emergencies
  • Obstetric Emergencies
  • Violence, Abuse, Sexual assault
  • Cardiopulmonary Resuscitation
  • Role of a nurse
  • Medicolegal Aspects
  • Crisis Intervention
  • Communication and Interpersonal relationship
 
UNIT VIII: NURSING CARE OF THE ELDERLY
  • Nursing assessment: History and Physical assessment
  • Aging
  • Demography: Myths and realities
  • Concepts and theories of aging
  • Cognitive Aspects of Aging
  • Normal biological aging
  • Age-related body system changes
  • Psychosocial Aspects of Aging
  • Medications and elderly
  • Stress and coping in older adults
  • Common Health Problems and Nursing Management
  • Cardiovascular, Respiratory, Musculoskeletal
  • Endocrine, genitourinary, gastrointestinal
  • Neurological, Skin and other Sensory organs
  • Psychosocial and Sexual
  • fm25Abuse of elderly person
  • Role of a nurse for care of elderly: ambulation, nutritional, communicational, psychosocial and spiritual
  • Role of a nurse for caregivers of elderly.
  • Role of a family and formal and nonformal caregivers,
  • Use of aids and prosthesis (hearing aids, dentures)
  • Legal and Ethical Issues
  • Provisions and programs for elderly; privileges, community programs and health services; Home and institutional care.
 
UNIT IX: NURSING MANAGEMENT OF PATIENTS IN CRITICAL CARE UNITS
  • Nursing assessment: History and physical assessment
  • Classification
  • Principles of critical care nursing
  • Organization: Physical setup, policies, staffing norms
  • Protocols, equipment and supplies
  • Special equipment: Ventilators, cardiac monitors, defibrillators
  • Resuscitation equipment
  • Infection Control Protocols; Nursing management of critically ill patients
  • Monitoring of critically ill patients
  • CPR: Advance Cardiac Life Support
  • Treatments and procedures
  • Transitional care
  • Ethical and legal aspects
  • Communication with patient and family
  • Intensive care records
  • Crisis Intervention
  • Death and Dying—coping with them
  • Drugs used in critical care unit
 
UNIT X: NURSING MANAGEMENT OF PATIENTS (ADULTS INCLUDING ELDERLY) WITH OCCUPATIONAL AND INDUSTRIAL DISEASES
  • Nursing assessment: History and Physical assessment
  • Etiology, pathophysiology, clinical manifestations, diagnosis, treatment modalities and medical and surgical nursing management of occupational and industrial health disorders
  • Role of a nurse
  • Special therapies, alternative therapies
  • Nursing procedures
  • Drugs used in treatment of occupational and industrial disordersfm26fm27

Cardiovascular Disorders1

 
CORONARY ARTERY DISEASE
Coronary artery disease (CAD) is characterized by atherosclerosis in the epicardial coronary arteries.
Atherosclerotic plaques, the hallmark of atherosclerosis, progressively narrow the coronary artery lumen and impair antegrade myocardial blood flow. The plaque becomes thick, calcified and solid, which causes obstruction in the coronary blood flow. The reduction in coronary blood flow may be symptomatic or asymptomatic, occur with exertion or at rest, and culminate in a myocardial infarction, depending on obstruction severity and the rapidity of development.
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Fig. 1.1: Atheroma in coronary artery
 
Etiology and Risk Factors
 
Nonmodifiable Major Risk Factors
  • Heredity (including race): Children whose parents had heart disease are at higher risk of CAD. This increased risk related to genetic predisposition to hypertension, elevated lipid levels, diabetes, and obesity, all of these conditions increase the risk of CAD.
  • Increasing age: Age influences both the risk and the severity of CAD. Symptomatic CAD appears predominantly in people older than 40, and four of five people who die of CAD are aged 65 years or older.
  • Gender: CAD is the number one killer of both men and women. In 1999, mortality from CAD was almost equal for men and women. Although, men are at higher risk for heart attacks at younger ages. The risk for women increases significantly at menopause, so that the CAD rates in women after menopause are two to three times that of women the same age before menopause.
 
Modifiable Major Risk Factors
  • Cigarette smoking: Both active and passive smoking have been strongly implicated as a risk factor in the development of CAD. Smoking triples the rate of heart attacks in women and doubles in men. Nonsmokers who are exposed to second-hand tobacco smoke at home or work may also have higher mortality rate from CAD.
  • Hypertension: High blood pressure increases the workload of heart by increasing afterload, enlarging and weakening the left ventricle over time. As blood pressure increases, the risk of serious cardiovascular event also escalates.
  • Elevated serum cholesterol level: The risk of CAD increases as blood cholesterol level increases. In an adult, total cholesterol levels of 240 mg/dl are classified as ‘HIGH’ and levels ranging from 200 to 239 mg/dl are classified as ‘BORDERLINE HIGH’.
  • Physical inactivity: Those who exercise reduce their risk of CHD because they have:
    • High HDL level
    • Lower LDL cholesterol, triglyceride and blood sugar levels
    • 3Greater insulin sensitivity
    • Lower blood pressure
    • Lower body mass index
    • Obesity: Obesity places an extra burden on the heart. In addition, it also increases the risk because it is often associated with elevated serum cholesterol and triglyceride levels, high bold pressure and diabetes.
    • Diabetes: A fasting blood glucose level of more than 126 mg/dl or routine blood glucose level of 180 mg/dl and glucosuria signal the presence of diabetes. Clients with diabetes have a 2 to 8-fold higher prevalence, incidence and mortality.
 
Contributing Factors include
  • Response to stress: A person's response to stress may contribute to the development of CAD. Some researchers have reported a relationship between CAD risk and stress level, e.g.:- some people response to stress by overeating or by starting or increasing smoking. Stress is also associated with elevated blood pressure.
  • Inflammatory responses: A newly identified risk factor currently being researched is the presence of any chronic inflammatory state that leads to increase in the body's production of CRP (C-reactive protein). Too much CRP tends to destabilize plaque inside too artery walls. When plaque lesions break, a clot is formed and this may lead to heart attack. So, this means that clients with chronic inflammatory disease, such as arthritis and autoimmune deficiency may be at higher risk for heart attack.
  • Menopause: The incidence of CHD increases among women after menopause. Before menopause, estrogen is thought to protect against CHD risk by releasing HDL and lowering LDL levels.
    Fig. 1.2: Plaque in coronary artery
 
Pathophysiology
  • CAD is a chronic process that begins during adolescence and slowly progresses throughout life. Independent risk factors include a family history of premature CAD, 4cigarette smoking, diabetes mellitus, hypertension, hyperlipidemia, sedentary lifestyle, and obesity. These risk factors accelerate or modify a complex and chronic inflammatory vascular process that ultimately manifests as fibrous atherosclerotic plaque.
  • The most widely accepted theory of atherosclerosis states that the process represents the body's attempt to heal in response to an endothelial injury. The first step in the atherosclerotic process is the development of fatty streaks, which contain atherogenic lipoproteins and macrophage foam cells. These streaks form between the endothelium and internal elastic lamina. Over time, an intermediate lesion composed of an extracellular lipid core and layers of smooth muscle and connective tissue matrix eventually forms a fibrous cap. The edge of the fibrous cap plays a critical role in the development of acute coronary syndromes. The shoulder region is the site where most plaques lose their integrity or rupture. Plaque rupture exposes the underlying thrombogenic core of lipid and necrotic material to circulating blood and its thrombogenic particulates. This exposure results in platelet adherence, aggregation, and progressive luminal narrowing, which can rapidly progress and–often in the absence of coronary artery collateral development–are associated with acute coronary syndromes.
  • Vascular inflammation has emerged as a critical and established component of atherosclerosis genesis, activity, and potential plaque instability. Patients with established CAD who possess a confluence of risk factors known as the metabolic syndrome remain at particularly high risk for a future vascular event, such as an acute MI or cerebrovascular accident. Biochemical markers such as elevated levels of high sensitivity or ultra-sensitive C-reactive protein in the absence of systemic inflammation are thought to signal an increased likelihood of vascular inflammation and to portend a higher risk of vascular events. This marker may also signal more rapidly advancing CAD and the need for aggressive preventive measures.
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Signs and Symptoms
The most common symptom of coronary artery disease is angina or chest pain. Angina can be described as a discomfort, heaviness, pressure, aching, burning, fullness, squeezing, or painful feeling in your chest. It can be mistaken for indigestion or heartburn. Angina may also be felt in the shoulders, arms, neck, throat, jaw, or back.
Other symptoms of coronary artery disease include:
  • Shortness of breath.
  • Palpitations (irregular heartbeats, or a ‘flip-flop’ feeling in your chest).
  • A faster heartbeat.
  • Weakness or dizziness.
  • Nausea
  • Discomfort, pressure, heaviness, or pain in the chest, arm, or below the breastbone.
  • Discomfort radiating to the back, jaw, throat, or arm.
  • Fullness, indigestion, or choking feeling (may feel like heartburn).
  • Sweating, nausea, vomiting, or dizziness.
  • Extreme weakness, anxiety, or shortness of breath.
  • Rapid or irregular heartbeats.
 
ANGINA
Angina (chest pain) that occurs regularly with activity, after heavy meals, or at other predictable times is termed as ‘stable angina’ and is associated with high-grade narrowings of the coronary arteries.
 
Stable Angina
Angina pectoris is said to be stable when its pattern of frequency, intensity, ease of provocation or duration does not change over a period of several weeks. Identification of activities that provoke angina and the amount of sublingual nitroglycerin required to relieve symptoms are helpful indicators of stability versus progression. A decrease in exercise tolerance or an increase in the need for nitroglycerin suggests that the angina is progressing in severity or transitioning to an accelerating pattern.
 
Accelerating Angina
Angina pectoris is said to be accelerating when there is a change in the pattern of stable angina. This may include a greater ease of provocation, more prolonged episodes, and episodes of greater severity, requiring a longer recovery period or more frequent use of sublingual nitroglycerin. This suggests a transition and most likely reflects a change in coronary artery blood flow and perfusion of the myocardium. This frequently portends unstable angina or an acute coronary syndrome, such as an acute MI.
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Unstable Angina
Unstable angina pectoris occurs when the pattern of chest discomfort changes abruptly. Signs of unstable angina are: symptoms at rest, a marked increase in the frequency of attacks, discomfort that occurs with minimal activity, and new-onset angina of incapacitating severity. Unstable angina usually is related to the rupture of an atherosclerotic plaque and the abrupt narrowing or occlusion of a coronary artery, representing a medical emergency with an incipient acute coronary syndrome and an MI to follow. Immediate medical attention is mandatory.
 
Variant Angina
Variant angina is also known as Prinzmetal's angina. Variant angina can occur while you are resting or sleeping. It can be relieved by taking appropriate medicines. It occurs usually between midnight and morning.
 
Microvascular Angina
Microvascular angina can be more severe and last longer than other types of angina. Medicine may not relieve this type of angina.
 
Decubitus Angina
The term ‘decubitus’ is derived from the latin word ‘decumbere’ meaning, ‘to lie down’. The angina decubitus means chest pain while lying down. It usually occur at night. It occurs because the fluid in the body are redistributed in this position due to gravity and the heart has to work harder. It occurs when the affected person assumes the left lateral decubitus position or basically lying on the left side with hypertrophied heart. The muscles are already at risk of ischemia. When the blood flow reduces, the angina occurs.
 
Risk Factors
 
Modifiable
  • Hyperlipidemia
  • Smoking
  • Hypertension
  • Diabetes
  • Stress
  • Inactivity
  • Obesity
 
Nonmodifiable
  • Age
  • Gender
  • Heredity
 
Etiology
  • Imbalance between myocardial oxygen supply and demand.
  • Obstruction of coronary blood flow due to arthrosclerosis, and coronary artery spasm.
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Pathophysiology
 
Diagnostic Evaluation
The initial diagnostic approach for CAD encompasses a detailed patient history including compiling a comprehensive list of CAD risk factors, a thorough physical examination to include an assessment of all peripheral pulses which, when abnormal, may signal the presence of underlying peripheral arterial disease, and an electrocardiogram. Once this initial evaluation is performed, laboratory blood tests, stress testing, and a cardiac catheterization may be necessary to obtain further diagnostic insight.
 
History
The history should include any current symptoms. An inventory of cardiac risk factors, and a complete family history are essential components. The history should also include information about the character and location of discomfort, radiation of discomfort, associated symptoms, and precipitating, exacerbating, or alleviating factors. The importance of the family history should not be underestimated.
 
Physical Examination
The results of the physical examination of a patient with stable or unstable angina may be entirely normal. The presence of multiple risk factors or atherosclerosis in the carotid or peripheral arteries increases the likelihood that a chest pain syndrome is related to myocardial ischemia. Evaluation should include measurements of blood pressure and the ankle-brachial index. Examination of the carotid arteries should include auscultation for bruits. Examination of the chest wall, neck, and shoulders for deformities and tenderness may be helpful in diagnosing musculoskeletal chest discomfort. Cardiac auscultation may detect murmurs caused by aortic stenosis or hypertrophic cardiomyopathy, either of which can cause angina in the absence of epicardial CAD. Assessment of the abdominal aorta for an aneurysm and palpation of lower extremity pulses is necessary to evaluate for peripheral vascular disease. Careful palpation of all peripheral pulses and assessment of symmetry 9versus diminution are also valuable noninvasive approaches for assessing the integrity of the arterial circulation. Finally, examination for xanthelasmas, tendon xanthomas, retinal arterial abnormalities, and peripheral neuropathy can be helpful.
 
Diagnostic and Imaging Studies
 
Electrocardiography
A resting 12-lead electrocardiogram should be obtained on all patients with suspected CAD. Electrocardiographic results are normal in approximately 50% of patients with chronic stable angina, and they can remain normal during an episode of chest discomfort. Importantly, a normal electrocardiogram does not exclude coronary artery disease. When abnormal, especially when Q-waves are present in a regional myocardial territory of diagnostic duration, it can signify the presence of a past MI with high accuracy.
Fig. 1.3: Abnormal ECG
 
Chest Radiograph
The usefulness of a routine chest radiograph in a patient with chest discomfort has not been established. Calcification of the aortic knob is a common finding in older patients and is a nonspecific indicator of flow-limiting obstructive coronary disease. Coronary calcification may also be present. A widened mediastinum may signify an aortic aneurysm and represent the first clue of unstable aortic disease as the cause of chest discomfort.
 
Cardiac Computed Tomography Angiography
A noninvasive imaging assessment of coronary atherosclerosis is now possible in the form of cardiac computed tomography angiography. When negative, this test possesses a high negative predictive value. The positive predictive value is also high, but exact stenosis quantification can be complicated. Associated calcification can cause a blooming artifact, resulting in an overestimation of stenosis.
 
Echocardiography
Echocardiography is recommended for patients with stable angina and physical findings suggesting valvular heart disease. It is invaluable for assessing the patient with suspected hypertrophic cardiomyopathy. It is also recommended for the assessment of global and regional left ventricular systolic functions in patients who have been diagnosed 10with congestive heart failure, complex ventricular arrhythmias, or a history of MI. The echocardiogram is in many ways an ideal test when assessing a patient with known CAD.
 
Laboratory Studies
Routine laboratory measurements recommended as a part of the initial evaluation of patients with CAD should include determination of fasting glucose and fasting lipid levels (total cholesterol, high-density lipoprotein [HDL] cholesterol, triglycerides, and calculated low-density lipoprotein [LDL] levels). Other markers, such as lipoprotein(a) and high-sensitivity C-reactive protein may be useful in assessing cardiac risk. High-sensitivity C-reactive protein is gaining greater prominence in assessing the inflammatory level of vascular disease and predicting future risk of vascular events, such as MIs and cerebrovascular accidents.
 
Stress Testing
Stress testing is another method for determining the presence of flow-limiting, functionally significant coronary artery disease. All stress-testing techniques include electrocardiography and blood pressure monitoring.
Absolute and Relative Contraindications to Exercise Stress Testing
Absolute Contraindications
  • Acute MI within 2 days
  • Symptomatic or severe aortic stenosis
  • Decompensated heart failure
  • Symptomatic or hemodynamically significant cardiac arrhythmias
  • Unstable angina not previously stabilized by medical therapy
  • Acute aortic dissection
  • Acute myocarditis or pericarditis
  • Acute pulmonary embolus or pulmonary infarction
Relative Contraindications
  • Left main coronary artery stenosis
  • Electrolyte imbalance
  • Systolic blood pressure >200 mm Hg
  • Diastolic blood pressure >110 mm Hg
  • Tachyarrhythmias or bradyarrhythmias
  • Hypertrophic cardiomyopathy, other forms of outflow tract obstruction
  • High-degree atrioventricular block
  • Moderate stenotic valvular heart disease
  • Mental or physical impairment leading to inability to exercise adequately
Cardiovascular stress testing takes 2 forms, exercise and pharmacologic administration. The preferred method of cardiovascular stress testing is exercise, using a treadmill or bicycle. Through aerobic exercise, a higher rate pressure product (peak systolic blood pressure multiplied by peak pulse rate), and, therefore, greater cardiovascular stress, can be obtained. This permits an assessment of a patient's functional capacity, providing prognostic data using the sole parameter of attained metabolic equivalents or oxygen uptake. Heart rate 11recovery—how fast the heart rate decreases after exercise cessation—is also a proven and prognostically important parameter. The most common pharmacologic agents used for nonexercise stress testing are dobutamine, dipyridamole, and adenosine or one of its derivatives.
 
Coronary Arteriography
Cardiac catheterization remains the gold standard for determining the presence of obstructive CAD. A cardiac catheterization yields a 2-dimensional rendering of the coronary artery circulation. To assist in circumventing the limitations of a 2-dimensional depiction of 3-dimensional anatomy, multiple views from varying angles are obtained with the extent of CAD severity, typically ascribed to the angulation with the greatest stenosis severity within the particular coronary arterial segment.
 
Treatment
Once a cardiac catheterization has been performed, the three most common therapeutic options are medical therapy, including lifestyle modification, percutaneous coronary intervention (PCI), and coronary artery bypass grafting (CABG).
 
Lifestyle Modification
Patients with documented CAD should actively pursue lifestyle modifications that reduce the risk of future cardiovascular events.
 
Smoking
Tobacco use is one of the most important reversible contributors to recurrent cardiovascular events. Tobacco use induces endothelial dysfunction, reduces coronary vasoreactivity, increases circulating carbon monoxide levels, impairs functional status, and raises blood pressure.
 
Exercise
Functional capacity is a strong predictor of major adverse cardiac events. Functional capacity can be improved by following an exercise program that includes at least 30 minutes of exercise 3 or 4 days a week (a daily regimen is considered optimal).
 
Weight Control
The best weight management strategy is diet and exercise. Ideal benchmarks are a body mass index between 19 and 25 kg/m2 and a waist circumference ≤ 40 inches for men and ≤ 35 inches for women. Weight loss has a favorable effect on the metabolic syndrome and associated cardiac risk factors, including hypertension, high LDL level, low HDL level, blood pressure, endothelial function, vascular inflammation, and glucose intolerance.
 
Pharmacologic Therapy
 
Antiplatelet Agents
Aspirin is the mainstay of antiplatelet therapy for patients who have known CAD or symptoms suggestive of CAD. Aspirin inhibits both cyclo-oxygenase and the synthesis of thromboxane A2.
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Antianginal Agents
Beta blockers, calcium channel blockers, and nitrates are the mainstays of antianginal therapy. Unless contraindications exist, all patients who have a history of angina pectoris should carry sublingual nitroglycerin. Beta blockers are recommended as first-line therapy for the management of stable angina in all patients with established CAD.
Patients who have a history suggestive of vasospastic angina should be treated with a calcium channel blocker or a long-acting nitrate as an initial therapy. Either treatment option can also serve as a substitute for a beta blocker in the presence of traditional angina when intolerable beta blocker effects ensue.
Nitrates improve exercise tolerance and prolong the time of onset of angina in patients with exertional angina. They are contraindicated in patients who have severe aortic stenosis or hypertrophic cardiomyopathy because they can adversely alter hemodynamics and exacerbate symptoms. Ranolazine may be useful for treating refractory angina pectoris. Unlike beta blockers, calcium channel blockers, nitrates, and ranolazine have not been demonstrated to reduce cardiac event rates or cardiac mortality.
 
Risk Factor Management
 
Hypertension
Management of hypertension in patients with CAD is exceedingly important. Control of blood pressure reduces myocardial oxygen consumption and thereby reduces angina, and it also lowers the incidence of cardiovascular events.
Beta blockers devoid of intrinsic sympathomimetic activity represent first-line antihypertensive therapy for patients with a history of MI or coronary artery disease with angina. Angiotensin-converting enzyme (ACE) inhibitors are indicated for all patients with diabetes mellitus or a history of MI with impaired left ventricular systolic function.
Calcium channel blockers are useful for patients with hypertension and angina despite maximum administration of beta blockers. The long-acting dihydropyridines are preferred; short-acting preparations should be avoided because they are suspected of increasing the risk of cardiac events via precipitous blood pressure reduction and induction of the coronary steal phenomenon, diverting coronary arterial blood flow from flow-limited myocardial regions.
 
Hyperlipidemia
Guidelines of the National Cholesterol Education Program (NCEP) have recommended an LDL cholesterol level > 70 mg/dl for all patients with coronary artery or other atherosclerotic diseases. Patients whose LDL levels are > 100 mg/dl should start pharmaceutical therapy. 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are the recommended first-line agents for patients who have CAD and elevated total and LDL cholesterol levels.
 
Diabetes Mellitus
Diabetic patients with CAD have a particularly high risk for recurrent cardiovascular events, and they should be targeted for aggressive risk-factor modification. The American Diabetes Association recommends enhanced blood glucose control and monitoring with a hemoglobin A1c level lower than 7%.
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Surgical Management: Revascularization
The primary revascularization options are PCI and CABG surgery. The most common PCI techniques are percutaneous transluminal coronary angioplasty and coronary stenting. A major limitation of PCI is restenosis at the intervention site. This represents the body's response to local injury with an exaggerated neointimal proliferative response. The use of drug-eluting stents, aspirin, clopidogrel, and glycoprotein IIb/IIIa inhibitors lowers the rate of restenosis to < 10% at 6 months in optimal circumstances.
The most common conduits for CABG are the saphenous vein and the internal thoracic (mammary) artery. The long-term patency rates of internal thoracic artery grafts are superior to those of venous grafts.
 
Percutaneous Transluminal Coronary Angioplasty (PTCA)
Percutaneous transluminal coronary angioplasty (PTCA) is performed to open blocked coronary arteries caused by coronary artery disease (CAD) and to restore arterial blood flow to the heart tissue without open-heart surgery. A special catheter (long hollow tube) is inserted into the coronary artery to be treated.
This catheter has a tiny balloon at its tip. The balloon is inflated once the catheter has been placed into the narrowed area of the coronary artery. The inflation of the balloon compresses the fatty tissue in the artery and makes a larger opening inside the artery for improved blood flow.
The use of fluoroscopy assists the physician in the location of blockages in the coronary arteries as the contrast dye moves through the arteries. A small sample of heart tissue (called a biopsy) may be obtained during the procedure to be examined later under the microscope for abnormalities.
A technique called intravascular ultrasound (IVUS), that uses a computer and a transducer that sends out ultrasonic sound waves to create images of the blood vessels, may be used during PTCA.
The use of IVUS provides direct visualization and measurement of the inside of the blood vessels and may assist the physician in selecting the appropriate size of balloons and/or stents, to ensure that a stent, if used, is properly opened, or to evaluate the use of other angioplasty instruments.
The physician may determine that another type of procedure is necessary. This may include the use of atherectomy (removal of plaque) at the site of the narrowing of the artery. In atherectomy, there may be tiny blades on a balloon or a rotating tip at the end of the catheter.
When the catheter reaches the narrowed spot in the artery, the plaque is broken up or cut away to open the artery. Atherectomy is used when the plaque is calcified, hardened, or if the vessel is completely closed. Another type of atherectomy procedure uses a laser, which opens the artery by ‘vaporizing’ the plaque.
Figs. 1.3A: Inflation of balloon inside a coronary artery
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Figs. 1.4 (A to C): Percutaneous transluminal coronary angioplasty (PTCA)
 
Procedure Completion, Both Methods
  • The sternum will be pushed back together and sewn together with small wires.
  • The skin over the sternum will be sewn back together.
  • Tubes will be inserted into your chest to drain blood and other fluids from around the heart. These tubes will be connected to a suction device to keep fluids pulled away from the heart.
  • A tube will be inserted through your mouth or nose into your stomach to drain stomach fluids.
  • A sterile bandage or dressing will be applied.
 
Coronary Artery Bypass Graft Surgery (CABG)
Coronary artery bypass graft surgery (CABG) is a procedure used to treat coronary artery disease in certain circumstances. Coronary artery disease (CAD) is the narrowing of the 15coronary arteries (the blood vessels that supply oxygen and nutrients to the heart muscle), caused by a buildup of fatty material within the walls of the arteries. This buildup causes the inside of the arteries to become narrowed, limiting the supply of oxygen-rich blood to the heart muscle.
Figs. 1.5: Coronary artery bypass graft (CABG)
One way to treat the blocked or narrowed arteries is to bypass the blocked portion of the coronary artery with another piece of blood vessel. Blood vessels, or grafts, used for the bypass procedure may be pieces of a vein taken from the legs or an artery in the chest. At times, an artery from the wrist may also be used. One end of the graft is attached above the blockage and the other end is attached below the blockage. Thus, the blood is rerouted around, or it bypasses the blockage through the new graft to reach the heart muscle. This bypassing of the blocked coronary artery can be done by performing coronary artery bypass surgery.
 
Risks of the Procedure
Possible risks associated with coronary artery bypass graft surgery include:
  • Bleeding during or after the surgery
  • Blood clots that can cause heart attack, stroke, or lung problems
  • Infection at the incision site
  • Pneumonia
  • Breathing problems
  • Cardiac dysrhythmias/arrhythmias (abnormal heart rhythms)
 
Coronary Artery Bypass Graft Surgery-on-Pump Procedure
  • In order to sew the grafts onto the very small coronary arteries, the heart must be stopped to allow the doctor to perform the very delicate procedure. Tubes will be inserted into the heart so that the blood can be pumped through your body by a cardiopulmonary bypass machine.
  • Once the blood has been diverted into the bypass machine for pumping, the heart will be stopped by injecting it with a cold solution.
  • When the heart has been stopped, the doctor will perform the bypass graft procedure by sewing one end of a section of vein over a tiny opening made in the aorta, and the other end over a tiny opening made in the coronary artery just below the blockage. If the internal mammary artery inside your chest is being used as a bypass graft, the lower end of the artery will be cut from inside the chest and sewn over an opening made in the coronary artery below the blockage.
  • You may have more than one bypass graft performed, depending on how many blockages you have and where they are located. After all the grafts have been completed, the doctor will examine them to make sure they are working.
  • 16Once the bypass grafts have been completed, the blood circulating through the bypass machine will be allowed back into your heart and the tubes to the machine will be removed. Your heart will be restarted.
  • Temporary wires for pacing may be inserted into the heart. These wires can be attached to a pacemaker and your heart can be paced, if needed, during the initial recovery period.
 
Coronary Artery Bypass Surgery-off-Pump Procedure
  • Once the chest has been opened, the area around the artery to be bypassed will be stabilized with a special type of instrument.
  • The rest of the heart will continue to function and pump blood through the body.
  • The cardiopulmonary bypass machine and the perfusionist who runs it may be kept on stand-by, should the procedure need to be completed on bypass.
  • The doctor will perform the bypass graft procedure by sewing one end of a section of vein over a tiny opening made in the aorta, and the other end over a tiny opening made in the coronary artery or internal mammary artery just below the blockage.
  • You may have more than one bypass graft performed, depending on how many blockages you have and where they are located.
  • Before the chest is closed, the doctor will examine the grafts to make sure they are working.
 
CABG Pre- and Post-operative Care
 
The Preoperative Phase
Education: Preoperative preparation of patients and significant others is a well-established protocol in most institutions. Research has shown that education of the patient prior to surgery assists with recovery, increases patient contentment, and decreases postoperative complications. Appropriate timing of preoperative preparation is helpful for the patient's information retention because impending open heart surgery is anxiety-provoking to most patients.
  • Assessment of learning ability: It is imperative for the nurse to assess the patient for individual learning needs and provide the information in a timely manner to minimize as much anxiety as possible. The skilled professional nurse individualizes preoperative instructions to meet the specific needs of that patient.
    • It has been suggested that anxiety state levels are lower 5 to 14 days prior to CABG surgery, which makes this an ideal time for teaching. A high anxiety level is not conducive to retention of information.
    • Some patients went to hospital for preadmission testing several days before surgery and completing the preoperative teaching during this time may be effective.
    • Some patients want specific details about the perioperative experience, whereas others seem to need only the reassurance that a knowledgeable and compassionate caregiver will provide the needed perioperative care.
  • Information: Focus Points for Preoperative Patient Education:
    • Sights and sounds in the perioperative environment
    • Insertion of monitoring lines
    • Preoperative medications and anticipated sensations
    • 17Use of incentive spirometer
    • Length of the operation
    • Expectations related to postoperative environment
    • Availability of postoperative pain medication and nursing staff: Assure the patient that a competent caregiver will be in close proximity during the immediate postoperative recovery period and will be able to anticipate and provide for needs.
    • Effectiveness of splinting incision for pain control.
    • Postoperative presence of an endotracheal tube: Patients should be informed that an endotracheal tube will probably be in place postoperatively, resulting in a temporary inability to speak.
    • Anticipated time of intubation: The patient should be assured that the endotracheal tube will be removed as soon as it is no longer needed.
    • Communication issues: The significant other may be anxious and this may intensify as his/her loved one is taken to surgery. Separation is inevitable, but communication with the significant other during the intraoperative period is helpful to minimize anxiety.
    • Postoperative activity: Pulmonary care is an important part of the postoperative care of the patient after CABG surgery.
  • Preoperative practice with the equipment (such as an incentive spirometer) that will be used postoperatively is helpful.
  • Teaching in the preoperative period assists the patient to comprehend the necessity of coughing effectively in spite of incisional pain to achieve positive outcomes postoperatively.
  • Preoperative teaching might include information related to the potential for mobilization to a chair during the first evening postoperatively. Early mobilization is effective in improving postoperative pulmonary outcomes.
  • Preparation of the significant other:
  • Nursing interventions important for significant others include teaching them about the expected patient appearance. The patient may appear pale, cool, and edematous.
  • The nurse should also discuss equipment that will be connected to the patient. This equipment will include the ventilator, chest tubes, nasogastric tube, invasive lines, and urinary catheter.
Risk Stratification
Various tests should be done to find and categorize risks.
Low-risk (< 1%)
Intermediate-risk (1–5%)
High-risk (> 5%)
  • Breast
  • Abdominal
  • Aortic and major vascular surgery
  • Dental
  • Carotid
  • Peripheral vascular surgery
  • Endocrine
  • Peripheral arterial angioplasty
  • Eye
  • Endovascular aneurysm repair
  • Gynecology
  • Head and neck surgery
  • Reconstructive
  • Neurological/orthopedic–major (hip and spine surgery)
  • Orthopedic-minor (knee surgery)
  • Pulmonary renal/liver transplant
  • Urologic–minor
  • Urologic–major
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Intraoperative Phase
The intraoperative events during cardiac surgery influence nursing care postoperatively:
  • Insertion of a large-bore peripheral intravenous catheter, an arterial line, and a pulmonary artery catheter. These are needed so intravenous fluids can be administered and hemodynamics monitored during the operation and in the postoperative period.
  • After the insertion of the invasive lines, anesthesia will be administered.
  • After the patient is anesthetized, there will be a head-to-toe surgical preparation and insertion of a urinary catheter.
  • Heparin is administered to promote anticoagulation. The activated clotting time is measured during surgery to determine the effectiveness of the anticoagulation and, therefore, guide the amount of heparin that is administered.
  • The patient may receive protamine to reverse the heparin at the end of the operation.
  • The patient's postoperative body temperature may be lower than a patient who was on bypass because the heat exchanger on the pump cannot be utilized for warming. Because of the reduced body temperature, bleeding may be exacerbated. So, it is the duty of a nurse to maintain the patient's body temperature.
 
Postoperative Phase
  • Postoperative care of the cardiac surgery patient is challenging in that changes can occur rapidly. The preoperative condition of the patient as well as intraoperative events should be considered in postoperative care.
  • It is essential for the nurse to anticipate the possible complications so that appropriate interventions are initiated in a timely manner in order to ensure a positive outcome for the patient.
  • There is a flurry of activity as the patient enters the recovery room/ICU and the admitting nurse connects the patient and the invasive lines to the monitoring equipment while another staff member connects drainage devices appropriately and draws admission blood work.
  • The operating room nurse and the anesthesiologist report the patient's condition to the receiving nurse.
Postoperative Pulmonary Management: Pulmonary dysfunction and hypoxemia may occur in 30% to 60% of patients after CABG.
  • Patient history and intraoperative factors must be considered in the postoperative pulmonary management. These are:
    • A history of smoking, obstructive pulmonary disease, steroid use, gastroesophageal reflux disease, heart failure, and poor nutrition may increase postoperative pulmonary complications.
    • There is potential for an increase in postoperative complications when patients are intubated longer than 24 hours. The length of hospital stay may also increase with longer intubation times.
    • The current trend is to extubate patients within the first 12 hours after surgery.
    • Routine postoperative care to promote oxygenation and ventilation involves prevention and treatment of atelectasis and pulmonary infection as well as maintenance of effective gas exchange and breathing patterns.
    • 19Nurse should assess several factors during heart surgery that increase the potential for pulmonary complications postoperatively. The length of the surgery and resultant increase in the amount of needed anesthetic agents, the amount of fluids administered during the intraoperative period, and prolonged time in the supine position increase the potential for pulmonary complications.
    • Nurse should be conscious about atelectasis. Atelectasis can be related to cardiopulmonary bypass, surfactant inhibition, and stimulation of the inflammatory response. Atelectasis as well as the inflammatory mediators inhibit diffusion of oxygen and carbon dioxide across the alveolar capillary membrane and impairs effective gas exchange.
    • Prolonged pump time causes fluid shifts, potentially increasing the amount of fluid in the pulmonary tissue, thus increasing the possibility of pulmonary complications.
    • Pain caused from the sternotomy can impair breathing patterns.
    • Some patients shiver after heart surgery and this response may lead to an increase in the carbon dioxide level or lead to lactic acidosis. Shivering may increase the body's oxygen consumption. Therefore, oxygen levels should be monitored and adjusted accordingly.
    • Shivering may be the result of the body compensating for the surgically induced hypothermia or a reaction to anesthetic agents. Shivering is usually managed by administration of sedation and neuromuscular blocking agents while the patient is being mechanically ventilated.
  • Postoperative management includes:
    • Accurate and frequent physical assessment
    • Arterial blood gas analysis
    • Continuous pulse oximetry
    • Pulmonary care (including suctioning while the patient is intubated and coughing and incentive spirometry after extubation)
    • Early mobilization
    • Control of pain and shivering.
  • Most protocols require a chest X-ray after heart surgery to determine placement of the endotracheal tube, thermodilution catheter, and nasogastric tube as well as information about the width of the mediastinum, amount of atelectasis, presence of hemothorax or pneumothorax, and size of the heart.
  • Pain control is usually achieved with intravenous narcotics while the patient is intubated. Oral and/or intravenous narcotics may be used after extubation. The nurse must balance the need for pain control without respiratory depression with the patient's need to have his/her pain minimized to allow an effective cough.
  • The nurse must assess the patient for readiness for early extubation. Extubation should be considered when the patient is arousable, able to follow commands, hemodynamically stable, and initiating spontaneous ventilations without excessive respiratory effort.
  • Typical intensive care protocols for the cardiac surgery patient include preprinted orders that facilitate the weaning process. As the patient is being weaned from the ventilator, ventilatory support is gradually withdrawn and the patient must sustain spontaneous ventilations.
  • 20Physical assessment of effective ventilation, and laboratory analysis of arterial blood gases and specific ventilatory parameters must be completed prior to extubation. Protocols may vary, but some standards require a PO2 80 mm of Hg on a FiO2 of 0.40 or less, a PCO2 less than 45 mm Hg, a pH between 7.35 and 7.45, and an oxygen saturation (SaO2) 99%. Ventilatory parameters include a maximum inspiratory pressure of at least 20, a tidal volume of at least 5 mL/kg body weight, and a minute volume of at least 5 liters per minute.
  • During the weaning process, the nurse should assess the patient for an increase in respiratory and/or heart rates, use of accessory muscles, fatigue, and color changes because these findings may indicate the patient is not ready for extubation.
  • An increase in pulmonary artery pressures can indicate an increase in PCO2 and give the nurse an early indication prior to arterial blood gas analysis that the patient is not ready for extubation. Early extubation is desirable but if parameters are not met and/or the patient is hemodynamically unstable, there may be detrimental effects of early extubation.
Postoperative Management of Hemodynamics: Movement of the patient from the operating room to the recovery room/ICU can create hemodynamic instability, and, thus, reconnection to the monitoring equipment in a timely manner is of the essence.
BP: A cuff BP is usually taken to provide correlation of the BP obtained from the arterial line.
  • The nurse must continually assess the patient for cardiac dysfunction and hemodynamic instability because intraoperative myocardial ischemia is a potential cause of low cardiac output (CO) during the immediate postoperative period. The receiving nurse must intensively monitor the interrelationship between heart rhythm and rate, preload, afterload, contractility, and myocardial compliance to achieve this outcome.
  • Blood pressure must be maintained within ordered parameters to provide tissue perfusion and prevent disruption of the surgical anastomoses.
  • The nurse must monitor the volume in the system, which is reflected by the right atrial pressure (RAP) and pulmonary capillary wedge pressure (PCWP).
  • If the BP is too low, there is either too little volume (preload), a decrease in contractility, or the SVR is too low (the patient's blood vessels are dilated).
  • If the BP, CO, and RAP/PCWP are all low, the patient probably needs volume.
  • Volume is generally replaced as needed with a colloid solution unless the hematocrit is low and then volume may be replaced with packed red blood cells.
  • If the BP and CO are low but the PCWP is high, the patient may be experiencing decreased contractility and inotropic support may be instituted with an agent, such as dopamine or dobutamine.
  • If the BP is low and the CO is adequate or elevated, the systemic vascular resistance may be low and the patient may need a constrictive agent, such as phenylephrine. Low BP can be temporarily increased by turning off positive end-expiratory pressure (to decrease intrathoracic pressure and augment preload) and by position changes.
  • The patient should be put in the supine position with legs elevated to allow the BP to increase until the cause of the low BP can be determined and corrective measures are taken. The Trendelenburg position can offer symptomatic relief from low BP, especially in the early postoperative phase, by shifting volume from the legs to the chest and increasing preload.
  • 21If the BP becomes too high, especially in the early postoperative period, the surgical anastomoses may become disrupted, which could cause significant intrathoracic bleeding, hemodynamic instability, poor tissue perfusion, and necessitate a return to the operating room.
  • The nurse has to carefully monitor the patient for high BP and quickly intervene per institution protocol. Nitroprusside, a vasodilator, is often administered to lower the BP to the ordered parameter. Nitroglycerine, a nitrate, may also be used to cause vasodilation and lower the BP. These medications should be started slowly so patient response can be evaluated. The patient must be monitored closely as the BP may drop as the patient's body temperature increases.
  • The nurse must rewarm the patient after surgery if hypothermia persists. The negative effects of hypothermia include depression of the myocardium, ventricular dysrhythmias, vasoconstriction, and depression of clotting factors (increasing the risk of bleeding postoperatively). Rewarming may be accomplished by the use of warm blankets, warm humidified oxygen, convective air mattresses, and other individual institutional approaches.
  • Vasoconstriction induced by hypothermia may increase BP. Because of the potential for issues with graft anastomoses and the importance of maintaining BP within the reference range, a vasodilator may be needed while the patient is rewarming. As normothermia is achieved, if the patient's systemic vascular resistance decreases significantly, additional intravenous fluids may need to be administered.
  • The nurse should carefully monitor the pulmonary artery pressures and the CO as well as the BP when interventions are instituted to assess the effect. Some references suggest that hemodynamic parameters be rechecked every 30 to 60 minutes after each intervention during the early postoperative period. It is important to maintain effective CO after open heart surgery to provide adequate tissue perfusion.
Ventricular dysrhythmias are more common in the early postoperative period and supraventricular dysrhythmias are more likely in 24 hours to 5 days postoperatively. The incidence of atrial fibrillation ranges from 10% to 65% depending on many factors.
These factors include:
  • Patient history
  • Preoperative medications, and type of surgery
  • Hypothermia
  • Inhaled anesthetics
  • Electrolyte disturbances (i.e. hypocalcemia, hypercalcemia, hypomagnesium, and hypokalemia)
  • Metabolic disturbances (such as acidosis)
  • Manual manipulation of the heart
  • Myocardial ischemia
  • Increase in catecholamine levels secondary to pain, anxiety, and inadequate sedation.
  • Management depends on the type of dysrhythmia and the patient's clinical response. The nurse must treat the patient effectively.
  • Effectiveness of BP and CO should be considered when evaluating dysrhythmias. Often, cardiac surgeons place epicardial wires on the atrium and/or the ventricle during the 22operation. Temporary pacing can be instituted to override a slow intrinsic rhythm so CI and BP can be maintained.
  • Atropine may be given to increase the heart rate in the absence of epicardial pacing wires.
  • Tachydysrhythmias are usually controlled pharmacologically. The specific medication utilized will depend on hospital protocols and physician preference.
  • The critical care nurse should utilize standing orders in the institution as well as current advanced cardiac life support protocols.
Postoperative Management of Bleeding: The postoperative period may be complicated by excessive bleeding. Many factors should be considered when assessing the patient's potential for bleeding.
  • Patients who were on anticoagulants and antiplatelet agents prior to surgery are at an increased risk of postoperative bleeding. Potential sites for bleeding include the internal mammary site, the chest wall, and chest tube sites.
  • Induced hypothermia, the use of the CPB machine, and the administration of heparin for anticoagulation can all contribute to postoperative bleeding.
  • The nurse should be aware that heparin can be stored in adipose tissue and some patients may have an increase in bleeding 4 hours postoperatively, depending on the body's adipose composition.
  • Some surgeons utilize an intravenous infusion of aprotinin intraoperatively to minimize the risk of postoperative bleeding. This drug is a protease inhibitor that inhibits fibrinolysis. Aprotinin may also have some anti-inflammatory effects and, therefore, be beneficial to the patient after CABG.
  • The nurse should monitor the patient for signs of bleeding from the chest tubes and the surgical sites as well as clinical signs of hypovolemia related to blood loss.
  • Hemoglobin and hematocrit should be monitored at regular intervals during the postoperative period.
  • If bleeding is an issue, drugs such as protamine sulfate (to reverse the effects of heparin) or antifibrinolytic agents, such as aminocaproic acid or desmopressin (DDAVP) may be ordered.
  • Blood products such as fresh frozen plasma and platelets may also be ordered.
  • When bleeding occurs, there is potential for the blood to accumulate in the pericardium, and, therefore, the nurse must be cognizant of the potential for cardiac tamponade.
  • The clinical manifestations of cardiac tamponade include lack of chest tube drainage, decreased BP, narrowed pulse pressure, increased heart rate, jugular venous distention, elevated central venous pressure, and muffled heart sounds.
  • Emergency reoperation would be required.
Postoperative Neurologic Management: Patients who require coronary artery bypass surgery are at an increased risk for neurologic complications.
  • Stroke can be caused by hypoperfusion or an embolic event during or after surgery.
  • Manipulation of the aorta has been implicated in embolic events. Other risk factors for stroke may include age, previous stroke, carotid bruits, and hypertension.
  • The nurse should be particularly astute to neurologic assessment in the postoperative period.
  • 23When the patient is admitted to the intensive care unit, he/she will likely be intubated and unconscious. The effects of the neuromuscular blocking agents will be apparent.
  • Pupils should be assessed initially; however, normal size and reactivity may not return until agents utilized intraoperatively have been metabolized.
  • Over the first few hours after surgery, the results of the neurologic assessment should improve gradually.
  • By the time the patient is ready for extubation, he/she should follow commands and have equal movement and strength of the extremities with neurologic function approaching the patient's normal condition.
  • It is difficult for significant others during this time because waiting during the awakening process can be anxiety-provoking. Patients and significant others are informed prior to surgery of the risk for stroke and want that to be definitively ruled out as soon as the patient returns to the intensive care unit.
  • The nurse should provide the needed comfort but not give false hope, as the neurologic status cannot be completely assessed until the patient is fully awake and extubated.
  • At that time, the patient should be assessed for orientation to person, place, time, and circumstance. A motor and sensory assessment should also be performed.
  • A positive result is a good indication that an intraoperative stroke can be ruled out.
  • Neurologic assessments must continue because the risk of stroke does not end with the operation.
Postoperative Renal Management: There is a potential for renal dysfunction in the postoperative cardiac surgery patient.
  • Renal insufficiency may be related to advanced age, hypertension, diabetes, decreased function of the left ventricle, and length of time on the CPB.
  • One indicator of effective CO is adequate renal perfusion as evidenced by urinary output of at least 0.5 mL/kg/h.
  • The nurse must monitor the urinary output at least hourly during the early postoperative period.
  • The urine should be assessed for color and characteristics as well as amount.
  • Diuresis is likely in the postoperative period when renal function is adequate, as the fluids mobilize from the interstitial to the intravascular space.
  • The patient's potassium level should be monitored at least every 4 to 6 hours for the first 24 hours, as potassium is lost with diuresis.
  • Intravenous potassium replacement should be administered to keep the serum potassium levels within the normal limits.
  • The patient should be astutely monitored for cardiac dysrhythmias if the serum potassium level is abnormal.
  • Other laboratory values that should be monitored at least daily are the blood urea nitrogen and serum creatinine.
Postoperative Gastrointestinal Management: Gastrointestinal complications include peptic ulcer disease, perforated ulcer, pancreatitis, acute cholecystitis, bowel ischemia, diverticulitis, and liver dysfunction.
  • Some risk factors for gastrointestinal dysfunction include age over 70, a history of gastrointestinal disease, a history of alcohol misuse, cigarette smoking, heart valve 24surgery, emergent operation, prolonged CPB, postoperative hemorrhage, use of vasopressors, and low postoperative CO.
  • If the gastroepiploic artery is used as a conduit for bypass, this may also increase the risk of gastrointestinal dysfunction.
  • Anesthetic agents, analgesics, and hypoperfusion of the gut during surgery can also contribute to gastrointestinal dysfunction.
  • The nurse should monitor the patient for bowel sounds, abdominal distention, and nausea and vomiting.
  • The intubated patient will have a nasogastric tube to low intermittent suction.
  • Placement and patency should be assessed as well as amount, color, and characteristics of the drainage.
  • Prior to extubation, if bowel sounds are present, the nasogastric tube will be discontinued and the nurse should continue to assess the patient for potential gastrointestinal disturbances.
  • The nurse should administer antiemetic agents as ordered.
  • Some surgeons order a histamine blocker to minimize acid secretion until normal dietary patterns are resumed.
  • When the nasogastric tube is removed, the patient will be started on a clear liquid diet and this can be advanced as tolerated by the patient.
Postoperative Pain Management: Dependent upon surgical approach, the patient may have a median sternotomy incision, leg incision(s), and/or a radial incision.
  • Manipulation of the chest cavity, use of retractors during surgery, and electrocautery may all contribute to postoperative pain.
  • In addition, positioning on the operating room table and length of time of the surgery may also be factors in pain experienced postoperatively.
  • Poorly controlled pain can stimulate the sympathetic nervous system and lead to cardiovascular consequences.
  • The heart rate and BP can increase and the blood vessels can constrict, causing an increase in the cardiac workload and myocardial oxygen demand.
  • Effective pain control is essential for patient comfort, hemodynamic stability, and prevention of pulmonary complications.
  • Nurses must individualize pain assessment and control for each patient as responses vary among individuals.
  • Opioid analgesics, positioning, mobilization, distraction, and relaxation techniques are among some of the methods of pain control.
  • Keeping serum levels of opioid analgesics in the therapeutic range is beneficial.
  • Nonsteroidal anti-inflammatory agents may be used in conjunction with opioid agents to control pain and minimize the amount of narcotics needed.
  • Pulmonary care is more effective for the patient when pain is effectively managed.
  • Teaching the patient to splint the incision when coughing and moving improves pain control.
  • The nurse should evaluate the effectiveness of pain management interventions regularly.
  • 25Significant others are often concerned about the postoperative pain experienced by the patient. Explanations about interventions utilized and outcomes achieved can decrease anxiety.
  • Another source of pain for the patient after CABG is the removal of the chest tubes. This usually occurs 24 to 48 hours postoperatively when the amount and characteristics of chest tube drainage meet ordered parameters as long as there is no air leak noted in the water seal chamber.
  • Pain medication should be administered prior to removal of chest tubes per institution protocol to minimize the trauma of the procedure.
Postoperative Management of Infection: The incidence of infection of sternal and leg incisions after cardiac surgery is less than 3%.
  • Risk factors for infection include diabetes, malnutrition, chronic diseases, and patients requiring emergent surgery or prolonged surgery.
  • Assessment for, and prevention of, infection is part of the nurse's role in the postoperative period.
  • The patient should be assessed for local and systemic signs of infection.
  • Postoperative antibiotics may be ordered.
  • Dressings should be removed and incision care should be completed according to institution protocols.
  • Control of blood glucose level may help with the prevention of infection. It is desirable to control blood glucose levels of greater than 150 mg/dL with a continuous intravenous infusion of insulin versus intermittent subcutaneous insulin injections. This practice is thought to be helpful in the prevention of deep sternal wound infection.
  • Some surgeons order corticosteroids postoperatively. When used, these drugs are intended to minimize the potential risks of inflammation after heart surgery.
  • Patients should be monitored for suppression of the immune system, as this can be an adverse effect of corticosteroid administration.
  • Patients need to be taught how to slowly discontinue the medication after discharge as per physician's orders. The other potential effect of corticosteroid administration is an elevation in serum glucose levels.
  • A sliding scale insulin order may be needed to maintain blood glucose levels within normal limits while the patient is in the hospital.
Additional Postoperative Management: The nurse must intensively care for the patient in the early postoperative period.
  • This intensive monitoring and postoperative discomfort can interfere with the patient's need for sleep. There is a potential for sleep disturbance as the patient is recovering from CABG.
  • Lack of sleep may negatively affect postoperative outcomes. Organization of needed care and provision of time for uninterrupted sleep cycles is important for effective outcomes.
  • Some of the postoperative confusion experienced by patients may be minimized and positive outcomes maximized when time for sleep is provided.
  • Hospital routines and too many visits by well-meaning significant others may add to the sleep deprivation problem.
  • 26Significant others should be able to spend time with the patient, but it is the role of the intensive care nurse to balance the need for visitation with the need for rest and sleep.
  • It can be frightening for significant others to visit the patient during the early postoperative period because of the monitoring equipment and appearance of their loved one. Explanations regarding the equipment and physical appearance may be helpful.
  • Often significant others need to overcome fear of touching the patient postoperatively and receive reassurance from the professional nurse that no harm will come from the touch.
 
Nursing Care
Acute pain related to an imbalance of oxygen supply to myocardial demands.
Outcome: The patient will express pain decreased
Intervention:
  • Assess pain location, duration, radiation, occurrence, a new phenomenon.
  • Review of previous activities that cause chest pain.
  • Create a 12-lead ECG during anginal pain episodes.
  • Assess signs of hypoxemia, give oxygen therapy if necessary.
  • Give analgesics as directed.
  • Maintain a rest for 24–30 hours during episodes of illness.
  • Check vital signs during periods of illness.
Decreased cardiac output related to electrical factors (dysrhythmias), Decrease in myocardial contraction, structural abnormalities (papillary muscular dysfunction and ventricular septal rupture).
Outcome: The patient will demonstrate a stable or better cardiac condition.
Intervention:
  • Maintain bed rest with head elevation of 30 degrees during the first 24–48 hours.
  • Assess and monitor vital signs and hemodynamic per 1–2 hours.
  • Monitor and record ECG continue to assess the rate, rhythm, and order to each change per 2 or 4 hours.
  • Review and report signs of CO reduction.
Anxiety related to the needs of the body is threatened.
Objectives: The patient will demonstrate reduced anxiety after nursing actions.
Intervention:
  • Assess signs and verbal expressions of anxiety.
  • Take action to reduce anxiety by creating a calm environment.
  • Accompany patient during periods of high anxiety.
  • Provide an explanation of procedures and treatments.
  • Encourage patients to express feelings.
  • Refer to the spiritual adviser if necessary.
27
 
CARDIOMYOPATHY
Cardiomyopathy is a weakening of the heart muscle or associated with other problems with the heart muscle. It may be associated with heart failure, endocarditis or other heart problems which alter the normal architecture of heart. Most patients with cardiomyopathy have heart failure.
 
Etiology
In the broadest sense, ‘cardiomyopathy’ (CM) refers to heart disease resulting from a primary abnormality of the myocardium (heart muscle). There are 3 types:
  • Dilated cardiomyopathy (also called ‘congestive’ cardiomyopathy)
  • Restrictive cardiomyopathy
  • Hypertrophic cardiomyopathy
    • Dilated cardiomyopathy is a condition in which the heart becomes weak and the chambers get large. As a result, the heart cannot pump enough blood out to the body. The heart with dilated cardiomyopathy is striking in appearance. Dilation (enlargement) of all 4 chambers (both atria and both ventricles). The total size of the heart is typically huge (cardiomegaly). The myocardium becomes ‘flabby’ and loses its ability to contract. Naturally, the heart chambers will lose their pumping function and the heart will ultimately undergo failure. Since blood flow within the chambers is sluggish, intracardiac mural thrombi are prone to form on the inner walls of the atria and ventricles. Pieces of these thrombi may break off and embolize to the lungs (pulmonary emboli), or any other organ and tissue (systemic emboli). This may lead to infarction of these organs.
    • Hypertrophic cardiomyopathy (HCM) is a condition in which the heart muscle becomes thick. The thickening makes it harder for blood to leave the heart. This type of cardiomyopathy is usually passed down through families. This is a disease of younger people (mean age 26). It is a genetically inherited disease. The classic anatomic feature is the profound hypertrophy of the myocardium of the left ventricle. The part of the LV wall that forms the interventricular septum (IVS) is more hypertrophic than the lateral part of the LV wall. This extra-thickened interventricular septum is referred to as asymmetric septal hypertrophy (ASH). The IVS can become so hypertrophied that it bulges into the lumen of the LV, thereby decreasing the volume of the LV chamber.
    • Restrictive cardiomyopathy is a group of disorders. Restrictive cardiomyopathy can either be idiopathic or can be caused by diseases that deposit abnormal substances within the myocardium. The classic example is amyloidosis, whereby the abnormal amyloid protein accumulates within the myocardium, resulting in stiffness.
    • Peripartum cardiomyopathy occurs during pregnancy or in the first 5 months afterwards.
 
Signs and Symptoms
  • Breathlessness with exertion or even at rest
  • Swelling of the legs, ankles and feet
  • 28Bloating of the abdomen due to fluid buildup
  • Fatigue
  • Irregular heartbeats that feel rapid, pounding or fluttering
  • Dizziness, lightheadedness and fainting
  • Palpitations (fluttering in the chest due to abnormal heart rhythms)
  • Fainting (usually caused by irregular heart rhythms or abnormal responses of the blood vessels during exercise
  • Chest pain or pressure (occurs usually with exercise or physical activity but can also occur with rest or after meals)
 
Diagnostic Evaluation
  • The health care provider may hear abnormal sounds, called murmurs, when listening to your heart with a stethoscope.
  • A physical exam may also reveal:
    • Enlarged spleen and enlarged heart size with atrophy
  • The following tests may be performed:
    • Blood culture and sensitivity (to detect bacteria)
    • Chest X-ray
    • Complete blood count (may show mild anemia)
    • CT scan of the chest
    • Echocardiogram (ultrasound of the heart)
    • ECG
 
Treatment
  • When possible, the cause of cardiomyopathy is treated. Medicines and lifestyle changes are often needed to treat the symptoms of heart failure, angina, and abnormal heart rhythms.
Different procedures or surgeries may also be used:
  • A defibrillator sends an electrical pulse to stop life-threatening abnormal heart rhythms.
  • A pacemaker treats a slow heart rate or helps both sides of your heart beat at the same time.
  • Coronary artery bypass (CABG) surgery or angioplasty can improve blood flow to the damaged or weakened heart muscle.
  • Heart transplant is used when all other treatments have failed.
 
Management
  • The overall goals of treatment for cardiomyopathy are to manage your signs and symptoms, prevent your condition from worsening, and reduce your risk of complications.
  • Angiotensin-converting enzyme (ACE) inhibitors to improve your heart's pumping capability, such as enalapril (Vasotec), lisinopril (Zestril, Prinivil), ramipril (Altace) and captopril (Capoten).
  • Angiotensin receptor blockers (ARBs) for those who can not take ACE inhibitors, such as losartan (Cozaar) and valsartan (Diovan).
  • 29Beta blockers to improve heart function, such as carvedilol (Coreg) and metoprolol (Lopressor, Toprol-XL).
  • Digoxin (Lanoxin). This drug, also referred to as digitalis, increases the strength of your heart muscle contractions. It also tends to slow the heartbeat. Digoxin reduces heart failure symptoms and improves your ability to live with cardiomyopathy.
  • Diuretics: Often called water pills, diuretics make you urinate more frequently and keep fluid from collecting in your body. Commonly prescribed diuretics for heart failure include bumetanide (Bumex) and furosemide (Lasix). The drugs also decrease fluid in your lungs, so you can breathe more easily. One diuretic, spironolactone (Aldactone), may also be helpful in treating scarring of your heart tissue.
  • Another option for some people with dilated cardiomyopathy is a special pacemaker that coordinates the contractions between the left and right ventricles (biventricular pacing). In people who may be at risk of serious arrhythmias, drug therapy or an implantable cardioverter-defibrillator (ICD) may be an option. An ICD is a small device—about the size of a box of matches—implanted in your chest to continuously monitor your heart rhythm and deliver electrical shocks when needed to control abnormal, rapid heartbeats. The device can also work as a pacemaker.
 
Surgical Management
  • Septal myectomy: This is an open-heart operation in which the surgeon removes part of the thickened, overgrown heart muscle wall (septum) that separates the two bottom heart chambers (ventricles). Removing the part of this overgrown muscle improves blood flow and reduces mitral regurgitation. Myectomy is used if medications do not relieve symptoms. Most people who have symptoms and undergo myectomy have no further symptoms. This type of surgery is available only in medical centers that specialize in the treatment of hypertrophic cardiomyopathy.
  • Septal ablation: Also called septal alcohol ablation, this is a treatment in which a small portion of the thickened heart muscle is destroyed by injecting alcohol through a catheter into the artery supplying blood to it. There are possible complications with this procedure, including heart block — a disruption of the heart's electrical system — which requires implantation of a pacemaker. The long-term success of this procedure is not yet known, but it is becoming more commonly used.
  • Pacemaker implantation: A pacemaker is a small electronic device inserted under your skin that sends electrical signals to your heart to monitor and regulate your heartbeat. Surgery to implant the pacemaker is usually performed during local anesthesia and typically takes less than three hours. Pacemaker implantation is generally not as effective as surgical options, but it is sometimes used in older people who want to avoid more invasive procedures.
  • Implantable cardioverter-defibrillator (ICD): This is a pager-sized device implanted in your chest like a pacemaker. An ICD continuously monitors your heartbeat. If a life-threatening arrhythmia occurs, the ICD delivers precisely calibrated electrical shocks to restore a normal heart rhythm. A small number of people with hypertrophic cardiomyopathy are at risk of sudden cardiac death because of abnormal heart rhythms. In these high-risk individuals, many doctors recommend the implantation of an ICD.
  • 30Heart transplant and ventricular assist devices (VADs): If you have severe cardiomyopathy and medications can not control your symptoms, a heart transplant may be an option. Because of the shortage of donor hearts, even people who are critically ill may have a long wait before having a heart transplant. In some cases, a mechanical heart assist device can help critically ill people as they wait for an appropriately matched donor. These devices, known as ventricular assist devices (VADs), can help blood circulate through your heart for months or even years.
 
Nursing Management
  • Acute pain related to an impaired ability of blood vessels to supply oxygen to the tissues.
  • Activity intolerance related to compromised oxygen transport system secondary to heart muscle dysfunction.
  • Risk for ineffective breathing pattern related to decreased respiratory depth secondary to pain.
 
Interventions
  • Bed rest is important because it reduces myocardial oxygen demand and usually continues until the following criteria are met:
    • Temperature remains normal without the use of salicylates.
    • Resting pulse rate remains less than 100 beats/min.
    • ECG tracings show no manifestations of myocardial damage.
    • Pericardial friction rub is not present.
  • 31Obtain a clear description of the pain or discomfort. Identify the source of greatest discomfort as a focus for intervention.
  • Administer analgesics as needed and use salicylates around the clock. Balance rest and activity according to the degree of pain and activity tolerance.
  • Provide psychosocial support while patient is confined to hospital or home with restrictive intravenous therapy.
  • If patient received surgical treatment, provide postsurgical care and instruction.
  • After surgery, monitor patient's temperature; a fever may be present for weeks.
  • A high-protein, high-carbohydrate diet helps maintain adequate nutrition in the presence of fever and infection.
  • Oral hygiene every 4 hours; small, attractive meal servings and foods that are not overly rich, sweet or greasy stimulate the appetite.
  • Instruct the client about how to reduce exposure to infection as follows:
    • Take good care of the teeth and gums, obtain prompt dental care for cavities and gingivitis
    • Prophylactic medication may be needed before invasive dental procedures, and individualized evaluation for prophylaxis medication is also needed.
      • Avoid people who have an upper respiratory tract infection.
      • Assess for signs and symptoms of organ damage, such as stroke (CVA, brain attack), meningitis, heart failure, myocardial infarction, glomerulonephritis, and splenomegaly.
      • Instruct patient and family about activity restrictions, medications, and signs and symptoms of infection.
      • Refer to home care nurse to supervise and monitor intravenous antibiotic therapy at home.
 
CONGESTIVE HEART FAILURE
The heart's pumping power is weaker than normal blood moves through the heart and body at a slower rate, and thus pressure in the heart increases. As a result, the heart cannot pump enough oxygen and nutrients to meet the body's needs. The chambers of the heart may respond by stretching to hold more blood to pump through the body or by becoming stiff and thickened.
 
Etiology
  • Coronary artery disease: Coronary artery disease (CAD), a disease of the arteries that supply blood and oxygen to the heart, causes decreased blood flow to the heart muscle. If the arteries become blocked or severely narrowed, the heart becomes starved for oxygen and nutrients.
  • Heart attack: A heart attack occurs when a coronary artery becomes suddenly blocked, stopping the flow of blood to the heart muscle. A heart attack damages the heart muscle, resulting in a scarred area that does not function properly.
  • Cardiomyopathy: Damage to the heart muscle from causes other than artery or blood flow problems, such as from infections or alcohol or drug abuse.
  • 32Conditions that overwork the heart: Conditions including high blood pressure, valve disease, thyroid disease, kidney disease, diabetes, or heart defects present at birth can all cause heart failure.
 
Categories of Heart Failure
  • Acute failure
  • Chronic failure
  • Left-sided heart failure
  • Right-sided heart failure
  • Forward failure
  • Backward failure
  • High-output failure
  • Low-output failure
  • Acute heart failure: It occurs in response to a sudden decrease in CO, resulting in rapid decrease in tissue perfusion. It can occur due to:
    • Cardiac tamponade
    • Massive pulmonary embolism
    • Acute viral myocarditis
    • Larger myocardial infarction
    • Valve rupture
  • Chronic heart failure: It occurs when body adjusts to decrease in CO through compensatory mechanisms, results in systemic congestion. It develops slowly as in:
    • 33Pulmonary embolism
    • Emotional stress
    • Progression of acute into chronic failure
    • Acute bacterial toxemia, myocardial ischemia from atherosclerotic coronary artery disease
    • Systemic arterial hypertension
    • Chronic lung disease resulting in hypoxia
  • Left-sided heart failure versus right-sided heart failure: Right-sided heart failure compromises pulmonary flow to the lungs. Left-sided heart failure compromises aortic flow to the body and brain. Mixed presentations are common. Left-sided heart failure often leads to right heart failure in the longer term.
Left-sided heart failure:
  • Left ventricle fails as effective pump
    • Left ventricle cannot eject blood delivered from right heart through pulmonary circulation
    • Blood backs up into pulmonary circulation
    • Increased pressure in pulmonary capillaries forces blood serum out of capillaries into interstitial spaces and alveoli
    • Increased respiratory work and decreased gas exchange occur.
 
Pathophysiology
34
 
Signs and Symptoms
Congested lungs: Fluid backup in the lungs can cause shortness of breath with exercise or difficulty breathing at rest or when lying flat in bed. Lung congestion can also cause a dry, hacking cough or wheezing.
Fluid and water retention: Less blood to your kidneys causes fluid and water retention, resulting in swollen ankles, legs, abdomen (called edema), and weight gain. Symptoms may cause an increased need to urinate during the night. Bloating in your stomach may cause a loss of appetite or nausea.
Dizziness, fatigue, and weakness: Less blood to your major organs and muscles makes you feel tired and weak. Less blood to the brain can cause dizziness or confusion.
Rapid or irregular heartbeats: The heart beats faster to pump enough blood to the body. This can cause a rapid or irregular heartbeat.
35Left heart failure—signs and symptoms:
  • Anxiety, confusion, restlessness
  • Persistent cough
  • Pink, frothy sputum
  • Tachycardia
  • Tachypnea
  • Noisy, labored breathing
  • Rales, wheezing (‘cardiac asthma’)
  • Dry hacking cough
  • Cyanosis (late)
  • Third heart sound (S3)
  • Dyspnea on exertion
  • Paroxysmal nocturnal dyspnea
  • Orthopnea
    Right-sided heart failure:
    • Right ventricle fails as effective pump
    • Right ventricle cannot eject blood returning through vena cava
    • Blood backs up into systemic circulation
    • Increased pressure in systemic capillaries forces fluid out of capillaries into interstitial spaces
    • Tissue edema occurs.
 
Compensatory Mechanism During CHF
  • Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus and aortic arch. This center in the brain increases sympathetic activity, releasing catecholamines into the bloodstream. Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heart rate and makes contractions more forceful, in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to perform.
  • Increased sympathetic stimulation also causes the hypothalamus to secrete vasopressin, which causes fluid retention at the kidneys. This increases the blood volume and blood pressure.
  • Reduced perfusion (blood flow) to the kidneys stimulates the release of renin – an enzyme which catalyzes the production of the potent vasopressor angiotensin. Angiotensin and its metabolites cause further vasoconstriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys, also increasing the blood volume.
 
Diagnostic Evaluation
  • Blood tests: Blood tests are used to evaluate kidney and thyroid function as well as to check cholesterol levels and the presence of anemia. Anemia is a blood condition that 36occurs when there is not enough hemoglobin (the substance in red blood cells that enables the blood to transport oxygen through the body) in a person's blood.
  • B-type Natriuretic Peptide (BNP) blood test: BNP is a substance secreted from the heart in response to changes in blood pressure that occur when heart failure develops or worsens. BNP blood levels increase when heart failure symptoms worsen, and decrease when the heart failure condition is stable.
  • Chest X-ray: A chest X-ray shows the size of your heart and whether there is fluid build-up around the heart and lungs.
  • Echocardiogram: This test is an ultrasound which shows the heart's movement, structure, and function.
  • Ejection Fraction (EF): It is used to measure how well heart pumps with each beat to determine if systolic dysfunction or heart failure with preserved left ventricular function is present.
  • Electrocardiogram (EKG or ECG)
  • Cardiac catheterization
  • Stress test: Noninvasive stress tests provide information about the likelihood of coronary artery disease.
 
Major criteria
  • Cardiomegaly on chest radiography
  • S3 gallop (a third heart sound)
  • Acute pulmonary edema
  • Paroxysmal nocturnal dyspnea
  • Crackles on lung auscultation
  • Central venous pressure of more than 16 cm H2O at the right atrium
  • Jugular vein distension
  • Positive abdominojugular test
  • Weight loss of more than 4.5 kg in 5 days in response to treatment
 
Minor criteria
  • Tachycardia of more than 120 beats per minute
  • Nocturnal cough
  • Dyspnea on ordinary exertion
  • Pleural effusion
  • Decrease in vital capacity by one-third from maximum recorded
  • Hepatomegaly
 
Management
 
General measures
  • Quit smoking
  • Exercise regularly
  • Reach and maintain your healthy weight
  • Treat high blood pressure
  • 37Treat lipid disorders
  • Discontinue alcohol or illegal drug use
  • Restrict dietary sodium (salt)
  • Monitor weight
  • Restrict fluids
  • Drugs that worsen the condition should be discontinued
  • Cardiac resynchronization therapy (biventricular pacemaker) may be recommended
  • An implantable cardiac defibrillator (ICD) may be recommended.
 
Pharmacological Management
  • Nonsteroidal anti-inflammatory medications, such as Motrin or Aleve. For relief of aches, pains or fever, take Tylenol instead.
  • Some antiarrhythmic agents, lidocaine, quinidine, etc.
  • Calcium channel blockers, amlodipine, naverapin, etc.
  • Some nutritional supplements, such as salt substitutes, and growth hormone therapies
  • Antacids that contain sodium (salt)
  • An angiotensin-converting-enzyme inhibitor (ACE inhibitor), enalapril
  • Beta blockers
  • Diuretics (water pills) and digoxin
  • An aldosterone inhibitor
  • Decongestants.
 
Surgical Management
  • Biventricular pacing: Cardiac resynchronization therapy (CRT) is used to treat the delay in heart ventricle contractions that occur in some people with advanced heart failure. The CRT pacing device (also called a biventricular pacemaker) is an electronic, battery-powered device that is surgically implanted under the skin. The device has 2 or 3 leads (wires) that are positioned in the heart to help the heart beat in a more balanced way. The leads are implanted through a vein in the right atrium and right ventricle and into the coronary sinus vein to pace the left ventricle. The CRT device can be implanted using the endocardial or epicardial approach. With the endocardial (transvenous) approach, a local anesthetic (pain-relieving medication) is injected to numb the area. The epicardial approach may also be used to place the CRT if you are already having surgery to treat another heart condition.
  • Coronary artery bypass grafting surgery: The most common surgery for heart failure caused by coronary artery disease is bypass surgery. Although surgery is more risky for people with heart failure, new strategies before, during and after surgery have reduced the risks and improved outcomes.
  • Heart valve surgery: Diseased heart valves can be treated both surgically (traditional heart valve surgery) and nonsurgically (balloon valvuloplasty).
  • Implantable left ventricular assist device (LVAD): The LVAD is known as the ‘bridge to transplantation’ for patients who have not responded to other treatments and are hospitalized with severe systolic heart failure. This device helps your heart pump blood 38throughout your body. It allows you to be mobile, sometimes returning home to await a heart transplant. It may also be used as destination therapy for long-term support in patients who are not eligible for transplant.
  • Stem cell transplantation: Stem cell transplantation represents a new therapeutic opportunity for such patients. Peripheral stem cells were mobilized and collected by apheresis. They were transplanted into areas of injury with open-heart surgery. To increase blood flow to the engrafted areas, coronary artery bypass surgery was also performed. This approach opens a new window in the treatment of ‘no hope’ patients with congestive heart failure.
  • Heart transplantation.
 
Complications
  • Cardiac asthma
  • Nonproductive cough due to lung congestion
  • Hemoptysis
  • Dysphagia due to distension of the pulmonary venous atrium or
  • Containment of systemic veins–JVP increased
  • Hepatomegaly
  • Peripheral edema
  • Ascites and anasarka
  • Increase in body weight due to water retention and sodium.
 
Nursing Management
  • Assessment: The nurse should assess the client for the clinical manifestations of CHF, especially in high-risk clients.
    • Impaired gas exchange related to fluid in the alveoli
      • Auscultation of breath sounds every 4 hours
      • Encourage to turn cough and deep breath
      • Maintain Fowler's position
      • Administer oxygen
      • Monitor ABG
      • Intubation and mechanical ventilation
    • Decreased cardiac output related to heart failure and Dysrhythmias
      • Vital signs every hour
      • Lung and heart sounds every 2 hours
      • Administer oxygen
      • Hourly urine output
      • Assess changes in mental status
      • Small meals
    • Fluid volume excess related to reduced cardiac output and Na and water retention
      • IO chart
      • Fowler's position
      • 39Frequent oral care
      • Daily weighing
      • Assess jugular vein distension, peripheral edema, hepatic engorgement
      • Fluid restriction
      • 2–4 gm salt diet
    • Decreased peripheral tissue perfusion related to reduced cardiac output
      • Monitor peripheral pulses
      • Color and temperature of skin
      • Keep extremities warm
      • Assess for thrombophlebitis
      • Active or passive ROM
      • High-risk for impaired skin integrity related to reduced peripheral tissue perfusion
    • Change position every 2 hours
    • Pressure mattress
    • Heel protectors
    • High-risk for digitalis toxicity related to impaired excretion
    • Assess for hypokalemia, heart block
    • Serum digitalis levels and potassium
    • Activity intolerance related to fatigue due to a decrease of cardiac output and pulmonary congestion as manifested by dyspnea, tachycardia, and feelings of weakness and shortness of breath.
      • Encourage alternative rest as well as activity periods to reduce cardiac workload.
      • Provide emotional and physical rest to reduce oxygen consumption and to relieve dyspnea and tiredness.
      • Observe cardiorespiratory response to activity to establish amount of activity that can be performed.
      • Educate patient and significant other particular approaches of self-care to decrease much needed oxygen consumption.
      • Assist to decide on activities in keeping with physical, psychological and social capabilities to establish the amount of activity that can be carried out.
 
ISCHEMIC HEART DISEASE
Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events, such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. This will further cause sudden loss of blood supply to an area of the heart, causing permanent heart damage or death called Acute Myocardial Infarction (AMI).
40
Fig. 1.6: Blocked coronary artery
Etiology and pathophysiology: The most common cause is atherosclerotic disease of coronary arteries, also arterial thrombi, spasm, and rarely coronary emboli. Myocardial ischemia can also occur if myocardial oxygen demands are abnormally increased, as in severe ventricular hypertrophy due to hypertension or aortic stenosis.
  • A reduction in the oxygen-carrying capacity of the blood: As in extremely severe anemia or in the presence of carboxyhemoglobin, is a rare cause of myocardial ischemia.
  • Occlusive intracoronary thrombus: A thrombus overlying a plaque causes 75% of myocardial infarctions, with superficial plaque erosion present in the remaining 25%.
  • Vasospasm: With or without coronary atherosclerosis and possible association with platelet aggregation.
  • Emboli: From left-sided mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale.
 
Pathophysiology
  • High-plasma LDL, low-plasma HDL, cigarette smoking, diabetes mellitus, and hypertension → dysfunction of vascular endothelium and an abnormal interaction with blood monocytes and platelets → subintimal collections of abnormal fat, cells, and debris (i.e. atherosclerotic plaques) → segmental reductions in cross-sectional area. When the luminal area is reduced by more than approximately 80 percent, blood flow at rest may be reduced, and further minor decreases in the stenotic orifice can reduce coronary flow dramatically and cause myocardial ischemia.
  • Severe coronary narrowing and myocardial ischemia are frequently accompanied by the development of collateral vessels, especially when the narrowing develops gradually.
The gross morphologic appearance of a myocardial infarction can vary. Patterns include:
  • Transmural infarct: Involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15–30%. Isolated infarcts of RV and right atrium are extremely rare.
  • 41Subendocardial infarct: Multifocal areas of necrosis confined to the inner 1/3–1/2 of the left ventricular wall. These do not show the same evolution of changes as seen in a transmural MI.
 
Clinical Manifestation
  • Chest pain that occurs suddenly and constantly does not subside. Usually above sterna region and upper abdomen, this is a major symptom.
  • The severity of pain can increase settled until unbearable pain.
  • Pain is very severe, such as punctured pain that can spread to shoulder and continue down to arm (usually left arm).
  • Pain starts spontaneously (does not occur after emotional disturbance or activity).
  • Pain does not disappear with the help of rest or nitroglycerin.
  • Pain spread to jaw and neck.
  • Pain is accompanied by shortness of breath, pale, cold, sever diaphoresis or head floating and nausea and vomiting.
  • Stomach, back and abdominal pain.
  • Shortness of breath and difficulty in breathing.
  • Unexplained anxiety.
  • Weakness and fatigue.
  • Palpitations.
 
Diagnostic Evaluation
  • Creatine Kinase: The total CK is a simple and inexpensive test that is readily available using many laboratory instruments. However, an elevation in total CK is not specific for myocardial injury, because most CK is located in skeletal muscle, and elevations are possible from a variety of noncardiac conditions.
  • Creatine Kinase–MB Fraction: Creatine kinase can be further subdivided into three isoenzymes: MM, MB, and BB. The MM fraction is present in both cardiac and skeletal muscles, but the MB fraction is much more specific for cardiac muscle: about 15 to 40% of CK in cardiac muscle is MB, while less than 2% in skeletal muscle is MB. The BB fraction (found in brain, bowel, and bladder) is not routinely measured. The creatine kinase-MB 42fraction (CK-MB) is part of total CK and more specific for cardiac muscle than other striated muscles. It tends to increase within 3 to 4 hours of myocardial necrosis, then peak in a day and return to normal within 36 hours. It is less sensitive than troponins.
  • Troponin I and T are structural components of cardiac muscle. They are released into the bloodstream with myocardial injury. They are highly specific for myocardial injury—more so than CK-MB. Troponins will begin to increase following MI within 3 to 12 hours. Troponins will remain elevated longer than CK—up to 5 to 10 days for troponin I and up to 2 weeks for troponin T. This makes troponins a superior marker for diagnosing myocardial infarction.
  • Myoglobin: Myoglobin is a protein found in skeletal and cardiac muscle which binds oxygen. It is a very sensitive indicator of muscle injury. However, it is not specific for cardiac muscle, and can be elevated with any form of injury to skeletal muscle. The rise in myoglobin can help to determine the size of an infarction.
  • CRP: C-reactive protein (CRP) is an acute phase protein elevated when inflammation is present. Since inflammation is part of atheroma formation, then CRP may reflect the extent of atheromatous plaque formation and predict risk for acute coronary events.
 
Management
  • Explanation and reassurance.
  • Reduction of risk factors (secondary prevention): The discontinuance of cigarette smoking is vital. The risk of coronary events is low when the total plasma cholesterol is less than 200 mg/100 mL, intermediate when it is 200 to 240 mg/100 mL, and abnormally increased when the plasma cholesterol is over 240 mg/100 mL.
  • Ideal weight should be attained and maintained. Aggravating factors (e.g. endocrine disorders, hypertension, and drugs such as glucocorticoids) should be treated and eliminated when possible. Diabetes mellitus and hypertension, when present, should be treated.
  • The administration of estrogen to postmenopausal women appears to provide significant protection with a reduction in coronary events.
  • Sensible adaptations of activities to minimize anginal attacks. Patients should reduce their energy requirements in the morning and immediately after meals. It may be necessary to recommend a change in employment to avoid physical stress.
 
Pharmacological Treatment
  • Nitrates act by causing systemic vesodilation, thereby reducing myocardial wall tension and oxygen requirements, as well as by dilating the epicardial coronary vessels and increasing blood flow in collateral vessels. Nitroglycerin is administered sublingually in tablets of 0.4 or 0.6 mg. Patients with angina should be instructed to take the medication both to relieve an attack and also in anticipation of stress (exercise or emotional). If relief is not achieved after the first dose of nitroglycerin, a second or third dose may be given at 5-minute intervals. These preparations can be swallowed, chewed, or administered as a patch or paste by the transdermal route.
  • Beta-adrenoceptor blockers reduce myocardial oxygen demand by inhibiting the increases in heart rate and myocardial contractility caused by adrenergic activity. Beta blockage reduces these variables most strikingly during exercise while causing only 43small reductions in heart rate, cardiac output, and arterial pressure at rest. Propranolol is usually administered in an initial dose of 20 to 40 mg four times a day.
  • Calcium antagonists: Verapamil (80 to 120 mg tid), diltiazem (30 to 90 mg qid) and other calcium antagonists are all coronary vasodilators that produce variable and dose-dependent reductions in myocardial oxygen demand, contractility, and arterial pressure
  • Aspirin is an irreversible inhibitor of platelet cyclooxygenase activity. Chronic administration of 100 to 325 mg orally per day reduces coronary events.
  • ACE inhibitors: Lower blood pressure, so the heart does not have to work as hard to pump blood. It is very useful in post heart-attack care.
  • Digitalis glycosides, such as digoxin, may be prescribed in some cases to strengthen heart muscle contraction.
  • Dopamine or dobutamine may be administered to increase blood flow to the heart and strengthen the heartbeat.
  • Thrombolytic, or clot-dissolving, drugs, such as tissue plasminogen activator (tPA), streptokinase or urokinase may be injected immediately to dissolve arterial blockage. This technique is most effective within three hours of the onset of a heart attack.
 
Surgical Management
 
Percutaneous Transluminal Coronary Angioplasty (PTCA)
  • Percutaneous transluminal coronary angioplasty (PTCA) is performed to open blocked coronary arteries caused by coronary artery disease (CAD) and to restore arterial blood flow to the heart tissue without open-heart surgery. A special catheter (long hollow tube) is inserted into the coronary artery to be treated.
  • This catheter has a tiny balloon at its tip. The balloon is inflated once the catheter has been placed into the narrowed area of the coronary artery. The inflation of the balloon compresses the fatty tissue in the artery and makes a larger opening inside the artery for improved blood flow.
  • The use of fluoroscopy assists the physician in the location of blockages in the coronary arteries as the contrast dye moves through the arteries. A small sample of heart tissue (called a biopsy) may be obtained during the procedure to be examined later under the microscope for abnormalities.
  • A technique called intravascular ultrasound (IVUS), a technique that uses a computer and a transducer that sends out ultrasonic sound waves to create images of the blood vessels, may be used during PTCA.
  • The use of IVUS provides direct visualization and measurement of the inside of the blood vessels and may assist the physician in selecting the appropriate size of balloons and/or stents, to ensure that a stent, if used, is properly opened, or to evaluate the use of other angioplasty instruments.
  • The physician may determine that another type of procedure is necessary. This may include the use of atherectomy (removal of plaque) at the site of the narrowing of the artery. In atherectomy, there may be tiny blades on a balloon or a rotating tip at the end of the catheter.
  • When the catheter reaches the narrowed spot in the artery, the plaque is broken up or cut away to open the artery. Atherectomy is used when the plaque is calcified, hardened, or if the vessel is completely closed. Another type of atherectomy procedure uses a laser, which opens the artery by ‘vaporizing’ the plaque.
44
Fig. 1.6A: Inflation of balloon inside a coronary artery
Fig. 1.7(A to C): Percutaneous transluminal coronary angioplasty (PTCA)
45
 
Procedure Completion, Both Methods
  • The sternum will be pushed back together and sewn together with small wires.
  • The skin over the sternum will be sewn back together.
  • Tubes will be inserted into your chest to drain blood and other fluids from around the heart. These tubes will be connected to a suction device to keep fluids pulled away from the heart.
  • A tube will be inserted through your mouth or nose into your stomach to drain stomach fluids.
  • A sterile bandage or dressing will be applied.
 
Coronary Artery Bypass Graft Surgery (CABG)
Coronary artery bypass graft surgery (CABG) is a procedure used to treat coronary artery disease in certain circumstances. Coronary artery disease (CAD) is the narrowing of the coronary arteries (the blood vessels that supply oxygen and nutrients to the heart muscle), caused by a buildup of fatty material within the walls of the arteries. This buildup causes the inside of the arteries to become narrowed, limiting the supply of oxygen-rich blood to the heart muscle.
One way to treat the blocked or narrowed arteries is to bypass the blocked portion of the coronary artery with another piece of blood vessel. Blood vessels, or grafts, used for the bypass procedure may be pieces of a vein taken from the legs or an artery in the chest. At times, an artery from the wrist may also be used. One end of the graft is attached above the blockage and the other end is attached below the blockage. Thus, the blood is rerouted around, or bypasses, the blockage through the new graft to reach the heart muscle. This bypass of the blocked coronary artery can be done by performing coronary artery bypass surgery.
 
Nursing Management
  1. Acute pain related to an imbalance of oxygen supply to myocardial demands.
    Intervention:
    • Assess pain location, duration, radiation, occurrence, a new phenomenon.
    • Review of previous activities that cause chest pain.
    • Create a 12-lead ECG during anginal pain episodes.
    • Assess signs of hypoxemia; give oxygen therapy, if necessary.
    • Give analgesics as directed.
    • Maintain a rest for 24–30 hours during episodes of illness.
    • Check vital signs during periods of illness.
  2. Decreased cardiac output related to electrical factors (dysrhythmias), decrease in myocardial contraction, structural abnormalities.
    Intervention:
    • Maintain bed rest with head elevation of 30 degrees during the first 24–48 hours
    • Assess and monitor vital signs and hemodynamic per 1–2 hours
    • 46Monitor and record ECG, continue to assess the rate, rhythm, and order to each change per 2 or 4 hours.
    • Review and report signs of CO reduction.
  3. Anxiety related to the needs of the body is threatened.
    Intervention:
    • Assess signs and verbal expressions of anxiety
    • Take action to reduce anxiety by creating a calm environment
    • Accompany the patient during periods of high anxiety
    • Provide an explanation of procedures and treatments
    • Encourage patients to express feelings
    • Refer to the spiritual adviser, if necessary
 
ENDOCARDITIS
Endocarditis is an infection of the heart's valves or its inner lining (endocardium). It is most common in people who have a damaged, diseased, or artificial heart valve, caused by bacterial infection
 
Etiology
Endocarditis is caused by bacteria that enter the bloodstream and settle on the inside of the heart, usually on the heart valves. Bacteria can invade in the bloodstream in the many ways, including during some dental and surgical procedures. If one does not take care of teeth, then chances of endocarditis increase. Streptococcus viridans is responsible for about 50% of all bacterial endocarditis cases. This is why dental procedures increase chances for developing this condition. Other common agents include Staphylococcus aureus and Enterococcus. Staphylococcus aureus can infect normal heart valves and is the most common cause of infectious endocarditis in intravenous drug users.
 
Risk Factors
  • Had endocarditis in the past.
  • Hemodialysis for kidney failure.
  • Abnormal or damaged heart valves.
  • An artificial heart valve.
  • A congenital heart defect.
  • Hypertrophic cardiomyopathy.
  • Injected illegal drugs using dirty needles or without cleaning the skin.
  • HIV
  • Coronary artery bypass graft surgery (bypass surgery).
  • Previous rheumatic fever without heart valve damage.
  • A pacemaker or an implantable cardioverter-defibrillator (ICD).
  • A heart attack without other complications.
  • Mitral valve prolapse without mitral valve regurgitation or unusually thickened valve leaflets.
  • A coronary artery stent.
47
 
Pathophysiology
 
Signs and Symptoms
  • Chills and fever
  • Fatigue
  • Weight loss
  • Night sweats
  • Painful joints
  • Persistent cough and shortness of breath
  • Bleeding under the fingernails
  • Tiny purple and red spots under the skin
  • Nail abnormalities (splinter hemorrhages under the nails)
  • Night sweats (may be severe)
  • Paleness
  • Red, painless skin spots on the palms and soles (Janeway lesions)
  • Red, painful nodes (Osler's nodes) in the pads of the fingers and toes
 
Diagnostic Evaluation
A physical examination may reveal:
  • Enlarged spleen
  • Splinter hemorrhages in the fingernails
  • A history of congenital heart disease raises the level of suspicion. An eye examination may show bleeding in the retina a central area of clearing. This is known as Roth's spots.
The following tests may be performed:
  • Blood culture and sensitivity (to detect bacteria)
  • Chest X-ray
  • 48Complete blood count (may show mild anemia)
  • CT scan of the chest
  • Echocardiogram (ultrasound of the heart)
  • Erythrocyte sedimentation rate (ESR)
  • Transesophageal echocardiogram
 
Management
The American Heart Association recommends preventive antibiotics for people at risk for infectious endocarditis before:
  • Certain dental procedures
  • Surgeries on respiratory tract or infected skin, skin structures, or musculoskeletal tissue
Antibiotics are more likely to be recommended to those with the following risk factors:
  • Artificial heart valves
  • Certain congenital heart defects, both before or possibly after repair
  • History of infective endocarditis
  • Valve problems after a heart transplant
 
Nursing Management
 
Nursing Diagnosis
  1. Hyperthermia related to infection of cardiac tissue as evidenced by temperature elevation, diaphoresis, chills, malaise, tachycardia, and tachypnea.
    Intervention
    • Monitor temperature as appropriate to determine effectiveness of therapy and to prevent treatment-induced hypothermia.
    • Administer antipyretic medication as appropriate or as ordered to reduce fever.
    • Administer medications as appropriate to treat the cause of the fever.
    • Monitor white blood cell count to evaluate a patient's response to treatment.
    • Monitor vital signs to assess cardiorespiratory response to fever.
    • Encourage intake of oral fluids to replace fluids lost as a result of fever.
  2. Activity intolerance related to generalized weakness, arthralgia, and alteration in oxygen transport secondary to valvular dysfunction.
    Intervention
    • Monitor cardiorespiratory response to activity (e.g. vital signs) to plan or alter activities.
    • Monitor patient for evidence of excess physical (e.g. tachycardia, hypertension, diaphoresis, dyspnea) or emotional fatigue to plan for changes in activity level.
    • Instruct patient/caregiver to recognize signs and symptoms of fatigue that require reduction in activity (e.g. pulse increases > 20 beats/min; no increase in activity if resting pulse > 100 beats/min) since these signs indicate excessive cardiac effort.
    • Encourage alternate rest and activity periods to reduce cardiac workload.
  3. Deficient knowledge related to lack of experience and exposure to information about disease and treatment process.
    • Review patient's and caregiver's knowledge about condition to identify teaching needs.
    • 49Discuss common signs and symptoms of the disease (e.g. fatigue, malaise, chills, elevated temperature, anorexia) so health care provider can be notified and treatment initiated promptly.
    • Discuss lifestyle changes that may be required to prevent future complications and/or control the disease process (e.g. avoiding persons with infection, taking prophylactic antibiotics before dental procedures) to reduce the risk of recurrent infective endocarditis.
    • Teaching: Prescribed Medication
    • Provide the patient and caregiver with information about the action, purpose, and side effects of the medications to promote safe medication therapy.
 
MYOCARDITIS AND PERICARDITIS
 
Introduction
Any of the heart's layer is affected by an infectious process. The infections are named for the layer of the heart most involved in the infectious process.
 
Definition of Myocarditis
Myocarditis or inflammatory cardiomyopathy is the inflammation of heart muscles (myocardium).
Or
Myocarditis is the inflammatory process involving the myocardium, can cause heart dilation, thrombi on the heart wall (mural thrombi), infiltration of circulating blood cells around the coronary vessels and between the muscle fibers, and degeneration of the muscle fibers themselves.
 
Etiology
  • Infections
    • Viral (HIV, rubella virus, poliovirus, cytomegalovirus, human herpesvirus 6 and possibly hepatitis C)
    • Protozoan (Toxoplasma gondii)
    • Bacterial (Brucella, Corynebacterium diphtheriae)
    • Fungal (Aspergillus)
    • Parasitic (Ascaris, Echinococcus granulosus)
  • Toxins
    • Drugs (ethanol, anthracyclines and some other forms of chemotherapy, and antipsychotics)
  • Immunological causes:
    • Allergic (acetazolamide, amitriptyline)
    • Rejection after a heart transplant
    • Autoantigens (scleroderma, systemic lupus erythematosus)
    • Toxins (arsenic, toxic shock syndrome toxin, carbon monoxide, or snake venom)
    • Heavy metals (copper or iron)
  • 50Physical agents
    • Electric shock, hyperpyrexia, and radiation
 
Pathophysiology
 
Signs and Symptoms
  • Chest pain (often described as ‘stabbing’ in character)
  • Palpitations
  • Fever and other signs of infection, including headache, muscle aches, sore throat, diarrhea or rashes
  • Fatigue
  • Dyspnea
  • Joints pain or swelling
  • Leg swelling
  • Dysrhythmias can also occur
  • Fainting (often related to irregular heart rhythms)
  • Low urine output.
 
Diagnostic Evaluations
Physical examination may reveal the following:
  • Abnormal heartbeat or heart sounds (murmurs, extra heart sounds)
  • Fever
  • Fluid in lungs
  • Rapid heartbeat (tachycardia)
  • Swelling in the legs.
  1. Chest X-ray: It shows enlarged cardiac silhouette resulting from ventricular enlargement or pericardial effusion.
  2. Blood Test: It shows moderate leukocytes.
  • Elevated cardiac enzymes.
  • Antibodies are found against the heart muscle and the body itself.
  1. ECG
  • It helps to identify heart chamber size and ventricular functioning.
  • 51It shows a bundle branch block or complete AV heart block, ST segment elevation or T-wave flattening.
  1. Biopsy: It shows features of myocardial interstitium with abundant edema and inflammatory infiltrates, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.
  • Cardiac Magnetic Resonance Imaging (cMRI or CMR): It helps in diagnosing myocarditis by visualizing markers for inflammation of the myocardium.
 
Treatment
  • As most viral infections cannot be treated with directed therapy, symptomatic treatment is the only form of therapy for those forms of myocarditis.
  • In the acute phase, supportive therapy, including bed rest, is indicated.
  • For symptomatic patients, digoxin and diuretics provide clinical improvement.
  • For patients with moderate to severe dysfunction, cardiac function can be supported by use of inotropes such as Milrinone in the acute phase, followed by oral therapy with ACE inhibitors (Captopril, Lisinopril) when tolerated.
  • People who do not respond to conventional therapy are given bridge therapy with left ventricular assist devices. Heart transplantation is reserved.
  • For patients who fail to improve with conventional therapy, heart transplantation is reserved. Others: Anti-embolism stockings and passive and active exercises should be used because embolization from venous thrombosis and mural thrombi can occur, especially in patients on bed rest.
 
Complications
  • Cardiomyopathy
  • Pulmonary congestion
  • Pericarditis
  • Heart failure
  • Sudden death
 
Prevention
Prevention of infectious diseases by means of appropriate immunizations (e.g. influenza, hepatitis) and early treatment appear to be important in decreasing the incidence of myocaridtis.
 
PERICARDITIS
 
Definition
Pericarditis is an inflammation of the pericardium (the fibrous sac surrounding the heart).
Or
  • Pericarditis is inflammation of the pericardium, which causes its two layers to rasp and rub against each other as the heart contracts and relaxes.
  • Classification: It is of two types:
    • Acute pericarditis.
    • Chronic pericarditis.
52
 
Classification on the Basis of Etiological Factors
  • Acute nonspecific (idiopathic)
  • Infective:
    • Bacterial
    • Viral
    • Other infections
  • Immunologic:
    • Rheumatic fever
    • Other connective tissue disorders
  • Neoplastic
  • Metabolic:
    • Uremic
    • Myxedema
    • Gout.
  • Traumatic (including after cardiac surgery)
  • Associated with myocardial infarction.
 
Infective
  • Bacterial pericarditis: This condition is potentially fatal without prompt medical treatment. Most cases of bacterial pericarditis are triggered by infections somewhere else in the body. For example, a person with pneumonia (lung infection) may be vulnerable to bacterial pericarditis if the bacteria access the pericardium directly or via the bloodstream. Some of the dangerous complications include:
    • Cardiac tamponade: Fluid builds up between the two layers of the pericardium. The heart is compressed and can not function properly.
    • Abscess: A buildup of pus either within the heart or in the pericardium.
    • Spread of infection: As with any infection, the infection can spread to other areas.
    • Constrictive pericarditis: The pericardium is scarred by the inflammation. Scar tissue does not stretch, so the heart can not function properly.
  • Viral pericarditis: Viral infections that cause cold or pneumonia, such as the echovirus or coxsackie virus (which are common in children) as well as influenza.
    • Chronic effusive pericarditis: Long-term inflammation causes a gradual buildup of fluid within the two layers of the pericardium. In most cases, the reasons for this are unknown. Some of the known causes of chronic effusive pericarditis include tuberculosis and hypothyroidism (underactive thyroid gland).
    • Constrictive pericarditis: As the pericardium recovers from injury or inflammation, scar tissue may form. Scar tissue makes the pericardium stiff and hard, so that the heart is unable to fill properly with blood. Symptoms include unexplained weight loss, fatigue, breathlessness, swelling of the abdomen and heart murmurs. Without treatment, constrictive pericarditis can lead to a range of complications including:
      • Irregular heartbeat (heart arrhythmia)
      • Heart failure
      • Liver damage.
  • 53Neoplastic: Cardiac myxoma, Cardiac rhabdomyoma, Papillary fibroelastoma, Cardiac fibroma, Cardiac lipoma, Cardiac hemangioma, Cardiac teratoma, Mesothelioma of atrioventricular node, Purkinje cell tumor.
  • Traumatic: Heart surgery or trauma to the chest, esophagus or heart.
  • Pericarditis following heart surgery: Pericarditis may be a complication of heart surgery. Operations on the heart involve opening the pericardium in order to apply coronary artery bypass grafts, open or replace heart valves, or undertake other corrective procedures.
  • Post-heart attack pericarditis: While pericarditis does not cause or contribute to heart attack, the injury to cardiac tissue caused by a heart attack can sometimes lead to pericarditis. This is known as postmyocardial infarction (post-MI) pericarditis. The symptoms may not appear for some weeks or months after the heart attack, and can include relatively mild chest pain, joints pain and fever. It is not possible to prevent post-MI pericarditis.
  • Acute pericarditis: It is the inflammation of the pericardium characterized by chest pain, pericardial friction rub and serial of ECG changes (ST evelations).
Types include: Pericarditis can be classified according to the composition of the inflammatory exudates.
  • Serous: This form usually consists of 50 to 200 ml of slowly accumulating exudates. Characteristically produced by nonbacterial involvement, including rheumatic fever, systemic lupus erythematosus, tumors, uremia and primary viral infection (e.g. coxsackie).
  • Purulent: This is due to bacteria, fungus or parasitic action. Infection reaches directly, through blood or through lymphatic route from the nearby areas of infection, e.g. pneumonia, empyema, lung abscess, etc. Most common causative organisms are Staphylococci, Streptococci, and Pneumococci. Purulent pericarditis is composed of 400 to 500 ml of a thin to creamy pus. The patient presents with fever, rigor and a friction rub. It usually organizes and may produce mediastinopericarditis or constrictive pericarditis.
  • Fibrinous: In this, exudates will be completely resolved or be organized, causing adhesive pericarditis.
  • Caseous: This form is due to tuberculosis by direct extension from neighboring lymph nodes.
  • Hemorrhagic: This is composed of an exudate of blood mixed with fibrinous to suppurative effusion. Most commonly, it occurs after cardiac surgeries.
 
Causes
  • Infectious: Pericarditis may be caused by:
    • Viral (coxsackievirus, influenza)
    • Bacterial (Pneumococcus, tuberculous, Staphylococcus or Streptococcus)
    • Fungal (Aspergillus, Candida, and Coccidioides)
 
Other
  • Idiopathic: No identifiable etiology found after routine testing.
  • Immunologic conditions including systemic lupus erythematosus (more common among women) or rheumatic fever
  • Myocardial infarction (Dressler's syndrome)
  • 54Trauma to the heart, e.g. puncture, resulting in infection or inflammation
  • Uremia (uremic pericarditis)
  • Malignancy (as a paraneoplastic phenomenon)
  • Side effects of some medications, e.g. isoniazide, cyclosporine, warfarin, and heparin
  • Radiation-induced
  • Aortic dissection
  • Tetracyclines
  • Postpericardiotomy syndrome: Usually after CABG surgery
 
Pathophysiology
 
Signs and Symptoms
  • Chest pain
  • Dry cough
  • Fever
  • Chills
  • Fatigue
  • Malaise
  • Anxiety
  • Joints pain
  • Anorexia
  • Increased heart rate (depends upon the degree of fever and anxiety)
  • Weight loss
Characteristic/Parameter
Pericarditis
Myocardial infarction
Pain description
Sharp, pleuritic, retrosternal (under the sternum) or left precordial (left chest) pain
Crushing, pressure-like, heavy pain. Described as ‘elephant on the chest’.
Radiation
Pain radiates to the trapezius ridge (to the lowest portion of the scapula on the back) or no radiation
Pain radiates to the jaw, or the left arm, or does not radiate
Exertion
Does not change the pain
Can increase the pain
Position
Pain is worse in the supine position or upon inspiration (breathing in)
Not positional
Onset/duration
Sudden pain that lasts for hours or sometimes days before a patient comes to the ER
Sudden or chronically worsening pain that can come and go in paroxysms or it can last for hours before the patient decides to come to the ER
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Diagnostic Evaluations
  • ECG: It indicates tachycardia but with underlying heart disease or uremia, bradycardia can occur.
  • Laboratory investigation shows:
    • Elevated ESR
    • Elevated WBC count
    • Cardiac enzymes are usually normal but may be elevated
  • Physical Examination: It reveals the classical symptom, that is friction rub.
  • Acute Complications: Pericarditis can progress to:
    • Pericardial effusion
    • Cardiac tamponade
    • Pulsus paradoxus (decrease of at least 10 mm Hg of the systolic blood pressure upon inspiration), hypotension (due to decreased cardiac index), JVD (jugular vein distention) from right-sided heart failure and fluid overload.
  • Treatment: The treatment in viral or idiopathic pericarditis is with Aspirin, or non-steroidal anti-inflammatory drugs (NSAIDs, such as naproxen). Severe cases may require:
  • Antibiotics to treat tuberculosis or other bacterial causes.
  • Steroids are used in acute pericarditis but are not favored because they increase the chance of recurrent pericarditis.
  • Colchicine is a very effective treatment option. If aspirin and NSAIDs are not sufficient, colchicine should be added to the regimen.
 
Surgical Management
Pericardiocentesis is done to treat pericardial effusion/tamponade. (Pericardiocentesis is a procedure in which puncture of pericardial sac is done and some of the pericardial fluid is removed to relieve cardiac tamponade, which restricts normal heart action. During the procedure, the patient is monitored by ECG and central venous pressure measurements are made. A defibrillator is turned on and other emergency resuscitative equipment should be kept ready).
 
CHRONIC PERICARDITIS
Definition: Chronic pericarditis is a condition in which there is chronic inflammatory thickening of the pericardium that changes the pericardium into thick fibrous band of tissues. Thus, the tissues encircle, encase and compress the heart and prevent it from expanding to normal size, causing restriction of ventricular filling.
 
Types
  • Adhesive pericarditis
  • Adhesive mediastinopericarditis
  • 56Constrictive pericarditis
  • Adhesive pericarditis: Chronic pericarditis with adhesions between visceral and parietal pericardium.
 
Causes
  • Shortness of breath
  • Pain: It may be steady and constant or it may occur in paroxysms, usually after unusal effort or after mental excitement or a fit of anger.
  • Pulse: Rapid and feasible; pulse tension and pressure greatly reduced; irregular pulse.
  • Palpitations
  • Ventricles become dilated and hypertrophied with its concomitant symptoms—dropsy, vertigo and venous stasis are present.
  • Treatment: It needs most careful and continuous oversight. Effusion should be retarded and its absorption and removal should be promoted by rational measures.
  • Adhesive mediastino pericarditis: Here pericardial sac is obliterated due to adhesion between two layers of pericardium as well as between parietal pericardium and surrounding mediastinal structures, chest wall and diaphragm.
  • Constrictive pericarditis: Constrictive pericarditis is a late sequela of an inflammatory condition of the pericardium. The inflammatory condition is usually an infection that involves the pericardium, but it may also occur after a heart attack or after heart surgery.
Almost half the cases of constrictive pericarditis in the developing world are idiopathic in origin. In regions where tuberculosis is common, it is the cause in a large portion of cases. Causes of constrictive pericarditis include:
  • Infectious:
    • Tuberculosis
    • Incomplete drainage of purulent pericarditis
    • Fungal and parasitic infections
  • Inflammatory and autoimmune:
    • Chronic pericarditis
    • Postviral pericarditis
    • Postsurgical
    • Following pericarditis associated with acute myocardial infarction
    • Following postmyocardial infarction (Dressler's) syndrome
    • In association with pulmonary asbestosis
  • Prior mediastinal radiation therapy
  • Chronic renal failure
  • Connective tissue disorders
  • Neoplastic pericardial infiltration
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Pathophysiology
 
Diagnostic Evaluation
  • Imaging will demonstrate a thickened pericardium. In contrast with restrictive cardiomyopathy, there is an increased resistance to ventricular filling due to increased myocardial stiffness. Imaging features of restrictive cardiomyopathy demonstrate an increased left ventricular thickness with infiltration of the myocardium.
  • Chest X-ray: Pericardial calcification, and pleural effusions are common findings.
  • Echocardiography: The echographic finding is an exaggerated anterior motion of the septum with the atrial filling. Since the posterior ventricular wall is unable to expand, an increase in left ventricular volume with the atrial systole produces a marked displacement of the septum.
  • CT and MRI: Useful in select cases.
  • BNP blood test: Tests for the existence of the cardiac hormone, brain natriuretic peptide which is only present in RCMP but not in CP, and is particularly helpful in determining the specific CHF type.
  • Pulmonary catheterization showed all four heart chambers having equal diastolic pressures.
 
Clinical Features
  • Kussmaul's sign (raised JVP on inspiration)
  • Increased JVP (almost universal), rapid descent (prominent diastolic collapse of JVP)
  • 58Pericardial knock in around 50% cases
  • Hepatomegaly and other signs of right heart failure; ascites; fatigue; peripheral edema
 
Treatment
Pericardial stripping: The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. This procedure has significant risk involved, with mortality rates of 6%. The high risk of the procedure is attributed to adherence of the thickened pericardium to the myocardium and coronary arteries. In patients who have undergone coronary artery bypass surgery with pericardial sparing, there is danger of tearing a bypass graft while removing the pericardium. Due to the significant risks involved with pericardial stripping, many patients are treated medically, with judicious use of diuretics.
 
Common Causes of Chronic Pericarditis
  • Long-standing pyogenic infections
  • Postviral infections
  • Tuberculosis
  • Hemopericardium.
 
Common Signs and Symptoms of Chronic Pericarditis
  • Congestive heart failure
  • Dyspnea
  • Chronic atrial fibrillation
  • Fatigue on exertion
  • Leg edema
  • Ascites
  • Low pulse pressure
  • Distended neck vein
  • Delay in capillary refill time
 
Common Treatment of Chronic Pericarditis
  • Medical treatment: Digitalis and diuretics
  • Surgical treatment: Surgical removal of the tough encasing pericardium (pericardiectomy) is the only treatment of benefit. The objective of the operation is to release both ventricles from the constrictive and restrictive inflammation. Surgery may be considered if the pericardium is scarred and inflexible, or if pericarditis keeps recurring.
  • The procedure begins when the surgeon makes an incision in the skin over the breastbone and divides it to expose the pericardium. During the surgery, the surgeon will grasp the pericardium, cut the top of this fibrous covering of the heart, drop it into the specimen bag, and re-cover the heart. The breastbone is then wired back together and the incision is closed, completing the procedure. When the portion of pericardium lying between the two phrenic nerves is excised, it is called total pericardiectomy. In cases where total pericardiectomy is not possible, subtotal pericardiectomy is performed or, in extreme cases, a cruciate incision on the pericardium is performed.
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Nursing Management
 
Assessment
  • Assess signs of pain.
  • Assess association of pain with respiratory movements, cough, swallowing.
  • Assess for pericardial friction rub (helps to distinguish between pericarditis and MI).
  • Frequently check client for temperature (pericarditis can cause abrupt onset of fever in a previously afebrile patient).
 
Nursing Diagnosis
  • Acute pain related to inflammation of layers of heart.
Goal: To relieve pain.
Interventions
  • Check the intensity of pain.
  • Assist the patient to sit upright or to lean forward to relieve pain.
  • Restrict the activities of patient.
  • Provide prescribed analgesics (morphine).
  • Hyperthermia related to inflammatory process.
Goal: To maintain normal temperature.
Interventions
  • Monitor temperature 2–4 hourly.
  • Observe for basic principles of asepsis like handwashing.
  • Provide cold compression if chills are not present along with fever.
  • Administer prescribed antibiotics and antipyretics.
    • Decreased cardiac output related to structural abnormality of valves.
Goal: To reduce risk of complications.
Interventions
  • Monitor BP and pulse (pulsus alternans indicates left-sided heart failure).
  • Evaluate jugular vein distension.
  • Check laboratory findings (ECG, cardiac enzymes).
  • Maintain intake.
  • Output chart.
  • Obtain daily weight.
  • Administer prescribed drugs like digitalis.
    • Risk for complications related to disease process.
Goal: To reduce risk of complications.
Interventions
  • Assess vital signs of patient.
  • Assess peripheral edema.
  • Check the laboratory findings (ECG, cardiac enzymes).
  • Administer digitalis and digoxin if signs of heart failure appear.
  • Prepare for emergency pericardiocentesis.
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RHEUMATIC HEART DISEASE
Rheumatic heart disease is a group of acute and long-term chronic heart disorders that can occur as a result of rheumatic fever. One common result of rheumatic fever is heart valve damage. This damage to the heart valves may lead to a valve disorder. It is caused by an autoimmune reaction to Group A β-hemolytic streptococci (GAS) that results in valvular damage characterized by fibrosis and scarring of valve leaflets, commissures and cusps leads to abnormalities that can result in valve stenosis or regurgitation.
 
Etiology
  • Autoimmune reaction to Group A β-hemolytic streptococci (GAS)
  • Rheumatic fever is a systemic disease affecting the periarteriolar connective tissue and can occur after an untreated Group A β-hemolytic streptococcal pharyngeal infection.
  • It is believed to be caused by antibody cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction and is termed as molecular mimicry.
  • Usually, self-reactive B-cells remain anergic in the periphery without T-cell co-stimulation. During a Streptococcus infection, mature antigen presenting cells such as B-cells present the bacterial antigen to CD4-T-cells which differentiate into helper T2 cells.
  • Helper T2-cells subsequently activate the B-cells to become plasma cells and induce the production of antibodies against the cell wall of Streptococcus.
  • The antibodies may also react against the myocardium and joints producing the symptoms of rheumatic fever.
 
Pathophysiology
61
 
Signs and Symptoms
  • Polyarthritis
  • Carditis
  • Subcutaneous nodules: Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees.
  • 62Erythema marginatum: A long-lasting reddish rash that begins on the trunk or arms as macules.
  • Chorea: A characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease for at least three months from the onset of infection.
  • Fever of 38.2–38.9 °C (101–102 °F)
  • Arthralgia: Joints pain without swelling.
  • Raised erythrocyte sedimentation rate or C-reactive protein
  • Leukocytosis
  • ECG showing features of heart block, such as a prolonged PR interval.
 
Diagnostic Evaluation
  • Signs and symptoms you report
  • Evidence of recent group A streptococcal infection
  • Physical examination:
    • Checking the joints for signs of inflammation
    • Examining the skin for nodules under the skin or a rash
    • Listening to the heart for abnormal rhythms, murmurs or muffled sounds that may indicate inflammation of the heart
    • Conducting a series of simple movement tests to detect indirect evidence of inflammation of the central nervous system
  • CBC
  • Electrocardiogram (ECG)
  • Echocardiography
 
Management
  • Antibiotics, penicillin, ampicillin and amoxicillin
  • A single dose of intramuscular benzathine penicillin G or benzathine/procaine penicillin combination can also be used.
  • Alternate drugs include narrow-spectrum cephalosporins, amoxicillin-clavulanate, dicloxacillin, erythromycin, or other macrolides.
  • Place hospitalized patients with Group A β-hemolytic streptococci on droplet precautions, as well as standard precautions, until 24 hours after initiation of appropriate antibiotics.
  • Salicylates and steroids can also be included in treatment regimen to decrease the inflammatory response.
  • Include digoxin and diuretics, afterload reduction, supplemental oxygen, bed rest, and sodium and fluid restriction as an additional treatment.
  • In patients with critical stenosis, mitral valvulotomy, percutaneous balloon valvuloplasty, or mitral valve replacement may be indicated.
 
Nursing management
 
Nursing assessment
  • About heart function.
  • Nutritional status of patients.
  • 63Tolerance to the activities and attitudes of patients toward limiting the activities undertaken.
  • Disturbances in sleep patterns.
  • Level of discomfort felt by rheumatic fever patients.
  • Ability of the patient in terms of troubleshooting.
  • Knowledge of patients and families will be suffered by rheumatic heart disease.
    • History of rheumatic heart disease.
    • Monitor cardiac complications in the event.
    • Auscultation of heart sounds.
    • Assessment of the patient's vital signs.
    • Assessment of pain.
    • Assessment of the presence of markers of inflammation in the joints.
    • Assessment of the presence of lesions on the skin.
      • Decreased cardiac output related to valvular stenosis
 
Nursing interventions
  • Monitor vital signs such as blood pressure, apical pulse and peripheral pulse.
  • Monitor cardiac rhythm and frequency.
  • Semi-Fowler bed rest in a position which is 45 degrees.
  • Encourage the patient to stress management techniques (quiet environment, meditation).
  • Medical collaboration in terms of oxygen delivery and therapy.
    • Activity intolerance related to decreased cardiac output, oxygen supply and demand imbalance.
 
Nursing interventions
  • Energy saving in case of acute patients.
  • Maintain bed rest until the results of laboratory and clinical status of patients are improved.
  • Monitor the gradual increase in the level of activity undertaken.
  • Teach to participate in activities of daily necessities.
  • Create a schedule of activities and also of the breaks.
 
VALVULAR HEART DISEASE
Heart valve disease occurs when heart's valves do not work properly. It includes narrowing of valve opening, stiff valve cusps and leaflets and contracture of valves. Valvular heart disease process involving one or more of the four valves of the heart affected by the functional alteration, stenosis and regurgitation.
 
Types
There are several types of valve diseases:
  • Valvular stenosis: This occurs when a valve opening is smaller than normal due to stiff or fused leaflets. The narrowed opening may make the heart work very hard to pump blood through it. This can lead to heart failure and other symptoms. All four valves 64can be stenotic (hardened, restricting blood flow). The conditions are called tricuspid stenosis, pulmonic stenosis, mitral stenosis or aortic stenosis.
 
Pathophysiology
  • Valvular insufficiency: Also called regurgitation, incompetence or ‘leaky valve’, this occurs when a valve does not close tightly. If the valves do not seal, some blood will leak backward across the valve. As the leak worsens, the heart has to work harder to make up for the leaky valve, and less blood may flow to the rest of the body. Depending on which valve is affected, the condition is called tricuspid regurgitation, pulmonary regurgitation, mitral regurgitation or aortic regurgitation.
 
Pathophysiology of Aortic Regurgitation
  • Congenital valve disease: Most often affects the aortic or pulmonic valve. Valves may be the wrong size, have malformed leaflets, or have leaflets that are not attached to the annulus correctly.
  • Acquired valve disease: This includes problems that develop with valves that were once normal. These may involve changes in the structure or valve due to a variety of diseases or infections, including rheumatic fever or endocarditis.
  • Mitral valve prolapse (MVP): MVP causes the leaflets of the mitral valve to flop back into the left atrium during the heart's contraction. MVP also causes the tissues of the valve to become abnormal and stretchy, causing the valve to leak.
  • Tricuspid regurgitation
  • Most common cause is annular dilatation due to RV failure of any cause.
  • 65Symptoms and signs result from a reduced cardiac output, ascites, painful congestive hepatomegaly and edema.
  • The pansystolic murmur of TR is usually loudest at the left sternal edge and augmented by deep inspiration.
  • Severe functional TR may be treated by annuloplasty or valve replacement. Severe TR due to intrinsic tricuspid valve disease requires valve replacement.
 
Etiology and Pathophysiology
There are many different types of valve disease; some types can be present at birth (congenital), while others may be acquired later in life.
  • Heart valve tissue may degenerate with age.
  • Rheumatic fever may cause valvular heart disease.
  • Bacterial endocarditis.
  • High blood pressure and atherosclerosis may damage the aortic valve.
  • A heart attack may damage the muscles that control the heart valves.
  • Other disorders, such as carcinoid tumors, rheumatoid arthritis, systemic lupus erythematosus, or syphilis may damage one or more heart valves.
 
Signs and Symptoms
  • Mitral valve stenosis:
    • Dyspnea on exertion
    • Hemoptysis
    • Fatigue
    • Palpitation
    • 66Diastolic murmur sound
    • Arterial fibrillation
  • Mitral valve regurgitation:
    • Acute poorly tolerated with fulminating pulmonary edema
    • Shock developing rapidly
    • Systolic murmur
  • Mitral valve prolapse:
    • Palpitation
    • Dyspnea
    • Chest pain
    • Activity intolerance
    • Syncope
  • Aortic valve stenosis:
    • Abrupt onset of profound dyspnea
    • Chest pain
    • Left ventricular failure
    • Shock
  • Chronic:
    • Fatigue
    • Exertional dyspnea
    • Orthopnea
    • High-pitched murmur sound
    • Absent S1 and S2 sound
  • Tricuspid and pulmonic stenosis:
    • Peripheral edema
    • Ascitis
    • Hepatomegaly
    • Diastolic low-pitched
    • Increased intensity during inspiration
  • Other signs and symptoms:
    • Low BP
    • Dizziness
    • Dysrythmia
 
Diagnosis
  • An electrocardiogram: Also called an ECG or EKG, to measure the electrical activity of the heart, regularity of heartbeats, thickening of heart muscle (hypertrophy) and heart-muscle damage from coronary artery disease.
  • Stress-testing: Also known as treadmill test, to measure blood pressure, heart rate, ECG changes and breathing rates during exercise. During this test, the heart's electrical activity is monitored through small metal sensors applied to your skin while you exercise on a treadmill.
  • 67Chest X-rays
  • Echocardiogram: To evaluate heart function. During this test, sound waves bounced off the heart are recorded and translated into images. The pictures can reveal abnormal heart size, shape and movement. Echocardiography can also be used to calculate the ejection fraction, or volume of blood pumped out to the body when the heart contracts.
  • Cardiac catheterization: Which is the threading of a catheter into the heart chambers to measure pressure irregularities across the valves (to detect stenosis) or to observe backflow of an injected dye on an X-ray (to detect incompetence).
 
Management
Medical management
  • Medical therapy
  • Antibiotic therapy: Clindamycin, ampicilline or cerazolin or ceftriaxone, clarithromycine
    • Treatment for heart faliure
    • Diuretics
    • Vasodilators: Nitrates, sorbitrate
    • ACE inhibitors: Captopril, enapril
    • Positive isotope: Digoxin
    • Anticoagulant therapy
    • Beta blockers: Metoprolol
 
Surgical Management
For mitral stenosis:
  • Closed mitral vulvotomy
  • Open mitral valvotomy
  • Mitral valve replacement
  • Balloon valvuloplasty (percutaneously):
    • For mitral insufficiency: (Mitral valve replacement or annuloplasty (the valve ring)
For aortic stenosis or insufficiency:
  • Replacement of aortic valve with prosthetic or tissue valves
  • Ballon valvuloplasty (aortic stenosis)
For tricuspid stenosis and insufficiency: Valvuloplasty replacement may be done at the time of surgical interventions for associated rheumatic mitral or aortic disease.
 
Complications
  • Left-sided heart failure
  • Possible, right-sided heart failure
  • Dysrythmia
 
Nursing Management
  • Mitral stenosis:
    • Auscultate the first heart sound, usually accompanied by an ‘opening snap’
    • Place patient in lateral recumbent position with bell to hear the low-pitched murmur (rumbling murmur)
    • Duration
  • 68Mitral insufficiency:
    • Auscultate for diminished first heart sound
    • Auscultate for systolic murmur
    • Note radiation of heart sound to axilla and left intrascapular region
    • Mild insufficiency may produce a systolic murmur
  • Aortic stenosis:
    • Auscultate for prominent fourth sound and possible splitting of second heart sound (LV dysfunction). First heart sound is normal.
    • Auscultate for midsystolic murmur at the base of the heart
    • Note harsh and rasping quality at base
    • Higher pitch at apex
  • Aortic insufficiency:
    • Auscultate for soft first heart sound
    • Place the stethoscope at the 3rd and 4th intercostal space
  • Tricuspid stenosis:
    • Auscultate for a blowing diastolic murmur at the lower left sternal border (increased with inspiration)
  • Tricuspid insufficiency:
    • Auscultate the third heart sound
    • Murmur usually listened at 4th intercostal space
    • Murmur usually high-pitched
 
Nursing Diagnosis
  • Decreased cardiac output related to altered preload, afterload, or contractility.
  • Activity intolerance related to reduced oxygen supply.
  • Ineffective coping related to acute and chronic illness.
 
Nursing Interventions
  • Maintaining adequate cardiac output:
    • Assess frequently for change in existing murmur or new murmur
    • Assess for right- and left-sided heart failure
    • Monitor and treat the dysrythmia as ordered
    • Prepare the patient for surgical interventions
  • Improve activity intolerance:
    • Maintain the bed rest while symptoms of heart failure are present.
    • Allow patient to rest between interventions
    • Allow chair-sitting activity
    • Assist or perform the hygiene needs for patient to reserve strength for ambulation
  • Strength-coping abilities:
    • Instruct the patient about specific valvular dysfunction, possible etiology and therapies
    • Include family members in any discussion
    • 69Stress the importance of adapting lifestyle to cope up with illness
    • Discuss with patient the surgical intervention as the treatment modality
    • Refer the patient to appropriate counseling services (vocational, social work and cardiac rehabilitation)
 
Health Education
  • Review activity restriction and schedule with the patient's family
  • Instruct the patient to report signs of impending or worsening heart failure—dyspnea, cough, increased fatigue, and ankle swelling
  • Review sodium and fluid restrictions
  • Inform adverse effects of drugs.
  • Keep regular appointments with the physician
  • Increase walking activity and other activities gradually.
 
ARTERIOSCLEROTIC VASCULAR DISEASE
Atherosclerosis (or arteriosclerotic vascular disease) is a condition where the arteries become narrowed and hardened due to an excessive buildup of plaque around the artery wall. The disease disrupts the flow of blood around the body, posing serious cardiovascular complications.
Arteriosclerosis is characterized by irregularly distributed lipid deposits in the intima of large and medium-sized arteries, causing narrowing of arterial lumens and proceeding eventually to fibrosis and calcification. Lesions are usually focal and progress slowly and intermittently. Limitation of blood flow accounts for most clinical manifestations, which vary with the distribution and severity of lesions.
Fig. 1.8: Arteriosclerosis
70
 
Risk Factors for Atherosclerosis
Any factor associated with a doubling in the incidence of ischemic heart disease has been defined as a ‘risk factor’. A major advance in the clinical assessment and treatment of atherosclerosis is a thorough screening for risk factors, followed by aggressive treatment to eliminate the risk factor. Risk factors can be categorized as genetic and environmental.
  • Hypertension: An increase in blood pressure is consistently associated with an increased risk of myocardial infarction. In fact, men with systolic blood pressure over 160 mm Hg have almost three times the incidence of myocardial infarction as compared to those with blood pressure under 120 mm Hg. Treatment of hypertension, which is usually clinically silent, especially in the early stages of hypertension, has resulted in a significant reduction in the incidence of myocardial infarction and stroke.
  • Serum cholesterol level: Numerous epidemiology and clinical studies have shown that the levels of serum cholesterol have been directly correlated with the incidence of ischemic heart disease. Indeed, of all the known risk factors, serum cholesterol seems to be the most important determinant of the geographical differences in the incidence of atherosclerotic coronary artery disease. In the absence of genetic disorders of lipid metabolism, such as familial hypercholesterolemia, the amount of cholesterol in the blood is related to the dietary intake of saturated fat. A number of studies have demonstrated a reduction in the incidence of myocardial infarction following treatment with cholesterol-lowering drugs.
  • Cigarette smoking: Atherosclerosis of the coronary arteries and the aorta is more severe and extensive among cigarette smokers than among nonsmokers, and the effect is dose-related. Second-hand smoking is a risk factor. As a result, the incidence of myocardial infarction, ischemic stroke, and abdominal aortic aneurysms is markedly increased among smokers. Smoking is an environmental risk factor that is best addressed by eliminating smoking in preteens and teens and eliminating environment with second-hand smoking.
  • Diabetes mellitus: Diabetics have a substantially greater risk of occlusive atherosclerotic vascular disease in many organs. The metabolic syndrome consisting of hypertension, glucose intolerance, truncal obesity and dyslipidemias has become an important target for early diagnosis and treatment.
  • Increasing age and male gender: These factors are strong determinants of the risk for myocardial infarction.
  • Physical inactivity and stressful life patterns: Both these factors have been correlated with an increased risk of ischemic heart disease.
  • Homocysteine: Homocystinuria is a rare autosomal recessive disease caused by mutations in the gene encoding cystathionine synthase. The disorder results in premature and severe atherosclerosis. Mild elevations of plasma homocysteine are common and represent an independent risk factor for atherosclerosis of the coronary arteries and other large vessels. Homocysteine is toxic to endothelial cells and inhibits several anticoagulant mechanisms in endothelial cells. It inhibits thrombomodulin on the endothelial cell surface, the antithrombin III-binding activity of heparan sulfate proteoglycan, the binding of tissue plasminogen activator, and the ecto-ADPase activity on the endothelial cell surface, which promotes the aggregation of platelets. A low dietary intake of folic acid may aggravate an underlying genetic predisposition to hyperhomocysteinemia, 71but it has not been established that treatment with folic acid actually protects against atherosclerotic vascular disease.
  • C-Reactive Protein and Inflammation Biomarkers: Elevated concentrations of C-reactive protein (CRP), an acute phase reactant produced mainly by hepatocytes, is a marker for systemic inflammation, and has been linked to an increased risk of myocardial infarction and ischemic stroke.
 
Pathophysiology
Natural history of atherosclerosis: Stable angina → unstable angina → MI → complications → death
 
Pathology of Atherosclerosis
  • Fatty streak (yellow streak of lipid-filled macrophage foam cells). Lipid gets deposited first, then macrophages infiltrate and ingest it.
  • Fibrous plaque (whitish yellow lump occluding lumen of coronary arteries, aorta, and carotids) leads to stable angina.
  • Thrombus (plaque rupture, platelet aggregation and thrombus) leads to unstable angina or MI.
 
Pathophysiology of Atherosclerosis
  • The intimal endothelium becomes dysfunctional, losing its ability to produce NO, and starting to express selectins for leukocyte recruitment.
  • Endothelial cells normally provide a permeability barrier, reduce clotting, and regulate vascular tone.
    • NO is a vasoprotective gas released by endothelium. NO is vasodilatory, anti-thrombotic, and anti-inflammatory.
    • NO activates guanylate cyclase to generate cGMP, which causes smooth muscle relaxation/dilation.
    • NO blocks vascular inflammation by inhibiting endothelial release of inflammatory granules. It also blocks platelet aggregation.
    • Endothelial cells lose ability to produce NO due to inflammation, toxins, atherosclerosis, or oxidized LDL.
    • Endothelial dysfunction leads to monocyte recruitment and atherosclerosis.
  • ACh stimulates NO release and dilation.
    • Initial inflammation → endothelial dysfunction → monocyte recruitment/differentiation to intima → growth factors stimulate smooth muscle proliferation → platelet activation/aggregation → atheroma formation.
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Signs and Symptoms
Carotid arteries: These arteries provide blood to the brain. When the blood supply is limited, patients can suffer stroke and may experience:
  • Weakness
  • Difficulty breathing
  • Headache
  • Facial numbness
  • Paralysis
Coronary arteries: These arteries provide blood to the heart. When the blood supply to the heart is limited, it can cause angina and heart attack. Symptoms include:
  • Vomiting
  • Extreme anxiety
  • Chest pain
  • Coughing
  • Feeling faint
Renal arteries: These supply blood to the kidneys. If the blood supply becomes limited, there is a serious risk of developing chronic kidney disease, and the patient may experience:
  • Loss of appetite
  • Swelling of the hands and feet
  • Difficulty concentrating
Peripheral arterial disease: The arteries to the limbs, usually the legs, are blocked. The most common symptom is leg pain, either in one or both the legs, usually in the calves, thighs or hips. The pain may be described as one of heaviness, cramp, or dullness in the leg muscles. Other symptoms may include:
  • Hair loss on legs or feet
  • Male impotence (erectile dysfunction)
  • Numbness in the legs
  • The color of the skin on the legs changes
  • 73The toenails get thicker
  • Weakness in the legs
 
Diagnostic Evaluation
  • Those who are at risk of developing atherosclerosis should be tested, as the symptoms do not show up until cardiovascular disease develops. A diagnosis will be based on the medical history of a patient, test results and a physical examination.
  • Blood tests: These measure how much sugar, fat and protein there is in your blood. If there are high levels of fat and sugar, it can be an indicator that you are at risk of developing the condition.
 
Physical Examination
  • The doctor will listen to the arteries using a stethoscope to see if there is an unusual ‘whooshing’ sound reflecting turbulence of flow, called a bruit. If a bruit is heard, then it can mean there is a plaque obstructing blood flow.
  • There may also be a very weak pulse below the area of the artery that has narrowed. Sometimes there is no detectable pulse.
  • An affected limb may have abnormally low blood pressure
  • There may be signs of an aneurysm (pulsating bulge) behind the patient's knee or in their abdomen
  • Where blood flow is restricted, wounds may not heal properly
  • Ultrasound: An ultrasound scanner is able to create a picture of the inside of your body using sound waves. It can check your blood pressure at distinct parts of the body; changes in pressure indicate where arteries may have obstruction of blood flow.
  • Computed tomography (CT) scan: A CT scan uses X-ray images to create detailed pictures of the inside parts of the body. It can be used to find arteries that are hardened and narrowed.
 
Complications of Atherosclerosis
  • Complicated atherosclerotic plaques: A complicated plaque is characterized by erosion, ulceration or fissuring of the surface of the plaque; plaque hemorrhage; mural thrombosis; calcification; and/or aneurysm formation.
  • Aneurysm formation: A complicated plaque extends into the media of an elastic artery and so weakens the wall to result in the formation of an aneurysm, typically in the abdominal aorta. At a certain size, these aneurysms may suddenly rupture and cause a vascular catastrophe.
  • Calcification occurs in areas of necrosis and elsewhere in the plaque. Calcification in the artery is thought to depend on focal mineral deposition and resorption, which is regulated by osteoblast-like and osteoclast-like cells in the vessel wall.
  • Mural thrombosis results from abnormal laminar and/or turbulent blood flow around the plaque that protrudes into the lumen. The disturbance in flow causes damage to the endothelial lining, which may become dysfunctional or locally denuded and is no longer an effective thrombus-resistant surface. Thrombi often form at sites of erosion and 74fissuring on the surface of the fibrous cap of the plaque. Mural thrombi may embolize to more distal sites. A thrombus formed over an atherosclerotic plaque may detach, become an embolism and lodge in a distal vessel. Ulceration of an atherosclerotic plaque may also dislodge atheromatous debris and produce so-called cholesterol crystal emboli, which appear as needle-shaped spaces in affected tissues, most commonly in the kidney.
  • Vulnerable atheroma has structural and functional alterations that predispose the fibroinflammatory lipid plaque to plaque destabilization.
  • Atheroma destabilization, resulting often in acute coronary syndromes, may occur at any time when the dynamic balance of opposing biological and physical processes is disrupted, leading to occlusive thrombosis, fibrous cap rupture, and occlusive thrombosis, or intraplaque hemorrhage. Plaque rupture has been associated with:
    • Areas of inflammation
    • Large lipid core size
    • Thin fibrous cap
    • Reduced number of smooth muscle cells owing to apoptosis, and
    • Imbalance of proteolytic enzymes and their inhibitors in the fibrous cap
    • Calcification in the plaque
    • Intraplaque hemorrhage leading to inside-out rupture of the fibrous cap.
  • Acute coronary syndromes: Coronary artery disease is the leading cause of mortality in the western world. Acute coronary syndromes (ACS) are characterized clinically into three groups, patients with unstable angina, those with non-ST elevation myocardial infarction and those with ST elevation myocardial infarction.
 
Treatment
  • Those who are at risk of developing atherosclerosis will likely be told by their doctors to change their lifestyle and maintain a healthy weight. In some cases, treatment may include medication or surgery.
  • Lifestyle changes: The changes will focus on weight management, physical activity and a healthy diet. Your doctor may recommend eating foods high in soluble fiber and limiting your intake of saturated fats, sodium and alcohol.
  • Medication: The doctor may prescribe medications to prevent the buildup of plaque or to help prevent blood clots (anteplatelets). Other medications such as statins may be prescribed to lower cholesterol, and angiotensin-converting enzyme (ACE) inhibitors to lower blood pressure.
  • Surgery: Severe cases of atherosclerosis may be treated by surgical procedures, such as angioplasty or coronary artery bypass grafting (CABG) and PTCA.
    • Percutaneous transluminal coronary angioplasty: It is a technique in which a balloon-tipped catheter is usually inserted into the femoral artery (although brachial or radial artery can be used) and threaded under guidance into a blocked coronary artery. The balloon is inflated several times to reshape the lumen by stretching the arterial wall.
    • Directional coronary atherectomy: It reduces the stenosis of coronary artery by excising and removing atheromatus plaque. The DCA cutter consists of a catheter that contain 75a rigid cylinder housing with a central rotating blade. The blade shaves the plaque and deposits it in the nose cone housing for later histopathologic study.
  • Intracoronary stents: Nowadays these are used instead of PTCA to eliminate the risk of acute closure and to improve long-term patency. Several different designs are available, but most are balloon-expandable or self-expandable tubes that, when placed in coronary artery, act as mechanical scaffold to reopen the blocked artery.
  • Laser ablation: In this the lasers are used with balloon angioplasty to vaporize the plaque. After the initial balloon angioplasty, a brief burst of laser radiation is administered and the additional remaining plaque is removed.
  • Transmyocardial revascularization: A new type of laser catheter is used called transmyocardial revascularization (TMR), which may be able to help clients who are not candidates for surgery or angioplasty because of ill health or degree of disease. The higher power laser is guided into left ventricle between heartbeat when the ventricle is filling with blood. The laser creates from 15 to 40 1-mm channels through the myocardium.
 
Prevention
The best way to prevent atherosclerosis is to eliminate any risk factors you might have. The best way to do this is by living a healthy lifestyle.
Diet: Try to avoid saturated fats. They increase your levels of bad cholesterol. The following foods are high in unsaturated fats and can help keep bad cholesterol levels down:
  • Olive oil
  • Avocados
  • Walnuts
  • Oily fish
  • Nuts
  • Seeds
  • Exercise: Exercise will improve your fitness level and lower your blood pressure. If you are overweight, then exercise can help you lose weight through activities, such as walking, swimming, and cycling.
  • Smoking: This is one of the major risk factors for atherosclerosis. It also raises your blood pressure. If you are a smoker, you should quit as soon as possible.
  • Flu vaccine: Researchers from the School of Public Health and Community Medicine in Australia say that the flu vaccination may reduce the risk of heart attack by 50% in middle-aged individuals with narrowed arteries.
 
Nursing Management
Acute pain related to an impaired ability of blood vessels to supply oxygen to the tissues.
 
Intervention and Rational
  • Monitor characteristics of pain through verbal and hemodynamic responses (crying, pain, grimacing, cannot rest, respiratory rhythm, blood pressure and changes in heat rate).
    • 76Rationale: Each patient has a different response to pain, verbal and hemodynamic changes in response to detecting a change in comfort.
  • Assess the description of pain experienced by patients which include: place, intensity, duration, quality, and distribution.
    • Rationale: Pain is a subjective feeling that is experienced and is described by the patient and should be compared with other symptoms to obtain accurate data.
  • Provide a comfortable environment, reduce the activity, limit visitors.
    • Rationale: Helps reduce external stimuli that can add to the tranquility so patients can rest in peace and the power of the heart is not too hard.
  • Teach relaxation techniques with a sigh.
    • Rationale: Helps relieve pain experienced by patients psychologically, which can distract the patient who is not focused on the pain experienced.
  • Observation of vital signs before and after drug administration.
    • Rationale: Knowing the patient's progress after being given the drug.
  • Knowledge deficit, ineffective management of therapeutic regimen, or altered health maintenance.
Inform the client that certain modifiable factors, such as elevated serum lipids, a sedentary lifestyle, cigarette smoking, and hypertension have been shown to increase the risk of atherosclerosis.
  • Assist client to identify changes in lifestyle that could reduce the risk for atherosclerosis (e.g. dietary modifications, smoking cessation, physical exercise on a regular basis).
  • Provide instructions on ways the client can reduce intake of saturated fat and cholesterol:
    • Reduce intake of meat fat (e.g. trim visible fat off meat; replace fatty meats such as fatty cuts of steak, hamburger, and processed meats with leaner products)
    • Reduce intake of milk fat (avoid dairy products containing more than 1% fat)
    • Reduce intake of trans-fatty acids (e.g. avoid stick margarine and shortening and foods such as commercially baked goods that are prepared with these products)
    • Use vegetable oil rather than coconut or palm oil in cooking and food preparation
    • Use cooking methods, such as steaming, baking, broiling, poaching, microwaving, and grilling rather than frying
    • Restrict intake of eggs (recommendations about the number of whole eggs allowed per week vary depending on the client's lipid levels).
Instruct client to take lipid-lowering agents (e.g. HMG-CoA reductase inhibitors [statins], gemfibrozil, niacin) as prescribed.
 
ARRHYTHMIA
The term ‘arrhythmia’ refers to any change from the normal sequence of electrical impulses. The electrical impulses may happen too fast, too slowly, or erratically – causing the heart to beat too fast, too slowly, or erratically. When the heart does not beat properly, it can not pump blood effectively. When the heart does not pump blood effectively, the lungs, brain and all other organs can not work properly and may shut down or be damaged.
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Fig. 1.9: Arrhythmia
Signs and Symptoms: Signs and symptoms depend on the type of heart block you have. First-degree heart block rarely causes symptoms.
Symptoms of second- and third-degree heart block include:
  • Fainting
  • Slow heartbeat
  • Dizziness or light-headedness
  • Irregular heartbeat
  • Fatigue (tiredness)
  • Arrhythmias
  • Shortness of breath
  • Blackouts (Stokes-Adams syndrome)
  • Chest pain
Symptoms of severe cases include:
  • Breathlessness
  • Breathlessness with exertion
  • Breathlessness caused by fever
  • Dizziness
  • Weakness
  • Fainting
  • Fatigue
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Classification
Arrhythmia may be classified by rate (normal sinus rhythm, tachycardia, bradycardia) or mechanism (automaticity, re-entry, junctional, fibrillation). It is also appropriate to classify by site of origin:
 
Sinus Node
  • Sinus bradycardia
  • Sinus tachycardia
  • Sinus arrhythmias
 
Atrial
  • Premature atrial contractions
  • Atrial flutter
  • Atrial fibrillation
 
Junctional Arrhythmias
  • Supraventricular tachycardia (SVT)
  • AV nodal re-entrant tachycardia is the most common cause of paroxysmal supra-ventricular tachycardia (PSVT)
  • Junctional rhythm
  • Junctional tachycardia
  • Premature junctional contraction
 
Ventricular
  • Premature ventricular contractions (PVC)
  • Premature ventricular fibrillation
  • Three premature ventricular grouped together is termed as ‘run of PVCs’. Runs lasting longer than three beats are generally referred to as ventricular tachycardia
    • Accelerated idioventricular rhythm
    • Monomorphic ventricular tachycardia
    • Polymorphic ventricular tachycardia
 
HEART BLOCK
  • First-degree heart block, which manifests as PR prolongation
  • Second-degree heart block:
    • Type 1 Second-degree heart block, also known as Mobitz I or Wenckebach
    • Type 2 Second-degree heart block, also known as Mobitz II
    • Third-degree heart block, also known as complete heart block.
      • SADS (sudden arrhythmic death syndrome)
  • Atrial fibrillation: In atrial fibrillation, the electrical activity of the heart is uncoordinated, with electricity travelling about the upper chambers in a chaotic fashion, causing the upper chambers to quiver (like a ‘bag of worms’) and contract inefficiently or not at all. Atrial fibrillation is common particularly in the elderly and those with heart disease. It 79is also common in patients with heart valve disease who may require surgery to repair or replace the mitral valve. There are a variety of treatment options for atrial fibrillation, including drugs, an ablation—a nonsurgical technique which eliminates the abnormal heart tissue with a catheter, or surgery in some cases.
Fig. 1.10: Atrial fibrillation
  • Atrial flutter: Atrial flutter causes a rapid but coordinated electrical stimulation of the upper chamber of the heart, often leading to a rapid pulse. The atria are stimulated so quickly that they cannot contract or squeeze. This arrhythmia is due to a loop of electricity in the upper chambers of the heart. It is often curable with ablation.
Fig. 1.11: Atrial flutter
  • Supraventricular tachycardia (PSVT): This is a fast heart rhythm from the top part of the heart. In this condition, repeated periods of very fast heartbeats begin and end suddenly. These arrhythmias are usually due to extra connections between the upper and lower chambers of the heart. They are often difficult to control with medication and are often curable with an ablation.
Fig. 1.12: Supraventricular tachycardia
  • Wolff-Parkinson-White syndrome: This is a special type of PSVT. This syndrome involves episodes of a rapid heart rate (tachycardia) caused by abnormal electrical connection in the heart. In people with Wolff-Parkinson-White syndrome, there is an extra (accessory) 80connection between the top and bottom chambers of the heart. Wolff-Parkinson-White syndrome occurs in approximately 4 out of 100,000 people, and is one of the most common causes of fast heart rate disorders (tachyarrhythmia) in infants and children.
  • Premature supraventricular contraction or premature atrial contraction (PAC): Premature beats or extra beats frequently cause irregular heart rhythms. Those that start in the upper chambers are called premature atrial contractions (PACs). Usually no cause can be found and no special treatment is needed.
Fig. 1.13: Premature supraventricular contraction
  • Sick sinus syndrome: The sinus node (heart's pacemaker) does not fire its signals properly, so that the heart rate slows down. Sometimes the rate changes back and forth between a slow (bradycardia) and fast (tachycardia) rate. This most often occurs in the elderly as a result of degenerative changes to the conduction pathways of the heart.
  • Sinus arrhythmia: Cyclic changes in the heart rate during breathing. Common in children and often found in normal, healthy adults. A pacemaker may be required for treatment.
Fig. 1.14: Sinus arrhythmia
  • Sinus tachycardia: The sinus node sends out electrical signals faster than usual, speeding up the heart rate. This is a normal response to exercise.
Fig. 1.15: Sinus tachycardia
  • Multifocal atrial tachycardia: In multifocal atrial tachycardia (MAT), multiple locations within the atria ‘fire’ and initiate an electrical impulse. Most of these impulses are conducted to the ventricles, leading to a rapid heart rate, anywhere from 100 to 250 beats per minute. MAT is most common in people 50 years old and over and it is often seen in patients with lung disease.
  • Premature ventricular contraction (PVC): An electrical signal from the ventricles causes an early heartbeat that generally goes unnoticed. The heart then seems to pause until the next beat of the ventricle occurs in a regular fashion. These are commonly detected in normal, healthy adults.
  • Ventricular fibrillation is where electrical signals in the ventricles fire in a very fast and uncontrolled manner. This causes the lower chambers to quiver, and not pump blood. 81If the person does not receive immediate medical attention and a normal rhythm is not restored quickly, the patient will suffer brain and heart damage and die. Patients who survive this should have a defibrillator (ICD) implanted.
  • Ventricular tachycardia is a rapid, regular heartbeat arising in the ventricles, and the bottom chamber of the heart. When it is occurs, it is usually fatal. About 400,000 people a year die from it. The treatment of choice for this invariably includes an implantable defibrillator and/or medication and/or interventions like ablation to try to minimize or limit the number of shocks.
  • Paroxysmal atrial tachycardia (PAT): PAT is a very rapid supraventricular rhythm that comes from the atria – usually it runs at a very rapid rate, about 250-300 bpm.
Fig. 1.16: Paroxysmal atrial tachycardia
 
HEART BLOCKS
 
Introduction
An atrioventricular block (AV block) involves the impairment of the conduction between the atria and ventricles of the heart. Under normal conditions, SA node in the atria sets the pace for the heart, and these impulses travel down to the ventricles. In an AV block, this message does not reach the ventricles or is impaired along the way. The ventricles of the heart have their own pacing mechanisms, which can maintain a lowered heart rate in the absence of SA stimulation.
Conduction block: Any obstruction of the normal pathways of electrical conduction is called as conduction block
 
Definition
A heart block is a disease of electrical system of the heart. This is opposed to coronary artery disease, which is disease of the blood vessels of the heart.
 
Etiology
The causes of pathological AV block are varied. The blocks may be complete or may only impair the signaling between the SA and AV nodes. Certain AV blocks can also be found as normal variants, such as in athletes or children, and are benign.
  • Ischemia
  • Infarction
  • Fibrosis
  • Drugs
  • Strong vagal stimulation may also produce AV block.
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Types
  • SA nodal block:
    • SA node arrest
    • SA node asystole
    • SA node exit block
  • AV nodal block: There are three types:
  • First-degree AV block: PR interval greater than 0.20 sec.
  • Second-degree AV block:
    • Type 1: Progressive prolongation of PR interval with dropped beats (the PR interval gets longer and longer; finally one beat drops).
    • Type 2: PR interval remains unchanged prior to the P wave which suddenly fails to conduct to the ventricles.
  • Third-degree AV blocks: No association between P waves and QRS complexes.
  • Infra-Hisian bundle block: Infra-Hisian block describes block of the distal conduction system. Types of infra-Hisian block include:
Type 2 second-degree heart block (Mobitz II):
  • Left bundle branch block:
    • Left anterior fascicular block
    • Left posterior fascicular block
  • Right bundle branch block
 
SA NODAL BLOCK
This is sinus exit block. The sinus node fires normally, but wave of depolarization is immediately blocked and is not transmitted into the arterial tissue. ECG shows just pause in normal cardiac cycle.
  • SA node arrest
  • SA node asystole
  • Sinus node stops firing or becomes silent
  • ECG shows flat line without prolongation and restoring electrical activity after one beat
  • ECG shows flat line without restoring electrical activity
  • SA node exit block
The sinus node continues to fire but the wave of depolarization is blocked immediately as it exits the node. Again, ECG shows no electrical activity.
Fig. 1.17: SA node block
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Atrioventricular Block
 
Definition
Conduction block between sinus node and up to and including AV node.
 
First-degree Atrioventricular Block
 
Introduction
  • The electrical impulses are slowed as they pass through the conduction system, but they all successfully reach the ventricles.
  • First-degree AV block occurs when all the impulses are conducted through AV node to ventricles at a rate slower than normal. It has a prevalence in the normal (young adult) population of 0.65–1.1% and the incidence is 0.13 per 1000 persons.
  • PR prolongation is a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.20 seconds.
 
Characteristics
  • Ventricular or arterial rate: Depends upon underlying rhythm
  • Ventricular or arterial rhythm: Depends upon underlying rhythm
  • QRS shape and duration: Usually normal, but may be abnormal
  • P-wave: In front of the QRS complex; shows sinus rhythm, regular rhythm
  • PR interval: Greater than 0.20 seconds
  • P : QRS ratio: 1:1
Fig. 1.18: AV block
Interpretation: 1st-degree AV block
--PR interval:- > 0.20 s
  • Rate: 60 bpm
  • Regularity: regular
  • P-wave: normal
  • PR interval: > 0.20 sec. (0.36 sec.)
  • QRS duration: Normal 0.08 sec.
  • Causes: The most common cause of first-degree heart block in an AV nodal disease is prolonged conduction delay in the AV node or bundle of His.
    • Enhanced vagal tone (for example, in athletes)
    • Myocarditis
    • Acute inferior wall myocardial infarction
    • Electrolyte disturbances
    • Medication
    • Drugs: Calcium channel blockers, beta-blockers, cardiac glycosides, and anything that increases cholinergic activity, such as cholinesterase inhibitors.
    • 84Hypokalemia or hyperkalemia
    • Hypothyroidism
    • Digitalis toxicity
 
Diagnostic Test
ECG: PR interval measurement
  • The normal PR interval is from 120 ms to 200 ms in length. This is measured from the initial deflection of the P-wave to the beginning of the QRS complex.
  • In first-degree heart block, the diseased AV node conducts the electrical activity more slowly. This is seen as a PR interval greater than 200 ms in length on the surface ECG. It is usually an incidental finding on a routine ECG.
  • Electrolyte and drug screens: First-degree heart block does not require any particular investigations except for electrolyte and drug screens, especially if an overdose is suspected.
 
Treatment
  • Cautious use of digitalis glycosides.
  • Atropine is effective if PR interval exceeds 0.26 sec. or bradycardia develops.
  • Identifying and correcting electrolyte imbalances and withholding any offending medications.
  • This condition does not require admission unless there is an associated myocardial infarction.
  • It may require outpatient follow-up
  • Regular monitoring of the ECG.
 
Prognosis
Isolated first-degree heart block has no direct clinical consequences. There are no symptoms or signs associated with it. It was originally thought of as having a benign prognosis. The presence of a prolonged PR interval or first-degree AV block doubled the risk of developing atrial fibrillation (irregular heartbeat), tripled the risk of requiring an artificial pacemaker, and was associated with a small increase in mortality. This risk was proportional to the degree of PR prolongation.
 
SECOND-DEGREE ATRIOVENTRICULAR BLOCK
 
Introduction
Second-degree AV block is a disease of the electrical conduction system of the heart. It refers to a conduction block between the atria and ventricles.
The presence of second-degree AV block is diagnosed when one or more (but not all) of the atrial impulses fail to conduct to the ventricles due to impaired conduction.
The electrical impulses are delayed further and further with each heartbeat until a beat fails to reach to the ventricles entirely. It sometimes causes dizziness and/or other symptoms. People with normal conduction systems may sometimes have type 1 second-degree heart block when they sleep.
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Types
There are two nondistinct types of second-degree AV called Type 1 and Type 2. In both types, a P-wave is blocked from initiating a QRS complex; but, in Type 1, there are increasing delays in each cycle before the omission, whereas in Type 2, there is no such pattern.
  • Type 1 second-degree heart block is considered a more benign entity than type 2 second-degree heart block. Both types are named after Woldemar Mobitz. Type I is also named for Karel Frederik Wenckebach and type II is also named for John Hay.
 
Second-degree AV block, Type 1/Mobitz I (Wenckebach)
  • Type 1 second-degree AV block, also known as Mobitz I or Wenckebach periodicity, is always a disease of the AV node. It occurs when there is repeating pattern in which all but one of a series of atrial impulses conducted through AV node into the ventricles (e.g. every 4 or 5 impulses are conducted). Each impulse takes a longer time for conduction than one before, until one impulse is fully blocked. Because AV node was not depolarized by the blocked atrial impulse, the AV node has a time to fully repolarize, so that next atrial impulse can be conducted within the shortest period of time.
 
Characteristics
  • Ventricular or arterial rate: Depends upon underlying rhythm
  • Ventricular or arterial rhythm: PP interval is regular if the patient has an underlying normal sinus rhythm; the RR interval characteristically reflects a pattern of change. Starting from the RR interval which is longest, the RR interval is gradually shorter until there is another long RR interval.
  • QRS shape and duration: Usually normal, but may be abnormal
  • P-wave: In front of the QRS complex, shape depends upon underlying rhythm
  • PR interval: PR interval becomes longer with each succeeding ECG complex until there is a P-wave not followed by a QRS. The changes in the PR interval are repeated between each dropped ‘QRS’, creating a pattern in the regular PR interval measurements.
  • P : QRS ratio: 3:2, 4:3, 5:4 and so on...
    Fig. 1.19: Second-degree AV block
  • Interpretation: Second degree AV block Type I
  • PR interval progressively lengthens, then the impulse is completely blocked (P-wave not followed by QRS).
  • Rate: 50 bpm
  • Regularity: Irregular (atrial rhythm regular and ventricular rhythm irregular)
  • P wave: normal
  • PR interval: lengthens
  • QRS duration: 0.08 sec.
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Causes
  • Inferior wall MI
  • Cardiac surgery
  • Acute rheumatic fever
  • Vagal stimulation
  • Digitalis toxicity; propranolol, quinidine, procainamide.
 
Treatment
  • This is almost always a benign condition for which no specific treatment is needed.
  • Atropine is effective for treating second degree type 1
  • Temporary pacemaker implantation for symptomatic bradycardia
  • Discontinuation of digitalis glycosides.
  • In symptomatic cases, intravenous atropine or proterenol may transiently improve conduction.
 
Second-degree AV block, Type II/Mobitz II
 
Introduction
Type 2 second-degree AV block, also known as ‘Mobitz II’, is almost always a disease of the distal conduction system (His-Purkinje System).
Type 2 second-degree AV block occurs when only some of the atrial impulses are conducted through the AV node into the ventricles. Mobitz II heart block is characterized on a surface ECG by intermittently nonconducted P-waves not preceded by PR prolongation and not followed by PR shortening. The medical significance of this type of AV block is that it may progress rapidly to complete heart block, in which no escape rhythm may emerge. In this case, the person may experience a Stokes-Adams attack, cardiac arrest, or sudden cardiac death.
With this condition, some of the electrical impulses are unable to reach the ventricles. This condition is less common than Type I, and is more serious.
 
Characteristics
  • Ventricular or arterial rate: Depends upon underlying rhythm
  • Ventricular or arterial rhythm: PP interval is regular if the patient has an underlying normal sinus rhythm; the RR interval is regular but may be irregular, depending on the ratio P : QRS.
  • QRS shape and duration: Usually abnormal, but may be normal.
  • P-wave: In front of the QRS complex; shape depends upon underlying rhythm.
  • PR interval: PR interval is constant for those P-waves just before QRS complexes.
  • P : QRS ratio: 2:1, 3:1, 4:1, 5:1 and so on...
    Fig. 1.20: Type 2 second-degree AV block
87Interpretation: 2nd-degree AV block Type II
Occasional P-waves are completely blocked (P-wave not followed by QRS).
  • Rate: 40 bpm
  • Regularity: Regular (both atrial or ventricular)
  • P-wave: Normal
  • PR interval: 0.14 sec.
  • PP interval: Constant
  • QRS duration: Periodically absent
 
Etiology
  • Conduction is all or nothing (no prolongation of PR interval)
  • Typically block occurs in the bundle of His
  • Severe coronary artery disease
  • Anterior wall MI
  • Acute myocarditis
  • Digitalis toxicity
 
Treatment
  • The definitive treatment for this form of AV block is an implanted temporary and permanent pacemaker
  • Isoproterenol for symptomatic bradycardia
  • Discontinuation of digitalis glycosides
Difference between Mobitz type-I and Mobitz type-II
Mobitz type-I
Mobitz type-II
  • Also known as Wenckebach block
  • Also known as John Hay block
  • Mobitz I is usually due to reversible conduction block at the level of the AV node
  • Mobitz II is usually due to conduction block below the level of the AV node and above from bundle branches
  • It is transient and benign
  • It occurs suddenly
  • More common type
  • Less common type
  • PR interval is prolonged followed by missing of QRS complex
  • PR interval is normal followed by missing of QRS complex
  • Rarely progressive 3rd-degree block
  • Progressively causes 3rd degree block
  • No need for treatment often
  • It requires pacemaker insertion
 
Third-degree Atrioventricular Block (Complete Heart Block)
 
Introduction
  • Third-degree AV block, also known as complete heart block, is a medical condition in which the impulse generated in the SA node in the atrium does not propagate to the ventricles.
  • Lead I and II demonstrating complete AV block. Note that the P-waves are not related to the QRS complexes (PP interval and QRS interval, both are constant), demonstrating 88that the atria are electrically disconnected from the ventricles. The QRS complexes represent an escape rhythm arising from the ventricle.
  • The QRS complexes with a regular R-to-R interval represent the second rhythm. The PR interval will be variable, as the hallmark of complete heart block is no apparent relationship between P waves and QRS complexes.
  • One of the pathognomonic characteristics of this block is the absolute absence of the opportunity for atrial impulses to enter and capture the ventricles (unlike AV dissociation with functional block) due to the organic nature of block (e.g. fibrosis, calcification, or infiltration of the node). In the presence of complete heart block, fusion or capture beats will never be seen. Patients with third-degree AV block typically experience bradycardia (an abnormally low measured heart rate), hypotension, and, at times, hemodynamic instability. In some cases, exercising may be difficult, as the heart cannot react quickly enough to sudden changes in demand or sustain the higher heart rates required for prolonged activity.
 
Characteristics
  • Ventricular or arterial rate: Depends upon escape rhythm and also upon underlying atrial rhythm.
  • Ventricular or arterial rhythm: PP interval is regular, RR interval is regular. PP interval is not equal to RR interval.
  • QRS shape and duration: Depends upon escape rhythm; with junctional rhythm, QRS shape and duration are usually normal; with idioventricular rhythm, QRS shape and duration are usually abnormal.
  • P-wave: Depends upon underlying rhythm
  • PR interval: Very irregular
  • P : QRS ratio: More P wave than QRS complexes
    Fig. 1.21: Third-degree AV block
  • Interpretation: 3rd-degree AV block
  • The P-waves are completely blocked in the AV junction; QRS complexes originate independently from below the junction.
  • Rate: 40 bpm
  • Regularity: Regular (atrial regular and ventricular rate slow and regular)
  • P-wave: No relation to QRS
  • PR interval: None
  • QRS duration: Wide (> 0.12 sec.)
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Etiology
  • There is complete block of conduction in the AV junction. So, the atria and ventricles form impulses independently of each other. Without impulses from the atria, the ventricles own intrinsic pacemaker kicks in at around 30–45 beats/minute.
  • Many conditions can cause third-degree heart block, but the most common cause is coronary ischemia. Progressive degeneration of the electrical conduction system of the heart can lead to third-degree heart block. This may be preceded by first-degree AV block, second-degree AV block, bundle branch block, or bifascicular block. In addition, acute myocardial infarction may present with third-degree AV block.
  • An inferior wall myocardial infarction: It may cause damage to the AV node, causing third-degree heart block. In this case, the damage is usually transitory. Studies have shown that third-degree heart block in the setting of an inferior wall myocardial infarction typically resolves within 2 weeks. The escape rhythm typically originates in the AV junction, producing a narrow complex escape rhythm.
  • An anterior wall myocardial infarction: It may damage the distal conduction system of the heart, causing third-degree heart block. This is typically extensive, permanent damage to the conduction system, necessitating a permanent pacemaker to be placed. The escape rhythm typically originates in the ventricles, producing a wide complex escape rhythm.
  • Third-degree heart block may also be congenital and has been linked to the presence of lupus in the mother. It is thought that maternal antibodies may cross the placenta and attack the heart tissue during gestation. The cause of congenital third-degree heart block in many patients is unknown.
 
PROGNOSIS
The prognosis of patients with complete heart block is generally poor without artificial pacemaker therapy.
 
Treatment
  • Pacemaker: Third-degree AV block can be treated by use of a dual-chamber artificial pacemaker. This type of device typically listens for a pulse from the SA node and sends a pulse to the AV node at an appropriate interval, essentially completing the connection between the two nodes. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation, two common secondary conditions that can accompany third-degree AV block.
  • Treatment may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce risk factors associated with heart attack and stroke.
  • Treatment in emergency situations ultimately involves electrical pacing. However, the American Heart Association states that giving a trial of atropine while waiting for the pacer to be set up is acceptable.
  • Atropine is effective for treating early heart blocks (1st-degree and 2nd-degree type 1) but generally thought to have no effect on 3rd-degree blocks.
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Difference Between 1, 2, 3-degree Block
Fig. 1.22: Types of heart blocks
 
BUNDLE BRANCH BLOCK
 
Anatomy and Physiology
The heart's electrical activity begins in the sinoatrial node (the heart's natural pacemaker), which is situated on the upper right atrium. The impulse travels next through the left and right atria and summates at the atrioventricular node. From the AV node, the electrical impulse travels down the Bundle of His and divides into the right and left bundle branches. The right bundle branch contains one fascicle. The left bundle branch subdivides into two fascicles: the left anterior fascicle and the left posterior fascicle.
Other sources divide the left bundle branch into three fascicles:
  • The left anterior
  • The left posterior
  • The left septal fascicle.
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Normal Conduction System
Sinoatrial node (SA node)→AV node→Bundle of His→Bundle branches→Purkinje fibers
 
Introduction
Bundle branch block is a condition in which there is a delay or obstruction along the pathway that electrical impulses travel to make the heart beat. The delay or blockage may occur on the pathway that sends electrical impulses to the left or the right side of the heart. Bundle branch block sometimes makes it harder for heart to pump blood efficiently through circulatory system.
When a bundle branch or fascicle becomes injured (due to underlying heart disease, myocardial infarction, or cardiac surgery), it may cease to conduct electrical impulses appropriately. This results in altered pathways for ventricular depolarization. Since the electrical impulse can no longer use the preferred pathway across the bundle branch, it may move instead through the muscle fibers in a way that both slow down the electrical movement and change the directional propagation of the impulses.
 
Definition
When a bundle branch or fascicle becomes injured, it may cease to conduct electrical impulses appropriately, resulting in altered pathways for ventricular depolarization called bundle block.
 
Types
  • Right bundle block
  • Left bundle block:
    • Left anterior fascicular block: In this case, only the anterior half of the left bundle branch (fascicle) is involved.
    • Left posterior fascicular block: In this case, only the posterior half of the left bundle branch (fascicle) is involved.
NOTE: A mnemonic to remember the ECG change is—in left bundle branch block, there is a W in V1 and an M in V6 and with an RBBB, there is an M in lead V1 and a W in lead V6.
 
RIGHT BUNDLE BRANCH BLOCK
 
Characteristics of QRS Complex
For RBBB, the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2).
  • The heart rhythm must originate above the ventricles (i.e. sinoatrial node, atria or atrioventricular node) to activate the conduction system at the correct point.
  • The QRS duration must be more than 100 ms (incomplete block) or more than 120 ms (complete block)
  • There should be a terminal R-wave in lead V1
  • There should be a slurred S wave in leads V1 and V6.
  • ST depression and T-wave inversion seen leads V1, V2
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Fig. 1.23: Bundle branch block
 
Causes
  • Congenital abnormalities: Such as atrial septal defect, a hole in the wall separating the upper chambers of the heart.
  • A heart attack (myocardial infarction)
  • A viral or bacterial infection of the heart muscle (myocarditis)
  • High blood pressure (hypertension)
  • Scar tissue that develops after heart surgery
  • A blood clot in the lungs (pulmonary embolism)
 
LEFT BUNDLE BRANCH BLOCK
Left bundle branch block (LBBB) is a cardiac conduction abnormality seen on the electrocardiogram (ECG). In this condition, activation of the left ventricle is delayed, which causes the left ventricle to contract later than the right ventricle.
 
Characteristics of QRS Complex
For LBBB, the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads—V1 and V2).
  • The heart rhythm must be supraventricular in origin
  • The QRS duration must be ≥ 120 ms
  • There should be a QS or rS complex in lead V1
  • There should be an RSR' wave in lead V6.
  • ST depression and T-wave inversion seen in leads V1, V2
Fig. 1.24: Left bundle branch block
 
Causes
  • Aortic stenosis
  • Dilated cardiomyopathy
  • 93Acute myocardial infarction
  • Extensive coronary artery disease
  • Primary disease of the cardiac electrical conduction system
  • Long-standing hypertension leading to aortic root dilatation and subsequent aortic regurgitation
 
Classification
 
Left Anterior Fascicular Block
Definition: It is caused by only the anterior half of the left bundle branch being defective. It is manifest on the ECG by left axis deviation. It is much more common than left posterior fascicular block.
  • In left anterior fascicular block, impulses are conducted to the left ventricle via the left posterior fascicle, which inserts into the inferoseptal wall of the left ventricle along its endocardial surface.
  • On reaching the left ventricle, the initial electrical vector is, therefore, directed downwards and rightwards (as excitation spreads outwards from endocardium to epicardium), producing small R-waves in the inferior leads (II, III, aVF) and small Q-waves in the left-sided leads (I, aVL).
  • The major wave of depolarization then spreads in an upward and leftward direction, producing large positive voltages (tall R-waves) in the left-sided leads and large negative voltages (deep S-waves) in the inferior leads.
  • This process takes about 20 milliseconds longer than simultaneous conduction via both fascicles, resulting in a slight widening of the QRS.
  • The impulse reaches the left-sided leads later than normal, resulting in an increased R-wave peak time (the time from onset of the QRS to the peak of the R-wave) in aVL.
    Fig. 1.25: Fascicular block
 
Characteristics
  • Left axis deviation (usually between –45 and –90 degrees)
  • Small Q-waves with tall R-waves (= ‘QR complexes’) in leads I and aVL
  • Small R-waves with deep S-waves (= ‘RS complexes’) in leads II, III, aVF
  • QRS duration normal or slightly prolonged (80–110 ms)
  • Prolonged R-wave peak time in aVL > 45 ms
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Left Posterior Fascicular Block
It is a condition where the left posterior fascicle, i.e. the backside of the left cardiac bundle, does not conduct electrical impulses from AV node. The electricity then has to go through the other fascicle and thus is a frontal right axis deviation seen on ECG.
 
Characteristics
  • Right axis deviation (> 120 degrees)
  • Small Q-waves with Tall R-waves: In leads II, III, aVF
  • Small R-waves with deep S-waves (= ‘RS complexes’) in leads I and aVL
  • QRS: Slightly widened or slightly prolonged (100–120 ms)
  • Prolonged R-wave peak time in aVF
  • Increased QRS voltage in limb leads
  • No evidence of right ventricular hypertrophy
    Fig. 1.26: Changes in fascicular block
Left anterior fascicular block
Left posterior fascicular block
  • Normal QRS duration and no ST segment or T-wave changes
  • Normal QRS duration and no ST segment or T-wave changes
  • Left axis deviation
  • Right axis deviation
  • No other cause of left axis deviation is present
  • No other cause of right axis deviation is present
  • Lead I is positive and Lead avF is negative
  • Lead I is negative and Lead avF is positive
 
Clinical Manifestations
  • Fainting (syncope)
  • Presyncope
  • Bradycardia
  • Light-headedness
  • Dizziness
 
DIAGNOSTIC TESTS
 
ECG
Depolarization of the Bundle Branches and Purkinje fibers are seen as the QRS complex on the ECG. Therefore, a conduction block of the bundle branches would be reflected as a change in the QRS complex. With bundle branch blocks, you will see two changes on the ECG.
  • 95QRS complex widens (> 0.12 sec).
  • QRS morphology changes (varies depending on ECG lead, and if it is a right vs. left bundle branch block).
    • A bundle branch block can be diagnosed when the duration of the QRS complex on the ECG exceeds 120 ms.
    • A right bundle branch block typically causes prolongation of the last part of the QRS complex, and may shift the heart's electrical axis slightly to the right.
    • The ECG will show a terminal R-wave in lead V1 and a slurred S-wave in lead I.
    • Left bundle branch block widens the entire QRS, and in most cases, shifts the heart's electrical axis to the left.
    • The ECG will show a QS or RS complex in lead V1 and a monophasic R-wave in lead I.
 
Treatment
  • Patients with LBBB require complete cardiac evaluation, and those with LBBB and syncope or near-syncope may require a pacemaker.
  • Some patients with LBBB, a markedly prolonged QRS (usually > 150 ms), and systolic heart failure may benefit from a biventricular pacemaker, which allows for better synchrony of heart contraction.
 
Combination of Bundle Branch Block and Hemiblock
It is also known as bi fascicular block refers to combination of either left anterior or left posterior fascicular or hemi block with right bundle branch block. Only one fascicle of left bundle branch supplying the bulk of both ventricle
Right bundle branch block
Left anterior hemiblock
  • QRS wider than 0.12 sec
  • Left axis deviation
  • RSR' in V1 and V2
  • Lead I is positive and Lead avF is negative
Right bundle branch block
Right anterior hemiblock
  • QRS wider than 0.12 sec
  • Right axis deviation
  • RSR' in V1 and V2
  • Lead I is negative and Lead avF is positive
Combination of AV block, bundle branch blocks and hemiblock:
  • Is there any AV block?: Relationship between P- and QRS-wave complex
  • Is there any bundle branch block?: Check pericardial leads for wide QRS complex and ST segment and T-wave changes
  • Is there any hemi block?: Check for axis deviation.
 
SUDDEN ARRHYTHMIC DEATH SYNDROME (SADS)
 
Introduction
SADS, or sudden arrhythmic death syndrome, is a term (sudden unexpected death syndrome) used to describe sudden death due to cardiac arrest brought on by an arrhythmia in the absence of any structural heart disease on autopsy. The most common cause of sudden death in the US is coronary artery disease.
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Etiology
  • Viral myocarditis
  • Long QT syndrome
  • Brugada syndrome
  • Catecholaminergic polymorphic ventricular tachycardia
  • Hypertrophic cardiomyopathy
  • Arrhythmogenic right ventricular dysplasia.
 
Signs and Symptoms
  • Some arrhythmias do not cause symptoms, and are not associated with increased mortality. However, some asymptomatic arrhythmias are associated with adverse events.
  • Palpitations: The most common symptom of arrhythmia is an abnormal awareness of heartbeat, called palpitations. These may be infrequent, frequent, or continuous.
Others include:
  • A higher risk of blood clotting within the heart
  • A higher risk of insufficient blood being transported to the heart because of weak heartbeat.
  • Increased risks of embolization and stroke
  • Heart failure
  • Sudden cardiac death
  • Lower blood pressure
  • Lightheadedness or dizziness, or syncope (fainting).
 
DIFFERENTIAL DIAGNOSIS
 
Normal Electrical Activity
  • Bradycardias: A slow rhythm (less than 60 beats/min) is bradycardia. This may be caused by a slowed signal from the sinus node (sinus bradycardia) or by blocking of the electrical impulse on its way from the atria to the ventricles (AV block or heart block). Heart block comes in varying degrees and severity. It may be caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node. Bradycardias may also be present in the normally functioning heart of endurance athletes or other well-conditioned persons.
    Fig. 1.27: Bradycardia in SADS
  • Tachycardias: In adults and children over 15, resting heart rate faster than 100 beats/minute is tachycardia. Tachycardia may result in palpitation; tachycardia is not an 97arrhythmia. Increased heart rate is a normal response to physical exercise or emotional stress. This is mediated by the sympathetic nervous system on the sinus node and is called sinus tachycardia. Other things that increase sympathetic nervous system activity in the heart include ingested or injected substances, such as caffeine or amphetamines, and an overactive thyroid gland (hyperthyroidism).
  • Abnormal impulses can begin by one of the three mechanisms: Automaticity, reentry or triggered activity:
    • Automaticity: Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus and is, by definition, a pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the atrioventricular node, are the least dangerous dysrhythmias; but they can still produce a decrease in the heart's pumping efficiency, because the signal reaches the various parts of the heart muscle with different timing than usual and can be responsible for poorly coordinated contraction.
    • Re-entry: Excitation in the myocardium is considered to be the main mechanism of life-threatening cardiac arrhythmias. In particular, the autowave reverberator is typical in thin walls of the atria, with the atrial flutter producing. Re-entry is also responsible for most paroxysmal supraventricular tachycardia, and dangerous ventricular tachycardia. These types of re-entry circuits are different from WPW syndromes in which the real pathways existed.
    • Triggered beats: Triggered beats occur when problems at the level of the ion channels in individual heart cells result in abnormal propagation of electrical activity and can lead to sustained abnormal rhythm. They are relatively rare and can result from the action of antiarrhythmic drugs.
 
Diagnostic Evaluation
  • Electrocardiogram (ECG or EKG): A picture of the electrical impulses travelling through the heart muscle. An ECG is recorded on graph paper, through the use of electrodes (small, sticky patches) that are attached to your skin on the chest, arms and legs.
  • Ambulatory monitors, such as:
    • Holter monitor: A small portable recorder that is attached to electrodes on your chest. It continuously records your heart's rhythm for 24 hours.
    • Transtelephonic monitor: A small monitor is attached to electrode leads, usually on your finger or wrist. With the help of this device, your heart's rhythm is transmitted over the phone line to your doctor's office.
    • Transtelephonic monitor with a memory loop: A small, portable recorder that is worn continuously for an extended period of time to record and save information about your heart's rhythm around the time you experience an arrhythmia. The recording is triggered by pushing a button (event button). The rhythm is recorded, saved and transmitted over the phone line.
  • Stress test: A test used to record arrhythmias that start or are worsened with exercise. This test may also be helpful in determining if there is underlying heart disease or coronary artery disease associated with an arrhythmia.
  • 98Echocardiogram: A type of ultrasound used to provide a view of the heart to determine if there is heart muscle or valve disease that may be causing an arrhythmia. This test may be performed at rest or with activity.
  • Cardiac catheterization: Using a local anesthetic, a catheter (small, hollow, flexible tube) is inserted into a blood vessel and guided to the heart with the help of an X-ray machine. A contrast dye is injected through the catheter so X-ray movies of your coronary arteries, heart chambers and valves may be taken. This test helps your doctor determine if the cause of an arrhythmia is coronary artery disease. This test also provides information about how well your heart muscle and valves are working.
  • Electrophysiology study (EPS): A special heart catheterization that evaluates your heart's electrical system. Catheters are inserted into your heart to record the electrical activity. The EPS is used to find the cause of the abnormal rhythm and determine the best treatment for you. During the test, the arrhythmia can be safely reproduced and terminated.
  • Tilt table test (also called a passive head-up tilt test or head upright tilt test): Records your blood pressure and heart rate on a minute-by-minute basis while the table is tilted in a head-up position at different levels. The test results may be used to evaluate heart rhythm, blood pressure and sometimes other measurements as you change position.
 
Management
 
Physical Maneuvers
A number of physical acts can increase parasympathetic nervous supply to the heart, resulting in blocking of electrical conduction through the AV node. This can slow down or stop a number of arrhythmias that originate above or at the AV node. Parasympathetic nervous supply to the heart is via the vagus nerve, and these maneuvers are collectively known as vagal maneuvers.
 
Antiarrhythmic Drugs
There are many classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within these classes. Although the goal of drug therapy is to prevent arrhythmia, nearly every antiarrhythmic drug has the potential to act as a proarrhythmic, and so must be carefully selected and used under medical supervision.
 
Other Drugs
Arrhythmias promote blood-clotting within the heart, and increase risk of embolus and stroke. Anticoagulant medications such as warfarin and heparins, and anti-platelet drugs such as aspirin can reduce the risk of clotting.
 
Cardioversion
It is either achieved pharmacologically or via the application of a shock synchronized to the underlying heartbeat. It is used for treatment of supraventricular tachycardias. In elective cardioversion, the recipient is usually sedated or lightly anesthetized for the procedure.
 
Defibrillation
It differs in that the shock is not synchronized. It is needed for the chaotic rhythm of ventricular fibrillation and is also used for pulseless ventricular tachycardia. Often, more 99electricity is required for defibrillation than for cardioversion. In most defibrillation cases, the recipient has lost consciousness; so there is no need for sedation.
 
Electrical cautery
In specialized catheter laboratories, they use fine probes inserted through the blood vessels to map electrical activity from within the heart. This allows abnormal areas of conduction to be located very accurately, and subsequently destroyed with heat, cold, electrical or laser probes.
 
Nursing Management
 
Nursing Assessment
  • General complaints: Palpitations, dizziness, light-headedness, chest pain, syncope
  • Physical examination:
    • Skin: Pallor, Diaphoresis
    • Arterial pulse: Normal, Tachycardia, Bradycardia
    • Rhythm: Normal, Irregular
    • Hypotension
    • Mental status: Confusion, Agitation, Anxiety
 
Drug History
  • Names, dosages of current antidysrhythmic drugs
  • Laboratory values: Electrolyte imbalance
  • Use of artificial stimulants: Narcotics, amphetamine
Nursing diagnosis: Decreased cardiac output related to electrical and mechanical dysfunction
Goal: To monitor and maintain cardiac output
Interventions
  • Assess the patient continuously for rate, rhythm and level of consciousness.
  • Monitor vital signs frequently.
  • Monitor and record ECG changes.
  • Notify the physician for if any change can occur in normal parameters.
  • Administer antidysrhythmic drugs as order or monitor serum blood level.
  • Administer oxygenation therapy.
Nursing diagnosis: Decreased tissue perfusion related to decreased cardiac output
Goal: To maintain tissue perfusion.
Interventions
  • Monitor pulse rate.
  • Monitor central venous pressure.
  • Provide sterile dressing on wound.
  • Give IV fluid to the patient.
  • Give oxygenation therapy.
  • Epinephrine drugs are first line drug used for its alpha adrenergic effect to increase perfusion pressure, e.g. adrenaline
  • 100Dopamine is given to stimulate beta adrenergic cell.
  • Norepinephrine drugs are used for its alpha adrenergic effect to increase perfusion pressure.
  • Vagal maneuver induces vagal stimulation of cardiac conduction system.
  • Massaging the carotid sinus causes vagal stimulation.
  • Sodium bicarbonate is used for those who are having hyperkalemia.
  • Pacemaker should be implanted.
Nursing diagnosis: Anxiety related to death secondary to altered heart rate.
Goal: To reduce anxiety level.
Interventions
  • Assess the anxiety level and level of understanding.
  • Provide continuous explanation about the health status and management.
  • Offer reassurance to the patient and their family members.
  • Administer sedation to reduce anxiety level.
  • Provide referral for continued supportive counseling to deal with fear and anxiety.
Nursing diagnosis: Chest pain related to electrical and mechanical dysfunction.
Goal: To reduce pain.
Interventions
  • Assess for the presence of pain, the scale and intensity of pain.
  • Teach the client about pain management and relaxation with distraction.
  • Secure the chest tube to restrict movement and avoid irritation.
  • Assess pain reduction measures.
Nursing diagnosis: Ineffective breathing pattern related to disease condition as evidenced by breathlessness.
Goal: To maintain breathing pattern.
Interventions
  • Open the airway with head tilt, chin lift, jaw thrust
  • Set the position to maximize ventilation
  • Use tools airway
  • Perform chest physiotherapy
  • Teach breathing deeply and coughing effectively
  • Perform suction
  • Auscultation of breath sounds
  • Give bronchodilators (collaboration)
  • Oxygenation therapy
Nursing diagnosis: Activity intolerance related to conduction problem as evidenced by tachycardia.
Goal: To maintain activity status of the patient.
101Interventions
  • Check the vital signs of the patient.
  • Check for the activity level of the patient.
  • Provide small activity.
  • Involve in activities of daily living.
  • Avoid staining activity.
Nursing diagnosis: Knowledge deficit about dysrhythmia and its treatment.
Goal: To provide knowledge about disease and its treatment.
Interventions
  • Explain the dysrhythmias and its side effects.
  • Describe the medications regimen and its rationale.
  • Explain the need for therapeutic serum level of the medication.
  • Describe the plan to eradicate or limit the factors that contribute to the dysrhythmias.
  • State the actions to take in the event of an emergency.
 
Management
The goal of management is to:
  • Prevent blood clots from forming to reduce stroke risk.
  • Control your heart rate within a relatively normal range.
  • Restore a normal heart rhythm, if possible.
  • Treat heart disease/condition that may be causing arrhythmia.
  • Reduce other risk factors for heart disease and stroke.
Medications: Common drugs used to treat arrhythmias are –
  • Antiarrhythmic drugs:
    • Amiodarone
    • Bepridil hydrochloride
    • Disopyramide
    • Dofetilide
    • Dronedarone
    • Flecainide
    • Ibutilide
    • Lidocaine (Xylocaine)
    • Procainamide
    • Propafenone
    • Propranolol
    • Quinidine
    • Sotalol
    • Tocainide
  • Beta-blockers decrease the heart rate and cardiac output, which lowers blood pressure by blocking the effects of adrenalin. They are also used with therapy for cardiac arrhythmias and in treating angina pectoris.
    • 102Acebutolol
    • Atenolol
    • Betaxolol
    • Bisoprolol/hydrochlorothiazide
    • Carteolol
    • Esmolol
    • Metoprolol
    • Nadolol
    • Penbutolol
    • Propranolol
    • Timolol
  • Anticoagulants
    • Anticoagulants (blood thinners) work by making it harder for the blood to clot, or coagulate, warfarin.
 
Avoid
Certain substances can contribute to an irregular heartbeat, including:
  • Caffeine
  • Tobacco
  • Alcohol
  • Cold and cough medications
  • Appetite suppressants
  • Psychotropic drugs
  • Beta-blockers for high blood pressure
  • Street drugs such as cocaine, marijuana and ‘speed’ or methamphetamines
 
Manage Your Risk Factor
Just having an arrhythmia increases your risk of heart attack, cardiac arrest and stroke. Work with your health care team and follow their instructions to control other risk factors:
  • Reduce high blood pressure
  • Control cholesterol levels
  • Lose excess weight
  • Eat a heart-healthy diet
  • Avoid tobacco smoke
  • Enjoy regular physical activity
 
ECG—ELECTRICAL CONDUCTION, BASIC ECG, 12-LEAD ECG, AXIS DETERMINATION
 
Normal Electrical Conduction of the Heart
The normal electrical conduction in the heart allows the impulse that is generated by the sinoatrial node (SA node) of the heart to be propagated to (and stimulate) the myocardium (cardiac muscle). The myocardium contracts after stimulation. It is the ordered stimulation 103of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped throughout the body.
 
Electrochemical Mechanism
Cardiac muscle has some similarities to neurons and skeletal muscle, as well as important unique properties. Like a neuron, a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening of voltage-gated ion channels and a flood of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels and release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay, potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state.
  • S-A node (sinoatrial node)—known as the heart's natural pacemaker, the S-A node has special cells that create the electricity that makes your heart beat.
  • A-V node (atrioventricular node)—the A-V node is the bridge between the atria and ventricles. Electrical signals pass from the atria down to the ventricles through the A-V node.
  • His-Purkinje system—the His-Purkinje system carries the electrical signals throughout the ventricles to make them contract. The parts of the His-Purkinje system include:
    • Right bundle branch
    • Left bundle branch
    • Purkinje fibers (the end of the system)
 
Conduction Pathway
Signals arising in the SA node stimulate the atria to contract and travel to the AV node. After a delay, the stimulus is conducted through the bundle of His to the Purkinje fibers and the endocardium at the apex of the heart, then finally to the ventricular epicardium.
 
Depolarization and the ECG
Fig. 1.28: Normal ECG
  • 104SA node: P-wave: Under normal conditions, electrical activity is spontaneously generated by the SA node, the physiological pacemaker. This electrical impulse is propagated throughout the right atrium, and through Bachmann's bundle to the left atrium, stimulating the myocardium of the atria to contract. The conduction of the electrical impulse throughout the atria is seen on the ECG as the P-wave.
  • As the electrical activity is spreading throughout the atria, it travels via specialized pathways, known as internodal tracts, from the SA node to the AV node.
 
AV Node/Bundles: PR Interval
The AV node functions as a critical delay in the conduction system. Without this delay, the atria and ventricles would contract at the same time, and blood would not flow effectively from the atria to the ventricles. The delay in the AV node forms much of the PR segment on the ECG. And part of atrial repolarization can be represented by PR segment.
The distal portion of the AV node is known as the bundle of His. The bundle of His splits into two branches in the interventricular septum, the left bundle branch and the right bundle branch. The left bundle branch activates the left ventricle, while the right bundle branch activates the right ventricle. The left bundle branch is short, splitting into the left anterior fascicle and the left posterior fascicle. The left posterior fascicle is relatively short and broad, with dual blood supply, making it particularly resistant to ischemic damage. The left posterior fascicle transmits impulses to the papillary muscles, leading to mitral valve closure. As the left posterior fascicle is shorter and broader than the right, impulses reach the papillary muscles just prior to depolarization, and therefore contraction, of the left ventricle myocardium. This allows pre-tensioning of the chordae tendinea, increasing the resistance to flow through the mitral valve during left ventricular contraction. This mechanism works in the same manner as pretensioning of car seatbelts.
 
Purkinje Fibers/Ventricular Myocardium: QRS Complex
The two bundle branches taper out to produce numerous Purkinje fibers, which stimulate individual groups of myocardial cells to contract. The spread of electrical activity through the ventricular myocardium produces the QRS complex on the ECG.
 
Ventricular Repolarization
The last event of the cycle is the repolarization of the ventricles. It is the restoring of the resting state. In the ECG, repolarization includes the J-wave, ST-segment, and T- and U-waves.
 
Electrical Signals and Blood Flow
The S-A node normally produces 60–100 electrical signals per minute —heart rate or pulse. With each pulse, signals from the S-A node follow a natural electrical pathway through heart walls.
 
(ECG) ELECTROCARDIOGRAPHY
 
Introduction
More than two electrodes are used, and they can be combined into a number of pairs for example: left arm (LA), right arm (RA) and left leg (LL) electrodes form the three pairs LA + RA, LA + LL, and RA + LL. The output from each pair is known as a lead. Each lead looks at the heart from a different angle. Different types of ECGs can be referred to by the 105number of leads that are recorded; for example, 3-lead, lead or 12-lead ECGs (sometimes simply ‘a 12-lead’). A 12-lead ECG is one in which 12 different electrical signals are recorded at approximately the same time and will often be used as a one-off recording of an ECG, traditionally printed out as a paper copy. Three- and 5-lead ECGs tend to be monitored continuously and viewed only on the screen of an appropriate monitoring device; for example, during an operation or whilst being transported in an ambulance. There may or may not be any permanent record of a 3- or 5-lead ECG, depending on the equipment used.
 
History
Alexander Muirhead is reported to have attached wires to a feverish patient's wrist to obtain a record of the patient's heartbeat while studying for his Doctor of Science (in electricity) in 1872 at St Bartholomew's Hospital. Einthoven assigned the letters P, Q, R, S and T to the various deflections, and described the electrocardiographic features of a number of cardiovascular disorders. In 1924, he was awarded the Nobel Prize in Medicine for his discovery.
 
Meaning
The word is derived from the Greek electro, because it is related to electrical activity, kardio, Greek for heart, and graph, a Greek root meaning ‘to write’.
 
Definition
Electrocardiography is a transthoracic interpretation of the electrical activity of the heart over a period of time, as detected by electrodes attached to the surface of the skin and recorded by a device external to the body. The recording produced by this noninvasive procedure is termed as an electrocardiogram and also ECG.
ECG: A galvanometer and electrodes with six limb leads and six chest leads. A graphic recording of the electric forces generated by the heart during depolarization and repolarization. The electrocardiogram is recorded on graph paper with divisions.
 
Other Definitions
  • Depolarization: Electrical activation of the myocardium.
  • Repolarization: Restoration of the electrical potential of the myocardial cell.
  • Sequence: Depolarization occurs in the sinoatrial (SA) node; current travels through internodal tracts of the atria to the atrioventricular (AV) node; then through bundle of His, which divides into right and left bundle branches; left bundle branch divides into left anterior and posterior fascicles.
 
Functions
  • To measure and diagnose abnormal rhythms of the heart.
  • Helps to diagnose properly, particularly abnormal rhythms caused by damage to the conductive tissue that carries electrical signals, or abnormal rhythms caused by electrolyte imbalances.
 
Characteristics of the Normal Basic ECG
It is important to remember that there is a wide range of normal variability in the 12-lead ECG. The following ‘normal’ ECG characteristics, therefore, are not absolute. It takes considerable ECG reading experience to discover all the normal variants. Only by following a structured ‘Method of ECG Interpretation’ (Lesson II) and correlating the various ECG findings with the particular patient's clinical status will the ECG become a valuable clinical tool.
  • 106Measurements
  • Rhythm
  • Conduction
  • Measurements:
    • Heart Rate: 60–90 bpm
    • PR Interval: 0.12–0.20 sec
    • QRS Duration: 0.06–0.10 sec
    • QT Interval (QTc ≤ 0.40 sec):
      • Bazett's Formula: QTc = (QT)/Sq Root RR (in seconds)
      • Poor Man's Guide to upper limits of QT: For HR = 70 bpm, QT ≤ 0.40 sec; for every 10 bpm increase above 70, subtract 0.02 sec, and for every 10 bpm decrease below 70, add 0.02 sec. For example:
        • QT ≤ 0.38 @ 80 bpm
        • QT ≤ 0.42 @ 60 bpm
    • Frontal Plane QRS Axis: +90° to –30° (in the adult)
  • Rhythm: Normal sinus rhythm
    • The P-waves in leads I and II must be upright (positive) if the rhythm is coming from the sinus node.
  • Conduction: Normal Sinoatrial (SA), Atrioventricular (AV), and Intraventricular (IV) conductions
Both the PR interval and QRS duration should be within the limits specified above.
 
ECG PAPER
Time is measured from the L to the R—one large box = 0.20 sec and one small one = 0.04 sec.
The rate of the ECG machine is 25 mm/sec. Marks on the upper or lower border of paper fall every 3 sec or 3 inches.
Voltage or current strength is determined from the magnitude or height of the various waveforms and is measured in mV or mm—one small box normally = 0.1 mV or 1 mm and one large box = 0.5 mV or 5 mm.
Fig. 1.29: ECG paper
Voltage strength can be adjusted when recording the ECG. Thus, if the waveform is especially large, as in the precordial leads of a patient with ventricular hypertrophy, or especially small, as in a patient with severe lung disease, the size of the waveforms can be adjusted to fit the paper. A calibration mark is thus made at the beginning of the recording to denote whether it is at full-, half-, or, occasionally, double-amplitude. The normal calibration mark should be a full 10 mm for a 0.1 mV calibration. At half-amplitude, each vertical block equals 0.2 mV; at double-amplitude, each vertical block equals 0.05 mV.
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Fig. 1.30: ECG blocks
If an electrical impulse is moving toward the sensing electrode, a positive (upright) deflection is recorded; if the impulse is moving away from the sensing electrode, a negative (downward) deflection is recorded; when an impulse travels perpendicular to (90° away from) the sensing electrode, a straight line (isoelectric deflection) or an equiphasic (small amplitude complex with approximately equal height of upward and downward deflections) deflection is recorded.
  • Monophasic waveform = complex (e.g. P or T) peaks in one direction, either all positive or all negative.
  • Biphasic = complex has a positive peak and a negative peak (nadir).
  • Triphasic = three points to the complex, e.g., RSR'.
  • Equiphasic = negative part of the waveform is equal in size to the positive portion.
Dimensions of grids on ECG paper: Horizontal axis represents time. Large blocks are 0.2 seconds in duration, while small blocks are 0.04 seconds in duration. Vertical axis represents voltage. Large blocks are 5 mm, while small blocks represent 1 mm.
 
Estimation of Heart Rate
  • Heart rates of 50 to 300 beats/min.: These can be estimated from the number of large squares in an R-R interval. Because there are 300 large blocks in one minute, the number of blocks between R-R intervals can be divided into 300 to approximate the rate. For example, one large block between R-R intervals would be determined thus:
  • Heart rates of < 50 beats/minute: These can be estimated with the aid of markings at 3-second intervals along the graph paper. To calculate the rate, the cycles on a 6-second interval (two 3-second markings) are multiplied by 10 (to give the rate per 60 seconds; i.e. per minute).
 
Layout
By definition, a 12-lead ECG will show a short segment of the recording of each of the 12-leads. This is often arranged in a grid of four columns by three rows, the first column being the limb leads (I, II and III), the second column being the augmented limb leads (aVR, aVL and aVF) and the last two columns being the chest leads (V1-V6). It is usually possible to change this layout, so it is vital to check the labels to see which lead is represented. Each column will usually record the same moment in time for the three leads and then the recording will switch to the next column, which will record the heartbeats after that point. It is possible for the heart rhythm to change between the columns of leads.
 
Leads
The term ‘lead’ in electrocardiography causes much confusion because it is used to refer to two different things. In accordance with common parlance, the word ‘lead’ may be used to refer to the electrical cable attaching the electrodes to the ECG recorder. As such, it may be 108acceptable to refer to the ‘left arm lead’ as the electrode (and its cable) that should be attached at or near the left arm. Usually, 10 of these electrodes are standard in a ‘12-lead’ ECG.
 
Placement of Electrodes
Ten electrodes are used for a 12-lead ECG. The electrodes usually consist of a conducting gel, embedded in the middle of a self-adhesive pad onto which cables clip. Proper placement of the limb electrodes, color-coded recommended by the American Heart Association (a different colour scheme).
Fig. 1.31: Placements of electrodes
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ELECTRODE LABEL (USA)
ELECTRODE PLACEMENT
RA
On the right arm, avoiding thick muscle
LA
In the same location where RA was placed, but on the left arm
RL
On the right leg, lateral calf muscle
LL
In the same location where RL was placed, but on the left leg
V1
In the fourth intercostal space (between ribs 4 and 5) just to the right of the sternum (breastbone)
V2
In the fourth intercostal space (between ribs 4 and 5) just to the left of the sternum
V3
Between leads V2 and V4
V4
In the fifth intercostal space (between ribs 5 and 6) in the midclavicular line
V5
Horizontally even with V4 in the left anterior axillary line
V6
Horizontally even with V4 and V5 in the midaxillary line
 
Additional Electrodes
The classical 12-lead ECG can be extended in a number of ways in an attempt to improve its sensitivity in detecting myocardial infarction involving territories not normally ‘seen’ well. This includes an rV4 lead, which uses the equivalent landmarks to the V4 but on the right side of the chest wall and extending the chest leads onto the back with a V7, V8 and V9.
The Lewis lead or S5 has the LA electrode placed in the second intercostal space to the right of the sternum with the RA at the fourth intercostal space. It is read as lead I and is supposed to demonstrate atrial activity much better to aid in identification of atrial flutter or broad-complex tachycardia.
A posterior ECG can aid in the diagnosis of a posterior myocardial infarction. This is performed by the addition of leads V7, V8 and V9 extending around the left chest wall toward the back.
 
Limb Leads
In both the 5- and 12-lead configurations, leads I, II and III are called limb leads. The electrodes that form these signals are located on the limbs—one on each arm and one on the left leg. The limb leads form the points of what is known as Einthoven's triangle.
  • Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode:
    I = LA–RA
  • Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode:
    II = LL–RA
  • Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode:
    III = LL–LA
Simplified electrocardiograph sensors designed for teaching purposes, e.g. at high school level, are generally limited to three arm electrodes serving similar purposes.
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  • Limb leads are usually labeled but also occasionally color coded so that:
    • Right arm—‘White is on the right’.
    • Right leg—‘Green is for go’. (Right leg is gas pedal.)
    • Left leg—‘Red is for stop’. (Some brake with left leg.)
    • Left arm—black lead.
    • Unipolar vs. bipolar leads
  • The two types of leads are unipolar and bipolar.
    • Bipolar leads have one positive and one negative pole. In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads.
    • Unipolar leads also have two poles, as a voltage is measured; however, the negative pole is a composite pole (Wilson's central terminal or WCT) made up of signals from multiple other electrodes. In a 12-lead ECG, all leads except the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).
  • Wilson's central terminal VW is produced by connecting the electrodes RA, LA, and LL together, via a simple resistive network, to give an average potential across the body, which approximates the potential at infinity (i.e. zero):
 
Augmented Limb Leads
Leads aVR, aVL, and aVF are augmented limb leads (after their inventor Dr Emanuel Goldberger known collectively as the Goldberger's leads). They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of Wilson's central terminal. This zeroes out the negative electrode and allows the positive electrode to become the ‘exploring electrode’. This is possible because Einthoven's Law states that I + (−II) + III = 0. The equation can also be written as I + III = II. It is written this way (instead of I - II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to view upright QRS complexes. Wilson's central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5 and V6.
  • 111Lead augmented vector right (aVR)' has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which ‘augments’ the signal strength of the positive electrode on the right arm:
  • Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which ‘augments’ the signal strength of the positive electrode on the left arm:
  • Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which ‘augments’ the signal of the positive electrode on the left leg:
The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson's central terminal. Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane. The aVR, aVL, and aVF leads can also be represented using the I and II limb leads:
 
Precordial Leads
  • The electrodes for the precordial leads (V1, V2, V3, V4, V5 and V6) are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. Wilson's central terminal is used for the negative electrode, and these leads are considered to be unipolar (recall that Wilson's central terminal is the average of the three limb leads. This approximates common, or average, potential over the body). The precordial leads view the heart's electrical activity in the so-called horizontal plane. The heart's electrical axis in the horizontal plane is referred to as the Z axis.
  • Unipolar leads (all have ‘V’ in their names) — aVR, aVL, aVF, and the precordial leads V1-V6.
  • Require more electrodes on the patient (a minimum of 4-5).
  • All have an ‘exploring’ electrode which ‘looks’ directly at the heart from its site of placement.
  • All also require three ‘indifferent’ electrodes (RA, LA, and LL) but which do not contribute toward the tracing.
112
 
Precordial Placement of Unipolar Electrodes for 12-lead ECGs
Fig. 1.32: Precordial placement of unipolar electrodes for 12-lead ECGs
*Addendum: V3 is placed halfway between V2 and V4.
All precordial leads bisect at AV node [point toward the AV node in a horizontal plane]:
  • Right chest (or anterior) leads — V1, V2; also aVR.
  • Septal leads—V3 and V4—located over the interventricular septum.
  • Left chest (or lateral) leads—V5, V6; also I and aVL.
  • V1 and V2 mirror changes occurring from the posterior side of the heart. None of the usual electrodes are directly adjacent to the posterior surface of the heart.
  • If additional posterior leads need to be seen (e.g. to diagnose a true posterior infarction) do another 12-lead ECG but move 3 electrodes to these positions:
    • V7 = same horizontal plane as V4–V6; PAL (posterior axillary line).
    • V8 = same horizontal plane as V4–V6; mid-scapula.
    • V9 = same horizontal plane as V4–V6; over spine.
    Fig. 1.33: Placements of ECG electrodes
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  • If additional right chest leads need to be seen (e.g. to diagnose a right ventricular infarction), do another 12-lead ECG but move 4 electrodes to these positions:
  • V3R = halfway between V1 and V4R.
  • V4R = 5 RICS at MCL.
  • V5R = same horizontal plane as V4R at AAL (anterior axillary line).
  • V6R = same horizontal plane as V4R at MAL (mid-axillary line).
  • PLACEMENT OF BIPOLAR LEADS (I, II, III, MCL1, MCL6) FOR MONITORING
  • RA = right arm; LA = left arm
  • RL = right leg; LL = left leg
  • Lead I — LA is +, RA is–, RL is ground.
    114
  • Lead II — LL is +, RA is–, RL is ground.
  • Lead III — LL is +, LA is–, RL is ground.
* NOTE: LL electrode should always be placed below the umbilicus in order to avoid problems in patients with ventricular hypertrophy.
* NOTE: In placing electrodes on the chest, always find the angle of Louis (palpable junction of the manubrium and body of the sternum). Slide to the side and you are on the second rib with the 2nd intercostal space just below it. Count down to the correct interspace from there.
  • Bipolar leads look from a positive pole toward a negative pole. The positive electrode ‘looks’ directly at the heart from the site where it is placed. Ground electrodes do not contribute to the tracing. ‘Quick look’ defibrillator paddles are also bipolar.
  • Lead MCL1— use lead I selection on monitor; positive electrode placed in 4ICS (4th intercostal space) at the RSB (right sternal border); negative electrode placed on L shoulder; ground may be placed anywhere.
  • V1 is the single best lead for diagnosing dysrhythmias; MCL1 is a substitute for V1 which can be recorded from 3 lead-wire patient cables.
  • MCL1 is very similar to, but not identical to, pattern seen in V1 precordial lead.
  • Rhythms which can be distinguished in V1 or MCL1 but not in other leads include those with a widened QRS complex, such as right versus left ventricular rhythms, right and left bundle branch blocks, and differentiation of supraventricular rhythms with aberration from ventricular rhythms. Also, P-waves are often visible in V1 and MCL1 when they are invisible in other leads because the exploring electrode is the one closest to the atria.
  • Lead MCL6 — almost the same electrode placement as MCL1, but the positive electrode is placed in the 5ICS in the left MAL (midaxillary line). MCL6 is very similar to, but not identical to, pattern seen in V6 precordial lead.
115
 
Clinical Lead Groups
Of the 12 leads in total, each records the electrical activity of the heart from a different perspective, which also correlates to different anatomical areas of the heart for the purpose of identifying acute coronary ischemia or injury. Two leads that look at neighboring anatomical areas of the heart are said to be contiguous. The relevance of this is in determining whether an abnormality on the ECG is likely to represent true disease or a spurious finding.
I Lateral
aVR
V1 Septal
V4 Anterior
II Inferior
aVL Lateral
V2 Septal
V5 Lateral
III
aVF Inferior
V3 Anterior
V6 Lateral
Category
Color on chart
Leads
Activity
Inferior leads
Yellow
Leads II, III and aVF
Look at electrical activity from the vantage point of the inferior surface (diaphragmatic surface of heart)
Lateral leads
Green
I, aVL, V5 and V6
Look at the electrical activity from the vantage point of the lateral wall of left ventricle
  • The positive electrode for leads I and aVL should be located distally on the left arm and because of which, leads I and aVL are sometimes referred to as the high lateral leads.
  • Because the positive electrodes for leads V5 and V6 are on the patient's chest, they are sometimes referred to as the low lateral leads.
Septal leads
Orange
V1 and V2
Look at electrical activity from the vantage point of the septal surface of the heart (interventricular septum)
Anterior leads
Blue
V3 and V4
Look at electrical activity from the vantage point of the anterior wall of the right and left ventricles (sternocostal surface of the heart)
 
Waves and Intervals
Upper limit of normal QT interval, corrected for heart rate according to Bazett's formula, Fridericia's formula and subtracting 0.02 s from QT for every 10 bpm increase in heart rate. Up to 0.42 s (≤ 420 ms) is chosen as normal QTc of QTB and QTF in this diagram.
Feature
Description
Duration
  • RR interval
The interval between an R-wave and the next R-wave; normal resting heart rate is between 60 and 100 bpm.
0.6 to 1.2 s
  • P wave
During normal atrial depolarization, the main electrical vector is directed from the SA node toward the AV node and spreads from the right atrium to the left atrium. This turns into the P-wave on the ECG.
80 ms
  • PR interval
The PR interval is measured from the beginning of the P-wave to the beginning of the QRS complex. The PR interval reflects the time the electrical impulse takes to travel from the sinus node through the AV node and entering the ventricles. The PR interval is, therefore, a good estimate of AV node function.
120 to 200 ms
116
  • PR segment
The PR segment connects the P-wave and the QRS complex. The impulse vector is from the AV node to the bundle of His to the bundle branches and then to the Purkinje fibers. This electrical activity does not produce a contraction directly and is merely traveling down toward the ventricles, and this shows up flat on the ECG. The PR interval is more clinically relevant.
50 to 120 ms
  • QRS complex
The QRS complex reflects the rapid depolarization of the right and left ventricles. The ventricles have a large muscle mass compared to the atria, so the QRS complex usually has a much larger amplitude than the P-wave.
80 to 120 ms
  • J-point
The point at which the QRS complex finishes and the ST segment begins. It is used to measure the degree of ST elevation or depression present.
N/A
  • ST segment
The ST segment connects the QRS complex and the T-wave. The ST segment represents the period when the ventricles are depolarized. It is isoelectric.
80 to 120 ms
  • T-wave
The T-wave represents the repolarization (or recovery) of the ventricles. The interval from the beginning of the QRS complex to the apex of the T-wave is referred to as the absolute refractory period. The last half of the T-wave is referred to as the relative refractory period (or vulnerable period).
160 ms
  • ST interval
The ST interval is measured from the J point to the end of the T wave.
320 ms
  • QT interval
The QT interval is measured from the beginning of the QRS complex to the end of the T-wave. A prolonged QT interval is a risk factor for ventricular tachyarrhythmias and sudden death. It varies with heart rate and, for clinical relevance, requires a correction for this, giving the QTc.
Up to 420 ms in heart rate of 60 bpm
  • U-wave
The U-wave is hypothesized to be caused by the repolarization of the interventricular septum. It normally has a low amplitude, and even more often is completely absent. It always follows the T-wave, and also follows the same direction in amplitude. If it is too prominent, suspect hypokalemia, hypercalcemia or hyperthyroidism.
  • J-wave
The J-wave, elevated J-point or Osborn wave appears as a late delta wave following the QRS or as a small secondary R-wave. It is considered pathognomonic of hypothermia or hypercalcemia.
 
Normal ECG Waveforms and Intervals
P-waves — represent depolarization of the atrial myocardium (Sinus node depolarization is too small in amplitude to be recorded from the body surface, so it is not seen.)
The normal P-wave is:
  • Not wider than 0.11 sec (under 3 little boxes on the ECG paper).
  • Not taller than 3 mm.
  • Not notched or peaked; does not have an excessive trough if biphasic.
  • Positive and rounded in leads I, II, and aVF in 94% of normals; usually upright in V4–V6.
Inverted P-waves in these leads are either abnormal or due to improper lead placement.
  • Negative in aVR.
  • Positive, negative, or biphasic in lead III, aVL, and V1–V3.
  • P-wave axis = + 60°.
  • Normally has 1:1 ratio with the QRS and should be regular.
    • Initial portion of P is largely a reflection of R atrial depolarization and the terminal portion reflects depolarization of the L atrium. The P-waves should all look alike.
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ECG Waveforms
Fig. 1.34: Normal ECG waves
PR Interval—represents atrial depolarization plus the normal delay at the AV node.
  • Normally = 0.12–0.20 sec. (No longer than one large box.)
  • Increased in length if AV conduction is prolonged (first-degree AV block).
PR Segment—begins at the end of the P-wave and ends with the onset of the QRS complex.
  • Should be isoelectric (flat).
  • Can be elevated with atrial infarction or pericarditis.
  • Can be depressed if there is a large repolarization wave (Tp) following the P-wave.
QRS Complex—represents depolarization of the ventricular myocardium. (Depolarization of the AV node, His bundle, bundle branches, and Purkinje fibers are too small in amplitude to be detected by electrodes on the body surface.)
  • All positive waves of the QRS complex are labeled R-waves. If there are more than one, the second one is labeled R'. An upper case capital letter describes a sizable R-wave (> 5 mm); a lower case letter describes a tiny R-wave (< 4 mm).
  • Negative waves of the QRS are labeled with Q-waves (preceding the R-wave) or S-waves (following the R-wave). Subsequent negative waves are labeled S' waves.
Relative size is denoted by upper- or lower-case letters.
  • Although termed the ‘QRS’ complex, many complexes do not contain all three waves.
  • Monomorphic = one shape; refers to a cardiac rhythm in which each QRS complex has a consistent pattern as, for example, monomorphic ventricular tachycardia which arises from one specific location. Older term, ‘unifocal’ means the same thing.
  • Polymorphic = multiple shapes such as polymorphic ventricular tachycardia which arise from multiple sites in the ventricles. Older term, ‘multifocal’ means the same thing.
  • 118Normal QRS characteristics:
  • 0.07–0.11 sec in width. QRS widths often vary in different leads. The widest QRS measurement on the 12-lead ECG is the correct one. Best leads to look at are usually leads I and V1.
  • Should neither be smaller than 6 mm in leads I, II, and III and nor should it be taller than 25–30 mm in the precordial leads.
  • R-wave Progression—in the precordial leads, the QRS starts off primarily negative (rS) in V1 and gradually becomes primarily positive (qRs) with the tallest R-wave in V5 or V6.
    • The transition from mostly negative to mostly positive normally occurs between V3 and V4. Normally, the R-wave in V6 is always less than the R-wave in V5. Precordial R-waves are very sensitive to lead placement and this must be considered in interpreting R-wave progression.
  • Early R-waves—R-waves in leads V1 and V2 as large as those in the next several leads can reflect posterior infarction, lateral MI, right ventricular hypertrophy (RVH), or septal hypertrophy.
  • Tall R-wave in V1—consider RVH, posterior MI, or Wolff-Parkinson-White (W-P-W).
  • ‘Low’ R-waves in the right precordial leads — most likely due to left ventricular hypertrophy (LVH) but also consider left anterior fascicular block (LAFB), COPD, or MI. R-wave < 2–3 mm in V3 is abnormal unless there is LVH. LVH causes loss of R height from V1–V3 without MI. Loss of R height between V1-2 or V2-3 in the absence of LVH suggests anterior MI.
  • Poor R-wave Progression—R-waves do not begin to dominate QRS until V5 or V6. This may represent infarction or injury of the anterior LV and carries almost as much significance as Q-waves.
  • Q-Wave — a negative wave preceding the R-wave. Not all leads normally record a Q-wave. Normal Q-waves represent septal depolarization and they must be distinguished from pathologic Q-waves which indicate myocardial infarction.
 
Normal Q-wave
  • Present only in leads I, aVL, V5, and V6 (left lateral leads).
  • Small in aVF and V5—normal variant.
  • If there is no Q where there should be one — septal fibrosis is present.
  • If large — myocardial damage. Large, diagnostic Q-waves represent altered electrical activity in the myocardium due to transmural myocardial damage.
  • Less than 0.04 sec.
  • 119Not deeper than one-third of the QRS complex.
  • ‘Diagnostic’ Q wave in V1, aVL, and III may be present without indicating myocardial damage.
  • ST segment — represents the time when ventricular cells are in the plateau phase (phase 2) of the action potential in which there is no current flow and thus little, if any transmembrane gradient (transmembrane potential hovers around zero). QRS and ST segment also represent a time when the ventricles are in their absolute refractory period and will not respond to stimulation.
  • ST segment starts at the J point (junction of the end of the QRS complex with the ST segment) and ends at the beginning of the T-wave.
  • ST segment (as well as the PR and TP segments) should be isoelectric (flat).
  • ST segment always has a smooth contour unless something else is added to it.
  • Clinical importance is related to its level relative to the isoelectric line rather than to its duration.
    • QT interval—measurement of the refractory period or the time during which the myocardium would not respond to a second impulse; measured from the beginning of the QRS complex to the end of the T-wave.
  • Best leads to measure the QT are V2 or V3.
  • If there is a U-wave visible, the measurement is made to the end of the U-wave and is called the Q-TU interval.
  • Q-T interval should be roughly less than half the preceding R-R interval.
  • It is longer with slower rates and shorter with faster rates. Normals also vary with age and gender.
  • If a Q-T table is not available, the Q-T interval can be corrected for heart rate using Basset's formula:
  • If a patient develops a wide QRS complex (a problem with depolarization) such as a bundle branch block, the QT interval will be increased. Thus, a long QT interval is not thought of as abnormal in patients with a wide QRS complex unless you have subtracted the extra width of the QRS from the QT interval and still found it prolonged.
  • If the rhythm is irregular, measure the QT relative to the rate of the prior R-R interval.
QT dispersion—QT is measured on the same beat in all 12 ECG leads and the shortest QT interval is subtracted from the longest QT interval. Recent evidence indicates that if there is much of a difference, heterogenous refractoriness exists in the heart muscle and the patient may be at higher risk of cardiac death from development of ventricular tachycardia/fibrillation, especially from any proarrhythmic effects of antiarrhythmic drugs.
JT Interval—JT interval reflects repolarization alone, not both depolarization and repolarization.
Sometimes used to measure the refractory period in patients who have been started on a Na+ channel blocker antiarrhythmic drugs (e.g. Quinidine, Pronestyl, and other class I agents). This is because such drugs slow depolarization, slightly prolonging the QRS complex.
  • 120T-wave—represents repolarization of the ventricles.
  • Earliest time ventricles can respond to another stimulus usually coinciding with the apex of the T-wave.
  • T-wave should have the same polarity as the QRS complex. Thus, if the QRS complex is primarily negative, the T-wave should be negative.
  • There are literally dozens of conditions that cause abnormal-looking T-wave in leads with positive QRS waveforms.
  • T-waves are very fickle; not as reliable as ST depression or elevation in diagnosis of ischemia.
  • Myocardial ischemia/non-Q-waves.
  • Normal variants (juvenile T-wave pattern; early repolarization).
  • Cerebrovascular accidents (especially intracranial bleeds) and related neurogenic patterns (e.g. radical neck dissection, Stokes-Adams syndrome).
  • Post-tachycardia or post-pacemaker T-wave pattern.
  • Intermittent left bundle branch block (LBBB).
  • Left or right ventricular overload (e.g. classic ‘strain’ patterns or apical hypertrophic cardiomyopathy.
  • Secondary T-wave alterations due to bundle branch blocks or Wolff-Parkinson-White patterns.
  • Respiratory alkalosis.
  • It is no longer believed that the first sign of infarction is T-wave inversion.
  • U-wave—A shallow, gently curved wave (in the same direction as the T-wave but smaller) following the T-wave. May not be visible at all.
  • It is not clear what the U-wave represents. May represent repolarization of intramural Purkinje conduction system.
  • Conditions which may cause a pronounced U-wave are antiarrhythmic drug effects, especially when the patient is prone to proarrhythmia (drug-induced arrhythmias such as polymorphic ventricular tachycardia or ‘torsades de pointes’).
  • Prominent U-wave—usually suggests digitalis toxicity or hypokalemia. Also seen in bradycardias.
 
Axis Determination
Definition: Direction of depolarization (vector) of the QRS complex.
  • The left ventricle is thicker, so the mean QRS vector is down and to the left (The origin of the vector is the AV node with the left ventricle being down and to the left of this).
  • The vector will point toward hypertrophy (thickened wall) and away from the infarct (electrically dead area).
    • The mean direction of electrical forces in the frontal plane (limb leads) as measured from the zero reference point (lead 1)
    • Normal values
      • P-wave: 0 to 75 degrees
      • QRS complex: 30 to 90 degrees
      • T-wave: QRS-T angle < 45 degrees frontal or < 60 degrees precordial
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Fig. 1.35: Direction of depolarization
  • It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the hex axial reference system, although -30° to +90° is considered to be normal.
  • If the left ventricle increases its activity or bulk, then there is said to be ‘left axis deviation’ as the axis swings round to the left beyond -30°; alternatively, in conditions where the right ventricle is strained or hypertrophied, then the axis swings round beyond +90° and ‘right axis deviation’ is said to exist. Disorders of the conduction system of the heart can disturb the electrical axis without necessarily reflecting changes in muscle bulk.
Normal
-30° to 90°
Normal
Normal
Left axis deviation
-30° to -90°
May indicate left anterior fascicular block or Q-waves from inferior MI.
Left axis deviation is considered normal in pregnant women and those with emphysema.
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Right axis deviation
+90° to +180°
May indicate left posterior fascicular block, Q-waves from high lateral MI, or a right ventricular strain pattern
Right deviation is considered normal in children and is a standard effect of dextrocardia.
Extreme right axis deviation
+180° to -90°
Is rare, and considered an ‘electrical no-man's land’
 
Measurement
 
Quick look tests
  • The simplest method of identifying gross deviations in axis is to look at the QRS complexes in leads I and aVF. Lead I is a left-sided lead, and as aVF is perpendicular to lead I, it can be considered a right-sided lead.
  • Both leads I and aVF have mainly positive QRS complexes.
  • Lead I is positive and aVF is negative left axis deviation (LAD).
  • Lead I is negative and aVF is positive right axis deviation (RAD).
  • Both leads negative extreme RAD or ‘North-West’ axis
 
Interpretation of QRS Axis
  • Normal: 0 to 90 degrees
  • Both leads I and aVF have mainly positive QRS complexes.
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Fig. 1.36: Interpretation of QRS complex
 
Normal Axis Deviation
 
Right Axis Deviation (RAD)
  • > 90 degrees (+90° to +180°)
    • Moderate RAD: 90 to 120 degrees
    • Marked RAD: 120 to 180 degrees
  • Differential diagnosis:
    • Right Ventricular Hypertrophy (RVH) — most common
    • Left Posterior Fascicular Block (LPFB) — diagnosis of exclusion
    • Lateral and apical MI
    • Acute Right Heart Strain, e.g. acute lung disease such as pulmonary embolus
    • Chronic lung disease, e.g. COPD
    • Hyperkalemia
    • Sodium-channel blockade, e.g. tricyclic toxicity
    • Secundum ASD
    • Normal in infants and children
Fig. 1.37: Normal axis deviation
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Right Axis Deviation (RAD)
 
Left Axis Deviation (LAD)
  • < –30 degrees (-30° to -90°)
  • Moderate LAD: –30 to –45 degrees
  • Marked LAD: –45 to –90 degrees
  • Differential diagnosis
    • Left ventricular hypertrophy (LVH)
    • Left Anterior Fascicular Block (LAFB)—diagnosis of exclusion
    • LBBB
    • Inferior MI
    • Primum ASD—rSR' pattern
      Fig. 1.38: Right axis deviation
 
Left Axis Deviation (LAD)
 
Extreme Axis Deviation
  • 180 to –90 degrees (rare)
  • Differential diagnosis:
    • Right Ventricular Hypertrophy (RVH)
    • Apical MI
    • VT
    • Hyperkalemia
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Fig. 1.39: Indeterminate axis of the QRS complex: Negative in lead I and negative in lead aVF
 
Rotation
  • Can be thought of as the axis of the heart in the transverse axis (the precordial leads)
  • Normal:
    • Isoelectric QRS in V3 and V4, indicating the transition point between the right and left ventricular electric forces
  • Clockwise rotation
    • Isoelectric QRS in V5, V6
  • Anticlockwise rotation:
    • Isoelectric QRS in V1, V2
 
AORTIC ANEURYSM
 
Definition
  • Aneurysm is a localized sac or dilation formed at a weak point in the wall of the aorta.
  • An aneurysm is an abnormal bulge in the wall of a blood vessel. A larger bulge, more than 1.5 times the size of normal aorta, is called an aneurysm.
 
Incidence
  • 30–60/1000
  • Increasing incidence over past 3 decades
  • Carotid Artery Stenosis –10%
  • Smoker: Nonsmoker –8:1
  • Male: Female –4:1
  • HTN: 40% of pts
Shapes: Aneurysm may be classified by its shape and form:
  • True aneurysms: One, two and all three layers of artery may be involved. It is classified into different types:
    • Fusiform aneurysms: Symmetric, spindle-shaped expansion of entire circumference of involved vessel. It appears as symmetrical bulges around the circumference of the aorta. They are the most common shape of aneurysm.
    • 126Saccular aneurysms: A bulbous protrusion, asymmetrical and appear on one side of the aorta. They are usually caused by trauma or a severe aortic ulcer.
    • Dissecting aneurysms: A bilateral out pouching in which layers of the vessels wall separate, creating a cavity. This is usually is a haematoma that split the layer of arterial wall.
  • False aneurysms: The wall rupture and a blood clot is retained in an out pouching of tissue or there connection between and artery that does not close.
Fig. 1.40: Types of aneurysms
Types: The two types of aortic aneurysms are:
  • Thoracic aortic aneurysms: Develop in the part of the aorta that runs through the chest. This includes the ascending aorta (the short stem of the cane); the aortic arch (the cane handle); and the descending thoracic aorta (the longer stem of the cane).
  • Abdominal aortic aneurysms: Develop in the part of the aorta that runs through the abdomen. Most abdominal aortic aneurysms develop below the renal arteries (the area where the aorta branches out to the kidneys). Sometimes aortic aneurysms extend beyond the aorta into the iliac arteries (the blood vessels that go to the pelvis and legs).
Causes: The exact cause is unknown. But recent evidence includes:
  • Atherosclerosis
  • Hypertension
Congenital:
Inflammatory (Noninfectious)
  • Primary connective tissue disorder (Marfan's syndrome)
  • Turner disorder
  • Takayasu's disease
  • Gaint cell arteries
  • Lupus erythematosus disease
  • BehÇet's disease
  • Pancreatitis
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Mechanical disorder:
Infectious:
  • Poststenotic and arteriovenous fistula
  • Amputation-related
  • Bacterial
  • Fungal
Traumatic (Psedoaneurysm):
Pregnancy related degenerative:
  • Penetrating arterial injuries
  • Blunt arterial aneurysm
  • Pseudoaneurysm
  • Nonspecific
  • Inflammatory disease
 
Risk Factors
  • CAD
  • Hypertension
  • Hypercholesterolemia
  • Hyperhomocysteinemia
  • Elevated C-reactive protein
  • Tobacco use
  • Peripheral vascular disease
  • Marfan's syndrome
  • Ehlers-Danlos type IV
  • Bicuspid aortic valve
 
Pathophysiology
 
Clinical Manifestations
  • Asymptomatic: 70–75%
  • Symptoms:
    • Early satiety, N, V
    • Abdominal, flank, or back pain
    • 1/3 of patients experience abdominal and flank pain
  • Abrupt onset of pain –> Rupture or expansion of aneurysm
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Diagnostic Evaluation
 
Physical Examination
  • If < 5 cm in diameter, then cannot be detected by routine physical examination
 
Radiographs
  • Calcified wall. Can determine size in 2/3
  • Cannot rule out and AAA
 
Arteriography
  • Cannot determine aneurysm size because of mural thrombus
  • Indications for obtaining arteriography
    • Suspicion of visceral ischemia
    • Occlusive disease of iliac and femoral arteries
    • Severe HTN, or impair renal function
    • Horseshoe kidney
    • Suprarenal of TAAA component
    • Femoropopliteal aneurysms
 
Ultrasound
  • Establishes diagnosis easily
  • Accurately measures infrarenal diameter
  • Difficult to visualize thoracic or suprarenal aneurysms
  • Difficult to establish relationship to renal arteries
  • Techniciandependent
  • Widely available, quick, no risk, cheap
 
CT Scan
  • Very reliable and reproducible
  • Can image entire aorta
  • Can visualize relationship to visceral vessels
  • Longer to obtain and is more costly than U/S
  • Most useful
  • Requires contrast agent—renal toxicity
 
Complications
  • Thrombosis
  • Distal embolization
  • Rupture
 
THORACIC AORTIC ANEURYSM
 
Introduction
Approximately 85% of all cases of thoracic aortic aneurysm are caused by atherosclerosis. They occur most frequently in men between ages 40 and 70 years. The thoracic area is the 129most common site for a dissecting aneurysm. About one-third of patients with thoracic aortic aneurysm die of rupture of aneurysm.
 
Clinical Manifestations
Symptoms are variable and depend on how rapidly the aneurysm dilates and how the pulsating mass affects the surrounding intrathoracic structures. Some of the patients are asymptomatic. But some are having:
  • Pain occurring in supine position
  • Dyspnea
  • Hoarseness
  • Stridor
  • Weakness
  • Aphonia
  • Dysphasia
 
Assessment and Diagnostic Tests
  • Physical Examination: superficial veins of neck, chest or arm dilated
  • Chest X-ray
  • Transesophageal echocardiography
  • CT scan
 
Treatment (Medical Management)
  • Antihypertensive: Hydralazine hydrochloride
  • Beta blocker: Atenolol, Timolol maleate
 
Surgical Management
 
Abdominal Aortic Aneurysm
 
Introduction
The most common cause of abdominal aortic aneurysm is arteriosclerosis. The condition which is more common among Caucasians population affects men 4 times more often than 130women and it is most prevalent in elderly patients. Most of this aneurysm occurs below renal arteries. Untreated, the eventual outcome may be rupture and death.
 
Causes
  • Congenital weakness
  • Trauma or disease
 
Risk Factors
  • Genetic predisposition
  • Smoking
  • Hypertension (50% cases)
 
Clinical Manifestations
  • Patient feels his heart beating in abdomen
  • Abdominal mass
  • Abdominal throbbing
 
Assessment and Diagnostic Tests
  • Physical Examination: Superficial veins of neck, chest or arm dilated
  • Duplex ultrasonography
  • CT scan: Determine size, length and location of aneurysm
 
Treatment (Medical Management)
  • Medical therapy of aortic aneurysms involves strict blood pressure control. This does not treat the aortic aneurysm per se, but control of hypertension within tight blood pressure parameters may decrease the rate of expansion of the aneurysm.
  • The tetracycline antibiotic doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen-stabilizing properties.
 
Prevention
Attention to patient's general blood pressure, smoking and cholesterol risks helps reduce the risk on an individual basis. There have been proposals to introduce ultrasound scans as a screening tool for those most at risk: men over the age of 65.
 
Surgical Management
For abdominal aortic aneurysms, suggest elective surgical repair when the diameter of the aneurysm is greater than 5 cm (2 in). However, suggest medical management for abdominal aneurysms with a diameter of less than 5.5 cm (2 in).
 
Open Surgery
Open surgery typically involves dissection of the dilated portion of the aorta and insertion of a synthetic (Dacron or Gore-Tex) patch tube. Once the tube is sewn into the proximal and distal portions of the aorta, the aneurysmal sac is closed around the artificial tube. Instead of sewing, the tube ends, made rigid and expandable by nitinol wireframe, can be much more 131simply, quickly and effectively inserted into the vascular stumps and there permanently fixed by external ligature.
 
Endovascular Surgery
The endovascular treatment of aortic aneurysms involves the placement of an endo-vascular stent via a percutaneous technique (usually through the femoral arteries) into the diseased portion of the aorta. This technique has been reported to have a lower mortality rate compared to open surgical repair, and is now being widely used in individuals with comorbid conditions that make them high-risk patients for open surgery.
 
DISSECTION/DISSECTING AORTA
 
Introduction
Occasionally, in an aorta diseased by atherosclerosis, a tear develops in the intima or the media degenerate, resulting in a dissection.
 
Definition
An aortic dissection is a serious condition in which a tear develops in the inner layer of the aorta, the large blood vessel branching off the heart. Blood surges through this tear into the middle layer of the aorta, causing the inner and middle layers to separate (dissect). If the blood-filled channel ruptures through the outside aortic wall, aortic dissection is often fatal.
 
Incidence
Arterial dissection is commonly associated with poorly controlled hypertension. It is 3 times more common in men than in women and occur most commonly in 50- to 70-year-old age group. Dissection is caused by rupture in the intima layer. A rupture may occur through adventitia or into the lumen through intima, allowing blood to re-enter the main channel and resulting in chronic dissection or occlusion of branches of the aorta.
 
Classification
 
Stanford Classification
The Stanford classification divides dissections into 2 types, type A and type B. Type A involves the ascending aorta (DeBakey types I and II); type B does not involve (DeBakey type III).
  • Type A dissections involve the ascending aorta and arch.
  • Type B involves the descending aorta.
  • A patient can have a type A dissection, type B dissection, or a combination of both.
 
DeBakey Classification
The DeBakey system, named after surgeon and aortic dissection sufferer Michael E. DeBakey, is an anatomical description of the aortic dissection. It categorizes the dissection based on where the original intimal tear is located and the extent of the dissection (localized to either the ascending aorta or descending aorta, or involves both the ascending and descending aorta. The DeBakey classification divides dissections into 3 types as follows:
  • Type I: Originates in ascending aorta, propagates at least to the aortic arch and often beyond it distally. It is most often seen in patients less than 65 years of age and is the most lethal form of the disease.
  • 132Type II: Originates in and is confined to the ascending aorta.
  • Type III: Originates in descending aorta, rarely extends proximally but will extend distally. It most often occurs in elderly patients with atherosclerosis and hypertension.
 
Etiology
  • High blood pressure: Most cases (over 70%) are associated with high blood pressure (hypertension).
  • Bicuspid aortic valve (a congenital abnormality of the aortic valve)
  • Marfan's syndrome
  • Ehlers-Danlos syndrome
  • Turner syndrome
  • Syphilis
  • Cocaine use
  • Pregnancy: Pregnancy is a rare associated risk factor, especially in the third trimester and early in the postpartum period.
  • Trauma: Blunt trauma is known to cause aortic dissection, which is often seen after car wrecks in which the patient's chest hits the steering wheel.
  • Surgical complications: Operations including coronary artery bypass grafting and aortic and mitral valve repairs. It can also be a complication of heart catheterization.
 
Risk Factors
The exact cause is unknown, but more common risks include:
  • Aging
  • Atherosclerosis
  • Blunt trauma to the chest, such as hitting the steering wheel of a car during an accident
  • High blood pressure
 
Pathophysiology
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Clinical Manifestations
  • Onset of symptoms is sudden
  • Severe and persistent pain—anterior chest or back extend to shoulder, epigastric region and abdomen
  • Sweating
  • Tachycardia
  • Appear pale
  • Increased blood pressure
The symptoms usually begin suddenly, and include severe chest pain. The pain may feel like a heart attack, and can:
  • Be described as sharp, stabbing, tearing, or ripping
  • Be felt below the chest bone, then move under the shoulder blades or to the back
  • Move to the shoulder, neck, arm, jaw, abdomen, or hips
  • Change position—pain typically moves to the arms and legs as the aortic dissection gets worse
The symptoms are caused by a decrease of blood flowing to the rest of the body, and can include:
  • Anxiety and a feeling of doom
  • Fainting or dizziness
  • Heavy sweating (clammy skin)
  • Nausea and vomiting
  • Shortness of breath—trouble breathing when lying flat (orthopnea)
Other symptoms may include:
  • Pain in the abdomen
  • Stroke symptoms
  • Swallowing difficulties from pressure on the esophagus
 
Assessment and Diagnostic Tests
  • Physical examination: Superficial veins of neck, chest or arm dilated.
  • D-dimer: A blood D-dimer level less than 500 ng/ml may be able to rule out the diagnosis of aortic dissection alleviating the need for further imaging.
  • Chest X-ray: Widening of the mediastinum on an X-ray of the chest has moderate sensitivity in the setting of an ascending aortic dissection. Pleural effusions may be seen on chest X-ray. They are more commonly seen in descending aortic dissections. Depression of the left main stem bronchus and tracheal deviation.
 
Computed Tomography
Computed tomography angiography is a fast noninvasive test that will give an accurate three-dimensional view of the aorta. These images are produced by taking rapid thin-cut slices of the chest and abdomen, and combining them in the computer to create cross-sectional slices. In order to delineate the aorta to the accuracy necessary to make the proper diagnosis, an iodinated contrast material is injected into a peripheral vein. Contrast is injected and the scan performed using a bolus tracking method. This is a type of scan timed to an injection 134to capture the contrast as it enters the aorta. The scan will then follow the contrast as it flows through the vessel.
It has a sensitivity of 96 to 100% and a specificity of 96 to 100%. Disadvantages include the need for iodinated contrast material and the inability to diagnose the site of the intimal tear.
 
Magnetic Resource Imaging
Magnetic resonance imaging (MRI) is currently the gold standard test for the detection and assessment of aortic dissection, with a sensitivity of 98% and a specificity of 98%. An MRI examination of the aorta will produce a three-dimensional reconstruction of the aorta, allowing the physician to determine the location of the intimal tear, the involvement of branch vessels, and locate any secondary tears. It is a noninvasive test, does not require the use of iodinated contrast material, and can detect and quantitate the degree of aortic insufficiency. The disadvantage of the MRI scan in the face of aortic dissection is that it has limited availability and is often located only in the larger hospitals, and the scan is relatively time-consuming. Due to the high-intensity magnetic fields used during MRI, an MRI scan is contraindicated in individuals with metallic implants. In addition, many individuals experience claustrophobia while in the MRI scanning tube.
 
Transesophageal Echocardiography
It is an echocardiogram displaying the true lumen and false lumen of an aortic dissection. In the image to the left, the intimal flap can be seen separating the two lumens. In the image to the right, color flow during ventricular systole suggests that the upper lumen is the true lumen.
The transesophageal echocardiogram (TEE) is a relatively good test in the diagnosis of aortic dissection, with a sensitivity of up to 98% and a specificity of up to 97%. It has become the preferred imaging modality for suspected aortic dissection. It is a relatively noninvasive test, requiring the individual to swallow the echocardiography probe. It is especially good in the evaluation of AI in the setting of ascending aortic dissection, and to determine whether the ostia (origins) of the coronary arteries are involved. While many institutions give sedation during transesophageal echocardiography for added patient comfort, it can be performed in cooperative individuals without the use of sedation. Disadvantages of the TEE include the inability to visualize the distal ascending aorta (the beginning of the aortic arch), and the descending abdominal aorta that lies below the stomach. A TEE may be technically difficult to perform in individuals with esophageal strictures or varices.
 
Aortogram
An aortogram involves placement of a catheter in the aorta and injection of contrast material while taking X-rays of the aorta. The procedure is known as aortography. Previously thought to be the diagnostic ‘gold standard’, it has been supplanted by other less–invasive imaging modalities.
 
Medical Management
  • Antibiotic: The tetracycline antibiotic Doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen stabilizing properties.
  • 135Antihypertensive: Hydralazine hydrochloride
  • Beta blocker: Atenolol, Timolol maleate
  • Vasodilators: Sodium nitroprusside
  • Calcium channel blockers: Verapamil and diltiazem
 
Surgical Management
Replacement of the damaged section with a tube graft (often made of dacron) when there is no damage to the aortic valve.
  • Bentall procedure: Replacement of the damaged section of aorta and replacement of the aortic valve.
  • David procedure: Replacement of the damaged section of aorta and reimplantation of the aortic valve.
  • Tevar: Insertion of a stent graft (covered stent), e.g. in TEVAR (thoracic endovascular aortic repair). It is usually combined with ongoing medical management.
  • Vascular ring connector (VRC): Replacement of the damaged section of aorta with a sutureless vascular ring connector-reinforced dacron graft. Vascular ring connector (VRC) is a titanic ring used as a stent in the vascular graft to achieve a quick, blood-sealed, and sutureless anastomosis. There are two furrows on the surface of the ring for fixation of the vascular graft and the aorta. The tapes used to tie against the ring provide a larger contact surface area than the traditional stitches, thus providing stronger anastomosis and better surgical results.
 
RAYNAUD'S PHENOMENON
 
Definition
Raynaud's phenomenon is a vasospastic disorder causing discoloration of the fingers, toes, and occasionally other areas. This condition may also cause nails to become brittle with longitudinal ridges. Due to vasospasm that decrease blood supply to the respective regions. Stress and cold are classic triggers of the phenomenon.
 
Types of Raynaud's Disease
There are two types of Raynaud's disease – Primary and Secondary:
  • Primary Raynaud's disease: In these cases, the cause of the condition is unknown. It does run in families, however, so a genetic cause is suspected. Primary Raynaud's disease is five times more common in women than it is in men, and usually starts between the ages of 20 and 45 years.
  • Secondary Raynaud's disease: Secondary Raynaud's disease is so-called because it occurs secondary to another condition or factor, such as:
    • Medications that narrow the blood vessels, e.g. beta blockers.
    • Hormone imbalances, e.g. hypothyroidism.
    • Injury, e.g. frostbite.
    • Occupational exposure to constant vibration (e.g. chainsaws) or repetitive movement (e.g. typing).
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Causes
  • Primary Raynaud's (disease): Raynaud's disease, or ‘Primary Raynaud's’, is diagnosed if the symptoms are idiopathic. It often develops in young women in their teens and early adulthood. Primary Raynaud's is hereditary.
  • Secondary Raynaud's (syndrome): Raynaud's syndrome, or ‘Secondary Raynaud's,’ occurs secondary to a wide variety of other conditions. Secondary Raynaud's has a number of associations:
    • Connective tissue disorders:
      • Scleroderma
      • Systemic lupus erythematosus
      • Rheumatoid arthritis
      • Polymyositis
      • Mixed connective tissue disease
      • Ehlers-Danlos Syndrome
    • Eating disorders
      • Anorexia nervosa
    • Obstructive disorders
      • Atherosclerosis
      • Buerger's disease
      • Takayasu's arteritis
      • Subclavian aneurysms
      • Thoracic outlet syndrome
    • Drugs
      • Betablockers
      • Cytotoxic drugs—particularly chemotherapeutics and most especially bleomycin
      • Cyclosporin
      • Bromocriptine
      • Ergotamine
      • Sulfasalazine
      • Anthrax vaccines whose primary ingredient is the anthrax protective antigen
    • Occupation
      • Jobs involving vibration, particularly drilling, suffer from vibration white finger
      • Exposure to vinyl chloride, mercury
      • Exposure to cold
    • Others
      • Physical trauma, such as that sustained in auto accident or other traumatic events
      • Lyme disease
      • Hypothyroidism
      • Cryoglobulinemia
      • Malignancy
      • 137Reflex sympathetic dystrophy
      • Carpal tunnel syndrome
      • Magnesium deficiency
      • Multiple sclerosis
      • Erythromelalgia (the opposite of Raynaud's, with hot and warm extremities)
 
Risk Factors
Smoking worsens frequency and intensity of attacks, and there is a hormonal component. Caffeine also worsens the attacks. Sufferers are more likely to have migraine and angina than controls.
 
Pathophysiology
 
Signs and Symptoms
  • Pain
  • Discoloration (paleness)
  • Sensations of cold and/or numbness
  • Swelling
  • Tingling
  • Raynaud's also has occurred in breastfeeding mothers, causing nipples to turn white and become extremely painful.
 
Diagnostic Tests
  • Digital artery pressure: Pressures are measured in the arteries of the fingers before and after the hands have been cooled. A decrease of at least 15 mm Hg is diagnostic (positive).
  • Doppler ultrasound: To assess blood flow.
  • Full blood count: This may reveal a normocytic anemia suggesting the anemia of chronic disease or renal failure.
  • 138Blood test for urea and electrolytes: This may reveal renal impairment.
  • Thyroid function tests: this may reveal hypothyroidism.
  • An autoantibody screen, tests for rheumatoid factor, erythrocyte sedimentation rate, and C-reactive protein, which may reveal specific causative illnesses or a generalized inflammatory process.
  • Nailfold vasculature: This can be examined under the microscope.
 
Treatment (General Care)
  • Environmental triggers should be avoided, e.g. cold, vibration, etc.
  • Emotional stress is another recognized trigger.
  • Extremities should be kept warm.
  • Consumption of caffeine and other stimulants and vasoconstrictors must be prevented.
 
Emergency Measures
  • Keeping warm and maintaining a constant body temperature.
  • Wearing gloves and warm socks when out in the cold.
  • Not smoking—nicotine can narrow the blood vessels.
  • Not directly handling cold things, e.g. bottles of milk, items just out of the freezer.
  • Keeping the skin supple by using moisturizers.
  • Learning how to manage stress and emotional situations.
  • Avoiding medications that can aggravate blood vessel spasm, e.g. some cold and flu medications.
  • Warming the hands and feet with clothing or in warm water.
  • Medications to widen the blood vessels and promote circulation (calcium channel blockers).
  • Medications to thin the blood, e.g. aspirin.
  • Treatment of underlying conditions in cases of secondary Raynaud's disease.
  • Alternative therapies, e.g. massage, acupuncture.
 
Drug Therapy
  • Calcium channel blockers: (Nifedipine) or diltiazem.
  • Side effects: Headache, flushing, and ankle edema; but these are not typically of sufficient severity to require cessation of treatment.
  • Angiotensin II receptor antagonists: (Losartan) reduce frequency and severity of attacks
  • Vasodilator therapy: Sildenafil (Viagra) improves both microcirculation and symptoms in patients with secondary Raynaud's phenomenon.
  • Selective serotonin reuptake inhibitor: Fluoxetine, a selective serotonin reuptake inhibitor.
  • Antidepressant medications: May reduce the frequency and severity of episodes if caused mainly by psychological stress.
 
Surgical Intervention
  • Sympathectomy: Procedure can be performed. The nerves that signal the blood vessels of the fingertips to constrict are surgically cut.
139
 
Nursing Management
Nursing diagnosis: Risk for hemorrhage related to graft procedure
Goal: To reduce risk of bleeding
Interventions
  • Monitor pulse rate.
  • Monitor central venous pressure.
  • Provide sterile dressing on wound.
  • Give vitamin K as per doctor's advice.
Nursing Diagnosis: Pain related to disease condition as evidences by verbal communication.
Goal: Pain is reduced or lost.
Intervention
  • Assess for the presence of pain, the scale and intensity of pain.
  • Teach the client about pain management and relaxation with distraction.
  • Secure the chest tube to restrict movement and avoid irritation.
  • Assess pain reduction measures.
  • Provide analgesics as indicated.
Nursing Diagnosis: Risk for impaired gas exchange related to cough and pain from incision.
Goal: To clear secretions from airway.
Interventions
  • Airway Management:
    • Open the airway with headtilt, chinlift, jaw thrust
    • Set the position to maximize ventilation
    • Use tools airway
    • Perform chest physiotherapy
    • Teach breathing deeply and coughing effectively
    • Perform suction
    • Auscultation of breath sounds
    • Give bronchodilators (collaboration)
  • Oxygenation Therapy:
    • Provide humidification system of oxygen equipment
    • Monitor the flow of oxygen and the amount given
    • Monitor signs of oxygen toxicity
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BIBLIOGRAPHY
  1. Ahmad EN. Cardiovascular diseases, conduction disturbances 2010. Aliabad University Hospital, Kabul Medical University,  Kabul,  Afghanistan.
  1. Basvanthappa BT. A textbook of medical surgical nursing, 2nd ed. Jaypee Brothers Medical publishers  1106–9.
  1. Black M. A textbook of medical surgical nursing. Elsevier.  Noida.  8th ed. 1307–40.
  1. Black M Joyce ‘Medical surgical nursing’, 8th ed., Elsevier  809–11.
  1. Brunner S. A Textbook of medical surgical nursing. Lippincott Company.  Philadelphia.  10th ed. 2007: 1052–60.
  1. ECG Conduction Abnormalities. Retrieved 2009-01-07.
  1. Edhag O, Swahn A. ‘Prognosis of patients with complete heart block or arrhythmic syncope who were not treated with artificial pacemakers. A long-term follow-up study of 101 patients’. Acta medica Scandinavica 1976. 200 (6): 457–63.
  1. Hopper P, William L. Understanding of medical surgical nursing. Devis.  ed. 2nd. 2003:286–97
  1. Lemone P, Burke K. A Textbook of medical surgical nursing. South Asia Dorling Kindersely  4th ed. 2007.
  1. Suddarth Brunner. A textbook of medical surgical nursing 10th ed., Lippincott Williams and Wilkins  713–24.

Cardiovascular Emergencies2

Cardiovascular emergencies are life-threatening disorders that must be diagnosed quickly to avoid delay in treatment and to minimize morbidity and mortality.
Cardiac emergencies includes:
  • Cardiopulmonary arrest
  • Hypertensive emergency
  • Aortic aneurysm (ruptured)
  • Aortic dissection
  • Air embolism (Arterial)
  • Cardiac tamponade
  • Cardiac arrhythmia
  • Ventricular fibrillation
  • Myocardial infarction (heart attack).
 
CARDIOPULMONARY ARREST
Cardiac arrest, also known as cardiopulmonary arrest or circulatory arrest, is the cessation of functional circulation of the blood due to failure of the heart to contract effectively.
A cardiac arrest is different from (but may be caused by) a heart attack, where blood flow to the muscle of the heart is impaired. It is different from congestive heart failure, where circulation is substandard, but the heart is still pumping sufficient blood to sustain life.
Cardiac arrest is a medical emergency that, in certain situations, is potentially reversible if treated early. Unexpected cardiac arrest can lead to death within minutes: this is called sudden cardiac death (SCD).
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Classification of Cardiopulmonary Arrest
Cardiac arrest is classified into two types:-
  1. Shockable
  2. Nonshockable
 
Shockable
  • In this type the rhythm is present but abnormal.
  • The two ‘shockable’ rhythms are ventricular fibrillation and pulseless ventricular tachycardia.
  • Ventricular fibrillation: It is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver rather than contract properly.
  • Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole (‘flatline’). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature), the patient could sustain irreversible brain damage and possibly become brain dead due to the effects of cerebral hypoxia. On the other hand, death often occurs if sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole.
  • Ventricular tachycardia: It is a type of tachycardia, or a rapid heartbeat that starts in the bottom chambers of the heart called the ventricles. The ventricles are the main pumping chambers of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death.
 
Nonshockable
  • When a patient's ECG shows flatlines it is called an asystole. It is not a shockable rhythm because there is no signal left to reset. This means the electrical impulse is gone and cannot be recovered.
  • ‘Nonshockable’ rhythms are asystole and pulseless electrical activity.
  • Asystole: A life-threatening cardiac condition characterized by the absence of electrical and mechanical activity in the heart. Clinical signs include apnea and lack of pulse. Without cardiac monitoring, asystole cannot be distinguished from ventricular fibrillation.
  • Pulseless electrical activity or PEA refers to a cardiac arrest situation in which a heart rhythm is observed on the electrocardiogram that should be producing a pulse, but is not.
 
Diagnosis and Treatment
The American Heart Association, in collaboration with the International Liaison Committee on Resuscitation, has established guidelines for resuscitation of cardiac arrest patients. In each resuscitation scenario, four concepts should always apply:
  1. Activate EMS or the designated code team.
  2. Perform basic life support (CPR).
  3. 143Evaluate heart rhythm and perform early defibrillation as indicated.
  4. Deliver advanced life support (e.g. intubation, intravenous [IV] access, and transfer to a medical center or intensive care unit).
 
VENTRICULAR TACHYCARDIA OR VENTRICULAR FIBRILLATION
  • Conduct a primary ABCD survey (airway, breathing, circulation, differential diagnosis). Place airway device as soon as possible. Confirm placement, secure device, and confirm oxygenation and ventilation. Establish IV access, identify rhythm, and administer drugs appropriate for rhythm and condition. Search for and treat identified reversible causes, with focus on basic CPR and early defibrillation.
  • On arrival to an unwitnessed cardiac arrest or downtime longer than 4 minutes, five cycles (approximately 2 minutes) of CPR are to be initiated before evaluation of rhythm. If the cardiac arrest is witnessed or downtime is shorter than 4 minutes, one shock may be administered immediately if the patient is in ventricular fibrillation or pulseless ventricular tachycardia.
  • If the patient is in ventricular fibrillation or pulseless ventricular tachycardia, shock the patient once using 200 J on biphasic (or equivalent monophasic, 360 J).
  • Resume CPR immediately after attempted defibrillation, beginning with chest compressions. Rescuers should not interrupt chest compression to check circulation (e.g. evaluate rhythm or pulse) until five cycles or 2 minutes of CPR have been completed.
  • If there is persistent or recurrent ventricular tachycardia or ventricular fibrillation despite several shocks and cycles of CPR, perform a secondary ABCD survey with a focus on more advanced assessments and pharmacologic therapy. Pharmacologic therapy should include epinephrine (1 mg IV push, repeated every 3 to 5 minutes) or vasopressin (a single dose of 40 U IV, one time only).
  • Consider using antiarrhythmics for persistent or recurrent pulseless ventricular tachycardia or ventricular fibrillation. These include amiodarone, lidocaine, magnesium and procainamide.
  • Resume CPR and attempts to defibrillate.
 
PULSELESS ELECTRICAL ACTIVITY
  • Assess the patient and conduct a primary ABCD survey.
  • Review for the most frequent causes of pulseless electrical activity, the five Hs and five Ts: hypovolemia, hypoxia, hydrogen ion (acidosis), hyperkalemia (or hypokalemia), and hypothermia and tablets (drug overdose, accidents), tamponade (cardiac), tension pneumothorax, thrombosis (coronary), and thrombosis (pulmonary embolism).
  • Administer epinephrine (1 mg IV push repeated every 3 to 5 minutes) or atropine (1 mg IV if the heart rate is slow, repeated every 3 to 5 minutes as needed, to a total dose of 0.04 mg/kg).
  • Conduct a secondary ABCD survey.
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BRADYCARDIA
  • Determine whether the bradycardia is slow (heart rate less than 60 beats/min) or relatively slow.
  • Conduct a primary ABCD survey.
  • Check for serious signs or symptoms caused by the bradycardia.
  • If no serious signs or symptoms are present, evaluate for a type II second-degree atrioventricular block or third-degree atrioventricular block.
  • If neither of these types of heart block is present, observe.
  • If one of these types of heart block is present, prepare for transvenous pacing. If symptoms develop, use a transcutaneous pacemaker until the transvenous pacer is placed.
  • If serious signs or symptoms are present, begin the following intervention sequence:
    • Atropine, 0.5 up to a total of 3 mg IV
    • Transcutaneous pacing, if available
    • Dopamine, 5 to 20 mcg/kg/min
    • Epinephrine, 2 to 10 mcg/min
    • Isoproterenol, 2 to 10 mcg/min
    • Conduct a secondary ABCD survey.
 
ASYSTOLE
  • Conduct a primary ABCD survey.
  • Perform transcutaneous pacing immediately if needed. Consider transvenous pacing if transcutaneous pacing fails to capture.
  • Administer epinephrine (1 mg IV push, repeated every 3 to 5 minutes) or atropine (1 mg IV repeated every 3 to 5 minutes, up to a total of 3 mg).
  • Conduct a secondary ABCD survey.
  • If asystole persists, consider withholding or ceasing resuscitative efforts.
 
HYPERTENSIVE EMERGENCY
A hypertensive emergency is an acute, severe elevation in blood pressure accompanied by end-organ compromise. In newly hypertensive patients, a hypertensive emergency is usually associated with a diastolic blood pressure higher than 120 mm Hg.
 
Etiology
  • Essential hypertension
  • Renal causes
  • Renal artery stenosis
  • Glomerulonephritis
  • Vascular causes
  • Vasculitis
  • Hemolytic-uremic syndrome
  • 145Thrombotic thrombocytopenia purpura
  • Pregnancy-related causes
  • Preeclampsia
  • Eclampsia
  • Pharmacologic causes
  • Sympathomimetics
  • Clonidine withdrawal, beta blocker withdrawal
  • Cocaine
  • Amphetamines
  • Endocrine causes
  • Cushing's syndrome
  • Pheochromocytoma
  • Renin-secreting adenomas
  • Thyrotoxicosis
  • Neurologic causes
  • Central nervous system trauma
  • Intracranial mass
  • Autoimmune cause
  • Scleroderma renal crisis.
 
Signs and Symptoms
Symptoms of end-organ involvement include:
  • Headache
  • Blurry vision
  • Confusion
  • Chest pain
  • Shortness of breath
  • Back pain (e.g. aortic dissection)
  • If severe, seizures and altered consciousness.
 
Treatment
  • Nitroprusside
  • Labetalol
  • Fenoldopam
  • Enalaprilat
 
AIR EMBOLISM
An air embolism, or more generally gas embolism, is a pathological condition caused by a gas bubble, or bubbles, in a vascular system.
An air embolism, also called a gas embolism is when an air bubble or air bubbles enter a vein or artery and block it. When the embolism enters a vein, it is called a venous air embolism. When the air enters an artery, it is called an arterial air embolism.
146These air bubbles can travel to brain, heart, or lungs and cause a heart attack, stroke, or respiratory failure.
 
Etiology
  • An air embolism can occur when veins or arteries are exposed and pressure allows air to travel into them. This can happen in several ways, such as:
    • Injections and Surgical Procedures
  • A syringe or IV can accidentally inject air into veins. Air can also enter veins or arteries through a catheter that is inserted into them.
  • Air can enter veins and arteries during surgical procedures. This is most common during brain surgeries.
    • Lung Trauma
    • Scuba Diving
    This is possible if a person hold his breath for too long when under water. These actions can cause the air sacs in lungs, called alveoli, to rupture. When the alveoli rupture, air may move to arteries, resulting in an air embolism.
    • Explosion and Blast Injuries
    • Air into the Vagina
In this case, the air embolism can occur if there is a tear or injury in the vagina or uterus. The risk is higher in pregnant women, who may have a tear in their placenta.
 
Signs and Symptoms
  • Loss of consciousness
  • Cessation of breathing
  • Vertigo
  • Convulsions
  • Tremors
  • Loss of coordination
  • Loss of control of bodily functions
  • Numbness
  • Paralysis
  • Extreme fatigue
  • Weakness in the extremities
  • Areas of abnormal sensation
  • Visual abnormalities
  • Hearing abnormalities
  • Personality changes
  • Cognitive impairment
  • Nausea or vomiting
  • Bloody sputum.
 
Diagnostic Evaluation
  • Ultrasound
  • CT scan
  • X-ray.
147
 
Treatment
  • A large bubble of air in the heart (as can follow certain traumas in which air freely gains access to large veins) will present with a constant ‘machinery’ murmur.
  • It is important to promptly place the patient in Trendelenburg position.
  • The Trendelenburg position keeps a left-ventricular air bubble away from the coronary artery ostia so that air bubbles do not enter and occlude the coronary arteries.
  • Left lateral decubitus positioning helps to trap air in the nondependent segment of the right ventricle (where it is more likely to remain instead of progressing into the pulmonary artery and occluding it).
  • Administration of high percentage oxygen is recommended for both venous and arterial air embolism. This is intended to counteract ischemia and accelerate bubble size reduction.
  • For venous air embolism the trendelenburg or left lateral positioning of a patient with an air-lock obstruction of the right ventricle may move the air bubble in the ventricle and allow blood flow under the bubble.
  • Hyperbaric therapy with 100% oxygen is recommended for patients presenting clinical features of arterial air embolism, as it accelerates removal of nitrogen from the bubbles by solution and improves tissue oxygenation. This is recommended particularly for cases of cardiopulmonary or neurological involvement. Early treatment has greatest benefits, but it can be effective as late as 30 hours after the injury.
 
CARDIAC TEMPONADE
Cardiac tamponade is pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium).
 
Etiology
Cardiac tamponade can occur due to:
  • Dissecting aortic aneurysm (thoracic)
  • End-stage lung cancer
  • Heart attack (acute MI)
  • Heart surgery
  • Pericarditis caused by bacterial or viral infections
  • Wounds to the heart.
Other possible causes include:
  • Heart tumors
  • Hypothyroidism
  • Kidney failure
  • Leukemia
  • Placement of central lines
  • Radiation therapy to the chest
  • Recent invasive heart procedures
  • 148Recent open heart surgery
  • Systemic lupus erythematosus.
 
Signs and Symptoms
  • Anxiety, restlessness
  • Chest pain
    • Radiating to the neck, shoulder, back, or abdomen
    • Sharp, stabbing
    • Worsened by deep breathing or coughing
  • Difficulty breathing
  • Discomfort, sometimes relieved by sitting upright or leaning forward
  • Fainting, light-headedness
  • Pale, gray, or blue skin
  • Palpitations
  • Rapid breathing
  • Swelling of the abdomen or other areas.
Other symptoms that may occur with this disorder:
  • Dizziness
  • Drowsiness
  • Weak or absent pulse.
 
Diagnostic Evaluation
  • Chest CT or MRI of chest
  • Chest X-ray
  • Coronary angiography
  • ECG.
 
Treatment
  • The fluid around the heart must be drained as quickly as possible.
  • Pericardiocentesis is a procedure that uses a needle to remove fluid from the pericardial sac, the tissue that surrounds the heart.
  • A procedure to cut and remove part of the pericardium (surgical pericardiectomy or pericardial window) may also be done.
  • Fluids are given to maintain normal blood pressure until Pericardiocentesis can be performed.
  • Medications that increase blood pressure may also help sustain the patient's life until the fluid is drained.
  • The patient may be given oxygen. This reduces the workload on the heart by decreasing tissue demands for blood flow.
  • The cause of tamponade must be identified and treated.
149
BIBLIOGRAPHY
  1. Brunner SA. Textbook of medical surgical nursing. Ed. 10th Lippincott Company.  Philadelphia.  2007; 597–601.
  1. Cinar B, Enc Y, Goksel O, et al. Chronic constrictive tuberculous pericarditis: risk factors and outcome of pericardiectomy. Int J Tuberc Lung Dis. 2006; 10 (6): 701–6.
  1. Chowdhury UK, Subramaniam GK, Kumar AS, et al. Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques. Ann Thorac Surg 2006 81 (2): 522–9.
  1. LeWinter MM, Tischler MD. Pericardial diseases. Braunwald's heart Disease: A textbook of cardiovascular medicine. 9th ed. Saunders Elsevier;  Philedelphia,  2011; P. 71–5.

Vascular Disorders of Heart3

 
 
Vascular Disease
 
Introduction
Vascular disease includes any condition that affects the circulatory system. As the heart beats, it pumps blood through a system of blood vessels called the circulatory system. The vessels are elastic tubes that carry blood to every part of the body. Arteries carry blood away from the heart while veins return it.
Vascular disease ranges from diseases of arteries, veins, and lymph vessels to blood disorders that affect circulation.
 
VASCULAR DISEASE
Vascular disease is a form of cardiovascular disease primarily affecting the blood vessels.
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Diagnostic Criteria
It can be very difficult to make a vascular disease diagnosis as there are a wide variety of symptoms that a person can carry.
  • The physical examination: May be slightly different depending on the type of vascular disease that is suspected. In the case of a peripheral vascular disease the physical examination consists in checking the blood flow in the legs or flow or the blood pressure.
  • Tests and examination:
    • Carotid angiogram: The coronary angiogram is basically the same procedure which is however utilized for detecting cardiovascular conditions.
    • Carotid duplex: Carotid ultrasound is another type of noninvasive test which uses ultrasound waves in order to detect plaque, blood clots or any other type of blood flow abnormalities in the carotid arteries.
    • The doppler ultrasound is a test used to diagnose both cerebrovascular disease and peripheral vascular disease. It utilizes high frequency soundwaves that are being directed to the vein or artery which presents abnormalities and are then detected on the Doppler.
    • Electroencephalography: May be required in order to detect electrical impulses in the brain by placing small metal disks called electrodes on the scalp of the patient.
    • MRI: Technique is able to obtain 3D images of the body structure. The images are very clear and they are produced by using magnetic fields and recent computer technology. Due to the clarity of the pictures, the MRI can detect any signs of prior strokes. The MRI may also be performed on the heart if a cardiovascular disease is suspected.
 
Common Vascular Disorders
  • Peripheral vascular disease
  • Buerger's disease
  • Takayasu's disease
  • Syphilitic disease
  • Arotic Aneurysm
  • Raynaud's disease or Raynaud's syndrome
  • Varicose veins
  • Deep vein thrombosis.
 
PERIPHERAL VASCULAR DISEASE
It refers to the obstruction of large arteries not within the coronary, aortic arch vasculature, or brain. PVD can result from atherosclerosis, inflammatory processes leading to stenosis, an embolism, or thrombus formation. It causes either acute or chronic ischemia. Often PVD is a term used to refer to atherosclerotic blockages found in the lower extremity.
 
Classification
  • Mild claudication
  • Moderate claudication
  • Severe claudication
  • 152Ischemic pain at rest
  • Minor tissue loss
  • Major tissue loss.
 
Etiology
  • Smoking: Tobacco use in any form is the single most important modifiable cause of PVD. Exposure to second-hand smoke from environmental exposure has also been shown to promote changes in blood vessel which is a precursor to atherosclerosis.
  • Diabetes mellitus: Causes between two and four times increased risk of PVD by causing endothelial and smooth muscle cell dysfunction in peripheral arteries.
  • Dyslipidemia: Elevation of total cholesterol, LDL cholesterol, and triglyceride levels each have been correlated with accelerated PAD.
  • Hypertension: Elevated blood pressure is correlated with an increase in the risk of developing PAD, as well as in associated coronary and cerebrovascular events (heart attack and stroke).
 
Clinical Manifestation
  • Claudication: Pain, weakness, numbness, or cramping in muscles due to decreased blood flow
  • Sores, wounds, or ulcers that heal slowly or not at all
  • Noticeable change in color (blueness or paleness)
  • Temperature (coolness)
  • Diminished hair and nail growth on affected limb and digits.
 
Diagnostic Evaluation
  • Ankle brachial pressure index: When the blood pressure readings in the ankles is lower than that in the arms, blockages in the arteries which provide blood from the heart to the ankle are suspected.
  • Doppler ultrasound examination: A lower limb doppler ultrasound examination to look at site and extent of atherosclerosis.
  • Angiography: Where a catheter is inserted into the common femoral artery and selectively guided to the artery in question. While injecting a radiodense contrast agent an X-ray is taken. Any flow limiting stenosis found in the X-ray can be identified and treated by atherectomy, angioplasty or stenting.
  • Computerized tomography (CT): CT provides complete evaluation of the aorta and lower limb arteries without the need for an angiogram's arterial injection of contrast agent.
 
Management
 
Medical Management
  • Smoking cessation (cigarettes promote PVD and are a risk factor for cardiovascular disease)
  • Management of diabetes
  • Management of hypertension
  • Management of cholesterol
  • 153Medication with antiplatelet drugs: Aspirin, clopidogrel and statins (which reduce clot formation and cholesterol levels)
  • Regular exercise: Treadmill exercise (35 to 50 minutes, 3 to 4 times per week)
  • Medication: Cilostazol or pentoxifylline treatment to relieve symptoms of claudication.
 
Surgical Management
  • Angioplasty: (PTA or percutaneous transluminal angioplasty) can be done on solitary lesions in large arteries, such as the femoral artery, but angioplasty may not have sustained benefits.
  • Plaque excision: In which the plaque is scraped off of the inside of the vessel wall.
  • Bypass grafting: The saphenous vein is used, although artificial (Gore-Tex) material is often used for large tracts when the veins are of lesser quality.
 
THROMBOANGIITIS (BUERGER'S DISEASE)
Thromboangiitis obliterans (Buerger's disease) is a recurring progressive inflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet.
 
Etiology
  • Current (or recent) history of tobacco use
  • Presence of distal extremity ischemia
  • Exclusion of other autoimmune diseases
  • Diabetes mellitus
  • Autoimmune reaction (one in which the body's immune system attacks the body's own tissues).
 
Clinical Manifestation
  • Acute and chronic inflammation
  • Thrombosis of arteries and veins of the hands and feet
  • Ulcerations and gangrene in the extremities
  • Claudication
  • Pain at rest
  • Ischemic ulcers or gangrene.
 
Pathophysiology
154
 
Diagnostic Evaluation
  • CT angiogram: Showing segmental stenosis of arteries of the lower leg. The changes are particularly apparent in the blood vessels in the lower right hand portion.
  • Angiograms: The upper and lower extremities can be helpful in making the diagnosis of Buerger's disease. Angiograms may also show occlusions or stenosis in multiple areas of both the arms and legs.
  • Skin biopsies: It affected extremities are rarely performed because of the frequent concern that a biopsy site near an area poorly perfused with blood will not heal well.
 
Prevention
  • Smoking cessation has shown to slow the progression of the disease and decrease the severity of amputation in most patients, but does not halt the progression.
  • Streptokinase has been proposed as adjuvant therapy.
  • Limaprost, oral PGE1 derivative, has shown efficacy.
 
RAYNAUD'S PHENOMENON
Raynaud's phenomenon is a vasospastic disorder causing discoloration of the fingers, toes, and occasionally other areas. This condition may also cause nails to become brittle with longitudinal ridges. The result of vasospasms that decrease blood supply to the respective regions. Stress and cold are classic triggers of the phenomenon.
 
Types
There are two types of Raynaud's disease—Primary and Secondary:
  1. Primary Raynaud's disease: In these cases, the cause of the condition is unknown. It does run in families, however, so a genetic cause is suspected. Primary Raynaud's disease is five times more common in women than it is in men, and usually starts between the ages of 20 and 45 years.
  2. Secondary Raynaud's disease: Secondary Raynaud's disease is so called because it occurs secondary to another condition or factor, such as:
    • Medications that narrow the blood vessels, e.g. beta-blockers.
    • Hormone imbalances, e.g. hypothyroidism.
    • Injury, e.g. frost bite.
    • Occupational exposure to constant vibration (e.g. chainsaws) or repetitive movement (e.g. typing).
 
Etiology
  • Primary Raynaud's (disease): Raynaud's disease, or ‘Primary Raynaud's’, is diagnosed if the symptoms are idiopathic, it often develops in young women in their teens and early adulthood. Primary Raynaud's is caused by Hereditary.
  • Secondary Raynaud's (syndrome): Raynaud's syndrome, or ‘Secondary Raynaud's’, occurs secondary to a wide variety of other conditions. Secondary Raynaud's has a number of associations:
  • Connective tissue disorders:
    • Scleroderma
    • Systemic lupus erythematosus
    • 155Rheumatoid arthritis
    • Sjögren's syndrome
    • Dermatomyositis
    • Polymyositis
    • Mixed connective tissue disease
    • Cold agglutinin disease
    • Ehlers-Danlos Syndrome.
  • Eating disorders
    • Anorexia nervosa
  • Obstructive disorders
    • Atherosclerosis
    • Buerger's disease
    • Takayasu's arteritis
    • Subclavian aneurysms
    • Thoracic outlet syndrome.
  • Drugs
    • Beta-blockers
    • Cytotoxic drugs—particularly chemotherapeutics and most especially bleomycin
    • Ciclosporin
    • Bromocriptine
    • Ergotamine
    • Sulfasalazine
    • Anthrax vaccines whose primary ingredient is the Anthrax Protective Antigen.
  • Occupation
    • Jobs involving vibration, particularly drilling, suffer from vibration white finger
    • Exposure to vinyl chloride, mercury
    • Exposure to the cold.
  • Others
    • Physical Trauma, such as that sustained in auto accident or other traumatic events
    • Lyme disease
    • Hypothyroidism
    • Cryoglobulinemia
    • Malignancy
    • Reflex sympathetic dystrophy
    • Carpal tunnel syndrome
    • Magnesium deficiency
    • Multiple Sclerosis
    • Erythromelalgia (the opposite of Raynaud's, with hot and warm extremities).
 
Clinical manifestation
  • Pain
  • Discoloration (paleness)
  • 156Sensations of cold and/or numbness
  • Swelling
  • Tingling
  • Raynaud's also has occurred in breastfeeding mothers, causing nipples to turn white and become extremely painful.
 
Diagnostic Evaluation
  • Digital artery pressure: Pressures are measured in the arteries of the fingers before and after the hands have been cooled. A decrease of at least 15 mm Hg is diagnostic (positive).
  • Doppler ultrasound: To assess blood flow.
  • Full blood count: This may reveal a normocytic anemia suggesting the anemia of chronic disease or renal failure.
  • Blood test for urea and electrolytes: This may reveal renal impairment.
  • Thyroid function tests: This may reveal hypothyroidism.
  • An autoantibody screen, tests for rheumatoid factor, Erythrocyte sedimentation rate, and C-reactive protein, which may reveal specific causative illnesses or a generalized inflammatory process.
  • Nail fold vasculature: This can be examined under the microscope.
 
Management
 
General Care
  • Environmental triggers should be avoided, e.g. cold, vibration, etc.
  • Emotional stress is another recognized trigger
  • Extremities should be kept warm
  • Consumption of caffeine and other stimulants and vasoconstrictors must be prevented.
 
Emergency Measures
  • Keeping warm and maintaining a constant body temperature.
  • Wearing gloves and warm socks when out in the cold.
  • Not smoking—nicotine can narrow the blood vessels.
  • Not directly handling cold things, e.g. bottles of milk, items out of the freezer.
  • Keeping the skin supple by using moisturisers.
  • Learning how to manage stress and emotional situations.
  • Avoiding medications that can aggravate blood vessel spasm, e.g. some cold and flu medications.
  • Warming the hands and feet with clothing or in warm water
  • Medications to widen the blood vessels and promote circulation (calcium channel blockers).
  • Medications to thin the blood, e.g. aspirin.
  • Treatment of underlying conditions in cases of secondary Raynaud's disease.
  • Alternative therapies, e.g. massage, acupuncture.
157
 
Pharmacological Management
  • Calcium channel blockers: Nifedipine or Diltiazem.
  • Angiotensin II receptor antagonists: Losartan, reduce frequency and severity of attacks
  • Vasodilator therapy: Sildenafil, improved both microcirculation and symptoms in patients with secondary Raynaud's phenomenon
  • Selective serotonin reuptake inhibitor: Fluoxetine, a selective serotonin reuptake inhibitor
  • Antidepressant medications: May reduce the frequency and severity of episodes if caused mainly by psychological stress.
 
Surgical Management
  • Sympathectomy: Procedure can be performed. Here, the nerves that signal the blood vessels of the fingertips to constrict are surgically cut.
 
TAKAYASU'S ARTERITIS
Takayasu's disease is a form of large vessel granulomatous vasculitis with massive intimal fibrosis and vascular narrowing.
 
Etiology
Due to obstruction of the main branches of the aorta, including the left common carotid artery, the brachiocephalic artery, and the left subclavian artery.
 
Pathophysiology
 
Clinical Manifestation
  • Malaise
  • Fever
  • Night sweats
  • Weight loss
  • Arthralgia
  • Fatigue
  • Anemia.
 
Diagnostic Evaluation
  • Elevation of the ESR or C-reactive protein
  • Magnetic resonance angiography (MRA)
  • 158Computed tomography angiography (CTA)
  • Arterial angiography (DSA).
 
Management
Steroids: Such as prednisone (starting dose is 1 mg/Kg/body weight/day).
 
Surgical Management
  • Bypass grafting: Grafting autologous tissue has the highest rates of success.
  • Percutaneous transluminal coronary angioplasty (PTCA) is not as effective in the longterm but has fewer risks.
 
SYPHILITIC AORTITIS
Syphilitic aortitis is a disease of the aorta associated with the tertiary stage of syphilis infection. SA begins as inflammation of the adventitia, including the vessels that supply the aorta itself with blood and the vasa vasorum.
Causes: It is caused by syphilis infection, which normally occurs in older people, syphilitic aortitis typically affects those under the age of 50.
 
Pathophysiology
 
Clinical Manifestation
  • Ischemia of the outer two-thirds of the aortic wall
  • Starved for oxygen and nutrients
  • Elastic fibers become patchy smooth muscle cells
  • Necrosis.
Treatment: Penicillin treatments is helpful.
 
AORTIC ANEURYSM
An aneurysm is an abnormal bulge in the wall of a blood vessel. A larger bulge, more than 1.5 times the size of normal aorta, is called an aneurysm.
 
Types
  • True aneurysms: In this vessels are dilate in following way:
    • Fusiform aneurysms: Appear as symmetrical bulges around the circumference of the aorta. They are the most common shape of aneurysm.
    • 159Saccular aneurysms are asymmetrical and appear on one side of the aorta. They are usually caused by trauma or a severe aortic ulcer.
    • Dissecting aneurysms: A bilateral out pouching in which layers of the vessels wall separate, creating a cavity.
  • False aneurysms: The wall rupture and a blood clot is retained in an out pouching of tissue or there connection between and artery that does not close.
  • Thoracic aortic aneurysms: Develop in the part of the aorta that runs through the chest. This includes the ascending aorta, the aortic arch and the descending thoracic aorta.
  • Abdominal aortic aneurysms: Develop in the part of the aorta that runs through the abdomen. Most abdominal aortic aneurysms develop below the renal arteries. Sometimes aortic aneurysms extend beyond the aorta into the iliac arteries.
 
Etiology
The exact cause is unknown. But recent evidence includes:
  • Atherosclerosis
  • Hypertension
 
Risk Factors
  • CAD
  • Hypertension
  • Hypercholesterolemia
  • Hyperhomocysteinemia
  • Elevated C-reactive protein
  • Tobacco use
  • Peripheral vascular disease
  • Marfan syndrome
  • Ehlers-Danlos type IV
  • Bicuspid aortic valve.
 
Pathophysiology
160
 
Management
 
Medical Management
Medical therapy of aortic aneurysms involves strict blood pressure control, but control of hypertension within tight blood pressure parameters may decrease the rate of expansion of the aneurysm.
The tetracycline antibiotic Doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen stabilizing properties.
 
Surgical Management
For abdominal aortic aneurysms suggest elective surgical repair when the diameter of the aneurysm is greater than 5 cm. However, suggest medical management for abdominal aneurysms with a diameter of less than 5.5 cm.
 
Open Surgery
Open surgery typically involves dissection of the dilated portion of the aorta and insertion of a synthetic (Dacron or Gore-Tex) patch tube. Once the tube is sewn into the proximal and distal portions of the aorta, the aneurysmal sac is closed around the artificial tube. Instead of sewing, the tube ends, made rigid and expandable by nitinol wireframe, can be much more simply, quickly and effectively inserted into the vascular stumps and there permanently fixed by external ligature.
 
Endovascular Surgery
The endovascular treatment of aortic aneurysms involves the placement of an endovascular stent via a percutaneous technique (usually through the femoral arteries) into the diseased portion of the aorta. This technique has been reported to have a lower mortality rate compared to open surgical repair, and is now being widely used in individuals with comorbid conditions that make them high-risk patients for open surgery.
 
VARICOSE VEINS
Veins are blood vessels that return deoxygenated blood from the outer parts of the body back to the heart and lungs. When veins become abnormally thick, full of twists and turns, or enlarged, they are called varicose veins. This happens most commonly in the veins in the legs and thighs.
 
Types
  • The superficial veins and their branches are close to the skin. Also included in this category are the communicator or perforator veins, which connect the superficial veins with the deep veins.
  • The deep veins are encased by muscle and connective tissue, which help to pump the blood in the veins and back to the heart. The veins have one-way valves to prevent them from developing varicosities.
 
Stages
  • C0 – no visible or palpable signs of venous disease
  • C1 – telangiectasia or reticular veins
  • 161C2 – varicose veins
  • C3 – edema
  • C4a – skin changes due to venous disorders: pigmentation, eczema
  • C4b – skin changes due to venous disorders: lipodermatosclerosis, atrophie blanche
  • C5 – as C4 but with healed ulcers
  • C6 – skin changes with active ulcers (venous insufficiency ulceration)
 
Etiology
  • Heredity
  • Pregnancy
  • Obesity
  • Menopause
  • Aging
  • Prolonged standing
  • Leg injury
  • Abdominal straining
  • Crossing legs at the knees or ankles
 
Risk Factors
  • Pregnancy is associated with an increase in blood volume.
  • Prolonged standing
  • Obesity or distended belly
  • Straining: Chronic constipation, urinary retention from an enlarged prostate, chronic cough
  • Prior surgery or trauma to the leg. These conditions interrupt the normal blood flow channels.
  • Age: Generally, most elderly individuals show some degree of varicose vein occurrence.
 
Clinical Manifestation
  • Aching, heavy legs.
  • Appearance of spider in the affected leg.
  • Ankle swelling, especially in evening.
  • A brownish-blue shiny skin discoloration near the affected veins.
  • Redness, dryness, and itchiness of areas of skin.
  • Cramps may develop especially when making a sudden move as standing up.
  • Minor injuries to the area may bleed more than normal and/or take a long time to heal.
  • Restless legs syndrome appears to be a common overlapping clinical syndrome in patients with varicose veins and other chronic venous insufficiency.
  • Whitened, irregular scar-like patches can appear at the ankles. This is known as atrophie blanche.
 
Diagnostic Evaluation
  • Duplex Doppler ultrasound scanning: All patients with varicose veins should now be investigated using ultrasound.
  • CT scanning.
162
 
Management
 
Conservative Management
  • Elevating the legs often provides temporary symptomatic relief.
  • Advice about regular exercise sounds sensible but is not supported by any evidence.
  • The wearing of graduated compression stockings with variable pressure to correct the swelling, nutritional exchange, and improve the microcirculation in legs affected by varicose veins.
  • The wearing of intermittent pneumatic compression devices have been shown to reduce swelling and increase circulation.
  • Diosmin/hesperidine and other flavonoids.
  • Anti-inflammatory medication, such as ibuprofen or aspirin can be used as part of treatment for superficial thrombophlebitis.
 
Surgical Management
Stripping
Stripping consists of removal of all or part of the saphenous vein (great/long and/or lesser/short) main trunk. The complications include deep vein thrombosis, pulmonary embolism, and wound complications including infection.
 
Nonsurgical Management
Sclerotherapy
A commonly performed nonsurgical treatment for varicose and ‘spider’ leg veins is sclerotherapy in which medicine is injected into the veins to make them shrink. The medicines that are commonly used as sclerosants are polidocanol (POL), sodium tetradecyl sulfate.
 
Complications
  • Pain, heaviness, inability to walk or stand for long hours, thus hindering work
  • Dermatitis which could predispose skin loss.
  • Skin ulcers especially near the ankle, usually referred to as venous ulcers.
  • Development of carcinoma or sarcoma in longstanding venous ulcers. Severe bleeding from minor trauma, of particular concern in the elderly.
  • Blood clotting within the affected veins.
  • Acute fat necrosis can occur especially at the ankle of overweight patients with varicose veins. Females are more frequently affected than males.
  • The afflicted person suffers tenderness in that region.
 
DEEP VEIN THROMBOSIS
Deep vein thrombosis or deep venous thrombosis (DVT) is a blood clot in a deep vein. A clot inside a blood vessel is called thrombus. Deep vein thrombosis (DVT) is a condition in which a blood clot forms in one or more of the deep veins in the body, usually in a calf or thigh muscle of legs.
163
 
Etiology
  • Combination of venous stasis
  • Hypercoagulability
  • Physical damage or endothelial activation
  • Genetic factors: Deficiencies in antithrombin, protein C
 
Risk Factors
  • Acquired:
    • Older age
    • Major surgery and orthopedic surgery
    • Cancers, especially pancreatic
    • Immobilization, as in orthopedic casts the sitting position, and travel, particularly by air
    • Pregnancy and the postpartum period
    • Antiphospholipid syndrome (such as lupus anticoagulant)
    • Trauma and minor leg injury
    • Previous oral contraceptives
    • Hormonal replacement therapy
    • Central venous catheters
    • Inflammatory diseases and some autoimmune diseases
    • Nephrotic syndrome
    • Obesity
    • Infection
    • HIV
    • Polycythemia vera
    • Chemotherapy
  • Inherited:
    • Antithrombin deficiency
    • Protein C deficiency
    • Protein S deficiency (type I)
    • Factor V Leiden
    • Prothrombin
    • Dysfibrinogenemia
    • Non-O-blood type
  • Mixed:
    • Low free protein S
    • Activated protein C resistance
    • High factor VIII levels
    • Hyperhomocysteinemia
    • High fibrinogen levels
    • High factor IX levels
    • High factor XI levels
164
 
Pathophysiology
 
Clinical Manifestation
  • Swelling in one or both legs
  • Pain or tenderness in one or both legs, which may occur only while standing or walking
  • Warmth in the skin of the affected leg
  • Red or discolored skin in the affected leg
  • Visible surface veins
  • Leg fatigue
 
Diagnostic Evaluation
  • Physical examination: Swelling in the leg from fluid can result in ‘pitting’ after pressure is applied.
  • CT scan: An abdominal CT scan shows a common iliac vein thrombosis.
  • D-dimer test: A type of blood test that detects pieces of blood clots that have broken down and are loose in the bloodstream.
  • Duplex ultrasound: During this test, high-frequency sound waves bounce off the inside of body, producing images of blood vessels. An ultrasound image demonstrates a blood clot in the left common femoral vein.
 
Management
  • Anticoagulation: Anticoagulation, which prevents further coagulation but does not act on existing clots, is the standard treatment for DVT. Parenteral anticoagulant (such as fondaparinux, or heparin) for at least five days and a vitamin K antagonist an oral anticoagulant.
  • 165Graduated compression stockings and walking: In addition to anticoagulation treatment, the graduated compression stockings, which apply higher pressure (30 to 40 mm Hg) at the ankles and a lower pressure around the knees is suggested. Walking is also suggested over bed rest for those without severe pain or edema.
 
Surgical Management
  • Inferior vena cava filters: Inferior vena cava filters (IVC filters) are used on the presumption that they reduce PE. They are only recommended in some high-risk scenarios.
  • Thrombolysis: Thrombolysis, which acts to break up clots, can be systemic or catheter-directed, patients may choose thrombolysis, if it concerns over the complexity, bleeding risk, and cost of the procedure.
  • Mechanical thrombectomy: A mechanical thrombectomy device can remove a thrombosis.
 
Nursing Management
Nursing diagnosis: Risk for hemorrhage related to graft procedure.
Interventions:
  • Monitor pulse rate
  • Monitor central venous pressure
  • Provide sterile dressing on wound
  • Give vitamin K as per doctor's advice
Nursing diagnosis: Pain related to disease condition as evidenced by verbal communication.
Interventions:
  • Assess for the presence of pain, the scale and intensity of pain
  • Teach the client about pain management and relaxation with distraction
  • Secure the chest tube to restrict movement and avoid irritation
  • Assess pain-reduction measures
  • Provide analgesics as indicated
Nursing diagnosis: Risk for impaired gas exchange related to cough and pain from incision.
Interventions:
  • Airway Management:
    • Open the airway with headtilt, chinlift, jaw thrust
    • Set the position to maximize ventilation
    • Use tools airway
    • Perform chest physiotherapy
    • Teach breathing deeply and coughing effectively
    • Perform suction
    • Auscultation of breath sounds
    • Give bronchodilators.
  • Oxygenation therapy:
    • Provide humidification system of oxygen equipment
    • Monitor the flow of oxygen and the amount given.
    • Monitor signs of oxygen toxicity.
166
 
HYPERTENSION
 
Introduction
Hypertension (HTN) or high blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated. Blood pressure is summarized by two measurements, systolic and diastolic, which depend on whether the heart muscle is contracting (systole) or relaxed between beats (diastole). This equals the maximum and minimum pressures, respectively. Normal blood pressure at rest is within the range of 100–140 mm Hg systolic and 60–90 mm Hg diastolic. High blood pressure is said to be present if it is often at or above 140/90 mm Hg.
Blood pressure is the pressure exerted by the blood on the walls of the blood vessels. High blood pressure is generally defined as a persistent elevation of systolic blood pressure above 140 mm Hg and diastolic pressure above 90 mm Hg.
 
Types of Blood Pressure
  • Systolic pressure: Systolic pressure is the highest when the blood is being pumped out of the left ventricle into the aorta during ventricular systole. The average high during systole is 120 mm Hg.
  • Diastolic pressure: Diastolic blood pressure lowers steadily to an average low of 80 mm Hg during ventricular diastole.
These measures of blood pressure are not static, but undergo natural variations from one heartbeat to another, and throughout the day (in a circadian rhythm), they also change in response to stress, nutritional factors, drugs, or disease.
 
Classification of Hypertension
Hypertension may be classified according to type (systolic and diastolic), cause, and degree of severity.
 
Classification on the basis of type
  • Systolic hypertension: Systolic hypertension is systolic pressure greater than 140 mm Hg. Clients over age 65 frequently have systolic pressure over 140 mm hg and diastolic pressure over 90 mm Hg. For these clients, hypertension is defined as systolic pressure over 160 mm Hg and/or diastolic pressure over 95 mm Hg.
  • Diastolic hypertension: Diastolic hypertension is diastolic pressure greater than 90 mm Hg.
 
On the basis of etiology
  • Primary hypertension: Primary hypertension, also known as essential or idiopathic hypertension, constitutes more than 90–95 percent of all cases of hypertension.
  • Secondary hypertension: Secondary hypertension results from an identifiable cause.
 
On the basis of severity
  • Borderline hypertension
  • Benign hypertension
  • Malignant hypertension
  • 167Borderline hypertension: Borderline or labile hypertension is defined as intermittent elevation of blood pressure interspersed with normal readings. Clients with borderline hypertension still carry an increased risk of developing cardiovascular disease.
  • Benign hypertension: Benign hypertension is a term used to describe uncomplicated hypertension, usually of long duration and mild to moderate severity.
  • Malignant hypertension: Malignant hypertension is a syndrome of markedly elevated BP (diastolic BP over 140 mm Hg) associated with papilledema. Accelerated hypertension is a syndrome of markedly elevated BP with retinal hemorrhage and exudates. Accelerated hypertension presumably develops into malignant hypertension if not well managed.
Blood pressure classification for adults*†
Blood pressure classification
SBP (mm Hg§)
DBP (mm Hg)
Normal
< 120
and < 80
Prehypertenslon
120–139
or 80–89
Stage 1 Hypertension
140–159
or 90–99
Stage 2 Hypertension
> 160
or ≥ 100
*Adapted from US Department of Health and Human Services; National Institutes of Health; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program
Treatment determined by highest blood pressure category
SBP: Systolic blood pressure
§ mm Hg millimeters of mercury
DBP: Diastolic blood pressure
 
Etiology
  • Primary hypertension has no single or specific cause but it is multifactorial. It develops in response to increased cardiac output or to a rise in peripheral resistance. Primary hypertensions occurs due to idiopathic causes.
  • Secondary hypertension is due to:
 
Renal Causes
  • Renal parenchymal disease
  • Acute glomerulonephritis
  • Chronic nephritis
  • Polycystic disease
  • Connective tissue disease
  • Diabetic nephropathy
  • Hydronephrosis
 
Endocrine Causes
  • Acromegaly
  • Hypothyroidism
  • Hyperthyroidism
  • Hypercalcemia
168
 
Adrenal Causes
  • Cortical
  • Cushing's syndrome
  • Primary aldosteronism
  • Congenital adrenal hyperplasia
 
Exogenous Hormones
  • Estrogen
  • Glucocorticoids
  • Mineralocorticoids
 
Other Causes
  • Acute stress, including surgery
  • Psychogenic hyperventilation
  • Hypoglycemia
  • Burns
  • Pancreatitis
  • Alcohol withdrawal
  • Postoperative
  • Increased intravascular volume
  • Alcohol, drugs, and so on
 
Risk Factors
  • Nonmodifiable risk factors
    • Family history: The genetic predisposition that makes certain families more susceptible to hypertension seems to be associated with elevated intracellular sodium levels and lowered potassium-to-sodium ratios. This is found more often in blacks. Clients with parents who have hypertension have a greater risk of developing hypertension at a younger age.
    • Age: The incidence of hypertension increases with age; 50–60 per cent of clients over 50 years of age have a blood pressure over 140/90 mm Hg.
    • Gender: Men experience hypertension at higher rates and at an earlier age than do women until after age 60. Men also have greater risk of cardiovascular morbidity and mortality. After age 50, hypertension is more prevalent in women.
    • Ethnic group: Hypertension is more prevalent in blacks, and at any given blood pressure level, with whites. The reason has been attributed to heredity, greater salt intake, and greater environmental stress.
  • Modifiable risk factors
    • Stress: It has been shown to cause increased peripheral vascular resistance and cardiac output and to stimulate sympathetic nervous system activity. Stress may be associated with occupational factors, socioeconomic levels, and personality characteristics.
    • 169Obesity: Obesity, in particular that located in the upper body with increased amounts of intra-abdominal fat, is an important cause of hypertension, the combination may be related to hyperinsulinemia secondary to insulin resistance.
    • Nutrients: Sodium is an important etiologic factor in essential hypertension. A high salt diet may induce excessive release of natriuretic hormone, which may indirectly increase blood pressure.
 
Pathophysiology
 
Clinical Manifestation
The early stages of hypertension have no clinical manifestations, other than elevations in blood pressure. This unfortunate fact means that there are no signs or symptoms to lead a person to seek health care.
As hypertension advances, without treatment, the clients may report morning occipital headache, fatigue, dizziness, palpitations, flushing, blurred vision, and epistaxis, vertigo.
 
Hypertensive Crisis
Severely elevated blood pressure (equal to or greater than a systolic of 180 or diastolic of 110—sometimes termed as malignant or accelerated hypertension) is referred to as a ‘hypertensive crisis’, as blood pressures above these levels are known to confer a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches and dizziness than the general population. Other symptoms accompanying a hypertensive crisis may include visual deterioration or breathlessness due to heart failure or a general feeling of malaise due to renal failure.
170
 
Treatment of Hypertension
The goal of treating clients with hypertension is to prevent morbidity and mortality associated with high blood pressure. The objective is to achieve and maintain arterial blood pressure below 140/90 mm Hg, if possible.
 
Nonpharmacologic Intervention
  • Weight reduction: The relationship between obesity and blood pressure has been clearly established from numerous studies. Weight reduction to within 15 per cent of ideal body weight is recommended for all obese hypertensive clients.
  • Sodium restriction: Studies demonstrate the antihypertensive efficacy of moderate sodium restriction to a level of approximately 1 to 2.5 g of sodium or 4 to 6 g of salt. These studies also demonstrate the ability of most clients to adhere to such a regimen. Moderate sodium restriction is not hazardous and may reduce the degree of potassium depletion accompanying diuretic therapy.
  • Modification of dietary fat: Modification of dietary intake of fat by decreasing the fraction of saturated fat and increasing that of polyunsaturated fat may decrease blood pressure and will decrease the cholesterol level, which is an important risk factor for coronary artery disease.
  • Exercise: A regular program of aerobic (isotonic) exercise facilitates cardiovascular conditioning, can aid the obese hypertensive client in weight reduction, and may provide some benefit in reducing blood pressure. Heavy isometric exercises such as weightlifting may be harmful, blood pressure often rises to very high levels because of vasovagal reflexes that occur during an isometric contraction.
  • Restriction of alcohol: The consumption of more than 1 to 2 ounces of alcohol per day is associated with a higher prevalence of hypertension, poor adherence to the antihypertensive therapy, and occasionally, refractory hypertension. Alcohol intake needs to be advised to do so in moderation (i.e., less than 1 to 2 ounces of ethanol per day).
  • Caffeine restriction: Although acute ingestion of caffeine may raise blood pressure, chronic moderate caffeine ingestion appears to have no significant effects on blood pressure. Instruct clients to limit caffeine to 250 mg (the amount in two to three cups of brewed coffee) because it probably raises blood pressure by activating the sympathetic nervous system. This sympathetic response particularly affects those not used to drinking coffee.
  • Relaxation techniques: A variety of relaxation therapies, including transcendental meditation, yoga, biofeedback, and psychotherapy, have been shown to reduce blood pressure in hypertensive clients at least transiently.
  • Smoking cessation: Nicotine definitely increases heart rate and produces peripheral vasoconstriction, which does raise arterial blood pressure for a short time. Smoking cessation is strongly recommended, however, to reduce the client's risk for cancer, pulmonary disease, and cardiovascular disease. Smokers appear to have a higher frequency of malignant hypertension and subarachnoid hemorrhage.
 
Pharmacological Management
  • Thiazide diuretics
    Mechanism: Inhibit Na/K pumps in the distal tubule
    Examples: Hydrochlorothiazide 12.5–25 mg daily
    Chlorthalidone 12.5–50 mg daily
  • 171Loop diuretics
    Mechanism: Inhibit Na/K/Cl ATPase in ascending loop of Henle
    Examples:
    Furosemide 20 mg BD
  • Aldosterone receptor antagonists
    Mechanism: Inhibit aldosterone's effect at the receptor, reducing Na and water retention
    Examples:
    Spironolactone 25 mg daily
  • Nitrates
    Mechanism: Direct vasodilatation by release of nitric oxide
    Examples:
    Isosorbide dinitrate 10 mg TID
  • Beta blockers
    Mechanism: Competitively inhibit the binding of catecholamines to beta-adrenergic receptors
    Examples:
  • Atenolol 25–100 mg PO daily
  • Metoprolol 25–100 mg PO daily or BID
  • Carvedilol 6.25–25 mg PO BID
  • Calcium channel blocker
    Mechanism: Decrease calcium influx into cells of vascular smooth muscle and myocardium
    Examples:
  • Diltiazem 60–480 mg q6h to daily
  • Verapamil 60–480 mg q8h to daily
  • Alpha2 agonists: Central acting agents
    Mechanism: It reduces sympathetic outflow by reducing sympathetic tone.
    Examples:
    Clonidine 0.1–0.6 mg PO BID-TID, Methyldopa
  • Vasodilators
    Mechanism: Direct vasodilation of arterioles via increased intracellular cAMP.
    Examples:
    Hydralazine 20–1000 mg BID-QID
    Minoxidil 2.5–40 mg PO daily-BID
 
Nursing Management
 
Nursing Assessment
  • History: Note the following points when interviewing the hypertensive client: Family history of hypertension, diabetes mellitus, or cardiovascular disease. Previous documentation of high blood pressure, including age of onset and currently prescribed medical regimen.
    • History of any disease or trauma to target organs. Results and side effects of previous antihypertensive therapy.
    • 172History of weight gain, exercise activities, sodium intake, fat intake, and alcohol use.
    • Psychosocial and environmental factors (e.g. emotional stress, cultural food practices, and economic status) that may influence blood pressure control.
    • Presence of other cardiovascular risk factors, including smoking, obesity, hyperlipidemia, and exercise levels.
 
Nursing Diagnosis
  • Altered nutrition status less than body requirement related to restriction in dietary pattern.
  • Knowledge deficit about the disease process, its consequences, and the rationale for intervention and proper administration of prescribed medications.
  • Lack of understanding about the seriousness of high blood pressure, cost of therapy, side effects of medications.
 
Nursing Intervention
  • Provide education to patient about proper diet management.
    • Cut sodium intake to 2.4 g or less per day.
    • Low-fat diet
  • Instruct the patient for regular exercise, and reduce the weight.
  • Smoking cessation.
 
HYPOTENSION
  • Low blood pressure means that blood pressure is lower (less than 90/60 mm Hg) than normal (< 120/80 mm Hg) called hypotension.
  • Low blood pressure occurs when blood pressure is much lower than normal. This means the heart, brain, and other parts of the body do not get enough blood. Normal blood pressure is usually between 90/60 mm Hg and 130/80 mm Hg.
 
Etiology
  • Dehydration: It is common among patients with prolonged nausea, vomiting, diarrhea, or excessive exercise which shunts blood away from the organs to the muscles. Large amounts of water are lost when vomiting and with diarrhea, especially if the person does not drink adequate amounts of fluid to replace the depleted water.
  • Moderate or severe bleeding: It can quickly deplete an individual's body of blood, leading to low blood pressure or orthostatic hypotension. Bleeding can result from trauma, surgical complications, from GI abnormalities, such as ulcers, tumors, or diverticulosis. Occasionally, the bleeding may be so severe and rapid (ruptured aortic aneurysm) that it causes shock and death rapidly.
  • Severe inflammation of organs inside the body: Such as acute pancreatitis can cause low blood pressure. In acute pancreatitis, fluid leaves the blood vessels to enter the inflamed tissues around the pancreas as well as the abdominal cavity, concentrating blood and reducing its volume.
  • Weakened heart muscle: Can cause the heart to fail and reduce the amount of blood it pumps. One common cause of weakened heart muscle is the death of a large portion of the heart's muscle due to a single, large heart attack or repeated smaller heart attacks.
  • 173Pericarditis: It is an inflammation of the pericardium. Pericarditis can cause fluid to accumulate within the pericardium and compress the heart, restricting the ability of the heart to expand, fill, and pump blood.
  • Pulmonary embolism: It is a condition in which a blood clot in a vein (deep vein thrombosis) breaks off and travels to the heart and eventually the lung. A large blood clot can block the flow of blood into the left ventricle from the lungs and severely diminish the blood returning to the heart for pumping. Pulmonary embolism is a life-threatening emergency.
  • Bradycardia: It can decrease the amount of blood pumped by the heart. The resting heart rate for a healthy adult is between 60 and 100 beats/minute. Bradycardia does not always cause low blood pressure. In fact, some highly trained athletes can have resting heart rates in the 40s and 50s (beats per minute) without any symptoms. The slow heart rates are offset by more forceful contractions of the heart that pump more blood than in nonathletes. But in many patients, bradycardia can lead to low blood pressure, light-headedness, dizziness, and even fainting.
  • Sick sinus syndrome: Sick sinus syndrome occurs when the diseased electrical system of the heart cannot generate electrical signals fast enough to maintain a normal heart rate.
  • Heart block: Heart block occurs when the specialized tissues that transmit electrical current in the heart are damaged by heart attacks, degeneration from atherosclerosis, and medications. Heart block prevents some or all of the electrical signals from reaching parts of the heart, and this prevents the heart from contracting as well as it otherwise would.
  • Drug toxicity: Drugs such as digoxin or beta blockers for high blood pressure can slow the transmission of electricity in the heart chemically and can cause bradycardia and hypotension.
  • Tachycardia: It also can cause low blood pressure. The most common example of tachycardia causing low blood pressure is atrial fibrillation. Atrial fibrillation is a disorder of the heart characterized by rapid and irregular electrical discharges from the muscle of the heart causing the ventricles to contract irregularly and rapidly. The rapidly contracting ventricles do not have enough time to fill maximally with blood before each contraction, and the amount of blood that is pumped decreases in spite of the faster heart rate. Other abnormally rapid heart rhythms such as ventricular tachycardia also can produce low blood pressure, sometimes even life-threatening shock.
  • Medications:
    • Medications, such as calcium channel blockers, beta blockers, and digoxin can slow the rate at which the heart contracts. Some elderly people are extremely sensitive to these medications since they are more likely to have diseased hearts and electrical conduction tissues. In some individuals, the heart rate can become dangerously slow even with small doses of these medications.
    • Medications used in treating high blood pressure (such as ACE inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers, and alpha blockers) can excessively lower blood pressure and result in symptomatic low blood pressure, especially among the elderly.
    • Diuretics, such as hydrochlorothiazide and furosemide (Lasix) can decrease blood volume by causing excessive urination.
    • Medications used for treating depression, such as amitriptyline, Parkinson's disease, such as levodopa-carbidopa and erectile dysfunction (impotence).
    • Alcohol and narcotics can also cause low blood pressure.
  • 174Vasovagal reaction: It is a common condition in which a healthy person temporarily develops low blood pressure, slow heart rate, and sometimes, fainting. A vasovagal reaction typically is brought on by emotions of fear or pain, such as having blood drawn, starting an intravenous infusion, or by gastrointestinal upset. Vasovagal reactions are caused by activity of the involuntary (autonomic) nervous system, especially the vagus nerve, which releases hormones that slow the heart and widen the blood vessels. The vagus nerve also controls digestive tract function and senses activity in the digestive system. Thus, some people can have a vasovagal reaction from straining at a bowel movement or vomiting.
  • Postural hypotension: It is a sudden drop in blood pressure when an individual stands up from a sitting, squatting, or supine (lying) position. When a person stands up, gravity causes blood to settle in the veins in the legs so that less blood returns to the heart for pumping, and, as a result, the blood pressure drops.
  • Micturition syncope: It is a temporary drop in blood pressure and loss of consciousness brought about by urinating. This condition typically occurs in elderly patients and may be due to the release by the autonomic nerves of hormones that lower blood pressure.
  • Adrenal insufficiency: Addison's disease can cause low blood pressure. It is a disorder in which the adrenal glands are destroyed. The destroyed adrenal glands can no longer produce sufficient adrenal hormones (specifically cortisol) necessary to maintain normal bodily functions. Cortisol has many functions, one of which is to maintain blood pressure and the function of the heart. Addison's disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, and sometimes, darkening of the skin.
  • Septicemia: It is a severe infection in which bacteria (or other infectious organisms such as fungi) enter the blood. The infection typically originates in the lungs, bladder, or in the abdomen due to diverticulitis or gallstones. The bacteria then enter the blood where they release toxins and cause life-threatening and profound low blood pressure (septic shock), often with damage to several organs.
  • Anaphylaxis (anaphylactic shock): It is a potentially fatal allergic reaction to medications, such as penicillin, intravenous iodine used in some X-ray studies, foods such as peanuts, or bee stings (insect stings). In addition to a severe drop in blood pressure, individuals may also experience hives and wheezing due to constriction of the airways, and a swollen throat which cause difficulty breathing. The shock is caused by enlargement of blood-containing blood vessels and escape of water from the blood into the tissues.
 
Pathophysiology
175
 
Clinical Manifestation
  • Chest pain
  • Shortness of breath
  • Irregular heartbeat
  • Fever higher than 38.3 °C (101 °F)
  • Headache
  • Stiff neck
  • Severe upper back pain
  • Cough with phlegm
  • Prolonged diarrhea or vomiting
  • Dyspepsia (indigestion)
  • Dysuria (painful urination)
  • Adverse effect of medications
  • Acute, life-threatening allergic reaction
  • Seizures
  • Loss of consciousness
  • Profound fatigue
  • Temporary blurring or loss of vision
  • Connective tissue disorder (Ehlers-Danlos syndrome)
  • Black tarry stools
 
Diagnostic Evaluation
  • Complete blood count: CBC may reveal anemia from blood loss or elevated white blood cells due to infection.
  • Blood electrolyte measurements: It may show dehydration and mineral depletion, renal failure or acidosis.
  • Cortisol levels: It can be measured to diagnose adrenal insufficiency and Addison's disease.
  • Blood and urine culture: It can be performed to diagnose septicemia and bladder infections, respectively.
  • Radiology studies: Such as chest X-rays, abdominal ultrasounds, and computerized tomography (CT or CAT) scans may detect pneumonia, heart failure, gallstones, pancreatitis, and diverticulitis.
  • Electrocardiogram: ECG can detect abnormally slow or rapid heartbeats, pericarditis, and heart muscle damage from either previous heart attacks or a reduced supply of blood to the heart muscle that has not yet caused a heart attack.
  • Holter monitor recordings: These are used to diagnose intermittent episodes of abnormal heart rhythms. A Holter monitor is a continuous recording of the heart's rhythm for 24 hours that often is used to chart and diagnose intermittent episodes of bradycardia or tachycardia.
  • Patient-activated event recorder: If the episodes of bradycardia or tachycardia are infrequent, a 24-hour Holter recording may not capture these sporadic episodes. In 176this situation, a patient can wear a patient-activated event recorder for up to 4 weeks. The patient presses a button to start the recording when he or she senses the onset of an abnormal heart rhythm or symptoms possibly caused by low blood pressure. The doctor then analyzes the recordings at a later date to identify the abnormal episodes.
  • Echocardiograms: Echocardiograms can detect pericardial fluid due to pericarditis, the extent of heart muscle damage from heart attacks, diseases of the heart valves, and rare tumors of the heart.
  • Tilt-table tests: It is used to evaluate patients suspected of having postural hypotension or syncope due to abnormal function of the autonomic nerves. During a tilt-table test, the patient lies on an examination table with an intravenous infusion administered while the heart rate and blood pressure are monitored. The table then is tilted upright for 15 minutes to 45 minutes. Heart rate and blood pressure are monitored every few minutes. The purpose of the test is to try to reproduce postural hypotension. Sometimes a doctor may administer epinephrine intravenously to induce postural hypotension.
 
Treatment Management
  • Trendelenburg position: Lying the person in dorsal decubitus position and lifting the legs increase venous return, thus making more blood available to critical organs in the chest and head.
  • Electrolytes to a diet can relieve symptoms of mild hypotension.
  • A morning dose of caffeine can also be effective.
  • Volume resuscitation (usually with crystalloid)
  • Blood pressure support with a vasopressor, e.g. dopamine.
  • Ensure adequate tissue perfusion (maintain SvO2 > 70 with use of blood or dobutamine)
  • Address the underlying problem [i.e. antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc.].
 
Medium-term treatments of hypotension include:
  • Blood sugar control (80–150 by one study)
  • Early nutrition (by mouth or by tube to prevent ileus)
  • Steroid support
 
According to diseases condition:
  • Dehydration: It is treated with fluids and minerals (electrolytes).
    • Mild dehydration without nausea and vomiting can be treated with oral fluids and electrolytes.
    • Moderate to severe dehydration usually is treated in the hospital or emergency room with intravenous fluids and electrolytes.
  • Blood loss: It can be treated by treating the cause of the bleeding, and with intravenous fluids and blood transfusions. Continuous and severe bleeding needs to be treated immediately.
  • Septic shock: It is a medical emergency and is treated with intravenous fluids and antibiotics.
  • 177Blood pressure medications or diuretics: There are adjusted, changed, or stopped by the doctor if they are causing low blood pressure symptoms.
  • Bradycardia: It may be due to a medication. Then change, or stop the medication.
  • Pacemaker: Bradycardia due to sick sinus syndrome or heart block is treated with an implantable pacemaker.
  • Tachycardia: It is treated depending on the nature of tachycardia. Atrial fibrillation can be treated with oral medications, electrical cardioversion, or a catheterization procedure called pulmonary vein isolation. Ventricular tachycardia can be controlled with medications or with an implantable defibrillator.
  • Pulmonary embolism and deep vein thrombosis are treated with blood thinners, intravenous initially with heparin. Later, oral warfarin or other oral medications are substituted for heparin.
  • Pericardial fluid from pericarditis can be removed by a procedure called pericardiocentesis.
  • Postural hypotension:
    • Changes in diet, such as increasing water and salt intake.
    • Increasing intake of caffeinated beverages (because caffeine constricts blood vessels).
    • Using compression stockings to compress the leg veins and reduce the pooling of blood in the leg veins.
    • Pyridostigmine, an anticholinesterase medication, works on the autonomic nervous system, especially when a person is standing up.
  • Postprandial hypotension refers to low blood pressure occurring after meals. Ibuprofen or indomethacin may be beneficial.
  • Vasovagal syncope: It can be treated with several types of drugs, such as:
    • Beta blockers: Propranolol
    • Selective serotonin reuptake inhibitors: Fluoxetine, escitalopram oxalate, paroxetine, sertraline, citalopram and fluvoxamine.
    • Fludrocortisone: A drug that prevents dehydration by causing the kidneys to retain water also may be used.
    • Pacemaker can also be helpful when a patient fails drug therapy.
 
Prevention
  • Stand up slowly.
  • Drink more water.
  • Drink little or no alcohol.
  • Limit or avoid caffeine.
  • Wear compression stockings.
 
CHRONIC VENOUS INSUFFICIENCY
Chronic venous insufficiency or CVI is a medical condition where the veins cannot pump enough oxygen and blood back to the heart. It is sometimes referred to as an ‘impaired musculovenous pump’. This is due to damaged or ‘incompetent’ valves as may occur after deep vein thrombosis.
178It is a condition that occurs when the venous wall or valves in the leg veins are not working effectively, making it difficult for blood to return to the heart from the legs. CVI causes blood to ‘pool’ or collect in these veins, and this pooling is called stasis.
 
Etiology
The cause of CVI is related either to poorly functioning vein valves or blockage in the veins. Vein valves are designed to allow blood to flow against gravity from the legs back to the heart. When the valves fail to close properly, gravity wins and the flow reverses. This is called venous reflux. Vein valves may fail to close due to:
  • Vein wall weakness that causes the vein to enlarge so that the valves cannot close, when these valves become damaged, allows the blood to leak backward. Valve damage may occur as the result of:
    • Aging
    • Extended sitting
    • Standing or a combination of aging
    • Reduced mobility.
  • A history of blood clots or deep vein thrombosis in the vein that damages the valve. DVT occurs when a blood clot blocks blood from flowing toward the heart, out of a deep or perforating vein. The blood trying to pass through the blocked veins can increase the blood pressure in the vein, which, in turn, overloads the valves. Vein valves that do not work properly are called incompetent because they stretch and no longer work efficiently, and incompetent valves contribute to CVI.
  • Phlebitis: It occurs when a superficial or deep vein becomes swollen and inflamed. This inflammation causes a blood clot to form, which can also lead to DVT.
  • An absence of vein valves since birth.
  • Varicose veins are hereditary most of the time and generally occur in several members of the same family.
  • Much less commonly, varicose veins develop after a trauma or injury.
 
Risk Factors
The most important risk factors are:
  • Deep vein thrombosis (DVT)
  • Varicose veins or a family history of varicose veins
  • Obesity
  • Pregnancy
  • Inactivity
  • Smoking
  • Extended periods of standing or sitting
  • Female sex
  • Age over 50
 
Clinical Manifestation
It is characterized by:
  • Chronic venous stasis
  • Edema in lower legs and ankles, especially after extended periods of standing.
  • 179Altered pigmentation
  • Pain
  • Tiredness in legs
  • Stasis dermatitis
  • Superficial veins may be dilated and tortuous
  • Skin ulceration causes skin to be dry, cracks and itching, subcutaneous tissue fibrosis and atrophy.
 
Pathophysiology
 
Diagnostic Evaluation
  • Physical examination: Inspection and palpation may reveal visual evidence for chronic venous disease. The surface of the skin is examined for irregularities or bulges to suggest the presence of varicose veins. Hyperpigmentation, stasis dermatitis, atrophic blanche may be observed.
  • Tourniquet test: A classic tourniquet (or Trendelenberg) test may be performed at bedside to help distinguish deep from superficial reflux. The test is performed with the patient lying down to empty the lower extremity veins. The upright posture is resumed after applying a tourniquet or using manual compression at various levels. In the presence 180of superficial disease, the varicose veins will remain collapsed if compression is more proximal to the point of reflux. With deep venous insufficiency, the varicose veins will appear despite the use of the tourniquet or manual compression. Although useful to help determine the distribution of venous insufficiency, this test does not help determine the extent or severity of disease or provide information about the cause.
  • Doppler study: The use of continuous wave Doppler has often been used to assist in the bedside evaluation. The presence and direction of flow in the veins may be determined after maneuvers, such as the Valsalva maneuver or the sudden release of thigh or calf compression. Minimal signal should be detected toward the feet with these maneuvers. This technique also has been used to assess the great and short saphenous veins, although this is technically more difficult because of the lack of direct visualization.
 
Noninvasive Testing
  • Venous duplex imaging: Venous duplex imaging is a well-established method to diagnoses DVT. The technique is also used to confirm the diagnosis of CVI and assess its etiology and severity. This provides information about the anatomic extent of disease involving the deep and superficial systems, as well as perforators. A standard venous duplex examination is performed to exclude DVT or venous obstruction. Venous compressibility complimented by flow characteristics is the key element of the examination to exclude thrombosis. The direction of flow may be assessed in a 30° reverse Trendelenburg position during provocative maneuvers, such as the Valsalva maneuver, or after augmenting flow with limb compression. The use of a cuff inflation-deflation method with rapid cuff deflation in the standing position is preferred to induce reflux.
  • Photoplethysmography: Photoplethysmography (PPG) may be used to establish a diagnosis of CVI. Relative changes in blood volume in the dermis of the limb can be determined by measuring the backscatter of light emitted from a diode with a photosensor. A PPG probe is placed on the foot with maneuvers to empty the foot with calf muscle contraction. Then return of blood is detected by increased backscatter of light and the refill time may be calculated. The venous refill time is the time required for the PPG tracing to return to 90% of the baseline after cessation of calf contraction.
  • Air plethysmography: Air plethysmography (APG) has the ability to measure each potential component of the pathophysiological mechanisms of CVI, reflux, obstruction, and muscle pump dysfunction. Changes in limb volume are measured by air displacement in a cuff surrounding the calf during maneuvers to empty and fill the venous system. Venous outflow is assessed during rapid cuff deflation on an elevated limb that has a proximal venous occlusion cuff applied. The outflow fraction at 1 second is the primary parameter used to evaluate the adequacy of outflow. The limb is then placed in the dependent position to evaluate the venous filling. The rate of refill is used to determine the presence and severity of reflux.
 
Invasive Testing
  • Phlebography: Phlebography or venography may be either ascending or descending.
    • Ascending phlebography involves the injection of contrast in the dorsum of the foot with visualization of contrast travelling up the lower extremity in the deep venous system. Although ascending phlebography is considered the gold standard to determine the patency of veins, it has been largely replaced by noninvasive imaging. It does provide details of venous anatomy that may be useful with surgical interventions and can help to distinguish primary from secondary disease.
    • 181Descending phlebography involves proximal injection of contrast in a semivertical posture on a tilt table with the use of the Valsalva maneuver. It is most useful to identify reflux in the common femoral vein and at the saphenofemoral junction, but it may be used to evaluate other locations.
  • Ambulatory venous pressure: Ambulatory venous pressure (AVP) monitoring is the hemodynamic gold standard in assessing CVI. The technique involves insertion of a needle into the pedal vein with connection to a pressure transducer. The pressure is determined at rest and after exercise is performed, usually in the form of toe raises. The pressure also is monitored before and after the placement of an ankle cuff to help distinguish deep from superficial reflux. The mean ambulatory venous pressure (normal range of 20 to 30 mm Hg) and refill time (normal range of 18 to 20 seconds) are the most useful measurements.
 
Management
The goals of treatment are to reduce the pooling of blood and prevent leg ulcers.
  1. Conservative treatment: The initial treatment of CVI involves conservative measures to reduce symptoms and help prevent the development of secondary complications and the progression of disease.
    Behavioral measures such as elevating the legs to minimize edema and reducing intra-abdominal pressure should be advocated.
    A simplified overview for the diagnosis and treatment of CVI based on pathophysiological mechanisms
  2. 182Compression stockings: The most conservative approach is to wear properly fitting support hose (also called compression stockings). They also come in different compressions varying from 8 to 10 mm Hg up to 40 to 50 mm Hg.
    When wearing compression stockings, be sure to take them off at the end of the day to wash and dry them, and to clean and check the skin. Make sure the stockings fit so there is no bunching. Elastic stockings that fit poorly can actually make the condition worse by blocking blood flow in the area where they have bunched up.
  3. Exercise: Abnormalities in the calf and foot muscle pump functions play a significant role in the pathophysiology of CVI. Graded exercise programs have been used in an effort to rehabilitate the muscle pump and improve the symptoms of CVI.
  4. Skin care: Practicing good skin hygiene is important. Keep skin moisturized so that it doesn't flake or crack easily. If the skin is not broken or leaking fluid but is inflamed, the doctor may recommend an anti-itch cream, such as the one containing hydrocortisone, a cream containing zinc oxide to protect the skin or an antifungal cream to prevent fungal infections.
  5. Wound care: The development of stasis dermatitis needs to be treated with a topical steroid. With venous ulcers, bacterial overgrowth control and aggressive wound care are required to minimize infectious complications. A variety of hydrocolloids and foam dressings are available to control wound fluid drainage and resultant maceration of the adjacent skin. In the presence of an infected ulcer bed, silver-impregnated dressings have been effective in controlling infection and restoring tissue integrity.
  6. Antibiotics: Antibiotics may be prescribed to clear skin infections related to CVI, but the underlying disease must be treated to prevent a recurrence. Deeper infections and ulcers may also be treated with antibiotics.
 
Other Medications
  • Diuretics may be used to reduce swelling.
  • Pentoxifylline, which improves the flow of blood through the vessels, may be used in combination with compression therapy to help heal leg ulcers.
  • Anticoagulation therapy may be recommended for those persons who have recurring problems with the veins in their legs.
  • A specially medicated wrap, known as an Unna Boot, combines multilayer compression with a zinc oxide gel-based wound cover that forms a semi-rigid bandage. Other multilayer compression systems are available and are often used in combination with topical wound care products.
 
Nonsurgical Management
Nonsurgical treatments include sclerotherapy and endovenous thermal ablation.
  1. Sclerotherapy involves the injection of a solution directly into spider veins or small varicose veins that causes them to collapse and disappear. Several sclerotherapy treatments are usually required to achieve the desired results. Sclerotherapy can eliminate the pain and discomfort of these veins and helps prevent complications such as venous hemorrhage and ulceration. It is also frequently performed for cosmetic reasons.
  2. 183Endovenous thermal ablation is a newer technique that uses a laser or high-frequency radio waves to create intense local heat in the affected vein. The technology is different with each energy source, but both forms of local heat close up the targeted vessel. This treatment closes off the problem veins but leaves them in place so there is minimal bleeding and bruising. Compared with ligation and stripping, endovenous thermal ablation results in less pain and a faster return to normal activities, with similar cosmetic results.
 
Surgical Treatment
  1. Ligation and stripping are often performed in combination.
    • Vein ligation is a procedure in which a vascular surgeon cuts and ties off the problematic veins. Most patients recover in a few days and can resume their normal activities.
    • Stripping is the surgical removal of larger veins through two small incisions. Stripping is a more extensive procedure and may require up to 10 days for recovery. It usually causes bruising for several weeks after surgery. Removing the saphenous vein with high ligation of the saphenofemoral junction is considered durable and the standard for many patients with CVI. In addition, large venous varicose clusters that communicate with the incompetent saphenous vein can be avulsed at the same setting by a technique called stab phlebectomy.
  2. Microincision or ambulatory phlebectomy or venous phlebectomy is a minimally invasive procedure in which small incisions or needle punctures are made over the veins, and a phlebectomy hook is used to remove the problem veins.
    This is a newer technique of transilluminated power phlebectomy to remove clusters of varicosities with fewer incisions and a decrease in operation time. The ligation and stripping of the great saphenous vein can be applied to all clinical cases with superficial venous reflux and have been shown to result in significant improvements in venous hemodynamic, possibly eliminate concomitant deep venous reflux, provide symptomatic relief of advanced stages of CVI, and assist in ulcer healing.
  3. Subfascial endoscopic perforator surgery: Subfascial endoscopic perforator surgery (SEPS) provides a means to ligate incompetent perforator veins by gaining access from a remote site on the leg that is away from the area with lipodermatosclerosis or ulcers.
  4. Valve reconstruction: Venous valve injury or dysfunction may contribute to the development and progression of CVI. Venous valve reconstruction of the deep vein valves has been performed in selected patients with advanced CVI who have recurrent ulceration with severe and disabling symptoms. An open technique for repairing the femoral vein valve that renders the valve leaflets competent has been described. This technique of open valvuloplasty has been refined, and closed techniques for venous repair developed with transcommissural valvuloplasty.
  5. Vein bypass in the leg is similar to heart bypass surgery, just in a different location. It involves using a portion of healthy vein transplanted from elsewhere in body to reroute blood around the vein affected by CVI. Bypass is used for treatment of CVI in the upper thigh and only in the most severe cases, when no other treatment is effective.
  6. 184Angioplasty and stenting: An angioplasty is the use of a balloon to push open a narrowed or blocked portion of the vein. A stent is a metal-scaffold tube that helps to keep the narrowed areas open. In some instances, depending on where the vein blockage is, this may be used to open up the blockage. The procedure is performed through small needle punctures in the veins, either behind the knee or in the groin.
 
Prevention
Like any disease, CVI is most treatable in its earliest stages. Vascular medicine or vascular surgery specialists typically recommend a combination of treatments for people with CVI. Some of the basic treatment strategies include:
  • Avoid long periods of standing or sitting: If you must take a long trip and will be sitting for a long time, flex and extend your legs, feet, and ankles about 10 times every 30 minutes to keep the blood flowing in the leg veins. If you need to stand for long periods of time, take frequent breaks to sit down and elevate your feet.
  • Exercise regularly
  • Lose weight
  • Elevate your legs
  • Wear compression stockings
  • Take antibiotics as needed to treat skin infections
  • Practice good skin hygiene.
 
VARICOSE VEINS
Varicose veins are veins that have become enlarged and tortuous. The term commonly refers to the veins on the leg, although varicose veins can occur elsewhere.
 
Etiology
  • Varicose veins are more common in women than in men
  • Heredity
  • Pregnancy
  • Obesity
  • Menopause
  • Aging (varicose veins usually affect people between the ages of 30 and 70)
  • Prolonged standing
  • High blood pressure inside your superficial leg veins
  • Leg injury
  • Abdominal straining
  • Not exercising enough, smoking
  • Postphlebitic obstruction or incontinence
  • Venous and arteriovenous malformations
  • Varicose veins could also be caused by elevated levels of homocysteine in the body
185
 
Pathophysiology
 
Clinical Manifestation
  • Aching, heavy legs (often worse at night and after exercise).
  • Appearance of spider veins (telangiectasia) in the affected leg.
  • Ankle swelling, especially in the evening.
  • A brownish-yellow shiny skin discoloration near the affected veins.
  • Redness, dryness, and itchiness of areas of skin, termed as stasis dermatitis or venous eczema, because of waste products building up in the leg.
  • Cramps may develop especially when making a sudden move as standing up.
  • Minor injuries to the area may bleed more than normal or take a long time to heal.
  • In some people, the skin above the ankle may shrink (lipodermatosclerosis) because the fat underneath the skin becomes hard.
  • 186Restless legs syndrome appears to be a common overlapping clinical syndrome in patients with varicose veins and other chronic venous insufficiency.
  • Whitened, irregular scar-like patches can appear at the ankles. This is known as atrophie blanche.
 
Diagnostic Evaluation
  • General health, medical history, physical examination and symptoms.
 
Stages
  • C0 not visible or palpable signs of venous disease
  • C1 telangiectasia or reticular veins
  • C2 varicose veins
  • C3 edema
  • C4a skin changes due to venous disorders: pigmentation, eczema
  • C4b skin changes due to venous disorders: lipodermatosclerosis, atrophie blanche
  • C5 as C4 but with healed ulcers
  • C6 skin changes with active ulcers (venous insufficiency ulceration)
 
Other Diagnostic Tests
  1. Trendelenburg test:
    • Used to assess the competence of SFJ (saphenofemoral junction).
    • Patient lies flat
    • Elevate the leg and gently empty the veins
    • Palpate the SFJ and ask the patient to stand whilst maintaining pressure.
      • Findings are: Rapid filling after thumb released—SFJ is incompetent.
      • Filling from below upwards without releasing thumb—presence of distal incompetent perforators
  2. Fegan's test:
    • Line of varicosities is marked.
    • Site where perforators pierce deep fascia—bulges on standing and circular depressions on lying.
  3. Perthe's test:
    • Empty the vein and place a tourniquet around the thigh, stand the patients up.
    • Ask them to rapidly stand up and down on their toes—filling of the veins indicates deep venous incompetence. This is a painful and rarely used test.
  4. Schwartz test: In standing position, tap the lower part of vein. Then impulse is felt on saphenofemoral junction.
  5. Duplex Doppler ultrasound scanning: Duplex ultrasound uses painless, high-frequency waves higher than human hearing can detect. Physician uses duplex ultrasound to measure the speed of blood flow and to see the structure of leg veins. The test can take approximately 20 minutes for each leg. Besides showing varicose veins, duplex ultrasound may help the physician decide whether varicose veins could be related to some other condition rather than the veins themselves.
187
 
Treatment Management
  • Compression stockings: For more severe varicose veins, the physician may prescribe compression stockings. Compression stockings are elastic stockings that squeeze veins and stop excess blood from flowing backward. In this way, compression stockings also can help heal skin sores and prevent them from returning. Patient may be required to wear compression stockings daily for the rest of life. For many patients, compression stockings effectively treat varicose veins and may be all that are needed to relieve pain and swelling and prevent future problems.
  • Sclerotherapy: During sclerotherapy, physician injects a chemical into varicose veins. The chemical irritates and scars veins from the inside out so abnormal veins can then no longer fill with blood. Blood that would normally return to the heart through these veins returns to the heart through other veins. The body will eventually absorb the veins that received the injection.
  • Vein stripping: To perform vein stripping, physician first makes a small incision in the groin area and usually another incision in calf below the knee. Then physician disconnects and ties off all major varicose vein branches associated with the saphenous vein, the main superficial vein in the leg. The physician then removes the saphenous vein from the leg. A procedure, called small incision avulsion, or sometimes ambulatory phlebectomy, can be done alone or together with vein stripping. Small incision avulsion allows physician to remove individual varicose vein clusters from the leg using hooks passed through small incisions. In a similar procedure called TIPP, physician shines an intense light on leg to show veins. Once physician locates a varicose vein, he or she passes a suction device through a tiny incision and suctions out the vein. Although these procedures sound painful, they cause relatively little pain and are generally well tolerated. Patient's vascular surgeon will advice regarding which procedure is the best for a particular situation.
  • Ablation and laser treatment: Ablation uses a thin, flexible tube called a catheter inserted into a vein in the leg. Tiny electrodes at the tip of the catheter heat the walls of the vein and destroy it. Similarly, laser treatment uses a tiny fiber that is placed in the vein through a catheter. The fiber sends out laser energy that kills the diseased portion of the vein, and the vein closes off. These two modes of treatment frequently replace the stripping that is performed on the saphenous vein that is described above. The objective is to destroy the saphenous vein that is providing the source for varicose vein development. It can be performed alone or in conjunction with ambulatory phlebectomy, which removes individual clusters of varicose veins from the leg.
 
Complications
Most varicose veins are reasonably benign, but severe varicosities can lead to major complications, due to the poor circulation through the affected limb.
  • Pain, heaviness, inability to walk or stand for long hours, thus hindering work.
  • Dermatitis which could predispose skin loss.
  • Skin ulcers especially near the ankle, usually referred to as venous ulcers.
  • Development of carcinoma or sarcoma in longstanding venous ulcers.
  • Severe bleeding from minor trauma, of particular concern in the elderly.
  • 188Blood clotting within affected veins called superficial thrombophlebitis.
  • Acute fat necrosis can occur, especially at the ankle of overweight patients with varicose veins.
  • The afflicted person suffers tenderness in that region.
 
Nursing Management
 
Nursing Assessment
  • Inspect for dilated, tortuous veins.
  • Perform the manual compression test to determine severity of disorder.
  • With the fingertips of one hand, feel dilated vein.
  • With your other hand, compress firmly at least 8 inches higher on the leg.
  • Feel for an impulse transmitted towards your lower hand.
  • Competent saphenous valves should block the impulse. If you feel the impulse, the patient has varicose veins with incompetent valves.
  • Perforating veins that are incompetent may be felt as bulging circles at intervals beneath the skin.
  • Assess for any ulceration, CVI or signs of infection.
 
Nursing Diagnosis
  • Impaired tissue integrity related to chronic changes and postoperative inflammation.
 
Nursing Interventions
  • Maintain elastic compression bandages from toes to groin.
  • Monitor neurovascular status of feet.
  • Elevate legs about 30 degrees, providing support for the entire leg.
  • Encourage ambulation.
  • Monitor for signs of bleeding, especially for first 24 hours.
  • If bleeding occurs, elevate the leg, apply pressure and notify the physician.
  • Be alert for complaints of pain over bony prominences; if elastic bandage is too tight, loosen it and then reapply it.
  • Observe the signs of cellulitis.
  • Acute pain related to surgical incisions, inflammation.
  • Encourage bedrest the first day with legs elevated, the second day, encourage ambulation for 5 to 10 min every 2 hours.
  • Advice to avoid prolonged standing, sitting, or crossing legs to prevent obstruction.
  • Administer analgesics as prescribed.
 
Health Education
  • Postoperative instructions: Instruct the patient to:
    • Wear pressure bandage or elastic stockings as prescribed—usually for 3 to 4 weeks after surgery.
    • Elevate legs about 30 degrees and provide adequate support for the entire leg.
    • Take analgesics for pain as ordered.
    • 189Report such signs as sensory loss, calf pain or fever to the health care providers.
    • Avoid dangling of legs.
    • Walk as able.
    • Note that complaints of patchy numbness can be expected but should disappear in less than 1 year.
    • Follow conservative management instructions to prevent recurrence.
  • Conservative management: Instruct the patient to:
    • Avoid activities that cause venous stasis by obstructing venous flow.
    • Control excessive weight gain.
    • Wear firm elastic support as prescribed, from toe to knee when in upright position.
    • Elevate foot of head 6 to 8 inches for night sleeping.
    • Avoid injuring legs.
BIBLIOGRAPHY
  1. Black M. A textbook of medical surgical nursing. Elsevier  Noida,  8th ed. 1307–40.
  1. Brunner S. A textbook of medical surgical nursing. Lippincott Company.  Philadelphia.  10th ed. 2007. 756–65.
  1. Hopper P, William L. Understanding of medical surgical nursing. Devis.  2nd ed. 2003. 286–97.
  1. Lemone P, Burke K. A textbook of medical surgical nursing. Dorling Kindersely.  South Asia.  4th ed. 2007.
  1. Wilkins and William L. Mannual of nursing practice. Elsevier  Noida,  8th ed.

Blood Disorders4

 
INTRODUCTION
Blood is a fluid connective tissue. It circulates continually around the body, allowing constant communication between tissues distant from each other.
It transports:
  • Oxygen from the lungs to the tissues and carbondioxide from the tissues to the lungs for excretion.
  • Nutrients from the alimentary tract to the tissues and cell wastes to the excretory organs principally the kidneys.
  • Hormones secreted by endocrine glands to their target glands and tissues.
  • Clotting factors that coagulate blood, minimizing bleeding from ruptured blood vessels.
191Blood is composed of a clear, straw-colored watery fluid called plasma in which several different types of blood cells are suspended. Plasma normally constitutes 55% of the volume of blood. The remaining 45% is accounted for by the cellular fraction of blood.
There are three types of blood cell:
  • Erythrocytes
  • Platelets
  • Leukocytes.
Blood cells are synthesized mainly in red bone marrow. Some lymphocytes additionally are produced in lymphoid tissue. In bone marrow all blood cells originate from pluripotent (i.e. capable of developing into one of a number of cell types) stem cells and go through several developmental stages before entering the blood.
Different types of blood cell follow separate lines of development. The process of blood cell formation is called hemopoiesis.
 
Erythrocytes
Red blood cells are biconcave disks they have no nucleus, and their diameter is about 7 micrometers. Their main function is in gas transport, mainly of oxygen, but they also carry some carbondioxide.
Life span and functions of erythrocytes.
Erythrocytes are produced in red bone marrow which is present in the ends of long bones and in flat and irregular bones. They pass through the different stages of development before entering the blood. Their life span in the circulation is about 120 days. The process of development of red blood cells from stem cells takes about 7 days and is called erythropoiesis. The immature cells are released from the blood stream as reticulocytes, and then mature into erythrocytes over a day or two within the circulation. Both vitamin B12 and folic acid are required for red blood cell synthesis. They are absorbed in the intestine, although vitamin B12 must be bound to intrinsic factor to allow absorption to take place.
Anemia refers to a deficiency in a number of circulating red blood cells available for oxygen transport. This condition is determined by an overall decrease in the number of RBCs, the concentration of RBCs (hematocrit), and the hemoglobulin concentration of the RBCs.
 
ANEMIA
Anemia is a reduction in red blood cells (erythrocytes) which inturn decreases the oxygen carrying capacity of the blood. Anemia reflects on abnormality in RBC number, structure and function.
 
Etiology
  • Loss of RBCs: Occurs with bleeding, potentially from a major source, such as the gastrointestinal tract, the uterus, the nose, or a wound.
  • Decreased production of RBCs: Can be caused by a deficiency in cofactors (including folic acid, vitamin B12, and iron) required for erythropoiesis, RBC production may also be reduced if the bone marrow is suppressed (e.g. by tumor, medication, toxin) or is in adequately stimulated because of a lack of erythropoietin (as occur in chronic renal disease).
  • 192Increased destruction of RBCs: May occur because of an overactive RES (reticuloendothelial system) or because the bone marrow produces abnormal RBCs that are then destroyed by the RES (sickle cell anemia).
 
Classification of Anemia
 
Morphologic Classification
  • Normocytic, normochromic
  • Macrocytic, normochromic
  • Microcytic, hypochromic.
 
Etiological Classification
1. Decreased erythrocyte production (hypoproliferative anemia)
  • Decreased hemoglobin production
    • Iron deficiency
    • Thalassemias.
  • Defective DNA synthesis
    • Cobalamin deficiency
    • Folic acid deficiency.
  • Decreased number of erythrocyte precursors
    • Aplastic anemia
    • Chronic diseases
    • Chemotherapy.
  • Blood loss
    • Acute: Trauma, blood vessel rupture
    • Chronic: Gastritis, menstrual flow, hemorrhoids.
  • Increased erythrocyte destruction (hemolytic anemia)
    • Intrinsic: Abnormal hemoglobin (sickle cell anemia), enzyme deficiency (G-6-PD)
    • Extrinsic: Physical trauma, medications, and toxins.
Relationship between morphologic classification and etiologies of anemia
Morphology
Etiology
Normocytic, normochromic (nomal size and color)
Acute blood loss, hemoptysis, chronic renal disease, cancer, aplastic anemia, sickle cell anemia
Macrocytic, normochromic (large size, normal color)
Cobalamin (vitamin B12) deficiency, folic acid deficiency
Microcytic, hypochromic (small size, pale color)
Iron deficiency anemia, thalassemia, and lead poisoning
193
 
Iron Deficiency Anemia
Iron deficiency anemia typically results when the intake of dietary iron is inadequate for hemoglobin synthesis. The body can store about one fourth to one third of its iron, and it is not until those stores are depleted that iron deficiency anemia actually begins to develop.
It is defined as anemia associated with either inadequate, absorption or excessive loss of iron; it is chronic, microcytic, and hypochromic anemia.
 
Etiology
  • In children, adolescents, and pregnant women, inadequate iron in diet; required to keep up with increased growth.
  • For adults, blood loss (from ulcers, gastritis, inflammatory bowel disease, or gastrointestinal tumors).
  • In premenopausal women, menorrhagia.
  • In chronic alcoholics, chronic blood loss from gastrointestinal tract.
  • Iron malabsorption after gastrectomy or with celiac disease.
 
Clinical Manifestation
Body system
Mild (10–14 g/dl)
Moderate (6–10 g/dl)
Severe (< 6 g/dl)
Integumentary
None
None
Pallor, jaundice, pruritis
Eyes
None
None
Icteric conjunctiva and sclera, blurred vission
Mouth
None
None
Glossitis, smooth tongue
Cardiovascular
Palpitation
Increased palpitations, bounding pulse
Tachycardia, systolic mummur, angina, MI
Pulmonary
Exertional dyspnea
Dyspnea
Tachypnea, orthopnea, dyspnea
Neurologic
None
Roaring in ears
Headache, vertigo, irritability, impaired thought process
Gastrointestinal
None
None
Anorexia, hepatomegaly, splenomegaly, difficulty in swallowing, sore mouth
Musculoskeletal
None
None
Bone pain
General
None
Fatigue
Sensitivity to cold, weight loss, lethargy
 
Diagnostic Evaluation
  • History and physical examination:
    • History: Ask the patient for socioeconomic status, any disease, injury, etc.
    • In physical examination check the vital signs temperature, pulse, respiration, blood pressure. Assess the skin color and signs of anemia. Check the body weight.
  • Red blood cell size and color: With iron deficiency anemia, red blood cells are smaller and paler in color than normal.
  • Hematocrit: This is the percentage of blood volume made up by red blood cells. Normal levels are generally between 34.9 and 44.5 percent for adult women and 38.8 to 50 percent for adult men. These values may change depending on age.
  • 194Hemoglobin: Lower than normal hemoglobin levels indicate anemia. The normal hemoglobin range is generally defined as 13.5 to 17.5 grams (g) of hemoglobin per deciliter (dL) of blood for men and 12.0 to 15.5 g/dL for women. The normal ranges for children vary depending on the child's age and sex.
  • Ferritin: This protein helps store iron in body, and a low level of ferritin usually indicates a low level of stored iron.
  • Endoscopy: To check for bleeding from a hiatal hernia, an ulcer or the stomach with the aid of endoscopy.
  • Colonoscopy: To rule out lower intestinal sources of bleeding.
  • Ultrasound: Women may also have a pelvic ultrasound to look for the cause of excess menstrual bleeding, such as uterine fibroids.
 
Management
To treat iron deficiency anemia, it is recommend to take iron supplements.
 
Medical Management
  • Oral iron preparations—ferrous sulfate, ferrous gluconate, and ferrous fumarate available.
  • In case, oral iron is poorly absorbed or poorly tolerated, or iron supplementation is needed in large amounts, intravenous or intramuscular administration of iron dextran needed.
  • Before parenteral administration, a small test dose administered to avoid risk of anaphylaxis.
  • Emergency medications (e.g. epinephrine) should be close at hand. If no signs of allergic reaction occurred after 30 minutes, remaining dose administered.
  • IM injection causes local pain and stain skin. Side effects minimized by using Z-track technique for administering iron dextran deep into gluteus maximus muscle.
  • Because of problems with IM administration, IV route is preferred.
 
Dietary Management
Foods rich in iron include:
  • Red meat
  • Pork
  • Poultry
  • Seafood
  • Beans
  • Dark green leafy vegetables, such as spinach
  • Dried fruit, such as raisins and apricots
  • Iron-fortified cereals, breads and pastas
  • Peas.
Choose foods containing vitamin C to enhance iron absorption.
To enhance the body's absorption of iron by drinking citrus juice or eating other foods rich in vitamin C at the same time. Vitamin C in citrus juices, like orange juice, helps body to better absorb dietary iron.
195Vitamin C is also found in:
  • Broccoli
  • Grapefruit
  • Kiwi
  • Leafy greens
  • Melons
  • Oranges
  • Peppers
  • Strawberries
  • Tangerines
  • Tomatoes.
 
MEGALOBLASTIC ANEMIA
Megaloblastic anemias are a group of disorders caused by impaired DNA synthesis and characterized by the presence of large RBCs. When DNA synthesis impaired, defective RBC maturation results. The RBCs are large (macrocytic) and abnormal and are referred to as megaloblasts.
It is caused by deficiencies of vitamin B12 or folic acid, this type of RBC deformity can also occur from suppression of DNA synthesis by drugs.
 
Types
  • Cobalamin (vitamin B12) deficiency.
  • Folic acid deficiency.
 
Cobalamine (Vit B12) Deficiency
It is also known as pernicious anemia. It is caused by decreased absorption of vitamin B12. Normally a protein termed intrinsic factor is secreted by the parital cells of the gastric mucosa. Intrinsic factor is required for cobalamin absorption. Therefore intrinsic factor is not secreted cobalamin will not be absorbed (cobalamin is normally absorbed in the distal ileum).
 
Etiology
 
Folic Acid Deficiency
  • People who rarely eat uncooked vegetables.
  • Alcohol increases folic acid requirements and have diet deficient in vitamin.
  • Patients with chronic hemolytic anemias and women who are pregnant.
  • Patients with malabsorptive diseases of the small bowel, such as sprue, may not absorb folic acid normally.
 
Vitamin B12 Deficiency
  • Inadequate dietary intake; who consume no meat or dairy products.
  • Faulty absorption from gastrointestinal tract such as Crohn's disease, or after ileal resection or gastrectomy.
  • Absence of intrinsic factor, as in pernicious anemia. Without intrinsic factor, orally consumed vitamin B12 cannot be absorbed, and RBC production is eventually diminished.
196
 
Clinical Manifestation
Signs and symptoms of vitamin deficiency anemia include:
  • Fatigue
  • Shortness of breath
  • Dizziness
  • Pale or yellowish skin
  • Irregular heartbeats
  • Weight loss
  • Numbness or tingling in your hands and feet
  • Muscle weakness
  • Personality changes
  • Unsteady movements
  • Mental confusion or forgetfulness.
Vitamin deficiencies usually develop slowly over several months to years. Vitamin deficiency symptoms maybe subtle at first, but they increase as the deficiency worsens.
 
Diagnostic Evaluation
  • The number and appearance of red blood cells: People with anemia have fewer red blood cells than normal. In vitamin deficiency anemia related to a lack of vitamin B12 and folate, the red blood cells appear large and underdeveloped. In advanced deficiencies, the numbers of white blood cells and platelets also might be decreased and look abnormal under a microscope.
  • The amount of folate, vitamin B12 and vitamin C in blood: Folate and vitamin B12 levels are measured at the same time because these deficiencies can cause similar signs and symptoms.
  • Antibodies test: A sample of blood to check for antibodies to intrinsic factor. Their presence indicates pernicious anemia.
  • Methylmalonic acid test: To measure the presence of a substance called methylmalonic acid. The level of this substance is higher in people with vitamin B12 deficiency.
  • Schilling test: In this test, first ingest a tiny amount of radioactive vitamin B12. Then blood is checked, if body absorbed the vitamin B12 or not. After that, ingest a combination of radioactive vitamin B12 and intrinsic factor. If the radioactive B12 is absorbed only when taken with intrinsic factor, it confirms that lack of intrinsic factor.
 
Management
 
Medical Management
  • Increasing amount of folic acid in diet and administering 1 mg of folic acid daily.
  • Folic acid administered intramuscularly only for people with malabsorption problems.
  • After hemoglobin level returns to normal, folic acid replacement can be stopped.
  • Vitamin B12 deficiency treated by vitamin B12 replacement.
  • Vegetarian supplements through vitamins or fortified soy milk.
  • If deficiency due to defective absorption or absence of intrinsic factor, replacement is by monthly intramuscular injections of vitamin B12, usually at a dose of 1000 μg. To prevent recurrence, vitamin B12 therapy must be continued for life.
197
 
FOLIC ACID DEFICIENCY ANEMIA
Folic acid deficiency also causes megaloblastic anemia. Folate deficiency anemia is a decrease in red blood cells (anemia) due to a lack of folate. Folate is a type of B vitamin. It is also called folic acid. Folic acid is required for DNA synthesis leading to RBC formation and maturation.
 
Etiology
  • Poor nutrition especially a lack of leafy green vegetables, lever, citrus fruits, nuts and grains.
  • Malabsorption syndrome particularly small bowel disorders.
  • Drugs that impede the absorption and use of folic acid (e.g. methotraxate), antiseizure drugs (e.g. phenobarbital), and others.
  • Alcohol abuse and anorexia.
  • Hemodialysis patients because folic acid is lost during dialysis.
  • Pregnancy.
 
Clinical Manifestation
  • Headache
  • Fatigue
  • Pallor
  • Sore mouth and tongue
  • Abnormal paleness or lack of color in the skin
  • Decreased appetite
  • Irritability
  • Diarrhea.
 
Diagnostic Evaluation
  • History and physical examination
  • Blood test
  • Complete blood count (CBC)
  • Serum folate level is low (3–25 mg/ml).
 
Management
Folic acid deficiency is treated by replacement therapy. The usual dose is 1 mg per day by month. In malabsorption states upto 5 mg per day by month may be required.
 
APLASTIC ANEMIA
Aplastic anemia is a disease in which the patient has peripheral blood pancytopenia (disease of all blood cell types–RBCs, white cells and platelets) and hypocellular bone marrow. It results bone marrow aplasia (markedly reduced hematopoiesis).
 
Etiology
There are various etiological classifications for aplastic anemia, but they can be divided into two major groups:
  • Congenital origin: Is caused by chromosomal alterations. Approximately 30% of the aplastic anemias that appear in childhood are inherited.
    • 198Fanconi syndrome
    • Congenital dyskeratosis
    • Amegakaryocytic thrombocytopenia
    • Shwachman-diamond syndrome.
  • Acquired aplastic anemia: Results from exposure to ionizing radiations, chemical agents, viral and bacterial infections (hepatitis, parvovirus, biliary tuberculosis) and prescribed medications (e.g. alkylating agents, antiseizure agents). Approximately 70% of the acquired plastic anemias are idiopathic.
    • Chemical agent and toxin
    • Drugs
    • Pregnancy
    • Radiation
    • Viral and bacterial infection.
 
Clinical Manifestation
  • Fatigue
  • Shortness of breath with exertion
  • Rapid or irregular heart rate
  • Pale skin
  • Frequent or prolonged infections
  • Unexplained or easy bruising
  • Nosebleeds and bleeding gums
  • Prolonged bleeding from cuts
  • Skin rash
  • Dizziness
  • Headache.
 
Diagnostic Evaluation
  • History and physical examination
  • Blood tests; Normally, red blood cell, white blood cell and platelet levels stay within a certain range. In aplastic anemia when all three of these blood cell levels are very low.
  • Bone marrow biopsy: To confirm a diagnosis, need a bone marrow biopsy. In this procedure, uses a needle to remove a small sample of bone marrow from a large bone. The bone marrow sample is examined under a microscope to rule out other blood-related diseases. In aplastic anemia, bone marrow contains fewer blood cells than normal.
 
Management
Treatments for aplastic anemia may include observation for mild cases, blood transfusions and medications for more serious cases, and in severe cases, bone marrow transplantation is required. Severe aplastic anemia in which blood cell counts are extremely low is life-threatening and requires immediate hospitalization for treatment.
  • Blood transfusions: Treatment for aplastic anemia usually involves blood transfusions to control bleeding and relieve anemia symptoms. Blood transfusions are not a cure for 199aplastic anemia. But they do relieve signs and symptoms by providing blood cells that bone marrow is not producing. A transfusion may include:
    • Red blood cells: Transfusions of red blood cells raise red blood cell counts. This helps relieve anemia and fatigue.
    • Platelets: Transfusions of platelets help prevent excessive bleeding.
  • Stem cell transplant: A stem cell transplant to rebuild the bone marrow with stem cells from a donor may offer the only successful treatment option for people with severe aplastic anemia. A stem cell transplant, which is also called a bone marrow transplant, is generally the treatment of choice for people who are younger and have a matching donor—most often a sibling.
  • Immunosuppressants: For people who cannot undergo a bone marrow transplant or for those whose aplastic anemia maybe due to an autoimmune disorder, treatment may involve drugs that alter or suppress the immune system. Drugs such as cyclosporine and anti-thymocyte globulin (Thymoglobulin) are examples.
  • Bone marrow stimulants: Certain drugs—including colony stimulating factors, such as sargramostim, filgrastim and pegfilgrastim may help stimulate the bone marrow to produce new blood cells. Growth factors are often used in combination with immune-suppressing drugs.
 
HEMOLYTIC ANEMIA
Hemolytic anemia is a condition is caused by the destruction of RBCs at a rate that exceeds production. Hemolysis can occur because of problems intrinsic or extrinsic to the RBCs.
Intrinsic hemolysis anemias results from defect in the RBCs themselves caused by abnormal Hb (sickle cells), enzyme deficiencies that alter glycolysis (glucose-6-phosphate dehydrogenase[G6PD] deficiency), or RBCs membrane abnormalities.
Sickle cell anemia is a severe hemolytic anemia that results from inheritance of the sickle hemoglobin gene. This gene causes the hemoglobin molecule to be defective. The sickle hemoglobin (HbS) acquires a crystal like formation when exposed to low oxygen.
 
Pathophysiology
200
 
Types of Hemolytic Anemia
  • Inherited: Abnormal hemoglobin, Sickle cell Anemia, Thalassemia, Hereditary spherocytosis, Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency.
  • Acquired: Antibody-related, Transfusion reaction, Autoimmune hemolytic anemia (AIHA), RBC membrane defects, Trauma, Mechanical heart valve, Infection, DIC, Hypersplenism.
 
Clinical Manifestation
  • Symptoms of sickle cell anemia vary and are only somewhat based on the amount of Hbs. The sickled RBCs have shortened life-span.
  • Patients always anemic: Hemoglobin value 7–10 g/dl
  • Jaundice
  • Bone marrow expands in childhood in a compensatory effort to offset the anemia.
  • Enlargement of bones of the face and skull.
  • Tachycardia, cardiac murmurs, and cardiomyopathy
  • Dysrhythmias and heart failure
  • Any organ may be affected by thrombosis, such as spleen, lungs, and CNS.
  • Susceptible to infection, particularly pneumonia and osteomyelitis.
 
Types of Hemolytic Anemia
 
Sickle Cell Crisis
There are three types of sickle cell crisis:
  • Sickle crisis: Results from the tissue hypoxia and nacrosis due to inadequate blood flow to a specific region of tissue or organ.
  • Aplastic crisis: It results from infection with human parvovirus. The hemoglobin level falls rapidly and the marrow cannot compensate as evidenced by absence of reticulocytes.
  • Sequestration crisis: It results when other organ pool the sickled cells. Although the spleen is the most common organ responsible for sequestration in children, by 10 years of age most childen with sickle cell anemia have had a splenic infarction and he spleen is then no longer functional (autosplenectomy). In adults, the common organs involved in sequestration are the liver and lungs.
201
 
Medical Management
There are three primary treatment modalities for sickle cell anemia:
  • Bone marrow transplantation
  • Hydroxyurea
  • Long-term RBC transfusion
  • Bone marrow transplantation: Bone marrow transplantation offers the potential for cure for this disease. However, this treatment modality is available to only a small subset of the patient population, because of the lack of a compatible donor or the severe organ (e.g. renal, liver, lungs) damage already present in the patient.
  • Hydroxyurea: A chemotherapy agent has been shown to be effective in increasing hemoglobin F levels in patients with sickle cell anemia and decreasing the permanent formation of sickled cells. Patients who receive hydroxyurea appears to have fewer painful episodes of sickle cell crisis, a lower incidence of acute chest syndrome and less need for transfusion. Side effects of hydroxyurea include chronic suppression of WBC formation, teratogenesis.
  • Transfusion therapy: Chronic transfusions with RBCs have been shown to be highly effective in several situations in sickle cell crisis and prevention of complications. The risk of complications from transfusion is important to consider. These risks include iron overload, infections, alloimmunization from repeated transfusions.
  • Patient with sickle cell anemia require daily folic acid replacements to maintain the supply required for increased for increased erythropoiesis from hemolysis.
  • Acute chest syndrome is managed by prompt initiation of antibiotic therapy.
 
GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY
The abnormality in this disorder is in the G-6-PD gene. This enzyme produces an enzyme within the RBC that is essential for membrane stability. A fewer patients have inherited an enzyme so defective that they have a chronic hemolytic anemia. All type of G-6-PD deficiency are inherited as X-linked defects, therefore many more men are at risk than women.
 
Clinical Manifestations
  • Patients are asymptomatic and have normal hemoglobin levels and reticulocyte counts most of the times.
  • Several days exposure to an offending medication they may develop
    • Pallor
    • Jaundice
    • Hemoglobinurea (hemoglobin in urine)
  • The reticulocyte count rises and symptoms of hemolysis develop. Special stains of the peripheral blood may then disclose Heinz bodies (degraded hemoglobin) within the RBCs.
 
Medical Management
  • Stop the offending medications.
  • Transfusion is necessary only in the severe hemolytic state.
202
 
HEREDITORY SPHEROCYTOSIS
  • Hereditary spherocytosisis relatively common hemolytic anemia characterized by an abnormal permeability of the RBC membrane; permits the cell to change into a spherical shape.
  • These RBCs are destroyed prematurely in the spleen.
  • The severity of this hemolytic anemia varies; jaundice can be intermittent and splenomegaly also can occur.
  • Surgical removal of the spleen is the principal treatment for this disorder.
 
IMMUNE HEMOLYTIC ANEMIA
Hemolytic anemia can result from exposure of the RBC to antibodies. Alloantibodies result from the immunization of an individual with foreign antigens (e.g. the immunization of an Rh-negative person with Rh-positive blood). Alloantibody tends to be large (IgM) and cause immediate destruction of the sensitized RBCs either within the blood vessels or within the liver.
The most common type of alloimmune hemolytic anemia in adults results from a hemolytic transfusion reaction.
 
Classification
Autoimmune hemolytic anemia can be classified based on the body temperature involved when the antibodies react with the RBC antigen.
  • Warm: Body antibodies bind to RBCs most actively in warm conditions (37 °C).
  • Cold: Body antibodies react in cold (0 °C).
Most autoimmune hemolytic anemia are the warm body type.
 
Etiology
  • Medication exposure
  • Lymphoma
  • Collagen vascular disease
  • Autoimmune disease
  • Infection
  • Idiopathic
  • All ages and genders are equally vulnerable.
 
Clinical Manifestation
  • Patient may be asymptomatic.
  • Hemolysis can be so severe that resultant anemia is life-threatening.
  • Fatigue and dizziness
  • Splenomegaly
  • Hepatomegaly
  • Lymphadenopathy
  • Jaundice.
 
Diagnostic Evaluation
  • Low hemoglobin level and hematocrit
  • RBCs appear abnormal; spherocytes common
  • 203Serum bilirubin level elevated
  • If hemolysis is severe, haptoglobin level low or absent.
  • Coombs test, which detects antibodies on the surface of RBCs, shows a positive result.
 
Management
  • Offending medication immediately discontinued
  • High doses of corticosteroids (1 mg/kg per day) until hemolysis decreases
  • In severe cases, blood transfusions required
  • Careful blood typing is necessary, and transfusion administered slowly and cautiously
  • Splenectomy (removal of the spleen) removes major site of RBC destruction
  • If nothing successful, immunosuppressive agents may be administered, e.g. cyclophosphamide and azathioprine.
 
HEREDITORY HEMOCHROMATOSIS
Hematochromatosis is a genetic condition in which iron is abnormally (excessively) absorbed from the gastrointestinal tract. The excessive iron is deposited in various organs, particularly the liver, myocardium, thyroid and pancreas. Eventually, the affected organs become dysfunctional.
 
Clinical Manifestation
  • Weakness, lethargy
  • Arthralgia,
  • Weight loss
  • Loss of libido
  • Skin hyperpigmented with melanin deposits (occasionally hemosiderin, an iron-containing pigment) and appears bronze in color
  • Cardiac dysrhythmias and cardiomyopathy is resulting dyspnea and edema
  • Endocrine dysfunction manifested as hypothyroidism, diabetes mellitus, and hypogonadism (testicular atrophy, diminished libido, and impotence).
 
Management
  • Therapeutic phlebotomy (removal of whole blood from a vein)
  • Each unit of blood removed results in decrease of 200–250 mg iron
  • Frequent phlebotomy schedule is required (1 to 2 units weekly), with gradual reduction in frequency over 1- to 3-year period
  • After 1 to 3 years, frequency reduced to 1 unit of blood every several months to prevent reaccumulation of iron deposits.
 
Nursing Management
 
Assessment
  • Health history and physical examination
  • Past health history (recent blood loss, trauma, chronic diseases); use of medications; surgery or other treatment; Family history; nutritional assessment (weight loss, nausea, vomoiting); activity level (fatigue, muscle weakness)
  • 204General (lethargy, apathy); integumentary (pale skin, poor skin turgor, jaundice); tachypnea; tachycardia; gastrointestinal (hepatosplenomegaly, glossitis); neurologic (confusion, impaired judgment).
 
Nursing Diagnosis
  • Activity intolerance related to weakness, fatigue, and general malaise
  • Imbalanced nutrition, less than body requirements, related to inadequate intake of essential nutrients, anorexia and treatment
  • Ineffective tissue perfusion related to inadequate blood volume
  • Ineffective therapeutic regimen management related to lack of knowledge, about appropriate nutrition and medication regimen.
 
Nursing Interventions
  • Activity intolerance related to weakness, fatigue, and general malaise
    • Assess activity level
    • Plan activity schedule
    • Alternate periods of activity of rest and activity
    • Assist patient with activities of daily living
    • Monitor vital signs to evaluate activity tolerance
    • Monitor hematocrit and hemoglobin as a guide to planning activity.
  • Imbalanced nutrition, less than body requirements, related to inadequate intake of essential nutrients, anorexia, and treatment
    • Assess food tolerance
    • Plan diet schedule
    • Offer the meal in attractive manner
    • Offer meal in calm and relaxed environment
    • Provide small, frequent meals
    • Provide high protein, iron, calorie diet
    • Teach about foods high in protein, iron, calories and other nutrients
    • Teach and monitor use of a food diary.
  • Ineffective tissue perfusion related to inadequate blood volume
    • Weigh daily
    • Administer blood transfusions or intravenous fluids as ordered
    • Administer supplemental oxygen
    • Monitor vital signs closely
    • Maintain intake output charting
    • Check for early sign of dehydration.
 
POLYCYTHEMIA VERA
Polycythemia vera is a chronic myoprolifrated disorder that involves all bone marrow elements, resulting in an increase in RBC mass or presence of increased in number of RBC and hemoglobin. Polycythemia is an abnormal increased in concentration of hemoglobin in the blood, either through reduction of plasma volume or increase in red cell numbers.
 
Etiology
  • Polycythemia vera is a bone marrow disease that leads to an abnormal increase in the number of blood cells (mainly RBCs), although the number of white blood cells and platelets are also increased.
  • 205It is associated with gene mutations. The cause of this mutation is unknown.
  • Polycythemia also associates with problems of the bone marrow.
  • Other causes may includes smoking, minning, or environmental factors.
 
Risk Factors
Some of the chronic risk factors:
  • Chronic hypoxia
  • Reduction of plasma volume
  • Splenomegaly
  • Long-term cigarette smoking
  • Familial and genetic predisposition
  • Living in high altitudes
  • Long-term exposure to carbon monoxide (tunnel worker, Car garbage attendants, Residents of highly polluted cities).
 
Pathophysiology
Polycythemia is due to excessive production of a single line of clonal stems cells present in the bone marrow. These cells interfere with or stimulate normal stem cells growth and maturation. Unregulated neoplastic proliferation is thought to be the etiology. The origin of the abnormal clonal cells is currently unknown however these cells have increased sensitivity to growth factors for maturations, indicating the presence of detect in the single pathway common to different growth factors. Clonal and cytogenic studies are currently under way in an attempt to determine the molecular basis of PV.
206
 
Types of Polycythemia
Polycythemia can be divided into two categories–primary and secondary. Polycythemia can result from internal problems with the production of red cells. This is termed primary polycythemia. If polycythemia is caused due to another underlying medical problem it is referred to as secondary polycythemia.
 
Primary Polycythemia
Polycythemia Vera is known as primary polycythemia. Its cause is unknown. Polycythemia Vera is a disorder of the proliferative bone marrow in which the myeloid cells stem cells seems to have escaped normal control mechanism. It is caused by much production of white blood cells, red blood cells and platelets. The bone marrow is hyper cellular and the WBCs, RBCs and platelet count in the peripheral blood are elevated the skin takes a ruddy appearance from the build up cells. PV is found in patients over age 50 years.
 
Secondary Polycythemia
Secondary Polycythemia is caused by excessive production of erythropoietin disease. Secondary Polycythemia generally occurs as a response to other factors or underlying conditions that promote red blood cells production. Secondary Polycythemia is usually due to increased erythropoietin production either in response to chronic hypoxia this may be caused in response to a reduced amount of oxygen, which acts as hypoxic stimulus, as in cigarette smoking, COPD or cyanotic heart failure, obstructive sleep apnea, poor blood flow to the kidney, living in high altitudes and smoking. Secondary Polycythemia is a compensatory mechanism rather than an actual disorder.
 
Relative Polycythemia
Relative polycythemia describes condition in which red cell volume is high due to increased blood concentration of red cells as a result of dehydration. In these situation (vomiting, diarrhea, excessive sweating) the number of red blood cells counts may seem elevated.
 
Stress Polycythemia
This is a condition that may be seen in hardworking, anxious, middle-aged men due to low plasma volume, although the red blood cells volume may be normal. Other names for this condition are pseudopolycythemia, stress erythrocytosis, or Gaisbock's disease
Fig. 4.1: Physiological changes related to PV
207Conditions which may result in a physiologically appropriate polycythemia include:
  • Altitude related: This physiologic polycythemia is a normal adaptation to living at high altitudes. Many athletes train at high altitude to take advantage of this effect—a legal form of blood doping. Some individuals believe athletes with primary polycythemia may have a competitive advantage due to greater stamina. However, this has yet to be proven due to the multifaceted complications associated with this condition.
  • Hypoxic disease: Aassociated–for example in cyanotic heart disease where blood oxygen levels are reduced significantly. May also occur as a result of hypoxic lung disease such as COPD and as a result of chronic obstructive sleep apnea.
  • Iatrogenic: Secondary polycythemia can be induced directly by phlebotomy, to withdraw some blood, concentrate the erythrocytes, and return them into the body.
  • Genetic: Heritable causes of secondary polycythemia also exist and are associated with abnormalities in hemoglobin oxygen release. This includes patients who have a special form of hemoglobin known as Hb Chesapeake, which has a greater inherent affinity for oxygen than normal adult hemoglobin. This reduces oxygen delivery to the kidneys, causing increased erythropoietin production and a resultant polycythemia. Hemoglobin Kempsey also produces a similar clinical picture. These conditions are relatively uncommon.
Conditions where the secondary polycythemia is not as a result of physiologic adaptation and occurs irrespective of body needs include:
  • Neoplasms: Renal cell carcinoma or liver tumors, and endocrine abnormalities including pheochromocytoma and adrenal adenoma with Cushing's syndrome.
  • People whose testosterone levels are high because of the use of anabolic steroids, including athletes who abuse steroids, or people on testosterone replacement for hypogonadism, as well as people who take erythropoietin may develop secondary polycythemia.
 
Clinical Manifestation
Many people have no symptoms when they are first diagnosed with Polycythemia vera. This disease is often discovered during a blood routine blood test and physical examination. If symptoms develop, they tend to do so over time.
  • Reddish purple skin and mucosa, pruritus (especially after bathing)
  • Breathing difficulty when lying down
  • Excessive bleeding (Hemorrhage)
  • Splenomegaly, hepatomegaly
  • Epigastric discomfort, abdominal discomfort
  • Painful fingers and toes paresthesia
  • Headache, fullness in head, dizziness, visual abnormalities, alter mutation from disturbed cerebral circulation
  • Weakness, fatigue, night sweats, bleeding tendency.
  • Hyperuricemia
  • Itching
  • High blood pressure.
208Some of these symptoms are due to increased blood thickness and clottinng
  • The Splenomegaly, hepatomegaly: The enlargement of the spleen is also common and occur in around 75% cases. Symptoms include feeling of fullness in the upper left-side of the abdomen. An enlarged spleen may also cause pressure on the stomach causing a feeling of fullness, indigestion and a loss of appetite. In some cases the liver is also enlarged called as hepatomegaly.
  • Painful inflammation of the toe or foot: This can results from build up for uric acid, a by-product of the increased production and breakdown of blood cells. Some individuals may develop erytheromelalgia, a rarely condition that primarily affects the feet and, less commonly the hands. It is characterized by intense, burning pain of affected extremities, and increased skin temperature that maybe episodic or almost continuous in nature.
  • Hemorrhage: This phenomenon caused by either vessel rupture from over distension or inadequate platelet function may results in ecchymosis, epistaxis, or GI bleeding. Hemorrhage can be acute and catastrophic.
 
Diagnostic Evaluation
The following laboratory manifestations are seen in a patient with polycythemia vera.
  • Elevated Hb and RBC count with microcytosis.
  • Low to normal EPO level (secondary polycythemia will have a high level)
  • Elevated WBC count with basophilia
  • Elevated platelets (thrombocytosis) and platelet dysfunction.
  • Elevated leukocyte alkaline phosphatase.
  • Elevated histamine levels.
  • Bone marrow in examination in polycythemia vera shows hypercelularity of RBCs, WBCs and platelets.
  • Splenomegaly is found in 90% of patient with primary polycythemia but does not accompany secondary polycythemia.
Routine blood work including:
  • Clotting profile, and metabolic panel.
  • Chest X-ray, electrocardiogram (ECG), echocardiogram, Hemoglobin analysis, Carbon monoxide measurement.
  • Evidence of long standing low body oxygen level (chronic hypoxia) in an important clue in patient with polycythemia.
  • Bone marrow examination (bone marrow aspiration or biopsy)
  • Full blood count (CBC): People with polycythemia vera have a high red cell count, hemoglobin level and hematocrit due to the excessive production of red cells. The hematocrit is the percentage of the whole blood that is made up of red cells. A raised white cell count (especially a raised neutrophil count) and a raised platelet count are also common findings.
  • JAK2 Mutation testing: JAK2 mutations (particularly the V617F mutation) can be found in more than 95% of people with polycythemia vera. This test can be performed on a blood sample and will help to confirm the diagnosis of a myeloproliferative neoplasm. It does not help distinguish polycythemia vera from essential thrombocythemia or primary myelofibrosis.
  • 209Bone marrow examination: In polycythemia vera the bone marrow is often very active with abnormally high numbers of normal cells. Iron stores maybe depleted since iron is being used to make more and more red cells.
Other possible blood tests
  • Serum vitamin B12 levels
  • Uric acid levels
  • Erythropoietin levels
  • Coagulation studies
  • Blood oxygen levels
  • Chest X-ray – to rule out lung disease
  • Abdominal ultrasound and/or CT scan – to rule out kidney disease and measure spleen or liver size.
 
Management
 
Medical Management
  • Phlebotomy: Venesection (or phlebotomy) is a procedure in which a controlled amount of blood is removed from bloodstream. This procedure is commonly used when people are first diagnosed with polycythemia vera because it can help to rapidly reduce a high red cell count. In a process similar to a blood donation, 450 to 500 ml of blood is removed, usually from a large vein in the arm. This is usually done in the outpatient's department of the hospital. It takes about 30 minutes to complete.
  • Marrow Hyperplasia (Myelosuppressive Drugs): Myelosuppressive (bone marrow suppressing) drugs or chemotherapy are commonly used to reduce blood cell production in the bone marrow. These drugs are commonly used for people with an extremely high platelet count, complications due to blood clotting or bleeding, or symptoms of an enlarged spleen. They are also used for some people who are unable to tolerate venesection or whose disease is no longer responding to venesection.
  • The most commonly used myelosuppressive agent is a chemotherapy drug called hydroxyurea. It is particularly useful in controlling a high platelet count and therefore reducing the risk of thrombosis. As hydroxyurea is a chemotherapy drug, it is known to affect fertility and should be avoided during pregnancy, for it can cause harm or may be fatal to the fetus.
  • Interferon: Interferon is a substance produced naturally by the body's immune system. It plays an important role in fighting disease. In polycythemia vera, interferon is sometimes prescribed for younger patients to help control the production of blood cells. Interferon is usually given three times a week as an injection under the skin (subcutaneous injection) using a very small needle. A weekly injection is also be given.
  • Aspirin: Many people are prescribed small daily doses of aspirin, which have been shown to significantly reduce the risk of thrombosis in people with polycythemia vera.
  • Radioactive phosphorus: Radioactive phosphorus (32P) is a radioisotope which maybe used for long-lasting control of blood counts in older people. One or two doses of 32P are usually given by injection into a vein in the hand or arm, in the nuclear medicine department of the hospital. This substance is taken up and concentrated in bone marrow where it suppresses the overactive bone marrow and helps to control blood counts.
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Assessment
The Patient who suffers from the polycythemia vera the family history and medical history and social history should be taken.
  • A comprehensive medical history, physical examination, family history, and social and occupational history is very important.
  • History include questions about smoking history, living at high altitudes for extended periods, breathing difficulties, sleep disturbances, or chronic cough.
  • A complete examination including the assessment of body habitus (stature), vital signs, oxygen saturation, heart and lungs exam, and evaluating for an enlarged spleen are essential in the evaluation of people with polycythemia.
 
Nursing Management
  • Assess for the ruddy cyanosis, reddened face with engorged retinal vein, tinnitus, weakness, fatigue and dizziness.
  • Assess for the signs of parasthesia, numbness, tingling, burning or weakness in hands, feet's or legs.
  • Assess for the hypertension, Nose bleeding.
  • Assess for any enlargement of liver and spleen.
  • The primary polycythemia is not preventable. However, because secondary polycythemia is generated by the source of hypoxia, maintaining adequate oxygenation may prevent problems. Therefore, controlling chronic pulmonary disease, stopping smoking and avoiding altitudes maybe important.
  • The nurse have a responsibilities to assist with or perform phlebotomy if acute exacerbation of polycythemia.
  • Fluid intake and fluid output should be evaluated during hydration therapy to avoid fluid overload and undehydration.
  • If the myelosuppressive agents are used the nurses must administer the drugs as ordered, observe the patient, and teach the patient about medication side effects.
  • Assessment of the patient's nutritional status in collaboration with the dietician may be necessary to of set the inadequate food intake that can result from GI symptoms of fullness, pain and dyspepsia.
  • Activities should be instituted to decreased thrombus formation. The relative immobility normally imposed by hospitalization puts the patient at risk for thrombus formation. Active and passive exercises and ambulation when possible should be initiated.
 
MULTIPLE MYELOMA
Multiple myeloma is the cancer of plasma cells. It is due to the unregulated proliferation of monoclonal plasma cells that are effective; accumulate in the bone marrow, and secret monoclonal immunoglobulin and cytokines. The monoclonal immunoglobulin and cytokines that are produced from the plasma cells leads to decreased bone marrow function and destruction of bone tissue.
211
 
Pathophysiology
212
 
Etiology
The causes of multiple myeloma are unknown, but research has shown possible associations with genetic factors, a decline in immune function, exposure to chemicals or radiation, and more recently a viral origin. Chronic immune stimulation and autoimmune disorders may also play a role in the pathogenesis of the disease.
 
Pathophysiology
213
 
Clinical Manifestation
  • Pain (an early symptom): Plasma cells accumulate within the bone marrow, causing destruction of bone, which result in fracture.
  • Renal compromise: Excessive movement of the protein excreted in the urine and hypercalcemia adversely affect renal function.
  • Infections: Abnormal plasma cells accumulate in the bone marrow, decreasing the production of normal WBCs. Decreased result in increased bacterial infections.
  • Weakness: The accumulation of abnormal plasma cells in the bone marrow prevents red blood cell production and results in anaemia.
  • Fatigue.
 
Diagnostic Evaluation
  • Urine and serum protein electrophoresis to determine the presence of abnormal protein, and number of normal immunoglobulin.
  • Bone marrow biopsy to determine the presence and number of cancerous plasma cells.
  • CT scan and radiography that show a ‘punched-out’ type of bone lesion or generalized osteoporosis of the axial skeleton.
  • CBC to determine the presence of anemia, leukopenia, or thrombocytopenia.
  • MRI to detect the presence of bone abnormalities and fracture.
  • Blood chemistries to detect the presence of hypercalcemia and elevated uric acid levels.
  • Estimate myeloma cell mass to estimate the tumor burden.
 
MANAGEMENT
 
Medical Management
Not all clients diagnosed with multiple myeloma should be treated. Symptoms, physical findings, and laboratory data must be considered.
In some cases, treatment might be withheld, and client is re-evaluated in 2 to 3 month.
Palliative radiations should be limited to client with disabling pain from a well-defined location that has not been responsive to chemotherapy.
 
Pharmacological Management
  • Prednisone and melphalan given orally for a period of 7 days and repeated at 6-week intervals produces positive results in 50 to 60 percents of the clients. (Leukocyte and platelet counts should check regularly and doses adjusted until modest cytopenia occurs).
  • Combination chemotherapy, commonly melphalan, cyclophosphamide, carmustine (BCNU), vincristine and prednisone, has shown a 70 to 75 percent response rate. This therapy may continue for 1 to 2 years, but relapse almost always occurs when chemotherapy is discontinued.
  • In addition the nurse should be alert to the possibility of spinal cord compression, another complication of multiple myeloma.
  • Treatment usually consists of radiation therapy and large doses of steroid, although a laminectomy maybe indicated.
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NURSING MANAGEMENT
 
Assessment
  • Obtain the health history, focusing on pain, fatigue.
  • Evaluate for evidence of bone deformities and bone tenderness or pain.
  • Assess patient's support system and personal coping skills.
 
Nursing Diagnosis
  • Chronic pain related to destruction of bone and possible pathologic fracture.
  • Impaired physical mobility related to pain and possible fracture.
  • Risk of infection related to internal defences due to disease process.
  • Activity intolerance related to fatigue.
  • Fear related to poor prognosis.
  • Anxiety related to hospitalization.
 
Nursing Interventions
To reduce the pain of the patient:
  • Assess the condition of the patient.
  • Assess the severity, duration and frequency of the pain.
  • Provide the heat/cold and relaxation therapy of the patient for pain relief.
  • Teach the use of nonpharmacologic methods such as music, relaxation breathing, music therapy and imagery, to help manage pain.
  • Administer nonsteroidal anti-inflammatory drugs to the patient.
  • Administer analgesics like tramadol for pain relief.
To promote the physical mobility of the patient:
  • Encourage patient to wear back brace for lumber lesions.
  • Recommend physical and occupational therapy consultation.
  • Discourage bed rest to prevent hypercalcemia but ensure safety of environment to prevent fracture.
  • Assist patient with measures to prevent injury and decrease risk of fractures. Advise avoidance of lifting and straining; use walker and other assistive devices as appropriate.
To reduce the risk of infection
  • Monitor the vital signs of the patient.
  • Teach the patient and its family member about the importance of the handwashing.
  • Avoid the extra visitor. Limit visitor only if needed.
  • Encourage the client about the frequent breathing, position changes and routine hygiene.
  • Encourage the patient to limit contact with the fresh plant and soil and to wash the fruits and vegetable thoroughly.
 
Health Education
  • Teach the patient about the risk of infection caused by impaired antibody production and chemotherapy.
  • 215Educate the patient how to take medications, as ordered and instruct to avoid adverse effect and progress of diseases.
  • Teach the patient to minimize the risk of fracture. Use proper body mechanics and assistive devices as appropriate; avoid bed rest, remain ambulatory.
  • Advise patient to report new onset of pain, new location, or sudden increase in pain intensity immediately.
  • Encourage the patient to maintain high fluid intake (2 to 3 L/day) to avoid dehydration.
 
LEUKEMIA
Leukemia is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called ‘blasts’. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms.
 
Etiology and Pathophysiology
There are different causes:
The following are either known causes, or strongly suspected causes:
  • Artificial ionizing radiation
  • Viruses–HTLV-1 (human T-lymphotropic virus) and HIV (human immunodeficiency virus)
  • Benzene and some petrochemicals
  • Alkylating chemotherapy agents used in previous cancers.
  • Maternal fetal transmission
  • Hair dyes
  • Genetic predisposition
  • Down syndrome–people with Down syndrome have a significantly higher risk of developing leukemia, compared to people who do not have Down syndrome.
 
Risk Factors
  • Gender: Men are more likely to develop CML, CLL and AML than women.
  • Age: The risk of most leukemias, with the exception of ALL, typically increases with age.
  • Genetics: Family history: Most leukemias have no familial link. However, first degree relatives of CLL patients, or having an identical twin who has or had AML or ALL, may at an increased risk for developing the disease.
  • Lifestyle: Smoking: Although smoking may not be a direct cause of leukemia, smoking cigarettes does increase the risk of developing AML.
  • Exposures: Exposure to high levels of radiation: Exposure to high-energy radiation (e.g. atomic bomb explosions) and intense exposure to low-energy radiation from electromagnetic fields (e.g. power lines).
  • Chemical exposure: Long-term exposure to certain pesticides or industrial chemicals like benzene is considered to be a risk for leukemia.
  • Previous Treatment: Previous cancer treatment: Certain types of chemotherapy and radiation therapy for other cancers are considered leukemia risk factors.
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Clinical Manifestation
  • Fever and night sweats
  • Headache
  • Bruising or bleeding
  • Bone or joint pain
  • A swollen or painful abdomen from an enlarged spleen
  • Swollen lymph nodes in the armpit, neck, or groin
  • Getting a lot of infections
  • Feeling very tired or weak
  • Losing weight and not feeling hungry
  • Fatigue
  • Night sweat, Lethargy
  • Fever.
 
Classification
  • ALL (Acute lymphatic leukemia).
  • ALM (Acute myelogenous leukemia)
  • CLL (Chronic lymphocytic leukemia)
  • CML (Chronic myelogenous Leukemia).
 
ALL (Acute Lymphatic Leukemia)
It is a type of leukemia that, all types of lukemia starts from white blood cells in the bone marrow, the soft inner part of bones. It develops from cells called lymphocytes, type of WBCs central to immune system, an immature type of lymphocyte.
 
Clinical Manifestation
  • Fever
  • Pallor
  • Bleeding
  • Anorexia
  • Fatigue
  • Weakness
  • Bone, joint and abdominal pain
  • Increase intracranial pressure.
 
Acute Myelogenous Leukemia (AML)
It is fast growing cancer of the blood and bone marrow where the bone marrow makes many cancerous cells called leukemic blasts, normally blasts develop into WBCs that fight infection, but in AML, leukemic blasts do not develop properly and cannot fight infection. In this there is proliferation of immature myloid cells.
 
Treatment
  • Use of cytarabine, 6-thioguanine, and doxorubicin
  • The same care of client as ALL, plus give adequate amounts of fluids (2000 to 3000 ml per day.)
  • Instruct client about medication, effects, side effects and nursing measures
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Chronic Lymphocytic Leukemia (CLL)
It is a type of cancer of the blood or bone marrow, normally bone makes blood stem cells (immature cells) that become mature blood cells over the time.
 
Pathophysiology
  • It is characterized by proliferation of small, abnormal, mature B lymphocytes, often leading to decreased synthesis of immunoglobulin and depressed antibody response.
  • The number of mature lymphocytes in peripheral blood smear and bone marrow are greatly increased.
 
Clinical Manifestation
  • Usually there is no symptoms
  • Chronic fatigue, weakness, anorexia, splenomegaly, lymphadenopathy, hepatomegaly
  • Skin lesions
  • Anemia
  • Thrombocytopenia.
  • The WBC count is elevated to a level between 20,000 to 100,000.
  • Increase blood viscosity and clotting episode.
 
Chronic Myelogenous Leukemia (CML)
It is a type of cancer that starts in certain blood forming cells of the bone marrow. And in this bone marrow produces too many white cells. It affects the blood and bone marrow.
  • Occurs between 25–60 years of age. Peak 45 year and it is caused by benzene exposure and high doses of radiation.
 
Clinical Manifestation
The classic symptoms of chronic types of leukemia, include:
  • Fatigue, weakness, fever, sternal tenderness
  • Weight loss, joint, and bone pain
  • Massive splenomegaly and increase in sweating
  • The accelerated phase of disease (blostic phase) is characterized by increasing number of granulocytes in the peripheral blood.
  • There is a corresponding anemia and thrombocytopenia.
 
Diagnostic Evaluation
  • History: Ask the patient for the presence of sign and symptoms. Assess the patient for the exposure of any risk factors or any history of risk factors.
  • Physical examination: During the physical examination, assess patient for sign and symptoms.
  • Assess patient for enlarged lymph nodes, areas of bruising, or any sign of infection.
  • Assess the vital signs of patient
  • Complete blood count: In complete blood count it measures the numbers of red blood cells, white blood cells and platelets. Most of patient with ALL have too many immature white cells. Low RBCs count, Hb, low platelet count, low to high WBC count.
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Treatment
Chemotherapeutic agent, it involve three phases
  • Induction: During the induction phase the client receives an intensive course of chemotherapy designed to induce a complete remission of the disease. Once the remission is achieved the consolidation phase begins. Using vincristine and prednisone.
  • Consolidation: Using modified course of intensive therapy to eradicate any remaining disease.
  • Maintenance: During the maintainence phase small doses of different combinations of chemotherapeutic agents are given every 3 to 4 weeks. It allows the client to live a normal life as possible.
 
Other Management
  • Eat diet that contains high in protein, fibers and fluids
  • Avoid infection (handwashing, avoid crowds), injury
  • Take measure to decrease nausea and to promote appetite, smoking, and spicy and hot foods.
  • Maintain oral hygiene.
 
Symptom Control
  • Chemotherapy with chlorambucil, cyclophosphamide, and prednisone to decrease lymphadenopathy and slpenomegaly.
  • Splenic irradiation or splenectomy for painful splenomegaly or platelet sequestration, hemolytic anemia.
  • Irradiation of painful enlarged lymph nodes.
 
Supportive Care
  • Transfusion therapy to replace platelets and RBCs.
  • IV immunoglobulins or gamma globulin to treat hypogamma globulinemia.
 
Chronic Phase
  • Palliative treatment, controlling symptoms, includes chemotherapy, irradiation, splenectomy.
  • Potentially curative treatment is offered by allogeneic (related or cumulated donor) BMT.
 
Accelerated Phase or Blast Crisis
Attempts to restore chronic phase through use of high dose chemotherapy, leukophoresis.
 
Nursing Intervention
  • Taking measures to prevent infection
  • Promoting safety
  • Providing oral hygiene
  • Preventing fatigue
  • Promoting effective coping
  • Client and family education.
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Nursing Assessment
 
History
  • Ask patient for their family history, past medical history
  • Ask for the presence of exposure to any risk factors and etiology factors
  • Ask client for the presence of sign and symptoms.
 
Physical Examination
  • Assess for swollen lymph nodes, spleen, or liver
  • Assess the client vital signs. Check client for presence of fever
  • Assess patient for the enlarged lymph nodes, sign of infection, and any signs of bruising or bleeding from any sites.
 
Blood Tests
The lab does a complete blood count to check the number of white blood cells, red blood cells, and platelets. Leukemia causes a very high level of white blood cells. It may also cause low levels of platelets and hemoglobin, which is found inside red blood cells.
 
Bone Marrow Aspiration
The doctor uses a thick, hollow needle to remove samples of bone marrow. The sample is taken from the back of the pelvic (hip) bone and with help of needle small amount of liquid bone marrow is sucked.
 
Bone Marrow Biopsy
It is usually done just after the aspiration. The doctor uses a very thick, hollow needle to remove a small piece of bone and bone marrow.
 
Nursing Diagnosis
  • Impaired tissue integrity related to high dose radiation therapy.
  • Risk for infection to decreased neutrophils, altered response to microbial invasion, and presence of environmental pathogens.
  • Impaired oral mucous membrane related to low platelet counts and effects of pathologic conditions and treatment as evidenced by oral bleeding.
  • Risk for injury related to low platelet counts and treatment.
  • Acute pain related to tumor growth, infection or adverse effects of chemotherapy.
  • Activity intolerance related to anemia and adverse effect of chemotherapy.
 
Nursing Interventions
 
Maintain Tissue Integrity
  • Avoid rubbing powders, deodorants, lotions or ointments (unless prescribed) or application of heat and cold to treated areas.
  • Encourage the patient to keep the treated area clean and dry.
  • Advise the patient to bath the area gently with tepid water and mild soap.
  • Encourage the patient to wear loose fitting cloths.
  • Advise the patient to protect skin from over and direct exposure to sun light, chlorine and temperature extremes.
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Prevent from Infection
  • Inspect the patient for the sign and symptoms of infection, e.g. redness, etc.
  • Maintain asepsis for patient at risk.
  • Instruct the patient to take antibiotics as prescribed by doctor to prevent microbial resistance.
  • Teach the patient and family how to avoid infections, e.g. about personal hygiene technique of handwashing, oral care, skin hygiene etc.
  • Educate the patient to report if there is any presence of signs of infection to the doctor immediately.
  • Monitor granulocyte count and WBC count to identify the presence of infection.
  • Screen all visitors for communicable diseases.
 
Free the Mucosa from Bleeding
  • Monitor lips, tongue, mucous membrane, and gums for moisture, color, texture, presence of infection.
  • Assist the patient to select soft, bland, and nonacidic foods to decrease irritation of oral mucosa.
  • Advise the patient to use soft toothbrush for removal of dental debris.
  • Instruct the patient to perform oral hygiene after eating and as often as needed to avoid breakdown of oral mucosa.
  • Advise the patient to avoid the use of lemon glycerin swabs to prevent excessive drying of the mucosa.
 
Health Education
  • Teach the patient about the risk of infection and how to prevent from infection.
  • Educate the patient how to take medications, as ordered and instruct to avoid adverse effect and progress of diseases.
  • Provide patient and family member information about resources in the community, such as the leukemia and lymphoma.
  • Educate the patient to maintain proper personal hygiene.
  • Teach the patient to avoid aspirin and NSAIDs which may interfere with platelet function.
 
Complication
  • Infections
  • Blood problems
  • Impaired body function
  • Other cancers
  • Leads to death
  • Infections: Leukemia causes abnormalities in the white blood cells. While healthy white blood cells protect the body against infections and disease, defective cells lose this ability. Without the protective properties of the white blood cells, people with leukemia become more susceptible to infections, which are the most common leukemia complications involved with the disease.
  • 221Blood Problems: People with leukemia may experience complications related to the blood. In some people, leukemia may lead to excess bleeding or bruising. Both may occur when leukemia causes a shortage in the number of platelets in the body. Other people experience an increase in the number of platelets, which can lead to clogging or excessive blood clotting.
  • Impaired Body Functions: When one part of the body begins to malfunction, it can lead to complications in other parts of the body. In the case of leukemia, the disease may adversely affect the spleen, kidneys, and renal areas. In a healthy body, the spleen stores excess blood cells. When levels increase due to leukemia, the spleen may attempt to store more than it can hold, which can cause an enlarged spleen.
  • Death: Like most diseases without a cure, possible death is another complication of leukemia.
 
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
DIC is an acquired thrombotic and hemorrhagic syndrome characterized by abnormal activation of the clotting cascade and accelerated fibrinolysis. This result in widespread clotting in small vessels with consumption of clotting factors and platelets, so that bleeding and thrombosis occur simultaneously.
 
Etiology
  • Venomous snake bites
  • Burns, trauma stimulates the changes in blood clotting process
  • Small blood clots form in the blood vessels
  • Inflammation, infection, or cancer (leukemia)
  • Bleeding or injury
  • Pancreatitis, blood transfusion reaction
  • Severe hepatic failure
  • Hemorrhagic skin necrosis
  • Sepsis and shock
  • Obstetric complications: Abruptio placenta, eclampsia, preeclampsia, septic abortion.
  • Viral, fungal, infections
  • Recent surgery or anesthesia
  • Severe tissue injury (as in burns and head injury)
  • Large hemangioma (a blood vessel that is not formed properly)
  • Client with incomplete miscarriage.
 
Risk Factors
  • Blood transfusion reaction
  • Cancer, especially certain types of leukemia
  • Inflammation of the pancreas (pancreatitis)
  • Infection in the blood, especially by bacteria or fungus
  • Liver disease
  • 222Pregnancy complications (such as placenta that is left behind after delivery)
  • Recent surgery or anesthesia
  • Severe tissue injury (as in burns and head injury)
  • Large hemangioma (a blood vessel that is not formed properly).
 
Types
  • Acute disseminated intravascular coagulation (Acute DIC)
  • Chronic disseminated intravascular coagulation (Chronic DIC)
  • Acute disseminated intravascular coagulation: Acute DIC begins with clotting in the small blood vessels and quickly leads to serious bleeding.
  • Chronic Disseminated intravascular coagulation: Chronic DIC causes blood clotting, but it usually does not lead to bleeding. Cancer is the most common cause of chronic DIC.
 
Pathophysiology
 
Clinical Manifestation
  • Bleeding, possibly from many sites in the body
  • Blood clots
  • Bruising
  • Drop in blood pressure
  • Coolness of extremities
  • Fever, breathing difficulty
  • Bloody stools
  • Joint pain
  • Headache, fatigue
  • Gum bleeding, excess bleeding from any wound
  • Nose bleeds, blood in urine, heavy menstrual bleeding
  • Tachycardia
  • Restlessness, Dyspnea, chest pain with deep inspirations
  • Altered mental status
  • Gangrene.
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Diagnostic Evaluation
  • History: Ask patient for the presence of any past history of disease. Ask him for the changes in the body and for the presence of sign and symptoms in the body.
  • Physical Examination: In physical examination assess patient for presence of sign and symptoms. Monitor patient vital signs. Observe for bleeding from any site of body.
  • Laboratory tests: Complete blood count, platelet count, normal value is 150,000–450,000/mm3. There is decrease in platelet count. A complete blood count measures the number of red blood cells, white blood cells, platelets in body. Abnormal platelet numbers may be a sign of a bleeding disorder.
    • Pro thrombin time, normal value is 11–12.5 sec, there is a increase in prothrombin time. This test measure how long it takes blood clot to form.
    • Thrombin time, normal value is 8–11 sec, there is increase in thrombin time.
    • Fibrinogen normal value is 170–340 mg/dl and there is decrease in fibrinogen. Fibrinogen is a protein help in blood clot. This test measures how much fibrinogen is in body.
 
Management
There is no specific treatment for DIC.
The goal is to determine and treat the underlying cause of DIC.
  • Supportive treatments may include:
    • Plasma transfusions to replace blood clotting factors, coagulation factors if a large amount of bleeding is occurring.
    • Blood thinner medicine (heparin) to prevent blood clotting if a large amount of clotting is occurring.
    • Transfusions of platelets or fresh frozen plasma can be considered in cases of significant bleeding.
    • Aspirin to stop blood clots, it helps to thin the blood to keep blood clots from forming.
 
Dietary Management
In case of disseminated intravascular coagulation provide vitamin K. Low level of vitamin K may lead to increased bleeding.
  • Vitamin K is found in green leafy vegetables.
  • Provide spinach, cabbage, cauliflower, green peas, beans, soybeans to the client.
 
Prevention
There is specific prevention for DIC.
  • Get the prompt treatment for the conditions known to bring on this disorder or results this disorder.
  • Eat healthy diet and take medicine properly.
  • Exercise regularly, it helps to maintain a healthy weight. Exercise help to keep the muscles flexible and prevent damage to muscles and joints.
  • Client need to rest in bed and breath through mouth if nosebleed.
  • Avoid playing sports such as football to prevent bleeding or bruising.
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Nursing Management
 
Nursing Assessment
Nurses need to be aware of patients who are at risk for DIC.
  • Assess the patient for bleeding from any of the site.
  • Nurse should assessed the patient thoroughly and frequently for the signs and symptoms of thrombi and bleeding.
  • Nurse should assess the patient for the progression of the signs and symptoms.
 
Nursing Diagnosis
  • Risk for deficient fluid volume related to bleeding
  • Risk for impaired skin integrity related to bleeding or ischemia
  • Risk for injury related to bleeding due to thrombocytopenia
  • Ineffective tissue perfusion related to microthrombi
  • Anxiety and fear related to disease condition
  • Deficient knowledge related to disease condition and treatment.
  1. Risk for Fluid Volume Deficient Related to Bleeding
    Interventions
    • Monitor vital signs closely
    • Monitor urine output of the patient
    • Avoid the medications that interfere with platelet count (NSAIDs)
    • Avoid IM injections because it decreases the chance for intramuscular bleeding
    • Monitor the external bleeding
    • Avoid dislodging any clots, including those around IV sites and injection sites
    • Blood components should be administered.
    • Provide packed red blood cells are to improve oxygen delivery by increasing the hemoglobin content of the blood.
    • Administer platelet transfusion when the platelet count falls below 100,000/mm3.
  2. Risk for impaired skin integrity related to bleeding or ischemia
    Interventions
    • Assess the skin of patient
    • Reposition the patient frequently
    • Use pressure reducing mattress
    • Perform skin care every 2 hour
    • Use prolonged pressure usually 5 min after injection because platelet plug is unstable and easily dislodged leads to increased bleeding
    • Provide oral care carefully
    • Maintain personal hygiene
  3. Anxiety and fear related to disease condition
    Interventions
    • Identify the patient previous coping mechanisms, if possible.
    • Encourage patient to use that coping mechanisms in this condition.
    • 225Explain all procedures and rationale for all procedures to patient.
    • Assist the family in supporting patient.
    • Explain about the causes and treatment of the disease to the patient.
    • Provide psychological support to the patient.
    • Advice to take medications at right time.
 
Health Education
  • When a bleeding disorder occurs in addition to another condition, the patient's and significant others’ coping skills and resiliency may be at a low point.
  • During this time, the patient and significant others need accurate information, honest reports about the patient's condition and prognosis, and an attentive nurse to listen to their concerns.
  • Provide emotional support and educate them as to the interventions and expected outcomes.
  • Help them understand the severity of the condition and the treatments; do not present false hopes.
  • The patient is usually maintained on complete bed rest.
  • Pad the side rails to help prevent injury. Reposition the patient every 2 hours, and provide skin care. Gently touch the skin when repositioning and bathing; vigorous rubbing could dislodge a clot and initiate fresh bleeding.
 
HEMOPHILIA (FACTOR VIII DEFICIENCY)
It is a group of hereditary genetic disorders that impair the body's ability to control blood clotting or coagulation, which is used to stop bleeding when a blood vessel is broken.
 
Incidence
  • Hemophilia A (clotting factor VIII deficiency) is the most common form of the disorder, present in about 1 in 5,000–10,000 male births.
  • Hemophilia B (factor IX deficiency) occurs in around 1 in about 20,000–34,000 male births.
 
Etiology
  • Hemophilia A is a recessive X-linked genetic disorder involving a lack of functional clotting Factor VIII and represents 80% of hemophilia cases.
  • Hemophilia B is a recessive X-linked genetic disorder involving a lack of functional clotting Factor IX. It comprises approximately 20% of hemophilia cases.
  • Hemophilia C is an autosomal genetic disorder (i.e. not X-linked) involving a lack of functional clotting Factor XI. Hemophilia C is not completely recessive, as heterozygous individuals also show increased bleeding.
 
Clinical Manifestation
  • Large bruises
  • Hematomas
  • Swelling and bruising from bleeding in the joints
  • Soft tissue.
226
 
Complications
  • Deep internal bleeding, e.g. deep-muscle bleeding, leading to swelling, numbness or pain of a limb.
  • Joint damage from hemarthrosis (hemophilic arthropathy), potentially with severe pain, disfigurement, and even destruction of the joint and development of debilitating arthritis.
  • Transfusion transmitted infection from blood transfusions that are given as treatment.
  • Adverse reactions to clotting factor treatment, including the development of an immune inhibitor which renders factor replacement less effective.
  • Intracranial hemorrhage is a serious medical emergency caused by the buildup of pressure inside the skull. It can cause disorientation, nausea, loss of consciousness, brain damage, and death.
 
LYMPHOMAS
 
Introduction
The lymphomas are neoplasms of cells of lymphoid origins. These tumors usually start in lymph nodes but can involve lymphoid tissue in the spleen, the gastrointestinal tract, the liver and the bone marrow.
They are often classified according to the cell differentiation and the origin of the predominant malignant cells. Lymphomas can be broadly classified into two categories:
  • Hodgkin's lymphoma
  • Non-Hodgkin's lymphoma
 
Hodgkin's Lymphoma
Hodgkin's lymphoma also called Hodgkin's disease. It is a chronic, progressive, neoplastic disorder of lymphatic tissue characterized by the painless enlargement of lymph nodes with progression to extralymphatic sites such as the spleen, and liver.
 
Etiology
  • Exact cause of Hodgkin's lymphoma remains unknown.
  • Infection with Epstin-Barr virus
  • Genetic predisposition
  • Exposure to occupational toxins
  • The incidence of hodgkin's lymphoma is increased among HIV infected patients.
 
Pathophysiology
227
 
Stages of Hodgkin's Lymphoma
  • Stage 1: Involvement of a single lymph node region on a lymphoid structure (e.g. spleen, thymus)
  • Stage 2: Involvement of two or more lymph node regions on the same side of the diaphragm
  • Stage 3: Involvement of lymph node regions or structure on both sites of the diaphragm
  • Stage 31: Involvement limited to the lymphatic structures in the upper abdomen that is spleen or splenic, celiac, or hepatic portal nodes.
  • Stage 32: Involvement of lower abdominal nodes, that is para-arotic, iliac, inguinal, with or without involvement of the splenic, ciliac or hepatic portal nodes.
  • Stage 4: Diffuse or disseminated involvement of one or more extra lymphatic organs or tissues with or without associated lymph node involvement.
 
Clinical Manifestation
  • Enlargement of cervical, axillary and inguinal lymph nodes
  • The enlarged lymph nodes are not painful unless they exert pressure on adjacent nerves
  • Pruritus: Is the common it can be extremely distressing and the cause is unknown
  • The symptoms results from compression of organs by the tumor
  • Cough and pulmonary effusion: From pulmonary filtration
  • Jaundice: From hepatic involvement or bile duct obstruction
  • Abdominal pain: From splenomegaly
  • Retroperitoneal adenopathy
  • Bone pain: From skeletal involvement
  • Fever
  • Unintentional weight loss
  • Anemia.
 
Diagnostic Evaluation
  • Physical examination: To assess swollen lymph nodes, including neck, axillary and groin, as well as a swollen spleen or liver.
  • Blood tests: A sample of blood is examined in a lab to see if anything in blood indicates the possibility of cancer.
  • Imaging tests: Imaging tests used to diagnose Hodgkin's lymphoma include X-ray, computerized tomography (CT) scan and positron emission tomography (PET).
  • Bone marrow biopsy: A bone marrow biopsy may be used to look for signs of cancer in the bone marrow. During this procedure, a small amount of bone marrow, blood and bone are removed through a needle.
 
Management
Treatment depends on the nature and extent of the disease. Once the stage of Hodgkin lymphoma is established management focuses on selecting a treatment plan.
  • The standard for chemotherapy is the ABVD regimen: Doxorubicin, Bleomycin, Vinblastine and Dacarbazine.
  • 228Patients with early stage disease will receive two to four cycles of chemotherapy.
  • Patient with early stage but unfavorable prognostic feature or intermediate stage disease will be treated with four to six cycles of chemotherapy.
  • Other chemotherapy regimens include MOPP alternating with ABVD. MOPP consist of Mechlorethamine, Vincristine, Procarbazine and Prednisone.
  • Role of radiation as a supplement to chemotherapy varies to depending on sites of disease and the presence of resistant disease after chemotherapy.
  • The most distressing and immediate side effect of the chemotherapeutic agents used to treat Hodgkin disease is severe nausea and vomiting. Symptoms may severe enough to force a client to discontinue therapy. Pancytopenia a toxic effect of these agents, usually occurs 10 to 14 days after intravenous therapy.
 
Non-Hodgkin Lymphoma
Non-Hodgkin lymphomas are a heterogeneous group of malignant neoplasms of primarily B- or T-cell origin affecting all ages. B-cell lymphomas constitute about 90% of all non-Hodgkin lymphoma. They are classified according to different cellular and lymph node characteristics.
 
Etiology
The cause of non-Hodgkin lymphoma is usually unknown.
 
Risk Factors
  • Immunosuppressive medicines: Used to prevent rejection following an organ transplant or to treat autoimmune disease.
  • Infection with certain viruses and bacteria: Certain viral and bacterial infections appear to increase the risk of non-Hodgkin's lymphoma. Viruses linked to increased non-Hodgkin's lymphoma risk include HIV and Epstein-Barr virus. Bacteria linked to an increased risk of non-Hodgkin's lymphoma include the ulcer-causing Helicobacter pylori.
  • Chemicals: Certain chemicals, such as those used to kill insects and weeds, may increase risk of developing non-Hodgkin's lymphoma. More research is needed to understand the possible link between pesticides and the development of non-Hodgkin's lymphoma.
 
Clinical Manifestation
  • Painless, swollen lymph nodes in your neck, axilla or groin
  • Abdominal pain or swelling
  • Chest pain, coughing or trouble breathing
  • Fatigue
  • Fever
  • Night sweats
  • Weight loss.
 
Diagnostic Evaluation
  • Physical examination: To determine the size and condition of lymph nodes and to find out whether liver and spleen are enlarged.
  • 229Blood and urine tests: Blood and urine tests may help rule out an infection or other disease.
  • Imaging tests: Imaging tests to look for tumors in body. Imaging tests may include X-ray, computerized tomography (CT) scan, magnetic resonance imaging (MRI) or positron emission tomography (PET).
  • Biopsy: A biopsy procedure to sample or remove a lymph node for testing. Analyzing lymph node tissue in a lab may reveal the cause.
  • Bone marrow biopsy: To find out whether the disease affects bone marrow.
 
Management
  • Chemotherapy: Chemotherapy is drug treatment—given orally or by injection—that kills cancer cells. Chemotherapy drugs can be given alone, in combination with other chemotherapy drugs or combined with other treatments.
  • Radiation therapy: Radiation therapy uses high-powered energy beams, such as X-rays, to kill cancerous cells and shrink tumors. Radiation therapy can be used alone or in combination with other cancer treatments.
  • Stem cell transplant: A stem cell transplant is a procedure that involves very high doses of chemotherapy or radiation with the goal of killing the lymphoma cells that may not be killed with standard doses. Later, healthy stem cells-own or from a donor—are injected into body, where they can form new healthy blood cells.
  • Medications that enhance immune system's ability to fight cancer: Biological therapy drugs help the body's immune system fight cancer. For example, one biological therapy called rituximab is a type of monoclonal antibody that attaches to B-cells and makes them more visible to the immune system, which can then attack. Rituximab lowers the number of B-cells, including healthy B-cells, but body produces new healthy B-cells to replace these. The cancerous B-cells are less likely to recur.
  • Medications that deliver radiation directly to cancer cells: Radioimmunotherapy drugs are made of monoclonal antibodies that carry radioactive isotopes. This allows the antibody to attach to cancer cells and deliver radiation directly to the cells. One radioimmunotherapy drug, ibritumomab tiuxetan is used to treat lymphomas.
 
Nursing Management
 
Nursing Diagnosis
  • Activity intolerance related to fatigue and anemia as evidence by inability to carry out activities of daily living.
  • Impaired tissue integrity related to high dose radiation therapy.
  • Risk of infection related to altered immune response because of lymphoma and leucopenia caused by chemotherapy or radiation therapy.
  1. Activity intolerance related to fatigue and anemia as evidence by in ability to carry out activities of daily living
    Interventions
    • Assess amount of activity that cause fatigue or dyspnea
    • Assessed patient with activities as needed
    • Provide oxygen therapy as ordered
    • Instruct pt to space rest with activities
  2. 230Impaired tissue integrity related to high dose radiation therapy
    Interventions
    • Avoid rubbing, powder, deodarnt, lotion or ointment (unless prescribed) or application of heat and cold to treated area.
    • Encourage pt to keep treated area clean and dry, bathing area gently with tepid water and mild soap.
    • Encourage wearing loose-fitting cloths.
    • Advise patient to protect skin from exposure to sun, chlorine, and temperature extremities.
  3. Risk of infection related to altered immune response because of lymphoma and leukopenia caused by chemotherapy or radiation therapy
    Interventions
    • Assess patient for risk factor for infection
    • Monitor patient for sign and symptoms of infection, such as cough, fever malaise erythema, pain or drainage and report immediately.
    • Teach patient and significant other sign and symptoms of infection to watch for and report
    • Teach the pt to avoid exposure to other with influenza or other infection.
    • Teach patient with proper handwashing and good oral and personal hygiene.
    • Teach hand hygiene and infection risk education to family member.
 
THALASSEMIA
Thalassemia is a group of inherited autosomal recessive blood disorders. In thalassemia the genetic defect which could be either mutation or deletion, results in reduced rate of synthesis or no synthesis of one of the globin chains that make up hemoglobin.
 
Types of Thalassemia
 
1. Alpha Thalassemia Facts
Alpha thalassemia is a blood disorder that reduces the production of hemoglobin, the protein in red blood cells that carries oxygen to cells throughout the body. Alpha thalassemia also occurs frequently in people from Mediterranean countries, North Africa, the Middle East, India, and Central Asia. Alpha thalassemia typically results from deletions involving the HBA1 and HBA2 genes. People who have alpha thalassemia trait can have mild anemia. However, many people with this type of thalassemia have no signs or symptoms.
Sign and Symptoms of Alpha Thalassemia
Reduction in the amount of hemoglobin prevents enough oxygen from reaching the body's tissues. Affected individuals also have a shortage of red blood cells (anemia), which can cause pale skin, weakness, fatigue, and more serious complications
 
2. Beta-Thalassemia
Beta thalassemias are due to mutations in the HBB gene on chromosome. It also inherited in an autosomal-recessive fashion. The severity of the disease depends on the nature of the 231mutation. Mutations are characterized as either β-thalassemia major if they prevent any formation of β-chains, the most severe form of β-thalassemia. Also, they are characterized as β+ or β-thalassemia intermediate if they allow some β-chain formation to occur. In either case, there is a relative excess of α-chains.
 
Diagnostic Evaluation
Microscopic examination of the blood, which shows many small, pale red blood cells.
 
Management
Normally, there are no treatments recommended. However, the doctor may suggest taking iron medication if they feel it is necessary. Additionally, splenectomy, bone marrow transplants and chelation therapy are being researched as possible treatments for thalassemia.
 
Medical therapy
Medical therapy involves iron chelation. Deferoxamine is the intravenously or subcutaneously administered chelation agent. Deferasirox is an oral iron chelation drug.
 
Standard Treatments
 
Blood Transfusions
Transfusions of red blood cells are the main treatment for people who have moderate or severe thalassemias. This treatment gives healthy red blood cells with normal hemoglobin.
Blood transfusions allow patient feel better, enjoy normal activities, and live into adulthood. This treatment is lifesaving, but it's expensive and carries a risk of transmitting infections and viruses (for example, hepatitis). However, the risk is very low in the United States because of careful blood screening.
 
Iron Chelation Therapy
Because the hemoglobin in red blood cells is an iron-rich protein, regular blood transfusions can lead to a buildup of iron in the blood. This condition is called iron overload. It damages the liver, heart, and other parts of the body. To prevent this damage, iron chelation therapy is needed to remove excess iron from the body. Two medicines are used for iron chelation therapy.
  • Deferoxamine is a liquid medicine that's given slowly under the skin, usually with a small portable pump used overnight. This therapy takes time and can be mildly painful. Side effects include problems with vision and hearing.
  • Deferasirox is a pill taken once daily. Side effects include headache, nausea (feeling sick to the stomach), vomiting, diarrhea, joint pain, and fatigue (tiredness).
 
Folic Acid Supplements
Folic acid is a vitamin B that helps build healthy red blood cells. Patient may need to take folic acid supplements in addition to treatment with blood transfusions and iron chelation therapy.
There are two kinds of iron in the diet:
  1. Iron which is present in red meat (meat iron)
  2. Iron which is widely distributed in the diet (non-meat).
232Iron chelators such as Desferal and Deferiprone not only bind iron but also some Zinc and excrete it in the urine. The main nutritional sources of Zinc are animal foods (meat and dairy products) and wholemeal cereals. Dairy products like milk, cheese and yoghurt, eggs, etc. contain a lot of Zinc.
In thalassemia, because of the excess iron in the body, there is a higher risk of oxidative damage. The four main antioxidants are vitamin E, vitamin C, carotenoids and flavonoids.
  • Vitamin E is mainly found in vegetable oils such as olive oil and safflower oil.
  • Vitamin C is present in fruit and vegetables.
  • Carotenoids are found in carrots, yellow squash, corn, tomatoes, papaya, oranged, and dark-green leafy vegetables. As these foods are also high in vitamin C.
  • Tea and Red wine contain Flavonoids. Tea also inhibits iron absorption.
 
Complication
  • Iron overload: People with thalassemia can get an overload of iron in their bodies, either from the disease itself or from frequent blood transfusions. Too much iron can result in damage to the heart, liver and endocrine system, which includes glands that produce hormones that regulate processes throughout the body. The damage is characterized by excessive iron deposition. Without adequate iron chelation therapy, almost all patients with beta-thalassemia will accumulate potentially fatal iron levels.
  • Infection: People with thalassemia have an increased risk of infection. This is especially true if the spleen has been removed.
  • Bone deformities: Thalassemia can make the bone marrow expand, which causes bones to widen. This can result in abnormal bone structure, especially in the face and skull. Bone marrow expansion also makes bones thin and brittle, increasing the risk of broken bones.
  • Enlarged spleen: The spleen aids in fighting infection and filters unwanted material, such as old or damaged blood cells. Thalassemia is often accompanied by the destruction of a large number of red blood cells, and the task of removing these cells causes the spleen to enlarge.
  • Slowed growth rates: Anemia can cause a child's growth to slow. Puberty also maybe delayed in children with thalassemia.
  • Heart problems: Such as congestive heart failure and abnormal heart rhythms (arrhythmias), may be associated with severe thalassemia.
 
Nursing Management
 
Nursing Diagnosis
  • Activity intolerance related impaired oxygen transport
  • High-risk for infection related decreased resistance secondary to hypoxia
  • Altered body image related skeletal changes
  • Altered nutrition: Less than body requirement related to inadequate nutritional intake and anorexia.
  • Ineffective management of therapeutic regimen related to lack of knowledge about appropriate nutrition and medication.
 
Nursing Interventions
  • Assess amount of activity that cause fatigue or dyspnea.
  • Assessed patient with activities as needed.
  • 233Provide oxygen therapy as ordered.
  • Instruct pt to space rest with activities.
  • Avoid rubbing, powder, deodrant, lotion or ointment (unless prescribed) or application of heat and cold to treated area.
  • Encourage pt to keep treated area clean and dry, bathing area gently with tepid water and mild soap.
  • Encourage wearing loose – fitting cloths
  • Advise patient to protect skin from exposure to sun, chlorine, and temperature extremities.
BIBLIOGRAPHY
  1. Basvanthapa BT. Medical surgical nursing, 2nd ed. Jaypee Brothers Medical Publishers;  New Delhi: 580–3.
  1. Brunner, Suddarth. Textbook of medical surgical nursing, 10th ed. Smelterzers;  456–8.
  1. Chintamani. Lewis's medical surgical nursing. 7th ed. Elseveir Limited;  New Delhi:  2010. 715–8.
  1. Joyce MB, Hawks JH. Medical surgical nursing clinical management for positive outcomes, 7th ed. Vol. 2, 2302–3.
  1. Joyce MB. Medical surgical nursing clinical management for positive outcomes, 7th ed. Elsevier;  1569–72.
  1. Kaur L, Kaur S, et al. Textbook of medical surgical nursing. 2nd ed. Vol. 1 Lotus publisher. 
  1. Lippincott. Textbook of manual nursing practice, 8th ed. 780–81.
  1. Phipps MS. Medical surgical nursing, 8th ed. Elsevier;  455–8.
  1. Porth. Pathphysiology, 4th ed.
  1. Phipps MS. Medical surgical nursing health and illness perspectives, 7th ed. Mosby;  1628–33.
  1. Polaski LA. Luckmann's core principles and practice of medical surgical nursing, Elsevier, a division of Reed Elsevier India Private Limited;  854–7.
  1. Polaski LA, Tatro SE. Luckmann's core principles and practice of medical surgical nursing, Elsevier;  687–9.
  1. Smelter CS, Bare BB, Suddarth. Textbook of medical surgical nursing, 10th ed. Lippincott Publishers;  Philadehia  (PA): 2006. 916–9.
  1. Usha RN. Textbook of medical surgical nursing, 1st ed. Jaypee Brothers Medical Publishers;  New Delhi: 2009. 345–7
  1. Williams LS, Hooper PD. Understanding medical surgical nursing, Jaypee Brothers Medical Publishers;  New Delhi: 478–80.

Respiratory Disorders5

235
 
RESPIRATORY FAILURE
 
Introduction
The most important function of the respiratory system is to provide oxygen to the body tissues and remove the carbon dioxide. The body relies primarily on the central nervous system, the pulmonary system, the heart, and the vascular system to accomplish the effective respiration. Respiratory failure develops when one or more of these systems or organs fail to maintain optimal functioning.
Respiratory failure is a sudden and life-threatening deterioration of the gas exchange functions of the lung and indicates failure of the lungs to provide adequate oxygenation or ventilation for the blood. Acute respiratory failure is defined as the decrease in the arterial oxygen tension to less than 50 mm Hg (hypoxemia) and increase in the arterial carbon dioxide tension, i.e. (hypercapina) to greater than 50 mm Hg, with an arterial pH of less than 7.35. It is a condition in which there is inadequate gas exchange by the respiratory system, with the result that arterial O2 and CO2 levels cannot be maintained within their normal ranges.
 
Definition
  • Acute respiratory failure is a condition in which the patient's breathing apparatus fails in the ability to maintain arterial blood gases within the normal range.
  • Ventilatory failure is the inability of the body to sustain respiratory drive or the inability of the chest wall and muscles to mechanically move air in and out of the lungs. The hallmark of ventilator failure is an elevated CO2 level.
  • A sudden inability of the lungs to maintain normal respiratory function. The condition may be caused by an obstruction in the airways or by failure of the lungs to exchange gases in the alveoli.
  • Acute respiratory failure is defined as the decrease in the arterial oxygen tension to less than 50 mm Hg (hypoxemia) and increase in the arterial carbon dioxide tension, i.e. (hypercapnia) to greater than 50 mm Hg, with an arterial pH of less than 7.35.
 
CLASSIFICATION OF RESPIRATORY FAILURE
It is divided into two types:
  • Acute respiratory failure
  • Chronic respiratory failure
 
Acute Respiratory Failure
Acute respiratory failure is characterized by hypoxemia (PaO2 less than 50 mm Hg) and acidemia (pH less than 7.35). Acute respiratory failure occurs rapidly, usually in minutes to hours or days.
 
Types of Acute Respiratory Failure
It is divided into two:
  1. Type 1 acute respiratory failure.
  2. Type 2 acute respiratory failures.
  • 236Type 1 acute respiratory failure: Type 1 respiratory failure is defined as hypoxia without, hypercapnia, and indeed the PaCO2 may be normal or low. It is typically caused by a ventilation/perfusion (V/Q) mismatch, the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs.
  • Type 2 acute respiratory failure: Type 2 respiratory failure is caused by inadequate ventilation, both oxygen and carbon dioxide are affected and buildup of carbon dioxide levels (PaCO2) that has been generated by the body.
 
Chronic Respiratory Failure
Chronic respiratory failure is characterized by hypoxemia and hypercapnea with the normal pH (7.35 to 7.45). Chronic respiratory failure occurs over a period of months to a year—allows for activation of compensatory mechanism.
Chronic respiratory failure may also be divided into:
  • Hypoxemic respiratory failure: When a lung disease causes respiratory failure, gas exchange is reduced because of changes in ventilation (the exchange of air between the lungs and the atmosphere), perfusion (blood flow), or both. Activity of the respiratory muscles is normal. This type of respiratory failure which results from a mismatch between ventilation and perfusion is called hypoxemic respiratory failure. Some of the alveoli get less fresh air than they need for the amount of blood flow, with the net result of a fall in oxygen in the blood. These patients tend to have more difficulty with the transport of oxygen than with removing carbon dioxide. They often overbreathe (hyperventilate) to make up for the low oxygen, and this results in a low CO2 level in the blood (hypocapnia). Hypocapnia makes the blood more basic or alkaline which is injurious to the cells.
  • Hypercapnic respiratory failure: Respiratory failure due to a disease of the muscles used for breathing (‘pump or ventilatory apparatus failure’) is called hypercapnic respiratory failure. The lungs of these patients are normal. This type of respiratory failure occurs in patients with neuromuscular diseases, such as myasthenia gravis, stroke, cerebral palsy, poliomyelitis, amyotrophic lateral sclerosis, muscular dystrophy, postoperative situations limiting ability to take deep breaths, and in depressant drug overdoses. Each of these disorders involves a loss or decrease in neuromuscular function, inefficient breathing and limitation to the flow of air into the lungs. Blood oxygen falls and the carbon dioxide increases because fresh air is not brought into the alveoli in needed amounts. In general, mechanical devices that help move the chest wall help these patients.
 
Etiology
 
Brain Disorders
  • Stroke: A stroke is sudden loss of brain function resulting from a disruption of blood supply to a part of the brain.
  • Brain tumors: A brain tumor is a localized intracranial lesion that occupies space within the skull and tends to cause a rise in intracranial pressure.
  • Depression of respiratory drive with drugs, e.g. narcotic tranquilizer.
237
 
Chest Wall Dysfunction and Neuromuscular Factor
  • Anesthetic blocking agent
  • Cervical spinal cord injury
  • Neuromuscular disorder
  • Neuromuscular blocking agent
 
Airway Obstruction
  • Airway inflammation
  • Tumor
  • Foreign bodies
  • Asthma
  • COPD
 
Interstitial Lung Diseases
  • Pneumonia
  • Pulmonary tuberculosis
  • Pulmonary edema
  • Pulmonary fibrosis
 
Pulmonary Dysfunction
  • Asthma
  • Emphysema
  • Chronic obstructive pulmonary disease
  • Pneumonia
  • Pneumothorax
  • Pulmonary contusion
  • Hemothorax
  • Acute respiratory distress syndrome (ARDS)
 
Cardiac Dysfunction
  • Pulmonary edema
  • Cerebrovascular accident
  • Arrhythmia
  • Congestive heart failure
  • Valve pathology
 
Other
  • Fatigue due to prolonged tachypnea in metabolic acidosis
  • Intoxication with drugs (e.g. morphine, benzodiazepines, alcohol) that suppress respiration.
 
Traumatic Causes
  • Direct thoracic injury may result in a number of abnormalities that can lead to respiratory failure.
  • Direct brain injury can result in loss of respiration.
238
 
Pathophysiology
239
 
Mechanism of Pathophysiology
  • Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, central nervous system (CNS), peripheral nervous system, respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure.
  • Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable PaCO.
  • Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller.
 
Clinical Manifestations
  • Paroxysmal nocturnal dyspnea
  • Orthopnea
  • Pulmonary edema
  • Confusion and reduced consciousness may occur.
  • Neurological features may include restlessness, anxiety, confusion, seizures or coma.
  • Tachycardia and cardiac arrhythmias
  • Cyanosis
  • Polycythemia
  • Cor pulmonale
  • Pulmonary hypertension
  • Right ventricular failure
  • Hepatomegaly
  • Peripheral edema
 
Diagnostic Evaluation
  • Arterial blood gas analysis: Confirmation of the diagnosis.
  • Renal function tests and LFTs: May provide clues to the etiology or identify complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ dysfunctions.
  • Serum creatine kinase and troponin I: To help exclude recent myocardial infarction. Elevated creatine kinase may also indicate myositis.
  • Thyroid function test: Hypothyroidism may cause chronic hypercapnic respiratory failure.
  • Spirometry: To evaluate lung capacity.
  • Echocardiography: If a cardiac cause of acute respiratory failure is suspected.
  • Pulmonary function tests are useful in the evaluation of chronic respiratory failure.
  • ECG: To evaluate a cardiovascular cause, it may also detect dysrhythmias resulting from severe hypoxemia or acidosis.
  • 240Right heart catheterization: Should be considered if there is uncertainty about cardiac function, adequacy of volume replacement, and systemic oxygen delivery.
  • Pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema.
 
Management
Management of acute respiratory failure is dependent upon the cause and its severity. The principle of management of acute respiratory failure is the following:
  • Treat the cause
  • Maintain a patient airway
  • Provide adequate ventilation
  • Provide optimum oxygen
  • Carry out chest physiotherapy.
    • The main goal of treating of respiratory failure is to get oxygen to lungs and organs and remove the carbon dioxide from the body.
    • The promoting effective airway clearance effective gas exchange.
    • Preventive complication of immobility.
    • Monitoring and documenting indication of altered tissue perfusion.
    • Promoting comfort.
    • Correction of hypoxemia.
    • Correction of hypercapnia.
    • Airway as another goal is to treat the underlying cause of the condition.
 
Administration of Oxygen
Nasal prongs, nasal catheters, or face masks are commonly used to administer oxygen to the spontaneously breathing patient.
The actual fraction of inspired oxygen depends upon:
  • Flow rate of oxygen
  • Degree of mouth breathing
  • Patency of nasal passage
  • Inspection of insertion of nasal catheter.
 
Positive End Expiratory Pressure (PEEP)
  • Used with mechanical ventilation
  • Increases interathoracic pressure
  • Keeps the alveoli open
  • Decreases shunting
  • Improves gas exchange.
 
Management of Upper Airway Obstruction
As soon as upper airway obstruction is diagnosed, measures must be taken to correct it.
  • The mouth is opened to see if tongue has fallen back or if there are secretions, blood clot or any particles obstructing the airway.
  • 241Extension of the head is the simplest way of relieving upper airway obstruction by the tongue falling back.
  • If simple extension of the head is not adequate to clear the airway, the mandible should be forced forward.
  • Maneuver is designed to put further tension on the musculature that supports the tongue. It is best executed by standing behind the patient.
  • If maneuver is not adequate and partial airway obstruction still exists, then oral airway may have to be inserted or end tracheal intubation be done.
  • If assisted ventilation is required, a resuscitator bag and mask are used initially prior to intubation and mechanical ventilation.
 
Medical Management
Medical management includes:
  • Antibiotics for pneumonia infection.
  • Bronchodilators: Reduce bronchospasm, COPD.
  • Diuretics for pulmonary edema.
  • Chest physical therapy and the hydration to mobilize secretions.
  • Maintain fluid and electrolytes and avoid fluid overload.
  • Intubation and mechanical ventilation.
 
Complications
  • Oxygen toxicity if prolonged high FIO2 required.
  • Barotrauma may occur from excessive intra-alveolar pressure.
  • Ventilator-associated pneumonia.
  • Infection to the lower respiratory tract due to intubation.
  • Dental or vocal cord trauma.
  • Gastric complications: Distention from air entering the GI tract, stress ulcers from hyperacidity and inadequate nutrition.
  • Other complications include deep venous thromboembolism, skin breakdown, malnutrition, stress and anxiety.
 
Nursing Management
 
Nursing Assessment
  • Note the changes suggesting increased work of breathing or pulmonary edema
  • Assess breathing sound
  • Assess sign of hypoxemia and hypercapnea
  • Analyze the ABG and compare the previous values
  • Determine hemodynamic status and compare it with previous value.
 
Nursing Diagnosis
  • Impaired gas exchange related to inadequate respiratory center activity or chest wall movement, airway obstruction, or fluid in lung.
  • Ineffective airway clearance related to increased or tenacious secretion.
  • 242Acute pain related to inflammatory process and dyspnea.
  • Anxiety related to pain, dyspnea and serious condition.
 
Nursing Intervention
  • Improve gas exchange:
    • Administer oxygen to maintain PaO2 of 60 mm Hg, using devices that provide increased oxygen concentration.
    • Monitor fluid balance by intake and output measurement, urine-specific gravity, daily weight measurement.
    • Provide measures to prevent atelectasis and promote chest extension and secretion clearance as per advice, spirometer.
    • Elevated head level to 30 degrees.
    • Monitor adequacy of alveolar ventilation by frequent measurement of respiratory system.
    • Administer antibiotic, cardiac medication, and diuretics as prescribed by doctor.
  • Maintain airway clearance:
    • Administer medication to increase alveolar function.
    • Perform chest physiotherapy to remove mucus.
    • Administer IV fluids
    • Suction patient as needed to assist with removal of secretions.
  • Relieving pain:
    • Watch patient for sign of discomfort and pain
    • Position the head elevated
    • Give prescribed morphine and monitor for pain-relieving sign
  • Reducing anxiety:
    • Correct dyspnea and relieve from physical discomfort
    • Speak calm and slowly
    • Explain diagnostic procedure.
 
CARE OF PATIENT ON VENTILATOR
 
Introduction
  • Mechanical ventilation (MV) is one of the core components of supportive therapy for critically ill patients and is often lifesaving. But its application may lead to numerous types of lung injury, known as ventilator-induced lung injury (VILI). Caring for a patient who needs MV requires sound knowledge of MV and pulmonary physiology.
  • Understanding the basics of MV can make all the difference for each patient.
 
Basics of Mechanical Ventilation
  • A breath cycle is classified into four phases—initiation of inspiration or a switch from expiration to inspiration, inspiration, a switch from inspiration to expiration, and expiration. With MV, the above four phases are controlled by phase variables, which include trigger, limit, and cycle variables, and can be manipulated on the ventilator.
  • 243The activation of inspiration or a switch from expiration to inspiration is triggered by a trigger variable, also called a triggering mechanism. After successful triggering, inspiration needs to be sustained and limited by at least one of the preset limit variables and terminated by a predefined cycle variable, also known as cycling mechanism.
 
Trigger Variables
  • A ventilator can be triggered by the machine itself, patient, or manual triggering. There are four common trigger variables—time, flow, pressure, and volume. With time triggering, mechanical inspiration occurs at a regular preset time-interval, which is determined by the preset respiratory rate (RR).
  • A patient's inspiratory effort causes changes in pressure, flow, or volume within the ventilator circuit.
  • When inspiration is initiated by a decrease in the baseline gas flow during exhalation, it is called flow triggering or flow-by on some ventilators.
  • If the ventilator is triggered to deliver inspiratory flow by a drop in baseline pressure resulting from a patient's inspiratory effort during exhalation, it is known as pressure triggering.
  • During exhalation, a decrease in volume to a certain extent within the ventilator circuit activates inspiration. It is referred to as volume triggering.
  • Other trigger variables such as flow waveform, chest-wall motion, transthoracic impedance, and diaphragm electrical activity are not available in most ventilators and seldom used.
  • Time triggering is also called machine triggering. Flow or pressure triggering is patient triggering and widely used. Flow triggering is claimed to reduce the work of breathing (WOB) compared with pressure triggering. With modern ventilators, these differences have minimal impact on a patient's condition.
  • After selecting a trigger variable, the operator has to set up a sensitivity setting that determines the extent of change in flow or pressure, or the amount of a patient's effort that is required to trigger the ventilator. In order to reduce the WOB and avoid patient-ventilator dyssynchrony, it is vital to adjust sensitivity settings to meet the needs of individual patients.
 
Limit Variables
  • Upon triggering a breath, inspiration needs to be sustained and limited by at least one of the following variables—volume, pressure, flow or time.
  • When the maximum tidal volume (VT) that can be delivered to a patient during inspiration is preset, it is called volume-controlled ventilation.
  • If the maximum pressure rise during inspiration is predetermined, it is referred to as pressure-controlled ventilation. With pressure-support ventilation, inspiration is limited by the preset level of pressure support.
  • The flow limit involves setting the maximum flow that can be delivered by the ventilator.
  • Setting a flow limit may cause patient-ventilator dyssynchrony if a patient's inspiratory flow demand exceeds the preset flow limit.
  • 244Most modern ventilators can increase flow rate in response to increasing patient demands. Time-limited ventilation is not commonly used and may be seen in high-frequency ventilation.
  • A limit variable specifies the relevant parameter that is reached during inspiration. However, it is not programmed to terminate inspiration. The termination of inspiration and initiation of expiration are controlled by a cycle variable.
 
Cycle Variables
  • Inspiration can be terminated by a predefined pressure, flow, volume or time variable.
  • With pressure-cycled ventilation, inspiration is ended once the peak inspiration pressure (PIP) reaches the targeted pressure.
  • In flow-cycled ventilation, the inspiratory flow ceases when its flow rate is dropped to the predetermined percentage of peak inspiratory flow rate.
  • Flow cycle criteria vary with different kinds of ventilators and are determined by a patient's clinical status. Appropriately set cycling threshold reduces autopositive end-expiratory pressure (auto-PEEP), also called intrinsic PEEP and the WOB.
  • With volume-cycled ventilation, inspiration is terminated once the preset VT is delivered. In time-cycled ventilation, the cycling between inspiration and expiration occurs at a regular preset time interval.
  • Both volume and time cycling are machine cycling. Both pressure and flow cycling are patient cycling. Flow cycling is commonly used in pressure support ventilation.
 
Breath Types
  • With MV, there are mandatory and spontaneous breaths. The mandatory breath is triggered, limited, and terminated by the ventilator (time-triggered and time-cycled). The spontaneous breath is initiated, controlled, and ended by the patient.
  • When the mandatory breath is triggered by the patient, it is called an assisted breath. If spontaneous breaths are assisted or supported by the ventilator, such as the pressure support mode, they are also classified as assisted breaths.
  • There are volume-controlled or pressure-controlled mandatory breaths. With volume-controlled ventilation, the inspiration of mandatory and assisted breaths is limited by the preset volume. Pressure is variable and affected by both anatomical and artificial airway resistance, chest wall, and lung compliance, as well as different flow patterns.
  • For pressure-controlled ventilation, mandatory, and assisted breaths are limited by the predetermined inspiratory pressure. Volume and flow are variable and influenced by the preset pressure, inspiratory time, respiratory resistance, chest wall, and lung compliance.
  • During spontaneous breathing, the patient controls his own tidal volumes and terminates his own inspiration. Both volume and pressure are variable and depend on the patient's inspiratory effort, respiratory resistance and lung compliance.
  • Spontaneous breaths can be supported by a preset pressure-supported or volume-supported ventilation to augment VT.
  • Pressure support is commonly prescribed for patients with spontaneous breaths to overcome the resistance created by the ventilator circuit, reduce the WOB, and improve a patient's comfort.
  • 245With volume-controlled ventilation, the mandatory breath is time-triggered, time-cycled, and volume limited; the assisted breath is patient triggered, limited, and cycled by the same mechanisms as the mandatory breath.
  • For pressure-controlled ventilation, the mandatory breath is time triggered, time cycled, and pressure-limited; the assisted breath is patient-triggered, limited, and cycled by the same variables as the mandatory breath.
  • Pressure-support ventilation is patient-triggered, pressure-limited and usually flow-cycled.
 
VILI and Other Complications
VILI includes barotrauma, volutrauma, atelectrauma, and biotrauma.
  • Barotrauma is evidenced by extra-alveolar air. It is induced by high airway pressure or large VT ventilation that damages the alveolar tissue and leads to alveolar rupture. Subcutaneous emphysema, pneumothorax, pneumomediastinum, and pneumoperitoneum are typical forms of barotrauma.
  • Volutrauma is caused by large VT ventilation that leads to alveolar overdistension, which may manifest itself as pulmonary edema.
  • Atelectrauma occurs with repeated recruiting and derecruiting unstable alveoli during each breath cycle. Ventilation with low positive end-expiratory pressure (PEEP) predisposes to the development of atelectrauma in patients with heterogenous damage of lung parenchyma, such as acute respiratory distress syndrome (ARDS).
  • Biotrauma results from the production, activation and release of both local and systemic inflammatory mediators secondary to lung parenchymal damage caused by volutrauma, barotrauma, and atelectrauma. Severe biotrauma may deteriorate to systemic inflammatory response syndrome (SIRS) and contribute to the development of multiple organ dysfunction syndromes (MODS).
 
Nursing Care of Ventilated Patients
Before caring for such patients, the questions to be kept in mind by a nurse are:
  • What do I need to know to plan my shift?
  • Which patient assessment parameters are crucial?
  • What evidence-based practice guidelines should I follow?
The nurse must be able to do the following:
  • Identify the indications for mechanical ventilation.
  • List the steps in preparing a patient for intubation.
  • Determine the FiO2, tidal volume, rate and mode of ventilation on a given ventilator.
  • Describe the various modes of ventilation and their implications.
  • Describe at least two complications associated with a patient's response to mechanical ventilation and their signs and symptoms.
  • Describe the causes and nursing measures taken when trouble-shooting ventilator alarms.
  • Describe preventative measures aimed at preventing other selected complications related to endotracheal intubation.
  • 246Give rationale for selected nursing interventions in the plan of care for the ventilated patient.
  • Complete the care of the ventilated patient checklist.
  • Complete the suctioning checklist.
    • To review indications for and basic modes of mechanical ventilation, possible complications that can occur, and nursing observations and procedures to detect and/or prevent such complications.
    • To provide a systematic nursing assessment procedure to ensure early detection of complications associated with mechanical ventilation.
The top ten essentials of nursing care for ventilated patients are as follows:
 
Care Essential 1
Review communications:
  • Communication among care providers promotes optimal outcomes. For mechanically ventilated patients, care providers may include primary care physicians, pulmonary specialists, hospitalists, respiratory therapists, and nurses.
  • To make sure nurse is aware of other team members' communications about the patient, find out the goals of therapy for her patient when obtaining report. Why is the patient on a ventilator? To improve oxygenation? Boost ventilation? Permit sedation? Reverse respiratory muscle fatigue? Why is the patient in this unit? Because the patient has an underlying condition that complicates weaning from the ventilator? What is the patient's do-not-resuscitate status?
  • Communicating with the patient is essential too. Provide writing tools or a communication board so patient can express his/her needs. Ask simple yes/no questions to which the patient can nod or shake his/her head.
 
Care Essential 2
Check ventilator settings and modes:
  • When the nurse enters the patient's room, take vital signs, check oxygen saturation, listen to breath sounds, and note the changes from previous findings.
  • Also assess the patient's pain and anxiety levels.
  • Read the patient's order and obtain information about the ventilator. Compare current ventilator settings with the settings prescribed in the order.
  • Familiarize self with ventilator alarms and the actions to take when an alarm sounds.
  • Locate suction equipment and review its use.
  • Look for a bag-valve mask, which should be available for every patient with an artificial airway; be sure to know how to hyperventilate and hyperoxygenate the patient.
 
Ventilator Settings and Modes
Generally, ventilators display ordered settings and patient parameters. Check the following settings:
  • Respiratory rate, the number of breaths provided by the ventilator each minute. Manually count the patient's respiratory rate, because the patient may be taking her own breaths at a rate above the ventilator setting.
  • 247Fraction of inspired oxygen (FiO2), expressed as a percentage (room air is 21%).
  • Tidal volume (TV or VT), the volume of air inhaled with each breath, expressed in milliliters.
  • Peak inspiratory pressure (PIP), the pressure needed to provide each breath. Target PIP is below 30 cm H2O. High PIP may indicate a kinked tube, a need for suctioning, bronchospasm, or a lung problem, such as pulmonary edema or pneumothorax.
  • To find out which ventilation mode or method patient is receiving, check the ventilator itself or the respiratory flow sheet. The mode depends on patient variables, including the indication for mechanical ventilation.
  • Modes include those that provide specific amounts of TV during inspiration, such as assist-control (A/C) and synchronized intermittent mandatory ventilation (SIMV) and those that provide a preset level of pressure during inspiration, such as pressure support ventilation (PSV) and airway pressure release ventilation.
  • PSV allows spontaneously breathing patients to take their own amount of TV at their own rate. A/C and continuous mandatory ventilation provide a set TV at a set respiratory rate. SIMV delivers a set volume at a set rate, but lets patients initiate their own breaths in synchrony with the ventilator.
  • Some patients may receive adjuvant therapy, such as positive end-expiratory pressure (PEEP). With PEEP, a small amount of continuous pressure (generally from +5 to +10 cm H2O) is added to the airway to increase therapeutic effectiveness. In many cases, PEEP is added to reduce oxygen requirements.
  • Finally determine if a capnography monitor is recording the patient's partial pressure of exhaled carbon dioxide (pCO2). Capnography, which reflects ventilation, can detect adverse respiratory events, such as tracheal-tube malpositioning, hypoventilation, and ventilator circuit problems. The capnography waveform should be square; generally, the value should be in the normal pCO2 range of 35 to 45 mm Hg. To better understand your patient's ventilation status, check for trends in waveforms and values rather than focusing solely on single events.
 
Care Essential 3
Suction appropriately:
  • Patients receiving positive-pressure mechanical ventilation have a tracheostomy, endotracheal, or nasotracheal tube. Most initially, have an endotracheal tube; if they stay on the ventilator for many days or weeks, a tracheotomy may be done.
  • Tracheotomy decisions depend on patient specifics. Controversy exists as to when a tracheotomy should be considered; generally, patients have tracheotomies before being managed on a med-surg unit.
  • Although specific airway management guidelines exist, always check the facility's policy and procedure manual of the concerned hospital.
  • General suctioning recommendations include the following:
    • Suction only as needed—not according to a schedule.
    • Hyperoxygenate the patient before and after suctioning to help prevent oxygen desaturation.
    • Do not instill normal saline solution into the endotracheal tube in an attempt to promote secretion removal.
    • 248Limit suctioning pressure to the lowest level needed to remove secretions.
    • Suction for the shortest possible duration.
    • If patient has an endotracheal tube, check for tube slippage into the right mainstem bronchus, as well as inadvertent extubation.
    • Other complications of tracheostomy tubes include tube dislodgment, bleeding, and infection.
    • To identify these complications, assess the tube insertion site, breath sounds, vital signs, and PIP trends.
    • For help in assessing and managing tube complications, consult the respiratory therapist.
    • If patient has a tracheostomy, perform routine cleaning and care according to facility policies and procedures.
 
Care Essential 4
  • Assess pain and sedation needs.
  • Even though patient cannot verbally express his/her needs, nurse will need to assess patient's pain level using a reliable scale.
  • Keep in mind that a patient's acknowledgment of pain means pain is present and must be treated.
  • Two scales that help to evaluate patient's sedation level are the Richmond Agitation Sedation Scale and the Ramsay Sedation Scale.
  • Should the nurse restrain an agitated ventilator patient to prevent extubation? It is best to treat agitation and anxiety with medication and nonpharmacological methods, such as communication, touch, presence of family members, music, guided imagery, and distraction.
 
Care Essential 5
Prevent infection:
  • Ventilator-associated pneumonia (VAP) is a major complication of mechanical ventilation. Much research has focused on how best to prevent VAP. The Institute for Healthcare Improvement includes the following components in its best-practices VAP prevention ‘bundle’:
    • Keep the head of the bed elevated 30 to 45 degrees at all times, if patient's condition allows. Health care providers tend to overestimate bed elevation, so gauge it by looking at the bed frame rather than by simply estimating.
    • Everyday, provide sedation ‘vacations’ and assess readiness to extubate, indicated by vital signs and arterial blood gas values within normal ranges as well as the patient taking breaths on her own.
    • Provide peptic ulcer disease prophylaxis, as with a histamine-2 blocker, such as famotidine.
    • Provide deep vein thrombosis prophylaxis, as with an intermittent compression device.
    • Perform oral care with chlorhexidine daily.
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Other measures that decrease VAP risk
  • Extubating the patient as quickly as possible
  • Performing range-of-motion exercises
  • Patient turning and positioning to prevent the effects of muscle disuse
  • Having the patient sit up when possible to improve gas exchange
  • Providing appropriate nutrition to prevent a catabolic state.
  • Assess the patient's tolerance when patient performs an activity by checking vital signs, oxygenation status, and pain and agitation levels.
  • Keeping bacteria out of oral secretions also reduces VAP risk. Use an endotracheal tube with a suction lumen above the endotracheal cuff to allow continuous suctioning of tracheal secretions that accumulate in the subglottic area. Do not routinely change the ventilator circuit or tubing. Brush the patient's teeth at least twice a day and provide oral moisturizers every 2 to 4 hours.
 
Care Essential 6
Prevent hemodynamic instability:
  • Monitor the patient's blood pressure every 2 to 4 hours, especially after ventilator settings are changed or adjusted.
  • Mechanical ventilation causes thoracic-cavity pressure to rise on inspiration, which puts pressure on blood vessels and may reduce blood flow to the heart; as a result, blood pressure may drop. To maintain hemodynamic stability, nurse may need to increase IV fluids or administer a drug such as dopamine or norepinephrine, if ordered.
  • High levels of inspiratory pressure with PSV and PEEP increase the risk of barotrauma and pneumothorax. To detect these complications, assess breath sounds and oxygenation status often. To help prevent these conditions, use the lowest pressure level for ventilator-delivered breaths and adjust the level as tolerated.
 
Care Essential 7
Manage the airway:
  • The cuff on the endotracheal or tracheostomy tube provides airway occlusion. Proper cuff inflation ensures the patient receives the proper ventilator parameters, such as TV and oxygenation.
  • Following hospital policy, inflate the cuff and measure for proper inflation pressure using the minimal leak technique or minimal occlusive volume.
  • These techniques help prevent tracheal irritation and damage caused by high cuff pressure; always practice them with an experienced nurse or respiratory therapist.
  • Never add air to the cuff without using proper technique.
  • When performing mouth care, suction oral secretions and brush the patient's teeth, gums, and tongue at least twice a day using a soft pediatric or adult toothbrush. Use a tonsil suction device if patient needs more frequent suctioning.
  • With assistance from an experienced colleague, change the tracheostomy tube or tracheostomy ties and endotracheal tube-securing devices if they become soiled or loose. Incorrect technique could cause accidental extubation.
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Care Essential 8
Meet the patient's nutritional needs:
  • For optimal outcomes, ventilator patients must be well-nourished and should begin taking nutrition early. But like any patient who cannot swallow normally, they need an alternative nutrition route. Preferably, they should have feeding tubes with liquid nutrition provided through the gut. If this is not possible, the health care team will consider parenteral nutrition.
  • Patients with tracheostomy tubes may be able to swallow food. Follow the physician's orders and consult speech and respiratory therapists.
 
Care Essential 9
Educate the patient and family:
  • Seeing a loved one attached to a mechanical ventilator is frightening. To ease distress in the patient and family, teach them why mechanical ventilation is needed and emphasize the positive outcomes it can provide.
  • Each time you enter the patient's room, explain what you are doing.
  • Reinforce the need and reason for multiple assessments and procedures, such as laboratory tests and X-rays.
  • Communicate desired outcomes and progression toward outcomes so the patient and family can actively participate in the plan of care.
  • Caring for a patient on mechanical ventilation requires teamwork, knowledge of care goals, and interventions based on best practices, patient needs, and response to therapy.
  • Mechanical ventilation has become a common treatment, and nurses must be knowledgeable and confident when caring for ventilator patients.
 
Care Essential 10
  • Wean the patient from the ventilator appropriately.
  • As patient's indications for mechanical ventilation resolve and he/she is able to take more breaths on his/her own, the health care team will consider removing them from the ventilator.
  • Weaning methods may vary by facility and provider preference. Although protocols may be used to guide ventilator withdrawal, the best methods involve teamwork, consistent evaluation of patient parameters, and adjustment based on these changes.
  • Some patients may need weeks of gradually reduced ventilator assistance before they can be extubated, others cannot be weaned at all.
  • Factors that affect ease of weaning include underlying disease processes, such as chronic obstructive pulmonary disease or peripheral vascular disease; medications used to treat anxiety and pain; and nutritional status.
Weaning criteria
Guide
Adequate oxygenation
PaO2/FiO2 ratio > 200 or FiO2 ≤ .40 and SpO2 ≥ 90% and/or PaO2 ≥ 60
Peep ≤ 8 cm H2O
Adequate ventilation
PH ≥ 7.30
RR ≤ 35 bpm
VE ≤ 15 lpm
Inspiratory effort by patient
251
Weaning criteria
Guide
Hemodynamic stability
HR ≤ 140 bpm
SBP 90–180 mm Hg
No or minimal vasopressors or inotropes*
Appropriate LOC
No continuous sedation infusion
No neuromuscular blocking agents
Afebrile
Temp > 36 °C and < 38 °C
Adequate hemoglobin
Hb ≥ 70 and/or no evidence of hemorrhage
*Dopamine < mcg/kg/min
The spontaneous breathing trial will be terminated if any of the following termination criteria occur:
Termination criteria
  • SpO2 < 90% with ↑ FiO2 ≥ .50
  • RR > 35 bpm
  • RSBI > 80
  • Blood pressure ↑ 20 mm Hg
  • HR ↑ 20 bpm
  • New arrhythmias
  • ↑ WOB
  • Patient agitation or anxiety
 
Weaning Procedure
Prior to and during weaning trial:
  • Obtain and document baseline mechanical and spontaneous measurements
  • Evaluate baseline vital signs and changes with each vent change
  • Titrate sedation to optimal level
  • Explain procedure to patient and family
  • Document mechanical and spontaneous efforts along with response
Sedation levels must be closely observed during the weaning period. Decreases in mechanical ventilation may result in hypoventilation if the patient is too sedate or is medicated with narcotics. Patient may need to be occasionally stimulated during weaning but if excessive stimulation is needed to maintain adequate rate, the patient is not ready to wean.
Slow wean
(Patient sleepy but ready to wean)
Moderate wean
(Patient awake but occasionally needs stimulation)
Quick wean
(Patient very awake and cooperative)
  • Decrease respiratory rate to 6/min, PSV 15 for 30 minutes
  • Decrease respiratory rate to 4/min, PSV 15 for 30 minutes
  • Decrease respiratory rate to 4/min, PSV 10 for 30 minutes (if endotube is less than 7.5 mm, keep PSV at 10)
  • Decrease respiratory rate to 4/min for 30 minutes (Do not change PSV pressure)
  • Decrease respirtory rate to 0/min for 30 minutes, patient in PSV Mode. (Do not change PSV pressures)
  • Decrease respiratory rate to 0/min PSV 5 for 30 minutes, patient in PSV mode (if endobute is less than 7.5 mm, keep PSV at 10)
252
  • Decrease respiratory rate to 0/min for 30 minutes, patient in PSV mode. (Do not change PSV pressure)
  • Decrease PSV to 10 or 5 for 30 minutes
  • Obtain spontaneous parameters and document. Evaluate patient readiness for for extubation using Burn‘s Wean Assessment Program
  • Decrease PSV to 10 for 30 minutes
  • Continue to wean to PSV 5 unless endotube size is less than 7.5 mm (if less than 7.5 mm, keep PSV at 10)
  • Obtain ABG and spontaneous parameters and report results to physician for extubation and oxygen orders
  • Continue to wean to PSV 5 unless endotube size is less than 7.5 mm (if less than 7.5 mm, keep PSV at 10)
  • Obtain spontaneous parameters and document. Evaulate patient readiness for extubation using Burn's Wean Assessment Program
  • Provide supplemental nasal cannula oxygen after extubation
  • Obtain and spontaneous parameters and document. Evaluate patient readiness for extubation using Burn's Wean Assessment Program
  • Obtain ABG and spontaneous parameters and report results to physician for extubation and oxygen orders
  • Obtain ABG and spontaneous parameters and report results to physician for extubation and oxygen orders
  • Provide supplemental nasal cannula oxygen after extubation
  • Provide supplemental nasal cannula oxygen after extubation
 
Other Care Essentials
 
Care of the Airway
  • It is of paramount importance that all cares and procedures are carried out with maintaining a patent airway always in mind.
  • Always check the patient first. Observe the patient's facial expression, color, respiratory effort, vital signs and ECG tracing.
  • Ensure the endotracheal tube (ETT) or tracheostomy tube is held securely in position but not too tightly to result in pressure area lesions.
  • Check the placement of the ETT by listening for equal bilateral breath sounds, checking the CXR and noting the distance marks on the tube, checking the previously documented level.
  • Check and adjust (if necessary) the cuff pressure of the ETT. In order to minimize tracheal damage, the cuff pressure should be at the lowest pressure necessary to prevent an air leak.
 
Check the Bedside Emergency Equipment
  • An alternative means of ventilation, e.g. Laerdal bag must be available and functional.
  • Yankauer sucker, suction catheters and functioning suction unit, airways and masks should be available.
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Ventilation
  • Ensure the ventilation tubing is not kinked and that it is adequately supported so as not to drag on the ETT. Take care of the tube while turning or moving the patient.
  • Check the ventilator and document the settings. Look at the alarm parameters and reset if necessary.
  • Ensure the ventilator and the cardiac monitor are plugged into emergency power supply in case of power failure.
  • Ensure that you have enough room to access the head of the bed in an emergency.
  • Check the type of humidification, and when the filters and ventilation tubing were last changed.
  • HME filters and end expiratory filters are changed routinely (and marked with the date and time) every 24 hours or more frequently if there is condensation visible.
  • Ventilator circuits are changed weekly.
  • Indications for an actively humidified circuit:
    • Minute volume greater than 10 liters
    • Chest trauma with pulmonary contusion
    • Airway burns
    • Severe asthma
    • Hypothermia (< 34 °C)
    • Pulmonary hemorrhage
    • Severe sputum plugging/pulmonary edema leading to HME occlusion
    • Consultant order
  • Pooled secretions above the ETT cuff are associated with ventilator-associated pneumonia (VAP). This is a result of aspiration of bacteria colonizing the oropharynx or GIT and subsequently leaking below the cuff into the trachea. Therefore, thorough oropharyngeal suctioning should be performed before letting down the cuff to reposition the ETT or to check cuff pressure.
 
Suction of an Artificial Airway
  • To maintain a patent airway.
  • To promote improved gas exchange.
  • To obtain tracheal aspirate specimens.
  • To prevent effects of retained secretions, e.g. infection, consolidation, atelectasis, increased airway pressures or blocked tube.
  • It is important to oxygenate before and after suctioning. Closed suction catheters should be rinsed post suctioning to remove mucus and to reduce the likelihood of bacterial growth.
  • Tracheal suctioning should be attended 2–3 hourly.
  • Suction the oropharynx to remove potentially infected secretions.
 
Monitors
  • Check the level of any invasive monitoring transducers and zero them.
  • Check the alarm parameters and reset if necessary.
  • 254Document the patient's vital signs hourly and when there is a deviation from the usual.
  • Check and document a manual blood pressure to assess the accuracy of the arterial trace once a shift.
 
Oral Care
  • The aim of oral care and assessment is to promote normal hygiene while preventing infection and trauma.
  • The presence of an ETT can cause hypersalivation in some patients and an uncomfortably dry mouth in others.
  • A soft toothbrush can be used for oral hygiene and a small amount of toothpaste can help the cleansing action. Using large amounts of toothpaste may leave a residual coating and produce a burning sensation if it is not rinsed away properly.
  • Properly diluted sodium bicarbonate may be used to remove resistant coating on the tongue, debris or tenacious secretions but again overuse may cause superficial burns.
  • The lips should be kept moisturized to stop them from becoming sore and cracked.
  • Second hourly oral care is recommended, using water, not saline, and oral swabs and thorough suctioning of oral secretions, a toothbrush and paste should be used at least once a shift and more often if indicated.
 
Eye Care
  • The unconscious, sedated or paralyzed patient is at risk of developing eye problems ranging from mild conjunctivitis to serious corneal injury and ulceration. Permanent eye damage may result from ulceration, perforation, vascularization and scarring of the cornea.
  • Sedation and muscle relaxants can lead to inadequate closure of the eye, lack of random eye movements and a loss of the blink reflex, all of which can lead to complications.
  • Fluid imbalances and increased permeability can promote conjunctival edema.
  • Constrictive securing tapes can compromise venous return from the head leading to venous congestion and may be an increase in interocular pressure and, therefore, an increase in conjunctival edema.
  • Second hourly eye care using saline soaked gauze to clean the eye and the application of lactrilube regularly in the ventilated patient is recommended to help reduce the risk of complications.
 
GIT
  • Intubated patients must have a nasogastric tube for gastric decompression or nutritional support.
  • The presence of bowel sounds and the turgor of the abdomen should be assessed during the initial assessment.
  • Nutrition and hydration are essential to build respiratory muscle strength necessary when a patient is being weaned from a ventilator. Patients who have inadequate nutritional stores are prone to infection, fluid and electrolyte imbalance, intestinal fluid retention, weight loss, pressure areas and poor wound healing.
  • Patients with a functioning GI tract should be fed enterally. TPN may be used if there are contraindications to enteral feeding.
  • 255The enterally fed patient should be monitored for diarrhea, dehydration, fluid overload, constipation or abdominal cramping. These observations can be a guide in determining the strength and rate of increase of the feeds.
  • NG tubes should be flushed with 20–30 ml of water before and after administering medications.
  • Fine bore tubes cannot be aspirated but should be flushed 4 hourly with water.
  • If the patient is not being fed enterally, the NG tube should be on free drainage and aspirated and flushed 6 hourly with water.
  • If the enterally fed patient has large aspirates (> 200 ml or > 4 hours feed), consult with medical staff regarding reducing the feed and/or discarding the aspirate. Otherwise the aspirate is generally returned if less that 200 ml or < 4 hours feed.
  • Elevating the head of the bed to 30–45 degrees (unless contraindicated) is effective in reducing the risk of aspiration.
  • Elimination should be recorded and aperients given if necessary.
 
Genital/Urinary Tract
  • IDCs predispose urinary tract infections.
  • Routine urinalysis should be done twice a day.
  • Regular penile/perineum catheter care should be done.
  • The catheter should be secured to the leg carefully and repositioned as necessary to prevent pressure areas.
  • Hourly urine monitoring is carried out and medical staff informed of abnormally high or low measurements. Aim for a urine output of 0.5 ml/kg.
 
Repositioning and Pressure Area Care
  • Attending to the patient's hygiene protects the skin and ensures dignity and comfort.
  • Ventilated patients are at a higher risk of developing nosocomial infections and pressure areas due to their immobility, their underlying disease process and the presence of invasive monitoring lines and equipment.
  • Repositioning the patient regularly has a number of positive effects:
    • Routine turning and positioning assist in the mobilization of secretions.
    • Prevents the development of pressure areas, joint stiffness and deformities.
    • Improves oxygenation and can encourage weaning from the ventilator.
    • Provides a different view on the environment for the patient
    • The patient should be repositioned second hourly if possible, taking care to position the limbs in proper alignment and supporting them to prevent dependent edema.
    • If the patient has leg splints on, they should be on for 2 hours and off for 2 hours. They should not be bandaged and the skin integrity should be checked with each turn.
  • The ETT and other lines should be safeguarded during turning and care should be taken to ensure that there are no lines or other equipment under the patient turned.
  • The skin should be kept dry and should be inspected with each change of position, including under restraints.
  • 256The head of the bed should be elevated if the patient's condition allows to help prevent aspiration and improve oxygenation.
  • If the patient has any signs of developing pressure areas, he/she should be nursed on an air mattress.
  • The ETT should be repositioned at alternate sides of the mouth to prevent pressure areas developing.
  • The NG tube should be secured in such a way as to minimize pressure on the nares and changed at least daily.
  • If the patient has a hard collar, it should be changed to an Aspen collar as soon as possible and the back of the head and neck checked once a shift for the presence of pressure areas.
 
Complications of Mechanical Ventilation
  • A thorough nursing assessment of patients requiring mechanical ventilation is crucial. MV has been associated with complications, such as ventilator-associated pneumonia, cardiovascular compromise, gastrointestinal disturbances, and renal impairment.
  • For example, asymmetric chest movement and decreasing oxygen saturation may indicate pneumothorax. The development of subcutaneous emphysema or pneumothorax suggests barotrauma. Fever, productive cough, decreased breath sounds, and dullness to percussion are signs of pneumonia. Oliguria may indicate decreased renal perfusion. Melena, pallor, and dizziness suggest upper gastrointestinal bleeding.
  • Critical care nurses assume an increasingly important role in early identification of complications and initiate appropriate measures to minimize adverse effects of MV.
 
Complications are of the Following Types
 
1. Associated with Patient's Response to Mechanical Ventilation
  1. Decreased Cardiac Output
    • Cause: Venous return to the right atrium impeded by the dramatically increased intrathoracic pressures during inspiration from positive pressure ventilation. Also reduced sympathoadrenal stimulation leading to a decrease in peripheral vascular resistance and reduced blood pressure.
    • Symptoms: Increased heart rate, decreased blood pressure and perfusion to vital organs, decreased CVP, and cool clammy skin.
    • Treatment: Aimed at increasing preload (e.g. fluid administration) and decreasing the airway pressures exerted during mechanical ventilation by decreasing inspiratory flow rates and TV, or using other methods to decrease airway pressures (e.g. different modes of ventilation).
  2. Barotrauma
    • Cause: Damage to pulmonary system due to alveolar rupture from excessive airway pressures and/or overdistention of alveoli.
    • Symptoms: May result in pneumothorax, pneumomediastinum, pneumoperitoneum, or subcutaneous emphysema.
    • Treatment: Aimed at reducing TV, cautious use of PEEP, and avoidance of high airway pressures resulting in development of auto-PEEP in high-risk patients [(patients with obstructive lung diseases (asthma, bronchospasm), unevenly distributed lung diseases (lobar pneumonia), or hyperinflated lungs (emphysema)].
  3. 257Nosocomial Pneumonia
    • Cause: Invasive device in critically ill patients becomes colonized with pathological bacteria within 24 hours in almost all patients. 20–60% of these develop nosocomial pneumonia.
    • Treatment: Aimed at prevention by the following:
      • Avoid cross-contamination by frequent handwashing
      • Decrease risk of aspiration (cuff occlusion of trachea, positioning, use of small-bore NG tubes)
      • Suction only when clinically indicated, using sterile technique
      • Maintain closed system setup on ventilator circuitry and avoid pooling of condensation in the tubing.
      • Ensure adequate nutrition
      • Avoid neutralization of gastric contents with antacids and H2 blockers
  4. Positive Water Balance
    • Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Due to vagal stretch receptors in right atrium sense a decrease in venous return and see it as hypovolemia, leading to a release of ADH from the posterior pituitary gland and retention of sodium and water. Treatment is aimed at decreasing fluid intake.
    • Decrease of normal insensible water loss due to closed ventilator circuit preventing water loss from lungs. This fluid overload is evidenced by decreased urine-specific gravity, dilutional hyponatremia, increased heart rate and BP.
  5. Decreased Renal Perfusion
    Can be treated with low dose dopamine therapy.
  6. Increased Intracranial Pressure (ICP)
    Reduce PEEP.
  7. Hepatic Congestion
    Reduce PEEP.
  8. Worsening of Intracardiac Shunts
    Reduce PEEP.
 
2. Associated with Ventilator Malfunction
Alarms Turned off or Nonfunctional
May lead to apnea and respiratory arrest.
Troubleshooting Ventilator Alarms
  • Low exhaled volume: Cuff leak, tubing disconnect, patient disconnected.
  • Evaluate cuff; reinflate PRN; if ruptured, tube will need to be replaced. Evaluate connections; tighten or replace as needed; check ETT placement, reconnect to ventilator.
  • High pressure: Secretions in airway, patient biting tubing, tube kinked, cuff herniation, increased airway resistance/decreased lung compliance (caused by bronchospasm, right mainstem bronchus intubation, pneumothorax, pneumonia), patient coughing and/or fighting the ventilator; anxiety; fear; pain.
  • 258Suction patient, insert bite block, reposition patient's head/neck; check all tubing lengths, deflate and reinflate cuff, auscultate breath sounds, evaluate compliance and tube position; stabilize tube, explain all procedures to patient in calm, reassuring manner; sedate/medicate as necessary.
  • Low oxygen pressure: Oxygen malfunction.
 
3. Other Complications Related to Endotracheal Intubation
  1. Sinusitis and Nasal Injury
    Obstruction of paranasal sinus drainage; pressure necrosis of nares:
    • Prevention: Avoid nasal intubations; cushion nares from tube and tape/ties.
    • Treatment: Remove all tubes from nasal passages; administer antibiotics.
  2. Tracheoesophageal Fistula
    Pressure necrosis of posterior tracheal wall resulting from overinflated cuff and rigid nasogastric tube:
    • Prevention: Inflate cuff with minimal amount of air necessary; monitor cuff pressures q. 8 h.
    • Treatment: Position cuff of tube distal to fistula; place gastrostomy tube for enteral feedings; place esophageal tube for secretion clearance proximal to fistula.
  3. Mucosal Lesions
    Pressure at tube and mucosal interface:
    • Prevention: Inflate cuff with minimal amount of air necessary; monitor cuff pressure q. 8 h.; use appropriate size tube.
    • Treatment: May resolve spontaneously; perform surgical interventions.
  4. Laryngeal or Tracheal Stenosis
    Injury to area from end of tube or cuff, resulting in scar tissue formation and narrowing of airway:
    • Prevention: Inflate cuff with minimal amount of air necessary; monitor cuff pressure q. 8.h.; suction area above cuff frequently.
    • Treatment: Perform tracheostomy; place laryngeal stint; perform surgical repair.
  5. Cricoid Abscess
    Mucosal injury with bacterial invasion:
    • Prevention: Inflate cuff with minimal amount of air necessary; monitor cuff pressure q. 8 h.; suction area above cuff frequently.
    • Treatment: Perform incision and drainage of area; administer antibiotics.
    • Other common potential problems related to mechanical ventilation: Aspiration, GI bleeding, inappropriate ventilation (respiratory acidosis or alkalosis, thick secretions, patient discomfort due to pulling or jarring of ETT or tracheostomy, high PaO2, low PaO2, anxiety and fear, dysrhythmias or vagal reactions during or after suctioning, incorrect PEEP setting, inability to tolerate ventilator mode.
 
Nursing Care Plan for the Ventilated Patient
Critical care nurses can identify subtle changes in a patient's clinical status and initiate appropriate nursing interventions rapidly and effectively. This includes the following:
259
 
Nursing Assessment
Primary surgery
Assessment parameters
Related numerical data
A: Airway
Is the airway patent and secure?
  • LIsten to air movement
  • Observe rise and fall of chest
  • Check if tube is secure and length is correct
B: Breathing
Is the patient breathing?
  • Observe chest rise and fall
  • Observe patient color
SpO2, tidal volume, respiratory rate
C: Circulation
Does the patient have adequate circulation?
  • Check for a pulse
  • Assess strength of pulse
  • Observe patient color
Heart rate and rhythm, arterial blood pressure
D: Disability
What is the patient's level of consciousness?
E: Exposure
What is the patient's surrounding environment?
Is the patient's dignity preserved?
 
Goals
  • Patient will have effective breathing pattern.
  • Patient will have adequate gas exchange.
  • Patient's nutritional status will be maintained to meet body needs.
  • Patient will not develop a pulmonary infection.
  • Patient will not develop problems related to immobility.
  • Patient and/or family will indicate understanding of the purpose for mechanical ventilation.
Nursing diagnosis
Nursing interventions
Rationale
Ineffective breathing pattern related to secretions/displacement of ET, etc.
Observe changes in respiratory rate and depth; observe for SOB and use of accessory muscles
An increase in the work of breathing will add to fatigue; may indicate patient fighting ventilator
Observe for tube misplacement—note and post cm. Marking at lip/teeth/nares after X-ray confirmation and q. 2 h
Indicates correct position to provide adequate ventilation
Prevent accidental extubation by taping tube securely, checking q. 2h restraining/sedating as needed
Avoids trauma from accidental extubation, prevent inadequate ventilation and potential respiratory arrest
Inspect thorax for symmetry of movement
Determines adequacy of breathing pattern; asymmetry may indicate hemothorax or pneumothorax.
Measure tidal volume and vital capacity
Indicates volume of air moving in and out of lungs
Assess for pain
Pain may prevent patient from coughing and deep breathing
Monitor chest X-rays
Shows extent and location of fluid or infiltrates in lungs
260
Maintain ventilator settings as ordered
Ventilator provides adequate ventilator pattern for the patient
Elevate head of bed 60–90 degrees
This position moves the abdominal contents away from the diaphragm, which facilitates its contraction
Impaired gas exchange related to alveolar-capillary membrane changes
Monitor ABGs
Determines acid-base balance and need for oxygen
Assess LOC, listlessness, and irritability
These signs may indicate hypoxia
Observe skin color and capillary refill
Determines adequacy of blood flow needed to carry oxygen to tissues
Monitor CBC
Indicates the oxygen-carrying capacity available
Administer oxygen as ordered
Decreases work of breathing and supplies supplemental oxygen
Observe for tube obstruction; suction PRN; ensure adequate humidification
May result in inadequate ventilation or mucous plug
Reposition patient q. 1–2 h
Repositioning helps all lobes of the lung to be adequately perfused and ventilated
Potential altered nutritional status: less than body requirements related to NPO status
Monitor lymphocytes and albumin
Indicates adequate visceral protein
Provide nutrition as ordered, e.g. TPN, lipids or enteral feedings
Calories, minerals, vitamins, and protein are needed for energy and tissue repair
Obtain nutrition consultation.
Provides guidance and continued surveillance
Potential for pulmonary infection related to compromised tissue integrity
Secure airway and support ventilator tubing
Prevents mucosal damage
Provide good oral care q. 4 h; suction when need indicated using sterile technique; handwashing with antimicrobial for 30 seconds before and after patient contact; do not empty condensation in tubing back into cascade
Measures aimed at prevention of nosocomial infections
Use disposable saline irrigation units to rinse in-line suction; ensure ventilator tubing changed q. 7 days, in-line suction changed q. 24 h.; ambu bags changed between patients and whenever becoming soiled
IAW Infection Control Policy and Respiratory Therapy Standards of Care for CCNS
261
Potential for complications related to immobility
Assess for psychosocial alterations
Dependency on ventilator with increased anxiety when weaning; decreased ability to communicate; social isolation/alteration in family dynamics
Assess for GI problems. Preventative measures include relieving anxiety, antacids or H2 receptor antagonist therapy, adequate sleep cycles, adequate communication system
Most serious is stress ulcer. May develop constipation
Observe skin integrity for pressure ulcers; preventative measures include turning patient at least q. 2 h.; keep HOB < 30 degrees with a 30-degree sidelying position; use pressure relief mattress or turning bed if indicated; follow prevention of pressure ulcers plan of care; maintain nutritional needs
Patient is at high risk for developing pressure ulcers due to immobility and decreased tissue perfusion
Maintain muscle strength with active/active-assistive/passive ROM and prevent contractures with use of span-aids or splints
Patient is at risk for developing contractures due to immobility, use of paralytics and ventilator-related deficiencies
Knowledge deficit related to intubation and mechanical ventilation
Explain purpose/mode and all treatments; encourage patient to relax and breathe with the ventilator; explain alarms; teach importance of deep breathing; provide alternate method of communication; keep call bell within reach; keep informed of results of studies/progress; demonstrate confidence
Reduce anxiety, gain cooperation and participation in plan of care
 
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
  • It is the clinical syndrome which is characterized by a sudden and progressive pulmonary edema, increased bilateral infiltrates on chest X-ray, the absence of an elevated atrial pressure.
  • Patient often demonstrates reduced lung compliance. A wide range of factors are associated with the development of ARDS. The main cause of death in ARDS is nonpulmonary multiple system organ failure, often with sepsis. Etiological factors related to acute respiratory distress syndrome:
    • Aspiration (gastric secretion, drowning)
    • Drug ingestion and overdose
    • Hematological disorder
    • Prolonged inhalation of high concentrations of oxygen, smoke and corrosive substance
    • 262Major surgery
    • Fat embolism
    • Systemic sepsis
    • Shock, trauma.
 
Clinical Manifestations
ARDS is an acute event that typically develops over 4 to 48 hours. The acute phase of ARDS is marked by a rapid onset of severe dyspnea that usually occurs 12 to 48 hours after initiating the event. Other signs and symptoms include:
  • Increased pulse rates
  • Low PaO2
  • Dyspnea
  • Marked restlessness
  • Decreased mental status
  • Tachycardia
  • Sudden breathlessness
  • Low blood oxygen levels
  • Lung inflammation
  • Tachypnea
  • Hypotension
 
Pathophysiology
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Assessment and Diagnostic Findings
On the physical examination, intercostal retraction and crackles may be present as the fluid begins to leak into the alveolar interstitial space. Common diagnostic tests performed in patient with potential ARDS include:
  • Echocardiography
  • ABG
  • CT scan of thorax
  • Chest X-ray
  • Sputum culture
  • Pulmonary artery catheterization.
 
Management
  • The primary focus in the management of ARDS includes identification and treatment of the underlying condition. The supportive therapy almost always includes intubation and mechanical ventilation. In addition, circulatory support, adequate fluid volume, and nutrition support are important.
  • Supplement oxygen is used by the patient to begin the initial spiral of hypoxemia. As the hypoxemia progresses intubation and mechanical ventilation are required.
 
Treatment of ARDS
  • Intravenous fluids are given to provide nutrition and prevent dehydration and are carefully monitored to prevent fluid from accumulating in lungs.
  • Antibiotic therapy is provided for infection.
 
Pharmacological Management
In pharmacological management following drugs are included:
  • Antianxiety to reduce the anxiety
  • Diuretics to eliminate fluid from lungs
  • Antibiotics for the infection
  • Anti-inflammatory drugs.
 
Nutritional Therapy
Adequate nutritional therapy support is vital in the treatment of ARDS. Patients with ARDS require 35 to 45 kcal/kg/day to meet caloric requirements. Enteral feeding is the first consideration; however, parental nutrition may also be required.
 
Complications
  • Dysrhythmias
  • Multiorgan failure
  • Renal failure
  • Infection
  • Stress ulcer
  • Decreased cardiac output.
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Nursing Management
 
General Measure
  • A patient with ARDS is critically ill and requires close monitoring in the intensive care unit because his/her conditions could quickly become life-threatening. The nurse must closely monitor the patient for deterioration in oxygenation with a change in position. Oxygenation is sometimes increased in the ARDS patient in prone position. The position is elevated for improvement of oxygenation.
  • A patient is extremely anxious and agitated because of the increase in hypoxemia and dyspnea. It is important to reduce the patient's anxiety because anxiety increases oxygen expenditure by preventing rest. Rest is essential to limit oxygen consumption and reduce oxygen need.
 
Nursing Assessment
  • Assess breathing sound
  • Assess sign of hypoxemia and hypercapnea
  • Note the changes suggesting increased work of breathing or pulmonary
  • Determine hemodynamic status and compare it with previous value
  • Analyze the ABG and compare the previous values
 
Nursing Diagnosis
  • Ineffective airway clearance related to increase or tenacious secretion
  • Impaired gas exchange related to inadequate respiratory center activity or chest wall movement, airway obstruction, or fluid in lung.
  • Acute pain related to inflammatory process and dyspnea
 
Nursing Intervention
  • Maintain airway clearance:
    • Administer medication to increase alveolar function
    • Perform chest physiotherapy to remove mucus
    • Administer IV fluids
    • Suction patient as needed to assist with removal of secretions
  • Relieving pain:
    • Watch patient for sign of discomfort and pain
    • Position the head elevated
    • Give prescribed morphine and monitor for pain-relieving sign
  • Reducing anxiety:
    • Correct dyspnea and relive physical discomfort
    • Speak calmly and slowly
    • Explain diagnostic procedure
    • Listen to the patient
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PULMONARY HYPERTENSION
 
Introduction
  • Pulmonary hypertension (PH) is high blood pressure in the arteries to lungs. It is a serious condition. The blood vessels that carry blood from heart to lungs become hard and narrow. Heart has to work harder to pump the blood through. Over time, heart weakens and cannot do its job and can develop failure.
  • Pulmonary hypertension (PH) is an increase of blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries, together known as the lung vasculature, leading to shortness of breath, dizziness, fainting, leg swelling and other symptoms.
 
Types of Pulmonary Hypertension
 
1. Idiopathic Pulmonary Hypertension
When an underlying cause for high blood pressure in the lungs cannot be found, the condition is called idiopathic pulmonary hypertension (IPH). Some people with IPH may have a gene that is a risk factor for developing pulmonary hypertension. But in most people with idiopathic pulmonary hypertension, there is no recognized cause of their pulmonary hypertension.
 
2. Secondary Pulmonary Hypertension
Pulmonary hypertension that is caused by another medical problem is called secondary pulmonary hypertension. This type of pulmonary hypertension is more common than idiopathic pulmonary hypertension. Causes of secondary pulmonary hypertension include:
  • Blood clots in the lungs (pulmonary emboli)
  • Chronic obstructive pulmonary diseases, such as emphysema
  • Connective tissue disorders, such as scleroderma or lupus
  • Sleep apnea and other sleep disorders
  • Congenital heart disease
  • Sickle-cell anemia
  • Chronic liver disease (cirrhosis)
  • AIDS
  • Lung diseases, such as pulmonary fibrosis
 
Other Types of Pulmonary Hypertension
The World Health Organization divides pulmonary hypertension (PH) into five groups. These groups are organized based on the cause of the condition and treatment options. In all groups, the average pressure in the pulmonary arteries is 25 mm Hg or higher. The pressure in normal pulmonary arteries is 8–20 mm Hg at rest.
 
Group 1 Pulmonary Arterial Hypertension
  • PAH that has no known cause.
  • PAH that is inherited (passed from parents to children through genes).
  • PAH that is caused by drugs or toxins, such as street drugs and certain diet medicines.
  • 266PAH that is caused by conditions such as:
    • Connective tissue diseases (connective tissue helps support all parts of your body, including your skin, eyes, and heart.).
    • HIV infection.
    • Liver disease.
    • Congenital heart disease. This is heart disease that is present at birth.
    • Sickle-cell disease.
  • PAH that is caused by conditions that affect the veins and small blood vessels of the lungs.
 
Group 2 Pulmonary Hypertension
Group 2 includes PH with left heart disease. Conditions that affect the left side of the heart, such as mitral valve disease or long-term high blood pressure, can cause left heart disease and PH. Left heart disease is likely the most common cause of PH.
 
Group 3 Pulmonary Hypertension
Group 3 includes PH associated with lung diseases, such as COPD (chronic obstructive pulmonary disease) and interstitial lung diseases. Interstitial lung diseases cause scarring of the lung tissue. It is also associated with sleep-related breathing disorders, such as sleep apnea.
 
Group 4 Pulmonary Hypertension
Group 4 includes PH caused by blood clots in the lungs or blood-clotting disorders.
 
Group 5 Pulmonary Hypertension
Group 5 includes PH caused by various other diseases or conditions. Examples include:
  • Blood disorders, such as polycythemia vera and essential thrombocythemia.
  • Systemic disorders, such as sarcoidosis and vasculitis.
  • Metabolic disorders, such as thyroid disease and glycogen storage disease.
  • Other conditions, such as tumors that press on the pulmonary arteries and kidney disease.
 
Etiology
  • Drugs: For example, dexfenfluramine and phentermine have been taken off the market. It increases risk of developing pulmonary hypertension.
  • Liver diseases, rheumatic disorders, lung conditions: Pulmonary hypertension can also occur as a result of other medical conditions, such as chronic liver disease and liver cirrhosis, rheumatic disorders, such as scleroderma or systemic lupus erythematosus (lupus) and lung conditions including tumors, emphysema, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis.
  • Certain heart diseases: Heart diseases including aortic valve disease, left heart failure, mitral valve disease, and congenital heart disease can also cause pulmonary hypertension.
  • Thromboembolic disease: A blood clot in a large pulmonary artery can result in the development of pulmonary hypertension.
  • 267Low-oxygen conditions: High-altitude living, obesity, and sleep apnea can also lead to the development of pulmonary hypertension.
  • Genetic predisposition: Pulmonary hypertension is inherited in a small number of cases. Knowing that someone in the family had or has pulmonary hypertension should prompt you to seek early evaluation should symptoms occur.
  • Pulmonary hypertension may also be caused by other conditions, and in some cases, the cause is unknown.
 
Pathophysiology
 
Clinical Manifestations
  • Fatigue
  • Dizziness
  • 268Fainting spells
  • Swelling in the ankles, abdomen or legs
  • Bluish lips and skin
  • Chest pain
  • Irregular heartbeat (palpitations or strong, throbbing sensation)
  • Tachycardia
  • Progressive shortness of breath
 
Diagnostic Tests
  • Physical examination:
    • Listen for abnormal heart sounds, such as a loud pulmonic valve sound, a systolic murmur of tricuspid regurgitation, or a gallop due to ventricular failure.
    • Examine the jugular vein in the neck for engorgement.
    • Examine the abdomen, legs, and ankles for fluid retention.
    • Examine nail beds for bluish tint.
    • Look for signs of other underlying diseases that might be causing pulmonary hypertension.
  • Blood tests:
    • Complete metabolic panel (CMP): Examines liver and kidney function.
    • Autoantibody blood tests, such as ANA, ESR, and others: Screens for collagen vascular diseases.
    • Thyroid stimulating hormone (TSH): A screening for thyroid problems.
    • HIV: A screening for human immunodeficiency virus.
    • Arterial blood gases (ABG): Determines the level of oxygen in arterial blood.
    • Complete blood count (CBC): Tests for infection, elevated hemoglobin, and anemia.
    • B-type natriuretic peptide (BNP): A marker for heart failure.
  • Doppler echocardiogram: Uses sound waves to show the function of the right ventricle, to measure blood flow through the heart valves, and then calculate the systolic pulmonary artery pressure.
  • Chest X-ray: Shows an enlarged right ventricle and enlarged pulmonary arteries.
  • 6-minute walk test: Determines exercise tolerance level and blood oxygen saturation level during exercise.
  • Pulmonary function tests: Evaluates for other lung conditions, such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis among others.
  • Polysomnogram or overnight oximetry: Screens for sleep apnea (results in low oxygen levels at night).
  • Right heart catheterization: Measures various heart pressures (i.e. inside the pulmonary arteries, coming from the left side of the heart), the rate at which the heart is able to pump blood, and finds any leaks between the right and left sides of the heart.
  • Ventilation perfusion scan (V/Q scan): Looks for evidence of blood clots along the pathway to the lungs.
  • Pulmonary angiogram: Looks for blood clot blockages in the pulmonary arteries.
  • Chest CT scan: Looks for blood clots and other lung conditions.
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Management
 
Nonpharmacological Management
  • Appropriate diagnosis and analysis of the problem is necessary before starting any treatment. Treatment varies per individual based on the different underlying causes but generally includes taking medications; making lifestyle and dietary changes.
  • Oxygen Therapy: Replaces the low oxygen in blood.
  • Nutrition: Fuel the body with a nutritious diet that is low in fat, cholesterol and sodium and rich in high-fiber, whole grain, foods, including fruits and vegetables and lean protein.
  • Physical activities: Regular activity may help improve the ability to be active.
  • Smoke-free living: Quit smoking. Avoid second-hand smoking. Smoking and breathing second-hand smoke make PPH symptoms worse.
 
Pharmacological Management
  • Anticoagulants or ‘blood thinners‘ such as warfarin sodium. It decreases blood clot formation, so blood flows more freely through blood vessels.
  • Diuretics: Furosemide, spironalactone, removes extra fluid from the tissues and bloodstream, which reduces swelling and makes breathing easier.
  • Potassium: Replaces potassium that may be lost with increased urination when taking diuretics.
  • Inotropic agents (such as Digoxin): Improves the heart's pumping ability.
  • Vasodilators and calcium channel blockers (Nifedipine or Diltiazem): Lowers pulmonary blood pressure and may improve the pumping ability of the right side of the heart.
  • Endothelin receptor antagonists (Bosentan): These help block the action of endothelin, a substance that causes narrowing of lung blood vessels.
  • Prostaglandins (Epoprostenol): Dilates pulmonary arteries and helps prevent blood clots from forming.
  • Phosphodiesterase type 5 inhibitors (Sildenafil): Relax pulmonary smooth muscle cells, which further leads to dilation of the pulmonary arteries.
 
Surgical Management
  • Atrial septostomy: It is a surgical procedure that creates a communication between the right and left atria. It relieves pressure on the right side of the heart, but at the cost of lower oxygen levels in blood (hypoxia).
  • Pulmonary thromboendarterectomy: If present, a large clot in the pulmonary artery may be surgically removed to improve blood flow and lung function.
  • Lung transplantation: Currently, this is the only cure for primary pulmonary hypertension. Transplantation is reserved for advanced pulmonary hypertension that is not responsive to medical therapy. The right side of the heart will generally return to normal after the lungs have been transplanted.
  • Heart/lung transplantation: This type of double organ transplant is very rare but is necessary for all patients who have combined lung and left heart failure.
 
Complications
  • Right-sided heart failure (Cor pulmonale): In cor pulmonale, heart's right ventricle becomes enlarged and has to pump harder than usual to move blood through narrowed or blocked pulmonary arteries. At first, the heart tries to compensate by thickening its 270walls and expanding the chamber of the right ventricle to increase the amount of blood it can hold. But this thickening and enlarging works only temporarily, and eventually the right ventricle fails from the extra strain.
  • Blood clots: A number of small clots or just a few large ones dislodge from these veins and travel to the lungs, leading to a form of pulmonary hypertension that is reversible with time and treatment.
  • Arrhythmia: Irregular heartbeats (arrhythmias) from the upper or lower chambers of the heart are complications of pulmonary hypertension. These can lead to palpitations, dizziness or fainting and can be fatal.
  • Bleeding: Pulmonary hypertension can lead to bleeding into the lungs and coughing up blood (hemoptysis). This is another potentially fatal complication.
 
Nursing Management
 
Nursing Assessment
  • Note the changes suggesting increased work of breathing or pulmonary edema
  • Assess breathing sound
  • Assess sign of hypoxemia and hypercapnea
  • Analyze the ABG and compare the previous values
  • Determine hemodynamic status and compare it with previous value
 
Nursing Diagnosis
  • Impaired gas exchange related to inadequate respiratory centre activity or chest wall movement, airway obstruction, or fluid in lung.
  • Ineffective airway clearance related to increased or tenacious secretion.
  • Acute pain related to inflammatory process and dyspnea.
  • Anxiety related to pain dyspnea and serious condition.
 
Nursing Intervention
  • Improve gas exchange:
    • Administer oxygen to maintain PaO2 of 60 mm Hg, using devices that provide increased oxygen concentration.
    • Monitor fluid balance by intake and output measurement, urine-specific gravity. Daily weight measurement.
    • Provide measures to prevent atelectasis and promote chest extension and secretion clearance as per doctor's prescription spirometer.
    • Elevate head level to 30 degrees.
    • Monitor adequacy of alveolar ventilation by frequent measurement of respiratory system.
    • Administer antibiotic, cardiac medication, and diuretics as prescribed by doctor.
  • Maintain airway clearance:
    • Administer medication to increase alveolar function.
    • Perform chest physiotherapy to remove mucus.
    • Administer IV fluids.
    • Suction patient as needed to assist with removal of secretions.
  • Relieving pain:
    • Watch patient for sign of discomfort and pain.
    • Position the head elevated.
    • Give prescribed morphine and monitor for pain relieving sign.
  • 271Reducing anxiety:
    • Correct dyspnea and relieve physical discomfort.
    • Speak calmly and slowly.
    • Explain diagnostic procedure.
 
COR PULMONALE
  • Cor pulmonale is a condition that most commonly arises out of complications from pulmonary hypertension.
  • Cor pulmonale refers to the altered structure (hypertrophy or dilatation) and impaired function of the right ventricle that results from pulmonary hypertension that is associated with diseases of the lungs (chronic obstructive pulmonary disease), vasculature (idiopathic pulmonary arterial hypertension), upper airway (obstructive sleep apnea), or chest wall (kyphoscoliosis).
 
Etiology
  • Blood clots in the lungs
  • COPD (chronic obstructive pulmonary disease)
  • Lung tissue damages
  • Sleep apnea
  • Cystic fibrosis
  • CHF
 
Pathophysiology
 
Clinical Manifestations
Common symptoms that may suggest the presence of cor pulmonale in a patient with pulmonary or cardiopulmonary disease include:
  • 272Worsening tachypnea (particularly at rest)
  • Fatigue and lassitude
  • Ankle swelling
  • Worsening exertional dyspnea
  • Worsening cough
  • Angina-type chest discomfort
  • Hemoptysis
  • Hoarseness
  • Exertional syncope
  • Late-stage hepatic congestion can cause symptoms (anorexia, jaundice and right upper quadrant abdominal discomfort)
  • Cyanosis and plethora
  • Chest markedly hyperexpanded
  • Labored respiratory effort
  • Intercostal recession
  • Decreased air entry, crackles and wheeze in the chest
  • Systolic bruits over lung fields
  • Left parasternal or subxiphoid heave (a sign of right ventricular hypertrophy)
  • Distended neck veins with raised and prominent JVP
  • 3rd/4th heart sounds and pansystolic murmur of tricuspid regurgitation over right heart
  • Split second heart sound with loud pulmonary component
  • Systolic ejection murmur with a sharp ejection click over the pulmonary artery
  • Diastolic pulmonary regurgitation murmur over the pulmonary artery
  • Marked hepatojugular reflux due to hepatic congestion
  • Hepatomegaly
  • Jaundice in advanced cases
  • Ascites in advanced cases
 
Diagnostic Evaluation
The following investigations are often used to delineate the cause of respiratory compromise that may lead to cor pulmonale and to inform optimal management:
  • Alpha-1 antitrypsin levels, if considered relevant.
  • Autoantibody screen if there is suspected collagen vascular disease.
  • Thrombophilia screen if there is suspected chronic venous thromboembolism.
  • Spirometry or lung function tests including gas transfer and flow volume loop.
  • CT and MRI scan of the chest.
  • Bronchoscopy
  • Lung biopsy (open or transbronchial)
  • Ventilation/perfusion scan/spiral-CT angiography/MRI-angiography
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Management
  • Long-term oxygen therapy or nocturnal oxygen therapy (NOT): It has been shown to improve quality of life and survival in patients with severe chronic hypoxia due to lung disease, by reducing pulmonary arteriolar constriction and improving and slowing the progression of cor pulmonale. They are usually recommended where PaO2 is < 55 mm Hg or SaO2 is < 88%.
  • Diuretics: Such as furosemide and bumetanide are frequently utilized, particularly where the right ventricular filling volume is markedly elevated, and in the management of associated peripheral oedema. Care must be taken to avoid overdiuresis which can impair the functioning of both the ventricles. It may also induce a hypokalemic metabolic alkalosis which can lessen respiratory drive through reducing the hypercapnea stimulus to breathe. Intravenous diuretics may be needed in patients with acute decompensation and severe peripheral edema, due to poor absorption of oral medication.
  • Vasodilators: Such as nifedipine and diltiazem can also be used to prevent chest pain.
  • Inotropic drugs, particularly digoxin, are frequently used to increase the cardiac output.
  • Methylxanthine bronchodilators: Such as theophylline are frequently used for their beneficial effect on bronchial tone.
  • Anticoagulation: It is used where patients have venous thromboembolism as the underlying cause of their cor pulmonale.
  • Venesection: It is used with caution in some patients who have severe secondary polycythemia due to chronic hypoxia.
  • Transplantation of lung and heart.
 
Complications
  • Exertional syncope
  • Hypoxia and significantly limited exercise tolerance
  • Peripheral edema
  • Peripheral venous insufficiency
  • Tricuspid regurgitation
  • Hepatic congestion and cardiac cirrhosis
  • Death
 
Nursing Management
 
Nursing Assessment
The nurse should assess the client for the clinical manifestations of CHF, especially in high-risk clients.
  • Impaired gas exchange related to fluid in the alveoli:
    • Auscultation of breath sounds every 4 hours
    • Encourage to turn cough and deep breath
    • Maintain Fowler's position
    • Administer oxygen
    • Monitor ABG
    • Intubation and mechanical ventilation.
  • 274Decreased cardiac output related to heart failure and dysrhythmias
    • Vital signs every hour
    • Lung and heart sounds every 2 hours
    • Administer oxygen
    • Hourly urine output
    • Assess changes in mental status
    • Small meals.
  • Fluid volume excess related to reduced cardiac output and Na and water retention:
    • IO chart
    • Fowler's position
    • Frequent oral care
    • Daily weighing
    • Assess jugular vein distension, peripheral edema, and hepatic engorgement
    • Fluid restriction
    • 2–4 g salt diet.
  • Decreased peripheral tissue perfusion related to reduced cardiac output:
    • Monitor peripheral pulses
    • Color and temperature of skin
    • Keep extremities warm
    • Assess for thrombophlebitis
    • Active or passive ROM.
  • High risk for impaired skin integrity related to reduced peripheral tissue perfusion:
    • Change position every 2 hours
    • Pressure mattress
    • Heel protectors.
  • High risk for digitalis toxicity related to impaired excretion:
    • Assess for hypokalemia, heart block
    • Serum digitalis levels and potassium.
 
BRONCHITIS
Bronchitis is a term that describes inflammation of the bronchial tubes (bronchi and the smaller branches termed as bronchioles) that results in excessive secretions of mucus into the tubes, leading to tissue swelling that can narrow or close off bronchial tubes.
 
Etiology
  • Acute bronchitis (also known as a chest cold) is typically a fairly minor illness that causes symptoms for a few days to a couple of weeks. It usually resolves on its own with rest without leaving any obvious long-term consequences. Viruses, such as influenza, respiratory syncytial virus (RSV), and rhinoviruses cause the majority of cases of acute bronchitis, while the remainder are caused by bacteria (for example, Mycoplasma, Pneumococcus) or short-term exposure to chemical irritants (for example, tobacco smoke, gastric reflux contents, inhaled solvents).
  • 275Chronic bronchitis is a cough with mucus for at least three months in each of the two consecutive years. It can indicate other health problems as well as lead to permanent damage to lungs. It may occur due to deficiency of alpha-1 antitripsinogen enzyme.
 
Risk Factors
  • Cigarette smoke: People who smoke or who live with a smoker are at higher risk of both acute bronchitis and chronic bronchitis.
  • Low resistance: This may result from another acute illness, such as a cold, or from a chronic condition that compromises the immune system. Older adults, infants and young children have greater vulnerability to infection.
  • Exposure to irritants: Risk of developing bronchitis is greater if exposed to certain lung irritants, such as grains or textiles, or are exposed to chemical fumes.
 
Pathophysiology
 
Clinical Manifestations
For either acute bronchitis or chronic bronchitis, signs and symptoms may include:
  • Cough
  • Production of mucus (sputum), which can be clear, white, yellowish-gray or green in color
  • Fatigue
  • 276Slight fever and chills
  • Chest discomfort
 
Complications
Although a single episode of bronchitis usually is not the cause for concern, it can lead to pneumonia in some people. Repeated bouts of bronchitis may signal:
  • Chronic bronchitis
  • Asthma
  • Bronchiectasis
  • Cystic fibrosis
  • Tuberculosis
  • Sinusitis
  • Dyspnea, sometimes severe
  • Respiratory failure
  • Pneumonia
  • Cor pulmonale
  • Pneumothorax
  • Polycythemia
  • COPD
  • Emphysema
  • Chronic advancement of the disease, and
  • High mortality rate
 
Diagnostic Evaluation
During the first few days of illness, it can be difficult to distinguish the signs and symptoms of bronchitis from those of a common cold.
  • Chest X-ray: A chest X-ray can help determine pneumonia or another condition that may explain cough.
  • Sputum culture: This test checks for the presence of bacteria in sputum produced when coughed. It is helpful in determining whether whooping cough or other illnesses would be helped by antibiotics.
  • Pulmonary function test: During a pulmonary function test, you blow into a device called a spirometer, which measures how much air your lungs can hold and how quickly you can get air out of your lungs. This test checks for signs of asthma or emphysema.
 
Management
The goal of treatment for bronchitis is to relieve symptoms and ease breathing. In most cases, acute bronchitis requires only self-care treatments, such as:
  • Getting more rest
  • Taking over-the-counter pain medications
  • Drinking fluids
  • Breathing in warm, moist air.
277
 
Medications
  • Antibiotics: Such as Fluoroquinolones, Macrolides, Sulfonamides, Tetracyclines.
  • Cough medicine: Such as expectorants, mucolytics, etc.
  • Bronchodilators: Such as theophyllin, etc. to dilate the bronchus and ease the sputum to come out.
  • Steroids: Such as prednisone, methylprednisolone to reduce the inflammatory reaction and thus decrease the bronchial swelling and secretions that, in turn, allows better airflow because of reduced airway obstruction.
  • PDE4 inhibitors are a class of anti-inflammatory agents for exacerbations of COPD. It is primarily for exacerbations that involve excessive bronchitis and mucus production. There is currently only one agent available called roflumilast a pill taken once per day.
 
Nursing Management
 
Nursing Diagnosis
  1. Impaired Gas Exchange related to altered oxygen supply
    Interventions
    • Assess respirations: Quality, rate, pattern, depth and breathing effort.
    • Assess for life-threatening problems (i.e. respiratory arrest, flail chest, sucking chest wound).
    • Auscultate lung sounds: Also assess for the presence of jugular vein distention (JVD) or tracheal deviation.
    • Assess for signs of hypoxemia.
    • Monitor vital signs.
    • Assess for changes in orientation and behavior.
    • Monitor ABGs.
    • Place the patient on continuous pulse oximetry.
    • Assess skin color for development of cyanosis, especially circumoral cyanosis.
    • Provide supplemental oxygen, via 100% O2 non-rebreather mask.
    • Prepare the patient for intubation.
  2. Ineffective Airway Clearance related to tracheobronchial obstruction
    Interventions
    • Assess airway for patency by asking the patient to state his name.
    • Inspect the mouth, neck and position of trachea for potential obstruction.
    • Auscultate lungs for presence of normal or adventitious lung sounds.
    • Assess respiratory quality, rate, depth, effort and pattern.
    • Assess for mental status changes.
    • Assess changes in vital signs.
    • Monitor arterial blood gases (ABGs).
    • Administer supplemental oxygen.
    • Position patient's head with bed at 45 degrees (if tolerated).
    • Assist patient with coughing and deep breathing techniques (positioning, incentive spirometry, frequent position changes).
    • 278Prepare for placement of endotracheal or surgical airway (i.e. cricothyroidectomy, tracheostomy).
    • Confirm placement of the artificial airway.
  3. Impaired Gas Exchange related to altered oxygen supply
    Interventions
    • Assess respirations: Quality, rate, pattern, depth and breathing effort.
    • Assess for life-threatening problems (i.e. respiratory arrest, flail chest, sucking chest wound).
    • Auscultate lung sounds. Also assess for the presence of jugular vein distention (JVD) or tracheal deviation.
    • Assess for signs of hypoxemia.
    • Monitor vital signs.
    • Assess for changes in orientation and behavior.
    • Monitor ABGs.
    • Place the patient on continuous pulse oximetry.
    • Assess skin color for development of cyanosis, especially circumoral cyanosis.
    • Provide supplemental oxygen, via 100% O2 nonrebreather mask.
    • Prepare the patient for intubation.
 
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
  • COPD is a condition of chronic dyspnea with expiratory airflow limitation that does not significantly fluctuate characterized by airway inflammation, mucous plugging, narrowed airway lumina, or airway destruction. The term ‘COPD’ includes chronic bronchitis and emphysema and asthma.
  • Asthma: It is a chronic reactive airway disease characterized by reversible inflammation and constriction of bronchial smooth muscle, hypersecretion of mucus, hyperventilation and edema.
  • Chronic bronchitis: It is an inflammation of airways with narrowing or blocking of airways that leads to increased production of mucoid sputum, and marked cyanosis.
    Fig. 5.1: Normal vs bronchitis lumen
  • 279Emphysema: Most severe form of COPD, characterized by recurrent inflammation that damages and destroys alveolar walls to create large blebs or bullae (air spaces) and collapsed bronchioles on expiration (air-trapping).
    Fig. 5.2: Normal vs emphysemic alveoli
 
Etiology
 
Primary Causes
  • Smoking
  • Alpha-1-Antitrypsin deficiency
  • Air pollution.
  • Smoking: Smoking remains the major cause of COPD. Cigarette smoking damages the cilia in the lungs which normally help clear away mucus and secretions. This creates blockage in the airways. Cigarette smoke also causes inflammation and irritation in the lungs, leading to an increase in mucus production. The primary cause of chronic obstructive pulmonary disease (COPD) is tobacco smoke (including second-hand or passive exposure).
  • Alpha-1-antitrypsin deficiency: These are susceptible to irritants in the environment, such as smoking, second-hand smoke, air pollution and allergens that, over time, cause symptoms of chronic obstructive pulmonary disease, such as emphysema.
  • Air pollution: It also plays a role in the development of COPD. Like that of its damaging counterpart smoking, air pollution causes airway inflammation and irritation that eventually destroys healthy lung tissue.
  • Environmental factors: COPD does occur in individuals who have never smoked. Although the role of air pollution in the etiology of COPD is unclear, the effect is small when 280compared with that of cigarette smoking. In developing countries, the use of biomass fuels with indoor cooking and heating is likely to be a major contributor to the worldwide prevalence of COPD. Long-term exposure to traffic-related air pollution and smoke is a factor in COPD in patients with diabetes and asthma.
  • Other causes:
    • Long-term exposure to lung irritants that damage the lungs and the airways usually is the cause of COPD.
    • The most common irritant that causes COPD is cigarette smoke. Pipe, cigar, and other types of tobacco smoke also can cause COPD, especially if the smoke is inhaled.
    • Breathing in second-hand smoke, air pollution, or chemical fumes or dust from the environment or workplace also can contribute to COPD. (Second-hand smoke is smoke in the air from other people smoking.)
    • In some cases, genetic condition called alpha-1 antitrypsin deficiency may play a role in causing COPD. People who have this condition have low levels of alpha-1 antitrypsin (AAT), a protein made in the liver.
    • Although uncommon, some people who have asthma can develop COPD. Asthma is a chronic (long-term) lung disease that inflames and narrows the airways. Treatment usually can reverse the inflammation and narrowing. However, if not, COPD can develop.
    • Occupational chemicals and dusts: The person who is exposed to dusts, vapors, irritants or fumes in the workplace may suffer from COPD.
    • Air pollution: High level of air pollution is harmful to the person with existing lung diseases.
    • Infections: Infections are a risk factor for developing COPD. The person with COPD is prone to acute exacerbations of the diseases.
    • Hereditary: Alpha 1-antitrypsin (AAT) deficiency is the genetic risk factor that leads to COPD.
    • Aging: Some degree of emphysema is common in the lungs of the older person, even a nonsmoker. Aging results in the change in the lung structure. Because as a person ages, there is gradual decrease in the elastic recoil of the lungs. The lungs become more rounded and smaller.
 
Pathophysiology
The COPD pathophysiology thus includes:
  • Narrowing of the airways
  • Damage to the lungs and other supportive tissues
  • Hyperactivity of the lungs
  • Dysfunction of the cilia in the airways
  • Constant damage of the alveolar walls
  • Air trapping—RV and FRC elevated
  • Hyperinflation—TLC elevated
  • Decreased elastic recoil pressure → dynamic collapse of airways during expiration → ineffective cough mechanism and pursed lips breathing (emphysema)
  • 281Decreased compliance (emphysema)
  • Increased airway resistance
  • Prolonged forced expiratory time.
 
Mechanism of Pathophysiology
  • COPD is a type of obstructive lung disease in which chronic incompletely reversible poor airflow (airflow limitation) and inability to breathe out fully (air trapping) exist.
  • The poor airflow is the result of breakdown of lung tissue (known as emphysema) and small airways disease known as obstructive bronchitis. The relative contributions of these two factors vary between people. Some also have a degree of airway hyper-responsiveness to irritants similar to those found in asthma.
  • COPD develops as a significant and chronic inflammatory response to inhaled irritants.
  • Chronic bacterial infections may also add to this inflammatory state. The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Those who smoke additionally have Tc1 lymphocyte involvement and some people with COPD have eosinophil involvement similar to that in asthma.
  • Part of this cell response is brought on by inflammatory mediators, such as chemotactic factors. Other processes involved with lung damage include oxidative stress produced by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, and breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited by protease inhibitors.
  • The destruction of the connective tissue of the lungs is what leads to emphysema, which then contributes to the poor airflow and, finally, poor absorption and release of respiratory gases. General muscle wasting that often occurs in COPD may be partly due to inflammatory mediators released by the lungs into the blood.
  • Narrowing of the airways occurs due to inflammation and scarring within them. This contributes to the inability to breathe out fully.
  • The greatest reduction in air flow occurs when breathing out, as the pressure in the chest is compressing the airways at this time.
  • This can result in more air from the previous breath remaining within the lungs when the next breath is started, resulting in an increase in the total volume of air in the lungs at any given time, a process called hyperinflation or air-trapping. Hyperinflation from exercise is linked to shortness of breath in COPD, as it is less comfortable to breathe in when the lungs are already partly full.
  • Low oxygen levels and, eventually, high carbon dioxide levels in the blood can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation and a reduced desire to breathe.
  • During exacerbations, airway inflammation is also increased, resulting in increased hyperinflation, reduced expiratory airflow and worsening of gas transfer. This can also lead to insufficient ventilation and, eventually, low blood oxygen levels.
  • Low oxygen levels, if present for a prolonged period, can result in narrowing of the arteries in the lungs, while emphysema leads to breakdown of capillaries in the lungs. Both these changes result in increased blood pressure in the pulmonary arteries, which may cause chronic pulmonary diseases.
282
 
Schematic Diagram of COPD
 
Risk Factors
283
 
Signs and Symptoms
Patients typically present with a combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease. Symptoms include the following:
  • Cough: Usually worse in the mornings and productive of a small amount of colorless sputum.
  • Acute chest illness.
  • Breathlessness: The most significant symptom, but usually does not occur until the sixth decade of life.
  • Wheezing: May occur in some patients, particularly during exertion and exacerbations.
  • The sensitivity of physical examination in detecting mild to moderate COPD is relatively poor, but physical signs are quite specific and sensitive for severe disease.
Findings in severe disease include the following:
  • Tachypnea and respiratory distress with simple activities
  • Use of accessory respiratory muscles and paradoxical indrawing of lower intercostal spaces (Hoover's sign)
  • Cyanosis
  • Elevated jugular venous pulse (JVP)
  • Peripheral edema
Thoracic examination reveals the following:
  • Hyperinflation (barrel chest)
  • Wheezing – Frequently heard on forced and unforced expiration
  • Diffusely decreased breath sounds
  • Hyper-resonance on percussion
  • Prolonged expiration
  • Coarse crackles beginning with inspiration in some cases
  • Certain characteristics allow differentiation between disease that is predominantly chronic bronchitis and that which is predominantly emphysema.
Chronic bronchitis characteristics include the following:
  • Patients may become obese.
  • Frequent cough and expectoration are typical.
  • Coarse bronchi and wheezing may be heard on auscultation.
  • Patients may have signs of right heart failure (i.e. cor pulmonale), such as edema and cyanosis.
Emphysema characteristics include the following:
  • Patients may be very thin with a barrel chest.
  • Patients typically have little or no cough or expectoration.
  • Breathing may be assisted by pursed lips and use of accessory respiratory muscles; patients may adopt the tripod sitting position.
  • The chest may be hyper-resonant, and wheezing may be heard.
  • Heart sounds are very distant.
284
 
Diagnostic Evaluation
  • Chest X-ray: It may indicate hyperinflation of lungs, flattened diaphragm, increased retrosternal air space, decreased vascular markings (emphysema), increased bronchovascular markings (bronchitis), normal findings during periods of remission (asthma).
  • Pulmonary function tests: It determines the cause of dyspnea, whether functional abnormality is obstructive or restrictive, to estimate degree of dysfunction and to evaluate effects of therapy, e.g. bronchodilators. Exercise pulmonary function may also be done to evaluate activity tolerance in those with known pulmonary impairment/progression of disease.
  • The forced expiratory volume over 1 second (FEV1): Reduced FEV1 not only is the standard way of assessing the clinical course and degree of reversibility in response to therapy, but also is an important predictor of prognosis.
  • Total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV): May be increased, indicating air-trapping. In COPD, the RV will make up the greater portion of the TLC.
  • Arterial blood gas (ABG) analysis: Determines degree and severity of disease process, e.g. PaO2 is decreased, and PaCO2 is normal or increased in chronic bronchitis and emphysema, but is often decreased in asthma, pH normal or acidosis, mild respiratory alkalosis secondary to hyperventilation.
  • DLCo test: Assesses diffusion in lungs. Carbon monoxide is used to measure gas diffusion across the alveocapillary membrane. Because carbon monoxide combines with hemoglobin 200 times more easily than oxygen, it easily affects the alveoli and small airways where gas exchange occurs.
  • Bronchogram: Can show cylindrical dilation of bronchi on inspiration, bronchial collapse on forced expiration (emphysema), enlarged mucous ducts (bronchitis).
  • Lung scan: Perfusion/ventilation studies may be done to differentiate between the various pulmonary diseases. COPD is characterized by a mismatch of perfusion and ventilation (i.e. areas of abnormal ventilation in area of perfusion defect).
  • Complete blood count (CBC): Increased hemoglobin (advanced emphysema), increased eosinophils (asthma).
  • Blood chemistry: Alpha1-antitrypsin is measured to verify deficiency and diagnosis of primary emphysema.
  • Sputum culture: Determines presence of infection, identifies pathogen.
  • Cytologic examination: Rules out underlying malignancy or allergic disorder.
  • Electrocardiogram (ECG): Right axis deviation, peaked P waves (severe asthma), atrial dysrhythmias (bronchitis), tall, peaked P waves in leads II, III, AVF (bronchitis, emphysema); vertical QRS axis (emphysema).
  • Exercise ECG, stress test: Helps in assessing degree of pulmonary dysfunction, evaluating effectiveness of bronchodilator therapy, planning/evaluating exercise program.
 
Complications
  • Pneumothorax: Air filled in the lungs
  • Cor pulmonale: It is heart disease associated with respiratory etiology.
  • 285Giant bullae: Empty spaces, called bullae develop in the lungs. Giant bullae are very large, sometimes half the size of the lung.
  • Recurring infections: Chest infections, pneumonia, influenza, cold and the common cold are likely to occur.
 
Management
An effective COPD plan includes four components:
  1. Assess and monitor disease
  2. Reduce risk factor
  3. Manage stable COPD
  4. Manage exacerbations.
The goals of effective COPD management are to:
  • Prevent progression
  • Relieve symptoms
  • Improve exercise tolerance
  • Improve health status
  • Prevent and treat complications
  • Prevent and treat exacerbations
  • Reduce mortality
 
Component 1: Assess and Monitor Disease
  • Diagnosis of COPD is based on a history of exposure to risk factors and the presence of airflow limitation that is not fully reversible, with or without the presence of symptoms.
  • Patients who have chronic cough and sputum production with a history of exposure to risk factors should be tested for airflow limitation.
  • Measurement of arterial blood gas tensions should be considered.
 
Component 2: Reduce Risk Factors
  • Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollution are important goals to prevent the onset and progression of COPD.
  • Smoking cessation is the single-most and cost-effective way to reduce the risk of developing COPD and stop its progression.
  • Three types of counseling are especially effective: Practical counseling, social support as part of treatment, and social support arranged outside of treatment.
  • Several effective pharmacotherapies for tobacco dependence are available, and at least one of these medications should be added to counseling if necessary and in the absence of contraindications.
  • Progression of many occupationally induced respiratory disorders can be reduced or controlled through a variety of strategies aimed at reducing the burden of inhaled particles and gases.
 
Component 3: Manage Stable COPD
  • The overall approach to managing stable COPD should be characterized by a stepwise increase in treatment, depending on the severity of the disease.
  • 286For patients with COPD, health education can play a role in improving skills, ability to cope with illness, and health status. It is effective in accomplishing certain goals, including smoking cessation.
  • None of the existing medications for COPD has been shown to modify the long-term decline in lung function that is the hallmark of this disease. Therefore, pharmacotherapy for COPD is used to decrease symptoms and complications.
  • Bronchodilator medications are central to the symptomatic management of COPD. They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms.
  • The principal bronchodilator treatments are 2-agonists, anticholinergics, theophylline, and a combination of one or more of these drugs.
  • Regular treatment with inhaled glucocorticosteroids should only be prescribed for symptomatic patients with COPD.
  • Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-to-risk ratio.
  • All patients with COPD benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue.
  • The long-term administration of oxygen (> 15 h per day) to patients with chronic respiratory failure has been shown to increase survival.
 
Component 4: Manage Exacerbations
  • Exacerbations of respiratory symptoms requiring medical intervention are important clinical events in COPD.
  • Inhaled bronchodilators (particularly inhaled 2-agonists or anticholinergics), theophylline, and systemic, preferably oral, glucocorticosteroids are effective for treatments for acute exacerbations of COPD.
  • Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g. increased volume and change of color of sputum, or fever) may benefit from antibiotic treatment.
  • Noninvasive positive pressure ventilation (NIPPV) in acute exacerbations improves blood gases and pH, reduces in-hospital mortality, decreases the need for invasive mechanical ventilation and intubation, and decreases the length of hospital stay.
 
Alpha1-Antitrypsin Deficiency Treatment
The treatment strategies for AAT deficiency involve reducing the neutrophil elastase burden. Available augmentation strategies include pharmacologic attempts to increase endogenous production of AAT by the liver (i.e. danazol, tamoxifen). Tamoxifen can increase endogenous production of AAT.
 
Management of Sputum Viscosity and Secretion Clearance
Mucolytic agents reduce sputum viscosity and improve secretion clearance. The oral agent N-acetyl cysteine has antioxidant and mucokinetic properties and is used to treat patients with COPD.
 
Others
  • Stop smoking: Smoking is the main cause of COPD in the first place. Stopping smoking will considerably slow down its progress.
  • 287Bronchodilators: Types of medications that relax airways that have become constricted, thus relieving shortness of breath, breathing problems, and coughing. These drugs are more effective for the treatment of chronic bronchitis or asthma.
  • Steroid aerosol sprays: Corticosteroids are effective for shortness of breath. However, they must be used under the careful monitoring of a doctor because long-term usage can result in weakened bones, elevated blood pressure and cataracts. Long-term steroid use also significantly raises the risk of developing diabetes.
  • Antibiotics: Patients with COPD generally get more infections, such as pneumonia or acute bronchitis than other people. Such conditions require antibiotic treatment.
  • Rehabilitation techniques: The patient can be taught certain breathing exercises that may help reduce shortness of breath and improve his/her ability to do exercise. Patients may undergo weight changes, which need to be addressed.
  • Oxygen: Those with severe symptoms may require supplemental oxygen, which is usually administered through the nostril via narrow tubing.
  • Surgery: A surgeon may surgically remove some of the damaged tissue, which helps the remaining lung tissue work better. This may help the patient breathe better.
  • Lung transplant: When other options have not worked and symptoms are very severe, lung transplant is recommended.
 
Pharmacological Therapy
  • Short-acting beta2-agonist bronchodilators (albuterol)
  • Long-acting beta2-agonist bronchodilators (salmeterol)
  • Respiratory anticholinergics (ipratropium)
  • Xanthine derivatives (theophylline)
  • Phosphodiesterase-4 inhibitors (roflumilast)
  • Inhaled corticosteroids (fluticasone, budesonide)
  • Oral corticosteroids (prednisone)
  • Beta2-agonist and anticholinergic combinations (ipratropium)
  • Beta2-agonist and corticosteroid combinations (budesonide)
 
Nursing Management
 
Nursing Diagnosis
  1. Ineffective Airway Clearance related to bronchospasm
    Intervention
    • Auscultate breath sounds. Note adventitious breath sounds, e.g. wheezes, crackles, rhonchi.
    • Assess/monitor respiratory rate. Note inspiratory/expiratory ratio.
    • Assist patient to assume position of comfort, e.g. elevate head of bed, have patient lean on overbed table or sit on edge of bed.
    • Keep environmental pollution to a minimum, e.g. dust, smoke, and feather pillows, according to individual situation.
    • Encourage/assist with abdominal or pursed-lip-breathing exercises.
    • 288Observe characteristics of cough, e.g. persistent, hacking, moist. Assist with measures to improve effectiveness of cough effort.
    • Increase fluid intake to 3000 ml/day within cardiac tolerance. Provide warm/tepid liquids. Recommend intake of fluids between, instead of during, meals. Monitor/graph serial ABGs, pulse oximetry, chest X-ray.
  2. Impaired Gas Exchange related to altered oxygen supply
    Intervention
    • Assess respiratory rate, depth. Note use of accessory muscles, pursed-lip breathing, and inability to speak.
    • Elevate head of bed, assist patient to assume position to ease work of breathing.
    • Include periods of time in prone position as tolerated.
    • Encourage deep-slow or pursed-lip breathing as individually needed.
    • Routinely monitor skin and mucous membrane color.
    • Encourage expectoration of sputum; suction when indicated.
    • Auscultate breath sounds, noting areas of decreased airflow and adventitious sounds.
    • Monitor level of consciousness/mental status.
    • Monitor vital signs and cardiac rhythm.
    • Evaluate level of activity tolerance. Provide calm, quiet environment.
    • Limit patient's activity or encourage bedrest during acute phase.
  3. Nutrition: Imbalanced, less than body requirements related to dyspnea and sputum production.
    Intervention
    • Assess dietary habits, recent food intake. Note degree of difficulty with eating.
    • Evaluate weight and body size.
    • Auscultate bowel sounds.
    • Give frequent oral care, remove expectorated secretions promptly, provide specific container for disposal of secretions and tissues.
    • Encourage a rest period of 1 hour before and after meals. Provide frequent small feedings.
    • Avoid gas-producing foods and carbonated beverages.
    • Avoid very hot or very cold foods.
    • Weigh as indicated.
    • Administer supplemental oxygen during meals as indicated.
  4. Risk for infection related to inadequate primary defense
    Intervention
    • Monitor temperature.
    • Review importance of breathing exercises, effective cough, frequent position changes, and adequate fluid intake.
    • Observe color, character, odor of sputum.
    • Demonstrate and assist patient in disposal of tissues and sputum. Stress proper hand-washing and use gloves when disposing of tissues, sputum containers.
    • 289Monitor visitors, provide masks as indicated.
    • Encourage balance between activity and rest.
    • Discuss need for adequate nutritional intake.
    • Recommend rinsing mouth with water and spitting, not swallowing, or use of spacer on mouthpiece of inhaled corticosteroids.
    • Obtain sputum specimen by deep coughing or suctioning for Gram's stain, culture/sensitivity.
    • Administer antimicrobials as indicated.
  5. Knowledge deficit related to lack of information
    Intervention
    • Discuss respiratory medications, side effects, adverse reactions.
    • Refer for evaluation of home care, if indicated.
    • Provide a detailed plan of care and baseline physical assessment to home care nurse as needed on discharge from acute care.
    • Provide information and encourage participation in support groups.
    • Instruct asthmatic patient in use of peak flow meter, as appropriate.
    • Review oxygen requirements and dosage for patient who is discharged on supplemental oxygen. Discuss safe use of oxygen and refer to supplier as indicated.
    • Discuss importance of medical follow-up care, periodic chest X-rays, sputum cultures.
    • Review the harmful effects of smoking, and advice cessation of smoking by patient as well as family member.
    • Provide information about activity limitations and alternating activities with rest periods to prevent fatigueness, ways to conserve energy during activities (e.g. pulling instead of pushing, sitting instead of standing while performing tasks), and use of pursed-lip breathing, sidelying position, and possible need for supplemental oxygen during sexual activity.
    • Discuss importance of avoiding people with active respiratory infections. Stress need for routine influenza and pneumococcal vaccinations.
    • Stress importance of oral care and dental hygiene.
    • Instruct rationale for breathing exercises, coughing effectively, and general conditioning exercises.
 
ASTHMA
Asthma is a condition in which the airways become narrow and swell and produce extra mucus and characterized by airway hyper-responsiveness, hyperventilation and mucosal edema.
 
Etiology
Exposure to various substances that trigger allergies and irritants can trigger signs and symptoms of asthma. Asthma triggers are different from person to person and can include:
  • 290Airborne allergens, such as pollen, animal dander, mold, cockroaches and dust mites
  • Respiratory infections, such as the common cold
  • Physical activity
  • Cold air
  • Air pollutants and irritants, such as smoke
  • Certain medications, including beta blockers, aspirin, ibuprofen
  • Strong emotions and stress
  • Menstrual cycle in some women
 
Risk Factors
A number of factors are thought to increase chances of developing asthma. These include:
  • Having a blood relative (such as a parent or sibling) with asthma
  • Having another allergic condition, such as atopic dermatitis or allergic rhinitis
  • Overweight
  • Smokers
  • Exposure to second-hand smoke
  • Mother who smoked while being pregnant
  • Exposure to exhaust fumes or other types of pollution
  • Exposure to occupational triggers, such as chemicals used in farming, hairdressing and manufacturing.
 
Pathophysiology
It involves the following mechanism:
  • Bronchoconstriction: In asthma, the dominant physiological event leading to clinical symptoms is airway narrowing and a subsequent interference with airflow. In acute exacerbations of asthma, bronchial smooth muscle contraction occurs quickly to narrow the airways in response to exposure to a variety of stimuli including allergens or irritants. Allergen-induced acute bronchoconstriction results from an IgE-dependent release of mediators from mast cells that includes histamine, tryptase, leukotrienes, and prostaglandins that directly contract airway smooth muscle. Aspirin and other nonsteroidal anti-inflammatory drugs can also cause acute airflow obstruction.
  • Airway edema: As the disease becomes more persistent and inflammation more progressive, other factors further limit airflow. These include edema, inflammation, mucous hypersecretion and the formation of mucus plugs, as well as structural changes including hypertrophy and hyperplasia of the airway smooth muscle.
  • Airway hyper-responsiveness: The mechanisms influencing airway hyper-responsiveness are multiple and include inflammation, dysfunctional neuroregulation, and structural changes.
  • Airway remodeling: In some persons who have asthma, airflow limitation may be only partially reversible. Permanent structural changes can occur in the airway. These are associated with a progressive loss of lung function.
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Fig. 5.3: Pathophysiology
 
Signs and Symptoms
  • Shortness of breath
  • Chest tightness or pain
  • Trouble sleeping caused by shortness of breath, coughing or wheezing
  • A whistling or wheezing sound when exhaling
  • Coughing or wheezing attacks
For some people, asthma symptoms flare up in certain situations:
  • Exercise-induced asthma, which may be worse when the air is cold and dry.
  • Occupational asthma, triggered by workplace irritants, such as chemical fumes, gases or dust.
  • Allergy-induced asthma, triggered by particular allergens, such as pet dander, cockroaches or pollen.
 
Diagnostic Evaluation
  • Spirometry: This test estimates the narrowing of bronchial tubes by checking how much air one can exhale after a deep breath.
  • Peak flow: A peak flow meter is a simple device that measures how hard you can breathe out. Lower than usual peak flow readings are a sign that lungs may not be working as well and that asthma may be getting worse.
  • 292Methacholine challenge: Methacholine is a known asthma trigger that, when inhaled, will cause mild constriction of airways. If a patient reacts to methacholine, then he/she is likely to have asthma.
  • Imaging tests: A chest X-ray and high-resolution computerized tomography (CT) scan of lungs and nose cavities (sinuses) can identify any structural abnormalities or diseases that can cause or aggravate breathing problems.
  • Allergy testing: This can be performed by skin test or blood test. Allergy tests can identify allergy to pets, dust, mold and pollen. If important allergy triggers are identified, this can lead to a recommendation for allergen immunotherapy.
  • Sputum eosinophils: This test looks for certain white blood cells in the mixture of saliva and mucus discharge during coughing. Eosinophils are present when symptoms develop and become visible when stained with a rose-colored dye.
 
Management
  • Long-term asthma control medications: Types of long-term control medications include:
    • Inhaled corticosteroids: These anti-inflammatory drugs include fluticasone, budesonide, flunisolide, ciclesonide, beclomethasone and mometasone.
    • Leukotriene modifiers: These oral medications include montelukast and zileuton. These help relieve asthma symptoms for up to 24 hours.
    • Long-acting beta agonists: These inhaled medications, which include salmeterol and formoterol, open the airways.
    • Theophylline: Theophylline is a daily pill that helps keep the airways open by relaxing the muscles around the airways.
  • Quick-relief (rescue) medications are used as needed for rapid, short-term symptom relief during an asthma attack—or before exercise. Types of quick-relief medications include:
    • Short-acting beta agonists: These inhaled, quick-relief bronchodilators act within minutes to rapidly ease symptoms during an asthma attack. They include albuterol, levalbuterol and pirbuterol. Short-acting beta agonists can be taken using a portable, hand-held inhaler or a nebulizer.
    • Ipratropium: Like other bronchodilators, ipratropium acts quickly to immediately relax the airways, making it easier to breathe.
    • Oral and intravenous corticosteroids: These medications include prednisone and methylprednisolone, relieve airway inflammation caused by severe asthma.
  • Allergy medications may help if asthma is triggered or worsened by allergies. These include:
    • Allergy shots (immunotherapy): Allergy shots gradually reduce immune system reaction to specific allergens. Patient generally receives shots once a week for a few months, then once a month for a period of three to five years.
    • Omalizumab: This medication, given as an injection every two to four weeks, is specifically for people who have allergies and severe asthma. It acts by altering the immune system.
    • Allergy medications: These include oral and nasal spray antihistamines and decongestants as well as corticosteroid and cromolyn nasal sprays.
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Lifestyle Management
  • Use air conditioner: Air conditioning reduces the amount of airborne pollen from trees, grasses and weeds that finds its way indoors. Air conditioning also lowers indoor humidity and can reduce exposure to dust mites.
  • Decontaminate the décor: Minimize dust that may worsen night-time symptoms by replacing certain items in the bedroom. For example, encase pillows, mattresses and box springs in dust proof covers. Remove carpeting and install hardwood or linoleum flooring. Use washable curtains and blinds.
  • Maintain optimal humidity: Dehumidify the room.
  • Prevent mold spores: Clean damp areas in the bath, kitchen and around the house to keep mold spores from developing. Get rid of moldy leaves or damp firewood in the yard.
  • Clean regularly: Clean home at least once a week.
  • Cover nose and mouth: If asthma is worsened by cold or dry air, wearing a face mask can help.
 
Nursing Management
 
Nursing Diagnosis
  1. Ineffective Airway Clearance related to tracheobronchial obstruction
    Interventions
    • Assess airway for patency by asking the patient to state his name.
    • Inspect the mouth, neck and position of trachea for potential obstruction.
    • Auscultate lungs for presence of normal or adventitious lung sounds.
    • Assess respiratory quality, rate, depth, effort and pattern.
    • Assess for mental status changes.
    • Assess changes in vital signs.
    • Monitor arterial blood gases (ABGs).
    • Administer supplemental oxygen.
    • Position patient with head of bed at 45 degrees (if tolerated).
    • Assist patient with coughing and deep breathing techniques (positioning, incentive spirometry, frequent position changes).
    • Prepare for placement of endotracheal or surgical airway (i.e. cricothyroidectomy, tracheostomy).
    • Confirm placement of the artificial airway.
  2. Impaired Gas Exchange related to altered oxygen supply
    Interventions
    • Assess respirations: quality, rate, pattern, depth and breathing effort.
    • Assess for life-threatening problems. (i.e. respiratory arrest, flail chest, sucking chest wound).
    • Auscultate lung sounds. Also assess for the presence of jugular vein distention (JVD) or tracheal deviation.
    • Assess for signs of hypoxemia.
    • Monitor vital signs.
    • Assess for changes in orientation and behavior.
    • Monitor ABGs.
    • Place the patient on continuous pulse oximetry.
    • 294Assess skin color for development of cyanosis, especially circumoral cyanosis.
    • Provide supplemental oxygen, via 100% O2 nonrebreather mask.
    • Prepare the patient for intubation.
 
PNEUMONIA
  • Pneumonia is an inflammation and consolidation of the lung parenchyma. It is an inflammatory process in lung parenchyma usually associated with marked increase in interstitial and alveoli fluid.
  • Pneumonitis: It is a more general term that describes an inflammatory process in lung tissues that may predispose a patient to or place a patient at risk for microbial invasions.
    OR
  • Pneumonia is an inflammatory condition of the lung, especially affecting the microscopic air sacs (alveoli), associated with fever, chest symptoms, and a lack of air space (consolidation) on a chest X-ray. The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs and other conditions.
 
Etiology and Risk Factors
The main cause of pneumonia is the:
  • Bacteria like Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus
  • Viruses like rhinoviruses, coronaviruses, influenzavirus
  • Fungal agents like Histoplasma capsulatum
  • Parasites: A variety of parasites can affect the lungs. These parasites typically enter the body through the skin or the mouth. Once inside the body, they travel to the lungs, usually through the blood. The most common parasites causing pneumonia are Toxoplasma gondii, Strongyloides stercoralis, and Ascariasis.
The major risk factors of pneumonia include:
  • Advanced age
  • A history of smoking
  • 295Upper respiratory infections
  • Tracheal intubation
  • Prolonged immobility
  • Immunosuppressive therapy
  • Malnutrition
  • Dehydration
  • Chronic disease states, like diabetes, heart disease, chronic lung disease, renal disease and cancer.
  • Exposure to air pollution
  • Alcoholism.
 
Pneumonia According to Site
  • Segmental pneumonia: It involves one or more segments of the lungs.
  • Lobar pneumonia: It involves one or more entire lobes.
  • Bilateral pneumonia: It involves lobes in both the lungs.
 
Pneumonia According to Location and Radiologic Appearance
  • Broncho or bronchial pneumonia: It involves terminal bronchials and alveoli.
  • Interstitial or reticular pneumonia: It involves inflammatory response within the lung tissues surrounding the air space or vascular structure rather than air passage.
  • Alveolar or acinar pneumonia: It involves fluid accumulation in a lung's distal air space.
  • Nacrotizing pneumonia: It causes the death of the lung tissue surroundings by viable tissue. It does not heal and cause permanent loss of functioning parenchyma.
 
Pneumonia According to Organism
  • Pneumococcal or streptococcal pneumonia: Caused by Streptococcus pneumoniae.
  • Staphylococcus pneumoniae: Caused by Staphylococcus aureus.
  • Influenza pneumonia: Caused by Haemophillus influenzae.
  • Gram-negative bacterial pneumonia: Caused by Klebsiella pneumoniae.
  • Legionnaires disease: Caused by Legionella pneumophilae.
  • Mycoplasma pneumonia: Caused by Mycoplasma microorganisms.
  • Viral pneumonia: Caused by influenza A virus and B virus, adenovirus, Cytomegalovirus, parainfluenza.
  • Fungal pneumonia: Caused by aspergillosis, candidiasis, blastomycosis.
  • Parasitic pneumonia: Caused by protozoa, nematodes.
 
Other Types of Pneumonia
  • Aspiration pneumonia: Due to aspiration of foreign particles, gastric content or food.
  • Hypostatic pneumonia: Caused by constantly remaining in same position and most common in weak or aged persons.
  • Ventilator-associated pneumonia (VAP): It is defined as pneumonia occurring in a patient within 48 hours or more after intubation with an endotracheal tube or tracheostomy tube and which was not present before. Early onset VAP occurs within 48 hours and late onset VAP beyond 48 hours of tracheal intubation.
 
Other Risk Factors
  • Previous stroke: People, who have had a stroke, have problems in swallowing, or are bedridden, can easily develop pneumonia.
  • 296Age: Infants from birth to age too are at risk for pneumonia, as are individuals aged 65 years or older.
  • Weakened immune system: This includes people who take medications (steroid drugs and anti-cancer drugs) that weaken the immune system and people with HIV, AIDS, or cancer.
  • Drug abuse: This includes excessive alcohol consumption and smoking.
  • Certain medical conditions: Asthma, cystic fibrosis, diabetes, and heart failure raise risks for pneumonia.
 
Pathophysiology of Pneumonia
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Signs and Symptoms
  • Productive cough
  • Fever accompanied by shaking chills
  • Shortness of breath
  • Sharp or stabbing chest pain during deep breaths
  • Confusion, and an increased respiratory rate
  • Malnutrition
  • Hemoptysis
  • Headache
  • Fatigue
  • Chest auscultation reveals bronchial breath sounds over the area of consolidation
  • Crackling sounds
  • Dull sound on percussion
  • Unequal chest wall expansion may occur during inspiration.
  • Pneumococcal pneumonia: Sudden onset with a single shaking chill, high fever, stabbing pleuritic chest pain, malaise, weakness, occasional vomiting, tachypnea, dyspnea, elevated WBC count.
  • Single or multiple lobar consolidations on the X-ray film. Cough productive of rusty brown or blood-streaked purulent sputum that turns yellow and mucoid.
  • Staphylococcus pneumonia: Sudden onset with fever, multiple chills, pleuritic pain, dyspnea, decreased breath sounds, elevated WBC counts, and productive cough with purulent golden yellow or blood-streaked sputum.
  • The chest X-ray may show patchy infiltrates, empyema, abscesses, and pneumothorax.
  • Influenzal pneumonia: Similar to those of pneumococcal pneumonia. Cough productive of apple or lime green purulent sputum, which may be blood-tinged.
  • Gram-negative: Sudden onset with high fever, multiple chills, pleuritic pain, dyspnea, cyanosis and elevated WBC count.
  • Lobar consolidation on chest X-ray and cough productive of red sputum.
  • Single or multiple lobe consolidation and small pleural effusion on chest X-ray film, dry cough productive of blood-tinged sputum.
  • Mycoplasma pneumonia: Insidious onset with slowly rising fever, headache, malaise, and normal WBC count.
  • Viral pneumonia: Headache and myalgia followed by high fever, dyspnea, normal breath sounds with occasional wheezing and crackles, elevated WBC count.
  • Diffused patchy infiltrates on the X-ray film.
  • Fungal pneumonia: Usually asymptomatic
  • Parasitic pneumonia: Cough, dyspnea, pleuritic chest pain, fever, night sweat, crackles.
  • Aspiration pneumonia: Asymptomatic with minor aspiration.
  • Major aspiration may lead to tachypnea, apnea, cyanosis, hypotension, lung sounds (crackles, rhonchi, wheezing), hypoxemia, respiratory failure, leukocytosis.
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Diagnostic Evaluation
  • Chest computed tomography: A CT scan is similar to an X-ray, but the pictures provided by this method are highly detailed. This painless test provides a clear and precise picture of the chest and lungs.
  • Sputum test: This test will examine the sputum to determine what type of pneumonia is present.
  • Pleural fluid test: If there is fluid apparent in the pleural space, a fluid sample can be taken to help determine if the pneumonia is bacterial or viral.
  • Pulse oximetry: This test measures the level of oxygen blood saturation by attaching a small sensor to finger. Pneumonia can prevent normal oxygenation of blood.
  • Bronchoscopy: When antibiotics fail, this method is used to view the airways inside the lungs to determine if blocked airways are contributing to pneumonia.
 
Management
Antibiotics are prescribed based on Gram stain results and antibiotic guidelines. Combination therapy may also be used.
  • Classifications: Antibiotics (Aminoglycosides: gentamicin, tobramycin, amoxicillin, erythromycin, penicillin, tetracycline).
  • Indications: Prevent or treat infections caused by pathogenic microorganisms.
  • Selected Interventions:
    • Before administering the first dose, assess the client for allergies and determine whether culture has been obtained.
    • After multiple doses, assess the client for superinfection (thrush, yeast infection, diarrhea). Notify the health care provider if superinfection occurs.
    • Assess the insertion site for phlebitis if antibiotics are being administered IV
    • To assess the effectiveness of antibiotic therapy, monitor the white blood cell count.
    • Monitor peaks and troughs for aminoglycosides.
 
Nursing Management
 
Nursing Diagnosis
  1. Ineffective airway clearance related to copious tracheobronchial secretions
    Interventions
    • Improving airway patency:
      • Encourage hydration: Fluid intake (2 to 3 l/day) to loosen secretions.
      • Provide humidified air using high-humidity face mask.
      • Encourage patient to cough effectively, and provide correct positioning, chest physiotherapy, and incentive spirometry.
      • Provide nasotracheal suctioning, if necessary.
      • Provide appropriate method of oxygen therapy.
      • Monitor effectiveness of oxygen therapy.
  2. 299Activity intolerance related to impaired respiratory function
    Interventions
    Promoting activity tolerance:
    • Counsel patient to rest and to avoid overexertion, which may exacerbate symptoms.
    • Assist patient into a comfortable position that maximizes breathing (e.g. semi-Fowler's)
    • Change position frequently (particularly in elderly patients).
  3. Risk for fluid volume deficit related to fever and dyspnea
    Interventions
    • Promoting fluid intake and maintaining nutrition
    • Encourage fluids (2 l/day minimum with electrolytes)
    • Administer intravenous fluids and nutrients, if necessary.
  4. Knowledge deficit about treatment regimen and preventive measures
    Interventions
    Informing patient:
    • Instruct on cause of pneumonia and management of symptoms
    • Explain treatments in simple manner and using appropriate language
    • Repeat instructions and explanations as needed.
 
Monitoring and Preventing Complications
  • Assess for signs and symptoms of shock and respiratory failure (e.g. evaluate vital signs, pulse oximetry, and hemodynamic monitoring parameters).
  • Administer intravenous fluids and medications and respiratory support as ordered.
  • Initiate preventive measures for atelectasis.
  • Assess for atelectasis and pleural effusion.
  • Assist with thoracentesis, and monitor patient for pneumothorax after procedure.
  • Monitor for superinfection (rise in temperature, increased cough), and assist in therapy.
  • Assess for confusion or cognitive changes; assess underlying factors.
 
Health Education
  • Instruct patient to continue taking antibiotics until complete.
  • Advice patient to increase activities gradually after fever subsides.
  • Advice patient that fatigue and weakness may linger on.
  • Encourage breathing exercises to promote lung expansion and clearing.
  • Encourage follow-up chest radiographs.
  • Instruct patient to avoid fatigue, sudden changes in temperature, and excessive alcohol intake, which lower resistance to pneumonia.
  • Review principles of adequate nutrition and rest.
  • Recommend influenza vaccine and pneumovax to all patients at risk (elderly, cardiac, and pulmonary disease patients).
  • Refer patient for home care to facilitate adherence to therapeutic regimen, as indicated.
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BRONCHIECTASIS
Bronchiectasis is a condition in which some of the bronchi have become scarred and permanently enlarged along with the loosening of integrity of bronchial wall. During the disease process, the cilia are damaged so that they are unable to effectively sweep away the mucus. As a result, mucus accumulates in parts of the lung that are affected and the risk of developing lung infections is increased.
 
Etiology and types
Currently bronchiectasis usually occurs as the result of an illness, such as pneumonia (approximately 25% of all cases). Other causes include:
  • Cystic fibrosis
  • Immune deficiency
  • Recurrent aspiration of fluid into the lungs (as occurs with gastroesophageal reflux)
  • Inhalation of a foreign object into the lungs
  • Inhalation of harmful chemicals, e.g. ammonia
  • In rare cases, it may be congenital
 
Types
  • Cylindrical bronchiectasis: Bronchi are enlarged and cylindrical.
  • Varicose bronchiectasis: Bronchi are irregular with areas of dilatation and constriction.
  • Saccular or cystic bronchiectasis: Dilated bronchi form clusters of cysts. This is the most severe form of bronchiectasis and is often found in patients with cystic fibrosis.
 
Signs and Symptoms
The main symptom of bronchiectasis is a mucus-producing cough. The cough is usually worse in the mornings and is often brought on by changes in posture. The mucus may be yellow-green in color and foul-smelling, indicating the presence of infection.
 
Other Symptoms
  • Coughing up blood (more common in adults)
  • Bad breath
  • Wheezing chest: A characteristic crackling sound may be heard when listening with a stethoscope
  • Recurring lung infections
  • A decline in general health
  • In advanced bronchiectasis, breathlessness can occur.
 
Diagnostic Evaluation
An initial diagnosis of bronchiectasis is based on the patient's symptoms, their medical history and a physical examination. Further diagnostic tests may include:
  • Chest X-ray
  • CT (computerized tomography) scan
  • Blood tests
  • 301Testing of the mucus to identify any bacteria present
  • Checking oxygen levels in the blood
  • Lung function tests (spirometry).
 
Management
Bronchiectasis is a chronic (long-term) condition that requires lifelong maintenance. Good management of the condition is vital to prevent ongoing damage to the lungs and worsening of the condition.
The ultimate goal of treatment is to clear mucus from the chest and prevent further damage to the lungs. The two main types of treatments used are:
 
Medications
Some or all of the following groups of medications may be used:
  • Antibiotics are used to treat acute lung infections. Where the infection is severe, hospitalization and treatment with intravenous antibiotics may be required.
  • Bronchodilators (as used in people with asthma) to improve the flow of air to the lungs.
  • Corticosteroids to reduce inflammation in the lungs.
  • Occasionally, medications to thin the mucus may be used.
  • Vaccination against flu and pneumococcous.
 
Physiotherapy and Exercise
  • Chest physiotherapy and postural drainage are used to remove secretions from the lungs.
  • Other factors important in managing the condition include avoiding dust, smoke and other respiratory irritants, and maintaining a balanced nutritious diet.
 
Prevention
The Ministry of Health recommends the following measures to help prevent bronchiectasis in children:
  • Not smoking during pregnancy and having a smoke free home
  • Breastfeeding your children
  • Eating a healthy balanced diet
  • Early detection and treatment of chest infections
  • Making sure homes are warm and dry (making chest infections less likely)
  • Immunization for diseases like measles and whooping cough.
 
Nursing Management
 
Nursing Intervention
  • Improve gas exchange
    • Administer oxygen to maintain PaO2 of 60 mm Hg, using devices that provide increased oxygen concentration.
    • Monitor fluid balance by intake and output measurement, urine-specific gravity. Daily weight measurement.
    • Provide measures to prevent atelectasis and promote chest extension and secretion clearance as per order, spirometer.
    • 302Elevate head level to 30 degrees.
    • Monitor adequacy of alveolar ventilation by frequent measurement of respiratory system.
    • Administer antibiotic, cardiac medication and diuretics as prescribed by doctor.
  • Maintain airway clearance
    • Administer medication to increase alveolar function
    • Perform chest physiotherapy to remove mucus
    • Administer IV fluids
    • Suction patient as needed to assist with removal of secretions.
  • Relieving pain
    • Watch patient for signs of discomfort and pain
    • Position the head elevated
    • Give prescribed morphine and monitor for pain-relieving sign.
  • Reducing anxiety
    • Correct dyspnea and relive physical discomfort
    • Speak calmly and slowly
    • Explain diagnostic procedure.
 
INTERSTITIAL LUNG DISEASE
 
Introduction
Interstitial lung disease describes a large group of disorders, most of which cause progressive scarring of lung tissue. The scarring associated with interstitial lung disease eventually affects ability to breathe and get enough oxygen into the bloodstream. It can be caused by long-term exposure to hazardous materials, such as asbestos. Some types of autoimmune diseases, such as rheumatoid arthritis, also can cause interstitial lung disease. In most cases, however, the causes remain unknown.
 
Definition
Interstitial lung disease refers to inflammation in the interstitial tissue of the lungs, the spaces that surround and separate the air sacs.
 
Types of Interstitial Lung Disease
  • Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumoniae is the most common cause.
  • Idiopathic pulmonary fibrosis: A chronic, progressive form of fibrosis of the interstitium. Its cause is unknown.
  • Nonspecific interstitial pneumonitis: Interstitial lung disease that is often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
  • Hypersensitivity pneumonitis: Interstitial lung disease caused by ongoing inhalation of dust, mold, or other irritants.
  • Cryptogenic organizing pneumonia (COP): Pneumonia-like interstitial lung disease but without an infection present. COP is also called bronchiolitis obliterans with organizing pneumonia (BOOP).
  • 303Acute interstitial pneumonitis: A sudden, severe interstitial lung disease, often requiring life support.
  • Desquamative interstitial pneumonitis: An interstitial lung disease that is partially caused by smoking.
  • Sarcoidosis: A condition causing interstitial lung disease along with swollen lymph nodes, and sometimes heart, skin, nerve, or eye involvement.
  • Asbestosis: Interstitial lung disease caused by asbestos exposure.
  • Silicosis: Silicosis is a condition caused by inhaling too much silica over a long period of time. Silica is a crystal-like mineral found in sand and rocks, such as granite. Silica can have deadly consequences for people who work with stone, concrete, glass, or other forms of rock.
  • Pneumoconiosis: Pneumoconiosis, also known as Black Lung Disease, is an occupational lung disease caused by inhaling coal dust.
 
Etiology
Interstitial lung disease can be triggered by many different things, including airborne toxins in the workplace, drugs and some types of medical treatments. In most cases, the causes are unknown.
  • Occupational and environmental factors: Long-term exposure to a number of toxins and pollutants can damage your lungs. These may include:
    • Silica dust
    • Asbestos fibers
    • Grain dust
    • Bird and animal droppings
  • Radiation treatments: Some people who receive radiation therapy for lung or breast cancer show signs of lung damage months or sometimes years after the initial treatment. The severity of the damage depends on:
    • How much of the lung was exposed to radiation
    • The total amount of radiation administered
    • Whether chemotherapy also was used
    • The presence of underlying lung disease
  • Medications: Many drugs can damage your lungs, especially:
    • Chemotherapy drugs: Methotrexate and cyclophosphamide
    • Heart medications: Amiodarone (cordarone) and propranolol
    • Some antibiotics: Nitrofurantoin and sulfasalazine
  • Medical conditions: Lung damage can also result from:
    • Systemic lupus erythematosus
    • Rheumatoid arthritis
    • Sarcoidosis
    • Scleroderma
  • Unknown causes: The list of substances and conditions that can lead to interstitial lung disease is long. Even so, in most cases, the causes are never found. Disorders without a known cause are grouped together under the label idiopathic pulmonary fibrosis or idiopathic interstitial lung disease.
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Risk Factors
  • Age: Interstitial lung disease is much more likely to affect adults, although infants and children sometimes develop the disorder.
  • Exposure to occupational and environmental toxins: If clients working in mines, farming or construction or for any reason are exposed to pollutants known to damage lungs, risk of interstitial lung disease greatly increases.
  • Smoking: Some forms of interstitial lung disease are more likely to occur in people with a history of smoking, and active smoking may make the condition worse.
  • Radiation and chemotherapy: Having radiation treatments to chest or using some chemotherapy drugs makes it more likely that will develop lung disease.
  • Oxygen: Continually inhaling very high levels of therapeutic oxygen for more than 48 hours can harm the lungs.
 
Pathophysiology
 
Signs and Symptoms
  • Shortness of breath
  • Dry cough
  • Cyanosis
  • Clubbing (a painless enlargement of the fingertips)
  • Enlarged heart
  • Weight loss
  • Loss of appetite
  • Muscle and joints pain
  • Fatigue
 
Diagnostic Evaluation
  • Medical history and physical examination
  • Blood tests: May help provide direction in the initial stage of diagnosis and rule out other conditions that may have similar symptoms. Measurement of the oxygen level in the arterial blood may also be performed.
  • 305Chest X-ray: A simple chest X-ray is the first test in the evaluation of most people with a breathing problem. Chest X-ray films in people with interstitial lung disease may show fine lines in the lungs.
  • Computed tomography (CT scan): A CT scanner takes multiple X-rays of the chest and a computer creates detailed images of the lungs and surrounding structures. Interstitial lung disease can usually be seen on a CT scan.
  • High-resolution CT scan: If interstitial lung disease is suspected, using certain CT scanner settings can improve the images of the interstitium.
  • Pulmonary function testing: A person sits in a sealed plastic booth and breathes through a tube. PFTs are noninvasive tests that measure the function of the lungs. The test involves blowing into a tube that is part of an instrument called a spirometer. This can measure the volume of the lungs as well as the air flow into and out of the lungs. People with interstitial lung disease may have a reduced total lung capacity. They may also have a decreased ability to transfer oxygen from their lungs into their blood.
  • Bronchoscopy: An endoscope is advanced through the mouth or nose into the airways. Tiny tools on the endoscope can take a sample of lung tissue.
  • Video-assisted thoracoscopic surgery (VATS): Using tools inserted through small incisions, a surgeon can sample multiple areas of lung tissue.
  • Lung biopsy: Obtaining lung tissue to examine under a microscope is the only way to determine which type of interstitial lung disease a person has. There are several ways to collect lung tissue, which is called a lung biopsy.
  • Open lung biopsy (thoracotomy): In some cases, traditional surgery with a large incision in the chest is needed to obtain a lung biopsy.
 
Management
  • Inhaled oxygen: In people with low oxygen blood levels due to interstitial lung disease, inhaled oxygen may improve symptoms. Regular use of oxygen might also protect the heart from damage caused by low oxygen levels.
  • Antibiotics: These are effective treatments for most interstitial pneumonias, e.g. azithromycin and levofloxacin eliminate the bacteria that cause most interstitial pneumonias.
  • Vaccines: Influenza vaccine and pneumococcal pneumonia vaccine.
  • Corticosteroids: In some forms of interstitial lung disease, ongoing inflammation in the lungs causes damage and scarring, e.g. prednisone and methylprednisolone reduce the activity of the immune system. This reduces the amount of inflammation in the lungs and the rest of the body.
  • Immune-suppressing drug: Such as azathioprine or cyclophosphamide are also given, either in combination with steroids or following a course of steroid treatment.
  • Smoking cessation: It is critical for those with interstitial lung disease.
 
Surgical Management
Lung transplant: In advanced interstitial lung disease causing severe impairment, a lung transplant may be the best option. Most people undergoing lung transplant for interstitial lung disease make large gains in quality of life and their ability to exercise.
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Contraindications
  • Current or recurring infection that cannot be treated effectively
  • Metastatic cancer
  • Severe cardiac or other medical problems preventing the ability to tolerate the surgical procedure
  • Serious conditions other than lung disease that would not improve after transplantation
  • Noncompliance with treatment regimen
 
Risks of the Procedure
  • Bleeding
  • Infection
  • Blockage of the blood vessels to the new lung(s)
  • Blockage of the airways
  • Severe pulmonary edema (fluid in the lung)
  • Blood clots
 
Transplant Requirements
Requirements for potential donors:
  • Healthy
  • Size match, the donated lung or lungs must be large enough to adequately oxygenate the patient, but small enough to fit within the recipient's chest cavity
  • Age
  • Blood type
 
Requirements for Potential Recipients
While a transplant center is free to set its own criteria for transplant candidates, certain requirements are generally agreed upon.
  • End-stage lung disease
  • Has exhausted other available therapies without success
  • No other chronic medical conditions (e.g. heart, kidney, liver)
  • No current infections or recent cancer
  • No HIV or hepatitis
  • No alcohol, smoking, or drug abuse
  • Within an acceptable weight range (marked undernourishment or obesity are both associated with increased mortality)
  • Age
  • Acceptable psychological profile
  • Has social support system
  • Financially able to pay for expenses
  • Able to comply with post-transplant regimen.
 
Medical Tests for Potential Transplant Candidates
  • Blood typing: The recipient's blood type must match the donor's, due to antigens that are present on donated lungs. A mismatch of blood type can lead to a strong response by the immune system and subsequent rejection of the transplanted organs.
  • 307Tissue typing: Ideally, the lung tissue would also match as closely as possible between the donor and the recipient, but the desire to find a highly compatible donor organ must be balanced against the patient's immediacy of need.
  • Chest X-ray: To verify the size of the lungs and the chest cavity.
  • Pulmonary function tests
  • CT scan (High resolution thoracic and abdominal)
  • Bone mineral density scan
  • Cardiac stress test (Dobutamine/thallium scan)
  • Ventilation/perfusion (V/Q) scan
  • Electrocardiogram
  • Cardiac catheterization
  • Echocardiogram
 
Types of Lung Transplant
  • Lobe: A lobe transplant is a surgery in which part of a living donor's lung is removed and used to replace part of recipient's diseased lung. This procedure usually involves the donation of lobes from two different people, thus replacing a single lung in the recipient. Donors who have been properly screened should be able to maintain a normal quality of life despite the reduction in lung volume.
  • Single-lung: Many patients can be helped by the transplantation of a single healthy lung. The donated lung typically comes from a donor who has been pronounced brain-dead.
  • Double-lung: Certain patients may require both lungs to be replaced. This is especially the case for people with cystic fibrosis, due to the bacterial colonization commonly found within such patients' lung, if only one lung were transplanted, bacteria in the native lung could potentially infect the newly transplanted organ.
  • Heart-lung: Some respiratory patients may also have severe cardiac disease which would necessitate a heart transplant. These patients can be treated by a surgery in which both lungs and the heart are replaced by organs from a donor or donors.
 
Procedure
  • Before operating on the recipient, the transplant surgeon inspects the donor lung(s) for signs of damage or disease.
  • If the lung or lungs are approved, then the recipient is connected to an IV line and various monitoring equipment, including pulse oximetry.
  • The patient will be given general anesthesia, and a machine will breathe for him or her.
It takes about one hour for the preoperative preparation of the patient. A single lung transplant takes about four to eight hours, while a double lung transplant takes about six to twelve hours to complete. A history of prior chest surgery may complicate the procedure and require additional time.
 
Single-lung
  • The process starts out after the donor lung has been inspected.
  • The decision to accept the donor lung for the patient has been made.
  • 308An incision is generally made from under the shoulder blade around the chest, ending near the sternum.
  • An alternate method involves an incision under the breastbone.
  • In the case of a singular lung transplant, the lung is collapsed, the blood vessels in the lung tied off, and the lung removed at the bronchial tube.
  • The donor lung is placed, the blood vessels reattached, and the lung reinflated. To make sure the lung is satisfactory and to clear any remaining blood and mucus in the new lung, a bronchoscopy will be performed.
  • When the surgeons are satisfied with the performance of the lung, the chest incision will be closed.
 
Double-lung
  • A double-lung transplant, also known as a bilateral transplant, can be executed sequentially or simultaneously. Sequential is more common. This is effectively like having two separate single-lung transplants done.
  • The transplantation process starts after the donor lungs are inspected and the decision to transplant has been made.
  • An incision is then made from under the patient's armpit, around the sternum, and then back towards the other armpit. This is known as a clamshell incision.
  • In the case of a sequential transplant, the recipient's lung with the poorest lung functions is collapsed, the blood vessels tied off, and cut at the corresponding bronchi.
  • The new lung is then placed and the blood vessels reattached. To make sure the lung is satisfactory before transplanting the other, a bronchoscopy is performed.
  • When the surgeons are satisfied with the performance of the new lung, surgery on the second lung will proceed.
  • In 10% to 20% of double-lung transplants, the patient is hooked up to a heart-lung machine which pumps blood for the body and supplies fresh oxygen.
 
Signs of Rejection
  • Fever
  • Flu-like symptoms, including chills, dizziness, nausea, general feeling of illness, night sweats
  • Increased difficulty in breathing
  • Worsening pulmonary test results
  • Increased chest pain or tenderness
  • Increase or decrease in body weight of more than 2 kilograms in a 24-hour period.
 
Prevention of Rejection
The antirejection medications most commonly used include:
  • Cyclosporine
  • Tacrolimus
  • Sirolimus
  • Azathioprine
  • Mycophenolate mofetil
  • Prednisone
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Complications
  • Pulmonary hypertension: Unlike systemic high blood pressure, this condition affects only the arteries in lungs. It begins when scar tissue restricts the smallest blood vessels, limiting blood flow in lungs. This, in turn, raises pressure within the pulmonary arteries. Pulmonary hypertension is a serious illness that becomes progressively worse.
  • Right-sided heart failure (Cor pulmonale): This serious condition occurs when right ventricle of heart which is less muscular than the left has to pump harder than usual to move blood through obstructed pulmonary arteries. Eventually the right ventricle fails from the extra strain.
  • Respiratory failure: In the end-stage of chronic interstitial lung disease, respiratory failure occurs when severely low blood oxygen levels along with rising pressures in the pulmonary arteries and the right ventricle cause heart failure.
 
SILICOSIS
Silicosis is a chronic lung disease caused by breathing in tiny bits of silica dust. When people breathe silica dust, they inhale tiny particles of silica that has crystallized. This silica dust can cause fluid buildup and scar tissue in the lungs that cuts down your ability to breathe.
 
Silica
  • Crystalline silica exists in 7 different forms (polymorphs), depending upon the temperature of formation. The main 3 polymorphs are quartz, cristobalite, and tridymite.
  • Microcrystalline silica consists of minute quartz crystals bonded together with amorphous silica. Examples include flint and chert.
  • Amorphous silica consists of kieselgur (diatomite) from the skeletons of diatoms, and vitreous silica, produced by heating and then rapid cooling of crystalline silica. Amorphous silica is less toxic than crystalline, but not biologically inert, and diatomite, when heated, can convert to tridymite or cristobalite.
 
Classification of Silicosis
There are three types of silicosis:
  • Chronic silicosis: The most common type of silicosis, usually occurs after 10 or more years of exposure to crystalline silica at low levels. This is the most common type of silicosis. Patients with this type of silicosis may not have obvious signs or symptoms of disease, but abnormalities may be detected by X-ray. Chronic cough and exertion dyspnea are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (< 10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.
  • Accelerated silicosis: It occurs 5 to 10 years after exposure and is caused by exposure to higher levels of crystalline silica. Symptoms and X-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).
  • Acute silicosis: It can occur after only weeks or months of exposure to very high levels of crystalline silica. Acute silicosis progresses rapidly and can be fatal within months. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The X-ray usually 310reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.
 
Etiology
Silica is a common, naturally occurring crystal. It is found in most rock beds and forms dust during mining, quarrying, tunneling, and working with many metal ores. Silica is a main part of sand, so glass workers and sand-blasters are also exposed to silica.
Risk factors: People who work in jobs where they are exposed to silica dust are at risk. These jobs include:
  • Glass manufacturing
  • Mining
  • Quarrying
  • Stone cutting
  • Highway and bridge construction, and repair
  • Building construction, demolition, and repair
  • Abrasive blasting
  • Masonry work
  • Concrete finishing
  • Drywall finishing
  • Rock drilling
  • Sand and gravel screening
  • Rock crushing (for road base)
 
Pathophysiology
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Signs and Symptoms
  • Dyspnea (shortness of breath) exacerbated by exertion
  • Cough, often persistent and sometimes severe
  • Fatigue
  • Tachypnea (rapid breathing) which is often labored
  • Loss of appetite and weight loss
  • Chest pain
  • Fever
  • Gradual dark shallow rifts in nails eventually leading to cracks as protein fibers within nail beds are destroyed.
In advanced cases, the following may also occur:
  • Cyanosis (blue skin)
  • Cor pulmonale (right ventricle heart disease)
  • Respiratory insufficiency
 
Diagnostic Test
  • Chest X-ray
  • Chest CT scan
  • Pulmonary function tests
  • Purified protein derivative (PPD) skin test (for tuberculosis)
  • Serologic tests for connective tissue diseases
 
Treatment
  • Stopping further exposure to silica and other lung irritants, including tobacco smoking.
  • Cough suppressants.
  • Antibiotics for bacterial lung infection.
  • TB prophylaxis for those with positive tuberculin skin test or IGRA blood test.
  • Prolonged anti-tuberculosis (multi-drug regimen) for those with active TB.
  • Chest physiotherapy to help the bronchial drainage of mucus.
  • Oxygen administration to treat hypoxemia, if present.
  • Bronchodilators to facilitate breathing.
  • Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.
  • 312For acute silicosis, bronchoalveolar lavage may alleviate symptoms, but does not decrease overall mortality.
 
Experimental Treatments
  • Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.
  • Corticosteroid therapy.
  • The herbal extract tetrandrine may slow progression of silicosis
 
Prevention
Specific steps to take while you are at work:
  • Avoid working in dust whenever possible.
  • Know what causes silica dust at your workplace.
  • Even if you cannot see dust, you can still be at risk from silica.
  • If there is visible dust, you are almost definitely at risk.
  • Use water sprays and ventilation when working in confined structures, to lower the amount of dust, including:
    • Use a water hose to wet dust before it becomes airborne
    • Use saws that add water to the blade
    • Use drills that add water through the stem or have dust collection systems
    • Use blast cleaning machines or cabinets to control dust
    • If you use a tight-fitting respirator for your particular work, you cannot have a beard or mustache. Beards and mustaches keep the respirator from sealing to your face.
    • Go to lung screenings and other health programs offered at work.
  • Practice good personal hygiene at the workplace:
    • Do not eat, drink, or use tobacco products in dusty areas.
    • If you smoke, do not smoke in dusty areas, and always wash your hands and face outside dusty areas before smoking. Make a plan to quit as soon as you are ready
      • smoking always makes lung disease worse.
    • Wash hands and face outside dusty areas before eating or drinking.
    • Park your car in an area where it would not be contaminated with silica.
    • At work, change into disposable or washable work clothes.
    • If possible, shower and change into clean clothes before leaving the worksite. This will prevent you from bringing silica into other work areas, your car and your home—and exposing your family and other people to silica.
    • Always remember that when you wear dusty clothing in your car, at home, or anywhere outside of your worksite, you may be exposing your family to potentially deadly silica!
    • Be sure you are using the proper respirator that fits well and is not uncomfortable. The National Institute of Occupational Safety and Health approves specific respirators for specific situations. The type of respirator you need depends on:
      • 313The amount of silica dust to which you are exposed.
      • The kind of work you need to do.
 
Complications
  • Connective tissue disease, including rheumatoid arthritis, scleroderma and systemic lupus erythematosus
  • Lung cancer
  • Progressive massive fibrosis
  • Respiratory failure
  • Tuberculosis
 
ASBESTOSIS
Asbestosis is a chronic inflammatory and fibrotic medical condition affecting the parenchymal tissue of the lungs caused by the inhalation and retention of asbestos fibers.
 
Etiology
Tiny asbestos fibers can get stuck deep inside the lungs. Inhaling asbestos fibers can cause scar tissue to form inside the lungs. This scar tissue does not expand and contract normally, which interferes with breathing. Asbestos fibers may remain in the lungs for a lifetime. In some cases, the fibers might damage the lungs or the membrane covering the lungs, leading to illness and even death.
 
Symptoms of Asbestosis
  • Dry inspiratory crackles: Which are clicking or rattling noises made by the lungs during inhalation.
  • ‘Clubbing’ of the fingers: Which may include softening of the fingernail beds, and bulging and of the end of the finger.
  • Misshapen nails: Caused by a decrease of oxygenated blood flow to the extremities.
  • Shortness of breath
  • A persistent, dry cough
  • Loss of appetite with weight loss
  • Chest tightness or pain
 
Other Symptoms of Asbestosis
  • Coughing
  • Chest pain
  • Blood in the sputum
  • Swelling in the neck or face
  • Difficulty swallowing
  • Loss of appetite
  • Weight loss
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Pathophysiology
 
Diagnosis
  • Complete physical examination
  • Chest X-ray
  • Lung function tests
  • A lung biopsy, in which tissue is removed by surgery, is the most reliable way to confirm the presence of microscopic asbestos fibers because X-rays cannot detect asbestos fibers in the lungs.
 
Treatment
  • Oxygen therapy to relieve shortness of breath
  • Respiratory physiotherapy to remove secretions from the lungs
  • Medications to thin secretions and relieve pain.
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COAL WORKER'S PNEUMOCONIOSIS
  • Coal worker's pneumoconiosis (CWP) can be defined as the accumulation of coal dust in the lungs and the tissue's reaction to its presence.
  • Pneumoconiosis, also known as Black Lung Disease, is an occupational lung disease caused by inhaling coal dust. There are two types of pneumoconiosis— simple, known as coal worker's pneumoconiosis (CWP) and complicated, known as progressive massive fibrosis (PMF).
 
Causes
  • Type of dust: More silica increases the risk of fibrosis. Coal rankings are as follows:
    • High: This coal is older and has the least amount of volatile matter (e.g. anthracite coal).
    • Medium: This coal is of moderate age and has a greater amount of volatile matter (e.g. bituminous coal).
    • Low: This coal is younger and has the greatest amount of volatile matter (e.g. lignite coal).
  • Age at first exposure
  • Length of time spent underground
  • Smoking
  • Size of dust particles
  • Type of job: Certain jobs require more exposure to dust. Most dust is found at the coal face; therefore, individuals who work directly on the cutting of the coal have the highest exposure. The following list details dust exposure related to job title, beginning with the highest exposure:
    • Cutting-machine operator: This worker cuts coal directly at the face. Respirable dust levels are highest here.
    • Roof bolters: These individuals drill through rock and thus are also exposed to silica. The continuous mine operator, loading machine operator, and shot firer are also exposed to higher amounts of respirable dust.
    • Train operators: They drop sand onto the tracks for traction and may, therefore, develop silicosis.
    • Motormen, brakemen, drivers, and shuttle car operators: These individuals have less dust exposure because the coal has already been cut by the time they work with it, thus decreasing their exposure to respirable dust.
    • Mechanics, electricians, and maintenance personnel: They have the least amount of dust exposure.
 
Pathophysiology
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Signs and Symptoms
  • First stage is called simple pneumoconiosis, which is characterized by chronic cough, fever, expectoration and dyspnea on exertion. This is associated with little ventilatory impairment. This stage will develop after 10–12 years of exposure.
  • Second stage is called progressive massive fibrosis: It is irreversible and continues even after cessation of the exposure. Prognosis is not good.
 
Diagnostic Evaluation
  • History of exposure.
  • Lung function test: Varies from normal to obstructive or restrictive or combination of both. Diffusion decreased. Dyspnea on exertion. X-ray chest: small nodules, 1–10 mm in upper lung zones, and ground glass appearance of the lung.
  • Radiograph of CWP
  • Pulmonary function tests: Used to test the ability of the lungs to take in air (inspiration). Often used in conjunction with the X-ray chest. Forced vital capacity (FVC) and FEV1 (forced expiratory volume in one second) are used to diagnose lung disease.
 
Management
Corticosteroids, pulmonary lavage, lung transplant.
 
Prevention and Control
  • Preplacement and periodic medical examination of workers
  • Use of protective equipment by the workers
  • Use of dust suppression measure
  • Gravimetric dust sampling in dusty areas
  • Exhaust ventilation.
 
Complications
  • Respiratory: Pneumothorax, chronic obstructive pulmonary disease, cor pulmonale.
  • Infectious diseases: Tuberculosis, vascular diseases.
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Nursing Management
 
Nursing Diagnosis
  1. Impaired gas exchange related to cough and pain from incision:
    • Open the airway with headtilt, chinlift, jaw thrust
    • Set the position to maximize ventilation
    • Use tools airway
    • Perform chest physiotherapy
    • Teach breathing deeply and coughing effectively
    • Perform suction
    • Auscultation of breath sounds
    • Give bronchodilators (collaboration).
 
Oxygenation therapy
  • Provide humidification system of oxygen equipment
  • Monitor the flow of oxygen and the amount given
  • Monitor signs of oxygen toxicity.
  1. Risk for hemorrhage related to transplant procedure:
    • Monitor pulse rate
    • Monitor central venous pressure
    • Provide sterile dressing on wound
    • Give vitamin K as per doctor's advice.
  2. Pain related to surgical condition as evidenced by verbal communication:
    • Assess for the presence of pain, the scale and intensity of pain
    • Teach the client about pain management and relaxation with distraction
    • Secure the chest tube to restrict movement and avoid irritation
    • Assess pain-reduction measures
    • Provide analgesics as indicated.
 
RESTRICTIVE LUNG DISEASES
 
Introduction
Restrictive lung diseases are characterized by reduced lung volume, either because of an alteration in lung parenchyma or because of a disease of the pleura, chest wall, or neuromuscular apparatus. In physiological terms, restrictive lung diseases are characterized by reduced total lung capacity (TLC), vital capacity, or resting lung volume. Accompanying characteristics are preserved airflow and normal airway resistance, which are measured as the functional residual capacity (FRC). If caused by parenchymal lung disease, restrictive lung disorders are accompanied by reduced gas transfer, which may be marked clinically by desaturation after exercise.
 
Definition
  • Restrictive lung disease is a chronic disorder that causes a decrease in the ability to expand the lung and sometimes makes it harder to get enough oxygen to meet the body's needs. The most common restrictive lung diseases are:
    • 318Interstitial pulmonary fibrosis or interstitial lung disease (including sarcoidosis-granulomatous disorder)
    • Extrapulmonary restrictive lung disease (including scoliosis)
  • Restrictive lung diseases are characterized by reduced lung volume, either because of an alteration in lung parenchyma or because of a disease of the pleura, chest wall, or neuromuscular apparatus. In physiological terms, restrictive lung diseases are characterized by reduced total lung capacity (TLC), vital capacity, or resting lung volume.
 
Etiology
Restrictive lung diseases may be due to specific causes which can be intrinsic to the parenchyma of the lung, or extrinsic to it.
 
Intrinsic
  • Radiation fibrosis, usually from the radiation given for cancer treatment.
  • Certain drugs such as bleomycin and methotrexate.
  • As a consequence of another disease such as rheumatoid arthritis.
  • Hypersensitivity pneumonitis due to an allergic reaction to inhaled particles.
  • Acute respiratory distress syndrome (ARDS), a severe lung condition occurring in response to a critical illness or injury.
  • Infant respiratory distress syndrome due to a deficiency of surfactant in the lungs of a baby born prematurely.
 
Extrinsic
  • Neuromuscular diseases, including Myasthenia gravis, and Guillain-Barré syndrome.
  • Nonmuscular diseases of the upper thorax, such as kyphosis and chest wall deformities.
  • Diseases restricting lower thoracic/abdominal volume (e.g. obesity, diaphragmatic hernia, or the presence of ascites).
  • Pleural thickening.
 
Pathophysiology
 
In Cases of Intrinsic Lung Disease
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In Cases of Extrinsic Disorders
 
Signs and Symptoms
Symptoms of restrictive lung disease include:
  • Cough
  • Shortness of breath
  • Wheezing and chest pain.
  • Difficulty in inhaling and exhaling
  • Wheezing and noisy breathing
  • Coughing up blood
 
Diagnostic Evaluation
Diagnostic testing for lung disease may include any of the following:
  • Physical examination
    • In patients with intrinsic lung disorders may yield distinguishing physical findings. Those with chest wall disorders show obvious massive obesity and an abnormal configuration of the thoracic cage (e.g. kyphoscoliosis, spondylitis).
    • Cyanosis at rest is uncommon in persons with interstitial lung diseases, and this is usually a late manifestation of advanced disease.
    • Digital clubbing is common in those with idiopathic pulmonary fibrosis.
  • Pulmonary function tests: Spirometry provides an objective assessment of airflow obstruction and is important in staging asthma severity. It should be done on initial diagnosis of asthma, after treatment is started and symptoms have stabilized, and every 1 to 2 years afterward. Spirometry is used to measure the rate of airflow during maximal expiratory effort after maximal inhalation. It can be useful in differentiating between obstructive and restrictive lung disorders.
  • Chest X-ray: Patient is made to stand in front of the X-ray machine. Patient will be told to hold breath when the X-ray is taken. Two images are usually taken. You will need to stand against the machine, and then sideways. Air-space opacities suggest pulmonary hemorrhage.
  • CT scans: High-resolution CT scanning of the chest can be helpful, but the expense and high dose of radiation makes it inappropriate for every patient. Generally, complete 320scans take only a few minutes. The newest multidetector scanners can image the entire body in less than 30 seconds.
  • Bronchoscopy: A bronchoscope is a device used to see the inside of the airways and lungs. The scope can be flexible or rigid. A flexible scope is almost always used. It is a tube less than one-half inch wide and about two feet long. In rare cases, a rigid bronchoscope is used. The scope is passed through mouth or nose through windpipe and into lungs. Going through the nose is a good way to look at the upper airways.
  • Pulse oximetry: Pulse oximeters are noninvasive devices used to measure a patient's blood-oxygen saturation level and pulse rate.
  • Lung biopsy: A lung biopsy is not always required to make a diagnosis in patients suggested to have interstitial lung diseases. A lung biopsy can provide information that may help lead to a specific diagnosis, help assess for disease activity, exclude neoplastic and infectious processes, establish a definitive diagnosis, and predict the prognosis.
 
Management
Few medicines are available to treat most causes of restrictive lung disease. In cases of restrictive lung disease caused by ongoing inflammation, medicines that suppress the immune system may be used, including:
 
Corticosteroids (such as prednisone)
Corticosteroids are a first-line therapy but are associated with myriad adverse effects. Corticosteroids, the most commonly used drugs, halt or slow the progression of pulmonary parenchymal fibrosis with variable success. The optimal duration of therapy is not known, but treatment for 1–2 years is suggested.
 
Cytotoxic Therapy
Immunosuppressive cytotoxic agents may be considered for patients who do not respond to steroids, experience adverse effects, or have contraindications to high-dose corticosteroid therapy. The failure of steroid therapy is defined as a fall in FVC or TLC by 10%, a worsened radiographic appearance, and a decreased gas exchange at rest or with exercise.
  • Azathioprine is less toxic than methotrexate or cyclophosphamide and may be preferred as a corticosteroid-sparing agent for disorders that are not life-threatening. A response to therapy may not occur for 3–6 months.
  • Because of potentially serious toxicities, cyclophosphamide is reserved for fulminant or severe inflammatory disorders refractory to alternate therapy.
  • Supplemental oxygen therapy may be necessary.
  • Mechanical breathing assistance may be helpful to some people with breathing difficulty from restrictive lung disease.
  • Inhalers
  • Expectorants
  • Antibiotics
  • Chemotherapy
  • In cases of obesity-related lung disease, weight loss and exercise can help reduce the resistance to breathing caused by excess fat.
  • Severe, end-stage restrictive lung disease (such as idiopathic pulmonary fibrosis) may be treated with lung transplantation.
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PULMONARY STENOSIS
Pulmonary valve stenosis is a condition in which the flow of blood from heart to lungs is slowed by a deformity or near pulmonary valve. In pulmonary valve stenosis, one or more of the leaflets may be defective or too thick, or the leaflets may not separate from each other properly. If this happens, the valve does not open correctly, restricting blood flow.
 
Etiology
  • Pulmonary valve stenosis usually occurs when the pulmonary valve does not grow properly during fetal development.
  • Other heart abnormalities also are often present at birth (congenital) in babies who have pulmonary valve stenosis. It is not known what causes the valve to develop abnormally.
 
OTHER CONTRIBUTING CONDITIONS
Sometimes other medical conditions or having an artificial valve can cause the condition in older people.
  • Carcinoid syndrome: This syndrome is a combination of signs and symptoms, including flushing of the skin and diarrhea. Carcinoid syndrome results from the release of a chemical, serotonin, from growths called carcinoid tumors located in the digestive system. People with carcinoid syndrome may develop problems with their heart valves from the serotonin.
  • Rheumatic fever: This is a complication of an infection caused by bacteria, such as strep throat or scarlet fever. Rheumatic fever may injure the heart valves.
 
Risk Factors
Because most causes of pulmonary valve stenosis develop before birth, there are not many known risk factors. However, certain conditions can increase your risk of developing pulmonary valve stenosis, including:
  • Carcinoid syndrome
  • Rheumatic fever
  • Noonan's syndrome
 
Sign and Symptoms
  • Pulmonary valve stenosis symptoms vary, depending on the extent to which the valve is obstructed. People with mild pulmonary stenosis will usually not have any symptoms. Those with more significant stenosis often first notice symptoms while exercising.
  • Pulmonary valve stenosis signs and symptoms may include:
    • Heart murmur — an abnormal whooshing sound heard using a stethoscope, caused by turbulent blood flow
    • Shortness of breath, especially during exertion
    • Chest pain
    • Loss of consciousness
    • Fatigue
    • Palpitations
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Diagnostic Evaluation
A variety of tests to confirm the diagnosis:
  • Electrocardiogram: An electrocardiogram records the electrical activity of heart each time it contracts. During this procedure, patches with wires are placed on chest, wrists and ankles. The electrodes measure electrical activity, which is recorded on paper. This test helps determine if the muscular wall of right ventricle is thickened (ventricular hypertrophy).
  • Echocardiography: Echocardiograms use high-pitched sound waves to produce an image of the heart. Sound waves bounce off the heart and produce moving images that can be viewed on a video screen. This test is useful for checking the structure of the pulmonary valve, the location and severity of the narrowing and the functioning of the right ventricle of the heart.
  • Other imaging tests: Magnetic resonance imaging and CT scans are sometimes used to confirm the diagnosis of pulmonary valve stenosis.
  • Cardiac catheterization: During this procedure, doctor inserts a thin, flexible tube into an artery or vein in groin and weaves it up to the heart or blood vessels. A dye is injected through the catheter to make blood vessels visible on X-ray pictures. Doctors also use cardiac catheterization to measure the blood pressure in the heart chambers and blood vessels.
 
Management
A physician may prescribe medications that make it easier for blood to flow through the heart's chambers. Examples of medications prescribed may include:
  • Prostaglandins to improve blood flow
  • Blood thinners to reduce clotting
  • Antiarrhythmic that prevents irregular heart rhythms.
 
Surgical Management
  • Some cases of pulmonary stenosis are mild and do not require treatment except for routine checkups. However, if the case is more serious, it may need either balloon valvuloplasty or open-heart surgery.
  • The decision to perform a balloon valvuloplasty or open-heart surgery depends on the extent to which the pulmonary valve is obstructed. Pulmonary stenosis is classified as mild, moderate or severe, depending on a measurement of the blood pressure difference between the right ventricle and pulmonary artery.
 
Balloon Valvuloplasty
This technique, which tends to be the first choice for treatment, uses cardiac catheterization to treat pulmonary valve stenosis. During this procedure, doctor threads a small tube through a vein in leg and up to heart. An uninflated balloon is placed through the opening of the narrowed pulmonary valve. Then he inflates the balloon, opening up the narrowed pulmonary valve and increasing the area available for blood flow. The balloon is then removed.
 
Open-Heart Surgery
  • Balloon valvuloplasty cannot be used for cases of pulmonary stenosis that occur above the pulmonary valve (supravalvular) or below the valve (subvalvular). Open-heart surgery is required for these types of stenosis and occasionally for valvular stenosis.
  • 323During the surgery, doctor repairs the pulmonary artery or the valve to allow blood to pass through more easily. In certain cases, doctor may replace the pulmonary valve with an artificial valve.
  • Some people with pulmonary stenosis have other congenital heart defects, and these may be repaired at the time of surgery. As with balloon valvuloplasty, there is a slight risk of bleeding, infection or blood clots associated with the surgery.
 
Nursing Management
 
Nursing Diagnosis
  • Ineffective airway clearance related to bronchoconstriction, increased mucus production Ineffective cough, possible bronchopulmonary infection.
  • Risk for infection related to compromised pulmonary function, retained secretions andcompromised defense mechanism.
  • Impaired gas exchange related to chronic pulmonary obstruction due to destruction of alveolar capillary membrane.
  • Imbalanced nutritional status less than body requirements related to increased work of breathing, air swallowing, drug effects with resultant wasting of respiratory and skeletal muscles.
  • Activity intolerance related to compromised pulmonary function, resulting in shortness of breath and fatigue.
  • Ineffective coping related to the stress of living with chronic disease, loss of independence, depression, anxiety disorder.
 
Nursing Interventions
  • Improving airway clearance:
    • Eliminate all pulmonary irritants, particularly cigarette smoking.
    • Cessation of smoking usually results in less pulmonary irritation, sputum production, and cough.
    • Keep patient's room as dust-free as possible.
    • Add moisture to indoor environment.
    • Administer bronchodilators to control bronchospasm and assist with raising sputum.
    • Assess for side effects—tremulousness, tachycardia, cardiac dysrhythmias, central nervous system stimulation, and hypertension.
    • Auscultate the chest after administration of aerosol bronchodilator to assess for improvement of aeration and reduction of adventitious breath sounds.
    • Observe if patient has reduction in dyspnea.
    • Monitor serum theophylline level as ordered, to ensure therapeutic level and prevent toxicity.
    • Use postural drainage position to aid in clearance of secretions, because mucopurulent secretions are responsible for airway obstruction.
    • Encourage the patient to take high-liquid fluids.
    • Provide inhalation-nebulized water to humidify bronchial tree and liquefy sputum.
  • Controlling infection:
    • Recognize early manifestations of respiratory infection—increased dyspnea, fatigue, and change in color, amount and character of sputum, nervousness, irritability, low-grade fever.
    • Obtain sputum for smear and culture.
    • 324Administer prescribed antimicrobial tree, thus clearing the airway.
    • Advice to live in proper ventilated room.
    • Advice to take medicine regularly as prescribed by doctor.
    • Advice to live in hygienic place, i.e. free from dust, etc.
  • Improving gas exchange:
    • Watch for restlessness, aggressiveness, anxiety, or confusion; central cyanosis and shortness of breath at rest, which frequently is caused by acute respiratory insufficiency and may signal respiratory failure.
    • Give low-flow oxygen therapy as ordered to correct hypoxemia in a controlled manner and minimize carbon dioxide retention.
    • Be prepared to assist with intubation and mechanical ventilation if acute respiratory failure and rapid carbon dioxide retention occur.
    • Advice to live in ventilated room and contact with fresh air daily.
    • Advice to do breathing exercise as prescribed by doctors.
  • Improving nutrition:
    • Take nutritional history, weight, and anthropometric measurements.
    • Encourage frequent small meal if patient is dyspneic, even small increase in abdominal contents may press on diaphragm and impede breathing.
    • Avoid food which causes abdominal discomfort.
    • Give supplemental oxygen therapy while patient is eating to relieve dyspnea, as directed.
    • Monitor body weight regularly.
  • Increased activity tolerance:
    • Encourage the patient for daily exercise and discuss about walking, bicycling, swimming and its benefits.
    • Encourage patient to carry out regular exercise program to increase physical endurances
    • Train patient in energy conservation techniques.
    • Educate about the benefits of exercise to patient as well as to family.
  • Enhancing coping:
    • Understand that the constant shortness of breath and fatigue make the patient irritable, anxious and depressed, with feeling of helplessness/hopelessness.
    • Assess the patient for reactive behavior (anger, depression, and acceptance).
    • Strengthen the patient's self-image.
    • Allow the patient to express feelings and retain the mechanisms of dental and repression.
    • Support spouse/family members.
 
PULMONARY EMBOLISM
  • Pulmonary embolism refers to the obstruction of one or more pulmonary arteries, by a thrombus that originates somewhere in the venous system or in the right heart. It may be associated with trauma, surgery, pregnancy CCF, advanced age (above 60 years), and immobility.
  • 325Pulmonary embolism is defined as an obstruction of one or more pulmonary arteries of the lungs which are blocked, or thrombus that originates somewhere in the venous system or right side of the heart.
 
Etiology
  • Venous stasis
  • Hypercoagulation
  • Damage to the endothelium of blood vessels
The predisposing factors of pulmonary embolism:
  • Prolonged immobilization
  • Concurrent phlebitis
  • Heart failure, strokes
  • Malignancy
  • Advancing age, estrogen therapy
  • Oral contraceptives
  • Obesity
 
Pathophysiology
326
 
Clinical Manifestation
  • Rapid onset of dyspnea at rest, pleuritic chest pain, cough and syncope, delirium, apprehension, tachypnea, diaphoresis, hemoptysis.
  • Chest pain with apprehension and a sense of impending doom occurs when most of the pulmonary artery is obstructed.
  • Tachycardia, rales, fever, hypotension, cyanosis, heart gallop, loud pulmonic component of S2.
  • Calf and thigh pain, edema, erythema, tenderness or palpable cord.
 
Diagnostic Evaluation
  • History-taking
  • Assess for signs and symptoms; blood study
  • Thrombotic imaging: V/Q scan or single photoemission computerized
  • Pulmonary angiography
  • D-Dimer assay for low intermediate probability of pulmonary embolism
  • ABG levels: Decreased PaO2 usually found due to perfusion abnormality of lung
  • Chest X-ray—normal or possible wedge-shaped infiltrate.
 
Management
 
Assessment
  • Assess the signs and symptoms of pulmonary embolism
  • Assess the vital signs of patient, especially respiration
  • Assess the chest pain intensity
  • Assess for edema and fever
  • Assess the hypotension and cyanosis of the patient
 
Medical Management
It is focused on anticoagulant to reduce the size of thrombus and maintain the cardiopulmonary stability.
  • Anticoagulant: It begins with heparin 5000 IU and warfarin, 2.5 mg/day, as maintained dose regulation upon prothrombin time.
  • Thrombolytic therapy: Cytokines resolve the thrombus or emboli quickly and restore normal hemodynamic therapy to reducing pulmonary hypertension improving pulmonary perfusion, oxygenation, and cardiac output.
  • Also to improve patient's respiratory and vascular status:
    • Oxygenation therapy to correct hypoxia.
    • Venous stasis is reduced by using elastic stoking
    • Elevating leg for increase venous flow
    • Hypotension relaxed with fluids.
    • Chest pain and apprehension one treated with analgesics
 
Surgical Management
When anticoagulation is contraindicated or patient has recurrent embolization or develops serious complication from drug therapy.
  • 327Interruption of vena cava: Reduces channel size to prevent lower extremity from reaching lungs. Accomplished by:
    • Ligation, placation or clipping of the inferior vena cava
    • Placement of transversely inserted intraluminal filter inferior vena cava to prevent migration of emboli
  • Embolectomy
 
Nursing Diagnosis
  • Ineffective breathing pattern related to increase in alveolar dead airspace and possible changes in lung mechanics from embolism.
  • Ineffective tissue perfusion (pulmonary) related to decreased blood circulation
  • Acute pain (pleuritic) related to congestion, possible pleural effusion, lung infraction.
  • Anxiety related to dyspnea to altered hemodynamic factors and anticoagulant therapy.
 
Nursing Interventions
 
Improve the Breathing
  • Assess for hypoxia, dyspnea, headache, restlessness, apprehension, pallor, cyanosis, behavioral changes.
  • Monitor vital signs, ECG, oximetry and ABG levels for adequacy of oxygenation.
  • Monitor patient's response to IV fluids/vasopressor.
  • Monitor oxygen therapy—used to relieve hypoxia.
  • Prepare—patient for assisted ventilation does not respond to supplemental oxygen. Hypoxia is due to abnormalities of V/Q mismatch.
 
Improving Tissue Perfusion
  • Closely monitor shock—decreasing BP, tachycardia, cool, clammy skin.
  • Monitor prescribed medication given to preserve right-sided heart filling pressure and increase BP.
  • Maintain patient on bed rest during acute phase to reduce oxygen demand and risk of bleeding.
  • Monitor urinary output hourly because this reduces renal perfusion.
  • Antiembolism compression stocking should provide a compression of 30–40 mm Hg.
 
Relieving Pain
  • Watch patient for sign of discomfort and pain.
  • Ascertain if pain worsens with deep breathing and coughing for friction rub
  • Give morphine as prescribed and monitor for pain relief.
  • Monitor signs of hypoxia thoroughly when anxiety, restlessness and agitation of new onset are noted.
 
Relieving Anxiety
  • Correct dyspnea and relieve physical discomfort.
  • Explain diagnostic procedure and the role and correct the misconception
  • 328Listen to the patient's concerns; attentive listing relieves anxiety and reduces emotional distress.
  • Speak calmly and slowly.
 
Complications
  • Bleeding as a result of treatment
  • Respiratory failure
  • Pulmonary hypertension.
 
Health Education
  • Advice patient for possible need to continue taking anticoagulant therapy for 6 weeks up to an indefinite period.
  • Teaching about sign of bleeding, especially of gum, nose, bruising, blood in urine and stool.
  • Instruct patient to tell dentist about taking anticoagulant therapy.
  • Warn against inactivity for prolonged periods or sitting with legs crossed to prevent recurrence.
  • Warn against support activity that may cause trauma or injury to legs and predispose to thrombus.
  • Encourage to wear medic alert bracelet, identifying as an anticoagulant user.
 
Prevention
Preventing clots in the deep veins in legs (deep vein thrombosis) will help prevent pulmonary embolism. For this reason, most hospitals are aggressive about taking measures to prevent blood clots:
  • Anticoagulants: Anticoagulants are given to people at risk of clots before and after an operation as well as to people admitted to the hospital with a heart attack, stroke or complications of cancer.
  • Graduated compression stockings: Compression stockings steadily squeeze your legs, helping veins and leg muscles move blood more efficiently. They offer a safe, simple and inexpensive way to keep blood from stagnating after general surgery.
  • Pneumatic compression: This treatment uses thigh-high or calf-high cuffs that automatically inflate with air and deflate every few minutes to massage and squeeze the veins in legs and improve blood flow.
  • Physical activity: Moving as soon as possible after surgery can help prevent pulmonary embolism and hasten recovery overall. This is one of the main reasons nurse may push to get up, even on your day of surgery, and walk despite pain at the site of your surgical incision.
 
PNEUMOTHORAX
  • Air in the pleural space occurring spontaneously or from trauma. Pneumothorax is the presence of air in the pleural space that prohibits complete lung expansion.
  • 329Pneumothorax is an abnormal collection of air or gas in the pleural space separating the lung from the chest wall which may interfere with normal breathing.
  • The lung expansion occurs when the pleural lining of the chest wall and the visceral lining of the lung maintain negative pressure in the pleural space. When the continuity of this system is lost, the lung collapses, resulting in pneumothorax.
 
Classification of Pneumothorax
  • Spontaneous pneomothorax: Sudden onset of air in the pleural space with deflation of the affected lung in the absence of trauma.
  • Open pneumothoax: Implies an opening in the chest wall large enough to allow air to pass freely in and out of thoracic cavity with each attempted respiration.
  • Tension pneumothorax: Build-up of air under pressure in the pleural space resulting in interference with filling of both the heart and lungs.
 
Etiology
Primary spontaneous: The exact cause of primary spontaneous pneumothorax is unknown.
 
Risk Factors
  • Male
  • Smoking
  • Family history
  • Secondary spontaneous pneumothorax occurs in the setting of a variety of lung diseases.
In children, additional causes include:
  • Measles
  • Echinococcosis
  • Inhalation of a foreign body
  • Congenital malformations
  • Marfan's syndrome
  • Homocystinuria
  • Ehlers-Danlos syndrome
  • Alpha 1-antitrypsin deficiency (which leads to emphysema)
 
Pathophysiology
  • When there is a large hole in the chest wall, the patient will have a steal in the ventilation of other lung.
  • A portion of the tidal volume will move back and forth through the hole in the chest wall, rather than the trachea as it normally does.
  • Spontaneous pneumothorax is usually due to rupture of a subpleural bleb.
  • May occur secondary to chronic respiratory disease or idiopathically.
  • May occur in healthy people, particularly in thin, white males and those with family history of pneumothorax.
 
Signs and Symptoms
  • Hyperresonance (tympany) to percussion on, diminished breath sounds on affected side.
  • Tracheal deviation away from affected side of tension pneumothorax.
  • 330Clinical picture of open or tension pneumothorax is one of air hunger, agitation, hypotension, and cyanosis.
  • Mild to moderate dyspnea and chest discomfort may be present with spontaneous pneumothorax.
  • Tachypnea
  • Asymmetrical chest expansion
 
Diagnostic Evaluation
  • Chest X-ray: Chest X-ray of left-sided pneumothorax. The left thoracic cavity is partly filled with air occupying the pleural space. The mediastinum is shifted to the opposite side.
  • Computed tomography: Computed tomography can be useful in particular situations. In some lung diseases, especially emphysema, it is possible for abnormal lung areas such as bullae (large air-filled sacs) to have the same appearance as a pneumothorax on chest X-ray, and it may not be safe to apply any treatment before the distinction is made and before the exact location and size of the pneumothorax is determined.
  • Ultrasound: Ultrasound is commonly used in the evaluation of people who have sustained physical trauma. Ultrasound may be more sensitive than chest X-rays in the identification of pneumothorax after blunt trauma to the chest.
 
Management
 
Conservative
Oxygen given at a high flow rate may accelerate resorption as much as fourfold.
 
Aspiration
Aspiration is equally effective as the insertion of a chest tube. This involves the administration of local anesthetic and inserting a needle connected to a three-way tap, up to 2.5 liters of air (in adults) are removed. If there has been significant reduction in the size of pneumothorax on subsequent X-ray, the remainder of the treatment can be conservative.
 
Chest Tube
A chest tube (or intercostal drain) is the most definitive initial treatment of pneumothorax. These are typically inserted in an area under the axilla called the ‘safe triangle’, where damage to internal organs can be avoided. This is delineated by a horizontal line at the level of the nipple and two muscles of the chest wall (latissimus dorsi and pectoralis major). Local anesthetic is applied. Two types of tubes may be used. In spontaneous pneumothorax, small-bore (smaller than 14 F, 4.7 mm diameter) tubes may be inserted by the Seldinger technique, and larger tubes do not have an advantage. In traumatic pneumothorax, larger tubes (28 F, 9.3 mm) are used.
 
Surgical Management
  • Pleurodesis and surgery.
  • Pleurodesis is a procedure that permanently obliterates the pleural space and attaches the lung to the chest wall.
  • 331Thoracotomy (surgical opening of the chest), with identification of any source of air leakage and stapling of blebs.
  • Pleurectomy (stripping of the pleural lining) of the outer pleural layer and pleural abrasion (scraping of the pleura) of the inner layer.
 
HEMOTHORAX
A hemothorax is a condition that results from blood accumulating in the pleural cavity.
 
Etiology
  • Penetrating trauma
  • Blunt trauma
  • Broken ribs
  • Shearing forces
  • Violent compression of pleural cavity
 
Pathophysiology
 
Signs and Symptoms
  • Tachypnea
  • Dyspnea
  • Cyanosis
  • Decreased or absent breath sounds on affected side
  • Tracheal deviation to unaffected side
  • Dull resonance on percussion
  • Unequal chest rise
  • Tachycardia
  • Hypotension
  • Pale, cool, clammy skin
  • Possibly subcutaneous emphysema
  • Narrowing pulse pressure.
 
Diagnostic Evaluation
  • Chest X-ray
  • CT scan
  • 332Pleural fluid analysis
  • Thoracentesis.
 
Management
  • Thoracostomy: A hemothorax is managed by removing the source of bleeding and by draining the blood already in the thoracic cavity. Blood in the cavity can be removed by inserting a drain (chest tube) in a procedure called tube thoracostomy.
  • Thrombolytic agents have been used to break up clot in tubes or when the clot becomes organized in the pleural space. However, this is risky as it can lead to increased bleeding and the need for reoperation.
 
Complications
  • Collapsed lung, leading to respiratory failure
  • Death
  • Fibrosis or scarring of the pleural membranes
  • Infection of the pleural fluid (empyema)
  • Pneumothorax
  • Shock.
 
PYOTHORAX OR EMPYEMA
  • Empyema is a collection of pus (dead cells and infected fluid) inside a body cavity. Usually, this term refers to pus inside the pleural cavity, or ‘pleural space’. The pleural cavity is the thin space between the surface of your lungs and the inner lining of chest wall.
  • Pleural empyema, also known as pyothorax or purulent pleuritis, is an accumulation of pus in the pleural cavity that can develop when bacteria invade the pleural space, usually in the context of a pneumonia.
 
Stages of Pyothorax
There are three stages:
  • Exudative: When there is an increase in pleural fluid with or without the presence of pus.
  • Fibrinopurulent: When fibrous septa form localized pus pockets.
  • Organizing stage: When there is scarring of the pleura membranes with possible inability of the lung to expand.
 
Etiology and Risk Factors
  • It is the complication of the other medical conditions.
  • Bacteria, fungi
  • Lung infections
  • After surgery of lung
  • COPD
  • Lung cancer
  • Procedure like thoracentesis.
333
 
Types
There are two classes of empyema: simple and complex.
 
Simple Empyema
  • Simple empyema is seen early in the course of the illness. In simple empyema, pus is present, but it is free flowing. Treatment at the simple stage is best, because the pleural cavity can easily be drained.
  • Complex Empyema
  • In complex empyema, the inflammation is more severe. The longer the patient have empyema that is left untreated, the greater the chance that it will develop complex empyema.
  • In cases of severe inflammation, body forms lots of scar tissue in the pleural space. Formation of scar tissue causes the cavity to become divided into multiple, smaller cavities. This is called loculation. Loculation creates complications, because infected areas that have been walled off can be difficult to drain. Complete drainage of pus from the pleural cavity is essential for treatment.
 
Signs and Symptoms
  • Fever
  • Cough
  • Shortness of breath
  • Pleurisy: Pleurisy is chest pain that occurs when you breathe and is caused by inflammation.
  • The shortness of breath experienced by patients with empyema occurs when the lungs cannot fully expand.
  • Fatigue
  • Loss of appetite
  • Weight loss.
  • The most severe signs of empyema are associated with sepsis (the presence of bacteria in the blood).
  • Signs of sepsis include high fever, chills, rapid breathing, a fast heart rate, and low blood pressure. Sepsis is life-threatening and requires emergency treatment.
Diagnostic Evaluation
Diagnosis of empyema begins with a complete medical history and physical examination.
Tests that are useful for diagnosing empyema include:
  • Blood tests, such as:
    • Blood cultures (to identify what bacterium or organism is causing the infection)
    • C-reactive protein (CRP) (elevated levels are seen in inflammatory conditions)
    • White blood cell count (WBC) (elevated levels in inflammatory and infectious conditions))
  • X-ray (to diagnose pneumonia, lung abscess document fluid accumulation)
  • Thoracentesis (aspiration of pleural fluid for microscopic examination and testing)
  • 334Thoracic ultrasound (use of sound waves to tell if loculations are present)
  • CAT scan of the chest (use of computerized X-ray analysis to evaluate the lungs and pleural space).
 
Treatment Options
  • Empyema is treated with intravenous antibiotics, such as cephalosporins, metronidazole, and penicillins with beta-lactamase (ampicillin/sulbactam). Clindamycin can be used for patients who are allergic to penicillin.
  • Fluids lost, due to lack of appetite and fever, are replaced, and medications such as acetaminophen.
  • Pleural fluid drainage: A chest tube is used to drain pus from the pleural space and allow the lungs to expand normally.
 
PLEURAL EFFUSION
  • Pleural effusion is a collection of fluid in the pleural space, is rarely a primary disease process but is usually occur secondary to other disease.
  • Normally small amount of fluid is present in the pleural space (5–15 ml) which acts as lubricant that allows the pleural surfaces to move without friction.
  • Pleural effusion may be a complication of heart failure, TB, pneumonia, pulmonary infection, connective tissue disease, pulmonary embolus, neoplastic tumors.
  • A pleural effusion is an abnormal amount of fluid around the lungs. A pleural effusion is a buildup of fluid between the layers of tissue that line the lungs and chest cavity.
 
Etiology
  • Some of the more common causes are:
    • Congestive heart failure
    • Pneumonia
    • Liver disease (cirrhosis)
    • End-stage renal disease.
 
Signs and Symptoms
  • Shortness of breath
  • Chest pain, especially on breathing in deeply (pleurisy, or pleuritic pain)
  • Fever
  • Cough.
 
Diagnostic Evaluation
  • Physical examination
  • Chest X-ray film
  • CT scan
  • Kidney and liver function blood tests
  • Pleural fluid analysis (examining the fluid under a microscope to look for bacteria, amount of protein, and presence of cancer cells)
  • 335Thoracentesis (a sample of fluid is removed with a needle inserted between the ribs)
  • Ultrasound of the chest and heart.
 
Management
 
Assessment
  • Obtain history of previous pulmonary conditions
  • Assess patient for dyspnea and tachypnea
  • Auscultation and percussion for lung abnormalities.
 
Medical and Surgical Management
  • Thoracocentesis is done to remove the fluid, collect a specimen, relieve dyspnea
  • Drug therapy: Analgesics, antibiotic, corticosteroid therapy.
For malignant effusion
  • Chest tube drainage, radiation and chemotherapy, surgical pleuralectomy, pleuroperitoneal shunt.
  • Pleurodesis: Production of adhesions between the parietal and visceral pleura accomplished by tube thoracostomy.
 
Nursing Management
 
Nursing Diagnosis
  • Ineffective airway breathing pattern related to collection of fluid after space.
  • Pain related to pleuritic fluid in lungs
  • Disturbed sleep pattern related to the pain and dyspnea
  • Anxiety related to the disease process
 
Nursing Interventions
  1. Ineffective airway breathing pattern related to collection of fluid after space.
    Interventions
    • Institute treatment to solve the underlying cause ordered
    • Assist with thoracocentesis if indicated
    • Maintain chest diseases.
    • Provide care after pleurodesis:
      • Monitor for excessive pain from the sclerosing agent, which may cause hypoventilation.
      • Administer prescribed analgesic
      • Administer oxygen to prevent hypoxemia and dyspnea
      • Observe patient's breathing pattern.
  2. Pain related to pleuritic fluid in lungs
    Interventions
    • Assess the pain intensity
    • Provide breathing exercises
    • Provide analgesics to relieve the pain.
  3. 336Disturbed sleep pattern related to the pain and dyspnea
    Interventions
    • Assess the sleeping hours of the patient
    • Provide oxygen administration
    • Provide analgesics to patient
    • Provide cool and calm environment
    • Provide sideline position to the patient to increase the lung capacity.
 
Complications
  • Infection that turns into an abscess, called an empyema, which will need to be drained with a chest tube
  • Pneumothorax (air in the chest cavity) after thoracentesis
  • Cancer
  • Pulmonary embolism
  • Lung damage
 
TUBERCULOSIS
Tuberculosis is an infectious bacterial disease caused by Mycobacterium tuberculosis, which most commonly affects the lungs. It is transmitted from person to person via droplets from the throat and lungs of people with the active respiratory disease.
 
Etiology
  • Mycobacterium tuberculosis
  • Immunocompromised person.
  • Chemical industries.
 
Risk Factors
  • Aging
  • Alcoholism
  • Crowded living conditions
  • Diseases that weaken the immune system
  • Health care workers
  • HIV infection
  • Homelessness
  • Low socioeconomic status
  • Malnutrition, migration from a country with a high number of cases
  • Nursing homes
  • Unhealthy immune system
 
Types
  • Pulmonary tuberculosis: If a tuberculosis infection does become active, it most commonly involves the lungs (in about 90% of cases). Symptoms may include chest pain and a prolonged cough-producing sputum.
  • Extrapulmonary tuberculosis: In 15–20% of active cases, the infection spreads outside the lungs, causing other kinds of TB. These are collectively denoted as ‘extrapulmonary tuberculosis’. Extrapulmonary TB occurs more commonly in immunosuppressed persons and young children.
  • 337Active tuberculosis: Active TB means the bacteria are active in the body. The immune system is unable to stop these bacteria from causing illness. People with active TB in their lungs can pass the bacteria on to anyone they come into close contact with. When a person with active TB coughs, sneezes or spits, people nearby may breathe in the tuberculosis bacteria and become infected.
  • Inactive Tuberculosis: Inactive TB infection is also called latent TB. If a person has latent TB, it means their body has been able to successfully fight the bacteria and stop them from causing illness. People who have latent TB do not feel sick, do not have symptoms and cannot spread tuberculosis
 
Pathophysiology and Clinical Manifestations
  • A cough lasting for more than 2–3 weeks
  • Chest pain
  • Chills
  • Discolored or bloody sputum
  • Fatigue
  • Loss of appetite
  • Night sweats
  • Pain with breathing
  • Severe headache
  • Shortness of breath
  • Slight fever
  • Tiredness or weakness
  • Weight loss
Fig. 5.4: Pathophysiology
338
 
Diagnostic Evaluation
  • Injection of Protein: By injecting a protein found in TB bacteria into the skin of an arm. If the skin reacts by swelling, then the person is probably infected with tuberculosis.
  • X-ray: Diagnosis of tuberculosis in the lungs may be made using an X-ray.
  • Sputum test: Sample of sputum is tested in laboratory to diagnose the TB.
  • Bacteria: A culture of TB bacteria can also be grown in a laboratory. However, this requires specialized and costly equipment and can take six to eight weeks to produce a result.
 
Management
 
Medical Management
The five basic or ‘first-line’ TB drugs are:
  • Isoniazid
  • Rifampicin
  • Pyrazinamide
  • Ethambutol
  • Streptomycin
 
Surgical Management
If medications are ineffective, there are three surgical treatments for pulmonary TB:
  • Pneumothorax, in which air is introduced into the chest to collapse the lung
  • Thoracoplasty, in which one or more ribs are removed
  • Removal of a diseased lung.
 
Nursing Management
 
Goals
The goals of management are:
  • To control the inflammatory process.
  • To relieve symptoms.
  • To correct metabolic and nutritional problems and promote healing.
  • To achieve the previous health status.
 
Nursing Assessment
  • Promoting airway clearance
  • Advocating adherence to treatment regimen
  • Promoting activity and adequate nutrition
  • Preventing spreading of tuberculosis infection
 
Nursing Diagnosis
  • Ineffective airway clearance related to increased sputum
  • Risk of infection related to lower resistance of others who are around people.
  • Ineffective breathing pattern related to inflammation.
  • Hyperthermia related to the infection process.
  • 339Fluid volume deficit related to fatigue due to lack of fluid intake.
  • Activity intolerance related to fatigue.
  • Imbalanced nutrition, less than body requirements related to decreased appetite.
  • Ineffective management, therapeutic regimen related to lack of knowledge about the disease process.
  • Impaired gas exchange related to alveoli function decline.
 
Intervention
  • Ineffective airway clearance:
    • Auscultate lungs for wheezing, decreased breath sounds, coarse sounds
    • Use universal precautions if secretions are purulent even before culture reports
    • Assess cough for effectiveness and productivity
    • Note sputum amount, color, odor, consistency
    • Send sputum specimens for culture as prescribed
    • Institute appropriate isolation precautions if cultures are positive
    • Use humidity to help loosen sputum
    • Administer medications, noting effectiveness and side effects
    • Teach effective deep breathing and coughing techniques
  • Risk for infection:
    • Monitor sputum for changes indicating infection
    • Monitor vital signs
    • Teach patient and family the purpose and techniques for infection control, such as handwashing, patient covering mouth when coughing, maintaining isolation if necessary
    • Teach patient the purpose, importance and how to take medications as prescribed consistently over the long-term therapy
  • Deficient knowledge:
    • Determine who will be the learner—patient or family
    • Assess ability to learn
    • Identify any existing misconceptions about the material to learn
    • Assist the learner to integrate the information into daily life
    • Give clear thorough explanations and demonstrations
  • Activity intolerance:
    • Assess patient's level of mobility
    • Observe and document response to activity
    • Assess emotional response to change in physical status
    • Anticipate patient's needs to accommodate
    • Teach energy conservation techniques
    • Refer to community resources as needed
  • Ineffective therapeutic regimen management:
    • Assess prior efforts to follow regimen
    • Assess patient's perceptions of their health problem
    • 340Assess other factors that may affect success in a negative way
    • Inform patient of the benefits of conforming with the regimen
    • Concentrate on the behaviors that will make the most difference to the therapeutic effect
    • Include family, support system in teachings and explanations.
 
Health Education
  • Explain about the disease condition's causes, risk factors
  • Use universal precautions if secretions are purulent even before culture reports
  • Assess cough for effectiveness and productivity
  • Note sputum amount, color, odor, consistency
  • Send sputum specimens for culture as prescribed or PRN
  • Institute appropriate isolation precautions if cultures are positive
  • Use humidity to help loosen sputum
  • Administer medications, noting effectiveness and side effects
  • Assess patient's perceptions of their health problem
  • Assess other factors that may affect success in a negative way
  • Inform patient of the benefits of conforming with the regimen
  • Concentrate on the behaviors that will make the most difference to the therapeutic effect.
 
Complications
  • Miliary tuberculosis
  • Pleural effusion
  • Emphysema
  • Tuberculosis pneumonia
 
CHEST INJURIES
Chest injuries (or thoracic trauma) are a serious injury of the chest. Thoracic trauma is a common cause of significant disability and mortality, the leading cause of death from physical trauma after head and spinal cord injury. Blunt thoracic injuries are the primary or a contributing cause of about a quarter of all trauma-related deaths.
 
Classification
Chest trauma can be classified as:
  • Blunt injuries
  • Crush injuries
  • Penetrating injuries.
 
Blunt Trauma
Mode of injury is important where there has been massive deformity of a car or a history of a fall of 5 meters or more major intrathoracic injuries should always be suspected. The physical nature of chest wall allows for considerable elastic recoil, especially in young patients and, therefore, degree of injury within chest may need to be judged initially by deformity to car rather than appearance of patient.
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Penetrating Injuries
  • Result in parenchymal damage related to track of missile or stabbing implement and velocity
  • More solid structures (e.g. heart and major vessels) suffer greater injury where high-velocity missiles are penetrating weapons
  • Most lethal complication is hemorrhage
  • Often associated with abdominal trauma.
 
Crush Injury
  • Occurs where elastic limits of chest and its contents have been exceeded
  • Patients usually have AP deformity
  • Majority have flail chests with multiple fractures, pneumothorax or hemothorax
  • Most have pulmonary contusion
  • Injuries of heart, aorta, diaphragm, liver, kidney and spleen are common.
 
Specific Types of Chest Trauma
  • Injuries to the chest wall:
    • Rib fractures
    • Flail chest
    • Sternal fractures.
  • Pulmonary injury (injury to the lung) and injuries involving the pleural space:
    • Pulmonary contusion
    • Pulmonary laceration
    • Pneumothorax
    • Hemothorax
    • Hemopneumothorax.
  • Injury to the airways:
    • Tracheobronchial tear.
  • Cardiac injury:
    • Pericardial tamponade.
 
Signs and Symptoms
  • Air hunger, use of accessory muscles, tracheal deviation, cyanosis or distended neck veins (evidence of tension pneumothorax, or tamponade)
  • Tracheal deviation (evidence of tension pneumothorax)
  • Major defects in the chest (sucking chest wounds)
  • Unilaterally diminished breath sounds or hyper-resonance to percussion (evidence of closed pneumothorax or tension pneumothorax)
  • Decreased heart sounds (pericardial tamponade)
  • Location of foreign bodies
  • Location of entry and exit wounds.
 
Diagnostic Evaluation
  • Chest X-ray:
    • CXR is most useful screening investigation
    • Look for subcutaneous air, foreign bodies, bony fractures, widening of mediastinum, atelectasis
    • Inspiratory and expiratory films for checking for pneumothorax.
  • 342CT scan:
    • Valuable tool
    • Aids in diagnosis and precise location of numerous lesions.
    • Contrast is useful particularly when looking for mediastinal hemorrhage and periaortic hematomas.
  • Echocardiography: Cardiac wall motion abnormalities and valve function and presence of pericardial fluid or blood.
  • ECG: Most common abnormality in thoracic trauma are S-T and T wave changes and findings indicative of bundle branch block.
  • Angiography: Remains the gold standard for defining thoracic vascular injuries.
  • Bronchoscopy: Indications include evaluation of airway injury, hemoptysis, segmental or lobar collapse, and removal of aspirated foreign bodies.
 
Management
 
Immediate Management
  • Assure patent airway, oxygenation and ventilation
  • Exclude or treat:
    • Pneumothorax
    • Hemothorax
    • Cardiac tamponade
  • Assess for extrathoracic injuries
  • Decompress stomach
  • Provide pain relief
  • Reconsider endotracheal intubation, ventilation. In particular, take into account gross obesity, significant pre-existing lung disease, severe pulmonary contusion or aspiration, need for surgery for thoracic or extrathoracic injuries.
 
General Management
  • Monitoring
    Following are danger signs requiring full reassessment:
  • Respiratory rate > 20/min
  • Heart rate > 100/min
  • Systolic BP < 100 mm Hg
  • Reduced breath sounds on affected side
  • PaO2 < 9 kPa on room air
  • PaCO2 > 8 kPa
  • Increased size of pneumothorax, hemothorax or increased width of mediastinum on CXR.
  • Deterioration in any of these signs must be followed by a search for evidence of blood loss, tension pneumothorax, head injury, sepsis or fat embolism. Chest drains should be checked for patency.
  • 343Chest drains: Indications for insertion of chest drains in stable patients:
    • Pneumothorax > 10% in nonventilated patients (i.e. > 1 intercostal space)
    • Hemothorax > 500 ml (i.e. above neck of 7th rib)
    • Surgical emphysema
  • Antibiotics:
    • Use of prophylactic antibiotics is controversial. Some recommend them for patients treated conservatively in whom a chest drain is inserted.
    • Cefuroxime and metronidazole for patients with perforated viscus (in addition to exploration and drainage)
  • Mechanical ventilation:
    • Most centers use PCV or PSV to reduce incidence of barotraumas
    • PCV and PSV also provide some compensation for air leaks
  • Analgesia:
    • IV opioids in frequent small doses or by continuous infusion
    • Entonox inhalation during physiotherapy
    • Intercostal nerve block
    • Multiple individual nerve blocks
    • Single large volume (e.g. 20 ml 0.5% bupivicaine) into one intercostal space. Spreads to block nerves above and below
    • Intrapleural bupivicaine via intercostal catheters using intermittent injections or continuous infusions
    • NSAIDs: fully resuscitated patients with normal renal function.
 
Postoperative Intensive Care
  • Following tracheobronchial, lung or diaphragmatic repair, high inflation pressures should be avoided
  • Tracheal suction must be minimal where there is a tracheobronchial suture line
  • Avoid fluid overload
  • Prevent gastric distension.
 
RIB FRACTURE
Fractures of the first and second ribs may be more likely to be associated with head and facial injuries than other rib fractures. The middle ribs are the ones most commonly fractured. Fractures usually occur from direct blows or from indirect crushing injuries. The weakest part of a rib is just anterior to its angle, but a fracture can occur anywhere. The most commonly fractured ribs are the 7th and 10th. A lower rib fracture has the complication of potentially injuring the diaphragm, which could result in a diaphragmatic hernia. Rib fractures are usually quite painful because the ribs have to move to allow for breathing. Even a small crack can inflame a tendon and cripple an arm. When several ribs are broken in several places, a flail chest results, and the detached bone sections will move separately from the rest of the chest.
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Definition
A rib fracture is a breaking or fracture in one or more of the bones making up the rib cage. The first rib is rarely fractured because of its protected position behind the clavicle. If it is broken, serious damage can occur to the brachial plexus of nerves and the subclavian vessels.
 
Etiology
  • Rib fractures can occur without direct trauma and have been reported after sustained coughing.
  • Various sports, for example, rowing and golf, often in elite athletes. They can also occur as a consequence of diseases such as cancer or infections.
  • Fragility fractures of ribs can occur due to diseased bone structure, e.g. osteoporosis and metastatic deposits.
 
Signs and Symptoms
  • Pain when breathing or with movement
  • A portion of the chest wall moving separately from the rest of the chest (flail chest)
  • A grating sound with breathing or movement
  • Where the mechanism of injury would indicate substantial force to the ribs.
 
Treatment
There is no specific treatment for rib fractures, but various supportive measures can be taken. In simple rib fractures, pain can lead to reduced movement and cough suppression. This can contribute to formation of secondary chest infection.
  • Adequate analgesia can avoid pain.
  • It is a potentially life-threatening injury and will often require a period of assisted ventilation.
  • Acute Innovations’ RibLoc is a titanium U-shaped plate that is sized to match rib thickness and uses screws that fixate to anterior and posterior of plate and provide fixation without needing purchase for screws and without risking damage to the neurovascular bundle. These plates can be contoured to match the rib segment being plated and come in various lengths.
  • Judet and/or Sanchez Plates/Struts are metal plates with strips that bend around the rib and then are further secured with sutures.
  • Synthes MATRIX RIB Fixation System has two options: A precontoured metal plate that uses screws to secure the plate to the rib and an intramedullary splint which is tunneled into the rib and secured with a set screw.
  • Anterior locking plates are metal plates that have holes for screws throughout the plate. The plate is positioned over the rib and screwed into the bone at the desired position. The plates may be bent to match the contour of the rib section.
 
FLAIL CHEST
A flail chest is a life-threatening medical condition that occurs when a segment of the rib cage breaks under extreme stress and becomes detached from the rest of the chest wall. It 345occurs when multiple adjacent ribs are broken in multiple places, separating a segment, so a part of the chest wall moves independently.
 
Characteristics
  • During normal inspiration, the diaphragm contracts and intercostal muscles push the rib cage out. Pressure in the thorax decreases below the atmospheric pressure, and air rushes in through the trachea. However, a flail segment will not resist the decreased pressure and will appear to push in while the rest of the rib cage expands.
  • During normal expiration, the diaphragm and intercostal muscles relax, allowing the abdominal organs to push air upwards and out of the thorax. However, a flail segment will also be pushed out while the rest of the rib cage contracts.
 
Etiology
This typically occurs when three or more adjacent ribs are fractured in two or more places, allowing that segment of the thoracic wall to displace and move independently of the rest of the chest wall. Flail chest can also occur when ribs are fractured proximally in conjunction with disarticulation of costal cartilages distally. For the condition to occur, generally there must be a significant force applied over a large surface of the thorax to create the multiple anterior and posterior rib fractures. Rollover and crushing injuries most commonly break ribs at only one point—for flail chest to occur, a significant impact is required, breaking the ribs in two or more places.
 
Signs and Symptoms
  • Fracture is extremely painful, and, untreated, the sharp broken edges of the ribs
  • Puncture in the pleural sac and lung
  • Pneumothorax.
 
Treatment
Treatment of the flail chest initially follows the principles of advanced trauma life support. Further treatment includes:
  • Good analgesia including intercostal blocks, avoiding narcotic analgesics as much as possible. This allows much better ventilation, with improved tidal volume, and increased blood oxygenation.
  • Positive pressure ventilation, meticulously adjusting the ventilator settings to avoid pulmonary barotrauma.
  • Chest tubes as required.
  • Adjustment of position to make the patient most comfortable and provide relief of pain.
  • Aggressive pulmonary toilet.
 
Surgical Fixation
  • Can help in significantly reducing the duration of ventilatory support and in conserving the pulmonary function.
  • A patient may be intubated with a double lumen tracheal tube. In a double lumen endotracheal tube, each lumen may be connected to a different ventilator. Usually one side of the chest is affected more than the other. So each lung may require drastically different pressures and flows to adequately ventilate.
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STERNAL FRACTURE
A sternal fracture is a fracture of the sternum located in the center of the chest. The injury that experiences significant blunt chest trauma may occur in vehicle accidents, when the still-moving chest strikes a steering wheel or dashboard, or is injured by a seatbelt. Sternal fractures may also occur as a fracture in people who have weakened bone in their sternum, due to another disease process.
 
Etiology
Vehicle collisions are the usual cause of sternal fracture. The injury is estimated to occur in about 3% of auto accidents. The chest of a driver who is not wearing a seatbelt may strike the steering wheel, and the shoulder component of a seatbelt may injure the chest if it is worn without the lap component.
 
Signs and Symptoms
  • Crepitus (a crunching sound made when broken bone ends rub together)
  • Pain
  • Tenderness
  • Bruising
  • Swelling over the fracture site.
  • Palpation.
 
Diagnostic Test
  • X-rays of the chest are taken in people with chest trauma and symptoms of sternal fractures
  • CT scanning
  • Electrocardiogram and radionucleotide abnormalities (abnormal test results indicating cardiac dysfunction).
 
Treatment
  • Tracheal intubation
  • Mechanical ventilation
 
PULMONARY CONTUSION
  • Contusion is a bruise of the lung caused by chest trauma. As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels or hypoxia.
  • Pulmonary contusion: It is usually caused directly by blunt trauma but can also result from explosion injuries or a shock wave associated with penetrating trauma.
 
Etiology
  • Motor vehicle accidents are the most common cause of pulmonary contusion.
  • Chest strikes the inside of the car
  • Falls
  • 347Assaults
  • Sports injuries
  • Explosions
 
Pathophysiology
 
Signs and Symptoms
  • Dyspnea (painful breathing or difficulty breathing)
  • Rapid breathing
  • Rapid heart rate
  • Rales (an abnormal crackling sound in the chest accompanying breathing)
  • Bronchorrhea (the production of watery sputum)
  • Wheezing and coughing are other signs
  • Coughing up blood or bloody sputum
  • Cardiac output (the volume of blood pumped by the heart)
  • Hypotension (low blood pressure)
  • Tender or painful.
 
Diagnostic Evaluation
  • X-ray: A chest X-ray showing right-sided pulmonary contusion associated with rib fractures and subcutaneous emphysema.
  • Computed tomography: A chest CT scan revealing pulmonary contusions, pneumothorax, and pseudocysts. Computed tomography (CT scanning) is a more sensitive test for pulmonary contusion, and it can identify abdominal, chest, or other injuries that accompany the contusion. CT scans also help differentiate between contusion and pulmonary hematoma.
  • Ultrasound: An ultrasound image showing early pulmonary contusion, at this moment not visible on radiography.
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Prevention
  • Airbags in combination with seat belts can protect vehicle occupants by preventing the chest from striking the interior of the vehicle during a collision.
  • Child restraints such as car seats protect children in vehicle collisions from pulmonary contusion.
  • Equipment exists for use in some sports to prevent chest and lung injury, for example, in softball, the catcher is equipped with a chest.
  • Protective garments can also prevent pulmonary contusion in explosions.
 
Treatment
  • Ventilation: Mechanical ventilation may be required if pulmonary contusion causes inadequate oxygenation.
  • Fluid therapy: The administration of fluid therapy in individuals with pulmonary contusion is controversial. Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal.
  • Supportive care: The use of suction, deep breathing, coughing, and other methods to remove material, such as mucus and blood from the airways. Chest physical therapy makes use of techniques, such as breathing exercises, stimulation of coughing, suctioning, percussion, movement, vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of the lungs.
 
Complications
  • Pneumonia
  • Acute respiratory distress syndrome
  • Pulmonary edema
  • Acute respiratory distress syndrome
  • Pneumonia
 
PULMONARY LACERATION
  • Pulmonary laceration: In which lung tissue is torn or cut, differs from pulmonary contusion in that the former involves disruption of the macroscopic architecture of the lung.
  • Pulmonary hematoma: When lacerations fill with blood, the result is pulmonary hematoma, a collection of blood within the lung tissue.
 
Etiology
Pulmonary laceration is a common result of:
  • Penetrating trauma
  • Blunt trauma
  • Broken ribs
  • Shearing forces
  • Violent compression of the chest
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Classification
  • Type 1 lacerations: Which occur in the mid-lung area, the air-filled lung bursts as a result of sudden compression of the chest. Also called compression-rupture lacerations, type 1 are the most common type and usually occur in a central location of the lung. They tend to be large, ranging in size from 2 to 8 cm.
  • Type 2 lacerations: Result when the lower chest is suddenly compressed and the lower lung is suddenly moved across the vertebral bodies. It is also called compression-shear, tends to occur near the spine and have an elongated shape. Type 2 lacerations usually occur in younger people with more flexible chests.
  • Type 3 lacerations: Which are caused by punctures from fractured ribs, occur in the area near the chest wall underlying the broken rib. Also called rib penetration lacerations, type 3 lacerations tend to be small and accompanied by pneumothorax.
  • Type 4 lacerations: Also called adhesion tears, occur in cases where a pleuropulmonary adhesion had formed prior to the injury, in which the chest wall is suddenly fractured or pushed inward.
 
Pathophysiology
 
Diagnostic Evaluation
  • X-ray: A chest X-ray of a right-sided pulmonary contusion associated with flail chest and subcutaneous emphysema. Contusion may mask pulmonary laceration on chest X-ray.
  • CT scanning: On a CT scan, pulmonary lacerations show up in a contused area of the lung typically appearing as cavities filled with air or fluid that usually have a round or ovoid shape due to the lung's elasticity.
  • Thoracoscopy may be used in both diagnosis and treatment of pulmonary laceration.
 
Management
  • As with other chest injuries, such as pulmonary contusion, hemothorax, and pneumothorax, pulmonary laceration can often be treated with just supplemental oxygen, ventilation, and drainage of fluids from the chest cavity.
  • A thoracostomy tube can be used to remove blood and air from the chest cavity. About 5% of cases require surgery, called thoracotomy.
 
Surgical Treatment
  • Lobectomy: In which a lobe of the lung is removed
  • Pneumonectomy: In which an entire lung is removed.
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Complications
  • Pulmonary abscess
  • Bronchopleural fistula (a fistula between the pleural space and the bronchial tree)
  • Air embolism: In which air enters the bloodstream, is potentially fatal, especially when it occurs on the left side of the heart.
 
TRACHEOBRONCHIAL INJURY
Tracheobronchial injury (TBI) is damage to the tracheobronchial tree (the airway structure involving the trachea and bronchi). It can result from blunt or penetrating trauma to the neck or chest, inhalation of harmful fumes or smoke, or aspiration of liquids or objects.
 
Etiology
  • Falls from height
  • Motor vehicle accidents
  • Explosions are another cause
  • Gunshot wounds
  • Knife wounds
  • Edema (swelling).
 
Clinical Manifestations
  • Dyspnea
  • Respiratory distress
  • Coughing
  • Hemoptysis
  • Stridor (an abnormal, high-pitched breath sound indicating obstruction of the upper airway can also occur)
  • Necrosis (death of the tissue)
  • Scar formation
  • Stenosis
  • Due to inhalation of foreign body aspiration
  • Medical procedure is uncommon.
 
Diagnostic Evaluation
  • Chest X-ray: Is the initial imaging technique used to diagnose TBI. X-rays may also show accompanying injuries and signs, such as fractures and subcutaneous emphysema.
  • CT scanning detects resulting from blunt trauma. CT are a replacement for bronchoscopy.
 
Prevention
Vehicle occupants who wear seatbelts have a lower incidence of TBI after a motor vehicle accident.
 
Treatment
  • Endotracheal tube: May be used to bypass a disruption in the airway
  • Tracheotomy: An incision can be made in the trachea (tracheotomy)
  • 351Mechanical ventilation: Such as positive end-expiratory pressure (PEEP) and ventilation at higher-than-normal pressures may be helpful in maintaining adequate oxygenation.
 
Complications
  • Bronchial stenosis
  • Pneumonia
  • Bronchiectasis.
BIBLIOGRAPHY
  1. Black M. A textbook of medical surgical nursing. Elsevier.  Noida.  8th ed. 1307–40.
  1. Brunner S. A textbook of medical surgical nursing. Lippincott Company.  Philadelphia.  10th ed. 2007. 756–65.
  1. Brunner S. Textbook of medical surgical nursing. Williams and willkins Wolter Kulvar.  Lippincott.  11 ed. 1200–1.
  1. Halks B. Textbook of medical surgical nursing. Jaypee Brothers Medical Publishers (P) Ltd.  1216–17.
  1. Hopper P, William L. Understanding of medical surgical nursing. Devis.  2nd ed. 2003. 286–97.
  1. Lemone P, Burke K. A textbook of medical surgical nursing. Dorling Kindersely.  South Asia.  4th ed. 2007.
  1. Lippincott Wiliam and Wilkins. Textbook of medical surgical nursing. Wolter Kulvers.  9th ed. 534–6.
  1. Wilkins and William L. Mannual of nursing practice. Elsevier.  Noida.  8th ed.

Neurological Disorders6

 
 
Introduction
The nervous system has been divided into two components: The central nervous system which is composed of the brain and the spinal cord, and the peripheral nervous system, which is composed of ganglia a peripheral nerves that lie outside the brain and spinal cord.
 
PERIPHERAL NERVOUS SYSTEM
The peripheral nervous system has been, in turn divided into two subsystem: Somatic and autonomic.
Somatic subsystem includes sensory neurons of the dorsal root and cranial ganglia that innervate the skin, muscles, and joints and provide sensory information to the central nervous system about muscle and limb position and about the environment.
Autonomic subsystem includes the motor system for the viscera, the smooth muscles and exocrine glands. It in turn consists of three segregated subdivisions: the sympathetic system which participates in the response of the body to stress. The parasympathetic system that 353acts to conserve de body's resources and restore homeostasis. The enteric nervous system which controls the function of smooth muscle of the gut.
 
CENTRAL NERVOUS SYSTEM
The central nervous system consists of six main regions:
 
The Spinal Cord
It extends from the base of the skull through the first lumbar vertebra. The spinal cord receives sensory information from the skin, joints, and muscles of the trunk and limbs, and contains the motor neurons responsible for both voluntary and reflex movements. It also receives sensory information from the internal organs and control many visceral functions. Within the spinal cord there is an orderly arrangement of sensory cell groups that receive input from the periphery and motor cell groups that control specific muscle groups. In addition, the spinal cord contains ascending pathway through which sensory information reaches the brain and descending pathways that relay motor command from the brain to motor neurons.
 
The Medulla
This structure is the direct rostral extension (this means toward the head and nose) of the spinal cord. Together with the pons it participates in regulating blood pressure and respiration. It resembles the spinal cord in both organization and function.
 
The Pons
It lies rostral to the medulla and contains a large number of neurons that relay information from the cerebral hemispheres to the cerebellum. The cerebellum lies dorsal to the pons and medulla. It has a distinctive corrugated surface. The cerebellum receives somatosensory input from the spinal cord, motor information from the cerebral cortex and balance information from the vestibular organs of the inner ear. The cerebellum integrates this information and coordinates the planning, timing and patterning of skeletal muscle contractions during movement. The cerebellum plays a major role in the control of posture, head and eye movements.
 
The Midbrain
This is the smallest brain stem component which lies rostral to the pons. The midbrain contains essential relay nuclei of the auditory and visual system. Several regions of this structure play an important role in the direct control of eye movement, whereas others are involved in motor control of skeletal muscles.
 
The Diencephalon
It consists of the thalamus and hypothalamus. Lies between the cerebral hemispheres and the midbrain. The thalamus distributes almost all sensory and motor information going to the cerebral cortex. In addition, it is thought to regulate levels of awareness and some emotional aspects of sensory experiences. The hypothalamus lies ventral to the thalamus and regulates autonomic activity and the hormonal secretion by the pituitary gland. It has extensive connections with the thalamus, midbrain and some cortical areas that process information from the autonomic system.
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The Cerebral Hemispheres
It forms, in humans, the largest region of the brain. They consist of the cerebral cortex, the white matter under the cortex and three deeply located nuclei: the basal ganglia, the hippocampus formation and the amygdala. The cerebral hemispheres are divided by the hemispheric fissure and are thought to be concerned with perception, cognition, emotion, memory and high motor functions.
 
The Basal Ganglia
The major components of the basal ganglia are the caudate nucleus, the putamen and the globus pallidus. The basal ganglia have an important role in regulation of movement and also contribute to cognitive functions.
 
The Hippocampus and Amygdala
The hippocampus and amygdala are part of the so called limbic system. The hippocampus is involved in memory storage. The amygdala coordinates the actions of the autonomic and endocrine systems and is involved in emotions.
 
BELL'S PALSY
Bell's palsy is a paralysis or weakness of the muscles on one side of face. Damage to the facial nerve that controls muscles on one side of the face causes that side of face to droop. The nerve damage may also affect sense of taste. The weakness usually affects one side of the face. Rarely, both sides are affected.
 
Etiology
It is thought that inflammation develops around the facial nerve as it passes through the skull from the brain. The inflammation may squash (compress) the nerve as it passes through the skull. The nerve then partly, or fully, stops working until the inflammation goes. If the nerve stops working, the muscles that the nerve supplies also stop working.
Fig. 6.1: Facial nerve
Cold sore (herpes simplex) virus.
Chickenpox (varicella-zoster) virus.
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Signs and Symptoms
  • Weakness of the face which is usually one-sided. The weakness normally develops quickly.
    • Face may droop to one side.
    • Food may get trapped between gum and cheek. Drinks and saliva may escape from the side of mouth.
    • Difficult to close the eye, this may cause a watery or dry eye.
    • Difficult able to wrinkle forehead, whistle or blow out cheek.
    • Difficulty with speech.
  • Painless or cause just a mild ache.
  • Loud sounds maybe uncomfortable and normal noises may sound louder than usual. This is because a tiny muscle in the ear may stop working.
  • Lose of sense of taste on the side of the tongue that is affected.
Fig. 6.2: Bell's Palsy
 
Management
  • Anti-inflammatory drugs
The steroid tablet most commonly used is called prednisolone. Steroids help to reduce inflammation, which is probably the reason they help.
  • Antiviral drugs
  • Eye protection
    • An eye pad or goggles to protect the eye.
    • Eye drops to lubricate the eye during the day.
    • Eye ointment to lubricate the eye overnight.
    • Tape the upper and lower lid together when you are asleep. Other procedures are sometimes done to keep the eye shut until the eyelids recover.
  • Physiotherapy; a treatment called, ‘facial retraining’ with facial exercises may help.
  • Injections of botulism toxin (Botox) may help if spasm develops in the facial muscles.
  • Various surgical techniques can help with the cosmetic appearance.
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Complications
  • Corneal ulcers
  • Blindness
  • Impaired nutrition.
 
Medical Management
The objectives of management are to maintain facial muscle tone and to prevent or minimize complication with the help of the following:
  • Corticosteroid therapy (prednisone) maybe initiated to reduce inflammation and edema, which reduces vascular compression and permits restoration of blood circulation to the nerve.
  • Early administration of corticosteroids appears to diminish severity, relieve pain, and minimize denervation.
  • Facial pain is controlled with analgesic agents or heat applied to the involved side of the face.
  • Additional modalities may include electrical stimulation applied to the face to prevent muscle atrophy, or surgical exploration of the facial nerve.
  • Surgery may be performed if a tumor is suspected, for surgical decompression of the facial nerve, and for surgical rehabilitation of a paralyzed face.
 
Surgical Management
 
1. Facial Nerve Decompression
The surgeon decides if the maxillary segment should be decompressed externally or if the labyrinthine segment and geniculate ganglion should be decompressed with a middle fossa craniotomy.
 
2. Subocularis Oculi Fat Lift (SOOF)
The SOOF is deep to the orbicularis oculi muscle and superficial to the periosteum below the inferior orbital rim. An SOOF lift is designed to lift and suspend the midfacial musculature. The procedure may also elevate the upper lip and the angle of the mouth to improve facial symmetry.
 
3. Lateral Tarsal Strip Procedure
An SOOF lift is commonly performed in conjunction with a lateral tarsal strip procedure to correct horizontal lower-lid laxity and to improve apposition of the lid to the globe. First, lateral canthotomy and cantholysis is performed. Then, the anterior lamella is removed and the lateral tarsal strip is shortened and attached to the periosteum at the lateral orbital rim.
 
4. Implants in Eyelid
Implantable devices have been used to restore dynamic lid closure in cases of severe, symptomatic lagophthalmos. These procedures are best for patients with poor Bell phenomenon and decreased corneal sensation. Gold or platinum weights, a weight-adjustable magnet, or palpebral springs can be inserted into the eyelids. Pretarsal gold-weight implantation is most commonly performed. The implants are easily removed if nerve function returns.
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5. Tarsorrhaphy
Tarsorrhaphy decreases horizontal lid opening by fusing the eyelid margins together, increasing support of the precorneal lake of tears and improving coverage of the eye during sleep. The procedure can be done in the office and is particularly suitable for patients who are unable or unwilling to undergo other surgery. It can be completed as either a temporary or a permanent measure. Permanent tarsorrhaphy is performed if nerve recovery is not expected.
Tarsorrhaphy can be performed laterally, centrally, or medially. The lateral procedure is the most common; however, it can restrict the monocular temporal visual field. Central tarsorrhaphy offers good corneal protection, but it occludes vision and can be cosmetically unacceptable. Medial or paracentral tarsorrhaphy is performed lateral to the lacrimal puncta and can offer good lid closure without substantially affecting the visual field.
 
Other surgeries
 
Muscle Transposition, Nerve Grafting, and Brow Lift
1. Transposition of temporalis
Transposition of the temporalis muscle can be used to reanimate the face and to provide lid closure by using the fifth cranial nerve. Strips from the muscle and fascia are placed in the upper and lower lids as an encircling sling. Patients initiate movement by chewing or clenching their teeth.
2. Facial nerve grafting or hypoglossal-facial nerve anastomosis
Reinnervation of the facial nerve by means of facial nerve grafting or hypoglossal-facial nerve anastomosis can be used in cases of clinically significant permanent paralysis to help restore relatively normal function to the orbicularis oculi muscle or eyelids.
3. Direct brow lift
Brow ptosis is repaired with a direct brow lift. Care should be taken in the presence of corneal decompensation because lifting the brow can cause worsening of lagophthalmos, especially if lid closure is poor. A gold-weight implant can be placed or lower-lid resuspension can be performed simultaneously to prevent this complication.
 
Nursing Management
Teaching patients with Bell's palsy to care for them at home is an important nursing priority.
 
Teaching Eye Care
Because the eye usually does not close completely, the blink reflex is diminished, so the eye is vulnerable to injury from dust and foreign particles. Corneal irritation and ulceration may occur. Distortion of the lower lid alters the proper drainage of tears. Encourage the client for the following:
  • Cover the eye with a protective shield at night.
  • Apply eye ointment to keep eyelids closed during sleep.
  • Close the paralyzed eyelid manually before going to sleep.
  • Wear wraparound sunglasses or goggles to decrease normal evaporation from the eye.
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Teaching about Maintaining Muscle Tone
  • Show patient how to perform facial massage with gentle.
  • Upward motion several times daily when the patient can tolerate the massage.
  • Demonstrate facial exercises, such as wrinkling the forehead.
  • Blowing out the cheeks, and whistling, in an effort to prevent muscle atrophy.
  • Instruct patient to avoid exposing the face to cold and drafts.
 
Diet and Nutrition
  • Instruct patient to chew on the unaffected side of his mouth.
  • Provide soft and nutritionally balanced diet. Eliminate hot fluids and foods.
  • Give frequent mouth care, being particularly careful to remove residues of food that collects between the cheeks and gums.
 
TRIGEMINAL NEURALGIA (‘TIC DOULOUREUX’)
Fig. 6.3: Trigeminal nerve
The trigeminal nerve (also called the fifth cranial nerve) is one of the main nerves of the face. It comes through the skull from the brain in front of the ear. It is called tri geminal as it splits into three main branches. Each branch divides into many smaller nerves. The nerves from the first branch go to scalp, forehead and around eye. The nerves from second branch go to the area around cheek. The nerves from the third branch go to the area around jaw. The branches of the trigeminal nerve take sensations of touch and pain to the brain from face, teeth, and mouth. The trigeminal nerve also controls the muscles used in chewing and the production of saliva and tears.
In trigeminal neuralgia (TN) sudden pains that come from one or more branches of the trigeminal nerve. The pains are usually severe. The second and third branches are the most commonly affected. Therefore, the pain is usually around the cheek or jaw or both. The first branch is less commonly affected, so pain over forehead and around eye is less common. Trigeminal neurolagia usually affects one side of face. Rarely.
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Etiology
  • Tumor
  • Multiple sclerosis
  • Abnormality of the base of the skull.
 
Signs and Symptoms
Triggers of pain attacks include the following:
  • Chewing, talking, or smiling
  • Drinking cold or hot fluids
  • Touching, shaving, brushing teeth, blowing the nose
  • Encountering cold air from an open automobile window.
Pain localization is as follows:
  • Patients can localize their pain precisely.
  • The pain commonly runs along the line dividing either the mandibular and maxillary nerves or the mandibular and ophthalmic portions of the nerve.
  • The pain shoots from the corner of the mouth to the angle of the jaw.
  • Pain jolts from the upper lip or canine teeth to the eye and eyebrow.
  • Pain involves the ophthalmic branch of the facial nerve.
The pain has the following qualities:
  • Characteristically severe, paroxysmal, and lancinating.
  • Commences with a sensation of electrical shocks in the affected area.
  • Begins to fade within seconds, only to give way to a burning ache lasting seconds to minutes.
  • Pain fully abates between attacks, even when they are severe and frequent.
  • Attacks may provoke patients to grimace, wince, or make an aversive head movement, as if trying to escape the pain, thus producing an obvious movement, or tic, hence called ‘tic douloureux’.
 
Types of ‘Tic Douloureux’
Trigeminal neuralgia can be split into different categories depending on the type of pain. These are:
  • Trigeminal neuralgia type 1 (TN1) is the classic form of trigeminal neuralgia. The piercing and stabbing pain only happens at certain times and is not constant. This type of neuralgia is known as idiopathic.
  • Trigeminal neuralgia type 2 (TN2) can be referred to as atypical trigeminal neuralgia. Pain is more constant and involves aching, throbbing and burning sensations.
  • Symptomatic trigeminal neuralgia (STN) is when pain results from an underlying cause, such as multiple sclerosis.
 
Management
 
Medical Management
  • The anticonvulsant carbamazepine is the first line treatment, second line medications include baclofen, lamotrigine, oxcarbazepine, phenytoin, gabapentin, pregabalin, and sodium valproate.
  • 360Low doses of some antidepressants such as amitriptyline are thought to be effective in treating neuropathic pain.
  • Duloxetine can also be used in some cases of neuropathic pain, and as it is also an antidepressant can be particularly helpful where neuropathic pain and depression are combined.
  • Opiates such as morphine and oxycodone can be prescribed, and there is evidence of their effectiveness on neuropathic pain, especially if combined with gabapentin.
  • Gallium maltolate in a cream or ointment base has been reported to relieve refractory postherpetic trigeminal neuralgia.
 
Deep Brain Stimulation
It involves delivering an electrical pulse to a part of the brain using a probe. A scanning technique (usually MRI or CT) is used to make sure the probe is in the right place.
 
Surgical Management
An operation is an option if medication does not work or causes troublesome side-effects. Basically, surgery for trigeminal neurolagia falls into two categories:
  • Decompression surgery: This means an operation to relieve the pressure on the trigeminal nerve. As trigeminal neurolagia are due to a blood vessel in the brain pressing on the trigeminal nerve as it leaves the skull. An operation can ease the pressure from the blood vessel (decompress the nerve) and therefore ease symptoms. This operation has the best chance of long-term relief of symptoms. However, it is a major operation involving a general anesthetic and brain surgery to get to the root of the nerve within the brain. Although usually successful, there is a small risk of serious complications, such as a stroke or deafness, following this operation.
  • Ablative surgical treatments: Ablative means to destroy. There are various procedures that can be used to destroy the root of the trigeminal nerve and thus ease symptoms. For example, one procedure is called stereotactic radiosurgery (gamma knife surgery). This uses radiation targeted at the trigeminal nerve root to destroy the nerve root. The advantage of these ablative procedures is that they can be done much more easily than decompression surgery as they do not involve formal brain surgery. So, there is much less risk of serious complications or death than there is with decompression surgery.
  • Balloon compression: It works by injuring the insulation on nerves that are involved with the sensation of light touch on the face. The procedure is performed in an operating room under general anesthesia. A tube called a cannula is inserted through the cheek and guided to where one branch of the trigeminal nerve passes through the base of the skull. A soft catheter with a balloon tip is threaded through the cannula and the balloon is inflated to squeeze part of the nerve against the hard edge of the brain covering and the skull. After about a minute the balloon is deflated and removed, along with the catheter and cannula. Balloon compression is generally an outpatient procedure, although sometimes the patient may be kept in the hospital overnight. Pain relief usually lasts one to two years.
  • Glycerol injection: It is also generally an outpatient procedure in which the individual is sedated with intravenous medication. A thin needle is passed through the cheek, next to the mouth, and guided through the opening in the base of the skull where the third 361division of the trigeminal nerve (mandibular) exits. The needle is moved into the pocket of spinal fluid that surrounds the trigeminal nerve center. The procedure is performed with the person sitting up, since glycerol is heavier than spinal fluid and will then remain in the spinal fluid around the ganglion. The glycerol injection bathes the ganglion and damages the insulation of trigeminal nerve fibers. This form of rhizotomy is likely to result in recurrence of pain within a year to two years. However, the procedure can be repeated multiple times.
  • Radiofrequency thermal lesioning (also known as ‘RF Ablation’ or ‘RF Lesion’): It is most often performed on an outpatient basis. The individual is anesthetized and a hollow needle is passed through the cheek through the same opening at the base of the skull where the balloon compression and glycerol injections are performed. The individual is briefly awakened and a small electrical current is passed through the needle, causing tingling in the area of the nerve where the needle tips rests. When the needle is positioned so that the tingling occurs in the area of TN pain, the person is then sedated and the nerve area is gradually heated with an electrode, injuring the nerve fibers. The electrode and needle are then removed and the person is awakened. The procedure can be repeated until the desired amount of sensory loss is obtained; usually a blunting of sharp sensation, with preservation of touch.
Fig. 6.4: RF Ablation
  • Stereotactic radiosurgery (Gamma Knife, Cyber Knife) uses computer imaging to direct highly focused beams of radiation at the site where the trigeminal nerve exits the brain stem. This causes the slow formation of a lesion on the nerve that disrupts the transmission of sensory signals to the brain.
  • Microvascular decompression (MVD): It is the most invasive of all surgeries for trigeminal neurolagia, but also offers the lowest probability that pain will return. About half of individuals undergoing MVD for trigeminal neurolagia will experience recurrent pain within 12 to 15 years. This inpatient procedure, which is performed under general anesthesia, requires that a small opening be made through the mastoid bone behind the ear. While viewing the trigeminal nerve through a microscope or endoscope, the surgeon moves away the vessel (usually an artery) that is compressing the nerve and 362places a soft cushion between the nerve and the vessel. Unlike rhizotomies, the goal is not to produce numbness in the face after this surgery. Individuals generally recuperate for several days in the hospital following the procedure, and will generally need to recover for several weeks after the procedure.
  • Neurectomy (also called partial nerve section): Which involves cutting part of the nerve, maybe performed near the entrance point of the nerve at the brain stem during an attempted microvascular decompression if no vessel is found to be pressing on the trigeminal nerve. Neurectomies also maybe performed by cutting superficial branches of the trigeminal nerve in the face. When done during microvascular decompression, a neurectomy will cause more long-lasting numbness in the area of the face that is supplied by the nerve or nerve branch that is cut. However, when the operation is performed in the face, the nerve may grow back and in time sensation may return. With neurectomy, there is risk of creating anesthesia dolorosa.
 
Nursing Management
 
Nursing Interventions
  • Instruct the client to avoid factors that can trigger the attack and result in exhaustion and fatigue.
  • Avoid foods that are too cold or too hot.
  • Chew foods in the affected side.
  • Use cotton pads gently, wash face and for oral hygiene.
  • Provide teaching to clients who have sensory loss as a result of a treatment.
  • Inspection of the eye for foreign bodies, which the client will not be able to feel, should be done several times a day.
  • Warm normal saline irrigation of the affected eye two to three times a day is helpful in preventing corneal infection.
  • Dental check ups every 6 months is encouraged, since dental caries will not produce pain.
  • Explain to the client and his family the disease and its treatments.
 
PARKINSONISM
Parkinson's disease is a neurodegenerative disorder which leads to progressive deterioration of motor function due to loss of dopamine-producing brain cells and is characterized by progressive loss of muscle control, which leads to trembling of the limbs and head while at rest, stiffness, slowness, and impaired balance.
 
Etiology and Risk Factors
  • Age is the largest risk factor for the development and progression of Parkinson's disease. Most people who develop Parkinson's disease are older than 60 years years of age.
  • Men are affected about 1.5 to 2 times more often than women.
  • A small number of individuals are at increased risk because of a family history of the disorder.
  • Head trauma, illness, or exposure to environmental toxins such as pesticides and herbicides maybe a risk factor.
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Signs and Symptoms
  • Tremors: Trembling in fingers, hands, arms, feet, legs, jaw, or head. Tremors most often occur while the individual is resting, but not while involved in a task. Tremors may worsen when an individual is excited, tired, or stressed.
  • Rigidity: Stiffness of the limbs and trunk, which may increase during movement. Rigidity may produce muscle aches and pain. Loss of fine hand movements can lead to cramped handwriting (micrographia) and may make eating difficult.
  • Bradykinesia: Slowness of voluntary movement. Over time, it may become difficult to initiate movement and to complete movement. Bradykinesia together with stiffness can also affect the facial muscles and result in an expressionless, ‘mask-like’ appearance.
  • Postural instability: Impaired or lost reflexes can make it difficult to adjust posture to maintain balance. Postural instability may lead to falls.
  • Parkinsonian gait: Individuals with more progressive Parkinson's disease develop a distinctive shuffling walk with a stooped position and a diminished or absent arm swing. It may become difficult to start walking and to make turns. Individuals may freeze in mid-stride and appear to fall forward while walking.
Fig. 6.5: Clinical manifestations
 
Secondary Symptoms of Parkinson's Disease
While the main symptoms of Parkinson's disease are movement-related, progressive loss of muscle control and continued damage to the brain can lead to secondary symptoms. Some of the secondary symptoms include:
  • Anxiety, insecurity, and stress
  • Confusion, memory loss, and dementia
  • 364Constipation
  • Depression
  • Difficulty swallowing and excessive salivation
  • Diminished sense of smell
  • Increased sweating
  • Male erectile dysfunction
  • Skin problems
  • Slowed, quieter speech, and monotone voice
  • Urinary frequency/urgency
  • Slow blinking
  • Stooped position.
 
Parkinson's Disease Stages
  • Stage one: During this initial phase of the disease, a patient usually experiences mild symptoms. These symptoms may inconvenience the day-to-day tasks the patient would otherwise complete with ease. Typically these symptoms will include the presence of tremors or experiencing shaking in one of the limbs.
  • Stage two: In the second stage of Parkinson's disease, the patient's symptoms are bilateral, affecting both limbs and both sides of the body. The patient usually encounters problems walking or maintaining balance and the inability to complete normal physical tasks becomes more apparent.
  • Stage three: Stage three symptoms of Parkinson's disease can be rather severe and include the inability to walk straight or to stand. There is a noticeable slowing of physical movements in stage three.
  • Stage four: This stage of the disease is accompanied by severe symptoms of Parkinson's. Walking may still occur, but it is often limited and rigidity and bradykinesia are often visible. During this stage, most patients are unable to complete day-to-day tasks, and usually cannot live on their own. The tremors or shakiness that takes over during the earlier stages however, may lessen or become nonexistent for unknown reasons during this time.
  • Stage five: The last or final stage of Parkinson's disease usually takes over the patients physical movements. The patient is usually unable to take care of himself or herself and may not be able to stand or walk during this stage. A patient at stage five usually requires constant one-on-one nursing care.
 
Pathophysiology
  • A substance called dopamine acts as a messenger between two brain areas—the substantia nigra and the corpus striatum—to produce smooth, controlled movements.
  • Most of the movement related symptoms of Parkinson's disease are caused by a lack of dopamine due to the loss of dopamine—producing cells in the substantia nigra.
  • When the amount of dopamine is too low, communication between the substantia nigra and corpus striatum becomes ineffective, and movement becomes impaired.
  • The greater the loss of dopamine, the worse the movement-related symptoms. Other cells in the brain also degenerate to some degree and may contribute to non—movement related symptoms of Parkinson's disease.
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Diagnostic Evaluation
  • At least two of the three major symptoms are present (tremor at rest, muscle rigidity, and slowness).
  • The onset of symptoms started on one side of the body.
  • Symptoms are not due to secondary causes such as medication or strokes in the area controlling movement.
  • Symptoms are significantly improved with levodopa.
 
Management
  • Medical management
  • Levodopa, Sinemet, levodopa and Carbidopa
  • Pramipexole, Ropinirole, Bromocriptine
  • Selegiline, Rasagiline
  • Amantadine or anticholinergic medications to reduce early or mild tremors
  • Entacapone
Other medications may include
  • Memantine, rivastigmine, galantamine for cognitive difficulties
  • Antidepressants for mood disorders
  • Gabapentin, duloxetine for pain
  • Fludrocortisone, Midodrine, Botox, Sidenafil for autonomic dysfunction
  • Armodafinil, clonazepam, zolpidem for sleep disorders.
 
Nursing Management
 
Nursing Diagnosis
  • Impaired Physical Mobility related to stiffness and muscle weakness
  • Self-care deficits related to neuromuscular weakness, decreased strength, loss of muscle control/coordination
  • Impaired bowel elimination: Constipation related to medication and decreased activity
  • Imbalanced nutrition: Less than body requirements related to tremor, slowing the process of eating, difficulty chewing and swallowing
  • Impaired verbal communication related to the decrease in the volume of speech, delayed speech, inability to move facial muscles
  • Ineffective individual coping related to depression and dysfunction due to disease progression
  • Knowledge deficit related to information resources inadequate maintenance procedures.
 
Interventions
  • Examine existing mobility and observation of an increase in damage
  • Do exercise program increases muscle strength
  • Encourage bath and massage the muscle
  • Help clients perform ROM exercises, self-care according to tolerance
  • 366Collaboration physiotherapists for physical exercise
  • Assess the ability and the rate of decline and the scale of 0–4 to perform ADL
  • Avoid what not to do the client and help if needed
  • Collaborative provision of laxatives and consult a doctor of occupational therapy
  • Teach and support the client during the client's activities
  • Environmental modifications
  • Refer to speech therapy
  • Teach clients to use facial exercises and breathing methods to correct the words, volume, and intonation
  • Breathe deeply before speaking to increase the volume and number of words in sentences of each breath
  • Practice speaking in short sentences, reading aloud in front of the glass or into a voice recorder (tape recorder) to monitor progress.
 
MYASTHENIA GRAVIS
  • Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia gravis, which is Latin and Greek in origin, literally means ‘grave muscle weakness’.
 
Etiology
 
Autoimmunity
In myasthenia gravis, the immune system produces antibodies that block or destroy muscles receptor sites for a neurotransmitter called acetylcholine. Antibodies may also block the function of a protein called a muscle-specific receptor tyrosine kinase. This protein is involved in forming the nerve-muscular junction. When antibodies block the function of this protein, it may lead to myasthenia gravis.
 
Thymus Gland
Tumors of the thymus (thymomas). Usually, thymomas are not cancerous. In some people myasthenia gravis is not caused by antibodies blocking acetylcholine or the muscle-specific receptor tyrosine kinase. This type of myasthenia gravis is called antibody-negative myasthenia gravis. Antibodies against another protein, called lipoprotein-related protein 4, may play a part in the development of this condition.
 
Genetic Factors
Rarely, mothers with myasthenia gravis have children who are born with myasthenia gravis (neonatal myasthenia gravis). If treated promptly, children generally recover within two months after birth.
 
Factors that can Worsen Myasthenia Gravis
  • Fatigue
  • Illness
  • Stress
  • 367Extreme heat
  • Some medications–such as beta blockers, quinidine gluconate, quinidine sulfate, quinine (Qualaquin), phenytoin (Dilantin), certain anesthetics and some antibiotics
 
Signs and Symptoms
Eye muscles
In more than half the people who develop myasthenia gravis, their first signs and symptoms involve eye problems, such as:
  • Drooping of one or both eyelids (ptosis)
  • Double vision (diplopia), which maybe horizontal or vertical, and improves or resolves when one eye is closed.
Face and throat muscles
In about 15 percent of people with myasthenia gravis, the first symptoms involve face and throat muscles, which can cause:
  • Altered speaking
  • Difficulty swallowing
  • Problems chewing
  • Limited facial expressions.
Neck and limb muscles
Myasthenia gravis can cause weakness in neck, arms, and legs, but this usually happens along with muscle weakness in other parts of body, such as eyes, face or throat.
The disorder usually affects arms more often than legs. However, if it affects legs, patient may waddle when walk. If neck is weak, it may be hard to hold up head
Patient may have difficulty in:
  • Breathing
  • Seeing
  • Swallowing
  • Chewing
  • Walking
  • Using arms or hands
  • Holding up head.
 
Diagnostic Evaluation
Diagnosis may be made on the basis of neurological health by testing:
  • Reflexes
  • Muscle strength
  • Muscle tone
  • Senses of touch and sight
  • Coordination
  • Balance.
The key sign that points to the possibility of myasthenia gravis is muscle weakness that improves with rest. Tests to help confirm the diagnosis may include:
  • 368Edrophonium test: Injection of the chemical edrophonium chloride (Tensilon) may result in a sudden, although temporary, improvement in muscle strength. This is an indication that the patient may have myasthenia gravis.
  • Edrophonium chloride blocks an enzyme that breaks down acetylcholine, the chemical that transmits signals from nerve endings to muscle receptor sites.
  • Ice pack test: In this test, a bag filled with ice is placed on eyelid. After two minutes, doctor removes the bag and analyzes droopy eyelid for signs of improvement.
  • Blood analysis: A blood test may reveal the presence of abnormal antibodies that disrupt the receptor sites where nerve impulses signal muscles to move.
  • Repetitive nerve stimulation: In this nerve conduction study, electrodes are attached to skin over the muscles to be tested.
  • Single-fiber electromyography (EMG): Electromyography (EMG) measures the electrical activity traveling between brain and muscle. It involves inserting a fine wire electrode through skin and into a muscle.
  • Imaging scans: CT scan or an MRI to check if there is a tumor or other abnormality in thymus.
  • Pulmonary function tests: To evaluate whether condition is affecting breathing.
 
Management
 
Medical Management
  • Cholinesterase inhibitors: Medications such as pyridostigmine enhance communication between nerves and muscles. These medications do not cure the underlying condition, but they may improve muscle contraction and muscle strength.
  • Corticosteroids: Corticosteroids such as prednisone inhibit the immune system, limiting antibody production.
  • Prolonged use of corticosteroids, however, can lead to serious side effects, such as bone thinning, weight gain, diabetes, and increased risk of some infections.
  • Immunosuppressants: Such as azathioprine, mycophenolate mofetil, cyclosporine or tacrolimus.
  • Side effects of immunosuppressants can be serious and may include nausea, vomiting, gastrointestinal upset, increased risk of infection, liver damage and kidney damage.
  • Plasmapheresis: This procedure uses a filtering process similar to dialysis. Blood is routed through a machine that removes the antibodies that block transmission of signals from nerve endings to muscles’ receptor sites.
  • Other risks associated with plasmapheresis include a drop in blood pressure, bleeding, heart rhythm problems or muscle cramps. Some people may also develop an allergic reaction to the solutions used to replace the plasma.
  • Intravenous immunoglobulin (IVIg): This therapy provides normal antibodies, which alters the immune system response. IVIg has a lower risk of side effects than do plasmapheresis and immune-suppressing therapy. Side effects, which usually are mild, may include chills, dizziness, headaches and fluid retention.
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Surgical Management
About 15 percent of the people with myasthenia gravis have a tumor in their thymus gland, a gland under the breastbone that is involved with the immune system. If patient is having a tumor, called a thymoma, thymectomy maybe performed as an open surgery or as a minimally invasive surgery.
Minimally invasive thymectomy may include:
Video-assisted thymectomy: In one form of this surgery, surgeons make a small incision in neck and use a long thin camera (video endoscope) and small instruments to visualize and remove the thymus gland through neck.
  • Robot-assisted thymectomy: In a robot-assisted thymectomy, surgeons make several small incisions in the side of chest. Surgeons conduct the procedure to remove the thymus gland using a robotic system, which includes a camera arm and mechanical arms
 
Nursing Management
 
Nursing Diagnosis
  • Ineffective breathing pattern related to respiratory muscle weakness
  • Impaired physical mobility related to weakness of voluntary muscles
  • Risk for aspiration related to the weakness of bulbar muscles
  • Self-Care deficit related to muscle weakness, general fatigue
  • Imbalanced Nutrition: Less than body requirements related to dysphagia, intubation, or muscle paralysis.
 
Interventions
  • Assess the breathing pattern
  • Administer oxygen in case of emergency arrest
  • Encourage deep breathing exercise to strengthen the respiratory muscle tone
  • Install grab bars or railings in places
  • Keep floors clean, and move any loose rugs out of areas.
  • Use electric appliances and power tools
  • Try using an electric toothbrush, electric can openers and other electrical tools to perform tasks when possible to save the energy
  • Wearing an eye patch if have double vision, as this can help relieve the problem
  • Try wearing the eye patch while you write, read or watch television. Periodically switch the eye patch to the other eye to help reduce eyestrain
  • Encourage to eat when patient have good muscle strength
  • Take time chewing the food, and take a break between bites of food
  • Encourage to eat small meals several times a day may be easier to handle
  • Encourage to eat mainly soft foods and avoid foods that require more chewing, such as raw fruits or vegetables.
 
GUILLAIN-BARRE SYNDROME OR INFECTIOUS POLYNEURITIS
  • Guillain-Barre Syndrome (GBS) is an acute condition that involves progressive muscle weakness or paralysis. It is an autoimmune disorder in which the body's immune 370system attacks its own nervous system, causing inflammation that damages the myelin sheath of the nerve. This damage (demyelinazation) slows or stops the conduction of impulses through the nerve. The impairment of nerve impulses to the muscles leads to symptoms that may include muscle weakness, paralysis, spasms, numbness, tingling or pins-and-needle sensations and tenderness.
 
Etiology
  • Campylobacter jejuni infection: Campylobacter infection is also the most common risk factor for Guillain-Barre. It is often found in undercooked food, especially poultry.
  • Influenza
  • Cytomegalovirus
  • Epstein-Barr virus infection
  • Mycoplasma pneumonia
  • HIV or AIDS
 
Pathophysiology
 
Signs and Symptoms
  • Loss of tendon reflexes in the arms and legs
  • Tingling or numbness (mild loss of sensation)
  • Muscle tenderness or pain (maybe a cramp-like pain)
  • Uncoordinated movement (cannot walk without help)
  • Low blood pressure or poor blood pressure control
  • Abnormal heart rate
  • Blurred vision and double vision
  • 371Clumsiness and falling
  • Difficulty moving face muscles
  • Muscle contractions
  • Feeling the heartbeat.
 
Emergency Symptoms
  • Breathing temporarily stops
  • Cannot take a deep breath
  • Difficulty breathing
  • Difficulty swallowing
  • Drooling
  • Fainting
  • Feeling light-headed when standing.
 
Diagnostic evaluation
  • Spinal tap: This test is also referred to as a lumbar puncture. A spinal tap involves taking a small amount of fluid from the spine in the lower back. The fluid is then tested to detect protein levels. People with Guillain-Barre typically have higher-than-normal levels of protein in their cerebrospinal fluid.
  • Electromyography: An electromyography is a nerve function test. It reads electrical activity from the muscles and help to learn if the muscle weakness is caused by nerve damage or muscle damage.
 
Management
  • Physical therapy: Before recovery, a caregiver may need to manually move the arms and legs. This will help keep the muscles strong and mobile. After recovery, physical therapy will helps to strengthen and flex the muscles again. Therapy includes massages, exercises, and frequent position changes.
  • Plasmapheresis: The immune system produces proteins called antibodies that normally attack harmful foreign substances, such as bacteria and viruses. Guillain-Barre occurs when the immune system mistakenly makes antibodies that attack the healthy nerves of the nervous system. Plasmapheresis is intended to remove the antibodies attacking the nerves from the blood. During this procedure, blood is removed from the body by machine that removes the antibodies from the blood and then the blood is returned to the body.
  • Intravenous immunoglobulin: High doses of immunoglobulin can also help to block the antibodies causing Guillain-Barre.
 
Nursing Management
 
Nursing Diagnosis
  • Ineffective breathing pattern and airway clearance related to respiratory muscle weakness or paralysis, decreased cough reflex, immobilization.
  • Impaired physical mobility related to paralysis, ataxia.
  • 372Risk for impaired skin integrity, pressure sores related to muscle weakness, paralysis, impaired sensation, changes in nutrition, incontinence.
  • Imbalanced nutrition, less than body requirements related to difficulty chewing, swallowing, fatigue, limb paralysis.
  • Impaired elimination: Constipation, diarrhea, related to inadequate food intake, immobilization.
  • Impaired verbal communication related to the VII cranial nerve paralysis, tracheostomy.
  • Ineffective coping related to the patient's disease state.
 
Interventions
  • Monitor respiratory status through vital capacity measurements, rate and depth of respirations, and breath sounds.
  • Monitor level of muscle weakness as it ascends toward respiratory muscles. Watch for breathlessness while talking which is a sign of respiratory fatigue.
  • Monitor the patient for signs of impending respiratory failure.
  • Monitor gag reflex and swallowing ability.
  • Position patient with the head of bed elevated to provide for maximum chest excursion.
  • Avoid giving opioids and sedatives that may depress respirations.
  • Position patient correctly and provide range-of-motion exercises.
  • Provide good body alignment, range-of-motion exercises, and change of position to prevent complications such as contractures, pressure sores, and dependent edema.
  • Ensure adequate nutrition without the risk of aspiration.
  • Encourage physical and occupational therapy exercises to help the patient regain strength during rehabilitation phase.
  • Provide assistive devices as needed (cane or wheelchair) to maximize independence and activity.
  • If verbal communication is possible, discuss the patient's fears and concerns.
  • Provide choices in care to give the patient a sense of control.
  • Teach patient about breathing exercises or use of an incentive spirometer to re-establish normal breathing patterns.
  • Instruct patient to wear good supportive and protective shoes while out of bed to prevent injuries due to weakness and paresthesia.
  • Instruct patient to check feet routinely for injuries because trauma may go unnoticed due to sensory changes.
  • Urge the patient to maintain normal weight because additional weight will further stress monitor function.
  • Encourage scheduled rest periods to avoid fatigue.
 
MULTIPLE SCLEROSIS (MS)
  • Multiple sclerosis (MS) is a disease in which immune system attacks the protective sheath (myelin) that covers nerves. Myelin damage disrupts communication between brain and the rest of body. Ultimately, the nerves themselves may deteriorate a process that is currently irreversible.
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Etiology and Risk Factors
These factors may increase risk of developing multiple sclerosis:
  • Age: MS can occur at any age, but most commonly affects people between the ages of 15 and 60.
  • Sex: Women are about twice as likely as men are to develop MS.
  • Family history: If one of parents or siblings has had MS, you are at higher risk of developing the disease.
  • Certain infections: A variety of viruses have been linked to MS, including Epstein-Barr, the virus that causes infectious mononucleosis.
  • Race: White people are at highest risk of developing MS.
  • Climate: MS is far more common in countries with temperate climates.
  • Certain autoimmune diseases: Like thyroid disease, type 1 diabetes or inflammatory bowel disease.
  • Smoking: Smokers who experience an initial event of symptoms that may signal MS are more likely than nonsmokers to develop a second event that confirms relapsing-remitting MS.
 
Pathophysiology
 
Signs and Symptoms
Signs and symptoms of multiple sclerosis vary, depending on the location of affected nerve fibers. Multiple sclerosis signs and symptoms may include:
  • Numbness or weakness in one or more limbs that typically occurs on one side of body at a time, or the legs and trunk
  • Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement
  • 374Double vision or blurring of vision
  • Tingling or pain in parts of body
  • Electric-shock sensations that occur with certain neck movements, especially bending the neck forward
  • Tremor, lack of coordination or unsteady gait
  • Slurred speech
  • Fatigue
  • Dizziness
  • Problems with bowel and bladder function.
 
Complications
People with multiple sclerosis also may develop:
  • Muscle stiffness or spasms
  • Paralysis, typically in the legs
  • Problems with bladder, bowel or sexual function
  • Mental changes, such as forgetfulness or mood swings
  • Depression
  • Epilepsy.
 
Diagnostic Evaluation
  • Blood tests: It helps to rule out infectious or inflammatory diseases with symptoms similar to MS.
  • Spinal tap (lumbar puncture): In which a small sample of fluid is removed from spinal canal for laboratory analysis. This sample can show abnormalities in white blood cells or antibodies that are associated with MS. Spinal tap can also help rule out viral infections and other conditions with symptoms similar to MS.
  • MRI: Which can reveal areas of MS (lesions) on brain and spinal cord.
 
Management
  • Corticosteroids: Such as oral prednisone and intravenous methylprednisolone, are prescribed to reduce nerve inflammation. Side effects may include insomnia, increased blood pressure, mood swings, and fluid retention.
  • Plasma exchange (plasmapheresis): The liquid portion of part of blood (plasma) is removed and separated from blood cells. The blood cells are then mixed with a protein solution (albumin) and put back into body.
  • Beta interferons: These medications, which are injected under the skin or into muscle, can reduce the frequency and severity of relapses. Beta interferons can cause side effects such as flu-like symptoms and injection-site reactions.
  • Glatiramer acetate: This medication may help block immune system's attack on myelin. The medication must be injected beneath the skin. Side effects may include skin irritation at the injection site.
  • Dimethyl fumarate: This twice-daily oral medication can reduce relapses. Side effects may include flushing, diarrhea, nausea and lowered white blood cell count.
  • 375Fingolimod: This once-daily oral medication reduces relapse rate. Heart rate must be monitored for six hours after the first dose because heartbeat may be slowed. Other side effects include high blood pressure and blurred vision.
  • Teriflunomide: This once-daily medication can reduce relapse rate. Teriflunomide can cause liver damage, hair loss and other side effects. It is also known to be harmful to a developing fetus.
  • Natalizumab: This medication is designed to block the movement of potentially damaging immune cells from bloodstream to brain and spinal cord. The medication increases the risk of a viral infection of the brain called progressive multifocal leukoencephalopathy. It is generally given to people who have more severe or active MS, or who do not respond to or cannot tolerate other treatments.
  • Mitoxantrone: This immunosuppressant drug can be harmful to the heart and is associated with development of blood cancers. Mitoxantrone is usually used only to treat severe, advanced M.
  • Physical therapy: A physical or occupational therapist can teach like stretching and strengthening exercises.
  • Muscle relaxants: Muscle relaxants such as baclofen and tizanidine may help.
  • Medications to reduce fatigue.
  • Other medications: Medications may also be prescribed for depression, pain, and bladder or bowel control problems that are associated with MS.
 
Nursing Management
 
Nursing Diagnosis
1. Fatigue related to decreased energy production, increased energy requirements to perform activities
Interventions
  • Note and accept presence of fatigue
  • Identify and review factors affecting ability to be active: Temperature extremes, inadequate food intake, insomnia, use of medications, time of day.
  • Schedule ADLs in the morning if appropriate.
  • Determine need for walking aids. Provide braces, walkers, or wheelchairs. Review safety considerations.
  • Accept when patient is unable to do activities.
  • Plan care consistent rest periods between activities. Encourage afternoon nap.
  • Assist with physical therapy. Increase patient comfort with massages and relaxing baths.
  • Stress need for stopping exercise or activity just short of fatigue.
  • Investigate appropriateness of obtaining a service dog.
  • Recommend participation in groups involved in fitness or exercise.
2. Self-care deficit related to neuromuscular, perceptual impairment
Interventions
  • Determine current activity level and physical condition. Assess degree of functional impairment using 0–4 scale.
  • 376Encourage patient to perform self-care to the maximum of ability as defined by patient. Do not rush patient.
  • Assist according to degree of disability allow as much autonomy as possible.
  • Encourage patient input in planning schedule.
  • Allot sufficient time to perform tasks, and display patience when movements are slow.
  • Encourage scheduling activities early in the day or during the time when energy level is best.
  • Note presence of fatigue.
  • Anticipate hygienic needs and calmly assist as necessary with care of nails, skin, and hair; mouth care; shaving.
  • Provide assistive devices and aids as indicated: Shower chair, elevated toilet seat with arm supports.
  • Provide massage and active or passive ROM exercises on a regular schedule. Encourage use of splints or footboards as indicated.
  • Reposition frequently when patient is immobile. Provide skin care to pressure points, such as sacrum, ankles, and elbows. Position properly and encourage to sleep prone as tolerated.
  • Consult with physical and occupational therapist.
  • Problem-solve ways to meet nutritional and fluid needs.
  • Encourage stretching and toning exercises and use of medications, cold packs, and splints and maintenance of proper body alignment, when indicated.
3. Low self-esteem related to change in structure and function
Interventions
  • Establish and maintain a therapeutic nurse-patient relationship, discussing fears and concerns.
  • Acknowledge reality of grieving process related to actual or perceived changes. Help patient deal realistically with feelings of anger and sadness.
  • Support use of defense mechanisms, allowing patient to deal with information in own time and way.
  • Note withdrawn behaviors and use of denial or over concern with body and disease process.
  • Review information about course of disease, possibility of remissions, prognosis.
  • Provide accurate verbal and written information about what is happening and discuss with patient.
  • Explain that labile emotions are not unusual. Problem-solve ways to deal with these feelings.
  • Assess interaction between patient. Note changes in relationship.
  • Note presence of depression and impaired thought processes, expressions of suicidal ideation.
  • Discuss use of medications and adjuncts to improve sexual function.
  • Provide open environment for patient to discuss concerns about sexuality, including management of fatigue, spasticity, arousal, and changes in sensation.
3774. Powerlessness and hopelessness related to Illness-related regimen, unpredictability of disease
Intervention
  • Note behaviors indicative of powerlessness or hopelessness. Patient may say statements of despair.
  • Discuss plans for the future. Suggest visiting alternative care facilities, taking a look at the possibilities for care as condition changes.
  • Encourage and assist patient to identify activities he or she would like to be involved in within the limits of his or her abilities.
  • Acknowledge reality of situation, at the same time expressing hope for patient.
  • Assist patient to identify factors that are under own control. List things that can or cannot be controlled.
  • Encourage patient to assume control over as much of own care as possible.
  • Discuss needs openly with patient, setting up agreed-on routines for meeting identified needs.
  • Incorporate patient's daily routine into home care schedule or hospital stay, as possible.
  • Refer to vocational rehabilitation as indicated.
5. Risk for ineffective coping related to physiological changes, psychological conflict and impaired judgment
Intervention
  • Assess current functional capacity and limitations; note presence of distorted thinking processes, labile emotions, cognitive dissonance.
  • Determine patient's understanding of current situation and previous methods of dealing with life's problems.
  • Discuss ability to make decisions, care for children or dependent adults, handle finances.
  • Maintain an honest, reality-oriented relationship.
  • Encourage verbalization of feelings and fears, accepting what patient says in a nonjudgmental manner.
  • Encourage patient to tape-record important information and listen to the recording periodically.
  • Provide clues for orientation: Calendars, clocks, notecards, and organizers.
  • Observe nonverbal communication: Posture, eye contact, movements, gestures, and use of touch. Compare with verbal content and verify meaning with patient as appropriate.
 
CEREBROVASCULAR ACCIDENT (STROKE)
  • A cerebrovascular accident is also called a CVA, brain attack, or stroke. It occurs when blood flow to a part of the brain is suddenly stopped and oxygen cannot get to that part. This lack of oxygen may damage or kill the brain cells. Death of a part of the brain may lead to loss of certain body functions controlled by that affected part and it last longer than 24 hours.
  • A transient ischemic attack (TIA)—also called a mini stroke, is a brief episode of symptoms similar to those have in a stroke. A transient ischemic attack is caused by a temporary decrease in blood supply to part of brain. It last less than five minutes.
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Etiology and Types
 
1. Ischemic Stroke
An ischemic stroke occurs when a blood clot blocks a blood vessel, preventing blood and oxygen from getting to a part of the brain. When a clot forms somewhere else in the body and gets lodged in a brain blood vessel, it is called an embolic stroke. When the clot forms in the brain blood vessel, it is called a thrombotic stroke.
 
2. Hemorrhagic Stroke
  • A hemorrhagic stroke occurs when a blood vessel ruptures, or hemorrhages, which then prevents blood from getting to part of the brain. The hemorrhage may occur in a blood vessel in the brain, or in the membrane that surrounds the brain. It maybe of the following types:
  • Intracerebral hemorrhage: In an intracerebral hemorrhage, a blood vessel in the brain bursts and spills into the surrounding brain tissue, damaging brain cells. Brain cells beyond the leak are deprived of blood and damaged. High blood pressure, trauma, vascular malformations, use of blood-thinning medications and other conditions may cause intracerebral hemorrhage.
  • Subarachnoid hemorrhage: In a subarachnoid hemorrhage, an artery on or near the surface of brain bursts and spills into the space between the surface of brain and skull. This bleeding is often signaled by a sudden, severe headache. A subarachnoid hemorrhage is commonly caused by the rupture of an aneurysm, a small sack-shaped or berry-shaped outpouching on an artery in the brain.
 
Risk Factors
  • High blood pressure
  • Cigarette smoking or exposure to second hand smoke
  • High cholesterol level
  • Diabetes
  • Overweight or obese
  • Physical inactivity
  • Obstructive sleep apnea
  • Cardiovascular disease, including heart failure, heart defects, heart infection or abnormal heart rhythm
  • Use of some birth control pills or hormone therapies that include estrogen
  • Heavy drinking
  • Use of drugs such as cocaine and methamphetamines
  • Having regular checkups after being diagnosed with preeclampsia
  • Personal or family history of stroke, heart attack or TIA.
  • Being age 55 or older
  • Race—Black has higher risk of stroke than people of other races
  • Gender—Stroke is more common in women than men, and more deaths from stroke occur in women.
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Pathophysiology
 
Signs and Symptoms
  • Difficulty walking
  • Dizziness
  • Loss of balance and coordination
  • Difficulty speaking or understanding others who are speaking
  • Numbness or paralysis in the face, leg, or arm, most likely on just one side of the body
  • Blurred or darkened vision
  • A sudden headache, especially when accompanied by nausea, vomiting, or dizziness.
 
Diagnostic Evaluation
  • Physical examination
  • Personal and family history of heart disease, TIA or stroke
  • Blood tests: To evaluate the clotting time, bleeding time, etc.
  • Computerized tomography scan: Brain imaging plays a key role in determining a stroke and what type of stroke maybe experiencing. A CT scan uses a series of X-rays to create 380a detailed image of brain. A CT scan can show a brain hemorrhage, tumors, strokes and other conditions. A dye is injected into blood vessels to view blood vessels in neck and brain in greater detail.
  • Magnetic resonance imaging: An MRI uses powerful radio waves and magnets to create a detailed view of brain. An MRI can detect brain tissue damaged by an ischemic stroke and brain hemorrhages.
  • Carotid ultrasound: In this test, sound waves create detailed images of the inside of the carotid arteries in neck. This test shows buildup of fatty deposits (plaques) and blood flow in carotid arteries.
  • Cerebral angiogram: In this test, a thin, flexible tube (catheter) is inserted through a small incision, usually in groin, and guides it through major arteries and into carotid or vertebral artery. A dye is injected into blood vessels to make them visible under X-ray imaging. This procedure gives a detailed view of arteries in brain and neck.
  • Echocardiogram: This imaging technique uses sound waves to create a picture of heart. It can help to find the source of blood clots.
 
Management
 
Prevention
There are many risk factors for having a stroke. Correspondingly, there are many measures that can be taken to help prevent them. These preventive measures are similar to the actions that you would take to help prevent heart disease, and include the following:
  • Maintain normal blood pressure
  • Limit saturated fat and cholesterol intake
  • Refrain from smoking and drink alcohol in moderation
  • Control diabetes
  • Maintain a healthy weight
  • Get regular exercise
  • Eat a diet rich in vegetables and fruits.
 
Medical Management
  • Aspirin, an antithrombotic drug, is an immediate treatment after an ischemic stroke to reduce the likelihood of having another stroke. Aspirin prevents blood clots from forming.
  • Other blood-thinning drugs, such as heparin, warfarin, or aspirin in combination with extended release dipyridamole may also be used, but these are not usually used in the emergency room setting.
  • Intravenous injection of tissue plasminogen activator (TPA): Some people who are having an ischemic stroke can benefit from an injection of a recombinant tissue plasminogen activator (TPA), also called alteplase, usually given through a vein in the arm. This potent clot-busting drug needs to be given within 4.5 hours after stroke symptoms begin if it is given into the vein. This drug restores blood flow by dissolving the blood clot causing stroke.
  • Carotid endarterectomy: In a carotid endarterectomy, a surgeon removes fatty deposits (plaques) from carotid arteries. In this procedure, a small incision along the front of neck, opens carotid artery, and removes fatty deposits that block the carotid artery.
  • 381Angioplasty and stents: In an angioplasty, a surgeon inserts a catheter with a mesh tube and balloon on the tip into an artery in groin and guides it to the blocked carotid artery in neck. Surgeon inflates the balloon in the narrowed artery and inserts a mesh tube into the opening to keep artery from becoming narrowed after the procedure.
  • Surgical clipping: A surgeon places a tiny clamp at the base of the aneurysm, to stop blood flow to it. This can keep the aneurysm from bursting.
  • Coiling (endovascular embolization): In this procedure, a surgeon inserts a catheter into an artery in groin and guides it to brain using X-ray imaging. Then guides tiny detachable coils into the aneurysm (aneurysm coiling). The coils fill the aneurysm, which blocks blood flow into the aneurysm and causes the blood to clot.
 
Nursing Management
 
Nursing Diagnosis
  1. Ineffective cerebral tissue perfusion related to interruption of blood flow.
    Interventions
    • Determine factors related to individual situation, cause for coma, decreased cerebral perfusion and potential for increased ICP.
    • Monitor and document neurological status frequently and compare with baseline.
    • Monitor vital signs, i.e. Hypertension/hypotension, compare BP readings in botharms, Heart rate and rhythm, auscultate for murmurs, respirations, noting patterns and rhythm, e.g., periods of apnea after hyperventilation, Cheyne-Stokes respiration.
    • Evaluate pupils, noting size, shape, equality, light reactivity.
    • Document changes in vision, e.g., reports of blurred vision, alterations in visual field and perception.
    • Assess higher functions, including speech, if patient is alert.
    • Position with head slightly elevated and in neutral position.
    • Maintain bedrest, provide quiet environment, and restrict visitors as indicated. Provide rest periods between care activities, limit duration of procedures.
    • Prevent straining at stool, holding breath.
    • Assess for nuchal rigidity, twitching, increased restlessness, irritability, onset of seizure activity.
    • Administer supplemental oxygen as indicated.
    • Administer medications as indicated: Alteplase, Anticoagulants, e.g., warfarin sodium, low-molecular-weight heparin, antiplatelet agents, aspirin, dipyridamole, ticlopidine. Antihypertensives, peripheral vasodilators, e.g., cyclandelate, papaverine, isoxsuprine, steroids, e.g., dexamethasone.
    • Prepare for surgery, as appropriate, e.g., endarterectomy, microvascular bypass, cerebral angioplasty.
    • Monitor laboratory studies as indicated, e.g., prothrombin time (PT), activated partial thromboplastin time (aPTT) time, dilantin level.
  2. Impaired physical mobility related to neuromuscular abnormality.
    Interventions
    • Assess functional ability of impairment initially and on a regular basis.
    • Change positions at least every 2 hour (supine, sidelying) and possibly more often if placed on affected side.
    • 382Position in prone position once or twice a day if patient can tolerate.
    • Prop extremities in functional position, use footboard during the period of flaccid paralysis. Maintain neutral position of head.
    • Use arm sling when patient is in upright position, as indicated.
    • Evaluate use and need for positional aids and splints during spastic paralysis, place pillow under axillae to abduct arm, elevate arm and hand.
    • Observe affected side for color, edema, or other signs of compromised circulation.
    • Inspect skin regularly, particularly over bony prominences. Gently massage any reddened areas and provide aids such as sheepskin pads as necessary.
    • Begin active/passive range of motion exercise to all extremities.
    • Assist to develop sitting balance (e.g. raise head of bed, assist to sit on edge of bed, having patient use the strong arm to support body weight and strong leg to move affected leg, increase sitting time) and standing balance (e.g. put flat walking shoes on patient, support patient's lower back with hands while positioning own knees outside patient's knees, assist in using parallel bars/walkers).
    • Get patient up in chair as soon as vital signs are stable, except following cerebral hemorrhage.
    • Pad chair seat with foam or water-filled cushion, and assist patient to shift weight at frequent intervals.
    • Provide egg-crate mattress, water bed, flotation device, or specialized beds (e.g. kinetic), as indicated.
  3. Disturbed sensory perceptions related to disturbed sensory reception and neuromuscular dysfunction.
    Interventions
    • Observe behavioral responses, e.g., hostility, crying, inappropriate affect, agitation, hallucination.
    • Eliminate extraneous noise and stimuli as necessary.
    • Speak in calm, quiet voice, using short sentences. Maintain eye contact.
    • Reorient patient frequently to environment, staff, and procedures.
    • Evaluate for visual deficits. Note loss of visual field, changes in depth perception (horizontal/vertical planes), and presence of diplopia.
    • Approach patient from visually intact side. Leave light on, position objects to take advantage of intact visual fields. Patch affected eye if indicated.
    • Assess sensory awareness, e.g. differentiation of hot/cold, dull/sharp, position of body parts/muscle, joint sense.
    • Stimulate sense of touch; e.g. give patient objects to touch, grasp.
    • Protect from temperature extremes, assess environment for hazards. Recommend testing warm water with unaffected hand.
  4. Ineffective coping related to situational crisis and cognitive perceptual changes.
    Interventions
    • Assess extent of altered perception and related degree of disability. Determine functional independence measure score.
    • 383Identify meaning of the loss, dysfunction and change to patient. Note ability to understand events, provide realistic appraisal of situation.
    • Determine outside stressors, e.g. family, work, social, future nursing/healthcare needs.
    • Encourage patient to express feelings, including hostility or anger, denial, depression, sense of disconnectedness.
    • Note whether patient refers to affected side as ‘it’ or denies affected side and says it is ‘dead’.
    • Identify previous methods of dealing with life problems. Determine presence and quality of support systems.
    • Emphasize small gains either in recovery of function or independence.
    • Support behaviors and efforts such as increased interest, participation in rehabilitation activities.
    • Monitor for sleep disturbance, increased difficulty concentrating, and statements of inability to cope, lethargy, and withdrawal.
    • Refer for neuropsychological evaluation and/or counseling if indicated.
  5. Self-care deficit related to neuromuscular impairment and decreases strength and endurance.
    Interventions
    • Assess abilities and level of deficit (0–4 scale) for performing ADLs.
    • Avoid doing things for patient that patient can do for self, but provide assistance as necessary.
    • Be aware of impulsive behavior and actions suggestive of impaired judgment.
    • Maintain a supportive, firm attitude. Allow patient sufficient time to accomplish tasks.
    • Provide positive feedback for efforts and accomplishments.
    • Create plan for visual deficits that are present, e.g. place food and utensils on the tray related to patient's unaffected side, situate the bed so that patient's unaffected side is facing the room with the affected side to the wall, position furniture against wall and out of travel path.
    • Provide self-help devices, e.g. button/zipper hook, knife-fork combinations, long-handled brushes, extensions for picking things up from floor, toilet riser, leg bag for catheter, shower chair.
    • Assist and encourage good grooming and makeup habits.
    • Encourage family member to allow patient to do as much as possible for self.
    • Assess patient's ability to communicate the need to void and ability to use urinal, bedpan. Take patient to the bathroom at frequent and periodic intervals for voiding if appropriate.
    • Identify previous bowel habits and re-establish normal regimen. Increase bulk in diet, encourage fluid intake, increased activity.
  6. Risk for impaired swallowing related to neuromuscular dysfunction.
    Intervention
    • Review individual pathology and ability to swallow, noting extent of paralysis, clarity of speech, facial, tongue involvement, ability to protect airway and episodes of coughing or choking, presence of adventitious breath sounds, amount and character of oral secretions.
    • 384Have suction equipment available at bedside, especially during early feeding efforts.
    • Promote effective swallowing, e.g. schedule activities, medications to provide a minimum of 30 min rest before eating, provide pleasant environment free of distractions, assist patient with head control and support, and position based on specific dysfunction.
    • Place patient in upright position during and after feeding as appropriate.
    • Provide oral care based on individual need prior to meal.
    • Season food with herbs, spices, lemon juice, etc. according to patient's preference, within dietary restrictions.
    • Place food of appropriate consistency in unaffected side of mouth.
    • Touch parts of the cheek with tongue blade and apply ice to weak tongue.
    • Feed slowly, allowing 30–45 min for meals.
    • Offer solid foods and liquids at different times.
    • Maintain upright position for 45–60 min after eating.
    • Maintain accurate intake output, record calorie count.
    • Encourage participation in exercise.
    • Administer IV fluids and or tube feedings.
    • Coordinate multidisciplinary approach to develop treatment plan that meets individual needs.
  7. Knowledge deficit related to lack of exposure and cognitive limitation
    Interventions
    • Evaluate type and degree of sensory-perceptual involvement.
    • Include family in discussions and teaching.
    • Discuss specific pathology and individual potentials.
    • Identify signs and symptoms requiring further follow-up, e.g. changes or decline in visual, motor, sensory functions, alteration in mentation or behavioral responses, severe headache.
    • Review current restrictions or limitations and discuss planned resumption of activities (including sexual relations).
    • Provide written instructions and schedules for activity, medication, important facts.
    • Encourage patient to refer to lists communications or notes instead of depending on memory.
    • Discuss plans for meeting self-care needs.
    • Refer to discharge planner, home care supervisor, visiting nurse.
    • Suggest patient reduce or limit environmental stimuli, especially during cognitive activities.
    • Recommend patient seek assistance in problem-solving process and validate decisions, as indicated.
    • Review importance of balanced diet, low in cholesterol and sodium if indicated. Discuss role of vitamins and other supplements.
    • Refer to reinforce importance of follow-up care by rehabilitation team, e.g. physical, occupational, speech, vocational therapists.
385
 
NARCOLEPSY
Narcolepsy is a neurological disorder that affects the control of sleep and wakefulness. People with narcolepsy experience excessive daytime sleepiness and intermittent, uncontrollable episodes of falling asleep during the daytime. These sudden sleep attacks may occur during any type of activity at any time of the day.
 
Etiology
  • The cause of narcolepsy is not known; however, scientists have made progress toward identifying genes strongly associated with the disorder. These genes control the production of chemicals in the brain that may signal sleep and awake cycles.
  • Some experts think narcolepsy maybe due to a deficiency in the production of a chemical called hypocretin by the brain.
 
Signs and Symptoms
  • Excessive daytime sleepiness (EDS): In general, EDS interferes with normal activities on a daily basis, whether or not a person with narcolepsy has sufficient sleep at night. People with EDS report mental cloudiness, a lack of energy and concentration, memory lapses, a depressed mood, and extreme exhaustion.
  • Cataplexy: This symptom consists of a sudden loss of muscle tone that leads to feelings of weakness and a loss of voluntary muscle control. It can cause symptoms ranging from slurred speech to total body collapse, depending on the muscles involved, and is often triggered by intense emotions such as surprise, laughter, or anger.
  • Usually, these delusional experiences are vivid and frequently frightening. The content is primarily visual, but any of the other senses can be involved. These are called hypnagogic hallucinations when accompanying sleep onset and hypnopompic hallucinations when they occur during awakening.
  • This symptom involves the temporary inability to move or speak while falling asleep or waking up. These episodes are generally brief, lasting a few seconds to several minutes. After episodes end, people rapidly recover their full capacity to move and speak.
  • Microsleep is a very brief sleep episode during which the patient continue to function (talk, put things away, etc.) and then awaken with no memory of the activities.
 
Diagnostic Evaluation
A physical exam and exhaustive medical history are essential for proper diagnosis of narcolepsy. Two tests that are considered essential in confirming a diagnosis of narcolepsy are the polysomnogram (PSG) and the multiple sleep latency test (MSLT).
  • Nocturnal polysomnogram: This overnight test measures the electrical activity of brain and heart, and the movement of muscles and eyes.
  • Multiple sleep latency test (MSLT): This test measures how long it takes to fall asleep during the day.
  • Spinal fluid analysis: The lack of hypocretin in the cerebrospinal fluid may be a marker for narcolepsy. Examining spinal fluid is a new diagnostic test for narcolepsy.
The Epworth Sleepiness Scale measures daytime sleepiness. Use the following scale to choose the most appropriate number for each situation:
3860 = would never sleep
1 = slight chance of dozing or sleeping
2 = moderate chance of dozing or sleeping
3 = high chance of dozing or sleeping
Situation
Chance of dozing or sleeping
Sitting and reading
---
Watching TV
---
Sitting inactive in a public place
---
Being a passenger in a motor vehicle for an hour or more
---
Lying down in the afternoon
---
Sitting and talking to someone
---
Sitting quietly after lunch (no alcohol)
---
Stopped for a few minutes in traffic while driving
---
Total score (add the scores up)
---
A total score of 10 or more is considered sleepy. A score of 18 or more is very sleepy.
 
Management
  • Schedule sleep periods: Take a few brief, scheduled naps during the daytime (10–15 minutes each). Try to get a good night's sleep during the same hours each night. Planned naps can prevent unplanned lapses into sleep.
  • Avoid caffeine, alcohol, and nicotine: These substances interfere with sleep.
  • Avoid over-the-counter drugs that cause drowsiness: Some allergy and cold medications can cause drowsiness, so should be avoided.
  • Involve employers, coworkers, and friends: Alert others so that they can help when needed.
  • Carry a tape recorder: Record important conversations and meetings, in case you fall asleep.
  • Break up larger tasks into small pieces: Focus on one small thing at a time.
  • Exercise on a regular basis: Exercise can make you feel more awake during the day and stimulate sleep at night. For example, take several short walks during the day.
  • Avoid activities that would be dangerous if you had a sudden sleep attack: If possible, do not drive, climb ladders, or use dangerous machinery. Taking a nap before driving may help you to manage any possible sleepiness.
  • Wear a medical alert bracelet or necklace: A bracelet or necklace will alert others if you suddenly fall asleep or become unable to move or speak.
  • Eat a healthy diet: Aim for a diet rich in whole grains, vegetables, fruits, low fat dairy, and lean sources of protein. Eat light or vegetarian meals during the day and avoid heavy meals before important activities.
  • Relax and manage emotions: Narcolepsy symptoms can be triggered by intense emotions, so you may benefit from practicing relaxation techniques, such as breathing exercises, yoga, or massage.
 
Medical Management
387Common medications used to treat narcolepsy symptoms include:
  • Stimulants: Stimulants are the mainstay of drug treatment for narcolepsy. These include modafinil, a stimulant used during the day to promote wakefulness and alertness.
  • Sodium oxybate: This strong drug maybe prescribed if one have severe cataplexy. Sodium oxybate is also known as GHB, or the ‘date rape drug’, but is considered safe for treating narcolepsy when used responsibly to promote sound sleep, diminish daytime sleepiness, and reduce incidences of cataplexy.
  • Antidepressants: Selective serotonin reuptake inhibitors (SSRIs) used to treat depression may also be used to help suppress REM sleep, and alleviate symptoms of cataplexy, hallucinations, and sleep paralysis.
 
Nursing Management
  • Instruct patient to follow as consistent a daily schedule for retiring and arising as possible.
  • This promotes regulation of the circadian rhythm, and reduces the energy required for adaptation to changes.
  • Instruct to avoid heavy meals, alcohol, caffeine, or smoking before retiring.
  • Though hunger can also keep one awake, gastric digestion and stimulation from caffeine and nicotine can disturb sleep.
  • Instruct to avoid large fluid intake before bedtime. For patients may need to void during the night.
  • Increase daytime physical activities as indicated, to reduce stress and promote sleep.
  • Instruct to avoid strenuous activity before bedtime. Over fatigue may cause insomnia.
  • Discourage pattern of daytime naps unless deemed necessary to meet sleep requirements or if part of one's usual pattern. Napping can disrupt normal sleep patterns. However the elderly do better with frequent naps during the day to counter their shorter night-time sleep schedule.
  • Suggest use of soporifics such as milk. Which contains L-tryptophan that facilitates sleep.
  • Recommend an environment conducive to sleep or rest (e.g. quiet, comfortable temperature, ventilation, darkness, closed door). Suggest use of earplugs or eye shades as appropriate.
  • Suggest engaging in a relaxing activity before retiring, such as warm bath, calm music, reading an enjoyable book, relaxation exercises.
  • Explain the need to avoid concentrating on the next day's activities or on one's problems at bedtime.
  • Suggest using hypnotics or sedatives as ordered.
  • If unable to fall asleep after about 30 to 45 minutes, suggest getting out of bed and engaging in a relaxing activity. Provide nursing aids (e.g. back rub, bedtime care, pain relief, comfortable position, relaxation techniques).
  • Organize nursing care: Eliminate nonessential nursing activities. Prepare patient for necessary anticipated interruptions/disruptions.
  • Attempt to allow for sleep cycles of at least 90 minutes.
  • 388Move patient to room farther from the nursing station if noise is a contributing factor.
  • Post a ‘Do not disturb’ sign on the door.
 
HEADACHE
Headache is pain in any region of the head. Headaches may occur on one or both sides of the head, be isolated to a certain location, radiate across the head from one point, or have a vise-like quality. A headache maybe a sharp pain, throbbing sensation or dull ache. Headaches may appear gradually or suddenly, and they may last less than an hour or for several days.
 
Types of Headache
Chronic Tension headache
Chronic tension-type headaches maybe the result of stress or fatigue, but more than likely, they can be attributed to physical problems, psychological issues, or depression.
A pattern of chronic tension-type headaches generally begins between the ages of 20 and 40, and every personality type can experience them.
 
Symptoms
  • The muscles between head and neck contract for hours or days.
    • A tightness around neck or even feel as if head and neck were in a cast and only certain positions seem to provide relief.
    • Feeling of soreness, a tightening band around head (a ‘vice-like’ ache), a pulling, or pressure sensations.
    • The pain is continuous, annoying, but not throbbing.
    • Headache primarily occurs in forehead, temples or the back of head and neck.
  • Changes in sleep patterns if headaches are related to anxiety, then you may have trouble falling asleep or may suffer from insomnia. If headaches are associated with depression, then you may awaken frequently during the night, awaken before you wanted to in the morning, or you maybe sleeping excessively (hypersomnia).
  • Shortness of breath
  • Constipation
  • Nausea
  • Weight loss
  • Ongoing fatigue
  • Decreased sexual drive
  • Palpitations
  • Dizziness
  • Unexpected crying
  • Menstrual changes.
 
Etiology and Risk Factors
  • Poor posture, close work under poor lighting conditions, or cramps from assuming an unnatural head or neck position for long periods of time
  • Arthritis, particularly cervical arthritis
  • 389Abnormalities in neck muscles, bones or disks
  • Eye strain caused when one eye is compensating for another eye's weakness
  • Misalignment of teeth or jaws
  • Noise or lighting
  • Job conflicts and family relationships
  • Grief
  • Depression.
 
Management
  • There are two goals when treating any type of headache: Prevent future attacks, abort or relieve current pain.
  • Prevention includes taking prescribed medications, avoiding or minimizing the causes, and learning self-help measures, such as biofeedback or relaxation exercises.
  • NSAIDs (Nonsteroidal Anti-inflammatory Agents), Fenoprofen, Flurbiprofen, Ketoprofen.
  • Antidepressants—Tricyclics (nonsedating), Protriptyline, Desipramine.
  • Antidepressants—Tricyclics (sedating), Amitriptyline, Doxepin.
 
MIGRAINE HEADACHE
Migraines deserve the attention they receive, one headache can put the life ‘on hold’ for a few hours or several days. Migraine is responsible for more job absenteeism and disrupted family life than any other headache type.
 
Symptoms
Migraine often begins as a dull ache and then develops into a constant, throbbing and pulsating pain at the temples, as well as the front or back of one side of the head. The pain is usually accompanied by nausea and vomiting, and sensitivity to light and noise.
The two most prevalent types of migraine are migraine with aura (formerly referred to as classic migraine) and migraine without aura (formerly referred to as common migraine).
 
Etiology
Physical and Environmental Causes
  • Stress
  • Fatigue
  • Oversleeping or lack of sleep
  • Fasting or missing a meal
  • Food or medication that affects the diameter of blood vessels.
  • Caffeine
  • Chocolate
  • Alcohol
  • Menses
  • Hormonal changes
  • 390Changes in barometric pressure
  • Changes in altitude.
Foods and Diet
Specific foods are suspected of triggering at least 30 percent of the migraine headaches. Foods that contain: Additives such as, Nitrates and nitrites (usually in processed meats), yellow (annatto) food coloring, and MSG (monosodium glutamate). Canned or processed foods, Chinese foods, tenderizer, and seasonings such as soy sauce may contain MSG.
Tyramine
  • Red wines and most alcoholic beverages, aged cheeses and processed meats (including pizza and hot dogs), peanuts, chicken livers, pickled foods, sourdough bread, bread and crackers containing cheese, broad beans, peas, lentils. Foods to eat in moderation include: avocados, bananas, citrus fruits, figs, raisins, red plums, raspberries, and chocolates.
 
Management
  • There are two goals when treating migraine, or any other headache: to relieve the pain and prevent future attacks.
  • Once migraine has been diagnosed, treatment will begin by identifying those circumstances or factors that trigger it.
  • Keep a daily calendar of activities, foods, beverages, prescription and over-the-counter medications, physical and environmental factors, stressful situations, sleep patterns, and characteristics of the headache itself.
  • Beta-Blockers, Propranolol, Timolol
  • Calcium Channel Blockers, Verapamil, Diltiazem
  • Antiepilepsy Medication, Divalproex sodium, Neurontin
  • NSAIDs, Fenoprofen, Flurbiprofen
  • Antidepressants—Tricyclics (nonsedating), Protriptyline, Desipramine
Self-Help Treatments for Migraine and Tension-Type Headaches
  • Counseling and pyschotherapy
  • Relaxation Training
  • Progressive muscle relaxation
  • Guided imagery
  • Biofeedback
  • Acupuncture
  • Physical and massage therapy.
 
CLUSTER HEADACHE
In this the attacks come in groups. The pain arrives with little, if any, warning, and it has been described as the most severe and intense of any headache type. It generally lasts from 30 to 45 minutes, although it might persist for several hours before it disappears.
Cluster headaches frequently surface during the morning or late at night, the cluster cycle can last weeks or months and then can disappear for months or years.
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Symptoms
  • The headache is usually unilateral and rarely switches sides from one attack to another.
  • One might feel the pain begin around one eye, ‘like a nail or knife stabbing or piercing’ the eye, or as if someone ‘were pulling out’ eye, it maybe accompanied by a tearing or bloodshot eye and a runny nose on the side of the headache.
  • It can radiate from the eye to the forehead, temple and cheek on the same side.
  • The pain of a cluster headache has been described as piercing, burning, throbbing, and pulsating.
 
Etiology
Unlike migraine headaches, cluster headaches are not the result of heredity. Sufferers, however, usually do have a history of chronic smoking, and alcohol frequently triggers a cluster headache.
Because the level of histamine increases in a person's blood and urine during a cluster headache, which dilate or expand blood vessels, influence a cluster headache.
 
Management
Verapamil, Prednisone, Ergotamine tartrate, Lithium carbonate, Divalproex sodium, Histamine acid phosphate.
 
HEAD INJURIES
Head injuries are dangerous. They can lead to permanent disability, mental impairment, and even death. To most people, head injuries are considered an acceptable risk when engaging in sports and other types of recreational activities.
Head injuries are injuries to the scalp, skull, or brain caused by trauma. Concussions are the most common type of sports-related brain injury. A concussion is a type of traumatic brain injury (TBI) that happens when the brain is jarred or shaken hard enough to bounce against the skull.
 
Types of Head Injuries
There are four common types of traumatic head injury
  • Closed injury: A closed injury does not break or open the skull or penetrate brain tissue. However, it can still cause bruising or swelling of the brain.
  • Open injury: An open injury is any damage that penetrates the skull. The damage may cause bleeding within the brain's tissues. It may also produce skull fractures or cause the skull bones to press into brain tissue.
  • Concussion: A concussion occurs when brain is shaken. It may lead to loss of consciousness and headache.
 
Causes of Head Injury
Many types of trauma can cause a head injury
  • Gunshot wounds can cause head injuries when the bullet penetrates the skull and enters the brain. This can damage the blood vessels and cause bleeding.
  • 392Vehicle accidents are common causes of traumatic head injuries
  • Violent shaking is a common cause of brain trauma in infants and young children.
  • Falling and hitting head can damage the skull, scalp, or brain. Falls may cause any type of head injury.
  • Assault can lead to a head injury. Being kicked, punched, or struck in the head can cause a concussion, closed or open brain injury.
 
Management
  • Check the person's level of response using the AVPU code:
    • A: Is the person alert, eyes open and responding to questions
    • V: Does the person respond to voice, obey simple commands
    • P: Does the person respond to pain (e.g. eyes open or movement in response to being pinched)
    • U: Is the person unresponsive.
  • Regularly monitor and record vital signs—level of response, breathing and pulse. Even if the person appears to recover fully, watch them for any deterioration in their level of response.
  • When the person has recovered, place them in the care of a responsible person. If a person has been injured on the sports field, never allow them to ‘play on’ without first obtaining medical advice.
  • Advise the person to go to hospital if, following a blow to the head, they develop symptoms such as headache, vomiting, confusion, drowsiness or double vision.
 
Treatment of Acute Head Injury
  • Cervical collar
  • Craniotomy, surgical incision into to cranium (maybe necessary to evacuate a hematoma or evacuate contents to make room for swelling to prevent herniation)
  • Oxygen therapy, intubation and mechanical ventilation (to provide controlled hyperventilation to decrease elevate ICP)
  • Restricted oral intake for 24 to 48 hours
  • Ventriculostomy, insertion of a drain into the ventricles (to drain CSF in the presence of hydrocephalus, which may occur as a result of head injury; can also be used to monitor ICP).
 
Pharmacological Management
  • Analgesic: Codein phosphate
  • Anesthetic: Lidocin
  • Anticonvulsant: Phenytoin
  • Barbiturate: Pentobarbital
  • Diuretic: Mannitol, furosemide to combat cerebral edema
  • Dopamine (Intropin) to maintain cerebral perfusion pressure above 50 mm Hg (if blood pressure is low and ICP is elevated)
  • Glucocorticoid: Dexamethasone to reduce cerebral edema
  • 393Histamin-2 (H2) receptor antagonist such as cimetidine, ranitidine, famotidine.
  • Mucosal barrier fortifiers: Sucralfate
  • Posterior pituitary: Vasopressin if client develops diabetes insipidus.
 
Nursing Management
 
Assessment
  • Assess neurologic status as follows: Level of consciousness as per Glasgow Coma Scale, pupil size, symmetry, and reaction to light, extraocular movement, gaze preference, speech and thought processes, memory, motor-sensory signs and drift, increased tone, increased reflexes, Babinski reflex, Deteriorating neurological signs indicate increased cerebral ischemia.
  • Evaluate presence or absence of protective reflexes (e.g. swallowing, gagging, blinking, coughing, and others).
  • Monitor vital signs.
  • Monitor arterial blood gases (ABGs) and pulse oximetry. Recommended parameters of PaO2 > 80 mm Hg and PaCO2 < 35 mm Hg with normal ICP. If patient's lungs are being hyperventilated to decrease ICP, PaCO2 should be between 25 and 30 mm Hg.
  • Monitor input and output with urine—specific gravity. Report urine—specific gravity > 1.025 or urine output < 1.50 ml/kg/hr, May indicate decreased renal perfusion and possible associated decrease in CPP.
  • Monitor ICP if measurement device is in place. Report ICP >15 mm Hg for 5 minutes.
  • Calculate cerebral perfusion pressure (CPP), Should be approximately 90 mm Hg to 100 mm Hg and not < 50 mm Hg to ensure blood flow to brain.
  • Monitor serum electrolytes, blood urea nitrogen (BUN), creatinine, glucose, osmolality, hemoglobin (HGB), and hematocrit (HCT) as indicated, to detect treatment complications such as hypovolemia.
  • Monitor closely when treatment of increased ICP begins to taper, ICP may increase as treatment is tapered.
 
Nursing Diagnosis
  • Ineffective airway clearance and impaired gas exchange related to brain injury
  • Ineffective cerebral tissue perfusion related to increased ICP, decreased CPP, and possible seizures
  • Deficient fluid volume related to decreased LOC and hormonal dysfunction
  • Imbalanced nutrition, less than body requirements, related to increased metabolic demands, fluid restriction, and inadequate intake
  • Risk for injury related to seizures, disorientation, restlessness, or brain damage
  • Risk for imbalanced body temperature related to damaged temperature-regulating mechanisms in the brain
  • Risk for impaired skin integrity related to bed rest, hemiparesis, hemiplegia, immobility, or restlessness
  • Disturbed thought processes (deficits in intellectual function, communication, memory, information processing) related to brain injury
  • 394Disturbed sleep pattern related to brain injury and frequent neurologic checks
  • Interrupted family processes related to unresponsiveness of patient, unpredictability of outcome, prolonged recovery period, and the patient's residual physical disability and emotional deficit
  • Deficient knowledge about brain injury, recovery, and the rehabilitation process.
Interventions
  • Asses neurologic and respiratory status to monitor for sign of increased ICP and respiratory distress
  • Monitor and record vital sign and intake and output, hemodynamic variables, ICP, cerebral perfusion pressure, specific gravity, laboratory studies, and pulse oximetry to detect early sign of compromise
  • Observe for sign of increasing ICP to avoid treatment delay and prevent neurologic compromise
  • Assess for CSF leak as evidenced by otorhea or rinorrhea. CSF leak could leave the patient at risk for infection
  • Assess for pain. Pain may cause anxiety and increase ICP
  • Check cough and gag reflex to prevent aspiration
  • Check for sign of diabetes insipidus (low urine specific gravity, high urine output) to maintain hydration
  • Administer IV fluids to maintain hydration
  • Administer oxygen to maintain position and patency of endotracheal tube if present, to maintain airway and hyperventilate the patient and to lower ICP
  • Provide suctioning; if patient is able, assist with turning, coughing, and deep breathing to prevent pooling of secretions
  • Maintain position, patency and low suction of NGT to prevent vomiting
  • Maintain seizure precautions to maintain patient safety
  • Administer medication as prescription to decrease ICP and pain
  • Allow a rest period between nursing activities to avoid increase in ICP
  • Encourage the patient to express feeling about changes in body image
  • Provide appropriate sensory input and stimuli with frequent reorientation to foster awareness of the environment
  • Provide means of communication, such as a communication board to prevent anxiety
  • Provide eye, skin, and mouth care to prevent tissue damage
  • Turn the patient every 2 hours or maintain in a rotating bed if condition allows preventing skin breakdown.
  • Monitor patient's neurologic status, ICP and vital signs at least every hour.
  • Notify physician for collaborative management or institute a protocol to respond to a sustained ICP greater than 20.
  • Maintain patient's head of the bed at 30 degrees elevation or higher and patient's body in a neutral position. Do not allow pronounced neck or hip flexion.
  • Monitor the patient's temperature and maintain it within designated parameters, aggressively treat hyperthermia.
  • 395Monitor patient's blood gases; collaborate with physician and respiratory therapist to resolve hypercarbia, hypocarbia, or hypoxia.
  • Suction only after preoxygenating the patient and for less than 10 seconds at a time.
  • Spread nursing activities out, do not cluster them.
 
SPINAL INJURY
A spinal cord injury is damage to any part of the spinal cord or nerves at the end of the spinal canal, often causes permanent changes in strength, sensation and other body functions below the site of the injury.
 
Types of Spinal Injuries
  1. Cervical spinal cord injury C1-C8–quadriplegia also known as tetraplegia: Cervical level injuries cause paralysis or weakness in both arms and legs (quadriplegia). All regions of the body below the level of injury or top of the back may be affected. Sometimes this type of injury is accompanied by loss of physical sensation, respiratory issues, bowel, bladder, and sexual dysfunction. This area of the spinal cord controls signals to the back of the head, neck and shoulders, arms and hands, and diaphragm. Since the neck region is so flexible it is difficult to stabilize cervical spinal cord injuries. Patients with cervical level injuries maybe placed in a brace or stabilizing device.
  2. Thoracic spinal cord injury T1-T12: Thoracic level injuries are less common because of the protection given by the rib cage. Thoracic injuries can cause paralysis or weakness of the legs (paraplegia) along with loss of physical sensation, bowel, bladder, and sexual dysfunction. In most cases, arms and hands are not affected. This area of the spinal cord controls signals to some of the muscles of the back and part of the abdomen. With these types of injuries most patients initially wear a brace on the trunk to provide extra stability.
  3. Lumbar spinal cord injury L1-L5: Lumbar level injuries result in paralysis or weakness of the legs (paraplegia). Loss of physical sensation, bowel, bladder, and sexual dysfunction can occur. The shoulders, arms and hand function are usually unaffected. This area of the spinal cord controls signals to the lower parts of the abdomen and the back, the buttocks, some parts of the external genital organs, and parts of the leg. These injuries often require surgery and external stabilization.
  4. Sacral spinal cord injury S1-S5: Sacral level injuries primarily cause loss of bowel and bladder function as well as sexual dysfunction. These types of injuries can cause weakness or paralysis of the hips and legs. This area of the spinal cord controls signals to the thighs and lower parts of the legs, the feet, and genital organs.
  5. Complete and incomplete: An incomplete injury means that the ability of the spinal cord to convey messages to or from the brain is not completely lost, some sensation and movement is possible below the level of injury. A complete injury is indicated by a total lack of sensory and motor function below the level of injury. But the absence of motor and sensory function below the injury site does not necessarily mean that there are no remaining intact axons or nerves crossing the injury site, just that they do not function appropriately following the injury.
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Types of Paralysis
  1. Complete paraplegia: Complete paraplegia is a condition that results in permanent loss of movement and sensation at the T1 level or below. At the T1 level there is normal hand function, and as the levels move down the spinal column improved abdominal control, respiratory function, and sitting balance may occur.
  2. Complete tetraplegia: Complete tetraplegia is a condition that results in permanent loss of movement and sensation in all four limbs. Spinal cord injuries that result in complete tetraplegia most often occur at levels C1 through C8. The degree of functionality is a direct result of where the injury to the spine occurred.
  3. Anterior cord syndrome: The injury occurs at the front of the spinal cord, leaving the person with partial or complete loss of ability to sense pain, temperature, and touch below the level of injury. Some people with this type of injury later recover some movement.
  4. Central cord syndrome: The injury occurs at the center of the spinal cord and usually results in the loss of arm function. Some leg, bowel, and bladder control maybe preserved. Some recovery from this injury may start in the legs, and then move upward.
  5. Posterior cord syndrome: The injury occurs toward the back of the spinal cord. Usually muscle power, pain, and temperature sensation is preserved. However, the person may have trouble with limb coordination.
  6. Brown-Sequard syndrome: This injury occurs on one side of the spinal cord. Pain and temperature sensation will be present on the injured side, but impairment or loss of movement will also result. The opposite side of the injury will have normal movement, but pain and temperature sensation will be affected or lost.
  7. Cauda equina lesion: Damage to the nerves that fan out of the spinal cord at the first and second lumbar region of the spine can cause partial or complete loss of movement and feeling. Depending upon the extend of initial damage, sometimes these nerves can grow back and resume functionality.
  8. Hemiplegia is a term used to describe paralysis, severe weakness, or rigid movement on either the right or left side of the body. Hemiplegia can also be associated with limited use of the hand, balance issues, speech issues, and visual field problems.
 
Etiology
The main cause of hemiplegia is:
  • Brain damage as the result of disrupted blood flow
  • Stroke
  • Cerebral palsy
  • Perinatal strokes in infants, and traumatic brain injury.
 
Types of Hemiplegia
There are several different types of hemiplegia. They include:
  • Facial hemiplegia—Paralysis occurs on one side of the face
  • Cerebral hemiplegia—A brain lesion disrupts the flow of blood to the brain
  • Spastic hemiplegia—Characterized by paralysis and spastic movements on the affected side
  • Spinal hemiplegia—Caused by lesions that have formed on the spine.
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Signs and Symptoms
  • Loss of movement
  • Loss of sensation, including the ability to feel heat, cold and touch
  • Loss of bowel or bladder control
  • Exaggerated reflex activities or spasms
  • Changes in sexual function, sexual sensitivity and fertility
  • Pain or an intense stinging sensation caused by damage to the nerve fibers in spinal cord
  • Difficulty breathing, coughing or clearing secretions from lungs.
Emergency signs and symptoms
Emergency signs and symptoms of spinal cord injury after an accident may include:
  • Extreme back pain or pressure in neck, head or back
  • Weakness, incoordination or paralysis in any part of body
  • Numbness, tingling or loss of sensation in hands, fingers, feet or toes
  • Loss of bladder or bowel control
  • Difficulty with balance and walking
  • Impaired breathing after injury
  • An oddly positioned or twisted neck or back
  • Loss of consciousness
  • Low breathing rate
  • Restlessness, clumsiness, or lack of coordination
  • Severe headache
  • Slurred speech or blurred vision
  • Stiff neck or vomiting
  • Sudden worsening of symptoms after initial improvement
  • Swelling at the site of the injury
  • Persistent vomiting.
 
Management
Treatment for spinal cord injuries can be divided into two stages: Acute and Rehabilitation. The acute phase begins at the time of injury, and lasts until the person is stabilized. The rehabilitation phase begins as soon as the person has stabilized and is ready to begin working toward his or her independence.
  1. The acute phase: During the acute phase, it is very important that the person receive prompt medical care. The faster the person accesses treatment, the better his or her chances are at having the least amount of impairment possible.
    The first few days of the acute stage are accompanied by spinal shock, in which the person's reflexes do not work. During this stage, it is very difficult to determine an exact prognosis, as some function beyond what is currently being seen may occur later. At this stage other complications from the accident or injury will also be present, such as brain injury, broken bones, or bruising.
  2. The rehabilitation phase: Once the acute phase is over and the person has been stabilized, he or she enters the rehabilitation stage of treatment. Treatment during this phase has 398the goal of returning as much function as possible to the person. Because all spinal cord injuries are different, a unique plan designed to help the person function and succeed in everyday life is designed. The plan often includes:
  • Helping the person understand his or her injuries
  • Helping the person understand the details regarding his or her care
  • Helping the person become as independent as possible in everyday activities such as bathing, eating, dressing, grooming, and wheelchair use
  • Helping the person learn to accept a new lifestyle, especially pertaining to sexual, recreational, and housing options
  • Helping the person learn how to instruct caregivers in how to assist them
  • Preparing them for vocational rehabilitation
  • In most cases, rehabilitation occurs at an approved and accredited spinal cord injury treatment center.
Specific level of spinal cord injury and rehabilitation potential
  • C2 or C3: Patient is completely dependent for all care.
  • C4: Dependent for all cares and usually needs a ventilator.
  • C5: Patient maybe able to feed himself using assistive devices, usually needs a type of respiratory support but maybe able to break without a ventilator.
  • C6: Patient maybe able to push himself on wheelchair indoors and maybe able to perform daily living tasks such as eating, grooming, and dressing.
  • C7: Patient maybe able to drive a car with special adaptations or can propel a wheelchair outside.
  • C8: Same as C7.
  • T1-T6: Patient maybe able to become independent with self-care and use of a wheelchair.
  • T6-T12: Patient may improve sitting balance and be able to participate in athletic activities with the use of a wheelchair.
  • L1-L5: Patient maybe able to walk short distances with assistive devices.
 
Nursing Intervention
  • Assess functional ability of impairment initially and on a regular basis.
  • Change positions at least every 2 hour (supine, sidelying) and possibly more often if placed on affected side.
  • Position in prone position once or twice a day if patient can tolerate.
  • Prop extremities in functional position, use footboard during the period of flaccid paralysis. Maintain neutral position of head.
  • Use arm sling when patient is in upright position, as indicated.
  • Evaluate use and need for positional aids and splints during spastic paralysis, place pillow under axillae to abduct arm, elevate arm and hand.
  • Observe affected side for color, edema, or other signs of compromised circulation.
  • Inspect skin regularly, particularly over bony prominences. Gently massage any reddened areas and provide aids such as sheepskin pads as necessary.
  • Begin active/passive range of motion exercise to all extremities.
  • 399Assist to develop sitting balance (e.g. raise head of bed, assist to sit on edge of bed, having patient use the strong arm to support body weight and strong leg to move affected leg, increase sitting time) and standing balance (e.g. put flat walking shoes on patient, support patient's lower back with hands while positioning own knees outside patient's knees, assist in using parallel bars/walkers).
  • Get patient up in chair as soon as vital signs are stable, except following cerebral hemorrhage.
  • Pad chair seat with foam or water-filled cushion, and assist patient to shift weight at frequent intervals.
  • Provide egg-crate mattress, water bed, flotation device, or specialized beds (e.g. kinetic) as indicated.
  • Assess abilities and level of deficit (0–4 scale) for performing ADLs.
  • Avoid doing things for patient that patient can do for self, but provide assistance as necessary.
  • Be aware of impulsive behavior and actions suggestive of impaired judgment.
  • Maintain a supportive, firm attitude. Allow patient sufficient time to accomplish tasks.
  • Provide positive feedback for efforts and accomplishments.
  • Create plan for visual deficits that are present, e.g. Place food and utensils on the tray related to patient's unaffected side, situate the bed so that patient's unaffected side is facing the room with the affected side to the wall, position furniture against wall and out of travel path.
  • Provide self-help devices, e.g. button/zipper hook, knife-fork combinations, long-handled brushes, extensions for picking things up from floor, toilet riser, leg bag for catheter, shower chair.
  • Assist and encourage good grooming and makeup habits.
  • Encourage family member to allow patient to do as much as possible for self.
  • Assess patient's ability to communicate the need to void and ability to use urinal, bedpan. Take patient to the bathroom at frequent and periodic intervals for voiding if appropriate.
  • Identify previous bowel habits and re-establish normal regimen. Increase bulk in diet, encourage fluid intake, increased activity.
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Eye Disorders7

 
 
Introduction
Eye is like a camera. The external object is seen like the camera takes the picture of any object. Light enters the eye through a small hole called the pupil and is focused on the retina, which is like a camera film. Eye also has a focusing lens, which focuses images from different distances on the retina. The colored ring of the eye, the iris, controls the amount of light entering the eye. It closes when light is bright and opens when light is dim. A tough white sheet called sclera covers the outside of the eye. Front of this sheet (sclera) is transparent in order to allow the light to enter the eye, the cornea. Ciliary muscles in ciliary body control the focusing of lens automatically. Choroid forms the vascular layer of the eye supplying nutrition to the eye structures. Image formed on the retina is transmitted to brain by optic nerve. The image is finally perceived by brain. A jelly like substance called vitreous humor fill the space between lens and retina. The lens, iris, and cornea are nourished by clear fluid, aqueous humor, formed by the ciliary body and fill the space between lens and cornea. This space is known as anterior chamber. The fluid flows from ciliary body to the pupil and is absorbed through the channels in the angle of anterior chamber. The delicate balance of aqueous production and absorption controls pressure within the eye.
 
REFRACTIVE ERRORS
A refractive error is a very common eye disorder. It occurs when the eye cannot clearly focus the images from the outside world. The result of refractive errors is blurred vision, which is sometimes so severe that it causes visual impairment.
402The four most common refractive errors are:
  1. Myopia: It is also known as nearsightedness. This occurs when the distance between the cornea and the retina is too long. Light rays entering the eye are focused in front of the retina causing the image that falls on the retina to be blurred.
  2. Hypermyopia: It is also known as farsightedness and occurs when the distance between the cornea and the retina is too short. Light rays entering the eye have not yet come into focus when they reach the retina. So again the image is blurred.
  3. Astigmatism: It is a condition in which the cornea is curved unevenly. A cornea that is curved the same in each direction is shaped like a basketball, while a cornea with astigmatism is more curved in one direction than the other like a football. Light passing through this uneven cornea is not properly focused on the retina.
  4. Presbyopia: It is a normal condition associated with age that causes problems with near vision.
Fig. 7.1: Types of refractive errors
 
Treatment of Refractive Errors
  • Eyeglasses: Eyeglass lenses correct refractive errors by focusing light directly on the retina. The type of lens depends on the type and severity of the refractive error. The type of refractive error determines the lens's shape. A concave lens is used to correct myopia. In myopia, light rays fall in front of the retina rather than on it. Because a concave lens is thin in the center and thicker on the edges, it diverges light rays so that the eye's lens focuses them directly on the retina.
    • A convex lens is used to correct hypermyopia. In hypermyopia, light rays fall behind the retina. The lens is thickest in the center and thinnest on the outer edges. The convex lens converges light rays so that the eye's lens focuses them on the retina.
    • To correct astigmatism, which is caused by distortions in the shape of the lens or cornea, a cylinder lens is frequently used. The cylinder lens has two refractive powers on one lens. One power is placed over the entire lens and the other is oriented in one direction. This corrects the scattered pattern in which light enters the eye and creates one focal point on the retina.
  • 403Multifocal Lenses: People that have more than one refractive error may require two pairs of eyeglasses or glasses with multifocal lenses. Multifocal lenses contain two or more vision-correcting prescriptions.
    • Bifocals are the most common type of multifocal lenses. The lens is split in two sections; the upper part is for distance vision and the lower part for near vision. They are usually prescribed for people over the age of 40 whose focusing ability has declined due to presbyopia.
    • Trifocals have a third section used for middle distance vision (i.e. objects within arm's reach, such as a computer screen).
  • Eyeglass Frames: The choice of frames usually depends on personal preference, fashion, comfort, and cost. Frames are made from metals, plastic, nylon, and other synthetics. Each material has its advantages.
  • Eyeglass Lenses: Traditionally, lenses have been made from glass, but today, they are more commonly made from plastic. Glass lenses are breakable and are about twice as heavy as plastic ones. They are more resistant to scratches. Plastic lenses scratch more easily, even with scratch-resistant coatings, but they are much lighter, less likely to break, and can be treated with ultraviolet filters and antiglare coatings.
    • Photochromic lens: This type of lens changes from colorless to dark, depending on the amount of ultraviolet exposure. The lenses are clear, but in sunlight a tint appears, eliminating the need for prescription sunglasses. Photochromic lenses are available in plastic and glass and for nearly every type of refractive error.
    • Polycarbonate lens: This is the most impact-resistant material available and is 10 times less likely to break than glass or plastic. They are the lenses of choice for children and adults who engage in activities (e.g. sports) or occupations in which eyeglasses can be easily broken. They are also recommended for those who are monocular (have only one eye) and those who have one functioning eye. Polycarbonate lenses are lighter and thinner than other types of lenses and absorb ultraviolet light, thus negating the need to treat eyeglasses with ultraviolet filters.
 
CATARACT
A cataract is a clouding or opacity of the normally clear lens of eye. The patient may have a cataract in one or both the eyes. Cataract is the third leading cause of preventable blindness.
Fig. 7.2: Difference between normal and cataract eye
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Risk Factors and Etiology
  • Increasing age
  • Diabetes
  • Drinking excessive amounts of alcohol
  • Excessive exposure to sunlight
  • Exposure to ionizing radiation, such as that used in X-rays and cancer radiation therapy
  • Family history of cataracts
  • High blood pressure
  • Obesity
  • Previous eye injury or inflammation
  • Previous eye surgery
  • Prolonged use of corticosteroid medications
  • Smoking.
 
Pathophysiology
Following are the various mechanisms involves in the occurrence of cataract:
  • Caused by degeneration and opacification of existing lens fibers, formation of aberrant fibers or deposition of other material in their place.
  • Loss of transparency occurs because of abnormalities of lens protein and consequent disorganization of the lens fibers.
  • Any factor that disturbs the critical intra and extra-cellular equilibrium of water and electrolytes, the colloid system within the fibers causing opacification.
  • Fibrous metaplasia of lens fibers occurs in complicated cataract.
  • Epithelial cell necrosis occurring in angle closure glaucoma leads to focal opacification of the lens epithelium.
  • Abnormal products of metabolism, drugs or metals can be deposited in storage diseases, metabolic diseases and toxic reactions
Three biochemical factors are evident in cataract formation:
  1. Hydration: Seen particularly in rapidly developing forms. Actual fluid droplets collect under the capsule forming lacunae between fibers, the entire tissue may swell and becomes opaque, and this process is reversible in early stage, as in juvenile insulin dependent diabetes. Hydration maybe due to osmotic changes in the lens or due to changes in the semipermeability of the capsule.
  2. Denaturation of lens proteins: If the proteins are denatured with an increase in insoluble protein, a dense opacity is produced. This stage is irreversible and opacity does not clear, this change is seen in young lens or the cortex of the adult nucleus where metabolism is active.
  3. Sclerosis: Inactive fibers of the nucleus suffer from degenerative change of slow sclerosis.
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Pathophysiology
 
Types of Cataract
  • Nuclear cataracts: A nuclear cataract may at first causes more nearsighted. But with time, the lens gradually turns more densely yellow and further cloudy. As the cataract slowly progresses, the lens may even turn brown. Advanced yellowing or browning of the lens can lead to difficulty distinguishing between shades of color.
  • Cortical cataracts: A cortical cataract begins as whitish, wedge-shaped opacities or streaks on the outer edge of the lens cortex.
  • Posterior subcapsular cataracts: A posterior subcapsular cataract starts as a small, opaque area that usually forms near the back of the lens, right in the path of light on its way to the retina.
  • Congenital cataracts (Aphakia): Some people are born with cataracts or develop them during childhood. Such cataracts maybe the result of the mother having an infection during pregnancy.
  • Hypermature shrunken cataract: when cortex disintegrate and transform into mass. The lens become inspissated and shrunken, the anterior capsule becomes thickened.
  • Morgagnian Hypermature Cataract: Sometimes cortex becomes liquefies and nucleus sink into the bottom. The liquefied cortex become milky and nucleus is seen as brown mass, visible as semicircular line in pupillary area altering its position with change in position of the head.
 
Signs and Symptoms
  • Clouded, blurred or dim vision
  • Increasing difficulty with vision at night
  • Sensitivity to light and glare
  • Seeing ‘halos’ around lights
  • Frequent changes in eyeglass or contact lens prescription
  • Fading or yellowing of colors
  • Double vision in a single eye.
 
Diagnostic Evaluation
  • Visual acuity test: A visual acuity test uses an eye chart to measure how well an eye can read a series of letters.
    406
    Fig. 7.3: Visual acuity test
  • Slit-lamp examination: With this examination, the eye can be visualizing at large scale by magnifying the eye. The microscope is called a slit lamp; it uses an intense line of light, a slit, to illuminate cornea, iris, lens, and the space between iris and cornea.
    Fig. 7.4: Slit lamp examination
  • Retinal examination: To visualize the retina.
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Other tests:
  • Snellen visual acuity test
  • Opthalmoscopy
  • Slit lamp bimicroscopic examination
  • Glare testing
  • Keratometry
  • Ocular examination
  • Perimetry: To determine the scope of visual fields.
 
Management
 
Objective of Cataract Surgery
  • The objective of cataract surgery is to remove the opacified lens.
  • Successful treatment of acute attack and prompt alleviation of manifestations.
  • Prevention of complications and further attacks.
  • Rehabilitation and education of the clients and significant others.
 
Pharmacologic Therapy
  • Beta carotene
  • Vitamin C and E
  • Antioxidant supplements
  • Selenium
  • Multivitamin supplements
  • Contact lenses
  • Strong bifocals
  • Glasses
  • Mydriatics: Phenylephrine HCL acid.
  • Cyloplegics: Tropicamide
  • Homatropine
  • Atropine.
 
Surgical Management
  • Phacoemulsification: In this method, surgery can usually be performed in less than 30 minutes and usually requires only minimal sedation. Numbing eyedrops or an injection around the eye is used and, in general, no stitches are used to close the wound, and often no eye patch is required after surgery.
  • Extracapsular cataract extraction surgery: This procedure is used mainly for very advanced cataracts where the lens is too dense to dissolve into fragments. This technique requires a larger incision so that the cataract can be removed in one piece without being fragmented inside the eye. An artificial lens is placed in the same capsular bag as with the phacoemulsification technique. This surgical technique requires a various number of sutures to close the larger wound, and visual recovery is often slower. Extra capsular cataract extraction usually requires an injection of numbing medication around the eye and an eye patch after surgery.
  • 408Intracapsular cataract surgery: This surgical technique requires an even larger wound than extracapsular surgery, and the surgeon removes the entire lens and the surrounding capsule together. This technique requires the intraocular lens to be placed in a different location, in front of the iris.
  • Aphakia: (absence of the lens) is corrected by the use of eyeglasses, contact lenses.
 
Nursing Management
 
Nursing Assessment
  • Assess knowledge level regarding procedure.
    • Assess the level of fear and anxiety.
    • Determine visual limitations.
 
Postoperative Assessment
  • Assess pain level
    • Sudden onset: Maybe due to ruptured vessel or suture and may lead to hemorrhage.
    • Severe pain: Accompanied by nausea and vomiting maybe caused by intraocular pressure.
    • Assess visual acuity in unoperated eye.
    • Assess patient's ability to ambulate.
    • Assess patient's level of independence.
 
Nursing Diagnoses
  • Self-care deficit related to visual deficit.
  • Anxiety related to lack of knowledge about the surgical and postoperative experience.
  • Risk for injury related to blurred vision.
  • Risk for infection related to trauma to incision.
  • Acute pain related to trauma to incision.
 
Nursing Intervention
 
Relieving Pain
  • Give medication to reduce pain as analgesics.
  • Give cold compression demand for blunt trauma.
  • Encourage to the use of sunglasses in strong light.
  • Vital signs must assess frequently.
  • Physical rest in bed with backrest elevated to provide comfort.
 
Relieving Anxiety
  • Assess the degree and duration of visual impairment.
  • Orient the patient to new environment.
  • Explain the preoperative routines.
  • Push to perform daily living habits when able.
  • Encourage the participation of family.
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Prevention of Injury
  • Provided a comfortable position to the patient.
  • Help the patient to set the environment.
  • Orient the patient in a room.
  • Discuss the need for use of goggles when instructed.
  • Do not put pressure over the affected eye trauma.
  • Used the proper procedures when providing eye drugs.
 
Promoting Self-Care
  • Cleared the all doubts of patient regarding the disease condition.
  • Maintained good IPR with the patient.
  • Provided calm cool environment to the patient.
  • Music therapy and pet therapy given to patient.
  • Relaxation therapy also provided to relieve the anxiety of patient.
 
Improving Knowledge
  • Provided adequate knowledge about a disease condition.
  • Provided the sunglasses to patient during exposure to sunlight.
  • Provided medications to patient on proper time.
  • Advised the patient to talk with doctor.
  • Followed the recommendations that ensure regular eye checkup by the ophthalmologist.
 
Health Education
  • Advised the patient to wear sunglasses during exposure.
  • Advised the patient to take analgesics to reduce pain.
  • Advised the patient to take proper diet.
  • Advised the patient to take care of eyes after surgery.
  • Advised patient to prevent eyes from dirt and dust.
  • Advised patient to preventing eyes from trauma.
  • Advised patient to report to doctor for early complications.
  • Advise patient to increase activities gradually as directed by health care provider.
  • Caution against activities that cause patient to strain.
  • Instruct patient and family in proper use of medications.
  • Advise patient to apply plastic shield over the eye at night to avoid accidental injury during sleep.
  • Infirm about fitting temporary corrective lenses for the first 6 weeks.
 
Complications
  • Capsular rupture
  • Vitreous loss
  • Endothalemitis
  • Pseudoexfoliation
  • Myopia.
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After Care
Before the patient goes home, may receive the following:
  • A patch to wear over eye until the follow-up exam
  • Eyedrops to prevent infection, treat inflammation, and help with healing
  • Wear dark sunglasses outside after removing the patch
  • Wash hands well before and after using eyedrops and touching eye. Try not to get soap and water in eye when are bathing or showering for the first few days.
 
GLAUCOMA
Glaucoma is a disease of the major nerve of vision, called the optic nerve. Glaucoma is characterized by a particular pattern of progressive damage to the optic nerve that generally begins with a subtle loss of side vision.
Fig. 7.5: Normal IOP vs Raised IOP
 
Etiology and Risk Factors
The most important risk factors include:
  • Age
  • Elevated eye pressure
  • Thin cornea
  • Family history of glaucoma
  • Nearsightedness
  • Past injuries to the eyes
  • Steroid use
  • A history of severe anemia or shock
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Pathophysiology
 
Types
  • Open-angle glaucoma (Chronic): Chronic open-angle glaucoma is the most common form of glaucoma. The ‘open’ drainage angle of the eye can become blocked leading to gradual increased eye pressure. If this increased pressure results in optic nerve damage, it is known as chronic open-angle glaucoma. The optic nerve damage and vision loss usually occurs so gradually and painlessly.
  • Angle-closure glaucoma: Angle-closure glaucoma results when the drainage angle of the eye narrows and becomes completely blocked. In the eye, the iris may close off the drainage angle and cause a dangerously high eye pressure. When the drainage angle of the eye suddenly becomes completely blocked, pressure builds up rapidly, and this is called acute angle-closure glaucoma.
  • Exfoliation syndrome: Exfoliation syndrome is a common form of open-angle glaucoma that results when there is a buildup of abnormal, whitish material on the lens and drainage angle of the eye. This material and pigment from the back of the iris can clog the drainage system of the eye, causing increased eye pressure.
  • Pigmentary glaucoma: Pigmentary glaucoma is characterized by the iris bowing backwards, and coming into contact with the support structures that hold the lens in place. This position disrupts the cells lining the back surface of the iris containing pigment, and results in a release of pigment particles into the drainage system of the eye. This pigment can clog the drain and can lead to an increase in eye pressure.
  • Low-tension glaucoma: This is another form that experts do not fully understand. Even though eye pressure is normal, optic nerve damage still occurs. Perhaps the optic nerve is over-sensitive or there is atherosclerosis in the blood vessel that supplies the optic nerve.
 
Signs and Symptoms
The signs and symptoms of primary open angle glaucoma and acute angle-closure glaucoma are quite different.
412Signs and Symptoms of Primary Open-angle Glaucoma
  • Peripheral vision is gradually lost. This nearly always affects both eyes.
  • In advanced stages, the patient has tunnel vision.
Signs and Symptoms of Closed Angle Glaucoma
  • Eye pain, usually severe
  • Blurred vision
  • Eye pain is often accompanied by nausea and sometimes vomiting
  • Lights appear to have extra halo-like glows around them
  • Red eyes
  • Sudden, unexpected vision problems, especially when lighting is poor.
Common symptoms are:
  • Unusual trouble adjusting to dark rooms
  • Difficulty focusing on near or distant objects
  • Squinting or blinking due to unusual sensitivity to light or glare
  • Change in color of iris
  • Red-rimmed, encrusted or swollen lids
  • Recurrent pain in or around eyes
  • Double vision
  • Dark spot at the center of viewing
  • Lines and edges appear distorted or wavy
  • Excess tearing or ‘watery eyes’
  • Dry eyes with itching or burning
  • Sudden loss of vision in one eye
  • Sudden hazy or blurred vision
  • Flashes of light or black spots
  • Halos or rainbows around light.
Fig. 7.6: Stages of glaucoma
 
Diagnostic Evaluation
  • Eye-pressure test: Tonometer, a device which measures intraocular pressure. Some anesthetic and a dye is placed in the cornea, and a blue light is held against the 413eye to measure pressure. This test can diagnose ocular hypertension; a risk factor for open-angle glaucoma.
    • Gonioscopy: This examines the area where the fluid drains out of the eye. It helps determine whether the angle between the cornea and the iris is open or blocked (closed).
    • Perimetry test: Also known as a visual field test. It determines which area of the patient's vision is missing. The patient is shown a sequence of light spots and asked to identify them. Some of the dots are located where the person's peripheral vision is; the part of vision that is initially affected by glaucoma. If the patient cannot see those peripheral dots, it means that some vision damage has already occurred.
    • Optic nerve damage: The ophthalmologist uses instruments to look at the back of the eye, which can reveal any slight changes which may also point towards glaucoma onset.
    • Visual acuity test: This eye chart test measures how well you see at various distances.
    • Visual field test: This test measures peripheral (side vision).
    • Dilated eye exam: In this exam, drops are placed in eyes to widen, or dilate, the pupils. Eye care professional uses a special magnifying lens to examine retina and optic nerve for signs of damage and other eye problems.
 
Management
 
Medical Management
  • Prostaglandin analogues: These medications have prostaglandin-like compounds as their active ingredient. They increase the outflow of the fluid inside the eye. Examples include Xalatan and Lumigan.
    • Beta blockers: These medications reduce the amount of fluid the eye produces. Some patients may experience breathing problems, hair loss, fatigue, depression, memory loss, a drop in blood pressure. Examples of such medications include timolol, betaxolol, and metipranolol.
    • Carbonic anhydrase inhibitors: These also reduce fluid production in the eye. Side effects may include nausea, eye irritation, dry mouth, frequent urination, tingling in the fingers or toes, and a strange taste in the mouth. Examples include brinzolamide and dorzolamide.
    • Cholinergic agents: Also known as miotic agents.
 
Surgery
  • Trabeculoplasty: A high-energy laser beam is used to unblock clogged drainage canals, making it easier for the fluid inside the eye to drain out. This procedure nearly always reduces inner eye pressure. However, the problem may come back.
  • Filtering surgery (viscocanalostomy): If eyedrops and laser surgery are not effective in controlling eye pressure, trabeculectomy is required. This procedure is performed in a hospital or an outpatient surgery center. Patient receives a medication to help relax and usually an injection of anesthetic to numb eye. Using small instruments under an operating microscope, an opening is created in the sclera and removes a small piece 414of eye tissue at the base of cornea through which fluid drains from eye (the trabecular meshwork). The fluid in eye can now freely leave the eye through this opening. As a result, eye pressure will be lowered.
  • Drainage implant (aqueous shunt implant): This option is sometimes used for children or those with secondary glaucoma. A small silicone tube is inserted into the eye to help it drain out fluids better.
  • Laser cycloablation (ciliary body destruction, cyclophotocoagulation or cyclocryopexy) is another form of laser treatment generally reserved for patients with severe forms of glaucoma with poor visual potential. This procedure involves applying laser burns or freezing to the part of the eye that makes the aqueous fluid. This therapy destroys the cells that make the fluid, thereby reducing the eye pressure.
  • Aqueous shunt devices: They are artificial drainage devices used to lower the eye pressure. They are essentially plastic microscopic tubes attached to a plastic reservoir. The reservoir is placed beneath the conjunctival tissue. The actual tube is placed inside the eye to create a new pathway for fluid to exit the eye. This fluid collects within the reservoir beneath the conjunctiva creating a filtering bleb. This procedure maybe performed as an alternative to trabeculectomy in patients with certain types of glaucoma.
 
Nursing Management
 
Nursing Assessment
  • Evaluate the patient for any of the clinical manifestations.
  • Assess patient's level of anxiety and knowledge base.
  • Assess the patient's knowledge of disease process.
 
Nursing Diagnosis
  • Pain related to increased to increased IOP.
  • Fear related to pain and potential loss of vision.
  • Self-care deficit related to visual deficit.
  • Anxiety related to lack of knowledge about the surgical and postoperative experience.
  • Risk for injury related to blurred vision.
  • Risk for infection related to trauma to incision.
  • Acute pain related to trauma to incision.
 
Intervention
 
Relieving Pain
  • Notify health care provider immediately.
  • Administer medications as directed.
  • Explain to patient that the goal of treatment is to reduce IOP as quickly as possible.
  • Explain procedures to patient.
  • Reassure patient that with reduction in IOP, Pain and other signs and symptoms should subside.
 
Relieving Fear
  • Provide reassurance and calm presence to reduce anxiety and fear.
  • Prepare patient for surgery, if necessary.
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Relieving Anxiety
  • Assess the degree and duration of visual impairment.
  • Orient the patient to new environment.
  • Explain the perioperatine routines.
  • Push to perform daily living habits when able.
  • Encourage the participation of family.
 
Prevention of Injury
  • Provided a comfortable position to the patient.
  • Help the patient to set the environment.
  • Orient the patient in a room.
  • Discuss the need for use of goggles when instructed.
  • Do not put pressure over the affected eye trauma.
  • Used the proper procedures when providing eye drugs.
 
Promoting Self-Care
  • Cleared the all doubts of patient regarding the disease condition.
  • Maintained good IPR with the patient.
  • Provided calm cool environment to the patient.
  • Music therapy and pet therapy given to patient.
  • Relaxation therapy also provided to relieve the anxiety of patient.
 
Improving Knowledge
  • Provided adequate knowledge about a disease condition.
  • Provided the sunglasses to patient during exposure to sunlight.
  • Provided medications to patient on proper time.
  • Advised the patient to talk with doctor.
 
Complications
If left untreated, glaucoma will cause progressive vision loss, normally in these stages:
  • Blind spots in peripheral vision
  • Tunnel vision
  • Total blindness.
 
RETINAL DETACHMENT
The retina is a light-sensitive membrane located at the back of the eye. When retina is detached from its pigmented epithelium is called retinal detachment. Characterized by partial or total loss of vision.
 
Types and Causes
  • Rhegmatogenous retinal detachment: It is characterized by tear or hole in retina. This allows fluid from within the eye to slip through the opening and get behind the retina. The fluid separates the retina from the membrane that provides it with nourishment and 416oxygen. The pressure from the fluid can push the retina away from the retinal pigment epithelium, causing the retina to detach.
  • Tractional retinal detachment: It occurs when scar tissue on the retina's surface contracts and causes the retina to pull away from the back of the eye. This is a less common type of detachment that typically affects people with diabetes.
  • Exudative detachment: This type of detachment is caused by retinal diseases such as inflammatory disorder or Coats disease, which causes abnormal development in the blood vessels behind the retina.
Fig. 7.7: Separation of retina from epithelium
 
Risk Factors
Risk factors for retinal detachment include:
  • Posterior vitreous detachment (PVD): A common condition in aging individuals, in which the fluid in the retina breaks down, putting strain on the retinal fibers
  • Extreme nearsightedness because
  • Family history of retinal detachment
  • Trauma to the eye
  • Being over 40 years old
  • Prior history of retinal detachment
  • Complications from cataract surgery
  • Diabetes.
 
Signs and Symptoms
There is no pain associated with retinal detachment, but there are usually symptoms before the retina becomes detached. Primary symptoms include:
  • Blurred vision
  • Partial vision loss
  • Flashes of light when looking to the side
  • Areas of darkness in field of vision
  • Suddenly seeing many floaters (small bits of debris that appear as black flecks or strings floating before the eye).
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Diagnostic Evaluation
  • Tonometry: To evaluate the eye pressure
  • Gonioscopy: To inspect the drainage angle of eye
  • Ophthalmolscopy: To evaluate the optic nerve.
 
Surgical Management
  • Photocoagulation: It is a laser burn around the tear site and the resulted scar will fixes the retina to the back of the eye.
  • Cryopexy: It consists of application of freezing probe to the tear site and the resulting scarring will help hold the retina in place.
  • Retinopexy: In this doctor will put a gas bubble in eye to help the retina move back into place. Once the retina is back in place, with the help of laser the holes are sealed out.
  • Scleral buckling: In this the sclera is pulled near the retina by decreasing the diameter of sclera. A small piece of silicone maybe sutured on or around the eye in a fashion that indents the eyeball and brings the retinal break that caused the detachment again in contact with it. This allows the subretinal fluid to reabsorb and the retina to reattach. Sometimes an air or gas bubble is injected at the time of surgery to aid reattachment of the retina.
  • Vitrectomy: By making tiny incisions into the eyeball, instruments are able to remove all the vitreous and subretinal fluid and reattach the retina. The retinal tear or tears that caused the detachment are then treated with laser to cause a permanent adhesive scar in this area and prevent a future detachment. A gas bubble, or less frequently an oil bubble, is instilled in the eye at the end of surgery to maintain the retina in contact with the eye wall as the laser scar matures.
 
Nursing Management
 
Nursing Diagnosis
  • Anxiety related to possible vision loss
  • Disturbed sensory perception related to visual impairment
  • Ineffective health maintenance related to knowledge deficit
  • Risk for injury related to impaired vision
  • Self-care deficit related to impaired vision.
 
Interventions
  • Prepare the patient for surgery.
    • Instruct the patient to remain quiet in prescribed (dependent) position, to keep the detached area of the retina in dependent position.
    • Patch both eyes.
    • Wash the patient's face with antibacterial solution.
    • Instruct the patient not to touch the eyes to avoid contamination.
    • Administer preoperative medications as ordered.
  • Take measures to prevent postoperative complications.
    • Caution the patient to avoid bumping head.
    • Encourage the patient no to cough or sneeze or to perform other strain-inducing activities that will increase intraocular pressure.
  • 418Encourage ambulation and independence as tolerated.
  • Administer medication for pain, nausea, and vomiting as directed.
  • Provide quiet diversional activities, such as listening to a radio or audio books.
  • Teach proper technique in giving eye medications.
  • Advise patient to avoid rapid eye movements for several weeks as well as straining or bending the head below the waist.
  • Advise patient that driving is restricted until cleared by ophthalmologist.
  • Teach the patient to recognize and immediately report symptoms that indicate recurring detachment, such as floating spots, flashing lights, and progressive shadows.
  • Advise patient to follow-up.
 
OTHER EYE DISORDERS
 
Stye (External and Internal Hordeolum)
An external stye or hordeolum is an infection of a lash follicle and its associated gland of zeis or moll. Internal styes are infections of the meibomian sebaceous glands lining the inside of the eyelids.
Fig. 7.8: Stye
 
Causes
  • Staphylococcus aureus bacterial infection
  • Blocking of an oil gland
  • Triggered by poor nutrition, sleep deprivation, lack of hygiene or rubbing of the eyes.
 
Signs and Symptoms
  • A lump on the top or bottom eyelid
  • Localized swelling of the eyelid
  • Localized pain
  • 419Redness
  • Tenderness to touch
  • Crusting of the eyelid margins
  • Sensation of a foreign body in the eye.
 
Treatment
  • Application of warm compresses.
  • Cleansing must be done gently.
  • Topical antibiotic ointments or antibiotic or steroid combination.
 
Prevention
  • Proper handwashing
  • Proper eye hygiene
  • Application of a warm washcloth
  • Never share cosmetics
  • Remove makeup every night before going to sleep
  • People are often advised to avoid touching their eyes or sharing towels and washcloths.
 
Chalazion (Meibomian Cyst)
A chalazion also known as a meibomian gland lipogranuloma, is a cyst in the eyelid that is caused by inflammation of a blocked duct of meibomian gland, usually on the upper eyelid.
Fig. 7.9: Chalazion
 
Signs and Symptoms
  • Swelling on the eyelid
  • Eyelid tenderness
  • Sensitivity to light
  • Increased tearing
  • Heaviness of the eyelid.
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Treatment
  • Chalazia will often disappear without further treatment within a few months and virtually all will resorb within two years.
  • Topical antibiotic eye drops or ointment (e.g. chloramphenicol or fusidic acid) are sometimes used.
  • A home remedy is to have a hot, wet flannel, and rub gently, until the heat has reached the cyst.
 
Blepharitis
Blepharitis is an ocular condition characterized by chronic inflammation of the eyelid.
Fig. 7.10: Blepharitis
 
Signs and Symptoms
  • Redness of the eyelids
  • Flaking of skin on the lids
  • Crusting at the lid margins, this is generally worse on waking
  • Cysts at the lid margin (hordeolum)
  • Red eye
  • Debris in the tear film, seen under magnification (improved contrast with use of fluorescein drops)
  • Gritty (sandy) sensation of the eye
  • Reduced vision.
 
Treatment
  • The single most important treatment principle is a daily routine of lid margin hygiene.
  • After lid margin cleaning, spread small amount of prescription antibiotic ophthalmic ointment with finger tip along lid fissure while eyes closed. Use prior to bed time as opposed to in the morning to avoid blurry vision.
  • Avoid the use of eye make-up until symptoms subside.
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Trichiasis
Trichiasis is a medical term for abnormally positioned eyelashes that grow back toward the eye, touching the cornea or conjunctiva.
  • This can be caused by infection, inflammation, autoimmune conditions, congenital defects, eyelid agenesis and trauma such as burns or eyelid injury.
  • Standard treatment involves removal or destruction of the affected eyelashes with electrology, specialized laser, or surgery.
Fig. 7.11: Trichiasis
 
Entropion
Entropion is a medical condition in which the eyelid (usually the lower lid) folds inward.
 
Ectropion
Ectropion is a medical condition in which the lower eyelid turns outwards.
Ectropion can occur due to any weakening of tissue of the lower eyelid. The condition can be repaired surgically.
 
Lagophthalmos
Lagophthalmos is defined as the inability to close the eyelids completely.
It leads to corneal drying and ulceration.
Lagophthalmos can arise from a malfunction of the facial nerve.
  • Lagophthalmos can also occur in comatose patients.
  • Blepharoplasty can be done as a treatment.
Fig. 7.12: Lagophthalamus
 
CONJUNCTIVAL DISORDERS
 
Conjunctivitis
Conjunctivitis (also called pink eye) refers to inflammation of the conjunctiva (the outermost layer of the eye and the inner surface of the eyelids).
 
Types of Conjunctivitis
  • Allergic conjunctivitis
  • Bacterial conjunctivitis
  • 422Viral conjunctivitis
  • Chemical conjunctivitis
  • Neonatal conjunctivitis
 
Signs and Symptoms
  • Red eye (hyperemia)
  • Irritation (chemosis)
  • Watering (epiphora)
  • Pain
  • Crusting of the eyelid margins
  • Burning in the eye
  • Droopiness of the eyelid
  • Scratchy sensation on the eyeball
  • Mucous discharge in the eye
  • Light sensitivity
  • Discomfort during blinking
  • Sensation of a foreign body in the eye
 
Management
  • Conjunctivitis resolves in 65% of cases without treatment, within two to five days. The prescribing of antibiotics to most cases is not necessary.
  • Symptomatic relief maybe achieved with cold compresses and artificial tears.
 
Prevention
  • People with conjunctivitis should not touch their eyes, regardless of whether or not their hands are clean, as they run the risk of spreading the condition to another eye.
  • With either type of conjunctivitis, handwashing is the best means of preventing the spread of disease.
  • People are often advised to avoid touching their eyes or sharing towels and washcloths.
  • During home care, eyes should be cleansed gently to remove exudates and the cleansing tissues disposed of using standard precautions.
  • Avoid shaking hands with other people.
  • Use separate medication bottles or tubes for each eye.
 
Pterygium
  • Pterygium (Surfer's Eye) most often refers to a benign growth of the conjunctiva.
  • A pterygium commonly grows from the nasal side of the sclera.
  • It is associated with, and thought to be caused by ultraviolet-light exposure (e.g. sunlight), low humidity, and dust.
 
Symptoms
  • Persistent redness
  • Inflammation
  • 423Foreign body sensation, which can cause bleeding, dry, and itchy eyes
  • Tearing
  • In advanced cases the pterygium can affect vision as it invades the cornea.
 
Treatment
  • Some of the irritating symptoms can be addressed with artificial tears.
  • However, no reliable medical treatment exists to reduce or even prevent pterygium progression.
  • Definitive treatment is achieved only by surgical removal i.e. irradiation, conjunctival autografting or amniotic membrane transplantation, along with glue and suture application.
  • Long-term follow-up is required as pterygium may recur even after complete surgical correction.
 
Prevention
  • As it is associated with excessive sun or wind exposure, wearing protective sunglasses with side shields and wide brimmed hats may help prevent their formation.
  • Surfers and other water-sport athletes should wear eye protection that blocks 100% of the UV rays from the water, as is often used by snow-sport athletes.
 
Subconjunctival Hemorrhage
  • A subconjunctival hemorrhage is bleeding underneath the conjunctiva.
  • Although its appearance maybe alarming, a subconjunctival hemorrhage is generally a painless and harmless condition.
  • It may be associated with high blood pressure, trauma to the eye, or a base of skull fracture.
 
Causes
  • Blood dyscrasia
  • Blood thinners. These can also make the vessels in the eye more susceptible to the pressure.
  • Diving accidents
  • Severe hypertension
  • LASIK
  • Minor eye trauma
  • Spontaneously with increased venous pressure
  • Strenuous exercising
  • Straining
  • Vomiting
  • Prolonged stress
  • Severe thoracic trauma, leading to increased pressure in the extremities, including around the eyes.
  • Subconjunctival hemorrhages in infants maybe associated with scurvy (a vitamin C deficiency), abuse or traumatic asphyxia syndrome.
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Treatment and Management
  • Self-limiting condition that requires no treatment in the absence of infection or significant trauma.
  • The elective use of aspirin and NSAIDs is typically discouraged.
 
CORNEAL DISORDERS
 
Keratitis
  • Keratitis is a condition in which the eye's cornea, the front part of the eye, becomes inflamed.
  • The condition is often marked by moderate to intense pain and usually involves impaired eyesight.
 
Types
  • Superficial keratitis involves the superficial layers of the cornea. After healing, this form of keratitis does not generally leave a scar.
  • Deep keratitis involves deeper layers of the cornea, and the natural course leaves a scar upon healing that impairs vision if on or near the visual axis. This can be reduced or avoided with the use of topical corticosteroid eyedrops.
 
Causes
  • Viral: Infection of herpes simplex virus secondary to an upper respiratory infection, involving cold sores.
  • Amebic Keratitis: Amebic infection of the cornea is the most serious corneal infection, usually affecting contact lens wearers. It is usually caused by Acanthameba.
  • Bacterial Keratitis: Bacterial infection of the cornea can follow from an injury or from wearing contact lenses. The bacteria involved are Staphylococcus aureus and for contact lens wearers, Pseudomonas aeruginosa. Pseudomonas aeruginosa contains enzymes that can digest the cornea.
  • Fungal Keratitis: Filamentous fungi are most frequently the causative organism for fungal keratitis.
  • Onchocercal keratitis: Which follows O. volvulus infection by infected blackfly bite. These blackfly usually dwell near fast-flowing African streams, so the disease is also called ‘river blindness’.
 
Treatment
  • Treatment depends on the cause of the keratitis. Infectious keratitis generally requires antibacterial, antifungal, or antiviral therapy to treat the infection.
  • In addition, contact lens wearers are typically advised to discontinue contact lens wear and discard contaminated contact lenses and contact lens cases.
  • With proper medical attention, infections can usually be successfully treated without long-term visual loss.
 
Corneal Dystrophies
  • Corneal dystrophies comprise a group of hereditary and acquired disorders of unknown cause, characterized by deposits in the layers of the cornea and alteration of the corneal structure.
  • 425Corneal dystrophies are associated with all five layers of the cornea. Although the disease usually originates in the inner layers (Descemet's membrane, the stroma, and Bowman's membrane), the degeneration, erosion, and deposits affect all layers.
 
Management
The goal of treatment is to restore visual clarity for both safety and improved quality of life.
 
Medical Management
Dystrophies cannot be cured; however, with certain medications, blurred vision resulting from corneal swelling can be controlled.
 
Surgical Management
 
Corneal Transplantation
  • Corneal transplantation (keratoplasty) is the use of donor corneas to improve the clarity of vision.
 
NURSING PROCESS—INFLAMMATION AND INFECTION OF THE EYE
 
Assessment
Assessment of symptoms for any eye problem includes asking the client for subjective data using the WHAT'S UP acronym:
  • Where is it? What part of the eye is affected? Eyelid, conjunctiva, cornea?
  • How does it feel? Pressure? Itchy? Painful? No pain? Irritated? Spasm?
  • Aggravating and alleviating factors. Worse when rubbing eyes, blinking? Photosensitivity?
  • Timing. Was there exposure to a pathogen? Previous infection or irritation? Length of time symptoms has persisted?
  • Severity. Is there visual impairment? Does pain affect ADL?
  • Useful data for associated symptoms. Immunosuppression drugs? Do other members of the family or peer group have symptoms? Are decongestant eyedrops used? Is there exudate? Are the eyelids sticks together on awakening? Does client wear contact lenses, soft contact lenses overnight, disposable contact lenses? Does client have dry eyes? Infection with tuberculosis, syphilis, HIV? What is typical eye hygiene?
  • Perception by the client of the problem. What does client think is wrong?
  • Assess the condition of conjunctiva, the condition of eyelids and eyelashes, the presence of exudate, whether tearing is occurring, any visible abscess on palpebral border, a palpable abscess in eyelid, opacity of the cornea, and visual acuity testing comparing unaffected and affected eyes.
 
Nursing Management
 
Nursing Assessment
History (subjective data):
  • Change in vision
  • Pain, itching, burning
  • 426Excessive watering
  • Blurred vision, double vision (diplopia)
  • Loss in field of vision, blind spots, floating spots
  • Difficulty with vision at night
  • Pain in bright light
  • Frontal headache
  • Halos around lights
  • Frequent reddening of eye–conjunctivitis
  • Discharge, eye crusted on awakening
  • Eyes feel dry–Wearing contact lenses, glasses
  • Regular medication
  • History of glaucoma in family
  • History of diabetes, hypertension
  • Date of last eye exam.
Physical Assessment (objective data):
  • Observe for redness of conjunctiva, swelling, secretions, excessive tearing
  • Change in visual acuity
  • Note any squinting, tilting head
  • Note ability to move eyebrows, eyes.
 
Nursing Diagnosis
  • Pain related to inflammation or infection of the eye or surrounding tissues.
  • Sensory-perceptual alteration (visual) related to blepharospasm, photophobia, diminished visual acuity, visual distortions.
  • Risk for injury related to visual impairment.
  • Risk for infection related to poor eye hygiene.
  • Knowledge deficit related to disease process, prevention and treatment.
 
Interventions
 
General Interventions for Visually Impaired
  • Speak as you enter the room and before touching patient
  • Tell the patient when you are leaving
  • Do not move objects without asking patient
  • Give special orientation to room on admission
  • Set-up meal tray and orient patient to food.
 
Preoperative
  • Describe procedure—local anesthetic
  • Discharge teaching—eye drops, activity restrictions
  • Start stool softeners to prevent constipation
  • Wash face well with surgical soap
  • Instill eye drops as order.
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Postoperative
  • Be gentle—no jarring movement
  • Treat nausea immediately with antiemetics
  • Monitor for pain or visual changes (sign of bleeding)
  • Eye patch with nonallergic tape
  • Patch both eye if restricting movement of eye
  • Metal eye shield at night for extra protection
  • Physician orders for positioning instilling eye drops
  • Wash hands, give patient tissue
  • Remove eye patch, gently cleanse with wet gauze
  • Patient supine or head tilted up, look up
  • Pull lower lid down
  • Do not touch dropper to patient's eye
  • Put pressure with finger over lacrimal duct to decrease systemic absorption
  • Ask to close eye gently and rotate eyeball to distribute medication. Do not squeeze eye shunt
  • Apply new patch with nonallergic tape.
 
EYE BANKING AND CORNEAL TRANSPLANTATION
It is an organization that deals with the collection, storage and distribution of donor eyes for the purpose of corneal grafting.
  • Corned blindness is a major form of visual deprivation in developing countries. A high percentage of these individuals can be visually rehabilitated by corneal transplantation (keratoplasty), a procedure that has very high rate of success among organ transplants. Quality of donor cornea, the nature of recipient pathology and the availability of appropriate postoperative care are the factors that determine the final outcome of this procedure.
  • In corneal grafting this diseased and opaque cornea is replaced by a healthy transparent cornea taken from a donor eye.
  • A corneal transplant can take one of two forms: A full-thickness penetrating keratoplasty, involving excision and replacement of the entire cornea, or a lamellar keratoplasty, which removes and replaces a superficial layer of corneal tissue.
 
Functions of Eye Bank
Procurement and supply of donor cornea to the corneal surgeons is the primary goal of eye banks
  • The eye bank collects the eyes of voluntary registered eye donors after their death of those deceased persons when enlightened relatives agree to donate the eyes as a service to humanity. From hospital deaths and from postmortem cases, after obtaining the consent from the next of kin.
  • 428These eyes are processed by the Eye Bank and are supplied to eye surgeons for corneal grafting and other sight restoring operations.
  • Before proceeding for recovery eye bank personnel should ascertain the following details: Location, Age of the donor, Cause of death and Time of death.
 
Contraindications for Donation
  • All eye banks have age limits both minimum and maximum
  • Previous corneal graft
  • Death of unknown cause
  • Dementia
  • Creutzfeldt–Jacob disease
  • Subacute sclerosing panencephalitis.
  • Congenital rubella
  • Reyes syndrome
  • Active viral encephalitis or encephalitis of unknown origin
  • Active septicemia
  • Rabies
  • Retinoblastomas, tumors of the anterior segment
  • Active ocular infections
  • Pterygia or other superficial disorders of the conjunctiva or corneal surface
  • Certain intraocular or anterior segment surgeries
  • Leukemia
  • Active disseminated lymphomas.
  • Hepatitis B and C, HTLV-1 or 2, HIV, syphilis.
  • Behavioral and or social issues, i.e. homosexual or other high-risk sexual behavior within the last 5 years.
  • Intravenous drug use for nonmedical reasons within the last 5 years
  • Exposure to infectious disease within the last year by contact with an open wound, needle stick, or mucous membrane.
  • Tattooing or piercing within the last 12 months using shared instruments.
 
Retrieval Procedure
  • Retrieval procedure could be either enucleation or corneal scleral rim excision.
  • Eye Bank team should carry only validated sterile instruments for retrieval.
  • Eye Bank team on arrival at the location should locate the next of kin and convey condolence and obtain death certificate.
  • In the absence of a death certificate the registered medical practitioner should satisfy self that life is extinct.
  • The eye bank team should obtain consent on a consent form from the legal custodian of the donor.
  • After obtaining consent the donor should be identified either through a tag or through the next of kin.
  • The eye bank team should then proceed to prepare the site.
  • Gross physical examination should be conducted with utmost respect for observations regarding build: Average, healthy or emaciated.
  • 429Eye bank team should look out for needle marks on the arm, skin lesions, etc.
  • Eye bank team should look out for ulcers or gangrene in exposed areas.
  • Ocular examination should be conducted.
  • Medical records and medical information should be obtained.
  • Information for hemodilution should be obtained.
  • Social history of the donor should be obtained wherever possible from the next of kin.
 
Role of Nurse During Corneal Transplantation
  • Explain the transplant procedure to the patient and answer any questions he may have.
  • Advise him that healing will be slow and that his vision may not be completely restored until the sutures are removed, which may be in about a year.
  • Tell the patient that most corneal transplants are performed under local anesthesia and that he can expect momentary burning during injection of the anesthetic.
  • Explain to him that the procedure will last for about an hour and that he must remain still until it has been completed.
  • Tell the patient that analgesics will be available after surgery because he may experience a dull aching.
  • Inform him that a bandage and protective shield will be placed over the eye.
  • As ordered, administer a sedative or an osmotic agent to reduce intraocular pressure.
  • Ensure that the patient has signed a consent form.
 
After Surgery
  • After the patient recovers from the anesthetic, assess for and immediately report sudden, sharp, or excessive pain, bloody, purulent, or clear viscous drainage or fever.
  • As ordered, instill corticosteroid eyedrops or topical antibiotics to prevent inflammation and graft rejection.
  • Instruct the patient to lie on his back or on his unaffected side, with the bed flat or slightly elevated as ordered. Also, have him avoid rapid head movements, hard coughing or sneezing, bending over, and other activities that could increase intraocular pressure; likewise, he should not squint or rub his eyes.
  • Remind the patient to ask for help in standing or walking until he adjusts to changes in his vision.
  • Make sure that all his personal items are within his field of vision.
 
Home Care Instructions
  • Teach the patient and his family to recognize the signs of graft rejection (inflammation, cloudiness, drainage, and pain at the graft site.)
  • Instruct them to immediately notify the doctor if any of these signs occur.
  • Emphasize that rejection can occur many years after surgery; stress the need for assessing the graft daily for the rest of the patient's life. Also, remind the patient to keep regular appointments with his doctor.
  • Tell the patient to avoid activities that increase intraocular pressure, including extreme exertion, sudden, jerky movements, lifting or pushing heavy objects and straining during defecation.
  • 430Explain that photophobia, a common adverse reaction, gradually decreases as healing progresses.
  • Suggest wearing dark glasses in bright light.
  • Teach the patient how to correctly instill prescribed eyedrops.
  • Remind the patient to wear an eye shield when sleeping.
  • Tell the patient to consult with the surgeon before driving or participating in sports or other recreational activities.
BIBLIOGRAPHY
  1. Black JM, Hawks JH. Medical surgical nursing: clinical management for positive outcomes, 8th ed. (vol 2). Elsevier;  New Delhi:  2010: 1704–15.
  1. Brunner, Suddarth. Textbook of medical surgical, 12th ed.
  1. Bucher L, Lewis SL, Heitkemper MM, Dirksen SR. Lewis's medical surgical nursing. Elsevier;  New Delhi:  2011: 416–23.
  1. Clark A, Morlet N, Jonathan Q, Preen DB, Semmens JB. Whole population trends in complications of cataract surgery over 22 years in Western Australia. Ophthalmology 2011 Jun; 118(6): 1055–61.
  1. Harsh M. Textbook of pathology, 6th ed. Jaypee Brothers Medical Publisher (p) Ltd.  New Delhi: 
  1. Joyce MB, Hawks HJ. Textbook of medical surgical nursing. 8th, ed. Vol. 1.
  1. Kanski JJ. Clinical ophthalmology: a systematic approach. 2nd ed. Hong Kong:1989: 1–12.
  1. Kaur L, Kaur S. Textbook of medical surgical. 2nd ed. Vol. 1 Lotus publisher. 
  1. Lewis's medical surgical nursing. Assessment and management of clinical problems, US editors, 421–8.
  1. Nettina SM. Lippincott manual of nursing practice, 9th ed. Wolters kluwer;  New Delhi:  2010: 594–8.
  1. The Lippincott. Manual nursing practice. 18th ed. 432–4.
  1. Williams LS, Hopper PD. Understanding medical surgical nursing. 7th ed. Davis company;  Philadelphia:  1999: 1040–57.

Ear, Nose and Throat Disorders8

 
INTRODUCTION
 
Outer Ear
The outer ear includes the portion of the ear that we see—the pinna or auricle and the ear canal.
 
Pinna
The pinna or auricle is a concave cartilaginous structure, which collects and directs sound waves traveling in air into the ear canal or external auditory meatus.
 
Ear Canal
The ear canal or external auditory meatus is approximately 1.25 inches long and .25 inch in diameter. The inner two-thirds of the ear canal is imbedded in the temporal bone. The outer one-third of the canal is cartilage. Although the shape of each ear canal varies, in general, the canal forms an elongated ‘S’ shaped curve. The ear canal directs airborne sound waves towards the tympanic membrane (eardrum). The ear canal resonates sound waves and increases the loudness of the tones in the 3000–4000 Hz range.
The ear canal maintains the proper conditions of temperature and humidity necessary to preserve the elasticity of the tympanic membrane. Glands, which produce cerumen and tiny hairs in the ear canal, provide added protection against insects and foreign particles from damaging the tympanic membrane.
432
 
Middle Ear
The middle ear is composed of the tympanic membrane and the cavity, which houses the ossicular chain.
 
Tympanic Membrane
The tympanic membrane or eardrum serves as a divider between the outer ear and the middle ear structures. It is gray-pink in color when healthy and consists of three very thin layers of living tissue.
The eardrum is very sensitive to sound waves and vibrates back and forth as the sound waves strike it. The eardrum transmits the airborne vibrations from the outer to the middle ear and also assists in the protection of the delicate structures of the middle ear cavity and inner ear.
 
Middle Ear Cavity
The middle ear cavity is located in the mastoid process of the temporal bone. The middle ear cavity extends from the tympanic membrane to the inner ear. It is approximately two cubic centimeters in volume and is lined with mucous membrane. The middle ear cavity is actually an extension of the nasopharynx via the eustachian tube.
 
Eustachian Tube
The eustachian tube acts as an air pressure equalizer and ventilates the middle ear. Normally the tube is closed but opens while chewing or swallowing. When the eustachian tube opens, the air pressure between the outer and middle ear is equalized. The transmission of sound through the eardrum is optimal when the air pressure is equalized between the outer and middle ear. When the air pressure between the outer and middle ear is unequal, the eardrum is forced outward or inward causing discomfort and the ability of the eardrum to transmit sound is reduced.
 
Ossicular Chain
The middle ear is connected and transmits sound to the inner ear via the ossicular chain. The ossicular chain amplifies a signal approximately 25 decibels as it transfers signals from the tympanic membrane to the inner ear.
The ossicular chain consists of the three smallest bones in the body: the malleus, incus, and stapes. The malleus is attached to the tympanic membrane. The footplate of the stapes inserts into the oval window of the inner ear. The incus is between the malleus and the stapes.
Attached to the ossicular chain are two tiny muscles, the stapedius and tensor tympani muscles. These muscles contract to protect the inner ear by reducing the intensity of sound transmission to the inner ear from external sounds and vocal transmission.
 
Inner Ear
The inner ear is composed of the sensory organ for hearing—the cochlea, as well as for balance—the vestibular system. The systems are separate, yet both are encased in the same bony capsule and share the same fluid systems.
433
 
Vestibular or Balance System
The balance part of the ear is referred to as the vestibular apparatus. It is composed, in part, of three semicircular canals located within the inner ear. The vestibular system helps to maintain balance, regardless of head position or gravity, in conjunction with eye movement and somatosensory input. The semicircular canals are innervated by the VIII cranial nerve.
 
Cochlea
The hearing part of the inner ear is the cochlea. The cochlea is spiral-shaped, similar to the shape of a snail.
The cochlea is composed of three fluid-filled chambers that extend the length of the structure. The two outer chambers are filled with a fluid called perilymph. Perilymph acts as a cushioning agent for the delicate structures that occupy the center chamber. It is important to note that perilymph is connected to the cerebrospinal fluid that surrounds the brain and the spinal column. The third fluid-filled chamber is the center chamber, called the cochlear duct. The cochlear duct secretes a fluid called endolymph, which fills this chamber.
The cochlear duct contains the basilar membrane upon which lies the organ of corti. The organ of Corti is a sensory organ essential to hearing. It consists of approximately 30,000 finger-like projections of cilia that are arranged in rows. These cilia are referred to as hair cells. Each hair cell is connected to a nerve fiber that relays various impulses to the cochlear branch of the VIII cranial nerve or auditory nerve. The ‘pitch’ of the impulse relayed is dependent upon which areas of the basilar membrane, and hence, which portions of the organ of Corti are stimulated. The apical portion of the basilar membrane (the most curled area of the cochlea) transfers lower frequency impulses. The basal end relays higher frequency impulses.
 
PHYSIOLOGY OF HEARING
The process of hearing begins with the occurrence of a sound. Sound is initiated when an event moves and causes a motion or vibration in the air. When this air movement stimulates the ear, a sound is heard.
In the human ear, a sound wave is transmitted through four separate mediums along the auditory system before a sound is perceived: in the outer ear—air, in the middle ear— mechanical, in the inner ear—liquid and to the brain—neural.
 
Sound Transmission through the Outer Ear
Air-transmitted sound waves are directed toward the delicate hearing mechanisms with the help of the outer ear, first by the pinna, which gently funnels sound waves into the ear canal, then by the ear canal.
 
Sound Transmission through the Middle Ear
When air movement strikes the tympanic membrane, the tympanic membrane or eardrum moves. At this point, the energy generated through a sound wave is transferred from a medium of air to that which is solid in the middle ear. The ossicular chain of the middle ear connects to the eardrum via the malleus, so that any motion of the eardrum sets the three little bones of the ossicular chain into motion.
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Sound Transmission through the Inner Ear
The ossicular chain transfers energy from a solid medium to the fluid medium of the inner ear via the stapes. The stapes is attached to the oval window. Movement of the oval window creates motion in the cochlear fluid and along the basilar membrane. Motion along the basilar membrane excites frequency-specific areas of the organ of Corti, which, in turn, stimulates a series of nerve endings.
 
Sound Transmission to the Brain
With the initiation of the nerve impulses, another change in medium occurs: from fluid to neural. Nerve impulses are relayed through the VIII CN through various nuclei along the auditory pathway to areas to the brain. It is the brain that interprets the neural impulses and creates a thought, picture, or other recognized symbols.
EAR DISORDERS
 
OTITIS MEDIA
Otitis media refers to inflammation of the middle ear. Acute otitis media occurs when a cold, allergy, or upper respiratory infection, and the presence of bacteria or viruses lead to the accumulation of pus and mucus behind the eardrum, blocking the Eustachian tube and characterized by earache and swelling.
When fluid accumulates in the middle ear, the condition is known as otitis media with effusion. This occurs in a recovering ear infection.
 
Types
  • Acute otitis media: It is usually of rapid onset and short duration. Acute otitis media is typically associated with fluid accumulation in the middle ear together with signs or symptoms of ear infection and may associate with drainage of purulent material (pus, also termed as suppurative otitis media).
  • Chronic otitis media: It is a persistent inflammation of the middle ear, typically for a minimum of a month. Following an acute infection, fluid may remain behind the eardrum for up to three months before resolving. Chronic otitis media may develop after a prolonged period of time with fluid or negative pressure behind the eardrum.
 
Etiology
Winter is high season for ear infections. They often follow a cold. Some factors that increase a risk for middle ear infections include:
  • Crowded living conditions
  • Attending daycare
  • Exposure to secondhand smoke
  • Respiratory illnesses such as common cold
  • Close contact with siblings who have cold
  • Having a cleft palate
  • Allergies that cause congestion on a chronic basis
  • 435Premature birth
  • Not being breastfed
  • Bottle-feeding while lying down
 
Signs and Symptoms
Symptoms of an ear infection may include:
  • Acute otitis media (AOM)
  • Pulling at ears
  • Excessive crying
  • Fluid draining from ears
  • Sleep disturbances
  • Fever
  • Headaches
  • Problems with hearing
  • Irritability
  • Difficulty balancing
Symptoms of fluid buildup may include:
 
Swimmer's Ear Symptoms
The symptoms of swimmer's ear include: Itching inside the ear Watery discharge from the ear Severe pain and tenderness in the ear, especially when moving your head or when gently pulling on the earlobe A foul-smelling, yellowish discharge from the ear Temporarily muffled hearing (caused by blockage of the ear canal).
Read the Understanding Swimmer's Ear Symptoms Article:
  • Popping, ringing, or a feeling of fullness or pressure in the ear
  • Trouble hearing
  • Balance problems and dizziness.
 
Diagnostic Evaluation
  • History, a physical examination and an ear examination
  • Pneumatic otoscope to look at the eardrum for signs of an ear infection or fluid buildup.
 
Ear Infection Symptoms
The symptoms of an ear infection in adults are: Earache (either a sharp, sudden pain or a dull, continuous pain); A sharp stabbing pain with immediate warm drainage from the ear canal; A feeling of fullness in the ear; Nausea Muffled hearing; Ear drainage. In children, the symptoms are: Tugging at the ear; Poor sleep Fever Irritability, restlessness; Ear drainage; Diminished appetite; Crying at night when lying down.
  • Tympanometry: Which measures how the eardrum responds to a change of air pressure inside the ear.
  • Hearing tests
  • Tympanocentesis: This test can remove fluid if it has stayed behind the eardrum (chronic otitis media with effusion).
  • Blood tests, which are done if there are signs of immune problems.
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Complications
Infratemporal infections can include:
  • Tympanic membrane perforation
  • Mastoiditis
  • Facial nerve palsy
  • Acute labyrinthitis
  • Petrositis
  • Acute necrotic otitis
  • Chronic otitis media.
Intracranial infections can include:
  • Meningitis
  • Encephalitis
  • Brain abscess
  • Otitic hydrocephalus
  • Subarachnoid abscess
  • Subdural abscess
  • Sigmoid sinus thrombosis.
 
Management
Antibiotic is the only treatment for otitis media.
 
Agents Used in the Treatment of Otitis Media
Agent
Dosage
Comments
Antimicrobials*
Amoxicillin
80 to 90 mg per kg per day, given orally in two divided doses
First-line drug. Safe, effective, and inexpensive
Amoxicillin (Augmentin)
90 mg of amoxicillin per kg per day given orally in two divided doses
Second-line drug. For patients with recurrent or persistent acute otitis media, those taking prophylactic amoxicillin, those who have used antibiotics within the previous month, and those with concurrent purulent conjunctivitis
Azithromycin
30 mg per kg, given orally
For patients with penicillin allergy. One dose is as effective as longer courses
Azithromycin (three-day course)
20 mg per kg once daily, given orally
For patients with recurrent acute otitis media
Azithromycin (five-day course)
5 to 10 mg per kg once daily, given orally
For patients with penicillin allergy (type 1 hypersensitivity)
Cefdinir
14 mg per kg per day, given orally in one or two doses
For patients with penicillin allergy, excluding those with urticaria or anaphylaxis to penicillin (i.e. type 1 hypersensitivity)
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Cefpodoxime
30 mg per kg once daily, given orally
For patients with penicillin allergy, excluding those with urticaria or anaphylaxis to penicillin (i.e. type 1 hypersensitivity)
Ceftriaxone (Rocephin)
50 mg per kg once daily, given intramuscularly or intravenously. One dose for initial episode of otitis media, three doses for recurrent infections
For patients with penicillin allergy, persistent or recurrent acute otitis media, or vomiting
Cefuroxime (Ceftin)
30 mg per kg per day, given orally in two divided doses
For patients with penicillin allergy, excluding those with urticaria or anaphylaxis to penicillin (i.e. type 1 hypersensitivity)
Clarithromycin
15 mg per kg per day, given orally in three divided doses
For patients with penicillin allergy (type 1 hypersensitivity). May cause gastrointestinal irritation
Clindamycin
30 to 40 mg per kg per day, given orally in four divided doses
For patients with penicillin allergy (type 1 hypersensitivity)
Topical agents
Ciprofloxacin/hydrocortisone
3 drops twice daily
Hydrocortisone/neomycin
4 drops three to four times daily
Ofloxacin
5 drops twice daily (10 drops in patients older than 12 years)
Analgesics
Acetaminophen
15 mg per kg every six hours
Antipyrine/benzocaine
2 to 4 drops three to four times daily
Ibuprofen
10 mg per kg every six hours
 
Nursing Management
 
Nursing Diagnosis
  • Acute pain related to inflammation of the middle ear tissue.
  • Disturbed sensory perception: Auditory conductive disorder related to the sound of the organ.
  1. Acute pain related to inflammation of the middle ear tissue
    Intervention
    • Assess the level of intensity of the client and client's coping mechanisms.
    • Give analgesics as indicated.
    • Distract the patient by using relaxation techniques: distraction, guided imagination, touching, etc.
  2. 438Disturbed sensory perception: Auditory conductive disorder related to the sound of the organ
    Intervention
    • Reduce noise in the client environment.
    • Looking at the client when speaking.
    • Speaking clearly and firmly on the client without the need to shout.
    • Providing good lighting when the client relies on the lips.
    • Using the signs of nonverbal (e.g. facial expressions, pointing, or body movement) and other communications.
    • Instruct family or the people closest to the client about the techniques of effective communication so that they can interact with clients.
    • If the client wants, the client can use hearing aids.
 
TYMPANIC MEMBRANE PERFORATION
The eardrum serves two important functions in the ear. It senses vibrating sound waves and converts the vibration into nerve impulses that convey the sound to brain. It also protects the middle ear from bacteria as well as water and foreign objects. Normally, the middle ear is sterile. But when the eardrum is ruptured, bacteria can get into the middle ear and cause an infection known as otitis media.
A ruptured eardrum is a tear in the thin membrane that separates outer ear from inner ear and when there is any abnormal opening or perforation in tympanic membrane, it is termed as perforated tympanic membrane.
 
Etiology
Traumatic causes of TM perforation include:
  • A number of things can cause the eardrum to rupture; one of the most common causes is an ear infection. When the middle ear is infected, pressure builds up and pushes against the eardrum. When the pressure gets too high, it can cause the eardrum to perforate.
  • Insertion of objects into the ear canal purposely: Another common cause of a ruptured eardrum is poking the eardrum with a foreign object, such as a cotton-tipped swab or a bobby pin that is being used to clean wax out of the ear canal. Sometimes children can puncture their own eardrum by putting objects, such as a stick or a small toy in their ears.
  • Concussion caused by an explosion or open-handed slap across the ear
  • Head trauma
  • Sudden negative pressure (e.g. strong suction applied to the ear canal)
  • Barotrauma: This happens when the pressure inside the ear and the pressure outside the ear are not equal. That can happen, for example, when an aeroplane changes altitude, causing the air pressure in the cabin to drop or rise. The change in pressure is also a common problem for scuba divers.
  • Iatrogenic perforation during irrigation or foreign body removal.
 
Signs and Symptoms
Some people do not notice any symptoms of a ruptured eardrum. Others complain only after several days of general discomfort in their ear and feeling that ‘something is not quite 439right with the ear’. Some people are surprised to hear air coming out of their ear when they blow their nose. Forcefully blowing nose causes air to rise up to fill the space in the middle ear. Normally this will cause the eardrum to balloon outward. But if there is a hole in the eardrum, air will rush out. Sometimes the sound is loud enough for other people to hear.
Other symptoms of a ruptured eardrum include:
  • Sudden sharp ear pain or a sudden decrease in ear pain
  • Drainage from the ear that may be bloody, clear, or resemble pus
  • Ear noise or buzzing
  • Hearing loss that may be partial or complete in the affected ear
  • Episodic ear infections
  • Facial weakness or dizziness
 
Diagnostic Evaluation
  • Audiometry: This hearing test checks how sensitive ears are to sounds at different volumes. The hearing tests may include pure-tone audiometry and speech audiometry tests. The tests help measure the quietest sounds or speech that can hear. They also help measure how well one can understand words when they are spoken at a normal sound level. These tests may check the type of hearing loss.
  • Otoscopy: An otoscope helps to see inside the ear and visualize the eardrum.
  • Tuning fork test: For this test, a vibrating tuning fork is held against the bone behind the ear. The tuning fork may also be held against the forehead, nose, or outside the opening of ear. You will be asked if you can hear certain sounds. Your hearing may be tested holding the tuning fork in more than one place. When this is done, you will be asked to state which area you heard the sound best.
 
Management
  • Ear kept dry
  • Oral or topical antibiotics
Often no specific treatment is needed. The ear should be kept dry, routine antibiotic ear drops are unnecessary. However, prophylaxis with oral broad-spectrum antibiotics or antibiotic ear drops is necessary if contaminants may have entered through the perforation as occurs in dirty injuries. If the ear becomes infected, amoxicillin 500 mg is given for 7 days. Although most perforations close spontaneously, surgery is indicated for a perforation persisting.
 
Surgical Management
Surgery is required to repair eardrum and prevent future ear infections. This is done when the hole in eardrum is large or does not heal on its own.
  • Myringoplasty: This type of surgery uses a tissue graft to cover torn eardrum. A tissue graft may be taken from own body, another person, an animal, or is man-made. A procedure called a mastoidectomy may also be done with a myringoplasty. A mastoidectomy is removal of infected bone from behind ear.
  • Tympanoplasty: This surgery repairs torn eardrum and any damage to inner ear. A tympanoplasty also helps prevent ear infections that stop and come back. The hole in eardrum will be covered with a tissue graft.
440
 
OTOSCLEROSIS AND HEARING LOSS
Otosclerosis is a term derived from oto, meaning ‘of the ear’ and sclerosis, meaning ‘abnormal hardening of body tissue’. The condition is caused by abnormal bone remodeling in the middle ear. Bone remodeling is a lifelong process in which bone tissue renews itself by replacing old tissue with new characterized by abnormal remodeling of ear bone that disrupts the ability of sound to travel from the middle ear to the inner ear.
 
Types of Hearing Impairment
The external ear and the middle ear conduct sound; the inner ear receives it. If there is some difficulty in the external or middle ear, a conductive hearing impairment occurs. If the trouble lies in the inner ear, a sensorineural or nerve hearing impairment is the result. When there is difficulty in both the middle and the inner ears a mixed or combined impairment exists. Mixed impairments are common in otosclerosis.
 
Cochlear Otosclerosis
When otosclerosis spreads to the inner ear, a sensorineural hearing impairment may result due to interference with the nerve function. This nerve impairment is called cochlear otosclerosis and once it develops it may be permanent. On occasions the otosclerosis may spread to the balance canals and may cause episodes of unsteadiness.
 
Stapedial Otosclerosis
Usually otosclerosis spreads to the stapes or stirrup, the final link in the middle ear transformer chain. The stapes rests in the small groove, the oval window, in intimate contact with the inner ear fluids. Anything that interferes with its motion results in a conductive hearing impairment. This type of impairment is called stapedial otosclerosis and is usually correctable by surgery.
 
Etiology
The most commonly affected portion of the bone around the inner ear (otic capsule) is the anterior oval window. It can also involve the round window niche, the internal auditory canal, and occasionally ossicles other than the stapes. Otosclerosis is thought to begin with otospongiosis, which is a localized softening of the normally very hard bone of the otic capsule. There appear to be three stages of otosclerosis—resorptive osteoclastic stages with signs of inflammation, followed by an osteoblastic stage involving immature bone, followed by mature bone formation.
  • Genetic
  • Viral
 
Diagnostic Evaluation
  • Tympanometry can show stiffening of the ossicular chain.
  • Acoustic reflexes are very useful in otosclerosis, as they show a characteristic ‘inversion’ pattern.
  • The temporal bone CT scan is both nonspecific and insensitive.
441
 
Treatment of Otosclerosis
There are four treatment options:
 
1. Doing Nothing is a Reasonable Option
Otosclerosis does not have to be treated, as there are no medications that have been shown to work, and it will progress or not independent of any treatment. It is advisable to have a formal hearing test repeated once a year.
 
2. Hearing Aids
Hearing aids are effective for conductive hearing loss and certainly are less risky than having ear surgery. Hearing aid technology has undergone tremendous advances since the invention of surgical treatment for otosclerosis. Bone-anchored hearing aids (BAHA), can be especially convenient.
 
3. Medical Treatment
Fluorides
Fluoride therapy is no longer a recommended primary treatment for otosclerosis, because of its effect on other bones including the possibility of increasing the risk of hip fractures. After two years of fluoride treatment, the dose of fluoride is reduced from three times a day to once a day. Once the otospongiosis phase of otosclerosis is over and there is a clear-cut otosclerosis documented by conductive hearing loss, fluoride may be stopped. The treatment is continued after surgery.
Bisphosphonates can also be recommended in some cases.
Other Approaches
Avoidance of estrogens or use of estrogen blockers might be helpful in an individual with otosclerosis as otosclerosis frequently worsens during pregnancy, suggesting hormonal modulation. Similarly, hormone supplements in menopause might be adverse to hearing in persons with otosclerosis.
 
4. Surgical treatment
For conductive hearing loss, stapedectomy can be done, which produces excellent hearing results, and which remain good for many years after the surgery. This procedure may allow avoidance of hearing aids. It, however, does not help the sensory component of the hearing loss and at best, may close the ‘air-bone’ gap.
The stapes operation (stapedectomy) is recommended for patients with otosclerosis who are candidates for surgery. This operation is usually performed under local anesthesia and requires but a short period of hospitalization and convalescence. Over 90 percent of these operations are successful in restoring the hearing permanently.
Stapedectomy or stapedotomy is performed through the ear canal under local or general anesthesia. A small incision may be made behind the ear to remove muscle or fat tissue for use in the operation.
 
Complications of Surgery
  • Hearing loss
  • Tinnitus: Most patients with otosclerosis notice tinnitus (head noise) to some degree. The amount of tinnitus is not necessarily related to the degree or type of hearing impairment. 442Following successful stapedectomy, tinnitus is often decreased in proportion to the hearing improvement, but occasionally may be worse.
  • Dizziness: It is normal for a few hours following a stapedectomy and may result in nausea and vomiting. Some unsteadiness is common during the first few postoperative days, and dizziness on sudden head motion may persist for several weeks.
  • Taste Disturbance and Mouth Dryness: They are not uncommon for a few weeks following surgery.
  • Eardrum Perforation: A perforation in the eardrum membrane is an unusual complication of the surgery. If healing does not occur, surgical repair (myringoplasty) may be required.
  • Weakness of the Face: A very rare complication of stapedectomy is temporary weakness of the face. This may occur as the result of an abnormality or swelling of the facial nerve.
 
Nursing Management
Successful communication requires the efforts of all people involved in a conversation. Even when the person with hearing loss utilizes hearing aids and active listening strategies, it is crucial that others involved in the communication process consistently use good communication strategies, including the following:
  • Face the hearing-impaired person directly, on the same level and in good light whenever possible. Position yourself so that the light is shining on the speaker's face, not in the eyes of the listener.
  • Do not talk from another room. Not being able to see each other when talking is a common reason people have difficulty understanding what is being said.
  • Speak clearly, slowly, distinctly, but naturally, without shouting or exaggerating mouth movements. Shouting distorts the sound of speech and may make speech reading more difficult.
  • Say the person's name before beginning a conversation. This gives the listener a chance to focus attention and reduces the chance of missing words at the beginning of the conversation.
  • Avoid talking too rapidly or using sentences that are too complex. Slowdown a little, pause between sentences or phrases, and wait to make sure you have been understood before going on.
  • Keep your hands away from your face while talking. If you are eating, chewing, smoking, etc. while talking, your speech will be more difficult to understand. Beards and moustaches can also interfere with the ability of the hearing impaired to speech read.
  • If the hearing-impaired listener hears better in one ear than the other, try to make a point of remembering which ear is better so that you will know where to position yourself.
  • Be aware of possible distortion of sounds for the hearing-impaired person. They may hear your voice, but still may have difficulty understanding some words.
  • Most hearing-impaired people have greater difficulty understanding speech when there is background noise. Try to minimize extraneous noise when talking.
  • Some people with hearing loss are very sensitive to loud sounds. This reduced tolerance for loud sounds is not uncommon. Avoid situations where there will be loud sounds when possible.
  • 443If the hearing-impaired person has difficulty understanding a particular phrase or word, try to find a different way of saying the same thing, rather than repeating the original words over and over.
  • Acquaint the listener with the general topic of the conversation. Avoid sudden changes of topic. If the subject is changed, tell the hearing impaired person what you are talking about now. In a group setting, repeat questions or key facts before continuing with the discussion.
  • If you are giving specific information—such as time, place or phone numbers—to someone who is hearing-impaired, make them repeat the specifics back to you. Many numbers and words sound alike.
  • Whenever possible, provide pertinent information in writing, such as directions, schedules, work assignments, etc.
  • Recognize that everyone, especially the hard-of-hearing, has a harder time hearing and understanding when ill or tired.
  • Pay attention to the listener. A puzzled look may indicate misunderstanding. Tactfully ask the hearing-impaired person if he/she understood you, or ask leading questions so you know your message got across.
  • Take turns speaking and avoid interrupting other speakers.
  • Enroll in aural rehabilitation classes with your hearing-impaired spouse or friend.
 
MENIERE'S DISEASE
Meniere's disease is a disorder of the inner ear that causes spontaneous episodes of vertigo, a sensation of a spinning motion, along with fluctuating hearing loss, ringing in the ear (tinnitus), and sometimes a feeling of fullness or pressure in ear.
 
Etiology
The cause of Meniere's disease is not well understood. It appears to be the result of the abnormal volume or composition of fluid in the inner ear.
The inner ear is a cluster of connected passages and cavities called a labyrinth. The outside of the inner ear is made of bone (bony labyrinth). Inside is a soft structure of membrane (membranous labyrinth) that is a slightly smaller, similarly shaped version of the bony labyrinth. The membranous labyrinth contains a fluid (endolymph) and is lined with hair-like sensors that respond to movement of the fluid.
Meniere's disease may occur because of the following reasons:
  • Improper fluid drainage, perhaps because of a blockage or anatomic abnormality
  • Abnormal immune response
  • Allergies
  • Viral infection
  • Genetic predisposition
  • Head trauma
  • Migraines
 
Signs and Symptoms
The primary signs and symptoms of Meniere's disease are:
  • Recurring episodes of vertigo: Vertigo is similar to the sensation experience if you spin around quickly several times and suddenly stop. Patient feels as if the room is still 444spinning, and he loses his balance. Episodes of vertigo occur without warning and usually last 20 minutes to two hours or more, up to 24 hours. Severe vertigo can cause nausea and vomiting.
  • Hearing loss: Hearing loss in Meniere's disease may fluctuate, particularly early in the course of the disease. Eventually, most people experience some degree of permanent hearing loss.
  • Ringing in the ear (tinnitus): Tinnitus is the perception of a ringing, buzzing, roaring, whistling or hissing sound in the ear.
  • Feeling of fullness in the ear: People with Meniere's disease often feel aural fullness or increased pressure in the ear.
 
Diagnostic Evaluation
A diagnosis of Meniere's disease requires:
  • Two spontaneous episodes of vertigo, each lasting 20 minutes or longer
  • Hearing loss verified by a hearing test on at least one occasion
  • Tinnitus or aural fullness
  • Exclusion of other known causes of these sensory problems
 
1. Physical examination and medical history
Physical examination may include:
  • The severity, duration and frequency of the sensory problems
  • History of infectious diseases or allergies
  • Medication use
  • Past ear problems
  • General health
  • History of inner ear problems in the family
 
2. Hearing assessment
A hearing test (audiometry) assesses how well you detect sounds at different pitches and volumes and how well you distinguish between similar-sounding words. The test not only reveals the quality of hearing but also may help determine if the source of hearing problems is in the inner ear or the nerve that connects the inner ear to the brain.
 
3. Balance assessment
Between episodes of vertigo, the sense of balance returns to normal for most people with Meniere's disease. But there may be some degree of ongoing balance problems.
There are several tests that assess functioning of the inner ear. Some or all of these tests can yield abnormal results in a person with Meniere's disease.
  • Videonystagmography (VNG): This test evaluates balanced function by assessing eye movement. Balance-related sensors in the inner ear are linked to muscles that control movement of the eye in all directions. This connection is what enables us to move head around while keeping our eyes focused on a single point.
  • In a VNG evaluation, warm and cool water or air are introduced into the ear canal. Measurements of involuntary eye movements in response to this stimulation are 445performed using a special pair of video goggles. Abnormalities of this test may indicate an inner ear problem.
  • Rotary-chair testing: Like a VNG, this measures inner ear function based on eye movement. In this case, stimulus to inner ear is provided by movement of a special rotating chair precisely controlled by a computer.
  • Vestibular evoked myogenic potentials (VEMP) testing: VEMP testing measures the function of sensors in the vestibule of the inner ear that help to detect acceleration movement. These sensors also have a slight sensitivity to sound. When these sensors react to sound, tiny measurable variations in neck or eye muscle contractions occur. These contractions serve as an indirect measure of inner ear function.
  • Posturography: This computerized test reveals the concerned part of the balance system, vision, inner ear function, or sensations from the skin, muscles, tendons and joints. While wearing a safety harness, you stand barefooted on a platform and keep your balance under various conditions.
  • Magnetic resonance imaging (MRI): This technique uses a magnetic field and radio waves to create images of soft tissues in the body. It can be used to produce either a thin cross-sectional ‘slice’ or a 3-D image of brain.
  • Computerized tomography (CT): This X-ray technique produces cross-sectional images of internal structures in the body.
  • Auditory brainstem response audiometry: This is a computerized test of the hearing nerves and hearing centers of the brain. It can help detect the presence of a tumor disrupting the function of auditory nerves.
 
Management
No cure exists for Meniere's disease, but a number of strategies may help to manage some symptoms.
 
Medications for vertigo
  • Motion sickness medications, such as meclizine or diazepam, may reduce the spinning sensation of vertigo and help control nausea and vomiting.
  • Anti-nausea medications, such as promethazine, may control nausea and vomiting during an episode of vertigo.
  • Diuretic, such as the drug combination triamterene and hydrochlorothiazide. It reduces the amount of fluid the body retains and helps to regulate the fluid volume and pressure in inner ear.
 
Noninvasive therapies and procedures
Some people with Meniere's disease may benefit from other noninvasive therapies and procedures, such as:
  • Rehabilitation: Problems with balance between episodes of vertigo may be reduced by vestibular rehabilitation therapy. The goal of this therapy, which may include exercises and activities that perform during therapy sessions and at home, is to help your body and brain regain the ability to process balanced information correctly.
  • Hearing aid: A hearing aid in the ear affected by Meniere's disease may improve hearing.
  • 446Meniett device: For vertigo that is hard to treat, this therapy involves the application of positive pressure to the middle ear to improve fluid exchange. A device called a Meniett pulse generator applies pulses of pressure to the ear canal through a ventilation tube. The treatment is performed at home, usually three times a day for five minutes at a time. Meniett device shows improvement in symptoms of vertigo, tinnitus and aural pressure.
 
Middle Ear Injections
Medications injected into the middle ear, and then absorbed into the inner ear, may improve vertigo symptoms. For example, Gentamicin, steroids, such as dexamethasone, also may help control vertigo attacks in some people.
 
Surgical Management
If vertigo attacks associated with Meniere's disease are severe and debilitating and other treatments do not help, surgery may be an option. Procedures may include:
  • Endolymphatic sac procedures: The endolymphatic sac plays a role in regulating inner ear fluid levels. These surgical procedures may alleviate vertigo by decreasing fluid production or increasing fluid absorption. In endolymphatic sac decompression, a small portion of bone is removed from over the endolymphatic sac. In some cases, this procedure is coupled with the placement of a shunt, a tube that drains excess fluid from inner ear.
  • Vestibular nerve section: This procedure involves cutting the nerve that connects balance and movement sensors in inner ear to the brain (vestibular nerve). This procedure usually corrects problems with vertigo while attempting to preserve hearing in the affected ear.
  • Labyrinthectomy: With this procedure, the surgeon removes the balance portion of the inner ear, thereby removing both balance and hearing functions from the affected ear. This procedure is performed only if one already has near-total or total hearing loss.
 
Nursing Management
 
Nursing Diagnosis
  • Risk for injury related to altered mobility because of gait disturbed and vertigo.
  • Impaired adjustment related to disability requiring change in lifestyle because of unpredictability of vertigo.
  • Risk for fluid volume imbalance and deficit related to increased fluid output, altered intake, and medications.
  • Anxiety related to threat of, or change in, health status and disabling effects of vertigo.
  • Ineffective coping related to personal vulnerability and unmet expectations stemming from vertigo.
  • Self-care deficits related to labyrinth dysfunction and episodes of vertigo.
 
Nursing Interventions
  • Provide nursing care during acute attack.
  • Provide a safe, quiet, dimly lit environment and enforce bed rest.
  • Provide emotional support and reassurance to alleviate anxiety.
  • Administer prescribed medications, which may include antihistamines, antiemetic, and possibly, mild diuretics. Instruct the client on self-care instructions to control the number of acute attacks.
  • 447Discuss the nature of the disorder.
  • Discuss the need for a low-salt diet.
  • Explain the importance of avoiding stimulants and vasoconstrictions (e.g. caffeine, decongestants, alcohol).
  • Discuss medications that may be prescribed to prevent attacks or self-administration of appropriate medications during an attack, which may include anticholinergics, vasodilation, antihsitamines, and possibly, diuretics or nicotinic acid.
  • Discuss, prepare and assist the client with surgical options.
  • A labyrinthectomy is the most radical procedure and involves resection of the vestibular nerve or total removal of the labyrinth performed by the transcanal route, which results in deafness in that eat.
  • An endolynmphatic decompression consists of draining the endolymphatic sac and inserting a shunt to enhance the fluid drainage.
 
LABYRINTHITIS
Labyrinthitis is a disorder of the inner ear. The two vestibular nerves in the inner ear send information to brain about head movement. When one of these nerves becomes inflamed, it creates a condition known as labyrinthitis.
 
Etiology
Labyrinthitis can happen to people of all ages. It can be caused by a variety of factors, including:
  • Respiratory illnesses (such as bronchitis)
  • Viruses of the inner ear
  • Stomach viruses
  • Herpes viruses
  • Bacterial infections (including bacterial middle ear infections)
  • Infectious organisms (like the one that causes Lyme disease)
 
Risk Factors
  • Smoking
  • Drink large quantities of alcohol
  • Have a history of allergies
  • Are habitually fatigued
  • Extreme stress
  • Over-the-counter medications
 
Signs and Symptoms
  • Dizziness
  • Nausea
  • Loss of hearing
  • Vertigo can interfere with driving, working, and other activities
  • 448Loss of balance
  • Tinnitus
  • Difficulty focusing eyes
 
Diagnostic Evaluation
Labyrinthitis can be diagnosed during a physical examination.
  • Hearing tests
  • CT or MRI scan of the head to record images of cranial structures
  • EEG (brain wave test)
  • ENG (eye movement test)
  • Blood tests
 
Management
Symptoms can be relieved with medications, including:
  • Antihistamines like clarinex or allegra, benadryl, and claritin.
  • Medications that can reduce dizziness and nausea, such as antivert
  • Sedatives like diazepam
  • Corticosteroids, to reduce the inflammation.
In addition to medications, there are several techniques use to relieve vertigo.
  • Avoid quick changes in position or sudden movements.
  • Sit still during a vertigo attack.
  • Get up slowly from a lying down or sitting position.
  • Avoid television, computer screens, and bright or flashing lights during a vertigo attack.
  • If vertigo occurs while you are in bed, try sitting up in a chair and keeping head still. Low lighting is better than darkness or bright lights.
 
Nursing Management
See nursing care plan for acute otitis media.
 
EPISTAXIS
The purpose of the nose is to warm and humidify the air that we breathe in. The nose is lined with many blood vessels that lie close to the surface where they can be injured and bleed.
Epistaxis is defined as bleeding from the nostril, nasal cavity, or nasopharynx. Nosebleeds are due to the bursting of a blood vessel within the nose.
 
Etiology
  • Dry, heated, indoor air, which dries out the nasal membranes and causes them to become cracked or crusted and bleed when rubbed or picked or when blowing the nose.
  • Dry, hot, low-humidity climates, which can dry out the mucus membranes
  • Colds (upper respiratory infections) and sinusitis, especially episodes that cause repeated sneezing, coughing, and nose-blowing
  • Vigorous nose-blowing or nose-picking
  • 449The insertion of a foreign object into the nose
  • Injury to the nose or face
  • Allergic and nonallergic rhinitis (inflammation of the nasal lining)
  • Use of drugs that thin the blood (aspirin, nonsteroidal anti-inflammatory medications, warfarin, and others)
  • High blood pressure
  • Chemical irritants (e.g. coccaine, industrial chemicals, others)
  • Deviated septum
  • Tumors or inherited bleeding disorders
  • Facial and nasal surgery
Nosebleeds can be divided into 2 categories based on the site of bleeding: anterior or posterior.
  • Anterior hemorrhage: The source of bleeding is visible in about 95% of cases—usually from the nasal septum, particularly Little's area which is where Kiesselbach's plexus forms (an anastomotic network of vessels on the anterior portion of the nasal septum).
  • Posterior hemorrhage: This emanates from deeper structures of the nose and occurs more commonly in older individuals. Nosebleeds from this area are usually more profuse and have a greater risk of airway compromise.
 
Diagnostic Evaluation
 
History
  • Determine if blood is running out of the nose and one nostril (usually anterior) or if blood is running into the throat or from both nostrils (usually posterior).
  • Ask about trauma (including nose picking).
  • Note family or past history of clotting disorders or hypertension.
  • Note whether there has been previous nasal surgery.
  • Discuss medication - especially, warfarin, aspirin.
  • Enquire about any facial pain or otalgia - these may be presenting signs of a nasopharyngeal tumor
  • In young male patients ask about nasal obstruction, headache, rhinorrhoea and anosmia - signs of juvenile nasopharyngeal angiofibroma.
 
Investigation
  • Coagulation studies and blood typing.
  • Quite marked anemia can result but a hematological malignancy may also be revealed.
 
Management
 
Initial assessment—first aid
  • Resuscitate the patient (if necessary)—remember the ABCD of resuscitation.
  • Ask the patient to sit upright, leaning slightly forward, and to squeeze the bottom part of the nose (NOT the bridge of the nose) for 10–20 minutes to try to stop the bleeding. The patient should breathe through the mouth and spit out any blood or saliva into a bowl. An ice-pack on the bridge of the nose may help.
  • 450Monitor the patient's pulse and blood pressure.
  • If bleeding has stopped after this time proceeds to inspect the nose, using a nasal speculum, consider cautery.
  • If the history is of severe and prolonged bleeding, get expert help and watch carefully for the signs of hypovolemia.
 
Cautery
  • Nasal cautery is a common treatment of epistaxis. A caustic agent such as silver nitrate or an electrically charged wire such as platinum is used to stop bleeding in the nasal mucous membrane.
  • Chemical cautery of the visible blood vessels on the anterior part of the nasal septum is the most popular treatment method for idiopathic recurrent nosebleeds.
  • Carefully examine the nasal cavity, looking for any bleeding points, which can usually be seen on the anterior septum–either an oozing point or a visible clot. Note whether there is any pus, suggesting local bacterial infection.
  • Blowing the nose decreases the effects of local fibrinolysis and removes clots, permitting a clearer examination. Applying a vasoconstrictor before examination may reduce hemorrhage and help locate the bleeding site. A topical local anesthetic reduces pain from examination and nasal packing.
  • Apply a silver nitrate cautery stick for ten seconds, working from the edge and moving radially–never on both sides of the septum at the same session.
  • Topical application with 0.5% neomycin + 0.1% chlorhexidine cream or with vaseline petroleum jelly is an alternative topical treatment.
  • If bleeding continues, packing may be considered.
  • A topical application of injectable form of tranexamic acid has been shown to be better than anterior nasal packing in the initial treatment of idiopathic anterior epistaxis.
  • It may be necessary to ligate the sphenopalatine artery endoscopically, or occasionally the internal maxillary artery and ethmoid arteries, or perform endovascular embolization of the internal maxillary artery, when packing fails to control a life-threatening hemorrhage. Ligation of the external carotid artery is the last resort.
 
Complications of packing
  • Anosmia
  • Pack falling out and continued bleeding
  • Breathing difficulties and aspiration of clots
  • Posterior migration of the pack, causing airway obstruction and asphyxia
  • Perforation of the nasal septum or pressure necrosis of cartilage.
 
Follow these steps to stop a nosebleed in emergency when you are alone
  • Relax
  • Sit down and lean your body and your head slightly forward. This will keep the blood from running down your throat, which can cause nausea, vomiting, and diarrhea.
  • Breathe through your mouth.
  • Use a tissue or damp washcloth to catch the blood.
  • 451Use your thumb and index finger to pinch together the soft part of your nose. Make sure to pinch the soft part of the nose against the hard bony ridge that forms the bridge of the nose. Squeezing at or above the bony part of the nose will not put pressure where it can help stop bleeding.
  • Keep pinching your nose continuously for at least 5 minutes before checking if the bleeding has stopped. If your nose is still bleeding, continue squeezing the nose for another 10 minutes.
  • You can spray an over-the-counter decongestant spray, such as oxymetazoline into the bleeding side of the nose and then applies pressure to the nose.
  • WARNING: These topical decongestant sprays should not be used over the long term.
  • Once the bleeding stops, do not bend over, strain or lift anything heavy and do not blow, rub, or pick your nose for several days.
 
Nursing Management
 
Provide nursing interventions to control bleeding
  • Have the client sit upright, breathe through the mouth, and refrain from talking.
  • Compress the soft outer portion of the nares against the septum for 5 to 10 minutes.
  • Instruct the client to avoid nose-blowing during or after the episode.
  • If pressure does not control bleeding, prepare to assist the health care provider in inserting an anterior packing or posterior packing as appropriate.
  • Keep scissors and a hemostat handy to cut the strings and remove the packing in the event of airway obstructions.
 
Provide ongoing assessment to monitor for bleeding
  • Inspect for blood trickling into the posterior pharynx.
  • Observe for hemoptysis, hematemesis and frequent swallowing or belching.
  • Instruct the client not to swallow but to spit out any blood into emesis basins.
  • Monitor the client's vital signs.
 
Provide oral and written instructions for treatment and prevention
  • Discuss ways to prevent epistaxis, including avoiding forceful nose-blowing, straining, high altitudes and nasal trauma.
  • Instruct the client to have adequate humidification to prevent drying of nasal passages.
  • Instruct the client on the proper way to stop bleeding.
  • Instruct the client not to put anything up the nasal passages.
  • Instruct the client to contact a health care provider if the bleeding does not stop.
 
LARYNX CANCER
Throat cancer refers to cancerous tumors that develop in throat (pharynx), voice box (larynx) or tonsils.
 
Types of Larynx Cancer
Throat cancer is a general term that applies to cancer that develops in the throat (pharyngeal cancer) or in the voice box (laryngeal cancer). The throat and the voice box are closely connected, with the voice box located just below the throat.
452Though most throat cancers involve the same types of cells, specific terms are used to differentiate the part of the throat where cancer originated.
  • Nasopharyngeal cancer begins in the nasopharynx.
  • Oropharyngeal cancer begins in the oropharynx.
  • Hypopharyngeal cancer (laryngopharyngeal cancer) begins in the hypopharynx.
  • Glottic cancer begins in the vocal cords.
  • Supraglottic cancer begins in the upper portion of the larynx and includes cancer that affects the epiglottis.
  • Subglottic cancer begins in the lower portion of voice box and below vocal cords.
  • Cancers that start in gland cells (adenocarcinoma): Adenocarcinoma is uncommon compared to squamous cell laryngeal cancer. It starts in the adenomatous cells that are scattered around the surface of the larynx. Adenomatous cells are gland cells that produce mucus.
  • Connective tissue cancers (sarcoma): Sarcomas are cancers that start in the body's connective tissues. These are the supporting tissues of the body, such as bone, muscle, and nerves. Cartilage is the supporting tissue of the larynx. Cancers that develop from cartilage are called chondrosarcomas.
 
TNM Stages of Cancer of the Larynx
TNM stands for Tumor, Node, and Metastasis. The system describes:
  • The size of a primary tumor (T)
  • Whether the lymph nodes have cancer cells in them (N)
  • Whether the cancer has spread to a different part of the body (M)
The exact T staging of laryngeal cancer varies depending on which part of the larynx is involved. The cancer may start on the vocal cords (glottis), above the vocal cords (supraglottis), or below the vocal cords (subglottis).
 
Early-stage Laryngeal Cancer (T0–T2)
 
(a) T stage 0, Tis
In very early cancer of the larynx, this means there are abnormal cells that may be precancerous. Tis (tumor in situ) means an early cancer that has not broken through the basement membrane of the tissue it is growing in.
 
(b) T stage 1
T stage 1 means the tumor is in only one part of the larynx and the vocal cords are able to move normally.
 
(c) T stage 2
T stage 2 means the tumor which may have started on the vocal cords (glottis), above the vocal cords (supraglottis), or below the vocal cords (subglottis) has grown into another part of the larynx. In cancer of the vocal cords (glottic cancer), stage T2a means that the vocal cords move normally.
 
Locally Advanced Laryngeal Cancer (T2b–T4)
 
(a) Glottic cancer T stage 2b
In T stage 2b in cancer that starts in the vocal cords (glottis), the vocal cord movement is limited.
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(b) T stage 3
T stage 3 means the tumor is throughout the larynx but has not spread further than the covering of the larynx.
 
(c) T stage 4
T stage 4 means the tumor has grown into body tissues outside the larynx. It may have spread to the thyroid gland, windpipe (trachea) or food pipe (oesophagus).
 
N-stages of Laryngeal Cancer
There are 4 main lymph node stages in cancer of the larynx. N2 is divided into N2a, N2b and N2c. The important points here are whether there is cancer in any of the nodes and, if so, the size of the node and which side of the neck it is on.
  • N0 means there are no lymph nodes containing cancer cells.
  • N1 means there are cancer cells in one lymph node on the same side of the neck as the cancer, but the node is less than 3 cm across.
  • N2a means there is cancer in one lymph node on the same side of the neck and it is between 3 cm and 6 cm across.
  • N2b means there is cancer in more than one lymph node, but none are more than 6 cm across. All the nodes must be on the same side of the neck as the cancer.
  • N2c means there is cancer in lymph nodes on the other side of the neck from the tumor, or in nodes on both sides of the neck, but none is more than 6 cm across.
  • N3 means that at least one lymph node containing cancer is larger than 6 cm across.
 
M-stages of Laryngeal Cancer
There are two stages to describe whether cancer of the larynx has spread:
  • M0 means there is no cancer spread.
  • M1 means the cancer has spread to other parts of the body, such as the lungs.
 
Grade of Cancer
The grade of a cancer tells how much the cancer cells look like normal cells under a microscope. There are 3 grades of laryngeal cancer:
  • Grade 1 (low grade): The cancer cells look very much like normal larynx cells (they are well-differentiated).
  • Grade 2 (intermediate grade): The cancer cells look slightly like normal larynx cells (they are moderately differentiated).
  • Grade 3 (high grade): The cancer cells look very abnormal and very little like normal larynx cells (they are poorly differentiated).
 
Etiology and Risk Factors
  • Age, as with most cancers, cancer of the larynx is more common in older people than in younger. There are very few cases in people under 40 years of age.
  • Drinking alcohol and smoking: Smoking tobacco and drinking a lot of alcohol are the main risk factors for cancer of the larynx in the western world.
  • Alcohol and cigarettes contain chemicals that increase the risk of cancer.
  • 454Heavy drinking and smoking are particularly linked to cancer above the vocal cords (the supraglottis) and the area around the vocal cords (the glottis). Compared to non-drinkers, heavy drinkers have about 3 times the risk of developing cancer of the larynx. Even drinking less than two drinks a day (for example, two pints of beer or two small glasses of wine) gives a slightly increased risk of laryngeal cancer. But nonsmokers are unlikely to have an increased risk of laryngeal cancer at this level of drinking.
  • HPV infection: HPV stands for human papilloma virus (HPV). There are many types of HPV. Some types can affect the lining of the larynx and cause small, wart-like growths.
  • Diet: Poor eating patterns are common in people who are heavy drinkers. This may be one reason why alcohol increases the risk of cancer. A poor diet may increase risk of cancer of the larynx. This may be due to a lack of vitamins and minerals. A diet high in fresh fruit and vegetables seems to reduce the risk of cancer of the larynx. This may be because these foods contain high levels of the antioxidant vitamins A, C and E. Vitamins and other substances in fresh foods may help to stop damage to the lining of the larynx that can lead to cancer.
  • Family history: People who have a first degree relative diagnosed with a head and neck cancer have double the risk of laryngeal cancer of someone without a family history.
  • Low immunity: HIV and AIDS lower immunity and so do drugs that people take after organ transplants.
  • Exposure to substances: Some chemicals may increase risk of cancer of the larynx, like wood dust, soot or coal dust, or paint fumes, exposure to coal as a fuel source at home.
  • Acid reflux: Reflux happens when stomach acid comes back up the esophagus and irritates the lining. In the long term this can cause damage to the cells in the oesophagus. This irritation and damage can extend to the larynx and may increase cancer risk.
 
Signs and Symptoms
  • A cough
  • Changes in voice, such as hoarseness
  • Difficulty swallowing
  • Ear pain
  • A lump or sore that does not heal
  • A sore throat
  • Weight loss
 
Diagnostic Evaluation
  • Flexible endoscopy of the larynx: This test means the back of mouth and throat (including the larynx) examined with a narrow, flexible telescope (a nasendoscope). This is passed up the nose to look at all upper air passages, including the larynx from above. This may be a bit uncomfortable, but can have an anesthetic spray to numb throat first. This test is sometimes called a nasoendoscopy.
  • Endoscopy: An endoscope is a series of connected telescopes that an ENT specialist uses to look at the back of throat. There are camera and light at one end, and an eyepiece at the other. Through the endoscope, doctor can see the inside of nose and throat very clearly and will take biopsies of any abnormally looking areas.
  • 455Transnasal esophagoscopy: The doctor inserts a flexible tube (endoscope) through nose and down the throat. This test is sometimes used instead of having an endoscope under general anesthetic. The tip of the tube has a digital video system and self-contained light. This test is done under a local anesthetic. It gives clear pictures of the inside of the throat and larynx.
  • Fine needle aspiration: This is sometimes written as FNA. A fine needle aspiration is done to aspirate the fluid to evaluate any cancerous property.
  • Physical examination
  • CT scan: This is a computerized scan using X-rays to evaluate the size of the cancer and any enlarged lymph nodes in the neck.
  • MRI scan
  • PET-CT scan
 
Management
 
The Main Treatments
The main treatments for cancer of the voice box are radiotherapy or surgery.
 
Radiotherapy
Radiotherapy can shrink a large tumor in the larynx and make it easier to remove. Or it can kill off any cancer cells that might have been left behind after surgery. This lowers the risk of the cancer coming back.
Radiotherapy may be used to treat the lymph nodes after surgery; if there is a risk, these may contain cancer cells. This may be instead of lymph node dissection.
 
Surgery
  • Partial laryngectomy (also called cordotomy): Tumors that are limited to one vocal cord are removed, and a temporary tracheotomy is performed to maintain the airway. After recovery from surgery, the patient will have a voice but it will be hoarse.
  • Hemilaryngectomy: When there is a possibility the cancer includes one true and one false vocal cord, they are removed along with an arytenoid cartilage and half of the thyroid cartilage. Temporary tracheotomy is performed, and the patient's voice will be hoarse after surgery.
  • Supraglottic laryngectomy: When the tumor is located in the epiglottis or false vocal cords, radical neck dissection is done and tracheotomy performed. The patient's voice remains intact; however, swallowing is more difficult because the epiglottis has been removed.
  • Total laryngectomy: Advanced cancers that involve a large portion of the larynx require removal of the entire larynx, the hyoid bone, the cricoid cartilage, two or three tracheal rings, and the strap muscles connected to the larynx. A permanent opening is created in the neck into the trachea, and a laryngectomy tube is inserted to keep the stoma open. The lower portion of the posterior pharynx is removed when the tumor extends beyond the epiglottis, with the remaining portion sutured to the esophagus after a nasogastric tube is inserted. The patient must breathe through a permanent tracheostomy, with normal speech no longer possible.
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BIOLOGICAL THERAPY
Biological therapy is treatment that changes the activity of substances made naturally in the body. These therapies can control or destroy cancer cells.
 
Cetuximab
Cetuximab (Erbitux) is a type of biological therapy known as a monoclonal antibody. It is designed to block areas on the surface of cancer cells that can trigger growth. These are called epidermal growth factor receptors (EGFRs). Blocking these receptors can stop the signals that tell the cancer to grow.
 
Side Effects of Biological Therapies
  • Tiredness (fatigue)
  • Diarrhea
  • Skin changes (rashes or discoloration) – rashes may be severe for some people
  • A sore mouth
  • Weakness
  • Loss of appetite
  • Low blood counts
  • Swelling of parts of the body, due to fluid build-up
 
Nursing Priorities
  • Maintain patent airway, adequate ventilation.
  • Assist patient in developing alternative communication methods.
  • Restore and maintain skin integrity.
  • Re-establish and maintain adequate nutrition.
  • Provide emotional support for acceptance of altered body image.
  • Provide information about disease process and prognosis and treatment.
 
Discharge Goals
  • Ventilation and oxygenation adequate for individual needs.
  • Communicating effectively.
  • Complications prevented or minimized.
  • Beginning to cope with change in body image.
  • Disease process, prognosis and therapeutic regimen understood.
 
Nursing Diagnosis:
  1. Ineffective airway clearance and risk for aspiration related to partial or total removal of the glottis, altering ability to breathe, cough, and swallow.
    Intervention
    • Monitor respiratory rate, depth. Auscultate breath sounds.
    • Elevate the head of the bed 30–45 degrees.
    • Encourage swallowing, if patient is able.
    • 457Encourage effective coughing and deep breathing.
    • Do suctioning and note the amount and color of secretions.
    • Demonstrate and encourage the patient to be in self-suction.
    • Maintain the proper positioning of laryngectomy tube.
    • Change patient position to check pooling of blood behind neck.
  2. Impaired verbal communication related to removal of vocal cord and tracheostomy.
    Intervention
    • Review preoperative instructions and discussion of why speech and breathing are altered, using anatomical drawings or models to assist in explanations.
    • Determine whether patient has other communication impairments, e.g. hearing, vision, literacy.
    • Provide immediate and continual means to summon nurse, e.g. call light/bell.
    • Let the patient know the summons will be answered immediately. Stop by to check on patient periodically without being summoned.
    • Post notice at central answering system or nursing station that patient is unable to speak.
    • Provide alternative means of communication appropriate to patient need, e.g., pad and pencil, magic slate, alphabet, picture board, sign language.
    • Allow sufficient time for communication.
    • Provide nonverbal communication, e.g., touching and physical presence. Anticipate needs.
    • Encourage ongoing communication with -outside world e.g., newspapers, television, radio, calendar, clock.
    • Refer to loss of speech as temporary after a partial laryngectomy and depending on availability of voice prosthetics, vocal cord transplant.
    • Caution patient not to use voice until physician gives permission.
    • Arrange for meeting with other persons who have experienced this procedure, as appropriate.
    • Prearrange signals for obtaining immediate help
  3. Skin and tissue integrity, impaired related to surgical removal of tissues and radiation or chemotherapeutic agents.
    Intervention
    • Assess skin color, temperature and capillary refill in operative and skin graft areas.
    • Keep head of bed elevated 30–45 degrees. Monitor facial edema (usually peaks by third to fifth postoperative day).
    • Protect skin flaps and suture lines from tension or pressure. Provide pillows, rolls and instruct patient to support head and neck during activity.
    • Monitor bloody drainage from surgical sites, suture lines, and drains.
    • Report any milky-appearing drainage.
    • 458Cleanse incisions with sterile saline and peroxide (mixed 1:1) after dressings has been removed.
    • Monitor donor site if graft is performed and check dressings as indicated.
    • Cleanse thoroughly around stoma and neck tubes, avoiding soap or alcohol. Show patient how to do self-stoma or tube care with clean water and peroxide, using soft, lint-free cloth, not tissue or cotton.
    • Monitor all sites for signs of wound infection, e.g. unusual redness, increasing edema, pain, exudates and temperature elevation.
  4. Oral mucous membrane, impaired related to dehydration, absence of oral intake, decreased saliva production secondary to radiation or surgical procedure.
    Intervention
    • Suction oral cavity gently and frequently.
    • Have patient perform self-suctioning when possible or use gauze wick to drain secretions.
    • Show patient how to brush inside of mouth, palate, tongue, and teeth frequently.
    • Apply lubrication to lips and provide oral irrigations as indicated.
    • Avoid alcohol-based mouthwashes.
    • Use normal saline or mixture of salt water and baking soda for rinsing.
    • Suggest use of artificial saliva preparations (e.g. pilocarpine hydrochloride) if mucous membranes are dry.
  5. Pain, acute related to surgical incisions and tissue swelling.
    Intervention
    • Support head and neck with pillows. Show patient how to support neck during activity.
    • Provide comfort measures (e.g. back rub, position change) and diversional activities (e.g. television, visiting, and reading).
    • Encourage patient to expectorate saliva or to suction mouth gently if unable to swallow.
    • Investigate changes in characteristics of pain. Check mouth, throat suture lines for fresh trauma.
    • Note nonverbal indicators and autonomic responses to pain.
    • Evaluate effects of analgesics.
    • Medicate before activity and treatments as indicated.
    • Schedule care activities to balance with adequate periods of sleep and rest.
    • Recommend use of stress management behaviors, e.g. relaxation techniques, guided imagery.
    • Provide oral irrigations, anesthetic sprays, and gargles. Instruct patient in self-irrigations.
    • Administer analgesics, e.g. codeine, acetylsalicylic acid (ASA), and propoxyphene as indicated.
  6. Nutrition: Imbalanced, less than body requirements related to temporary or permanent alteration in mode of food intake.
    Intervention
    • Auscultate bowel sounds.
    • Maintain feeding tube, e.g. check for tube placement, flush with warm water as indicated.
    • Monitor intake and weigh as indicated. Show patient how to monitor and record weight on a scheduled basis.
    • 459Instruct patient in self-feeding techniques, e.g. bulb syringe, bag and funnel method, and blending soft foods if patient is to go home with a feeding tube. Make sure patient and family member are able to perform this procedure before discharge and that appropriate food and equipment are available at home
    • Begin with small feedings and advance as tolerated. Note signs of gastric fullness, regurgitation, and diarrhea.
    • Provide supplemental water by feeding tube or orally if patient can swallow.
    • Encourage patient when relearning swallowing, e.g. maintain quiet environment, have suction equipment on standby, and demonstrate appropriate breathing techniques.
    • Encourage patient when relearning swallowing, e.g., maintain quiet environment, have suction equipment on standby, and demonstrate appropriate breathing techniques.
    • Resume oral feedings when feasible. Stay with patient during meals the first few days.
    • Develop and encourage a pleasant environment for meals.
    • Help patient to develop nutritionally balanced home meal plans.
    • Consult with dietitian and nutritional support team as indicated. Incorporate and reinforce dietitian's teaching.
    • Provide nutritionally balanced diet (e.g. semisolid/soft foods) or tube feedings (e.g. blended soft food or commercial preparations) as indicated.
    • Monitor laboratory studies, e.g. blood urea nitrogen (BUN), glucose, liver function, prealbumin, protein, electrolytes.
  7. Disturbed body image and role performance related to loss of voice.
    Intervention
    • Discuss meaning of loss or change with patient, identifying perceptions of current situation and future expectations.
    • Note nonverbal body language, negative attitudes and self-talk.
    • Assess for self-destructive and suicidal behavior.
    • Note emotional reactions, e.g. grieving, depression, anger.
    • Allow patient to progress at own rate.
    • Maintain calm, reassuring manner. Acknowledge and accept expression of feelings of grief, hostility.
    • Allow but do not participate in patient's use of denial, e.g. when patient is reluctant to participate in self-care (e.g. suctioning stoma). Provide care in a nonjudgmental manner.
    • Set limits on maladaptive behaviors, assisting patient to identify positive behaviors that will aid recovery.
    • Encourage family member to treat patient normally and not as an invalid.
    • Alert staff that facial expressions and other nonverbal behaviors need to convey acceptance and not revulsion.
    • Encourage identification of anticipated personal and work conflicts that may arise.
    • Recognize behavior indicative of overconcern with future lifestyle and relationship functioning.
    • Encourage patient to deal with situation in small steps.
    • Provide positive reinforcement for efforts and progress made.
    • Encourage patient and family to communicate feelings to each other.
  8. 460Knowledge, deficient regarding prognosis, treatment, self-care, and discharge needs related to lack of information.
    Intervention
    • Ascertain amount of preoperative preparation and retention of information.
    • Assess level of anxiety related to diagnosis and surgery.
    • Provide and repeat explanations at patient's level of acceptance.
    • Provide written directions for patient to read and have available for future reference.
    • Discuss inaccuracies in perception of disease process and therapies with patient and family.
    • Educate patient and family about basic information regarding stoma, shower with stoma collar, shampoo by leaning forward, no swimming or water sports.
    • Cover stoma with foam or fiber filter (e.g. cotton or silk).
    • Cover stoma when coughing or sneezing.
    • Reinforce necessity of not smoking.
    • Discuss inability to smell and taste as before surgery.
    • Discuss importance of reporting to caregiver and physician immediately such symptoms as stoma narrowing, presence of lump in throat, dysphagia, or bleeding.
    • Recommend wearing medical-alert identification tag or bracelet identifying patient as a neck breather.
    • Encourage family members to become certified in cardiopulmonary resuscitation (CPR) if they are interested or are able to do so.
    • Give careful attention to the provision of needed rehabilitative measures, e.g. temporary, permanent prosthesis, dental care, speech therapy, surgical reconstruction. Vocational, sexual or marital counseling and financial assistance.
    • Identify homecare needs and available resources.
 
SPEECH DISORDERS
 
Types of Speech Impairment
Speech impairments may be present in different forms. Adult-impaired speech is a symptom of several different speech disorders. They include:
  • Spasmodic dysphonia: Identified by involuntary movements of the vocal cords when speaking. Voice may be hoarse, airy, and tight.
  • Aphasia: The inability to express and comprehend language. Individuals with aphasia may find it difficult to think of words. They may also mispronounce words.
  • Dysarthria: Weak vocal muscles. These weak muscles cause slurred and slow speech. The larynx and vocal cords have difficulty coordinating to make a fluent sound.
  • Vocal disturbances: Any factor that changes the function or shape of vocal cords can cause changes in the sound and ease of speech.
 
Etiology
Speech impairment can occur suddenly or can gradually progress. Each speech impairment type has a different cause.
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Spasmodic Dysphonia
This is abnormal brain functioning. Though scientists are not sure, it is believed this condition originates in the basal ganglia (part of the brain that controls muscle movement in the body).
 
Aphasia
Brain damage from a stroke or blood clot is a common cause of aphasia. Other causes include:
  • Head trauma
  • Brain tumor
  • Cognitive degenerative conditions, such as Alzheimer's disease or dementia
 
Dysarthria
Degenerative muscle and motor conditions, such as multiple sclerosis, muscular dystrophy, cerebral palsy, and Parkinson's disease may cause this condition. Other causes may include:
  • Stroke
  • Head trauma
  • Brain tumor
  • Lyme disease
  • Drinking alcohol
  • Facial weakness, such as Bell's palsy
  • Tight or loose dentures
 
Vocal Disturbances
  • Throat cancer can affect the sound of the voice.
  • Polyps, nodules, or other growths on vocal cords can cause vocal concerns.
  • Heavy use of the voice can cause a hoarse voice, as in the case of a singer, performer, or coach.
  • Ingestion of certain drugs, such as caffeine, antidepressants, and amphetamines can cause a dry, tight voice.
 
Clinical Manifestations
Changes in speech will depend on the type of speech disorder
 
Apraxia of Speech
Individuals with apraxia may demonstrate:
  • Difficulty imitating and producing speech sounds, marked by speech errors, such as sound distortions, substitutions, or omissions
  • Inconsistent speech errors
  • Groping of the tongue and lips to make specific sounds and words
  • Slow speech rate
  • Impaired rhythm
  • Better automatic speech (e.g. greetings) than purposeful speech
  • Inability to produce any sound at all in severe cases.
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Dysarthria
A person with dysarthria may demonstrate the following speech characteristics:
  • ‘Slurred’, ‘choppy’, or ‘mumbled’ speech that may be difficult to understand
  • Slow rate of speech
  • Rapid rate of speech with a ‘mumbling’ quality
  • Limited tongue, lip, and jaw movement
  • Abnormal pitch and rhythm when speaking
  • Changes in voice quality, such as hoarse or breathy voice or speech that sounds ‘nasal’ or ‘stuffy’.
 
Stuttering
Signs and symptoms of stuttering:
  • The person is having difficulty moving from the ‘w’ in ‘where’ to the remaining sounds in the word. On the fourth attempt, he successfully completes the word.)
  • The person is having difficulty moving from the ‘s’ in ‘save’ to the remaining sounds in the word. He continues to say the ‘s’ sound until he is able to complete the word.
  • The person expects to have difficulty smoothly joining the word ‘you’ with the word ‘around’. In response to the anticipated difficulty, he produces several interjections until he is able to say the word ‘around’ smoothly.
 
Aphasia
Signs or symptoms of aphasia
  • Difficulty producing language.
  • Experience difficulty coming up with the words they want to say.
  • Substitute the intended word with another word that may be related in meaning to the target (e.g. ‘chicken’ for ‘fish’) or unrelated (e.g., ‘radio’ for ‘ball’).
  • Switch sounds within words (e.g. ‘wish dasher’ for ‘dishwasher’).
  • Use made-up words (e.g. ‘frigilin’ for ‘hamburger’).
  • Have difficulty putting words together to form sentences.
  • String together made-up words and real words fluently but without making sense.
  • Difficulty understanding language.
  • Misunderstand what others say, especially when they speak fast (e.g. radio or television news) or in long sentences.
  • Find it hard to understand speech in background noise or in group situations.
  • Misinterpret jokes and take the literal meaning of figurative speech (e.g. it is raining cats and dogs').
  • Difficulty reading forms, pamphlets, books, and other written material.
  • Problems spelling and putting words together to write sentences.
  • Difficulty understanding number concepts (e.g. telling time, counting money, adding/subtracting).
 
Management
  • Augmentative and alternative communication (AAC): It includes all forms of communication (other than oral speech) that are used to express thoughts, needs, wants, and ideas. We all use AAC when we make facial expressions or gestures, use symbols or pictures, or write. 463People with severe speech or language problems rely on AAC to supplement existing speech or replace speech that is not functional. Special augmentative aids, such as picture and symbol communication boards and electronic devices, are available to help people express themselves. This may increase social interaction, school performance, and feelings of self-worth.
 
Types of AAC Systems
When children or adults cannot use speech to communicate effectively in all situations, there are options:
  1. Unaided communication systems: These rely on the user's body to convey messages. Examples include gestures, body language, and sign language.
  2. Aided communication systems: These require the use of tools or equipment in addition to the user's body. Aided communication methods can range from paper and pencil to communication books or boards to devices that produce voice output (speech-generating devices or SGDs) and written output. Electronic communication aids allow the user to use picture symbols, letters, or words and phrases to create messages. Some devices can be programmed to produce different spoken languages.
 
Hearing aids and cochlear implant
Hearing aids differ in design, size, and the amount of amplification, ease of handling, volume control, and availability of special features. However, they do have similar components that include the following:
  • Microphone to pick up sound
  • Amplifier circuitry to make the sound louder
  • Receiver (miniature loudspeaker) to deliver the amplified sound into the ear
  • On/off switch and batteries to power the electronic parts
 
Types of Hearing Aid
 
In-the-Canal (ITC) and Completely-in-the-Canal (CIC) Aids
These aids are contained in a tiny case that fits partly or completely into the ear canal. They are the smallest aids available and offer some cosmetic and listening advantages.
Fig. 8.1: In-the-canal aids
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In-the-Ear (ITE) Aids
All parts of the aid are contained in a shell that fills in the outer part of the ear. These aids are larger than canal aids and, for some people, may be easier to handle than smaller aids.
Fig. 8.2: In-the-ear aids
 
Behind-the-Ear (BTE) Aids
All parts of the aid are contained in a small plastic case that rests behind the ear. The case is connected to an earmold by a piece of clear tubing. This style is often chosen for young children for safety and growth reasons.
Fig. 8.3: Behind-the-ear aids
 
Behind-the-Ear Aid: Open Fitting
A small plastic case rests behind the ear, and a very fine clear tube runs into the ear canal. Inside the ear canal, a small, soft silicone dome or a molded, highly vented acrylic tip holds 465the tube in place. These aids offer cosmetic and listening advantages and are used typically for adults.
Fig. 8.4: BTE with open fitting
 
Receiver-in-Canal Aids
These aids look very similar to the behind-the-ear hearing aid with a unique difference. The speaker of the hearing aid is placed inside the ear canal, and thin electrical wires replace the acoustic tube of the BTE (behind the ear) aid. These aids also offer cosmetic and listening advantages and are typically used for adults.
Fig. 8.5: Receiver-in-canal aids
 
Extended Wear Hearing Aids
These aids are devices that are nonsurgically placed in the ear canal by an audiologist. These are worn up to several months at a time without removal. The devices are made of soft 466material designed to fit the curves of the ear. They are worn continuously and then replaced with a new device. They are very useful for active individuals because their design protects against moisture and earwax, and they can be worn while exercising, showering, etc.
 
Middle Ear Implants
These hearing systems are implanted in the space behind the eardrum that mechanically vibrate the middle ear structures. This device has two parts—an external portion and an implanted portion.
 
Features Available in Hearing Aids
Many hearing aids have optional features that can be built in to assist in different communication situations. Some options are:
 
Directional Microphone
Some hearing aids have a switch to activate a directional microphone that responds to sound coming from a specific direction. When set to the normal, nondirectional (omnidirectional) setting, the aid picks up sound almost equally from any direction. When the directional microphone is activated, the aid focuses on a sound coming from in front of you and reduces sound coming from behind you. This can be especially helpful in a noisy room or for face-to-face conversation.
 
Telephone (Telecoil) Switch
This feature is something that everyone should consider adding to their hearing aid. This switch allows you to move from the normal microphone ‘on’ setting to a ‘T’ (telecoil) setting to hear better on the telephone. You can talk on the phone without your hearing aid ‘whistling’ because the hearing aid's microphone is turned off! This feature can also be used with another hearing assistive technology that is telecoil-compatible. The T-setting can be used in settings, such as theaters, auditoriums, and houses of worship that have induction loop or frequency modulation (FM) installations. Some hearing aids have a combination ‘M/T’ (microphone/telephone) switches so that, while listening with an induction loop, you can still hear the nearby conversation.
 
Direct Audio Input
Some hearing aids have a direct audio input capability that allows you to plug in a remote microphone or an FM-assistive listening system. This enables you to connect directly to a TV or other device, such as your computer, CD player, MP3 player, or radio.
 
Advantages of Hearing Aids
  • Greater control over the prosthetic device.
  • Can try different hearing aids to see which is qualitatively preferred, so that user can conceivably purchase a new device.
  • Can take advantage of new technology as it becomes available (improved earmolds, tubing, telecoils, digital/analog programming strategies.
  • Greater affordability.
  • Can have a back-up hearing aid for times when device malfunctions.
  • 467Cost of accessories is minimal.
  • Greater flexibility and accessibility for repairs.
  • Can use hearing-aid dispenser or audiologist in just about any neighborhood.
  • Can adjust controls on some personal device.
  • Easier maintenance.
  • Can easily change the tubing at home.
  • Battery gives a few hours' warning that it is ‘dying’ with sufficient time to change batteries at a more convenient time or place.
 
Disadvantages of Hearing Aids
  • Limited hearing assistance in high-frequency range.
  • Earmolds and their acoustic feedback issues may be repetitive, time-consuming, aggravating.
  • Loud noises are bothersome for those using linear amplification.
  • Hearing aids for those with severe loss need to be fitted carefully, assertively, and well-monitored.
 
Daily Care for the Hearing Aid
Hearing aids require special care to ensure that they function properly. It includes:
  • Perform listening checks: Listen to the hearing aid everyday. Using a listening tube, you can listen to the hearing aids to be sure that they sound clear and not weak or scratchy.
  • Check batteries: Batteries should last about 1 or 2 weeks. Using a battery tester, check that the batteries are at full strength so that the hearing aids are working at a peak performance. Always keep spare batteries with you. Store them in a cool, dry place. Discard batteries one at a time.
  • Clean the hearing aids regularly with a soft, dry cloth: Check for dirt and grime. Earmolds can be removed from the hearing aids and cleaned with a mild soap solution. Dry them carefully using a forced air blower (not a hair dryer). Be sure they are dry before reattaching them to the hearing aids.
  • Minimize moisture in the hearing aids: This is important for proper functioning. A hearing aid drying container will help keep moisture from building up inside the hearing aids and will lengthen their life. Be sure to take the batteries out of the hearing aid before placing them in the storage containers.
  • Avoid feedback: Feedback is the whistling sound that can be heard from the hearing aid. It occurs when amplified sound comes out of the earmold and re-enters the microphone.
 
Cochlear Implant
A cochlear implant is a small, complex electronic device that can help to provide a sense of sound to a person who is profoundly deaf or severely hard of hearing. The implant consists of an external portion that sits behind the ear and a second portion that is surgically placed under the skin. An implant has the following parts:
  • A microphone, which picks up sound from the environment.
  • A speech processor, which selects and arranges sounds picked up by the microphone.
  • 468A transmitter and receiver or stimulator, which receive signals from the speech processor and convert them into electric impulses.
  • An electrode array, which is a group of electrodes that collects the impulses from the stimulator and sends them to different regions of the auditory nerve.
 
Functioning of a Cochlear Implant
A cochlear implant is very different from a hearing aid. Hearing aids amplify sounds so they may be detected by damaged ears. Cochlear implants bypass damaged portions of the ear and directly stimulate the auditory nerve. Signals generated by the implant are sent by way of the auditory nerve to the brain, which recognizes the signals as sound. Hearing through a cochlear implant is different from normal hearing and takes time to learn or relearn. However, it allows many people to recognize warning signals, understand other sounds in the environment, and enjoy a conversation in person or by telephone.
 
Advantages of a Cochlear Implant
  • Can enable one to hear conversation and thus learn spoken language with relative ease, particularly for those with severe-profound hearing loss
  • May enable one to use a regular telephone when otherwise not possible
  • Avoids problems of acoustic feedback and earmold issues
  • Greater ease in high-frequency consonant perception
  • Distance hearing is likely better than with hearing aids
  • May be greater potential for incidental learning
  • Greater opportunity for natural sounding voice
  • Understanding women on the telephone may be easier as compared to understanding them with a cochlear implant for a severe-profound loss.
 
Disadvantages of a Cochlear Implant
  • Environmental and practical living issues
  • Static: radar detector, playgrounds, trampolines, computers, carpeting
  • Pressure: some recommended restrictions such as scuba diving
  • Magnetic: suggested MRI restriction
  • Trauma: some restrictions from rough sports, such as football
  • Surgical issues, such as staph infection, vertigo, tinnitus, partial facial nerve paralysis
 
Hearing-assistive Technology
Hearing-assistive technology systems (HATS) are devices that can help to function better in day-to-day communication situations. HATS can be used with or without hearing aids or cochlear implants to make hearing easier and thereby reduce stress and fatigue. Hearing aids + HATS = better listening and better communication.
 
Role of a Nurse with Hearing-impaired and Mute Clients
  • Face the client directly: Be sure to look directly at the client. They must be able to see you to hear you. Avoid talking from behind the client, or from another room and never turn away face when speaking. Smiles, frowns, head shakes, and hand signals are great conversational aides.
  • 469Spotlight your face: Face a window or a lamp so the light illuminates your mouth as you speak. If the room is dark, move to another area with more lighting. People with hearing loss rely a great deal on lip-reading.
  • Avoid noisy backgrounds: A conversation is difficult to hear over background noises. Do not try to talk above loud noises. Always ask to suggest things you can do, such as speaking to a better ear or moving to a better light, to facilitate communication.
  • Get attention first: Be sure that client is aware of you before you start talking. One can get their attention by gently touching them, flicking on a light switch, or moving a window shade.
  • Do not shout: Shouting only makes things worse. It can distort the face, making lip-reading impossible. Also, shouting which is amplified by a hearing aid can greatly shock and upset the client.
  • Clearly speak at a moderate pace: Speak more slowly and pause occasionally to help the client keep up with the word flow. Do not mouth or exaggerate expressions, as this simply makes it harder for the client to understand.
  • Give clues when changing subjects: Hearing-impaired people may become confused if you change the subject without warning. Keep them on track by saying something like, ‘Now I want to talk to you about our upcoming family night’ so that they can become ready for a new topic.
  • Use longer phrases: Which tend to be easier to understand and give more ‘meaning’ clues than shorter phrases. For example, ‘Will you get me a drink of water?’ presents much less difficulty than ‘Will you get me a drink?’
  • Use a different choice of words: After repeating something a second time without the client understanding, try a different choice of words for the third try.
  • Face the hearing-impaired person directly: On the same level and in good light whenever possible. Position yourself so that the light is shining on the speaker's face, not in the eyes of the listener.
  • Do not talk from another room, not being able to see each other when talking is a common reason people have difficulty understanding what is said.
  • Speak clearly, slowly, distinctly, but naturally, without shouting or exaggerating mouth movements. Shouting distorts the sound of speech and may make speech reading more difficult.
  • Say the person's name before beginning a conversation: This gives the listener a chance to focus attention and reduces the chance of missing words at the beginning of the conversation.
  • Avoid talking too rapidly or using sentences that are too complex: Slow-down a little, pause between sentences or phrases, and wait to make sure you have been understood before going on.
  • Keep your hands away from your face while talking: If you are eating, chewing, smoking, etc. while talking, your speech will be more difficult to understand. Beards and moustaches can also interfere with the ability of the hearing-impaired to speech read.
  • If the hearing-impaired listener hears better in one ear than the other, try to make a point of remembering which ear is better so that you will know where to position yourself.
  • Be aware of possible distortion of sounds for the hearing-impaired person. They may hear your voice, but still may have difficulty understanding some words.
  • 470Most hearing impaired people have greater difficulty understanding speech when there is background noise. Try to minimize extraneous noise when talking.
  • Some people with hearing loss are very sensitive to loud sounds. This reduced tolerance for loud sounds is not uncommon. Avoid situations where there will be loud sounds when possible.
  • If the hearing impaired person has difficulty understanding a particular phrase or word, try to find a different way of saying the same thing, rather than repeating the original words over and over.
  • Acquaint the listener with the general topic of the conversation. Avoid sudden changes of topic. If the subject is changed, tell the hearing impaired person what you are talking about now. In a group setting, repeat questions or key facts before continuing with the discussion.
  • If you are giving specific information: Such as time, place or phone numbers, to someone who is hearing impaired, have them repeat the specifics back to you. Many numbers and words sound alike.
  • Whenever possible, provide pertinent information in writing, such as directions, schedules, work assignments, etc.
  • Recognize that everyone, especially the hard-of-hearing, has a harder time hearing and understanding when ill or tired.
  • Pay attention to the listener: A puzzled look may indicate misunderstanding. Tactfully ask the hearing impaired person if they understood you, or ask leading questions so you know your message got across.
  • Take turns speaking and avoid interrupting other speakers.
  • Enroll in aural rehabilitation classes with your hearing impaired spouse or friend.
471
BIBLIOGRAPHY
  1. Acuin J, for the World Health Organization. Chronic Suppurative Otitis Media. Burden of Illness and Management Options. World Health Organization,  Geneva:  2004. Accessed online July 23, 2007 at: http://www.who.int/child-adolescent-health/publications/CHILD_HEALTH/ISBN_92_4_159158_7.htm.
  1. Acuin J. Extracts from ‘Concise clinical evidence’: chronic suppurative otitis media. BMJ. 2002;325:1159.
  1. American Academy of Pediatrics Subcommittee on Management of Acute Otitis Media. Diagnosis and management of acute otitis media. Pediatrics. 2004;113:1451–65.
  1. American Academy of Family Physicians, American Academy of Otolaryngology—Head and Neck Surgery, American Academy of Pediatrics Subcommittee on Otitis Media with Effusion. Otitis media with effusion. Pediatrics. 2004;113:1412–29.
  1. Arrieta A, Singh J. Management of recurrent and persistent acute otitis media: new options with familiar antibiotics. Pediatr Infect Dis J. 2004;23(2 suppl):S115–24.
  1. Gehanno P, Lenoir G, Barry B, et al. Evaluation of nasopharyngeal cultures for bacteriologic assessment of acute otitis media in children. Pediatr Infect Dis J. 1996;15:329–32.
  1. Hendley JO. Clinical practice. Otitis media. N Engl J Med. 2002;347:1169–74.
  1. Karma PH, Penttila MA, Sipila MM, et al. Otoscopic diagnosis of middle ear effusion in acute and non-acute otitis media. I. The value of different otoscopic findings. Int J Pediatr Otorhinolaryngol. 1989;17:37–49.
  1. Kemaloglu YK, Sener T, Beder L, et al. Predictive value of acoustic reflectometry (angle and reflectivity) and tympanometry. Int J Pediatr Otorhinolaryngol. 1999;48:137–42.
  1. Klein JO, Pelton S. Epidemiology, pathogenesis, clinical manifestations, and complications of acute otitis media. Accessed May 15, 2007 at: http://patients.uptodate.com/topic.asp?file=pedi_id/2870&title=Acute+Otitis+media[Subscription required].
  1. Kontiokari T, Koivunen P, Niemela M, et al. Symptoms of acute otitis media. Pediatr Infect Dis J. 1998;17:676–9.
  1. Marcy M, Takata G. Management of acute otitis media. Evidence report/technology assessment no. 15. Agency for Healthcare Research and Quality, Southern California Evidence-based Practice Center/RAND,  Rockville,  Md.: 2001. AHRQ publication no. 01-E 010.
  1. McCracken GH Jr. Diagnosis and management of acute otitis media in the urgent care setting. Ann Emerg Med. 2002;39:413–21.
  1. Niemela M, Uhari M, Jounio-Ervasti K, et al. Lack of specific symptomatology in children with acute otitis media. Pediatr Infect Dis J. 1994;13:765–8.
  1. Onusko E. Tympanometry. Am Fam Physician. 2004;70:1713–20.
  1. Rovers MM, Schilder AG, Zielhuis GA, et al. Otitis media [Published correction appears in Lancet 2004;363:1080]. Lancet. 2004;363:465–73.
  1. Rothman R, Owens T, Simel DL. Does this child have acute otitis media. JAMA. 2003;290:1633–40.
  1. University of Michigan Health System. Guidelines for clinical care. Otitis media. Accessed May 15, 2007 at: http://cme.med.umich.edu/pdf/guideline/om.pdf.

Endocrine Disorders9

 
INTRODUCTION
Anatomy of thyroid gland: The butterfly shaped of thyroid gland is located just inferior to the larynx (voice box). It is composed of right and left lateral lobes, one on either side of the trachea, that is connected with isthmus anterior to trachea, a small, pyramidal-shaped lobe something extend upward from the isthmus.
Weight: The normal weight of thyroid gland is 30 gm.
Blood supply: It is highly vascularized and receives 80–120 ml of blood per minute.
Hormones: Mainly three types of hormones are produced by thyroid gland:
473
  • T3 or Triiodothyroxine: It contain 3 atoms of iodine
    Normal value: T3 = 10–26 mcg/dl
    T3 Total = 75 ng/dl
  • T4 or Tertaiodiothyroxine or Thyroxine: It contains 4 atoms of iodine. It is secreted by follicular cells of Thyroid gland.
    Normal value: T4 = 4–11 mcg/dl
    T4 Free = 0.8–1.8 mg/dl
  • Calcitonin: It is secreted by parafolicullar cells or C-cells
    Function: Lower the level of blood calcium and phosphates by inhibiting bone resorption by osteoclast cell.
    Normal value: 19 mg/L.
 
Function
  • Increased the metabolic rate
  • Stimulate synthesis of protein
  • Increase use of glucose and fatty acids production for ATP production
  • Increased lipolysis
  • Enhance cholesterol excretion
  • Increased body growth
  • Contribute to development of nervous system
  • Lower the calcium and phosphate level in blood.
 
Common Diseases Related to Thyroid Gland
  • Hyperthyroidism: It is a state in which the thyroid gland secretions of excessive thyroid hormone.
  • Hypothyroidism: It is a state in which the thyroid gland does not make enough thyroid hormone.
  • Goiter: It is due to deficiency of iodine causes enlargement of thyroid gland.
  • Thyroiditis: It is the inflammation of thyroid gland.
  • Thyroid cancer: In this abnormal growth of tissues of thyroid gland.
 
HYPOTHYROIDISM
Hypothyroidism is a deficiency of TH resulting in slowed body metabolism, decreased heat production, and decrease oxygen consumption by the tissues. Or it is a state in which the thyroid gland does not make enough thyroid hormone (T3 and T4).
 
Causes
  • Iodine deficiency: It is the most common cause of hypothyroidism worldwide. In iodine-replete individuals hypothyroidism is frequently caused by Hashimoto's thyroiditis, or otherwise as a result of either an absent thyroid gland or a deficiency in stimulating hormones from the hypothalamus or pituitary.
  • Congenital hypothyroidism: It is very rare accounting for approximately 0.2% and can have several causes such as thyroid aplasia or defects in the hormone metabolism. Thyroid hormone insensitivity (most often T3 receptor defect) also falls into this 474category although in this condition the levels of thyroid hormones may be normal or even markedly elevated.
  • Postpartum thyroiditis: Hypothyroidism can result from postpartum thyroiditis, a condition that affects about 5% of all women within a year of giving birth. The first phase is typically hyperthyroidism; the thyroid then either returns to normal, or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring lifelong treatment.
  • Genetic factor: Hypothyroidism can also result from inheritance, sometimes autosomal recessive.
  • Temporary hypothyroidism: Can be due to the Wolff–Chaikoff effect. A very high intake of iodine can be used to temporarily treat hyperthyroidism, especially in an emergency situation. Although iodide is a substrate for thyroid hormones, high levels reduce iodide organification in the thyroid gland, decreasing hormone production. The antiarrhythmic agentamiodarone can cause hyper- or hypothyroidism due to its high iodine content.
  • Mood stabilizers: Hypothyroidism can be caused by lithium-based mood stabilizers, usually used to treat bipolar disorder (previously known as manic depression). In fact, lithium has occasionally been used to treat hyperthyroidism. Other drugs that may produce hypothyroidism include interferon alpha, interleukin-2, and thalidomide.
 
Primary
  • Gland destruction
  • Surgical removal
  • Irradiation (therapeutic radioiodine, external irradiation)
  • Autoimmune disease (Hashimoto's, atrophic thyroiditis)
  • Idiopathic atrophy
  • Infiltrative process
  • Inhibition of thyroid hormone synthesis and release
  • Iodine deficiency
  • Excess iodide in susceptible persons
  • Drugs: interferon alpha, lithium, amiodarone
  • Inherited enzyme defects
  • Transient
  • After surgery or therapeutic radioiodine
  • Postpartum
  • Thyroiditis.
 
Secondary
  • Hypothalamic disease and Pituitary disease
  • Genetic forms of pituitary hormone deficiencies
  • Infiltrative disorders
  • Surgery
  • Irradiation
  • Trauma
  • Tumors
  • Resistance to thyroid hormone.
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Classification
Hypothyroidism is often classified by association with the indicated organ dysfunction.
Type
Origin
Primary
Thyroid gland
The most common forms include Hashimoto's thyroiditis (an autoimmune disease) and radioiodine therapy for hyperthyroidism.
Secondary
Pituitary gland
Occurs if the pituitary gland does not create enough thyroid-stimulating hormone (TSH) to induce the thyroid gland to produce enough thyroxine and triiodothyronine. Although not every case of secondary hypothyroidism has a clear-cut cause, it is usually caused by damage to the pituitary gland, as by a tumor, radiation, or surgery. Secondary hypothyroidism accounts for less than 5% or 10% of hypothyroidism cases.
Tertiary
Hypothalamus
Results when the hypothalamus fails to produce sufficient thyrotropin-releasing hormone (TRH). TRH prompts the pituitary gland to produce thyroid-stimulating hormone (TSH). Hence may also be termed hypothalamic-pituitary-axis hypothyroidism. It accounts for less than 5% of hypothyroidism cases.
 
Pathophysiology
 
Primary Hypothyroidism
 
Secondary Hypothyroidism
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Signs and Symptoms
  • Early hypothyroidism: It is often asymptomatic and can have very mild symptoms.
  • Subclinical hypothyroidism: It is a state of normal thyroid hormone levels, thyroxine (T4) and triiodothyronine (T3), with mild elevation of thyrotropin, thyroid-stimulating hormone (TSH).
  • Clinical (or overt) hypothyroidism: With higher TSH levels and low free T4 levels, symptoms become more readily apparent in this type.
Fig. 9.1: Clinical manifestations
 
Early
  • Cold intolerance, increased sensitivity to cold
  • Constipation
  • Weight gain and water retention
  • Bradycardia (low heart rate – fewer than sixty beats per minute)
  • Fatigue
  • Decreased sweating
  • Muscle cramps and joint pain
  • Dry, itchy skin
  • Thin, brittle fingernails
  • Rapid thoughts
  • Depression
  • Poor muscle tone (muscle hypotonia)
  • Female infertility; any kind of problems with menstrual cycles
  • Hyperprolactinemia and galactorrhea
  • Elevated serum cholesterol.
477
 
Late
  • Goiter
  • Slow speech and a hoarse, breaking voice – deepening of the voice can also be noticed, caused by Reinke's edema
  • Dry puffy skin, especially on the face
  • Thinning of the outer third of the eyebrows (sign of Hertoghe)
  • Abnormal menstrual cycles
  • Low basal body temperature
  • Thyroid-related depression.
 
Uncommon
  • Impaired memory
  • Impaired cognitive function
  • A slow heart rate with ECG changes including low voltage signals. Diminished cardiac output and decreased contractility
  • Sluggish reflexes
  • Hair loss
  • Anemia caused by impaired hemoglobin synthesis (decreased EPO levels), impaired intestinal iron and folate absorption or B12 deficiency from pernicious anemia
  • Difficulty swallowing
  • Shortness of breath with a shallow and slow respiratory pattern
  • Increased need for sleep
  • Irritability and mood instability
  • Yellowing of the skin due to impaired conversion of beta-carotene to vitamin A (carotoderma)
  • Impaired renal function with decreased glomerular filtration rate
  • Acute psychosis (myxedema madness) (a rare presentation of hypothyroidism)
  • Decreased libido in men due to impairment of testicular testosterone synthesis
  • Decreased sense of taste and smell (anosmia)
  • Puffy face, hands and feet (late, less common symptoms)
  • Gynecomastia
  • Deafness
  • Enlarged tongue.
 
According to System
  1. Cardiovascular system:
    1. Bradycardia
    2. Decreased cardic output
    3. Cool skin
    4. Cold intolerance
  2. 478Neurological:
    1. Lethargy
    2. Slowed movement
    3. Memory loss
    4. Confusion
  3. Pulmonary:
    1. Dyspnea
    2. Hypoventilation
  4. Integumentary:
    1. Cool
    2. Skin, brittle
    3. Dry hair
  5. Gastrointestinal:
    1. Decreased appetite
    2. Weight gain
    3. Constipation
    4. Increased serum lipid levels
  6. Reproductive:
    1. Decreased libido
    2. Erectile dysfunction
 
Diagnostic Evaluation
Thyroid function tests: To measure thyroid-stimulating hormone (TSH): High levels of TSH indicate that the thyroid is not producing sufficient levels of thyroid hormone (mainly as thyroxine (T4) and smaller amounts of triiodothyronine (T3). However, measuring just TSH fails to diagnose secondary and tertiary hypothyroidism, thus leading to the following suggested blood testing if the TSH is normal and hypothyroidism is still suspected.
  • TSH: 0.4-4.2 mlU/L
  • Free triiodothyronine (fT3): Normal value: T3 = 10–26 mcg/dl
  • Total T3: Normal value: T3 Total = 75 ng/dl
  • Free thyroxine (fT4): Normal value T4 = 4–11 mcg/dl
    T4 Free = 0.8–1.8 ng/dl
  • Antithyroidantibodies: For evidence of autoimmune diseases that maybe damaging the thyroid gland
  • Serum cholesterol: Which may be elevated in hypothyroidism
    Normal value: 150–200 mg/dl
  • Prolactin: As a widely available test of pituitary function
    Normal value: 4–30 ng/dl
  • Testing for anemia, including ferritin
    Normal value: Hb: Male: 13–18 gm/dl
    Female: 12–16 gm/dl
  • Basal body temperature
479
 
Management
 
Medical Treatment
Thyroid hormones:
Hypothyroidism is treated with the levorotatory forms of thyroxine (levothyroxine) (L-T4) and triiodothyronine (liothyronine) (L-T3). This medicine can improve symptoms of thyroid deficiency such as slow speech, lack of energy, weight gain, hair loss, dry skin, and feeling cold. It also helps to treat goiter. Levothyroxine is best taken 1 hour before breakfast, as some food can diminish absorption. Calcium can inhibit the absorption of levothryoxin. Compared to water, coffee reduces absorption of levothyroxine.
Dose: It depends on level of TSH 1.6 μg/kg of body weight. In elderly patients and patients with cardiac disease, we recommend starting at a lower dose (25–50 μg/day) and increase by 25 μg/d until the patient is clinically and biochemically euthyroid.
T4 Only
This treatment involves supplementation of levothyroxine alone, in a synthetic form. It is currently the standard treatment in mainstream medicine. T4 and T3 in combination.
This treatment protocol involves administering both synthetic L-T4 and L-T3 simultaneously in combination.
 
Supportive Management
Aterial blood gases measures specially CO2 retention and treat with oxygenation.
 
Complication
 
Mild Hypothyroidism
Clients with mild hypothyroidism maybe asymptomatic or may experience vague manifestations, such as:
  • Cold
  • Lethargy
  • Dry skin
  • Forgetfulness
  • Depression
  • Some weight gain
480
 
Myxedema
Myxedema may develop in client with undiagnosed or undertreated hypothyroidism that experience stress such as:
  • Infection
  • Drug use
  • Respiratiory failure
  • Heart failure
  • Trauma.
It is characterized by a dry, waxy type of swelling with abnormal deposits of mucin in the skin and other tissues. The edema in nonpitting. Clients with myxedema may also have hypercholes-terolemia, hyperlipidemia and proteinemia as a result of T4 changes in the synthesis, mobilization and degradation of serum lipids levels may contribute to the later devopement of cardiac problems. Dilutional hypoatremia may develop as a result of the marked impairment of water excretion because of decreased delivery of sodium and volume to the distal renal tubules associated with decreased renal blood flow.
 
Myxedema Coma
Hypercalcemia, hypercalcemia secondary to adrenal insufficiency, hypoglycemia and water intoxication. It maybe triggered by stress as from surgery or infection or by noncompliance with thyroid.
The most severe complication of hypothyroidism is myxedema coma. This emergency state is characterized by a drastic decrease in metabolic rate, hypoventilation leading to respiratory acidosis, hypothermia, and hyponatremia, hypotension.
 
Cretinism
It is caused by a decreased production of T4 and results in mental retardation, stunted growth and coarse facial features. The signs of cretinism are constant drooling, a swayback, a potbelly, short stature, and irregularly placed and poorly formed teeth.
481
 
Nursing Management
 
Assessment
  • Physical assessment findings include a palpable and bilaterally enlarged thyroid; dry, yellowish skin, nonpitting edema of the face and lower legs and slow, constipation, slurred speech.
  • Diagnostic tests revealed the following abnormal findings: T3, (normal range: 80 to 200 ng/dL); T4, (normal range: 5 to 12 mg/dL); TSH increased.
 
Diagnosis
  • Constipation, related to decreased peristalsis, as evidenced by hard, formed stools every 4 days.
  • Impaired verbal communication, related to changes in speech patterns and enlarged tongue.
  • Low self-esteem, related to changes in physical appearance and activity intolerance.
 
Planning and Implementation
  • Teach to increase fluids, bulk, and fiber in the diet to help regain a normal bowel elimination pattern of a soft, formed stool every other day.
  • Take medication as prescribed and do not expect immediate reversal of symptoms affecting speech.
  • Plan activities around rest periods. Encourage husband and daughter to help with house cleaning and cooking.
  • Monitor vital signs, including heart rate and rhythm.
  • Administer thyroid replacement, levothyroxine sodium (Synthroid) is most commonly prescribed.
  • Instruct the client about thyroid replacement therapy.
  • Instruct the client in low-calorie, low-cholesterol, low-saturated-fat diet.
  • Assess the client for constipation; provide roughage and fluids to prevent constipation.
  • Provide a warm environment for the client.
  • Avoid sedatives and narcotics because of increase sensitivity to these medications.
  • Monitor for overdose of thyroid medications, characterized by tachycardia, restlessness, nervousness, and insomnia.
  • Instruct the client to report episodes of chest pain immediately.
 
HYPERTHYROIDISM
Hyperthyroidism is a condition in which thyroid gland produces too much of the hormone thyroxine, characteristic by elevated T3 and T4 level that result in accelerate body's metabolism, causing sudden weight loss, a rapid or irregular heartbeat, sweating, and nervousness or irritability.
 
Etiology
  • Graves' disease: Graves' disease, an autoimmune disorder in which antibodies produced by immune system stimulate thyroid to produce too much T4, is the most common cause of hyperthyroidism. It may lead to graves ophthalmopathy and graves dermopathy.
  • 482Hyper functioning thyroid nodules (toxic adenoma, toxic multinodular goiter, Plummer's disease): Hyperthyroidism occurs when one or more adenomas of thyroid produce too much T4.
  • Thyroiditis: Thyroid gland can become inflamed for unknown reasons. The inflammation can cause excess thyroid hormone stored in the gland to leak into bloodstream. It may be subacute thyroiditis or postpartum thyroiditis.
 
Pathophysiology
Any disturbance in the normal homeostatic mechanism at hypothalamus and pituitary gland leads to hypersecretion of thyroid hormone. It may occur due to certain tumor or any defect of thyroid gland that may lead to hypersecretion of T3 and T4. Hypersecretion of T3 and T4 lead to hypermetabolism state.
 
Symptoms
Hyperthyroidism can mimic other health problems, which may make it difficult to diagnose. It can also cause a wide variety of signs and symptoms
  • Sudden weight loss
  • Rapid heartbeat (tachycardia)
  • Increased appetite
  • Nervousness, anxiety and irritability
  • Tremor
  • Sweating
  • Changes in menstrual patterns
  • 483Increased sensitivity to heat
  • Changes in bowel patterns
  • An enlarged thyroid gland (goiter)
  • Fatigue, muscle weakness
  • Difficulty sleeping
  • Skin thinning
  • Fine, brittle hair
  • Exophthalamus
  • Fast tendon reflex
  • Reduce eye movement.
 
Complications
  • Heart problems: These include a rapid heart rate, a heart rhythm disorder called atrial fibrillation and congestive heart failure
  • Brittle bones: Untreated hyperthyroidism can also lead to weak, brittle bones (osteoporosis) because of over secretion of calcitonine.
Eye problems: Graves' ophthamlopathy characterized by bulging, red or swollen eyes, sensitivity to light, and blurring or double vision.
 
Clinical Features
The characteristic symptoms of Graves' eye disease feature the inflammation of the eye tissues. The eyes are painful, red and watery—particularly in sunshine or wind. The covering of the eye is inflamed and swollen. The lids and tissues around the eyes are swollen with fluid. The eyeballs bulge out of their sockets. Because of eye muscle swelling, the eyes are unable to move normally and there may be blurred or double vision. Some patients have decreased color vision as well.
  • Red, swollen skin: People with Graves' disease develop Graves' dermopathy, which affects the skin, causing redness and swelling, often on the shins and feet.
  • Thyrotoxic crisis: This leads to a fever, a rapid pulse and even delirium.
 
Diagnostic Evaluation
  • Radioactive iodine (RAI) uptake test: High in Graves' disease and toxic nodular goiter, low in thyroiditis.
  • Serum T4 and T3: Increased in hyperthyroidism. Normal T4 with elevated T3 indicates thyrotoxicosis.
  • Thyroid-stimulating hormone (TSH): Suppressed.
  • Thyroglobulin: Increased.
  • TRH stimulation: Hyperthyroidism is indicated if TSH fails to rise after administration of TRH.
  • Thyroid T3 uptake: Normal to high.
  • Protein-bound iodine: Increased.
  • Serum glucose: Elevated (related to adrenal involvement).
  • Plasma cortisol: Low levels (less adrenal reserve).
  • 484Alkaline phosphatase and serum calcium: Increased.
  • Liver function tests: Abnormal.
  • Electrolytes: Hyponatremia may reflect adrenal response or dilutional effect in fluid replacement therapy. Hypokalemia occurs because of GI losses and diuresis.
  • Serum catecholamines: Decreased.
  • Urine creatinine: Increased.
  • ECG: Atrial fibrillations; shorter systole time, cardiomegaly, heart enlarged with fibrosis and necrosis.
  • Needle or open biopsy: May be done to determine cause of hyperthyroidism, differentiate cysts or tumors, diagnose enlargement of thyroid gland.
  • Thyroid scan: Differentiates between Graves' disease and Plummer's disease, both of which result in hyperthyroidism.
Physiologic state
Serum TSH
Serum free T4
Serum T3
24-h radioiodine uptake
Hyperthyroidism, untreated
Low
High
High
High
Hyperthyroidism, T3 toxicosis
Low
Normal
High
Normal or High
Primary hypothyroidism, untreated
Low or Normal
Low
Low or Normal
Low or Normal
Hypothyroidism secondary to pituitary disease
Low or Normal
Low
Low or Normal
Low or Normal
Euthyroid, on exogenous thyroid hormone
Normal
Normal on T4, Low on T3
High on T3, Normal on T4
Low
 
Management
 
Beta Blockers
Beta blockers offer prompt relief of the adrenergic symptoms of hyperthyroidism such as tremor, palpitations, heat intolerance, and nervousness. Propranolol has been used most widely, but other beta blockers can be used. Nonselective beta blockers such as Propranolol are preferred because they have a more direct effect on hypermetabolism. Therapy with propranolol should be initiated at 10 to 20 mg every six hours. The dose should be increased progressively until symptoms are controlled. Calcium channel blockers such as diltiazem can be used to reduce heart rate in patients who cannot tolerate beta blockers.
 
Iodides
Iodides block the peripheral conversion of thyroxine (T4) to triiodothyronine (T3) and inhibit hormone release. Iodides also are used as adjunctive therapy before emergency nonthyroid surgery, if beta blockers are unable to control the hyperthyroidism, and to reduce gland vascularity before surgery for Graves' disease. Iodides are not used in the routine treatment of hyperthyroidism because of paradoxical increases in hormone release that can occur with prolonged use. Organic iodide radiographic contrast agents (e.g. iopanoic acid or ipodate sodium) are used more commonly than the inorganic iodides (e.g. potassium iodide). The dosage of either agent is 1 g per day for up to 12 weeks.
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Antithyroid Drugs
Antithyroid drugs act principally by interfering with the organification of iodine, thereby suppressing thyroid hormone levels. Methimazole and propylthiouracil are the two agents available which are commonly used.
 
Methimazole
Methimazole usually is the drug of choice in nonpregnant patients because of its lower cost, longer half-life, and lower incidence of hematologic side effects. The starting dosage is 15 to 30 mg per day, and it can be given in conjunction with a beta blocker. The beta blockade can be tapered after four to eight weeks and the methimazole adjusted. Maintenance dosage of 5 to 10 mg per day.
 
Propylthiouracil
PTU is preferred for pregnant women because methimazole has been associated with rare congenital abnormalities. The starting dosage of PTU is 100 mg three times per day with a maintenance dosage of 100 to 200 mg daily.
 
Radioactive Iodine
Radioactive iodine is the treatment of choice for most patients with Graves' disease and toxic nodular goiter. It is inexpensive, highly effective, easy to administer, and safe. There has been reluctance to use radioactive iodine in women of childbearing years because of the theoretical risk of cancer of the thyroid, leukemia, or genetic damage in future offspring.
Thyroidectomy: Removal of thyroid gland, it may be subtotal thyroidectomy, hemi thyroidectomy, or total thyroidectomy.
 
Nursing Management
  1. Decrease cardiac output related to uncontrolled hyperthyroidism and hypermetabolic state
    Interventions
    • Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure.
    • Monitor central venous pressure (CVP), if available.
    • 486Investigate reports of chest pain or angina.
    • Assess pulse and heart rate while patient is sleeping.
    • Monitor ECG, noting rate and rhythm. Document dysrhythmias.
    • Auscultate heart sounds, note extra heart sounds, development of gallops and systolic murmurs.
    • Monitor temperature, provide cool environment, limit bed linens or clothes, administer tepid sponge baths.
    • Observe signs and symptoms of severe thirst, dry mucous membranes, weak or thready pulse, poor capillary refill, decreased urinary output, and hypotension.
    • Weigh daily. Encourage chair-rest or bedrest. Limit unnecessary activities.
  2. Fatigueness related to hypermetabolic state or altered body chemistry
    Intervention
    • Monitor vital signs, noting pulse rate at rest and when active.
    • Note development of tachypnea, dyspnea, pallor, and cyanosis.
    • Encourage patient to restrict activity and rest in bed as much as possible.
    • Provide for quiet environment, cool room, decreased sensory stimuli, soothing colors, quiet music.
    • Encourage patient to restrict activity and rest in bed as much as possible.
    • Provide comfort measures: Touch therapy or massage, cool showers. Patient with dyspnea will be most comfortable sitting in high Fowler's position.
    • Provide for diversional activities that are calming, e.g. reading, radio, television.
    • Avoid topics that irritate or upset patient. Discuss ways to respond to these feelings.
  3. Disturbed thought processes related to altered sleep pattern.
    Intervention
    • Assess thinking process. Determine attention span, orientation to place, person, or time.
    • Note changes in behavior.
    • Assess level of anxiety.
    • Reorient to person, place, or time as indicated.
    • Provide quiet environment; decreased stimuli, cool room, dim lights.
    • Reorient to person, place, or time as indicated.
    • Provide, calendar, room with outside window, alter level of lighting to simulate day or night.
    • Present reality concisely and briefly without challenging illogical thinking.
    • Administer medication as indicated: Sedatives, antianxiety agents, antipsychotic drugs.
    • Provide safety measures. Pad side rails, close supervision, applying soft restraints as last resorts as necessary.
  4. Risk for imbalanced nutrition: Less than body requirements related to nausea, vomiting, diarrhea.
    Intervention
    • Monitor daily food intake. Weigh daily and report losses.
    • Encourage patient to eat and increase number of meals and snacks. Give or suggest high-calorie foods that are easily digested.
    • 487Provide a balance diet, with six meals per day.
    • Avoid foods that increase peristalsis and fluids that cause diarrhea.
    • Administer medications as indicated: Glucose, vitamin B complex, insulin.
    • Consult with dietitian to provide diet high in calories, protein, carbohydrates, and vitamins.
  5. Anxiety related to CNS stimulation (hypermetabolic state)
    Intervention
    • Observe behavior indicative of level of anxiety.
    • Monitor physical responses, noting palpitations, repetitive movements, hyperventilation, and insomnia.
    • Stay with patient, maintaining calm manner. Acknowledge fear and allow patient's behavior to belong to patient.
    • Describe and explain procedures, surrounding environment, or sounds that may be heard by patient.
    • Speak in brief statements. Use simple words.
    • Discuss with patient reasons for emotional lability and psychotic reaction.
    • Reduce external stimuli: Place in quiet room, provide soft, soothing music; reduce bright lights, reduce number of persons contacting patient.
    • Reinforce expectation that emotional control should return as drug therapy progresses.
    • Administer antianxiety agents or sedatives and monitor effects.
  6. Impaired tissue integrity related to alternation in protective mechanism of eye
    Intervention
    • Encourage use of dark glasses when awake and taping the eyelids shut during sleep as needed. Suggest use of sunglasses or eye patch. Moisten conjunctiva often with isotonic eye drops.
    • Elevate the head of the bed and restrict salt intake if indicated.
    • Instruct patient in extraocular muscle exercises if appropriate.
    • Provide opportunity for patient to discuss feelings about altered appearance and measures to enhance self-image.
    • Administer medications as indicated:
      Adrenocorticotropic hormone (ACTH), prednisone, Methylcellulose drops.
  7. Knowledge deficit regarding condition, prognosis, treatment, self-care, and discharge needs
    Intervention
    • Provide information appropriate to individual situation.
    • Provide information about signs and symptoms of hypothyroidism and the need for continuing follow-up care.
    • Identify stressors and discuss precipitators to thyroid crises: Personal or social and job concerns, infection, pregnancy.
    • Monitor CBC periodically.
    • Identify signs and symptoms requiring medical evaluation: fever, sore throat, and skin eruptions.
    • 488Discuss drug therapy, including need for adhering to regimen, and expected therapeutic and side effects.
    • Explain need to check with physician before taking other prescribed or OTC drugs.
    • Review need for nutritious diet and periodic review of nutrient needs. Tell patient to avoid caffeine, artificial preservatives.
    • Emphasize importance of planned rest periods.
 
Other Possible Nursing Diagnosis
  • Imbalanced nutrition less than body requirements related intake less than metabolic needs secondary to excessive metabolic rate.
  • Risk for injury related to tremors.
  • Risk for hyperthermia related to lack of metabolic compensatory mechanisms secondary to hyperthyroidism.
  • Activity intolerance related to fatigue, exhaustion secondary to excessive metabolic rate.
  • Diarrhea related to increased peristalsis secondary to excessive metabolic rate.
  • Impaired comfort related to heat intolerance and profuse diaphoresis.
 
THYROIDITIS
Thyroiditis is inflammation, or swelling of the thyroid.
 
Etiology
  • Postpartum thyroiditis postpartum thyroiditis seems to be caused by a problem with the immune system.
  • Silent or painless thyroiditis, symptoms is the same as in postpartum thyroiditis, but they are not related to having given birth.
  • Subacute thyroiditis, symptoms are the same as in postpartum and silent thyroiditis, but the inflammation in the thyroid leads to pain in the neck, jaw, or ear. Unlike the other types of thyroiditis, subacute thyroiditis maybe caused by an infection. Subacute thyroiditis is a rare condition. It is thought to be caused by a viral infection. The condition often occurs after a viral infection of the upper respiratory tract, such as mumps and influenza.
  • Chronic thyroiditis or Hashimoto's disease is a common thyroid gland disorder. It can occur at any age, but is most often seen in middle-aged women. It is caused by a reaction of the immune system against the thyroid gland.
    • Adrenal insufficiency (poor function of the adrenal glands)
    • Fungal infections of the mouth and nails
    • Hyperparathyroidism (underactive parathyroid gland).
 
Signs and Symptoms
The most obvious symptom of subacute thyroiditis is pain in the neck. Sometimes the pain can spread (radiate) to the jaw or ears. Painful enlargement of the thyroid gland may last for weeks or months.
489Other symptoms include:
  • Difficulty swallowing
  • Fatigue
  • Fever
  • Hoarseness
  • Tenderness when gentle pressure is applied to the thyroid gland (palpation)
  • Weakness
  • Cold intolerance
  • Constipation.
 
Diagnostic Evaluation
  • Low serum thyroid stimulating hormone (TSH) level
  • High serum free T4 (thyroid hormone, thyroxine) level
  • Low radioactive iodine uptake
  • High serum thyroglobulin level
  • High erythrocyte sedimentation rate (ESR)
  • High serum TSH level
  • Low serum free T4.
 
Management
The purpose of treatment is to reduce pain and inflammation and treat hyperthyroidism.
  • Anti-inflammatory medications such as aspirin or ibuprofen are used to control pain in mild cases.
  • Steroids (prednisone) to control inflammation.
  • Symptoms of hyperthyroidism are treated with a class of medications called beta blockers (propranolol, and atenolol).
  • Antithyroid drugs or thionamides are not effective in treating this condition.
 
HYPOPARATHYROIDISM
Hypoparathyroidism is decreased function of the parathyroid glands with under production of parathyroid hormone. This can lead to low levels of calcium in the blood, often causing cramping and twitching of muscles or tetany (involuntary muscle contraction), and several other symptoms.
Hypoparathyroidism is a condition in which body secretes abnormally low levels of parathyroid hormone (parathormone). This hormone plays a key role in regulating and maintaining a balance of body's levels of two minerals, calcium and phosphorus. This leads to abnormally low ionized calcium levels in blood and bones and to an increased amount of phosphorus.
 
Etiology
  • Acquired hypoparathyroidism: This most common cause of hypoparathyroidism develops after accidental damage to or removal of the parathyroid glands during surgery. Surgery maybe a treatment for diseases of the nearby thyroid gland, or for throat cancer or neck cancer.
  • 490Hereditary hypoparathyroidism (DeGeorge syndrome): In this form, either the parathyroid glands are not present at birth, or they do not work properly.
  • Autoimmune disease: In this condition in which immune system creates antibodies against the parathyroid tissues, and treats them as antigen. In the process, the parathyroid glands stop manufacturing their hormone.
  • Extensive cancer radiation treatment of face or neck, which can result in destruction of parathyroid glands.
  • Low levels of magnesium in blood, which can affect the function of parathyroid glands. Normal magnesium levels are required for optimum secretion of parathyroid hormone.
 
Risk Factors
  • Recent neck surgery, particularly if the thyroid was involved
  • A family history of hypoparathyroidism
  • Having certain autoimmune or endocrine conditions, such as Addison's disease–a condition characterized by a deficit in hormone production by the adrenal glands.
 
Diagnostic Evaluation
  • History: It begins with the diagnostic process by taking a medical history and asking about symptoms, such as muscle cramps or tingling of the extremities, recent surgeries, particularly operations involving the thyroid or neck.
  • Physical examination, looking for signs that suggest hypoparathyroidism, such as facial muscle twitching.
  • Blood tests will reveal low blood—calcium level, low parathyroid hormone level, high blood—phosphorus level, and low blood—magnesium level.
  • Electrocardiogram (ECG): This test involves taking electrical readings of heart's activity. It can detect arrhythmias associated with hypocalcemia, and in turn, hypoparathyroidism.
  • Urine test: Evaluation of a sample of urine can show whether body is excreting too much calcium.
  • X-rays and bone density tests these can determine whether abnormal calcium levels have affected the strength of bones.
 
Complication
  • Tetany: These cramp-like spasms of hands and fingers may be prolonged and painful. Tetany also may include muscle discomfort and twitches or spasms of the muscles of face, throat or arms. When these spasms occur in your throat, they can interfere with breathing, creating a possible emergency.
  • Paresthesias: These are characterized by sensory symptoms of odd, tingling sensations or pins and needles feelings in your lips, tongue, fingers and feet.
  • Loss of consciousness with convulsions (grand mal seizures).
  • Malformation of the teeth.
  • Impaired kidney function.
  • Heart arrhythmias and fainting
  • Stunted growth (short stature)
  • Slow mental development (or mental retardation) in children
  • 491Calcium deposits in the brain
  • Cataracts.
 
Management
 
Treatments and Drugs
Oral calcium carbonate tablets.
Vitamin D, which can help your body absorb calcium and eliminate phosphorus. The forms of vitamin D called ergocalciferol or calcitriol are recommended most often because they have a longer duration of action or are more potent than are other forms of this vitamin. Often, the required doses of vitamin D are much higher than are those used for a typical daily vitamin supplement.
 
Diet That is:
  • Rich in calcium. This includes dairy products, green leafy vegetables, broccoli, kale, and fortified orange juice and breakfast cereals.
  • Low in phosphorus-rich items. This means avoiding carbonated soft drinks, which contain phosphorus in the form of phosphoric acid. Eggs and meats also tend to be high in phosphorus.
  • Intravenous infusion: In some cases, when immediate relief of symptoms are required, administer of calcium by intravenous (IV) infusion.
  • Regular monitoring, regularly assessment of blood to monitor levels of calcium and phosphorus. Initially, these tests will be weekly to monthly.
  • Nutrition and Supplements
  • Following these nutritional tips may help reduce symptoms of hypoparathyroidism.
  • Eliminate all potential food allergens, including dairy, wheat (gluten), soy, corn, preservatives, and food additives.
  • Eat calcium rich foods, including beans, almonds, and dark green leafy vegetables (such as spinach).
  • Avoid refined foods, such as white breads, pastas, and sugar.
  • Eat fewer red meats and more lean meats, cold water fish, tofu (soy), or beans for protein.
  • Use healthy cooking oils, such as olive oil or vegetable oil.
  • Reduce or eliminate trans-fatty acids, found in commercially baked goods such as cookies, crackers, cakes, and doughnuts. Also avoid French fries, onion rings, processed foods.
  • Limit carbonated beverages. They are high in phosphates, which can leach calcium from your bones.
  • Avoid coffee and other stimulants, alcohol, and tobacco.
  • Drink 6–8 glasses of filtered water daily.
  • Drink soy milk for bone health unless allergic to soy.
  • Exercise moderately at least 30 minutes daily, 5 days a week.
  • A multivitamin daily, containing the antioxidant vitamins A, C, E, the B-complex vitamins, and trace minerals such as magnesium, calcium, zinc and selenium.
  • 492Ipriflavone (soy isoflavones) standardized extract, 200 mg 3 times a day, for bone loss. Ipriflavone can interfere with many different medications and may not be suitable for certain people with immune deficiencies.
  • Omega-3 fatty acids, such as fish oils, 1–2 capsules or 1–2 tablespoonfuls of oil daily, to help decrease inflammation and support healthy metabolism. Omega-3 fatty acids can have a blood-thinning effect and may increase the effect of blood-thinning drugs, such as warfarin (Coumadin) and aspirin.
 
Nursing Management
  • Activity intolerance related to fatigue and decreased cognitive process.
  • Constipation related to decreased gastrointestinal function.
  • Knowledge deficit related to exposure to information about treatment program for lifelong thyroid replacement therapy.
  • Ineffective breathing pattern related to depression of ventilation.
  • Disturbed thought process related to metabolic disorder and cardiovascular and respiratory status changes.
 
HYPERPARATHYROIDISM
Hyperparathyroidism is an excess of parathyroid hormone in the bloodstream due to over activity of parathyroid glands. These oval, grain-of-rice-sized glands are located in your neck. The parathyroid glands produce parathyroid hormone, which helps maintain an appropriate balance of calcium in the bloodstream and in tissues that depend on calcium for proper functioning.
 
Etiology
  • Primary hyperparathyroidism: It occurs because of some problem with one or more of the four parathyroid glands: A noncancerous growth (adenoma) on a gland is the most common cause, Enlargement (hyperplasia) of two or more parathyroid glands accounts for most other cases. A cancerous (malignant) tumor is a rare cause of primary hyperparathyroidism.
  • Secondary hyperparathyroidism: It is the result of another condition that lowers calcium levels.
  • Severe calcium deficiency.
  • Severe vitamin D deficiency.
  • Chronic kidney failure: Kidneys convert vitamin D into a form that body can use. If kidneys function poorly, useable vitamin D may decline and calcium levels drop. Chronic kidney failure is the most common cause of secondary hyperparathyroidism.
 
Risk Factors
  • Woman who has gone through menopause
  • Severe calcium or vitamin D deficiency
  • Inherited disorder, such as multiple endocrine neoplasia, type I, which usually affects multiple glands
  • Radiation treatment for cancer that has exposed neck to radiation a drug most often used to treat bipolar disorder.
493
 
Signs and Symptoms
  • Fragile bones that easily fracture (osteoporosis)
  • Kidney stones
  • Excessive urination
  • Abdominal pain
  • Tiring easily or weakness
  • Depression or forgetfulness
  • Bone and joint pain
  • Frequent complaints of illness with no apparent cause
  • Nausea, vomiting or loss of appetite.
 
Diagnostic Evaluation
  • Blood tests: If the result of a blood test indicates elevated calcium in your blood.
  • Bone mineral density test (bone densitometry): The most common test to measure bone mineral density is dual energy X-ray absorptiometry, or a DXA scan. This test uses special X-ray devices to measure how many grams of calcium and other bone minerals are packed into a segment of bone.
  • Urine tests: A 24-hour collection of urine can provide information on how well kidneys function and how much calcium is excreted in urine. This test may help in judging the severity of hyperparathyroidism or diagnosing a kidney disorder causing hyperparathyroidism.
  • Ultrasound: Ultrasound uses sound waves to create images of your parathyroid glands and surrounding tissue. A small device held against your skin (transducer) emits high-pitched sound waves and records the sound wave echoes as they reflect off internal structures. A computer converts the echoes into images on a monitor.
  • Sestamibi scan: Sestamibi is a specially designed radioactive compound that is absorbed by overactive parathyroid glands and can be detected on computerized tomography (CT) scans. A small dose of the compound is injected into your bloodstream before the imaging test is done.
 
Complications
  • Osteoporosis: The loss of calcium often results in osteoporosis, or weak, brittle bones that fracture easily.
  • Kidney stones: The excess of calcium in blood may cause small, hard deposits of calcium and other substances to form in kidneys. A kidney stone usually causes significant pain as it passes through the urinary tract.
  • Cardiovascular disease: Although the exact cause-and-effect link is unclear, high calcium levels are associated with cardiovascular conditions, such as high blood pressure (hypertension) and certain types of heart disease.
  • Neonatal hyperparathyroidism: Severe, untreated hyperparathyroidism in pregnant women may cause dangerously low levels of calcium in newborns.
 
Management
Your doctor may recommend no treatment and regular monitoring if:
  • Your calcium levels are only slightly elevated
  • Your kidneys are functioning normally
  • 494Your bone density is normal or only slightly below normal
  • You have no other symptoms that may improve with treatment
  • If you choose this watch-and-wait approach, you will likely need a test to check your blood-calcium levels at least twice a year and have other monitoring tests done at least once a year.
 
Surgical Management
Surgery is the most common treatment for primary hyperparathyroidism and provides a cure in at least 90 percent of all cases. A surgeon will remove only those glands that are enlarged or have a tumor (adenoma). If all four glands are affected, a surgeon will likely remove only three glands and perhaps a portion of the fourth—leaving some functioning parathyroid tissue.
Complications from surgery are not common. Risks include:
  • Damage to nerves controlling the vocal cords
  • Long-term low calcium levels requiring the use of calcium and vitamin D supplements
 
Drugs
  • Calcimimetics: A calcimimetic is a drug that mimics calcium circulating in the blood. Therefore, the drug may trick the parathyroid glands into releasing less parathyroid hormone. This drug is sold as cinacalcet (Sensipar). The Food and Drug Administration approved cinacalcet to treat hyperparathyroidism caused by chronic kidney disease or parathyroid cancer.
  • Hormone replacement therapy: For women who have gone through menopause and have signs of osteoporosis, hormone replacement therapy may help bones retain calcium. This treatment, usually a combination estrogen and progestin, does not address the underlying problems with the parathyroid glands. Prolonged use of hormone replacement therapy can increase the risk of cardiovascular disease and some cancers. Work with your doctor to evaluate the risks and benefits to help you decide what is best for you.
  • Bisphosphonates: Bisphosphonates also prevent the loss of calcium from bones and may lessen osteoporosis caused by hyperparathyroidism.
 
Lifestyle and Home Remedies
  • Monitor how much calcium and vitamin D you get in your diet. The Institute of Medicine recommends 1,000 milligrams (mg) of calcium a day for adults ages 19 to 50 and men ages 51 to 70. That calcium recommendation increases to 1,200 mg a day if you are a woman age 51 or older or a man age 71 or older. The Institute of Medicine also recommends 600 international units (IUs) of vitamin D a day for adults ages 19 to 70 and 800 IUs a day for adults age 71 and older.
  • Drink plenty of water. Drink six to eight glasses of water daily to lessen the risk of kidney stones.
  • Exercise regularly. Regular exercise, including strength training, helps maintain strong bones.
  • 495Do not smoke. Smoking may increase bone loss as well as increase your risk of a number of serious health problems.
  • Avoid calcium-raising drugs. Certain medications, including some diuretics and lithium, can raise calcium levels.
 
Nursing Management
  • Protect the patient from injury,
  • Monitor for possible complications
  • Provide patient education independent
  • Adjust activities and reduce intensity
  • Provide positive atmosphere, while acknowledging the difficulty of situation for the client.
  • Assist patients with activities/monitor clients use of assistive device such as walker.
  • Helps minimize frustration, rechanneling of energy
  • To protect client from injury
  • To remove cause of hypersecretion of parathormones
  • Loop diuretic used with normal saline to cause diuresis and to reduce calcium levels
  • Obtain baseline serum potassium, calcium, phosphate, and magnesium levels before treatment.
  • Provide at least 3 liters of fluid per day, including cranberry or prune juice, to increase urine acidity and help prevent calculus formation.
  • Take safety precaution to minimize the risk for injury from fall.
  • Schedule care to allow the patient with muscle weakness as much rest as possible.
  • Provide comfort measures to alleviate bone pain.
  • Administer antacids, as appropriate to prevent pelvic ulcers.
  • Auscultate the lungs regularly. Check for signs of pulmonary edema in the patient receiving large amounts of normal saline solution, especially if he has pulmonary or cardiac disease.
  • Check for elevated serum calcium levels if the patient is receiving cardiac glycosides.
  • Assess the patient for parathyroid poisoning, musculoskeletal changes, and renal impairment.
  • Observe the patient for signs of pain and monitor him for effectiveness of analgesics and comfort measures.
 
CUSHING SYNDROME AND ADDISON DISEASE
The adrenal glands are two flat canary yellow structures lying above the upper pole of each kidney. Each gland consist of a cortical and a medullary portion which, although anatomically joined are physiologically separate. Blood containing the secreted hormones drains into the adrenal veins–the right draining directly into the inferior vena cava. The left into the left renal vein which, in turn, joins the inferior vena cava.
Disease of adrenal glands may cause over or under activity of the cortex or of the medulla. Under activity from disease or surgical excision for therapeutic reasons will require replacement therapy.
496
 
The Cortical Hormones
  • The mineralocorticoids: Which regulates water and electrolyte balance, the most important being aldosterone which conserve sodium in the body.
  • The glucocorticoids: Which converts body protein to carbohydrates in addition hydrocortisone (which is converted in the body from cortisone) enables the body to response in stress, inhibits the action of insulin and is important in maintaining blood pressure. In excess it inhibits the inflammation reaction and also the rejection reaction in tissue transplantation.
  • The sex hormone: Androgens and estrogens are secreted ACTH stimulates the adrenal cortex to secretes glucocorticoids and an the sex hormone. Excess of hydrocortisone in the blood inhibit the secretion of ACTH. The secretion of mineralocorticoids is independent of the pituitary.
Fig. 9.2: Adrenal gland
 
CUSHING SYNDROME
Cushing syndrome occurs when body is exposed to high levels of the hormone cortisol for a long time. The most common cause of Cushing syndrome, sometimes called hypercortisolism, is the use of oral corticosteroid medication. The condition can also occur when body makes too much cortisol.
Too much cortisol can produce some of the hallmark signs of Cushing syndrome—a fatty hump between shoulders, a rounded face, and pink or purple stretch marks on skin are the classical sign of cushing syndrome.
 
Etiology
  • A pituitary gland tumor (pituitary adenoma): A noncancerous tumor of the pituitary gland, located at the base of the brain, secretes an excess amount of ACTH, which in turn stimulates the adrenal glands to make more cortisol.
  • An ectopic ACTH-secreting tumor: Rarely, when a tumor develops in an organ that normally does not produce ACTH, the tumor will begin to secrete this hormone in excess, resulting in Cushing syndrome.
  • A primary adrenal gland disease: In some people, the cause of Cushing syndrome is excess cortisol secretion that doesn't depend on stimulation from ACTH and is associated with disorders of the adrenal glands. The most common of these disorders is a noncancerous tumor of the adrenal cortex, called an adrenal adenoma.
  • Familial Cushing syndrome: Rarely, people inherit a tendency to develop tumors on one or more of their endocrine glands, affecting cortisol levels and causing Cushing syndrome.
497
 
Pathophysiology
498
 
Signs and Symptoms
  • Common signs and symptoms involve progressive obesity and skin changes, such as:
    Weight gain and fatty tissue deposits, particularly around the midsection and upper back, in the face (moon face), and between the shoulders (buffalo hump).
  • Pink or purple stretch marks (striae) on the skin of the abdomen, thighs, breasts and arms
  • Thinning, fragile skin that bruises easily
  • Slow healing of cuts, insect bites and infections
  • Acne
  • Women with Cushing syndrome may experience: Thicker or more visible body and facial hair (hirsutism)
  • Irregular or absent menstrual periods.
    Fig. 9.3: Clinical manifestations
  • Men with Cushing syndrome may experience: Decreased libido, Decreased fertility, Erectile dysfunction
  • Other signs and symptoms include:
    • Fatigue
    • Muscle weakness
    • Depression, anxiety and irritability
    • 499Loss of emotional control
    • Cognitive difficulties
    • New or worsened high blood pressure
    • Glucose intolerance that may lead to diabetes
    • Headache
    • Bone loss, leading to fractures over time.
 
Complications
  • Bone loss (osteoporosis), which can result in unusual bone fractures, such as rib fractures and fractures of the bones in the feet
  • High blood pressure (hypertension)
  • Diabetes
  • Frequent or unusual infections
  • Loss of muscle mass and strength.
 
Diagnostic Evaluation
 
24-Hour Urinary Free Cortisol Level
This is the most specific diagnostic test. The patient's urine is collected over a 24-hour period and tested for the amount of cortisol. Levels higher than 50–100 micrograms a day for an adult suggest Cushing's syndrome. The normal upper limit varies in different laboratories, depending on which measurement technique is used.
 
Dexamethasone Suppression Test
This test helps to distinguish patients with excess production of ACTH due to pituitary adenomas from those with ectopic ACTH-producing tumors. Patients are given dexamethasone, a synthetic glucocorticoid, by mouth every 6 hours for 4 days. For the first 2 days, low doses of dexamethasone are given, and for the last 2 days, higher doses are given. Twenty-four hour urine collections are made before dexamethasone is administered and on each day of the test. Since cortisol and other glucocorticoids signal the pituitary to lower secretion of ACTH, the normal response after taking dexamethasone is a drop in blood and urine cortisol levels. Different responses of cortisol to dexamethasone are obtained depending on whether the cause of Cushing's syndrome is a pituitary adenoma or an ectopic ACTH-producing tumor.
 
CRH Stimulation Test
This test helps to distinguish between patients with pituitary adenomas and those with ectopic ACTH syndrome or cortisol-secreting adrenal tumors. Patients are given an injection of CRH, the corticotropin-releasing hormone which causes the pituitary to secrete ACTH. Patients with pituitary adenomas usually experience a rise in blood levels of ACTH and cortisol. This response is rarely seen in patients with ectopic ACTH syndrome and practically never in patients with cortisol-secreting adrenal tumors
 
Direct Visualization of the Endocrine Glands (Radiologic Imaging)
Imaging tests reveal the size and shape of the pituitary and adrenal glands and help determine if a tumor is present. The most common are the CT scan and MRI). A CT scan 500produces a series of x-ray pictures giving a cross-sectional image of a body part. MRI also produces images of the internal organs of the body but without exposing the patient to ionizing radiation.
 
Petrosal Sinus Sampling
This test is not always required, but in many cases, it is the best way to separate pituitary from ectopic causes of Cushing's syndrome. Samples of blood are drawn from the petrosal sinuses, veins which drain the pituitary, by introducing catheters through a vein in the upper thigh or groin region, with local anesthesia and mild sedation. X-rays are used to confirm the correct position of the catheters. Often CRH, the hormone which causes the pituitary to secrete ACTH, is given during this test to improve diagnostic accuracy. Levels of ACTH in the petrosal sinuses are measured and compared with ACTH levels in a forearm vein. ACTH levels higher in the petrosal sinuses than in the forearm vein indicate the presence of a pituitary adenoma similar levels suggest ectopic ACTH syndrome.
 
The Dexamethasone-CRH Test
Some individuals have high cortisol levels, but do not develop the progressive effects of Cushing's syndrome, such as muscle weakness, fractures and thinning of the skin. These individuals may have Pseudo Cushing's syndrome, which was originally described in people who were depressed or drink excess alcohol, but is now known to be more common. Pseudo Cushing's does not have the same long-term effects on health as Cushing's syndrome and does not require treatment directed at the endocrine glands. Although observation over months to years will distinguish Pseudo Cushing's from Cushing's, the dexamethasone-CRH test was developed to distinguish between the conditions rapidly, so that Cushing's patients can receive prompt treatment. This test combines the dexamethasone suppression and the CRH stimulation tests. Elevations of cortisol during this test suggest Cushing's syndrome.
 
Management
 
Assessment
Hyper functioning of the adrenal cortex can result in excessive production of glucocoriticoid, mineralocorticoids, and androgens. Cushing syndrome is a condition in which the plasma cortisol levels are elevated, causing signs and symptoms of hypercortisolism.
The assessment of Cushing syndrome includes
  • The health history and examination focus on the effects on the body of high concentrations of adrenal cortex hormones or the inability of the adrenal cortex to respond to changes in cortisol and aldosterone levels.
  • The history includes information about the patient's level of activity and ability to carry out routine and self-care activities.
  • The skin is observed and assessed for trauma, infection, breakdown, bruising edema.
  • Changes in physical appearance are noted like weight gain or obesity, Heavy trunk, thin extremities, Buffalo hump in neck and supra clavicular area, Muscles wasted, osteoporosis—characteristics kyphosis, backache.
  • Assess the patients mental function, including mood changes, responses to question, awareness of environment, and level of depression, psycosis.
  • 501The family are the good source of information about gradual changes in the patient's physical appearance as well as emotional status.
  • Assess all the lab investigations like as increase in plasma cortisol levels, an increase in blood glucose levels and glucose tolerance, decreased potassium level, X-rays, etc.
 
Medical Management
Depending on the specific patient and the etiology of the disease various therapies may be used. These include drug therapy, radiation, and surgery. If Cushing syndrome is caused by synthetic glucocoriticoids, the physician may gradually withdraw them most patients affected with hyperaldernalism due to single benign tumor undergo single intervention. Bilateral benign tumors may often are treated with aldosterone antagonist, that is a drug reduces aldosterone secretion or blocks its effects.
Treatments for Cushing syndrome are designed to lower the high level of cortisol in body. The best treatment for you depends on the cause of the syndrome. Treatment options include:
  • Reducing corticosteroid use: If the cause of Cushing syndrome is long-term use of corticosteroid medications, the doctor maybe able to keep Cushing signs and symptoms under control by reducing the dosage of the drug over a period of time, while still adequately managing asthma, arthritis or other condition. For many of these medical problems, the doctor can prescribe noncorticosteroid drugs, which will allow him or her to reduce the dosage or eliminate the use of corticosteroids all together.
  • Surgical Management: If the cause of Cushing syndrome is a tumor, doctor may recommend complete surgical removal because the remaining adrenal gland may have atrophied and stopped producing adrenocortical hormones pituitary tumors are typically removed by a neurosurgeon, which may perform the procedure through nose. If a tumor is present in the adrenal glands, lungs or pancreas, the surgeon can remove it through a standard operation or in some cases by using minimally invasive surgical techniques, with smaller incisions.
 
Preoperative Care
  • Begin by obtaining a careful history from a client with possible Cushing syndrome.
  • The client may exhibit the characteristics clinical manifestation identified previously.
  • Support the client during the diagnostic phase of care. Explain to the client why these tests are important to perform before the treatment.
  • During this phase the client with Cushing syndrome require expert nursing assessment and care.
  • The crucial problems of hypertension, edema, possibility, diabetes mellitus, resistance to stress and emotional lability or instability must all be assessed and brought under the control before the surgery.
 
Postoperative Care
After the operation, patient need to take cortisol replacement medications to provide body with the correct amount of cortisol. In most cases, patient eventually experience a return of normal adrenal hormone production, and doctor can taper off the replacement drugs. However, this process can take up to a year or longer. In some instances, people with 502Cushing syndrome never experience a resumption of normal adrenal function; they then need lifelong replacement therapy.
  • Radiation therapy: In case in which a pituitary adenomas because excessive secretions of ACTH, the adenomas be treated with the radiation therapy. If the surgeon cannot totally remove a pituitary tumor, he or she will usually prescribe radiation therapy to be used in conjunction with the operation. Additionally, radiation maybe used for people who are not suitable candidates for surgery. Radiation can be given in small doses over a six-week period or by a technique called stereotactic radio surgery. It is administered externally or internally. Internally radiation involves the transsphenoidal implantation of radioactive material that remains in place for specified period of time. Radiotherapy is not always effective and can destroy healthy tissue. The radiation therapy is used to treat a patient with pituitary adenomas
  • Medications: Medications can be used to control cortisol production when surgery and radiation do not work. Medications may also be used before surgery in people who have become very sick with Cushing syndrome. Doctors recommend drug therapy before surgery to improve signs and symptoms and minimize surgical risk. Medications to control excessive production of cortisol include ketoconazole, mitotane, and metyrapone.
  • Metyrapone to control steroid hypersecretion in patient who does not respond to mitotane therapy.
  • Aminoglutethemide blocks cholesterol conversion of pregenolone, effectively blocking cortisol production. Adverse affect include GI disturbances, somnolence, skin rashes.
  • Increase activities slowly: Work-up to a reasonable level of exercise or activity that feels comfortable without overdoing it. Patient improves little by little, and prevent obesity.
  • Eat sensibly: Nutritious, wholesome foods provide a good source of fuel for recovering body and can help to lose the extra pounds that you gained from Cushing syndrome. Make sure the patient getting enough calcium and vitamin D. Taken together, they help body absorb calcium, which can help strengthen bones, counteracting the bone density loss that often occurs with Cushing syndrome.
  • Monitor your mental health: Depression can be a side effect of Cushing syndrome, but it can also persist or develop after treatment begins. Do not ignore depression or wait it out. Seek help promptly from doctor or a therapist if you are depressed, overwhelmed or having difficulty coping during your recovery.
  • Gently soothe aches and pains: Hot baths, massages and low-impact exercises, such as water aerobics and tai chi, can help alleviate some of the muscle and joint pain that accompanies Cushing syndrome recovery.
  • Exercise your brain: If the patient is recovering from any cognitive difficulties as a result of Cushing syndrome, mental exercises, such as math problems and crossword puzzles, may improve brain function.
 
Nursing Management
 
Nursing Diagnosis
  • Risk for injury related to weakness
  • Risk for infection related to altered protein metabolism and inflammatory response
  • Impaired skin integrity related to edema, impaired healing, and thin and fragile skin
  • 503Self-care deficit related to weakness, fatigue, muscle wasting and altered sleeping pattern
  • Disturbed body image related to altered physical appearance, decreased activity level
  • Disturbed thought process related to mood swings, irritability, and depression.
 
Nursing Interventions
  1. Risk for injury related to weakness
    Intervention
    • Establishing a protective environment help falls, fracture, and others injuries to bones and soft tissues.
    • The patient who is very week may require assistance from the nurse in ambulating to avoid falling or bumping into sharp corners of the furniture.
    • Food high in protein, vitamin D, calcium are recommended to minimize muscle wasting and osteoporosis.
    • Referral to the dietician may assist the patient in selecting appropriate foods that are also low in sodium and calories.
  2. Risk for infection related to altered protein metabolism and inflammatory response.
    Intervention
    • The patient should avoid unnecessary exposure to other with infection.
    • The nurse frequently assesses the patient for subtle signs of infection, because the anti inflammatory effect of corticosteroids may mask the common signs of inflammation and infection.
  3. Impaired skin integrity related to edema, impaired healing, and thin and fragile skin.
    Intervention
    • Meticulous skin care is necessary to avoid traumatizing the patient's fragile skin.
    • Use of adhesive tape is avoided, because it can irritate the skin and tear the fragile tissue when the tape is removed.
    • The nurse frequently assesses the skin and bony prominence and encourages and assists the patient to change positions frequently to prevent skin break down.
  4. Self-care deficit related to weakness, fatigue, muscle wasting and altered sleeping pattern.
    Intervention
    • Weakness, fatigue, and muscles wasting make it difficult for the patient with Cushing syndrome to carry out normal activities, the nurse should encourage out normal activity to prevent complications and promote increased self-esteem.
    • Insomnia often contribution to prevent complication and promote to increased self-esteem. Insomnia often contributes to the patient's fatigue.
    • It is important to help the patient plan and space rest periods throughout the day.
    • Efforts are made to promote a relaxing, quite environment for rest and sleep.
  5. Disturbed body image related to altered physical appearance, decreased activity level.
    Intervention
    • The Cushing syndrome is treatable the major physical changes disappear in time.
    • The patient may discussion of the effect the changes of had on his or her self-concept and relationships with other.
    • 504Weight gain and edema maybe modified by low carbohydrate, low sodium diet and high protein intake may reduce some of the other bother some symptoms.
  6. Disturbed thought process related to mood swings, irritability, and depression.
    Intervention
    • Explanation of the family members and patient about the cause of emotional instability are important in helping them and cope-up with the mood swings, irritability and depression that may occur.
    • Psychotic behavior and depression that may occur in a few patients and should be reported.
    • The nurse encourages the patients and family members to verbalize their feelings and concern.
 
ADDISON'S DISEASE (ADRENAL INSUFFICIENCY)
Addison's disease is a disorder that occurs when the body produces insufficient amounts of certain hormones produced by adrenal glands. In Addison's disease, adrenal glands produce too little cortisol and often insufficient levels of aldosterone as well.
Glucocorticoids: These hormones, which include cortisol, influence our body's ability to convert food fuels into energy, play a role in immune system's inflammatory response and help our body respond to stress.
Mineralocorticoids: These hormones, which include aldosterone, maintain body's balance of sodium and potassium to keep blood pressure normal.
Androgens: These male sex hormones are produced in small amounts by the adrenal glands in both men and women. They cause sexual development in men and influence muscle mass, libido and a sense of well-being in both men and women.
 
Etiology
  • Primary Adrenal Insufficiency: Addison's disease occurs when the cortex is damaged and does not produce its hormones in adequate quantities. The failure of adrenal glands to produce adrenocortical hormones is most commonly the result of the body attacking itself (autoimmune disease). For unknown reasons, immune system views the adrenal cortex as foreign, something to attack and destroy.
    Other causes of adrenal gland failure may include:
    • Tuberculosis
    • Other infections of the adrenal glands
    • Spread of cancer to the adrenal glands
    • Bleeding into the adrenal glands
  • Secondary Adrenal Insufficiency: Adrenal insufficiency can also occur if pituitary gland is diseased. The pituitary gland makes a hormone called adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to produce its hormones. Inadequate production of ACTH can lead to insufficient production of hormones.
  • Another more common cause of secondary adrenal insufficiency occurs when people who take corticosteroids for treatment of chronic conditions, such as asthma or arthritis, abruptly stop taking the corticosteroids.
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Pathophysiology
  • Addison's disease is a chronic condition that results from partial or complete adrenal destructon.
  • ACTH acts primarily to regulate the adrenal release of glucocorticoids, primarily cortisol, mineralocorticoids including aldosterone; and sex steroids that supplement those produced by the gonads.
  • ACTH secretion is controlled by corticotrophin releasing hormone from the hypothalamus and by negative feedback control by the glucocorticoids.
  • Cortisol deficiency causes decreased liver gluconeogenesis. Glucose levels of patients on insulin maybe dangerously low.
  • Aldosterone deficiency causes increased renal sodium loss and enhances potassium reabsorption. Sodium excretion causes a reduction in water volume that leads to hypotension.
  • Androgen deficiency may result in decreased hair growth in axillary and pubic areas, loss of erectile function, or decreased libido.
 
Signs and Symptoms
Addison's disease symptoms usually develop slowly, often over several months, and may include:
  • Muscle weakness and fatigue
  • Weight loss and decreased appetite
  • Darkening of your skin (hyperpigmentation)
  • Low blood pressure, even fainting
  • Salt craving
  • Low blood sugar (hypoglycemia)
  • Nausea, diarrhea or vomiting
  • Muscle or joint pains
  • 506Irritability
  • Depression
  • Body hair loss or sexual dysfunction in women.
In acute adrenal failure (Addisonian crisis), the signs and symptoms may also include:
  • Pain in lower back, abdomen or legs
  • Severe vomiting and diarrhea, leading to dehydration
  • Low blood pressure
  • Loss of consciousness
  • High potassium (hyperkalemia).
 
Diagnostic Evaluation
  • Blood test: Measuring blood levels of sodium, potassium, cortisol and ACTH gives an initial indication of whether adrenal insufficiency may be causing signs and symptoms. A blood test can also measure antibodies associated with autoimmune Addison's disease.
  • ACTH stimulation test: This test involves measuring the level of cortisol in blood before and after an injection of synthetic ACTH. ACTH signals adrenal glands to produce cortisol. If adrenal glands are damaged, the ACTH stimulation test shows that output of cortisol in response to synthetic.
  • Insulin-induced hypoglycemia test: Occasionally, this test has to be done if pituitary disease is a possible cause of adrenal insufficiency (secondary adrenal insufficiency). The test involves checking blood sugar and cortisol levels at various intervals after an injection of insulin. In healthy people, glucose levels fall and cortisol levels increase.
  • Imaging tests: Computerized tomography (CT) scan of abdomen to check the size of adrenal glands and look for other abnormalities that may give insight to the cause of the adrenal insufficiency.
 
Management
  • Oral corticosteroids, fludrocortisone to replace aldosterone. Hydrocortisone, prednisone or cortisone acetate maybe used to replace cortisol.
  • Corticosteroid injections.
  • Androgen replacement therapy: To treat androgen deficiency in women, dehydroepiandrosterone can be prescribed.
  • An ample amount of sodium is recommended, especially during heavy exercise, when the weather is hot, or gastrointestinal upsets, such as diarrhea.
 
Management of Addisonian Crisis
Addisonian crisis is a life-threatening situation that results in low blood pressure, low blood levels of sugar and high blood levels of potassium. This situation requires immediate medical care. Treatment typically includes intravenous injections of:
  • Hydrocortisone
  • Saline solution
  • Sugar (dextrose).
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Nursing Management
 
Assessment
Assessing the Patient
  • Assess the daily weights or intake and output to monitor fluid volume.
  • Check the pulse carefull, at least every 4 hours.
  • Assess bone prominences for pressure ulcers in immobilized clients.
  • Monitor for exposure to cold and infections.
  • Assess for manifestations of sodium and potassium imbalance.
  • Skin should be assessed for changes in color and turgor which could indicate chronic adrenal insufficiency.
 
Diagnosis
  1. Risk for injury: Addisonian crisis related to adrenal insufficiency.
    Interventions
    • Monitor for sudden profound weakness, severe abdominal, back and leg pain.
    • Immediately on admission, 1000 ml of normal saline with water soluble glucocorticoid added is rapidly infused.
    • Hypoglycemia is controlled by a glucose infusion.
    • Monitor BP, administer IV infusion and medication.
    • Monitor hourly urine output and minimize exposure to emotional and physical stress.
    • Observe for manifestation of glucocorticoid overdose and overhydration, such as generalized edema, hypertension, psychosis and loss of consciousness.
    • When the client can tolerate food and fluids by mouth, steroid replacement can be administered orally.
    • Keep bed in lowest position, to increase ease with which patient can get into bed and decrease the possibility of falling.
    • Keep side rails up to all times unless patient refuses.
    • Instruct patient to call for assistance when getting into or out of bed.
  2. Deficient fluid volume related to inability to conserve fluid secondary to glucocorticoid deficiency.
    Interventions
    • Monitor intake and output hourly.
    • Monitor blood pressure and heart rate hourly until normal.
    • Monitor weigh daily: to determine fluid and nutritional needs. Fluid deficit results in weight loss. Fluid restoration results in weight gain.
    • Administer intravenous fluids as prescribed.
    • Monitor hemoglobin, blood urea nitrogen and serum creatinine daily.
    • Administer cortisol as prescribed.
  3. 508Ineffective coping related to inability to respond to stressors secondary to adrenal insufficiency.
    Interventions
    • Decrease environmental stressors (noise, lights, temperature changes) patient has reduced ability to respond to any stressors. External stressors need to be controlled until patient is able to cope in his usual manner.
    • Explain all procedures and interventions to the patient this will helps to reduce the fair and anxiety.
    • Maintain consistency of care providers for first 24 hrs. Consistency of personnel increases the patient trust and reduce stress.
    • Provide care in calm and unhurried manner. If the nurse is calm the patient is more likely to be calm.
    • Encouraging family members to remain with patient, if they are comforting to him. The presence of family members often increases comfort and security and reduce stress.
 
DIABETES MELLITUS
Diabetes mellitus is a group of metabolic diseases in which a person has high blood sugar, either because the pancreas does not produce enough insulin, or because cells do not respond to the insulin that is produced. This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger). Hyperglycemia does not cause symptoms until glucose values are significantly elevated—above 200 milligrams per deciliter (mg/dL).
Diabetes mellitus is a group of chronic disorder of endocrine pancreas. This disease characterized by increased levels of glucose in blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, both.
There are three main types of diabetes mellitus (DM).
  1. TYPE-1 Diabetes Mellitus: Type 1 DM results from the body's failure to produce insulin, and currently requires the person to inject insulin or wear an insulin pump. It is also called ‘insulin-dependent diabetes mellitus’ (IDDM) or ‘juvenile diabetes’. The immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients’ own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies.
  2. TYPE-2 Diabetes mellitus: Type 2 DM results from insulin resistance, also referred to as non-insulin-dependent diabetes mellitus (NIDDM) or ‘adult-onset diabetes’. In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs. In many cases the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).
  3. Gestational diabetes: Gestational diabetes, occurs when pregnant women without a previous diagnosis of diabetes develop a high blood glucose level. Gestational diabetes 509(or gestational diabetes mellitus, GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy (especially during their third trimester).
510
 
Type 1 Diabetes Mellitus
 
Type 2 Diabetes Mellitus
 
Signs and Symptoms
  • Increased thirst (Polydepsia)
  • Frequent urination (polyuria)
  • 511Increased hunger (polyphagia)
  • Weight loss
  • Fatigue
  • Blurred vision
  • Slow-healing sores or frequent infections
  • Dark skin.
 
Diagnostic Evaluation
  • Glycated hemoglobin test: This blood test indicates average blood sugar level for the past two to three months. It measures the percentage of blood sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells. A normal level is below 5.7 percent.
  • Random blood sugar test: A blood sample will be taken at a random time. Regardless of when you last ate, a random blood sugar level of 200 mg/dL (11.1 mmol/L) or higher suggests diabetes, a blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal.
  • Fasting blood sugar test: A blood sample will be taken after an overnight fast. A fasting blood sugar level less than 100 mg/dL (5.6 mmol/L) is normal. A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If it is 126 mg/dL (7 mmol/L) or higher on two separate tests, indicates diabetes.
  • Oral glucose tolerance test: It is rarely used test for hyperglycimia, patient is asked to fast overnight, and the fasting blood sugar level is measured. Then drink a sugary liquid, and blood sugar levels are tested periodically for the next two hours. A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal. A reading of more than 200 mg/dL (11.1 mmol/L) after two hours indicates diabetes. A reading between 140 and 199 mg/dL (7.8 mmol/L and 11.0 mmol/L) indicates prediabetes.
  • Urine glucose and ketone levels: These are not as accurate in monitoring, changes in blood glucose as serum or blood levels. The presence of glucose in urine indicate hyperglycemia.
 
Complications
  • Cardiovascular disease
  • Nerve damage (neuropathy)
  • Kidney damage (nephropathy) or kidney failure
  • Damage to the blood vessels of the retina (diabetic retinopathy), potentially leading to blindness
  • Clouding of the normally clear lens (cataract)
  • Feet problems caused by damaged nerves or poor blood flow that can lead to serious infections
  • Bone and joint problems, such as osteoporosis
  • Skin problems, including bacterial infections, fungal infections and non healing wounds
  • Teeth and gum infections
  • Dawn phenomenon: It is rise of blood glucose between 4 am to 8 am that is not a response to hypoglycemia. This condition occurs in people both DM1 and DM2. Cause is unknown but due to hormone variation.
  • 512Diabetic ketoacidosis: Diabetic ketoacidosis develops when there is too little insulin in body. Without enough insulin, sugar cannot enter in cells for energy. Blood sugar level rises and body begins to break down fat for energy. This process produces toxic acids known as ketones. Excess ketones accumulate in the blood and eventually ‘spill over’ into the urine. Diabetic ketoacidosis can lead to diabetic coma that can be life-threatening.
  • Diabetic hyperosmolar syndrome: This condition occurs when production of insulin is normal, but it does not work properly. Blood glucose levels may become very high—greater than 600 mg/dL(33 mmol/L). Because insulin is present but not working properly, the body cannot use either glucose or fat for energy. Glucose is then dumped in the urine, causing increased urination. If left untreated, diabetic hyperosmolar syndrome can lead to coma and life-threatening dehydration.
 
Management
 
Nutritional Therapy
Nutrition, meal planning and weight control are the foundation of diabetes management.
The main objective to control dietary caloric intake to maintain normal weight. Medical nutrition therapy (MNT), nutritional management of diabetes is complex, a registered dietician who understand dietary management has major responsibilities for designing and teaching aspect of therapeutic plan.
  • Regular blood sugar monitoring
  • Regular exercise
  • Regular diabetes medication or insulin therapy
  • Alcohol: Alcohol and the substances use to make mixed drinks can cause either high or low blood sugar.
  • Stress: The hormones body may produce in response to prolonged stress may prevent insulin from working properly.
  • For women, fluctuations in hormone levels: As hormone levels fluctuate during menstrual cycle, so can blood sugar level also, particularly in the week before period. Menopause may trigger fluctuations in blood sugar level as well.
 
Pharmacological Management
  • Biguanides
  • Sulfonylureas
  • Meglitinide derivatives
  • Alphaglucosidase inhibitors
  • Thiazolidinediones (TZDs)
  • Glucagonlike peptide-1 (GLP-1) agonists
  • Dipeptidyl peptidase IV (DPP-4) inhibitors
  • Selective sodium-glucose transporter-2 (SGLT-2) inhibitors
  • Insulins
  • Amylinomimetics
  • Bile acid sequestrants
  • Dopamine agonists.
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Insulin Therapy
Some people who have type 2 diabetes need insulin therapy as well. Because normal digestion interferes with insulin taken by mouth, insulin must be injected. Insulin injections involve using a fine needle and syringe or an insulin pen injector—a device that looks like an ink pen, except the cartridge is filled with insulin.
Types of insulin are many and include rapid-acting insulin, long-acting insulin and intermediate options. Examples include:
  • Insulin lispro (Humalog)
  • Insulin aspart (Novolog)
  • Insulin glargine (Lantus)
  • Insulin detemir (Levemir)
  • Insulin isophane (Humulin N, Novolin N)
 
Lifestyle and Home Remedies
  • Commit to managing your diabetes: Make healthy eating and physical activity part of your daily routine. Establish a relationship with a diabetes educator, and ask your diabetes treatment team for help when you need it.
  • Wear a tag or bracelet that says you have diabetes. Keep a glucagon kit nearby in case of a low blood sugar emergency and make sure your friends and loved ones know how to use it.
  • Schedule a yearly physical exam and regular eye exams.
  • Keep your immunizations up-to-date. Get a flu shot every year, and get a tetanus booster shot every 10 years.
  • Take care of your teeth. Diabetes may leave you prone to gum infections. Brush your teeth at least twice a day, floss your teeth once a day, and schedule dental exams at least twice a year.
  • Pay attention to your feet. Wash your feet daily in lukewarm water. Dry them gently, especially between the toes, and moisturize with lotion. Check your feet everyday for blisters, cuts, sores, redness or swelling.
  • Keep your blood pressure and cholesterol under control.
  • Quit smoking.
  • If you drink alcohol, do so responsibly.
  • Take stress seriously.
 
Nursing Management
 
Nursing Diagnosis
  1. Fluid volume deficit related to osmotic diuresis, gastric loss, excessive diarrhea, nausea, and vomiting, limited input.
    Intervention
    • Monitor vital signs, note the presence of orthostatic blood pressure.
    • Assess breathing and breathe patterns.
    • Assess temperature, color and moisture.
    • Assess peripheral pulses, capillary refill, skin turgor and mucous membranes.
    • 514Monitor intake and output. Record the urine specific gravity.
    • Measure body weight everyday.
    • Collaboration fluid therapy as indicated
  2. Imbalanced nutrition, less than body requirements related to insulin insufficiency.
    Intervention
    • Measure body weight per day as indicated.
    • Determine the diet program and diet of patients compared with food that can be spent on the patient.
    • Auscultation of bowel sounds, record the presence of abdominal pain/abdominal bloating, nausea, vomiting, keep fasting as indicated.
    • Observation of the signs of hypoglycemia, such as changes in level of consciousness, cold/humid, rapid pulse, hunger and dizziness
    • Collaboration in the delivery of insulin, blood sugar tests and diet.
  3. Risk for infection related to inadequate peripheral defense, changes in circulation and high blood sugar levels
    Intervention
    • Observation for signs of infection and inflammation such as fever, redness, pus in the wound, purulent sputum, urine color cloudy and foggy.
    • Increase prevention efforts by performing good handwashing, each contact on all items related to the patient, including his or her own patients.
    • Maintain aseptic technique in invasive procedures (such as infusion, catheter foley, etc.)
    • Attach catheter/perineal care do well.
    • Give skin care with regular and earnest. Massage depressed bone area, keep skin dry, dry linen and tight (not wrinkled).
    • Position the patient in semifowler position.
    • Collaboration antibiotics as indicated.
  4. Knowledge deficit: About condition, prognosis and treatment needs related to misinterpretation of information; do not know the source of information.
    Intervention
    • Assess the level of knowledge of the client and family about the disease.
    • Give an explanation to the client about diseases and conditions now.
    • Encourage clients and families to pay attention to her diet.
    • Ask the client and reiterated family of materials that have been given.
BIBLIOGRAPHY
  1. Ananthakrishnan S. Diabetes insipidus in pregnancy: etiology, evaluation, and management. Endocr Pract. 2009 May-Jun; 15 (4): 377–82. doi: 10.4158/EP09090.RA.
  1. Brunner and Suddarth. Textbook of medical surgical nursing, 12th ed. 1245.
  1. Brunner and Siddarth. Textbook of medical surgical nursing, Lippincott Williams and Willkins Wolter Kulvar.  11th ed. 1483–6.
  1. Colmer RM. Textbook of moroney's surgery for nurses, Elsevier.  16th ed. 224–5.
  1. Diabetes Insipidus. The Pituitary Foundation.
  1. Di Iorgi N, Napoli F, AE, et al. Diabetes insipidus—diagnosis and management. Horm Res Pediatr. 2012; 77 (2): 69–84. doi: 10.1159/000336333. Epub 2012 Mar 16.
  1. Grunfeld JP, Rossier BC; Lithium nephrotoxicity revisited. Nat Rev Nephrol. 2009 May; 5 (5): 270–6. doi: 10.1038/nrneph. 2009.43.
  1. Halks B. Textbook of medical surgical nursing, 1221–2.
  1. Khardori R. Diabetes insipidus, Medscape, Oct 2012.
  1. Lederer E. Lithium nephropathy, Medscape, Jan 2012.
  1. Levis. Textbook of medical surgical nursing, 1023–5.
  1. Lewis. Textbook of medical surgical nursing, assessment and management of clinical problems, Chintamani Elsiver.  2011.
  1. Lewiv H, Dirksen. Medical surgical nursing, assessment and management of clinical problems, Elsevier,  1294.
  1. Linda SW, Paula DH. Textbook of understanding medical surgical nursing, 4th ed. 587–9.
  1. Lippincott manual of nursing practice. South Asian 10th ed. 792–5.
  1. Lippincott. Textbook of manual of nursing practice, 9th ed. 658–1660.
  1. Lippincott W and Wilkins. Textbook of medical surgical nursing, Wolter Kulvers,  9th ed. 934–5.
  1. Luckmann. Textbook of core principles and practice of medical surgical nursing, 786–9.
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Burn and Cosmetic Surgeries10

 
BURN
 
Introduction
Burns may be treated with first aid, in an out-of-hospital setting, or may require more specialized treatment such as those available at specialized burn centers. Managing burn injuries properly is important because they are common, painful and can result in disfiguring and disabling scarring, amputation of affected parts or death in severe cases. Complications such as shock, infection, multiple organ dysfunction syndrome, electrolyte imbalance and respiratory distress may occur. The treatment of burns may include the removal of dead tissue (debridement), applying dressings to the wound, fluid resuscitation, administering antibiotics, and skin grafting.
 
Definition
A burn is a type of injury to flesh or skin caused by heat, electricity, chemicals, light, radiation or friction. Most burns affect only the skin (epidermal tissue). Rarely, deeper tissues, such as muscle, bone, and blood vessels can also be injured.
517
 
Cause
Burns are caused by a wide variety of substances and external sources such as exposure to chemicals, friction, electricity, radiation, and heat.
 
Chemical
Most chemicals that cause chemical burns are strong acids or bases. Chemical burns can be caused by corrosive chemical compounds such as sulfuric acid and sodium hydroxide. Hydrofluoric acid can cause damage down to the bone and its burns are sometimes not immediately evident. Chemical burns can be either first, second, or third degree burns, depending on duration of contact, strength of the substance, and other factors.
 
Electrical
Electrical burns are caused by either an electric shock or an uncontrolled short circuit (a burn from a hot, electrified heating element is not considered an electrical burn).
The true incidence of electrical burn injury is unknown. This is sufficient to cause cardiac arrest and ventricular fibrillation but generates relatively low heat energy deposit into skin, thus producing few or no burn marks at all. High voltage electricity, on the other hand, is a common cause of third and fourth degree burns due to the extreme heat yielded by high temperature arcs and flashover associated with voltages over 1000v.
 
Radiation
Radiation burns are caused by protracted exposure to UV light (as from the sun), radiation therapy (in people undergoing cancer therapy), sunlamps, and X-rays. By far the most common burn associated with radiation is sun exposure.
 
Scalding
Scalding is caused by hot liquids (water or oil) or gases (steam), most commonly occurring from exposure to high temperature tap water in baths or showers or spilled hot drinks. A so-called immersion scald is created when an extremity is held under the surface of hot water. A blister is a ‘bubble’ in the skin filled with serous fluid as part of the body's reaction to the heat and the subsequent inflammatory reaction. The blister ‘roof’ is dead and the blister fluid contains toxic inflammatory mediators. Generally scald burns are first or second degree burns, but third degree burns can result, especially with prolonged contact.
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Inhalational injury
Steam, smoke, and high temperatures can cause inhalational injury to the airway and/or lungs.
 
Types of Burns
Burns can be classified by mechanism of injury, depth, extent and associated injuries and comorbidities.
 
According to depth
Currently, burns are described according to the depth of injury to the dermis and are loosely classified into first, second, third, and fourth degrees.
The following tables describe degrees of burn injury under this system as well as provide pictorial examples.
Names
Layers involved
Appearance
Texture
Sensation
Time to healing
Complications
Example
First degree
Epidermis
Redness (erythema)
Dry
Painful
1 wk or less
Increased risk to develop skin cancer later in life
Second degree (superficial partial thickness)
Extends into superficial (papillary) dermis
Red with clear blister. Blanches with pressure
Moist
Painful
2–3 wks
Local infection/cellulitis
Second degree (deep partial thickness)
Extends into deep (reticular) dermis
Red-and-white with bloody blisters. Less blanching.
Moist
Painful
Weeks - may progress to third degree
Scarring, contractures (may require excision and skin grafting)
Third degree (full thickness)
Extends through entire dermis
Stiff and white/brown
Dry, leathery
Painless
Requires excision
Scarring, contractures, amputation
Fourth degree
Extends through skin, subcutaneous tissue and into underlying muscle and bone
Black; charred with eschar
Dry
Painless
Requi-res excision
Amputation, significant functional impairment, possible gangrene, and in some cases death
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Fig. 10.1: Types of burn, according to depth
 
According to Burn Severity
Burn are classified as minor, moderate, or severe.
  • Minor burn: All first degree burns as well as second degree burns that involve less than 10% of the body surface usually are classified as minor.
  • Moderate burn: Burns invol-ving the hands, feet, face or genitals, second degree burns involving more than 10% of body surface area.
  • Severe burn: Burn surface involvement of 25% body surface area. All third degree burn are classified as severe burn.
Fig. 10.2: Total Burn Surface Area (TBSA)
 
According to the Extent of Body Surface Area
Burns can also be assessed in terms of total body surface area (TBSA), which is the percentage affected by partial thickness or full thickness burns. The rule of nine is used as a quick and useful way to estimate the affected area.
520The rule of nine: It was introduced by Alexander Wallace. The rule of nine is the quick way to calculate the extent of burn.
 
Pathophysiology
 
Clinical Manifestation
  • Fluid and electrolyte imbalance: The burn wound become rapidly edematous due to microvascular changes induced by direct thermal injury and by release of chemical mediators of inflammation. This results in systemic intravascular losses of water, sodium, albumin, and red blood cells. Unless the intravascular volume is rapidly restored, shock develops.
  • Metabolic disturbance: This is evidenced by increased resting oxygen consumption, an excessive nitrogen loss, and a pronounced weight loss.
  • Bacterial contamination of tissues: The damaged integument creates a vast area for surface infection and invasion of microorganisms. Increased risk of septic shock.
  • Complications from vital organs: All the major organ system are affected by the burn injury. Renal insufficiency can result from nephron obstruction with myoglobulin and hemoglobulin. Multi system organ failure is a common final pathway leading to late burn mortality.
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Diagnostic Studies in Burn
  • Complete blood count: Initial increased hematocrit suggests hemoconcentration due to fluid shift/loss. Later decreased Hct and RBCs may occur because of heat damage to vascular endothelium. Leukocytosis can occur because of loss of cells at wound site and inflammatory response to injury.
  • Arterial blood gases: Reduced PaO2, increased PaCO2 may seen with carbon monoxide retention. Acidosis may occur because of reduced renal function and loss of respiratory compensatory mechanism
  • Carboxyhemoglobin: Elevation of more than 15% indicates carbonmonoxide poisoning
  • Alkaline phosphate: Elevated because of interstitial fluid shift
  • Serum glucose: Elevated
  • Blood urea nitrogen: Elevated
  • Urine: Reddish black color of urine is due to presence of myoglobin
  • ECG: Sign of myocardial ischemia/dysrhythmias may occur with electrical burn
  • Electrolyte imbalance.
 
Burn Management and Plastic Surgeries
The burns patient has the same priorities as all other trauma patients.
  • Assess:
    • Airway
    • Breathing: beware of inhalation and rapid airway compromise
    • Circulation: fluid replacement
    • Disability: compartment syndrome
    • Exposure: percentage area of burn.
  • Essential management points:
    • Stop the burning
    • ABCDE
    • Determine the percentage area of burn (Rule of 9's)
    • Good IV access and early fluid replacement.
  • The severity of the burn is determined by:
    • Burned surface area
    • Depth of burn
    • Other considerations.
  • Morbidity and mortality rises with increasing burned surface area. It also rises with increasing age so that even small burns may be fatal in elderly people.
 
Burn Management in Adults
  • The ‘Rule of 9's’ is commonly used to estimate the burned surface area in adults.
  • The body is divided into anatomical regions that represent 9% (or multiples of 9%) of the total body surface (Figure 10.3). The outstretched palm and fingers approximates to 1% of the body surface area.
  • 522If the burned area is small, assess how many times patient's hand covers the area.
  • Morbidity and mortality rises with increasing burned surface area. It also rises with increasing age so that even small burns may be fatal in elderly people.
 
Rule of Nines for Establishing Extent of Body Surface Burned
Anatomic Surface
Percentage of total body surface
Head and neck
9%
Anterior trunk
18%
Posterior trunk
18%
Arms, including hands
9% each
Legs, including feet
18% each
Genitalia
1%
Fig. 10.3: Rule of Nine as per TBSA for adult
 
Burn Management in Children
  • The ‘Rule of 9's’ method is too imprecise for estimating the burned surface area in children because the infant or patient child's head and lower extremities represent different proportions of surface area than in an adult (see Figure 10.4).
  • Burns greater than 15% in an adult, greater than 10% in a child, or any burn occurring in the very patient or elderly are serious.
523
Fig. 10.4: Rule of Nine as per TBSA for children
 
Depth of Burn
  • It is important to estimate the depth of the burn to assess its severity and to plan future wound care. Burns can be divided into three types, as shown below.
    Depth of burn
    Characteristics
    Cause
    First degree burn
    • Erythema
    • Pain
    • Absence of blisters
    • Sunburn
    Second degree
    (Partial thickness)
    • Red or mottled
    • Flash burns
    • Contact with hot liquids
    Third degree
    (Full Thickness)
    • Dark and leathery
    • Dry
    • Fire
    • Electricity or lightning
    • Prolonged exposure to hot liquids/objects
  • 524It is common to find all three types within the same burn wound and the depth may change with time, especially if infection occurs. Any full thickness burn is considered serious.
 
Serious Burn Requiring Hospitalization
  • Greater than 15% burns in an adult
  • Greater than 10% burns in a child
  • Any burn in the very patientng, the elderly or the infirm
  • Any full thickness burn
  • Burns of special regions: face, hands, feet, perineum
  • Circumferential burns
  • Inhalation injury
  • Associated trauma or significant preburn illness, e.g. diabetes.
 
Treatment
  • General information
    • All burn patients should initially be treated with the principles of Advanced Burn and/or Trauma Life Support
  • The ABC's (airway, breathing, circulation) of trauma take precedent over caring for the burn
  • Search for other signs of trauma
  • Verified Burn Centers provide advanced support for complex cases.
 
Airway
  • Extensive burns may lead to massive edema
  • Obstruction may result from upper airway swelling
  • Risk of upper airway obstruction increases with
  • Massive burns: All patients with deep burns > 35–40% TBSA should be endotracheally intubated
  • Burns to the head and Burns inside the mouth:
    • Intubate early if massive burn or signs of obstruction
    • Intubate if patients require prolonged transport and any concern with potential for obstruction
    • If any concerns about the airway, it is safer to intubate earlier than when the patient is decompensating.
Signs of airway obstruction
  • Hoarseness or change in voice
  • Use of accessory respiratory muscles
  • High anxiety
    • Tracheostomies not needed during resuscitation period
    • Remember: Intubation can lead to complications, so do not intubate if not needed.
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Breathing
  • Hypoxia: Fire consumes oxygen so people may suffer from hypoxia as a result of flame injuries
  • Carbon monoxide (CO)
    • Byproduct of incomplete combustion
    • Binds hemoglobin with 200 times the affinity of oxygen
    • Leads to inadequate oxygenation
    • Diagnosis of CO poisoning
      • Nondiagnostic
      • PaO2 (partial pressure of O2 dissolved in serum)
      • Oximeter (difference in oxy- and deoxyhemoglobin)
      • Patient color (‘cherry red’ with poisoning)
    • Diagnostic
      • Carboxyhemoglobin levels
      • <, 10% is normal
      • > 40% is severe intoxication
Treatment: Remove source, 100% oxygen until CO levels are <, 10%.
  • Smoke inhalation injury
    • Pathophysiology
      • Smoke particles settle in distal bronchioles
      • Mucosal cells are die
      • Sloughing and distal atelectasis
      • Increase risk for pneumonia
  • Diagnosis
    • History of being in a smoke-filled enclosed space
    • Bronchoscopy
      • Soot beneath the glottis
      • Airway edema, erythema, ulceration
  • Nondiagnostic clinical tests
    • Early chest X-ray
    • Early blood gases
  • Nondiagnostic clinical findings
    • Soot in sputum or saliva, Singed facial hair
Treatment: Supportive pulmonary management and aggressive respiratory therapy.
 
Circulation
  • Obtain IV access anywhere possible
    • Unburned areas preferred
    • Burned areas acceptable
    • Central access more reliable if proficient
    • Cut-downs are last resort.
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Resuscitation in burn shock (first 24 hours)
  • Massive capillary leak occurs after major burns
  • Fluids shift from intravascular space to interstitial space
  • Fluid requirements increase with greater severity of burn (larger % TBSA, increase depth, inhalation injury, associate injuries - see above)
  • Fluid requirements decrease with less severe burn (may be less than calculated rate)
  • IV fluid rate dependent on physiologic response
  • Place Foley catheter to monitor urine output
  • Goal for adults: urine output of 0.5 ml/kg/hour
  • Goal for children: urine output of 1 ml/kg/hour
  • If urine output below these levels, increase fluid rate
  • Preferred fluid: Lactated Ringer's Solution
  • Isotonic
  • Cheap
  • Easily stored
  • Resuscitation formulas are just a guide for initiating resuscitation.
 
RESUSCITATION FORMULAS
Parkland formula most commonly used
  1. IV fluid - Lactated Ringer's Solution
  2. Fluid calculation
    • 4 × weight in kg × %TBSA burn
      • Give 1/2 of that volume in the first 8 hours
      • Give other 1/2 in next 16 hours
      • Warning: Despite the formula suggesting cutting the fluid rate in half at 8 hours, the fluid rate should be gradually reduced throughout the resuscitation to maintain the targeted urine output, i.e. do not follow the second part of the formula that says to reduce the rate at 8 hours, adjust the rate based on the urine output.
      • Example of fluid calculation
    • 100 kg man with 80% TBSA burn
    • Parkland formula:
      • 4 × 100 × 80 = 32,000 ml
      • Give 1/2 in first 8 hours = 16,000 ml in first 8 hours
      • Starting rate = 2,000 ml/hour
    • Adjust fluid rate to maintain urine output of 50 ml/hr
    • Albumin may be added toward end of 24 hours if not adequate response.
Resuscitation Endpoint: maintenance rate
  • When maintenance rate is reached (approximately 24 hours), change fluids to D50.5NS with 20 mEq KCl at maintenance level
  • Maintenance fluid rate = basal requirements + evaporative losses
  • 527Basal fluid rate
    • Adult basal fluid rate = 1500 × body surface area (BSA) (for 24 hours)
    • Pediatric basal fluid rate (<, 20 kg) = 2000 × BSA (for 24 hours)
  • May use
    • 100 ml/kg for 1st 10 kg
    • 0 ml/kg for 2nd 10 kg
    • 20 ml/kg for remaining kg for 24 hours
  • Evaporative fluid loss
    • Adult: (25 + % TBSA burn) × (BSA) = ml/hour
    • Pediatric (<, 20 kg): (35 + % TBSA burn) × (BSA) = ml/hour
 
COMPLICATIONS OF OVER-RESUSCITATION
 
Compartment Syndrome
  • Best dealt with at Verified Burn Centers
  • If unable to obtain assistance, compartment syndromes may require management
  • Limb compartments
    • Symptoms of severe pain (worse with movement), numbness, cool extremity, tight feeling compartments
    • Distal pulses may remain palpable despite ongoing compartment syndrome (pulse is lost when pressure > systolic pressure)
    • Compartment pressure > 30 mm Hg may compromise muscle/nerves
    • Measure compartment pressures with arterial line monitor (place needle into compartment)
    • Escharotomies may save limbs
  • Performed laterally and medially throughout entire limb
  • Performed with arms supinated
  • Hemostasis is required
    • Fasciotomies may be needed if pressure does not drop to <, 30 mm Hg
  • Requires surgical expertise
  • Hemostasis is required.
 
Chest Compartment Syndrome
  • Increased peak inspiratory pressure (PIP) due to circumferential trunk burns
  • Escharotomies through mid-axillary line, horizontally across chest/abdominal junction.
 
Abdominal Compartment Syndrome
  • Pressure in peritoneal cavity > 30 mm Hg
  • Measure through Foley catheter
    • Signs: increased PIP, decreased urine output despite massive fluids, hemodynamic instability, tight abdomen
    • Treatment
  • 528Abdominal escharotomy
  • NG tube
  • Possible placement of peritoneal catheter to drain fluid
  • Laparotomy as last resort.
 
Acute Respiratory Distress Syndrome (ARDS)
  • Increased risk and severity if over-resuscitation
  • Treatment supportive.
 
Medications
  • All pain meds should be given IV
  • Tetanus prophylaxis should be given as appropriate
  • Prophylactic antibiotics are contraindicated
  • Systemic antibiotics are only given to treat infections.
 
SPECIAL BURNS
  • General information
    • Often require specialized care
    • Calling a verified burn center is advised
  • Electrical injuries
    • Extent of injury may not be apparent
      • Damage occurs deep within tissues
      • Damage frequently progresses
      • Electricity contracts muscles, so watch for associated injuries
    • Cardiac arrhythmias may occur
      • If arrhythmia present, patient needs monitoring
      • CPR may be lifesaving
    • Myoglobinuria may be present
      • Color best indicator of severity
      • If urine is dark (black, red), myoglobinuria needs to be treated
        • Increase fluids to induce urine output of 75-100 ml/hour in adults
        • In children, target urine output of 2 ml/kg/hour
        • Alkalinize urine (give NaHCOi3)
        • Check for compartment syndromes
        • Mannitol as last resort
    • Compartment syndromes are common
    • Long-term neuropsychiatric problems may result
  • Chemical Burns
    • Brush off powder
    • Prolonged irrigation required
    • Do not seek antidote
      • Delays treatment
      • May result in heat production
    • Special chemical burns require contacting a Verified Burn Center, e.g. hydrofluoric acid burn.
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WOUND CARE
 
First Aid
  • If the patient arrives at the health facility without first aid having been given, drench the burn thoroughly with cool water to prevent further damage and remove all burned clothing.
  • If the burn area is limited, immerse the site in cold water for 30 minutes to reduce pain and edema and to minimize tissue damage.
  • If the area of the burn is large, after it has been do used with cool water, apply clean wraps about the burned area (or the whole patient) to prevent systemic heat loss and hypothermia.
  • Hypothermia is a particular risk.
  • First 6 hours following injury are critical; transport the patient with severe burns to a hospital as soon as possible.
 
Initial Treatment
  • Initially, burns are sterile. Focus the treatment on speedy healing and prevention of infection.
  • In all cases, administer tetanus prophylaxis.
  • Except in very small burns, debride all bullae. Excise adherent necrotic (dead) tissue initially and debride all necrotic tissue over the first several days.
  • After debridement, gently cleanse the burn with 0.25% (2.5 g/liter) chlorhexidine solution, 0.1% (1 g/liter) cetrimide solution, or another mild water-based antiseptic.
  • Do not use alcohol-based solutions.
  • Gentle scrubbing will remove the loose necrotic tissue. Apply a thin layer of antibiotic cream (silver sulfadiazine).
  • Dress the burn with petroleum gauze and dry gauze thick enough to prevent seepage to the outer layers.
 
Daily Treatment
  • Change the dressing daily (twice daily if possible) or as often as necessary to prevent seepage through the dressing. On each dressing change, remove any loose tissue.
  • Inspect the wounds for discoloration or hemorrhage, which indicate developing infection.
  • Fever is not a useful sign as it may persist until the burn wound is closed.
  • Cellulitis in the surrounding tissue is a better indicator of infection.
  • Give systemic antibiotics in cases of hemolytic streptococcal wound infection or septicemia.
  • Pseudomonas aeruginosa infection often results in septicemia and death. Treat with systemic aminoglycosides.
  • Administer topical antibiotic chemotherapy daily. Silver nitrate (0.5% aqueous) is the cheapest, is applied with occlusive dressings but does not penetrate eschar. It depletes electrolytes and stains the local environment.
  • 530Use silver sulfadiazine (1% miscible ointment) with a single layer dressing. It has limited eschar penetration and may cause neutropenia.
  • Mafenide acetate (11% in a miscible ointment) is used without dressings. It penetrates eschar but causes acidosis. Alternating these agents is an appropriate strategy.
  • Treat burned hands with special care to preserve function:
    • Cover the hands with silver sulfadiazine and place them in loose polythene gloves or bags secured at the wrist with a crepe bandage;
    • Elevate the hands for the first 48 hours, and then start hand exercises;
    • At least once a day, remove the gloves, bathe the hands, inspect the burn and then reapply silver sulfadiazine and the gloves;
    • If skin grafting is necessary, consider treatment by a specialist after healthy granulation tissue appears.
 
Healing phase
  • The depth of the burn and the surface involved influence the duration of the healing phase. Without infection, superficial burns heal rapidly.
  • Apply split thickness skin grafts to full-thickness burns after wound excision or the appearance of healthy granulation tissue.
  • Plan to provide long-term care to the patient.
  • Burn scars undergo maturation, at first being red, raised and uncomfortable. They frequently become hypertrophic and form keloids. They flatten, soften and fade with time, but the process is unpredictable and can take up to two years.
 
In children
  • The scars cannot expand to keep pace with the growth of the child and may lead to contractures.
  • Arrange for early surgical release of contractures before they interfere with growth.
  • Burn scars on the face lead to cosmetic deformity, ectropion and contractures about the lips. Ectropion can lead to exposure keratitis and blindness and lip deformity restricts eating and mouth care.
  • Consider specialized care for these patients as skin grafting is often not sufficient to correct facial deformity.
 
Other Wound Care Methods
  1. Exposure method: Leaving a burn open is a poor option but where dressings are not possible it may be the only option. The patients is washed daily and kept of clean dry sheets with another sheet or mosquito net draped over a frame to reduce the pain from air currents and to reduce contamination from the environment. Ambient temperature control is important to maintain normothermia. Exposure is less painful for full-thickness burns than for partial thickness burns but has little else to recommend it.
  2. Tubbing: Most modern burn units avoid the regular immersion of patients in water both because they practice early excision and grafting and because of the high-risks developing resistant strains of bacteria in the tub environment and of patient cross-infection. That said, tubbing can be helpful to clean the wounds and gently remove eschar as it separates. When early wound infections develop suspect the tub! Avoid 531the routine immersion of infected patients in filthy bathtubs of cold water on the basis of ignorance and tradition.
  3. Bland dressings: These provide a clean, moist wound healing environment, absorb exudates protect from contamination and provide comfort at a fraction of the cost of antibiotic dressings. Where antibiotic dressings are scarce bland dressings are a very acceptable solution for burns. Expensive topical antibiotic dressings may be reserved for infected wounds. Paraffin gauze is widely available and can be manufactured locally. Honey and Ghee dressings were first advocated in Ayurvedic texts two thousand years ago and remain an excellent choice for bland burn dressings. Mix two parts honey with one part Ghee (clarified butter) and pour over a stack of gauze dressings in a tray. Cover and store. Vegetable oil or mineral oil may be substituted for Ghee. Gauze sheets can be applied directly to the wound in a single layer and covered with plain dry gauze to absorb exudates, then wrapped. Dressings should be changed at least ever second day, or when soiled.
  4. Antimicrobial dressing: There exist numerous topical antimicrobial agents that are effective in delaying the onset of invasive wound infections, but none prevent them entirely. This is why they must be used in conjunction with a goal of early surgical wound closure when possible. A brief review of the agents most likely to be available to low and middle income countries will follow. There are also alternative synthetic wound coverings and newer silver-ionized agents that can be used; however they are often very costly and inaccessible in low-income countries. A more detailed review, as well as instructions for preparation, can be found in these references.
 
Burn Wound Dressings
Antimicrobial Salves
Silver sulfadiazine (Flamazine, Silvadene)
Broad-spectrum antimicrobial, painless and easy to use, does not penetrate eschar, deeply may leave black tattoos from silver ion; mild inhibition of epithelialization
Mafenide acetate (Sulfamylon)
Broad-spectrum antimicrobial; penetrates eschar well; may cause pain in sensate skin; wide application causes metabolic acidosis, therefore only suitable for small areas; mild inhibition of epithelialization.
Bacitracin
Ease of application; painless; antimicrobial spectrum not as wide as above agents
Neomycin
Ease of application; painless; antimicrobial spectrum not as wide
Polymyxin B
Ease of application; painless; antimicrobial spectrum not as wide
Nystatin (Mycostatin)
Effective in inhibiting most fungal growth; cannot be used in combination with mafenide acetate
Mupirocin (Bactroban)
More effective staphylococcal coverage; does not inhibit epithelialization; expensive
Antimicrobial Soaks
0.5% Silver nitrate
Effective against all microorganisms; stains contacted areas; leaches sodium from wounds; may cause methemoglobinemia
5% Mafenide acetate
Wide antibacterial coverage; no fungal coverage; painful on application to sensate wound; wide application associated with metabolic acidosis, and therefore generally used for small high-risk areas such as cartilage coverage in nose and ears.
532
0.025% Sodium hypochlorite (Dakin solution)
Effective against almost all microbes, particularly gram-positive organisms; mildly inhibits epithelialization
0.25% Acetic acid
Effective against most organisms, particularly gram-negative ones; mildly inhibits epithelialization
Synthetic Coverings
Opsite
Provides a moisture barrier; inexpensive; decreased wound pain; use complicated by accumulation of transudate and exudate requiring removal; no antimicrobial properties
Biobrane
Provides a wound barrier; associated with decreased pain; use complicated by accumulation of exudate risking invasive wound infection; no antimicrobial properties
Transcyte
Provides a wound barrier; decreased pain; accelerated wound healing; use complicated by accumulation of exudate; no antimicrobial properties
Integra
Provides complete wound closure and leaves a dermal equivalent; sporadic take rates; no antimicrobial properties. Allows for coverage with a very thin skin graft with no dermis. Very expensive product
Biologic Coverings
Xenograft (pig skin)
Completely closes the wound; provides some immunologic benefits; must be removed or allowed to slough
Allograft (homograft, cadaver skin)
Provides all the normal functions of skin; can leave a dermal equivalent; epithelium must be removed or allowed to slough
 
Surgical Treatment of Burns/Plastic Surgery for Burns or Wounds
Urgent procedures
  • Exposure of vital structures (such as eyelid releases)
  • Entrapment or compression of neurovascular bundles
  • Fourth degree contractures
  • Severe microstomia
Essential procedures
  • Reconstruction of function (such as limited range of motion)
  • Progressive deformities not correctable by ordinary methods
Desirable procedures
  • Reconstruction of passive areas
  • Esthetics
 
Time of performing procedure
 
Techniques for burn reconstruction
Without deficiency of tissue
  • Excision and primary closure
  • Z-plasty
With deficiency of tissue
  • Simple reconstruction
  • Skin graft
  • Dermal templates and skin grafts
533
Transposition flaps (Z-plasty and modifications)
  • Reconstruction of skin and underlying tissues
  • Axial and random flaps
  • Myocutaneous flaps
  • Tissue expansion
  • Free flaps
 
Essentials of burn reconstruction
  • Strong patient-surgeon relationship
  • Psychological support
  • Clarify expectations
  • Explain priorities
  • Note all available donor sites
  • Start with a ‘winner’ (easy and quick operation)
  • As many surgeries as possible in preschool years
  • Offer multiple, simultaneous procedures
  • Reassure and support patient.
 
ESCHAROTOMY
Definition: An escharotomy is defined as a surgical incision through burn eschar (necrotic skin). This procedure is usually performed within the first 24 hours of burn injury. Burn eschar has an unyielding, leathery consistency and is characterized by denatured proteins and coagulated vessels in the skin, which are the result of thermal, chemical or electrical injury.
Technique: Escharotomy (incision through the eschar) releases the constricting tissue allowing the body tissues and organs to maintain their normal perfusion and function. In most cases a single incision is inadequate to provide release of the constricting burn eschar. Escharotomy incisions are routinely performed on both sides of the torso or the medial and lateral sides of each affected limb. For the abdomen and chest, transverse incisions are often required to permit restoration of respiratory movement. The escharotomy procedure is most commonly performed using conscious sedation at bedside, in emergency room, hydrotherapy room, or ICU but may be done in operating room if general anesthesia is required.
Escharotomies release the constriction caused by burn eschar but do not remove the eschar. Once the patient is stable enough to be taken to the operating room, generally between the second to seventh days postburn, the burn eschar is excised to the level of viable underlying tissue. (Please see also Burn Wound Excision in a subsequent section.) In some cases, escharotomies are performed through partial thickness burns (second degree burns), which will eventually heal without the need for excision and grafting. Delayed primary closure of escharotomy incisions may produce better functional and cosmetic results than those achieved if the escharotomies are allowed to close by secondary intention.
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DEBRIDEMENT OF BURN WOUNDS
Definition: Debridement is the removal of loose, devitalized, necrotic, and/or contaminated tissue, foreign bodies, and other debris on the wound using mechanical or sharp techniques (such as curetting, scraping, rongeuring, or cutting). The level of debridement is defined by the level of the tissue removed, not the level exposed by the debridement process.
Purpose: Debridement cleans the wound and allows it to heal more rapidly with reduced risk of infection.
Technique: Debridement can be accomplished in a no. of ways using same surgical instruments used for excision.
 
EXCISION OF BURN WOUNDS
Definition: Excision is a surgical procedure requiring incision through the deep dermis (including subcutaneous and deeper tissues) of open wounds, burn eschar, or burn scars. This entails surgical removal of all necrotic tissue. Burn scars can also be excised in preparation for surgical reconstruction.
Purpose: Excision is typically performed on deep burns that would not heal on their own. The goal is to remove all necrotic and nonviable tissue and to prepare the wound for immediate or delayed wound closure. The skin and subcutaneous tissues are removed followed by wound care (such as application of topical antimicrobials, temporary biologic or synthetic wound covers), immediate or later grafting, flap closure, and other reconstructive procedures. Unlike debridement, excisional techniques create a wound surface that is fully vascularized and ready for application of temporary or permanent skin replacement or substitute.
Technique: Burn debridement (cleaning) and excision (escharectomy) are routinely performed by experienced burn surgeons. Though the techniques and instruments used for debridement and excision are often similar, burn excision is significantly more difficult and requires greater time and physical effort to achieve meticulous burn wound preparation for subsequent grafting with synthetic or biological materials.
The excisional technique may vary but is typically performed in one of two ways: tangential excision (which is usually performed on deep partial thickness burns) and full thickness excision.
  • Tangential excision: Involves surgical removal of successive layers of the burn wound down to viable dermis.
  • Full thickness excision: Often using electrocautery—involves removal of the burn wound down to viable subcutaneous tissue or to fascia.
 
SKIN GRAFTS
This is often used for burn patients; skin is removed from one area of the body and transplanted to another. There are two types of skin graft: split-thickness grafts in which just a few layers of outer skin are transplanted and full-thickness grafts, which involve all of the dermis. There is usually permanent scarring that is noticeable.
During a skin graft, a special skin-cutting instrument known as a dermatone removes the skin from an area (the donor site) usually hidden by clothing such as the buttocks or inner 535thigh. Once removed, the graft is placed on the area in need of covering and held in place by a dressing and a few stitches. The donor site is also covered with a dressing to prevent infection from occurring. Recovery time from a split-thickness skin graft is generally fairly rapid, often less than three weeks. For full-thickness skin graft patients the recovery time is a few weeks longer. Aside from burn patients, skin grafts can also be used during breast or nose reconstruction.
 
Single-and Multiple-Stage Excision and Grafting
Single-stage excision and grafting: Surgical closure of burn wounds achieves two goals. The first is to facilitate optimal and rapid healing of the wound, minimizing deleterious consequences such as scar contracture while maximizing the best functional and cosmetic outcomes. The second is to ameliorate the adverse influence of the burn wounds on the body's systemic responses, especially the immune and metabolic systems. Meticulous wound preparation and application of skin grafts leads to excellent functional and cosmetic results, but this becomes progressively more difficult in patients with more extensive burn injuries. In life-threatening burns, procedures which improve patient survival by reducing wound infection, hypermetabolism and immunosuppression, assume priority over those which may optimize later functional and cosmetic results.
The single-stage approach to excision and grafting of burn wounds includes seven intraoperative components:
  • Initial decision-making: Which is modified as necessary throughout the procedure including:
    • Area(s) to be excised usually based on the patient's physiologic state as well as the degree to which the anticipated blood loss will be tolerated.
    • Depth of the excision, a complex decision involving the anticipated blood loss, the ability of the patient's excised wounds to support the growth of a newly-transplanted skin graft, and considerations regarding long-term cosmetic results.
    • Location of donor sites, including the thickness of the skin to be harvested, the ease of dressing application, and the degree to which the donor site scar will remain masked by clothing in the future.
  • Excision of the burn wound, with close monitoring of the patient's vital signs because of intraoperative blood loss.
  • Achieving hemostasis with electrocautery and topical application of solutions containing vasoconstrictive agents (such as epinephrine or phenylephrine) and/or procoagulants (such as thrombin).
  • Harvesting the donor skin (which may be preceded by subcutaneous injection of an electrolyte solution containing vasoconstrictive agents to reduce blood loss, as well as local anesthestics to reduce postoperative pain).
  • Modification/expansion of the skin graft by meshing. Expansion is often necessary for patients with extensive burns and/or limited skin graft donor sites.
  • Applying and securing the skin graft to the excised wound bed with some combination of absorbable or nonabsorbable sutures, staples, fibrin glue, synthetic adhesives, and/or tapes.
  • Placement of dressings and splints to avoid mechanical shear of the grafts and to maintain proper positioning.
536It is clear that single-stage excision and grafting is a complex, time-consuming process, which is often physiologically stressful on the patient and may be poorly tolerated in patients with large burn injuries. It is ideal treatment for small burns in healthy patients.
 
Multiple-Stage Excision and Grafting
The alternative to single-stage excision and grafting is to perform the necessary steps in a planned sequence where part of the burn wound is excised initially and the remainder is removed in one or more subsequent operations. This is often done with cosmetically important areas such as the face, as well as with more extensive burns or burns in physiologically less stable patients.
For patients with small burns that are located in functionally and cosmetically important areas, the excision is done on the initial operative day and the freshly excised wound bed is protected with a temporary covering to prevent desiccation and infection. This is followed in one to two days by harvesting and placement of the skin autografts. Staged skin grafting of face burns allows inspection for hematomas or inadequately excised areas that would lead to graft loss and can result in nearly 100% graft take.
  • For patients with physiological challenges that increase the risk of complications with excision, concluding the initial operation after obtaining hemostasis reduces the chance of hypotensive complications. Temporary wound coverings can be expeditiously applied because they are prepackaged to simplify placement and because there is less need for careful placement of temporary coverings that will be removed within a few days.
  • For patients with burns too extensive to be completely excised and grafted in one stage, multiple procedures allow safe removal of the eschar with improved graft take. Most often, the burn eschar is excised on the first few visits to the operating room, and the goal is for complete eschar removal within the first five to seven days after injury. At the next operative procedure, the results of the first excision can be viewed, with further excision being performed and temporary dressings, skin substitutes or skin replacements applied if needed. Sometimes by the time the last areas of burn are being excised on the third or fourth visit to the OR, the first areas of excision are ready for permanent autografting. The other advantage of staging the excision and grafting procedures is that donor sites are given time to reepithelialize between harvesting sessions.
 
BURN WOUND COVERAGE
Burn wound coverage is a unique surgical process. Simple, small burn wounds are excised and covered by either a full thickness skin graft, in which the donor site is primarily closed, or by a split-thickness skin graft. Even though it seems a simple procedure, the surgeon must first choose the thickness to harvest the graft. He will then decide whether to mesh the graft (which would allow the drainage of fluid from beneath) or apply it as a sheet graft without perforations. The thicker the graft, the less it will contract, yet the more difficult it is to obtain 100% engraftment and the more difficult it is for the donor site to heal.
As the extent of the burn increases, the operative procedures and decision-making become more complex. Early excision of burn wounds improves patient survival. However, excision alone without grafting leaves an open wound that must be covered in order to prevent infection, decrease fluid losses, and reduce the risk of scar contractures.
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Skin Substitutes and Skin Replacements
Skin substitute: A biomaterial, engineered tissue or combination of materials and cells or tissues that can be substituted for skin autograft or allograft in a clinical procedure.
Skin replacement: A tissue or graft that permanently replaces lost skin with healthy skin.
 
Temporary Wound Coverage
Temporary skin substitutes are used when the wound is too extensive to be closed in one stage because there is not enough donor skin available, because the patient is too ill to undergo the creation of another wound that results when skin is harvested from a donor site, because there is a question regarding the viability of the recipient bed, or because of a concern regarding potential infectious complications. The gold standard temporary skin substitute is cadaver allograft.
  • Allograft: Allograft is obtained from skin banks to ensure quality and safety. Allograft may be used as fresh, refrigerated tissue or as frozen tissue, which is thawed immediately prior to use will. Allograft adhere and induce vascularization on an appropriately prepared wound bed. It will decrease the loss of fluids, proteins, and electrolytes and drying of the recipient bed. It also decreases bacterial contamination, diminishes pain, improves the patient's ability to participate in all types of therapy, is a marker for the ability of the wound to accept an autograft, and promotes wound healing in partial thickness wounds. In some patients, cultured keratinocytes can be applied onto the vascularized allodermis once the alloepidermis has been removed.
    Other temporary skin substitutes are used to provide transient wound coverage and to create a physiologically homeostatic environment. Skin Xenografts—also termed heterografts.
  • Xenograft (pigskin) is used at many institutions in the same manner as allograft. The application of xenograft on a debrided mid-dermal burn might prevent/obviate the need for excision and autografting.
 
Permanent Wound Coverage
  • A full-thickness skin graft contains all components of the skin: epidermis, dermis, hair follicles and nerve endings. The most important advantage of full-thickness grafts is decreased scar formation; however, because there is no dermis to regenerate epithelial coverage, the donor site of a full-thickness skin graft must be closed either with primary direct closure or with a split-thickness skin graft; local advancement of skin flaps is a rarely used option. Full-thickness grafts are thus usually used to cover small, functionally and cosmetically important areas (such as eyelids and digits).
  • The split-thickness skin graft is the most common method used to achieve permanent wound coverage. It includes the entire epidermis but the dermal layer is split by the dermatome blade. With thicker split-thickness grafts, more dermis is transferred with the skin graft (such as 15/1000 of inch or greater). This reduces the risk of scar formation at the recipient site, but it takes longer for the donor site to heal. Furthermore, the thicker the graft, the more likely the donor site will heal with a scar and the less likely the donor site may be reharvested for further grafts.
There are a number of commercially available products to facilitate permanent wound coverage.
  • 538Acellular human dermal allograft is devoid of epidermis and must be covered by a thin split-thickness autograft at the time of the initial operation; however, it replaces a portion of the missing dermis on the newly covered wound, thus reducing postoperative scarring. Another permanent wound coverage product is a dermal regenerative template constructed with bovine collagen and shark chondroitin sulfate with a silicone surface layer. This is applied to an excised wound bed that is well vascularized and free from infection, and provides wound coverage much like other skin substitutes; however, after the template becomes vascularized, it forms a neodermis (usually within 10 days to three weeks) and when the silicone layer is removed, an epidermal autograft (< 0.008 inch thickness) can be applied. This intermingling of autograft on a biosynthetic neodermis is permanent, unlike the wound coverage provided by temporary skin substitutes. This approach may be lifesaving and provides quality skin coverage.
  • Cultured epidermal autograph also referred to as ‘test tube’ skin, was introduced to provide permanent skin coverage for patients with extensive burns. This product has limitations including sensitivity to infection and the lack of a dermis, which leads to fragility of the healed skin and severe scarring. However, the short- and long-term results of CEA application can be improved by the use of a sandwich technique, in which CEA is applied over a vascularized allogeneic dermis or Alloderm. If the CEA is applied to a well-vascularized dermal bed. The dermis is created by using allograft that is allowed to engraft and removing the epidermis after the dermis is vascularized.
 
Others
  • Microsurgery: Have patient lost a finger, toe, ear, or even a lip? Microsurgery may allow for those to be reattached. Simply stated, it is a procedure in which the surgeon uses a microscope for surgical assistance in reconstructive procedures. By using a microscope, the surgeon can actually sew tiny blood vessels or nerves, allowing him or her to repair damaged nerves and arteries. This may also be a method to relieve facial paralysis or reconstruct breasts. Microsurgery is frequently used with other surgical procedures such as the free flap procedure.
  • Free flap procedure: A free flap procedure is often performed during breast reconstruction or following surgery to remove head or neck cancer. During the procedure, muscle, skin, or bone is transferred along with the original blood supply from one area of the body (donor site) to the surgical site in order to reconstruct the area. The procedure often involves the use of microsurgery. Healing of the surgical site can be slow and require frequent wound care. Total recovery may take six to eight weeks or longer.
  • Tissue expansion: Tissue expansion is a medical procedure that enables patient's body to ‘grow’ extra skin for use in reconstructive procedures. This is accomplished by inserting an instrument known as a ‘balloon expander’ under the skin near the area in need of repair. Overtime, this balloon will be gradually filled with saline solution (salt water), slowly causing the skin to stretch and grow, much the same way a woman's skin stretches during pregnancy.
Once enough extra skin has been grown, it is then used to correct or reconstruct a damaged body part. This procedure is especially common for breast reconstruction.
Tissue expansion has many advantages in that the skin color and texture are a near perfect match for the area in which it is needed and there is little scarring since there is no removal 539of skin from one area to another. The major drawback to tissue expansion is the length of the procedure, which can be as long as four months. During this period, as the balloon expander grows, the bulge under the skin grows with it. This bulge may be desirable for a breast reconstruction patient; however, for patients undergoing this procedure for scalp repair, the bulge may be uncomfortably noticeable.
 
Dealing with Deficiency of Tissue
At this point, the burn injury must be assessed for deficiency in tissue. If there is no deficiency and local tissues can be easily mobilized, excision and direct closure or Z-plasties can be performed.
Traditional Z-plasty to release a burn scar contracture. (1) The burn scar, showing the skin tension lines. (2) Z-plasty is performed by rotating two transposition flaps with an angle of 60° with the middle limb of the Z on the scar. (3) Final appearance after insetting of flaps. Note the lengthening of the tissue and the change of scar pattern. Z-plasties can be combined with other flaps (five limb Z-plasty, seven limb Z-plasty, etc.)
 
Skin Changes after Cosmetic Surgery
As patient continues to heal, patient will notice changes in the color, appearance, and feeling of patient's skin at the surgical site. Patient also may notice numbness, a tingling sensation, or minimal feeling around patient's incisions. This is normal. These sensations will continue to improve over the next few months.
 
Perfusion and Circulation after Cosmetic Surgery
After patient's cosmetic surgery, it is important to monitor perfusion (passage of fluid) and circulation of the wound site. Avoid wearing clothing that constricts or applies pressure around patient's wound. Also, patient's doctor may give patient additional instructions to help with circulation to the wound.
 
Signs of Infection at the Surgical Site
The following are signs indicating that there may be an infection at the surgical site. Notify patient's doctor right away if patient experience any of the following symptoms:
  • White pimples or blisters around incision lines.
  • An increase in redness, tenderness, or swelling of the surgical site.
  • Drainage from the incision line. Occasionally, a small amount of bloody or clear yellow-tinged fluid may drain. Notify patient's doctor if it persists or if it changes in consistency.
  • A marked or sudden increase in pain not relieved by the pain medication.
Patient may experience some other, more general signs of infection that will require medical treatment. If patient notice any of the following symptoms of infection, it is important that patient call patient's health care provider as soon as possible.
  • A persistent elevation of body temperature greater than 100.5 degrees Fahrenheit (Take patient's temperature daily, at the same time each day
  • Sweats or chills
  • Skin rash
  • Sore or scratchy throat or pain when swallowing
  • Sinus drainage, nasal congestion, headaches, or tenderness along the upper cheekbones
  • 540Persistent, dry or moist cough that lasts more than two days
  • White patches in patient's mouth or on patient's tongue
  • Nausea, vomiting, or diarrhea.
  • Trouble urinating: pain or burning, constant urge or frequent urination
  • Bloody, cloudy, or foul-smelling urine
 
Postoperative Daily Evaluation and Management
 
Operated Burn Wounds
Despite the most attentive precautions in the operating room, many patients will return to the burn intensive care unit with hypothermia which is treated by increasing the ambient temperature of the patient's room and positioning portable heating units over the patient's bed. As the patient's body temperature begins to rise towards normal, vasoconstriction in the periphery abates and the patient becomes tachycardic, hypovolemic and oliguric. The hypovolemia of rewarming can be anticipated and treated with the infusion of additional crystalloid fluids run through a fluid warmer.
In most cases, the postoperative care of burn patients following excision and grafting is uncomplicated. Any fluid and electrolyte replacements are corrected and adequate nutritional intake is assured. Many patients can begin a regular diet the morning following surgery unless they are ventilator-dependent. Continuation and/or resumption of enteral feedings begins in critically ill patients as soon as there is evidence of bowel function. Combinations of short- and long-acting narcotics and benzodiazepines are used for pain relief and sedation.
The dressings and splints are typically removed on the fourth or fifth day following skin grafting; they may, however, be reapplied for a more lengthy period of time in order to maintain proper positioning. Physical and occupational therapy resumes at this time, and patients are encouraged to resume as much independent activity as possible. For patients with smaller burns, discharge typically occurs within 48 hours of removing the dressings.
Many options are available for postoperative care of skin grafts. Grafts and donor sites should be kept clean, moist and covered. After discharge, patients return weekly to the outpatient clinic until all wounds, including donor sites, have reepithelialized and satisfactory progress is being made in therapy. Monthly or bimonthly visits for up to six months are necessary to ensure that patients achieve optimal restoration of functional capabilities, including range of motion, strength and endurance, and return to their pre-injury work status.
 
Care of Burn Wounds Unrelated To Previously Operated Wounds
Not all burn wounds require surgical intervention. Superficial second degree burns will close within two weeks and require only moist antimicrobial dressings. These second degree burns need to be monitored closely by experienced nurses and burn doctors since infections such as cellulitis are common and can result in extension of the depth of the burn. In addition, the progress of patients in physical and occupational therapy must be monitored, and pain medications frequently adjusted. For these reasons, daily evaluation and management of nonoperatively treated burn wounds merits recognition in the reimbursement process.
 
Unrelated Conditions
Thermal injuries result in perturbation of many systemic processes. Metabolic rate is increased, sometimes to double that of the uninjured healthy person. Because of increased541 metabolism, carbon dioxide production is greatly increased, resulting in the need for augmented minute ventilation. The immune system is impaired, and bacterial and fungal infections are common. Management of pain and anxiety are challenging because of the magnitude of physical discomfort and emotional distress.
Many patients with extensive thermal injuries, inhalation injuries or multiple comorbid conditions require intensive care in specialized units. ICU care includes management of fluids and electrolytes, assessment of airway, management of mechanical ventilators, establishment and evaluation of nutritional supplementation, and monitoring and treatment of infectious processes. The physician skills required for the management of these complex patients comes only with residency and fellowship training programs that emphasize critical care. The surgical skills needed to treat burn patients in the perioperative period are related but not identical to the requisite critical care skills. For this reason, billing for critical care services during the 90 day global period for skin grafting is a legitimate and well-recognized service for the treatment of medical conditions unrelated to the management of the postoperative burn wound.
 
POST-DISCHARGE BURN WOUND MANAGEMENT
 
Discharge and Follow-Up
Following discharge from the hospital, the condition of the burn patient ranges from fully independent at home to completely dependent in a skilled nursing facility. At the point of discharge the patient is typically breathing without continuous ventilatory support, is hemodynamically stable, and is showing no signs of sepsis. However, there may be resolving conditions still requiring treatment, such as infections, open wounds, and the need for nutritional support. Some patients are discharged on intravenous antibiotics; others finish their prescribed courses with oral agents. Most burn patients still have open wounds or donor sites at the time of discharge; more discussion follows below. Some are still receiving enteral feedings through feeding tubes, often because they have not successfully passed a swallowing evaluation. The resolution of these issues may require three months or more, and progress is monitored in the outpatient clinic or at the rehabilitation/skilled nursing facility.
Open wounds are present in nearly all patients discharged from burn centers. These maybe second degree burns which are being allowed to epithelialize on their own without surgery. There may also be unhealed donor sites that were created for split-thickness autografting. In addition, many third degree burns that have been grafted do not have 100% graft take (adherence and vascularity leading to viable incorporation of the graft), and there maybe areas of granulation tissue that eventually heal by secondary intention (horizontal migration of epithelial cells and contraction of the wound). These open areas of third degree burns may be small (1–2 mm) or much larger. Most wounds require daily care which may range from 1 to 3 dressing changes daily.
 
Follow-up
 
Scar prevention
For burns that take longer than 3 weeks to heal, or for wounds that have been grafted, hypertrophic scarring can be minimized with the use of compression therapy with custom-made garments that apply 25–30 mm Hg pressure to all wounds. Gel pads can be added 542underneath or sewn into the garments to apply extra compression. Compression therapy is continued throughout the wound healing process (approximately 12–18 months). Lotion application with massage therapy is used to keep the healed or grafted areas soft and supple.
 
Contracture prevention
Contractures refer to hypertrophic scar formation over joints that result in decreased range of motion. Aggressive attention to occupational and physical therapy, with appropriate consultation, is necessary to ensure optimal results. Active and passive range of motion exercises are instituted and splints are worn at night and between exercise periods. Patients with burns are at risk for contractures are followed for years to monitor for the development of these complications.
 
Psychological sequelae
Burn scarring can lead to significant psychological sequelae and the assistance of a trained psychologist or psychiatrist can be an important addition to the overall care of these patients.
 
NUTRITIONAL MANAGEMENT
 
Assessment
All inpatients with a deep burn injury are assessed by a dietitian, in order to establish whether a need exists for nutritional intervention.
 
Goals of Nutritional Management
  • To promote optimal wound healing and rapid recovery from burn injuries
  • To minimize risk of complications, including infections during the treatment period
  • To attain and maintain normal nutritional status
  • To minimize metabolic disturbances during the treatment process.
 
Objectives of Nutritional Management
  • Provide nutrition via enteral route within 6–18 hours postburn injury
  • Maintain weight within 5–10% of preburn weight
  • Prevent signs and symptoms of micronutrient deficiency
  • Minimize hyperglycemia
  • Minimize hypertriglyceridemia.
 
Enteral Feeding Should be Commenced Early
Appropriate nutritional management of the severely burned patient is necessary to ensure optimal outcome. Initiation of early enteral feeding, within 6 to 18 hours postburn injury, is recognized as beneficial, and has been shown to be safe in children as well as adults. Advantages of utilizing the enteral route, as opposed to the parenteral route, include improved nitrogen balance, reduced hypermetabolic response, and reduced immunological complications and mortality.
 
Aggressive Nutritional Support is often Required
Although oral nutrition is encouraged, young children with severe burn injuries often require nasogastric feeding as they tend to have difficulty meeting their nutritional goals with oral intake alone.
543
 
Energy Requirements are Elevated by the Burn Injury
The hypermetabolic response associated with severe burn injury results in high calorie requirements to allow optimal healing and outcome. Several predictive equations exist which enable estimations of energy requirements. Changes in management of these patients in the past decade have resulted in some reduction in the metabolic response and care must be taken to avoid overfeeding. Variation in energy needs between individuals, as well as with time, means that indirect calorimetry is recommended where practical to aid in determining energy expenditure.
 
Protein Requirements are Substantially Increased
Aggressive protein delivery, providing approximately 20% of calories from protein, has been associated with improved mortality and morbidity.
 
An Increased Requirement Exists for Nutrients Associated with Healing and Immune Function
Provision of those nutrients known to be associated with healing and immune function, particularly vitamins A, C, E, some B vitamins and zinc, is especially important. Recent studies have indicated that benefits may also be achieved by supplementation with various additives, including fish-oil and arginine.
 
Complications of Surgeries for Burn Management
Complications to surgery in patients with burns include bleeding, infection, or graft loss. If infection is suspected, dressings can be changed to include broad spectrum aqueous Sulfamylon solution.
 
Outcome and Prognosis
With the exception of infants, the prognosis for survival in children and adolescents is quite good. In the past decade, the size of a survivable injury has increased from 70% BSA burned to more than 95% BSA burned in children younger than 15 years.
 
Nursing Management
 
Assessment
  • Obtain thorough history including: Causative agent, duration of exposure, circumstances of injury, age, initial treatment taken, pre-existing medical problems, allergies, tetanus immunization, height, weight.
  • Perform ongoing assessment of hemodynamic and respiratory status, condition of wounds and signs of infection.
 
Nursing Diagnosis
1. Ineffective gas exchange related to inhalation injury.
Goal: Achieve adequate oxygenation and respiratory functions.
Interventions
  • Provide humidified 100% oxygen until CO level is known
  • Assess for signs of hypoxemia
  • Note character and amount of respiratory secretions
  • Provide mechanical ventilation when required.
5442. Decreased cardiac output related to fluid shift and hypovolemic shock
Goal: Support cardiac output.
Intervention
  • Position the patient to increase venous return
  • Give fluids as prescribed
  • Monitor vital signs
  • Check level of conscious.
Ineffective peripheral tissue perfusion related to edema
Goal: Promote peripheral circulation.
Intervention
  • Remove all jewelry and clothing
  • Elevate extremities
  • Monitor peripheral pulses hourly
  • Monitor tissue pressure.
Risk for infection related to reconstructive surgeries
Goal: Prevent risk for infections.
Interventions
  • Check vital signs
  • Assess signs of wound infection: Redness and discharge
  • Change dressing as prescribed
  • Apply antibiotic topically and also administer through IV route
  • Risk for excess fluid volume related to fluid resuscitation
  • Impaired skin integrity related to burn injury and surgical intervention
  • Impaired urinary elimination related to indwelling catheter
  • Ineffective thermoregulation related to loss of skin surface
  • Impaired physical mobility related to edema, pain, skin and joint contractures
  • Impaired nutrition: Less than body requirement related to hypermetabolic response to burn injury
  • Risk for injury related to decreased gastric mobility and stress response
  • Acute pain related to injured nerves in burn wound and skin tightness
  • Ineffective coping related to fear and anxiety
  • Disturbed body image related to cosmetic and functional sequelae of burn wound.
545
BIBLIOGRAPHY
  1. Achauer BM. Burn reconstruction. Thiene,  New York:  1991.
  1. American Medical Association. CPT Assistant. Skin replacement surgery and skin substitutes. Volume 16, October 2006. Herndon DN, Total burn care. 2nd ed. WB Saunders,  London:  2002.
  1. Barret JP, Herndon DN. Color atlas of burn care. WB Saunders,  London:  2001.
  1. Basavanthappa BT. A Textbook of medical surgical nursing, 2nd ed. Jaypee Brothers Medical Publishers.  New Delhi. 
  1. Black MA. Textbook of medical surgical nursing. 8th ed. Elsevier.  Noida. 
  1. Brou JA, Robson MC, McCauley RL. Inventory of potential reconstructive needs in the patient with burns. J Burn Care Rehabil 1989;10: 555–60.
  1. Brunner SA. Textbook of medical surgical nursing. 5th ed. Lippincott Company.  Philadelphia.  1982.
  1. Engrav LH, Donelan MB. Operative techniques in plastic and reconstructive surgery. Face burns: acute care and reconstruction. WB Saunders,  London:  1997.
  1. Greenwood JE. Burn injury and explosions: an Australian perspective. Eplasty 2009 Sep 16;9:e40.
  1. Holmes JH 4th. Critical issues in burn care. J Burn Care Res 2008 Nov-Dec;29 (6 Suppl 2):S180–7.
  1. Orgill DP. Excision and skin grafting of thermal burns. N Engl J Med 2009 Feb 26;360(9):893–901.

Oncological Conditions11

 
CANCER
Cancer is an important public health concern in India and throughout the world. Body is composed of many millions of tiny cells, each a self-contained living unit. Normally, each cell coordinates with the others that compose tissues and organs of your body. One way that this coordination occurs is reflected in how cells reproduce themselves. Normal cells in the body grow and divide for a period of time and then stop growing and dividing. Thereafter, they only reproduce themselves as necessary to replace defective or dying cells.
Cancer occurs when this cellular reproduction process goes out of control. In other words, cancer is a disease characterized by uncontrolled, uncoordinated and undesirable cell division. Unlike normal cells, cancer cells continue to grow and divide for their whole lives, replicating into more and more harmful cells.
Neoplasm means new growth that extends beyond the normal tissue boundaries.
The abnormal growth and division observed in cancer cells is caused by damage in these cells' DNA (genetic material inside cells that determines cellular characteristics and functioning). There are a variety of ways that cellular DNA can become damaged and defective. For example, environmental factors (such as exposure to tobacco smoke) can initiate a chain of events that results in cellular DNA defects that lead to cancer. Alternatively, 547defective DNA can be inherited from your parents. As cancer cells divide and replicate themselves, they often form into a clump of cancer cells known as a tumor. Tumors cause many of the symptoms of cancer by pressuring, crushing and destroying surrounding non-cancerous cells and tissues.
The scope, responsibilities and goals of cancer nursing, also called oncology nursing, are as diverse and complex as those of any nursing specialties.
 
Terminology Related to Cancer
  • Hypertrophy: Hypertrophy is the increase in the volume of an organ or tissue due to the enlargement of its component cells.
  • Atrophy: It is shrinkage in cell size leading to decrease in organ size. The decrease in cell size is due to less blood supply, nutrition, etc. it is mostly associated with aging.
  • Hyperplasia: It is an increase in the number of the new cells in an organ or tissue, as cells multiply volume also increases. It is a mitotic response, but it is reversible when the stimulus is removed. This distinguishes it from malignant growth, which continues after the stimulus is removed. Hyperplasia may be hormonally induced. Example is breast changes of a girl in puberty or of a pregnant woman.
  • Metaplasia: It is a cell transformation in which a highly specialized cell changes to a less specialized cell.
  • Differentiation: It is the processes by which immature cells become mature cells with specific functions. In cancer, this describes how much or how little tumor tissue looks like the normal tissue it came from. Well-differentiated cancer cells look more like normal cells and tend to grow and spread more slowly than poorly differentiated or undifferentiated cancer cells. Differentiation is used in tumor grading systems, which are different for each type of cancer.
 
Characteristics of Cancer Cells
  • Pleomorphism: Refers to variability in size and shape of cells and their nuclei
  • Hyperchromatism: It refers to the development of excess chromatin or of excessive nuclear staining.
  • Polymorphism: The nucleus is large and varies in shape
  • Aneuploidy: It is a term used to describe a chromosome problem that is caused by an extra or missing chromosome
  • Abnormal Chromosome Arrangements
  • Loss of proliferative control: In normal cell, cell production stops when stimulus is gone, producing balance between cells growing and dying but in cancer proliferation continue once the stimulus initiate the process and progress to uncontrolled growth.
  • Loss of capacity to differentiate: It is the processes by which immature cells become mature cells and acquire specific structural and functional characteristics. In cancer, this describes how much or how little tumor tissue looks like the normal tissue it came from. Well-differentiated cancer cells look more like normal cells and tend to grow and spread more slowly than poorly differentiated or undifferentiated cancer cells.
  • Chromosomal insatiability: Cancer cells are genetically less stable than normal cells because of the development of abnormal chromosome arrangement.
  • 548Capacity of metastasis: It is the capacity of cancer cells that they may spread from a primary site to distant sites and it is aided by production of enzymes on the surface of the cancer cell.
 
Classification of Cancer
1. Tumors according to behavior come in two forms; benign and malignant
Characteristics
Benign
Malignant
Cell characteristics
Well differentiated cell
Undifferentiated
Mode of growth
Does not infiltrate the surrounding tissues; usually encapsulated
Infiltrate and destroy the surrounding tissues
Rate of growth
Sow
Fast
Metastasis
Does not spread by metastasis
Metastasis occurs
General effects
Local effects
Generalized effects
Ability to cause death
Usually not cause death
Usually cause death
Reoccurrence
Rarely occur after removal
may occur after removal
Shape
Regular in shape
Irregular
Vascularity
slight
Moderate to marked
Encapsulated
Usually
Rarely
2. Tumors according to histological analysis (appearance of cell and degree of differentiation)
  • Grade I: Cell differs slightly from parent cells
  • Grade II: Cells are more abnormal and less differentiated
  • Grade III: Very abnormal cells and poorly differentiated
  • Grade IV: Cells will immature and undifferentiated.
Clinical staging
  • Stage 0: Carcinoma in situ
  • Stage 1: Tumor is limited to tissue of origin
  • Stage 2: Limited local spread
  • Stage 3: Extensive local and regional spread
  • Stage 4: Metastasis.
 
Etiology of Cancer
The etiology of cancer can be viewed from two perspectives: its molecular origins within individual cells and its external causes in terms of personal and community risks. Together, these perspectives form a multidimensional web of causation by which cancers arise from the interplay of casual events occurring in overtime.
 
Host Factors
Genetic Factors: 5–10% of adult cancers arise in hereditary setting. Genes underlying hereditary cancer are involved in control of cell growth and differentiation or in DNA repair and maintenance of genomic integrity. They are oncogenes, tumor suppressor genes 549and DNA repair genes. Characteristics of hereditary cancers also include early age onset, family history, and evidence of autosomal dominant transmission of cancer susceptibility.
Hormones: Endogenous hormones have received considerable research attention with respect to cancers of breast, ovary and endometrium in women and those of prostate and testis in men. Neoplasia is a consequence of prolonged hormonal stimulation of the particular target organ, the normal growth and function of which is controlled by one or more steroid or polypeptide hormones.
Female cancer sites, demonstrate a clear etiologic role for endogenous estrogen (estradiol) in both breast and endometrial cancers and probable role for gonadotropin in ovarian cancer. In breast cancer, association of increased cancer risk with low parity, late age at first birth, early menarche, late menopause, all of which are due to heightened exposure to endogenous estrogen.
In endometrial cancer, the etiological role of estrogen is supported strongly by the fact that postmenopausal risk in increased greatly by estrogen replacement therapy in the absence of progesterone replacement.
For ovarian cancers, estrogens do not appear to increase risk with oral contraceptive use suggest a role for gonadotropin.
Immune mechanisms: The occurrence of particular types of cancer under various conditions of immunological impairment supports the general concept that normal mechanism of immune-surveillance are important for control of carcinogenesis. Certain cancers, especially non-Hodgkin's lymphoma (NHL) occur with increased frequency in persons treated with immune-suppression for tissue transplantation, etc.
 
Environmental Factors
Chemical Factors: Chemical origin of human malignancies—observation of unusual cancer incidences in certain occupational groups. Chemical carcinogens are organ specific and target epithelial cells. They are genotoxic or nongenotoxic. Genotoxic carcinogens have high chemical reactivity, can be metabolized to reactive intermediate by the host, target DNA in nucleus and mitochondria. Mechanism action of nongenotoxic carcinogens is controversial.
Known Chemical Carcinogens in Humans
  • Lung: Tobacco smoke, arsenic, asbestos
  • Pleura: Asbestos
  • Oral Cavity: Tobacco smoke, alcohol, nickel compounds
  • Esophagus: Tobacco, alcohol, smoke, salted, pickled foods
  • Colon: Hetrocyclic amines
  • Liver: Alfatoxin, vinylchloride, tobacco, alcohol
  • Kidney: Tobacco smoke, phenacetin
  • Prostate: Cadmium
  • Skin: Arsenic, coal tar, soot, PUVA
  • Bone Marrow: Benzene, tobacco smoke, antineoplastic agents.
  • Physical Factors: Radiation are of two types:
    • Ionizing radiation: X-rays, electrons, protons
    • Nonionizing radiation: UV rays
  • 550Diet: Major role of diet and nutrition in influencing cancer risk is well established.
    • Naturally occurring dietary carcinogens
      • Natural pesticides: Allyl isothiolynate in cabbage, cauliflower, etc. hydrazine in mushrooms and pyrrolidine in herbal tea.
      • Mycotoxins: Alfatoxins in corn, peanut and ochratoxins in grains.
    • Products of food preparation and processing: Urethane in all fermented foods, heterocyclic aromatic amines in barbecued chicken, etc. and nitroso-compounds in cured meat and dairy cheese products.
    • Synthetic carcinogens in diet (synthetic derivatives):
      • Intentional: colorants, flavorants, sweetness
      • Unintentional: pesticides, solvents, and packaging derived chemicals.
 
Detection and Prevention of Cancer
Cancer develops in the body very silently until it becomes to certain stage, patient lead a normal life without any complaints. Initially it produces mild symptoms as found in other ailments. Disease detected at early stage produces better results on treatment and even cure whereas advanced disease shows poor results on treatment.
Primary prevention: The goal is to protect healthy people from developing a disease to reduce the impact of carcinogens.
  • Reducing the risk of cancer
  • Lifestyle modification to reduce the exposure to suspected carcinogens and promoting agents
  • Eating balanced diet specially Green Yellow (cabbage family) whole grains, fresh fruits
  • Adequate fiber diet
  • Regular exercise regime
  • Adequate rest period in between work periods
  • Have health examination regularly after 30 years
  • Reduce the stress
  • Enjoy consistent period of relaxation and leisure
  • Increase intake of Vit A and Vit C
  • Reduce dietary fat, alcohol consumption and smoking.
 
Caution
C: Changes in bathroom habits. This can be anything from changes in the bowel movements (watery or too hard) to frequency (going more often or infrequently). Any long-term changes in bathroom habits should be told to your doctor.
A: A sore that does not heal. This can also be a sign of diabetes, but sores that do not heal within a usual amount of time need to be checked.
U: Unusual discharge and bleeding. Moles and freckles should not bleed or drain. Other unusual draining issues should be checked out as well.
T: Thickness or lumps in the breast or other places. Breast lumps can be cysts that are normal in the course of your menstrual cycle, or they can be the beginnings of breast tumors. If you notice a lump, have a mammogram to see if there is something there other than fluid.
551I: Indigestion and difficulty in swallowing. Indigestion can come from many things, even very frequent indigestion can be a sign of acid reflux or other normal conditions. However, it can also be a sign of some cancers.
O: Obvious changes in moles or warts. Warts and moles should not change shapes or colors or thickness. Any of these changes can signal a chance of skin cancer.
N: Nagging cough and hoarseness. This can go along with the difficulty in swallowing. It can also be a sign of lung and other cancers.
 
Secondary Prevention (Early Detection and Screening of Cancer)
Secondary prevention is an approach to detect the abnormal changes at the beginning of the development of malignancy. It involves screening and early detection methods like mammogram, pap test and so on. This can help us to identify any abnormal changes of our body before they become cancerous. Therefore, it is effective to prevent cancer from fully developing. Sometimes, secondary cancer prevention can involve the treatment of precancerous lesions in an attempt to reverse carcinogenesis so that the lesion can regress.
 
Diagnostic Tests
  • Blood tests (CBC, RFT, LFT, electrolytes)
  • Radioimmuno assay
  • Tumor markers
  • Stool test (colon and rectal cancer)
  • Cytological tests
  • Pap smear
  • Endometrial tissue sampling
  • Monoclonal antibodies
  • Radiographic and imaging studies
  • PET, SPET
  • Biopsy
  • Sigmoidoscopy
  • Proctoscopy
  • Bone marrow examination.
According to american cancer society recommendations for early detection of cancer in asymptomatic people
Cancer Related Check-up: A cancer related check-up is recommended every 3 years for people aged 20–40 and every year for people age 40 and older. This exam should include health counseling and depending on a person's age, might include examination for cancer of the thyroid, oral cavity, skin, lymph nodes, testes and ovaries.
Breast: Women 40 and older should have a annual mammogram, an annual clinical breast examination (CBE) by a health care professional, and should perform monthly breast self examination (CSE). Women ages 20–39 should have a CBE by a health care professional every 3 years and should perform monthly BSE.
Colon and Rectum: Beginning at age 50, men and women should follow one of the examination schedules below:
  • 552A fecal occult blood test every year and a flexible sigmoidoscopy every 5 years
  • A colonoscopy every 10 years
  • A double contrast barium enema every 5–10 years
Prostate: The ACS recommends that both the prostate specific antigen (PSA) blood test and the digital rectal examination be offered annually, beginning at age of 50. Men in high-risk groups, such as those with a strong familial predisposition or African Americans may begin at a younger age (45 years).
Uterus Cervix: All women who are or have been sexually active or who are 18 and older should have an annual PAP test and pelvic examination. After 3 or more consecutive satisfactory examinations with normal findings, the PAP test may be performed less frequently.
Endometrium: Women at high-risk for cancer of the uterus should have a sample of endometrial tissue examined when menopause begins.
 
Tertiary Prevention
Tertiary prevention is an approach to control the cancer and prevention of disease-related complications. It involves a variety of aspects of patient care such as quality of life, adjuvant therapies, surgical intervention and palliative care.
 
Various Treatment Modalities of Cancer
There are various cancers in the body and all cancer had various and different treatment modalities to treat them. Although various modalities are present but common are chemotherapy, radiation therapy, surgeries and palliative therapy.
 
CHEMOTHERAPY
Chemotherapy is the use of chemical agents to kill cells. In conversational usage, the term chemotherapy refers to the chemical treatment of cancer.
 
Mechanism of Action of Chemotherapeutic Drugs
Chemotherapeutic drugs inhibit the process of mitosis, or cell division. Since malignant (cancer) cells divide without control or order, these drugs effectively target cancerous growths. Some chemo drugs cause cancer cells to die altogether by stimulating a process known as apoptosis (programmed cell-death). Although chemotherapeutic drugs are designed to target fast-dividing cancer cells, they inadvertently damage healthy cells. The faster a healthy cell divides, the more likely it is to be affected by chemotherapy. Chemotherapeutic drugs have been developed to target various rates of mitosis (cell division), but the slower the rate of division, the greater the risk of healthy cell damage.
 
The Focus of Chemotherapy Treatment
  • Curative: Curative chemotherapy is intended to kill all the cancer cells in the body, curing the patient of cancer.
  • Palliative: This approach involves prolonging the patient's life by controlling cancer growth, spread, and invasion into other tissues. Palliative treatments are also used to help relieve cancer-related symptoms, improving the patient's quality of life.
  • 553Adjuvant: This treatment strategy involves using chemotherapy alongside other cancer treatment options. Adjuvant chemotherapy is usually administered after surgery or radiotherapy to kill any remaining cancer cells in the body.
  • Neoadjuvant Chemotherapy: The focus of neoadjuvant chemotherapy is to reduce the size of a tumor preceding surgery or other treatment options.
 
Classification of Chemotherapeutic Drugs
Chemotherapy drugs can be divided into several groups based on factors such as how they work, their chemical structure, and their relationship to another drug.
 
Alkylating Agents
These chemical agents utilize the cellular property of electronegativity to add alkyl groups to cells. Electronegativity is a cell's ability to attract electrons. When a cell inadvertently attracts alkyl groups, the alkyl alters the cell's DNA, resulting in cell death or impaired mitosis.
Alkylating agents directly damage DNA to prevent the cancer cell from reproducing. As a class of drugs, these agents are not phase-specific; in other words, they work in all phases of the cell cycle. Alkylating agents are used to treat many different cancers, including leukemia, lymphoma, Hodgkin disease, multiple myeloma, sarcoma, as well as cancers of the lung, breast, and ovary.
Because these drugs damage DNA, they can cause long-term damage to the bone marrow. In rare cases, this can eventually lead to acute leukemia. The risk of leukemia from alkylating agents is ‘dose-dependent’, meaning that the risk is small with lower doses, but goes up as the total amount of the drug used gets higher. The risk of leukemia after getting alkylating agents is highest about 5 to 10 years after treatment.
There are different classes of alkylating agents, including:
  • Nitrogen mustards: Such as mechlorethamine (nitrogen mustard), chlorambucil, cyclophosphamide, ifosfamide, and melphalan
  • Nitrosoureas: Which include streptozocin, carmustine (BCNU), and lomustine
  • Alkyl sulfonates Busulfan
  • Triazines: Decarbazine (DTIC) and temozolomide (Temodar)
  • Ethylenimines: Thiotepa and altretamine (hexamethylmelamine).
 
Antimetabolites
These chemical agents mask themselves as purine (one of the building blocks of DNA). When a cell accepts the masked anti-metabolites, it becomes unable to incorporate genuine purine into its DNA. This results in cellular DNA damage. These agents damage cells during the S phase. They are commonly used to treat leukemias, cancers of the breast, ovary, and the intestinal tract, as well as other types of cancer.
Examples of antimetabolites include:
  • 5-fluorouracil (5-FU)
  • 6-mercaptopurine (6-MP)
  • Capecitabine (Xeloda)
  • Cladribine
  • Clofarabine
  • 554Cytarabine (Ara-C)
  • Floxuridine
  • Fludarabine
  • Gemcitabine (Gemzar)
  • Hydroxyurea
  • Methotrexate
  • Pemetrexed (Alimta)
  • Pentostatin.
 
Antitumor Antibiotics
Anthracyclines
Anthracyclines are antitumor antibiotics that interfere with enzymes involved in DNA replication. These drugs work in all phases of the cell cycle. They are widely used for a variety of cancers. A major consideration when giving these drugs is that they can permanently damage the heart if given in high doses. For this reason, lifetime dose limits are often placed on these drugs.
Examples of anthracyclines include:
  • Daunorubicin
  • Doxorubicin (Adriamycin)
  • Epirubicin
  • Idarubicin
Other Antitumor Antibiotics
Antitumor antibiotics that are not anthracyclines include:
  • Actinomycin-D
  • Bleomycin
  • Mitomycin-C
Mitoxantrone is an antitumor antibiotic that is similar to doxorubicin in many ways, including the potential for damaging the heart. This drug also acts as a topoisomerase II inhibitor, and can lead to treatment-related leukemia. Mitoxantrone is used to treat prostate cancer, breast cancer, lymphoma, and leukemia.
 
Topoisomerase Inhibitors
These drugs interfere with enzymes called topoisomerases, which help separate the strands of DNA so they can be copied. They are used to treat certain leukemias, as well as lung, ovarian, gastrointestinal, and other cancers.
  • Examples of topoisomerase I inhibitors include topotecan and irinotecan (CPT-11).
  • Examples of topoisomerase II inhibitors include etoposide (VP-16) and teniposide. Mitoxantrone also inhibits topoisomerase II.
  • Treatment with topoisomerase II inhibitors increases the risk of a second cancer — acute myelogenous leukemia (AML). With this type of drug, a secondary leukemia can be seen as early as 2 to 3 years after the drug is given.
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Mitotic Inhibitors
Mitotic inhibitors are often plant alkaloids and other compounds derived from natural products. They can stop mitosis or inhibit enzymes from making proteins needed for cell reproduction.
These drugs work during the M phase of the cell cycle, but can damage cells in all phases. They are used to treat many different types of cancer including breast, lung, myelomas, lymphomas, and leukemias. These drugs are known for their potential to cause peripheral nerve damage, which can be a dose-limiting side effect.
Examples of mitotic inhibitors include:
  • Taxanes: paclitaxel and docetaxel
  • Epothilones: ixabepilone
  • Vinca alkaloids: vinblastine, vincristine
  • Estramustine (Emcyt).
 
Corticosteroids
Steroids are natural hormones and hormone-like drugs that are useful in treating some types of cancer (lymphoma, leukemias, and multiple myeloma), as well as other illnesses. When these drugs are used to kill cancer cells or slow their growth, they are considered chemotherapy drugs.
Corticosteroids are also commonly used as anti-emetics to help prevent nausea and vomiting caused by chemotherapy. They are used before chemotherapy to help prevent severe allergic reactions (hypersensitivity reactions), too. When a corticosteroid is used to prevent vomiting or allergic reactions, it is not considered chemotherapy.
Examples include prednisone, methylprednisolone (Solumedrol), and dexamethasone (Decadron).
 
Miscellaneous Chemotherapy Drugs
Some chemotherapy drugs act in slightly different ways and do not fit well into any of the other categories.
Examples include drugs like L-asparaginase, which is an enzyme, and the proteosome inhibitor bortezomib (Velcade).
 
Hormone Therapy
Drugs in this category are sex hormones, or hormone-like drugs, that change the action or production of female or male hormones. They are used to slow the growth of breast, prostate, and endometrial (uterine) cancers, which normally grow in response to natural hormones in the body. These cancer treatment hormones do not work in the same ways as standard chemotherapy drugs, but rather by preventing the cancer cell from using the hormone it needs to grow, or by preventing the body from making the hormones.
Examples include:
  • The antiestrogens: Fulvestrant, tamoxifen, and toremifene
  • Aromatase inhibitors: Anastrozole (Arimidex), exemestane (Aromasin), and letrozole (Femara)
  • Progestins: Megestrol acetate
  • 556Estrogens
  • Anti-androgens: Bicalutamide, flutamide and nilutamide
  • Gonadotropin-releasing hormone (GnRH), also known as luteinizing hormone-releasing hormone (LHRH) agonists.
 
SIDE EFFECTS OF CHEMOTHERAPY
Although side effect management has come along way in recent years, chemotherapy drugs still affect healthy cells. Sometimes the effects of cell damage are temporary, but sometimes they are long-term or even permanent.
 
Short-term Side Effects
  • Hair loss
  • Bleeding
  • Fatigue
  • Infertility
  • Cognitive impairment
  • Sensory abnormalities: Food tastes different, odors are perceived differently, etc.
  • Lung damage
  • Nervous tissue damage
  • Liver damage
  • Gastrointestinal damage: Damage to the fast-dividing cells of your gastrointestinal tract (stomach, intestines, esophagus, and other digestive components) may result in a myriad of side effects, such as temporary effects may include:
    • Nausea
    • Vomiting
    • Diarrhea
    • Dry mouth
    • Constipation
    • Mouth Sores
    • Difficulty swallowing
    • Loss of appetite.
Most of these side effects will diminish or disappear completely after chemo treatment stops.
 
Long-term Side Effects
Long-term Chemo effects are rare. As cancer patients live longer and longer lives, doctors are uncovering side effects that do not show until many years after treatment ends. Long-term effects may include:
  • Nervous tissue damage: This may result in sensory abnormalities and impaired cognitive function. This is rare.
  • Hematuria: Blood in the urine.
  • Organ damage: This typically involves heart, lung, or kidney impairment.
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Role of Nurse in Chemotherapy
Prior to Chemotherapy Administration
  • Review: The chemotherapy drugs prescription which should have
    • Name of antineoplastic agent
    • Dosage
    • Route of administration
    • Date and time that each agent to be administered.
  • Accurately identify the client
  • Medications to be administered in conjunction with the chemotherapy e.g. antiemetic, sedatives, etc.
  • Assess the clients condition including:
    • Most recent report of blood counts including hemoglobin, hematocrit, white blood cells and platelets.
    • Presence of any complicating condition which could contraindicate chemotherapeutic agent administration, i.e. infection, severe stomatitis, decreased deep tendon reflexes, or bleeding.
    • Physical status, level of anxiety and psychological status.
  • Prepare for potential complications
    • Review the policy and have medication and supplies available for immediate intervention the event of extravasation.
    • Review the procedure and have medication available for possible anaphylaxis
  • Assure accurate preparation of the agent
    • Accuracy of dosage calculation
    • Expiry date of the drug to be checked
    • Procedure for correct reconstitution
    • Recommended procedures for administration
  • Assess patients understanding of the chemotherapeutic agents and administration procedures.
 
Calculation of Drug Dosage
It is calculated based on body surface area.
 
Drug Reconstitution/Preparation
Pharmacy staff should reconstitute all drugs preprime the intravenous tubing under a class II biologic safety cabinet (BSC). In certain conditions nurses may be required to reconstitute medications. When preparing and reconstituting safe handling guidelines to be followed.
  • Aseptic technique should be followed
  • Personal protective equipment includes disposable surgical gloves, long sleeves gown and elastic cuffs
  • Protective eye goggles if no BSC
  • To minimize exposure
  • Wash hands before and after drug handling
  • 558Limit access to drug preparation area
  • Keep labeled drug spill kit near preparation area
  • Open drug vials/ampoules away from body
  • Place absorbent pad on work surface
  • Wrap alcohol wipe around neck of ampoule before opening
  • Label all chemotherapeutic drugs.
The following guidelines to be kept in mind:
  • Inspect the solution, container and tubing for signs of contamination including particles, discoloration, cloudiness, and cracks or tears in bottle or bag
  • Aseptic technique to be followed
  • Prepare medicines according to manufacturer's directions
  • Select a suitable vein
  • Large veins on the forearm are the preferred site.
  • Use distal veins first, and choose a vein above areas of flexion.
  • For nonvesicant drugs, use the distal veins of the hands (metacarpal veins): then the veins of the forearms (basilic and cephalic veins)
  • For vesicants, use only the veins of the forearms. Avoid using the metacarpal and radial areas
  • Avoid the antecubital fossa and the wrist because an extravasation in these areas can destroy nerves and tendons, resulting in loss of function
  • Peripheral sites should be changed daily before administration of vesicants
  • Avoid the use of small lumen veins to prevent damage due to friction and the decreased ability to dilute acidic drugs and solutions
  • Select the shortest catheter with the smallest gauge appropriate for the type and duration of the infusion
  • Apply a small amount of iodine based antiseptic ointment over the insertion site and cover the area with sterile gauze.
 
Documentation
  • Chemotherapeutic drugs, dose, route, and time .
  • Premedications, postmedications, prehydration and other infusions and supplies used for chemotherapy regimen.
  • Any complaints by the patient of discomfort and symptoms experienced before, during, and after chemotherapeutic infusion.
 
Disposal of Supplies and Unused Drugs
  • Do not clip or recap needles or break syringes.
  • Place all supplies used intact in a leak proof, puncture proof, appropriate labeled container.
  • Place all unused drugs in containers in a leak proof, puncture proof, appropriately labeled container.
  • Dispose of containers filled with chemotherapeutic supplies and unused drugs in accordance with regulations of hazardous wastes.
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Management of Chemotherapeutic Spills
  • Chemotherapy spills should be cleaned up immediately by properly protected personnel trained in the appropriate procedure.
  • A spill should be identified with a warning sign so that other person will not be contaminated.
 
Staff Education
  • All personnel involved in the care should receive an orientation to chemo.
  • Drugs including their known risk, relevant techniques and procedures for handling, the proper use of protective equipment and materials, spill procedures, and medical policies covering personnel handling chemo agents.
  • Personnel handling blood, vomitus, or excreta from patients who have received chemotherapy should wear disposable gloves and gowns to be appropriately discarded after use.
  • All personnel involved in the care should receive an orientation to chemo.
  • Drugs including their known risk, relevant techniques and procedures for handling, the proper use of protective equipment and materials, spill procedures, and medical policies covering personnel handling chemotherapeutic agents.
  • Personnel handling blood, vomitus, or excreta from patients who have received chemotherapy should wear disposable gloves and gowns to be appropriately discarded after use.
 
Extravasation Management
Extravasation is the accidental infiltration of vesicant or irritant chemotherapeutic drugs from the vein into the surrounding tissues at the IV site. A vesicant is an agent that can produce a blister or tissue destruction. An irritant is an agent that is capable of producing venous pain at the site of and along the vein with or without an inflammatory reaction. Injuries that may occur as a result of extravasation include sloughing of tissue, infection, pain, and loss of mobility of an extremity.
 
Prevention of Extravasation
Nursing responsibilities for the prevention of extravasation include the following:
  • Knowledge of drugs with vesicant potential
  • Skill in drug administration
  • Identification of risk factors, e.g. multiple vene punctures
  • Anticipation of extravasation and knowledge of management protocol
  • New venepuncture site daily if peripheral access is used
  • Administration of drug in a quiet, unhurried environment
  • Testing vein patency without using chemotherapeutic agents
  • Providing adequate drug dilution
  • Careful observation of access site and extremity throughout the procedure
  • 560Ensuring blood return from IV site before, during, and after vesicant drug infusion.
  • Educating patients regarding symptoms of drug infiltration, e.g. pain, burning, stinging sensation at IV site.
 
Extravasation Management at Peripheral Site
  • According to agency policy and approved antidote should be readily available
  • The following procedure should be initiated
  • Stop the drug
  • Leave the needle or catheter in place
  • Aspirate any residual drug and blood in the IV tubing, needle or catheter, and suspected infiltration site
  • Instill the IV antidote
  • Remove the needle
  • If unable to aspirate the residual drug from the IV tubing, remove needle or catheter
  • Inject the antidote subcutaneously clockwise into the infiltrated site using 25 gauge needle; change the needle with each new injection
  • Avoid applying pressure to the suspected infiltration site
  • Apply topical ointment if ordered
  • Cover lightly with an occlusive sterile dressing
  • Apply cold or warm compresses as indicated
  • Elevate the extremity
  • Observe regularly for pain, erythema, induration, and necrosis
  • Documentation of extravasation management
  • All nursing personnel should be alert and prepared for the possible complication of anaphylaxis.
 
RADIATION THERAPY
Radiation therapy is the medical use of ionizing radiation, generally as part of cancer treatment to control or kill malignant cells. Radiation therapy maybe curative in a number of types of cancer if they are localized to one area of the body. It may also be used as part of curative therapy, to prevent tumor recurrence after surgery to remove a primary malignant tumor, e.g. early stages of breast cancer. Radiation therapy is synergistic with chemotherapy, and has been used before, during, and after chemotherapy in susceptible cancers.
Radiotherapy maybe used for curative or adjuvant cancer treatment. It is used as palliative treatment (where cure is not possible and the aim is for local disease control or symptomatic relief) or as therapeutic treatment (where the therapy has survival benefit and it can be curative). Total body irradiation (TBI) is a radiotherapy technique used to prepare the body to receive a bone marrow transplant.
 
Types of Radiation
Radiation has a wide range of energies that form the electromagnetic spectrum. The spectrum has two major divisions:
  1. Nonionizing radiation
  2. Ionizing radiation
561Nonionizing Radiation or Electromagnetic Radiation: Nonionizing radiation ranges from extremely low frequency radiation. These are indirectly ionizing. They do not themselves produce chemical and biological damage, but when absorbed in the medium through which they pass, they give up their energy to produce fast moving electrons by either the Compton, photoelectric or pair production processes.
Ionizing Radiation: Higher frequency ultraviolet radiation begins to have enough energy to break chemical bonds. X-ray and gamma ray radiation, which are at the upper end of magnetic radiation, have very high frequencies (in the range of 100 billion Hertz) and very short wavelengths of about 1 picometer. Ionization is the process in which a charged portion of a molecule is given enough energy to break away from the atom. This process results in the formation of two charged particles or ions: the molecule with a net positive charge and the free electron with a negative charge.
There are three main kinds of ionizing radiation:
  • Alpha particles, which include two protons and two neutrons
  • Beta particles, which are essentially high-speed electrons
  • Gamma rays and X-rays, which are pure energy (photons).
Alpha Radiation: Alpha radiation is a heavy, very short-range particle and is actually an ejected helium nucleus. Some characteristics of alpha radiation are:
  • Most alpha radiation is not able to penetrate human skin.
  • Alpha-emitting materials can be harmful to humans if the materials are inhaled, swallowed, or absorbed through open wounds.
  • Alpha radiation travels only a short distance (a few inches) in air, but is not an external hazard.
  • Alpha radiation is not able to penetrate clothing.
  • Examples of some alpha emitters: radium, radon, uranium, thorium.
 
Beta Radiation
Beta radiation is a light, short-range particle and is actually an ejected electron. Some characteristics of beta radiation are:
  • Beta radiation may travel several feet in air and is moderately penetrating.
  • Beta radiation can penetrate human skin to the ‘germinal layer’, where new skin cells are produced. If high levels of beta-emitting contaminants are allowed to remain on the skin for a prolonged period of time, they may cause skin injury.
  • Beta-emitting contaminants may be harmful if deposited internally.
  • Clothing provides some protection against beta radiation.
  • Examples of some pure beta emitters: strontium 90, carbon 14, tritium, and sulfur 35.
 
Gamma and X-Radiation
Gamma radiation and X-rays are highly penetrating electromagnetic radiation. Some characteristics of these radiations are:
  • Gamma radiation or X-rays are able to travel many feet in air and many inches in human tissue. They readily penetrate most materials and are sometimes called ‘penetrating’ radiation.
  • 562X-rays are like gamma rays. X-rays, too, are penetrating radiation. Sealed radioactive sources and machines that emit gamma radiation and X-rays respectively constitute mainly an external hazard to humans.
  • Gamma radiation and X-rays are electromagnetic radiation like visible light, radiowaves, and ultraviolet light. These electromagnetic radiations differ only in the amount of energy they have. Gamma rays and X-rays are the most energetic of these.
  • Dense materials are needed for shielding from gamma radiation. Clothing provides little shielding from penetrating radiation, but will prevent contamination of the skin by gamma-emitting radioactive materials.
  • Gamma radiation is easily detected by survey meters with a sodium iodide detector probe.
  • Gamma radiation and characteristic X-rays frequently accompany the emission of alpha and beta radiation during radioactive decay.
  • Examples of some gamma emitters: iodine 131, cesium 137, cobalt 60, radium 226, and technetium 99m.
Treatment: Radiation is used to treat a carefully defined area of the body to achieve local control of disease. As radiation has an effect on tissues only within the treatment field, it is not appropriate as an independent modality for patients with systemic disease. However, radiation maybe used, independently or in combination with chemotherapy, to treat primary tumors or for palliative control of metastatic lesions. Radiation can be delivered externally (teletherapy) or internally (brachytherapy). As with other cancer therapies, the goals of radiation therapy are cure, control, or palliation. There are multiple settings in which radiation maybe used, including:
  • Definitive or primary therapy: Used an independent treatment modality with curative intent (e.g. the cancers of the lung, prostate, bladder, head/neck, Hodgkin's lymphoma).
  • Neoadjuvant therapy: Given (with or without chemotherapy) preoperatively to minimize the tumor burden and improve the likelihood of complete surgical resection, making a previously inoperable tumor.
  • Adjuvant therapy: Administered following surgery or chemotherapy to improve local control of disease and reduce the risk of local disease recurrence.
  • Prophylaxis: Administered to high-risk areas to prevent future cancer development (such as prophylactic cranial irradiation to prevent brain metastasis secondary to small cell lung cancer).
  • Disease control: Limiting tumor growth to extend the symptom-free period as much as possible.
  • Palliation: Given to prevent or relieve distressing symptoms such as pain (bone metastasis) or shortness of breath (obstructing bronchial tumor), and for prevention of neurologic function (brain metastasis or spinal cord compression).
External Radiation: Teletherapy (external beam radiation) is the most common form of radiation treatment delivery. With this technique, the patient is exposed to radiation from a megavoltage treatment machine. Machines that used to deliver treatment may include the cobalt 60 machine, which emits gamma rays from a radioactive source, which produces neutrons or protons, linear accelerator, which generates ionizing radiation from electricity and can have multiple energies.
563Internal Radiation: Brachytherapy which means ‘close’. It consists of the implantation or insertion of radioactive materials directly into the tumor or in close proximity adjacent to the tumor (intracavitary or intraluminal). This allows for direct dose delivery to the target with minimal exposure to the surrounding health tissues. Brachytherapy is commonly used in combination with external radiation as a supplemental ‘boost’ treatment.
Sources of brachytherapy include temporary sealed sources such as iridium 192 and cesium 137 and permanent sealed sources such as iodine 125, gold 198, and palladium 103. These are supplied in the form of seeds or ribbons. With a temporary implant, the source maybe placed into a special catheter or metal tube that has been inserted into the tumor area. This method is commonly used for tumors of the head and neck cancer, lung and gynecologic malignancies.
 
New in Radiation Therapy
New ways of delivering radiation therapy are making it safer and more effective. Some of these methods are already being used, while others need more study before they can be approved for widespread use. And scientists around the world continue to look for better and different ways to use radiation to treat cancer. Here are just a few areas of current research interest:
  • Hyperthermia is the use of heat to treat cancer. Heat has been found to kill cancer cells, but when used alone it does not destroy enough cells to cure the cancer. Heat created by microwaves and ultrasound is being studied in combination with radiation and appears to improve the effect of the radiation.
  • Radiosensitizers are drugs that make cancer cells more sensitive to radiation. Some chemotherapy drugs already in use (such as 5-fluorouracil or 5-FU) are known to be radiosensitizers.
  • Radioprotectors are substances that protect normal cells from radiation. These types of drugs are useful in areas where it is hard not to expose vital normal tissues to radiation when treating a tumor, such as the head and neck area. Some radioprotectors, such as amifostine (Ethyol), are already in use, while others are being studied in clinical trials.
 
Side Effects of Radiation Therapy
  • Radiodermatitis: Radiation may cause an acute or chronic inflammatory condition of the skin. The first symptom, erythema, may appear a few days after administration of a sufficient single dose or days later after administration of repeated small doses. When the injury is severe, the patient experiences pain and itching. Areas of necrosis develop, and subcutaneous and deeper tissues are involved. If hairy surfaces are involved, permanent baldness may result.
  • Cancer of the skin: Exposure to X-ray and radium has induced cancer of the skin in many research workers in the specialty, especially in the early or pioneer years when the need for protection for workers was not known.
  • Growth retardation and bone lesions: The growing fetus may be injured by radiation of the mother's pelvis, especially during the early months of pregnancy. Serious deformity of the skeletal and nervous systems of the unborn child.
  • Gastrointestinal response to radiation induced damage: Particularly where RT is directed at any patient of the gastrointestinal tract, it may have marked effects on an individual's ability to ingest, digest or absorb nutrients.
  • 564Radiation cystitis.
  • Urethritis
  • Permanent infertility in child bearing age.
 
Nursing Management
  • Anxiety related to prescribed radiation therapy and insufficient knowledge of treatments and self-care measures.
    • Encouage the client to share fears and beliefs regarding radiation. Delay teaching if the client is experiencing severe anxiety.
    • Review general principles of RT as necessary. Provide written materials such as client education booklets.
    • Reinforce the treatment plan covering the following items–area to be administered, marking and tattoos, shielding of vital organs.
    • Explain the fatigue that accompanies RT.
    • Explain skin reactions and precautions.
    • Encourage family to share concerns.
  • High-risk for altered oral mucous membrane related to dry mouth or inadequate oral hygiene or radiation tooth decay.
    • Explain the signs and symptoms of mucositis and stomatitis.
    • Stress the need to have caries filled and bad or loose teeth extracted before initiation of RT to head and neck.
    • Emphasize the need for regular oral hygiene during and after therapy.
    • Brush with fluoridated toothpaste after meals.
    • Use a soft toothbrush.
    • Rinse mouth with topical fluoride solutions after brushing.
    • Encourage oral fluid intake, moistening lips.
    • Avoid commercial mouth washes, very spicy or hot drinks, alcoholic beverages, tobacco, highly seasoned food and acidic foods like oranges, grapes and tomatoes.
    • Offer topical relief of pain with lidocaine ointment or ice chips.
    • Explain the need for dental examinations during and after the course of treatment.
  • Impaired skin integrity related to effects of radiation on the epithelial and basal cells:
    • Explain the effects of radiation of skin (redness, tanning, peeling, and itching, hairless, decreased perspiration) and monitor skin in the irradiated areas.
    • For alopecia: Help patient plan for a wig or scraf or hat before hair loss. Have patient gently wash and gently comb remaining hair, reassure that hair will grow back after therapy.
    • For dermatitis: Observe irradiated area daily, teach them not to wash the treated area until therapist tells. Avoid hard soap, ointments, creams, cosmetics and deodrants on treated skin unless approved by therapist.
    • For moist desquamation: Shower or irradiate the area frequently, use moist wound healing dressing. Avoid the use of adhesive tapes, assist patient with bathing to maintain marking, have patient avoid excessive heat, sunlight, tightly restrictive 565clothing and soap. Provide skin care to special skin folds such as buttocks, perinum, groin, and axilla.
    • Use an electric razor only-no blades: to shave the irradiate area.
    • Instruct the client to report any skin changes promptly.
    • After the skin properly healed, teach precautions in sun.
      • Use a sunscreen lotion.
      • Increase exposure time very slowly.
      • Discontinue sun exposure if redness occurs.
      • Protect treated skin with hats, etc.
  • Altered comfort related to stimulation of vomiting center and damage to the GIT mucosa cells secondary to radiation.
    • Promote a positive attitude about radiotherapy and reinforce its killing effects.
    • Explain the possible reasons of nausea and vomiting.
    • Encourage to have small, frequent meals.
    • Instruct to avoid hot/cold liquids, high fat, high fiber diet, spicy food and caffeine.
    • Teach stress reduction techniques like relaxation techniques and guided imagery.
  • Impaired mobility related to fatigue and altered motor function.
    • Plan frequent rest periods.
    • Avoid injury.
    • Use assistive devices for ambulation as required.
    • Assess reflexes, tactile sensation, and movement in extremities and report abnormal findings.
    • Observe for Lhermittes's sign (sensation of electric shock-running down back and over extremities), which shows cervical cord compression.
  • Altered nutrition, less than body requirements related to decreased oral intake, reduced salivation, dysphagia, nausea and vomiting, increase BUN and diarrhea.
    • Help the client identify reasons for inadequate nutrition and explain possible causes.
    • Stress the need to increase calorie intake.
    • Encourage resting before meals.
    • Offer small frequent meals.
    • Maintain good oral hygiene before and after meals.
    • Instruct the client to avoid high fatty and oily foods.
    • Consider clients likes and dislikes pertaining food intake.
  • Grieving related to changes in lifestyle, role, finances, functional capacity, body image and health losses.
    • Provide opportunity to ventilate feelings, discuss loss openly.
    • Encourage to use positive coping strategies.
    • Encourage to express feeling to worth.
    • Promote grief at each stage.
    • 566Maintain safe and secure environment.
    • Explore reasons for and meaning of fears.
    • Reduce environmental stimuli and provide safe environment.
  • Altered family process related to imposed changes in family roles, responsibilities, and relationship.
    • Convey an understanding of the situation and its impact on the family.
    • Explore the family's perception of the situation.
    • Try to promote family bonding by involving family in client's care, encouraging humor, encouraging humor.
    • Prepare the family members for signs of stress, depression, anxiety, anger and dependency in the client.
    • Encourage family to call on its social network for emotional and other support.
    • Direct to community agencies and other sources of assistance as needed.
 
SURGICAL THERAPY
Surgical removal of the entire cancer remains the ideal and most frequently used treatment method. Surgical treatment is used in oncology nursing for diagnosis of disease, reconstruction, prevention of disease, type and extent of the disease, etc.
  • Primary treatment: It involves removal of a malignant tumor and a margin of adjacent normal tissue. Main goal of primary treatment is to reduce the total body tumor burden.
  • Adjuvant treatment: It is also called debulking. It is the removal of large portion of tumor and remaining cancer cells are destroyed by other systemic treatments.
  • Salvage treatment: It involve the use of an extensive surgical approach to treat local recurrence after a less extensive approach has been implemented, e.g. mastectomy after lumpectomy and radiation therapy.
  • Palliative treatment: It is used to minimize disease or cancer related symptoms without trying to surgically cure the cancer. The goal of palliative treatment is to just relieve the symptoms and make the patient more comfortable.
  • Combination treatment: In this surgery is combined with other treatment modalities to improve the treatment outcome. Example includes preoperative and postoperative chemotherapy, radiation therapy.
 
Surgical Techniques
Several techniques are used in the treatment of cancer. It include as follows
  • Electrosurgery: In this type of surgery cancer cells are destroyed by high frequency electrical current applied by electrodes, needle, etc. It is used in cancer of skin, oral cavity, etc.
  • Cryosurgery: Cryosurgery technique is used for destruction of cancer cells by producing temperature below 166.2 °F (200 °C). It causes freezing in cells, as freezing continues, cells membranes rupture. Carbondioxide, nitrous oxide and Freon are the three common gases used as freezing agents in cryosurgery.
  • 567Lasers: In this technique laser light is used for destruction. In this process, photons are emitted which causes various interactions in tissues or cells which include photocoagulation, vaporization, photochemical reactions and ablation.
  • Photodynamic therapy: It involves intravenous injection of a photosensitizing drug, followed by exposure to a laser light within 24 to 48 hours of injection which results in fluorescence of cancer cells and cell death.
 
Nursing Management
  • Disturbed body image related to surgical procedure
  • Ineffective family coping related to diagnosis of cancer
  • Ineffective individual coping related to diagnosis of cancer
  • Risk of fluid volume deficit related to extensive surgery
  • Risk for infection related to immunocompromised status from disease condition
  • Knowledge deficit related to areas of self-care activities.
 
Preoperative Care
  • Reducing anxiety
  • Enhancing physical well-being
  • Health education.
 
Postoperative Care
 
Palliative Therapy
Palliative care is care given to improve the quality of life of patients who have a serious or life-threatening disease, such as cancer. The goal of palliative care is to prevent or treat, as early as possible, the symptoms and side effects of the disease and its treatment, in addition to the related psychological, social, and spiritual problems. The goal is not to cure. Palliative care is also called comfort care, supportive care, and symptom management.
Palliative care is given throughout a patient's experience with cancer. It should begin at diagnosis and continue through treatment, follow-up care, and the end of life. Any medical professional may provide palliative care by addressing the side effects and emotional issues of cancer; some have a particular focus on this type of care. A palliative care specialist is a health professional who specializes in treating the symptoms, side effects, and emotional problems experienced by patients. The goal is to maintain the best possible quality of life.
Often, palliative care specialists work as part of a multidisciplinary team to coordinate care. This palliative care team may consist of doctors, nurses, registered dieticians, pharmacists, and social workers. Palliative care specialists may also make recommendations to primary care physicians about the management of pain and other symptoms. People do not give up their primary care physician to receive palliative care.
Palliative care can address a broad range of issues, integrating an individual's specific needs into care. The physical and emotional effects of cancer and its treatment may be very different from person to person. For example, differences in age, cultural background, or support systems may result in very different palliative care needs.
568Comprehensive palliative care will take the following issues into account for each patient:
  • Physical: Common physical symptoms include pain, fatigue, loss of appetite, nausea, vomiting, shortness of breath, and insomnia. Many of these can be relieved with medicines or by using other methods, such as nutrition therapy, physical therapy, or deep breathing techniques. Also, chemotherapy, radiation therapy, or surgery maybe used to shrink tumors that are causing pain and other problems.
  • Emotional and coping: Palliative care specialists can provide resources to help patients and families deal with the emotions that come with a cancer diagnosis and cancer treatment. Depression, anxiety, and fear are only a few of the concerns that can be addressed through palliative care. Experts may provide counseling, recommend support groups, hold family meetings, or make referrals to mental health professionals.
  • Practical: Cancer patients may have financial and legal worries, insurance questions, employment concerns, and concerns about completing advance directives. For many patients and families, the technical language and specific details of laws and forms are hard to understand. To ease the burden, the palliative care team may assist in coordinating the appropriate services. For example, the team may direct patients and families to resources that can help with financial counseling, understanding medical forms or legal advice, or identifying local and national resources, such as transportation or housing agencies.
  • Spiritual: With a cancer diagnosis, patients and families often look more deeply for meaning in their lives. Some find the disease brings them more faith, whereas others question their faith as they struggle to understand why cancer happened to them. An expert in palliative care can help people explore their beliefs and values so that they can find a sense of peace or reach a point of acceptance that is appropriate for their situation.
 
COLORECTAL CANCER
Definition: Colorectal cancer, commonly known as colon cancer or bowel cancer, is a cancer from uncontrolled cell growth in the colon or rectum (parts of the large intestine), or in the appendix. Colorectal Cancer refers to the malignancies of colon and rectum.
 
Cause
  • High intake of fat
  • Alcohol
  • Red meat
  • Obesity
  • Smoking
  • Lack of physical exercise
  • Older age
  • Male gender
  • Family history of colorectal cancer and polyps
  • Presence of polyps in the large intestine
  • 569Inflammatory bowel diseases
  • Chronic ulcerative colitis.
 
Stages of Colorectal Cancer
Colon and rectal cancer are staged according to how far they have spread through the walls of the colon and rectum and whether they have spread to other parts of the body.
 
Staging Colon Cancer
Stage 0: Stage 0 cancer of the colon is very early cancer. The cancer is found only in the innermost lining of the colon.
Stage I: The cancer has spread beyond the innermost lining of the colon to the second and third layers and involves the inside wall of the colon. The cancer has not spread to the outer wall of the colon or outside the colon.
Stage II: The tumor extends through the muscular wall of the colon, but there is no cancer in the lymph nodes (small structures that are found throughout the body that produce and store cells that fight infection).
Stage III: The cancer has spread outside the colon to one or more lymph nodes (small structures that are found throughout the body that produce and store cells that fight infection).
Stage IV: The cancer has spread outside the colon to other parts of the body, such as the liver or the lungs. The tumor can be any size and may or may not include affected lymph nodes (small structures that are found throughout the body that produce and store cells that fight infection).
 
Staging Rectal Cancer
Rectal cancer is staged much the same way as colon cancer, but because the tumor is much lower down in the colon, the treatment options may vary.
Stage 0: In stage 0 rectal cancer, the tumor is located only on the inner lining of the rectum. To treat this early stage cancer, surgery can be performed to remove the tumor or a small section of the rectum where the cancer is located can be removed.
Stage I: This is an early form or limited form of cancer. The tumor has broken through the inner lining of the rectum but has not made it past the muscular wall.
Stage II: This cancer is a little more advanced. The tumor has penetrated all the way through the bowel wall and may have invaded other organs, such as the bladder, uterus, or prostate gland.
Stage III: The tumor has spread to the lymph nodes (small structures that are found throughout the body that produce and store cells that fight infection).
Stage IV: The tumor has spread to distant parts of the body (metastasized). The tumor can be any size and sometimes is not that large. The liver and lung are two favoured places for rectal cancer to spread.
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Pathophysiology
 
Signs and Symptoms
The symptoms and signs of colorectal cancer depend on the location of tumor in the bowel, and whether it has spread elsewhere in the body (metastasis). The classic warning signs include:
  • 571Worsening constipation
  • Blood in the stool
  • Weight loss, fever
  • Loss of appetite
  • Nausea and vomiting in someone over 50 years old
  • Rectal bleeding
  • Anemia
  • Weight loss
  • Change in bowel habits.
 
Diagnostic Tests
  • Stool test for colon cancer: Finding colon cancer early is key to beating it. That is why doctors recommend a yearly fecal occult blood test, which tests for invisible blood in the stool, an early sign of colon cancer.
  • Fecal occult blood test: Fecal occult blood is tested for the presence of microscopic or invisible blood in the stool, or feces. Fecal occult blood can be a sign of a problem in digestive system, such as a growth, or polyp, or cancer in the colon or rectum. If microscopic blood is detected, it is important for doctor to determine the source of bleeding to properly diagnose and treat the problem.
What Causes Blood to Appear in Stool?
Blood may appear in the stool because of one or more of the following conditions:
  • Benign (noncancerous) or malignant (cancerous) growths or polyps of the colon
  • Hemorrhoids (swollen blood vessels near the anus and lower rectum that can rupture causing bleeding)
  • Anal fissures (splits or cracks in the lining of the anal opening)
  • Intestinal infections that cause inflammation
  • Ulcers
  • Ulcerative colitis
  • Crohn's disease
  • Diverticular disease, caused by outpouchings of the colon wall
  • Abnormalities of the blood vessels in the large intestine
  • Colonoscopy for colon cancer: One of the best tools for detecting colon cancer is a colonoscopy. Colonoscopy is an outpatient procedure during which large bowel (colon and rectum) is examined from the inside. Colonoscopies are usually used to evaluate symptoms like abdominal pain, rectal bleeding, or changes in bowel habits. They are also used to screen for colorectal cancer.
 
How is a Colonoscopy Performed?
The procedure is performed by a doctor experienced in colonoscopy and lasts approximately 30 to 60 minutes. Medications will be given into vein to make patient feel relaxed and drowsy. Patient will be asked to lie on his/her left side on the examining table. During a colonoscopy, the doctor uses a colonoscope, a long, flexible, tubular instrument about 1/2 inch in diameter that transmits an image of the lining of the colon so the doctor can examine it for any abnormalities. The colonoscope is inserted through the rectum and advanced to the other end of the large intestine.
572The scope bends, so the doctor can move it around the curves of his/her colon. Patient may be asked to change position occasionally to help the doctor move the scope. The scope also blows air into the colon, which expands the colon and helps to visualize better.
Patient may feel mild cramping during the procedure. Patient can reduce the cramping by taking several slow, deep breaths during the procedure. When the doctor has finished, the colonoscope is slowly withdrawn while the lining of bowel is carefully examined.
  • Sigmoidoscopy for colorectal cancer screening: Sigmoidoscopy enables the physician to look at the inside of the large intestine from the rectum through the last part of the colon, called the sigmoid colon.
  • CT scan and MRI for colon cancer
  • Genetic testing for colon cancer
 
Medical Management
 
Chemotherapy
Chemotherapy uses drugs to destroy cancer cells. Chemotherapy can be used to destroy cancer cells after surgery, to control tumor growth or to relieve symptoms of colon cancer.
 
Radiation therapy
Radiation therapy uses powerful energy sources, such as X-rays, to kill any cancer cells that might remain after surgery, to shrink large tumors before an operation so that they can be removed more easily, or to relieve symptoms of colon cancer and rectal cancer. Radiation therapy is rarely used in early-stage colon cancer, but is a routine part of treating rectal cancer, especially if the cancer has penetrated through the wall of the rectum or travelled to nearby lymph nodes. Radiation therapy, usually combined with chemotherapy, may be used after surgery to reduce the risk that the cancer may recur in the area of the rectum where it began.
 
Targeted Drug Therapy
Drugs that target specific defects that allow cancer cells to proliferate are available to people with advanced colon cancer, including bevacizumab (Avastin), cetuximab (Erbitux) and panitumumab (Vectibix). Targeted drugs can be given along with chemotherapy or alone. Targeted drugs are typically reserved for people with advanced colon cancer.
 
Alternative Treatment
Alternative treatments may help you cope with a diagnosis of colon cancer. Nearly all people with cancer experience some distress. Common signs and symptoms of distress after diagnosis might include sadness, anger, difficulty concentrating, difficulty sleeping and loss of appetite. Alternative treatments may help redirect thoughts away from your fears, at least temporarily, to give some relief.
Alternative treatments that may help relieve distress include:
  • Art therapy
  • Dance or movement therapy
  • Exercise
  • Meditation
  • Music therapy
  • Relaxation exercises.
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SURGERY FOR COLORECTAL CANCER
The types of surgery used to treat colon and rectal cancers are slightly different, so they are described separately.
  • Open colectomy: A colectomy (sometimes called a hemicolectomy, partial colectomy, or segmental resection) removes part of the colon, as well as nearby lymph nodes. The surgery is referred to as an open colectomy if it is done through a single incision in the abdomen.
    The day before surgery, patient will most likely be told to completely empty his/her bowel. This is done with a bowel preparation, which may consist of laxatives and enemas. Just before the surgery, patient will be given general anesthesia, which puts patient into a deep sleep.
    During the surgery, surgeon will make an incision in his/her abdomen and remove the part of the colon with the cancer and a small segment of normal colon on either side of the cancer. Usually, about one-fourth to one-third of colon is removed, but more or less may be removed depending on the exact size and location of the cancer. The remaining sections of colon are then reattached. Nearby lymph nodes are removed at this time as well. Most experts feel that taking out as many nearby lymph nodes as possible is important, but at least 12 should be removed.
    When patient wake-up after surgery, patient will have some pain and probably will need pain medicines for 2 or 3 days. For the first couple of days, patient will be given intravenous (IV) fluids. During this time patient may not be able to eat or patient may be allowed limited liquids, as the colon needs sometime to recover. But a colon resection rarely causes any major problems with digestive functions, and patient should be able to eat solid food again in a few days.
    It is important that patient are as healthy as possible for this type of major surgery, but in some cases an operation may be needed right away. If the tumor is large and has blocked the colon, it may be possible for the doctor to use a colonoscope to put a stent (a hollow metal or plastic tube) inside the colon to keep it open and relieve the blockage for a short time and help prepare for surgery a few days later.
    Fig. 11.1: Open colectomy
  • 574Laparoscopic-assisted colectomy: This newer approach to removing part of the colon and nearby lymph nodes may be an option for some earlier stage cancers. Instead of making one long incision in the abdomen, the surgeon makes several smaller incisions. Special long instruments are inserted through these incisions to remove part of the colon and lymph nodes. One of the instruments, called a laparoscope, has a small video camera on the end, which allows the surgeon to see inside the abdomen. Once the diseased part of the colon has been freed, one of the incisions is made larger to allow for its removal. This type of operation requires the same type of preparation before surgery and the same type of anesthesia during surgery as an open colectomy. Because the incisions are smaller than with an open colectomy, patients may recover slightly faster and have less pain than they do after standard colon surgery.
  • Polypectomy and local excision: Some early colon cancers (stage 0 and some early stage I tumors) or polyps can be removed by surgery through a colonoscope. When this is done, the surgeon does not have to cut into the abdomen. For a polypectomy, the cancer is removed as part of the polyp, which is cut at its stalk (the area that resembles the stem of a mushroom). Local excision removes superficial cancers and a small amount of nearby tissue.
 
Rectal Surgery
Surgery is usually the main treatment for rectal cancer, although radiation and chemotherapy will often be given before or after surgery. Several surgical methods can be used for removing or destroying rectal cancers.
  • Polypectomy and local excision: These procedures, described in the colon surgery section, can be used to remove superficial cancers or polyps. They are done with instruments inserted through the anus, without making a surgical opening in the skin of the abdomen.
  • Local transanal resection (full thickness resection): As with polypectomy and local excision, local transanal resection (also known as transanal excision) is done with instruments inserted through the anus, without making an opening in the skin of the abdomen. This operation cuts through all layers of the rectum to remove cancer as well as some surrounding normal rectal tissue, and then closes the hole in the rectal wall. This procedure can be used to remove some stage I rectal cancers that are relatively small and not too far from the anus. It is usually done with local anesthesia (numbing medicine) patient is not asleep during the operation.
  • Transanal endoscopic microsurgery (TEM): This operation can sometimes be used for stage I cancers that are higher in the rectum than could be reached using the standard transanal resection. A specially designed magnifying scope is inserted through the anus and into the rectum, allowing the surgeon to do a transanal resection with great precision and accuracy. This operation is only done at certain centers, as it requires special equipment and surgeons with special training and experience.
  • Low anterior resection: Some stage I rectal cancers and most stage II or III cancers in the upper third of the rectum (close to where it connects with the colon) can be removed by low anterior resection. In this operation, the part of the rectum containing the tumor is removed without affecting the anus. The colon is then attached to the remaining part of the rectum so that after the surgery, patient will move his/her bowels in the usual way.
  • 575Proctectomy with coloanal anastomosis: Some stage I and most stage II and III rectal cancers in the middle and lower third of the rectum require removing the entire rectum (proctectomy). The colon is then connected to the anus (coloanal anastomosis). The rectum has to be removed to do a total mesorectal excision (TME), which is required to remove all of the lymph nodes near the rectum. This is a harder procedure to do, but modern techniques have made it possible. Sometimes when a coloanal anastomosis is done, a small pouch is made by doubling back a short segment of colon (colonic J-pouch) or by enlarging a segment (coloplasty). This small reservoir of colon then functions as a storage space for fecal matter like the rectum did before surgery.
  • Abdominoperineal (AP) resection: This operation is more involved than a low anterior resection. It can be used to treat some stage I cancers and many stage II or III rectal cancers in the lower third of the rectum (the part nearest to the anus), especially if the cancer is growing into the sphincter muscle (the muscle that keeps the anus closed and prevents stool leakage). Here, the surgeon makes one incision in the abdomen, and another in the perineal area around the anus. This incision allows the surgeon to remove the anus and the tissues surrounding it, including the sphincter muscle. Because the anus is removed, patient will need a permanent colostomy to allow stool a path out of the body.
  • Pelvic exenteration: If the rectal cancer is growing into nearby organs, a pelvic exenteration may be recommended. This is an extensive operation. Not only will the surgeon remove the rectum, but also nearby organs such as the bladder, prostate (in men), or uterus (in women) if the cancer has spread to these organs. Patient will need a colostomy after pelvic exenteration. If the bladder is removed, patient will also need a urostomy (opening where urine exits the front of the abdomen and is held in a portable pouch).
 
Side Effects of Colorectal Surgery
Potential side effects of surgery depend on several factors, including the extent of the operation and a person's general health before surgery. Most people will have at least some pain after the operation, but it usually can be controlled with medicines if needed. Eating problems usually resolve within a few days of surgery.
Other problems may include bleeding from the surgery, blood clots in the legs, and damage to nearby organs during the operation. Rarely, the new connections between the ends of the intestine may not hold together completely and may leak, which can lead to infection. It is also possible that the abdominal incision might open up, becoming an open wound. After the surgery, patient might develop scar tissue in the abdomen that can cause organs or tissues to stick together. These are called adhesions. In some cases, adhesions can block the bowel, requiring further surgery.
  • Colostomy or ileostomy: Some people may need a temporary or permanent colostomy (or ileostomy) after surgery. This may take some time to get used to and may require some lifestyle adjustments. If patient have a colostomy or ileostomy, patient will need help learning how to manage it. Specially trained ostomy nurses or enterostomal therapists can do this. They will usually see patient in the hospital before his/her operation to discuss the ostomy and to mark a site for the opening. After the operation they may come to his/her house or an outpatient setting to give patient more training.
  • 576Sexual function and fertility after colorectal surgery: If patient are a man, an AP resection may stop his/her erections or ability to reach orgasm. In other cases, the pleasure at orgasm may become less intense. Normal aging may cause some of these changes, but they may be made worse by the surgery.
 
Surgery and Other Local Treatments for Colorectal Cancer Metastases
Sometimes, surgery for cancer that has spread (metastasized) to other organs can help patient live longer or, depending on the extent of the disease, may even cure patient. If only a small number of metastases are present in the liver or lungs (and nowhere else), they can sometimes be removed by surgery. This will depend on their size, number, and location.
In some cases, if it is not possible to remove the tumors with surgery, nonsurgical treatments may be used to destroy (ablate) tumors in the liver. But these methods are less likely to be curative. Several different techniques may be used.
  • Radiofrequency ablation: Radiofrequency ablation (RFA) uses high-energy radio waves to kill tumors. A thin, needle-like probe is placed through the skin and into the tumor under CT or ultrasound guidance. An electric current is then run through the tip of the probe, releasing high-frequency radio waves that heat the tumor and destroy the cancer cells.
  • Ethanol (alcohol) ablation: Also known as percutaneous ethanol injection (PEI), this procedure injects concentrated alcohol directly into the tumor to kill cancer cells. This is usually done through the skin using a needle, which is guided by ultrasound or CT scans.
  • Cryosurgery (cryotherapy): Cryosurgery destroys a tumor by freezing it with a metal probe. The probe is guided through the skin and into the tumor using ultrasound. Then very cold gasses are passed through the probe to freeze the tumor, killing the cancer cells. This method can treat larger tumors than either of the other ablation techniques, but it sometimes requires general anesthesia.
 
Nursing Assessment
  • Interview patient regarding dietary habits and family and medical history to identify risk factors.
  • Question the patient regarding symptoms of colorectal cancer, changes in bowel habits, rectal bleeding tarry stools, abdominal discomfort, weight loss, anemia, etc.
  • Palpate abdomen for tenderness and presence of mass.
  • Test stool for occult blood.
 
Nursing Diagnosis
  1. Chronic pain related to malignancy, inflammation and possible intestinal obstruction.
    Goal: Relieving pain.
    Intervention
    • Assess type and severity of pain
    • Administer prescribed analgesics
    • Evaluate effectiveness of analgesics
    • Use alternative therapies to relieve pain like relaxation therapy, etc.
  2. 577Imbalance nutrition less than body requirements related to malignancy effects and weight loss.
    Goal: Achieving adequate nutrition.
    Intervention
    • Serve high calorie, low-residue diet
    • Observe and record fluid losses
    • Maintain hydration through IV therapy
    • Check weight of patient.
  3. Constipation or diarrhea related to change in bowel lumen and disease process.
    Goal: Relieving constipation and diarrhea.
    Intervention
    • Monitor amount, consistency, frequency and color of stool
    • For constipation use laxatives or enema as needed and encourage exercise and adequate fluids and fibers
    • For diarrhea encourage adequate fluid intake to prevent fluid volume deficit and electrolyte imbalance
    • Administer antidiarrheal drugs to treat diarrhea related to radiation and chemotherapy.
  4. Fatigue related to anemia, radiation and chemotherapy.
    Goal: Maintain energy level.
    Interventions
    • Assess the patient's ability to perform activities.
    • Make an activity plan to reduce workload.
    • Allow frequent rest periods to regain energy.
    • Administer blood products to combat anemia.
  5. Risk for complications related to metastatic nature of disease.
    Goal: Prevent complications.
    Interventions
    • Check for signs of complications such as acute pain in any other organ, breathing difficulty, etc.
    • Educate patient for MRI or CT Scan of chest, liver, etc.
    • Check the lab values of CEA.
    • Educate for follow-up care.
  6. High-risk for infection related to colostomy.
    Goal: prevent infections.
    Interventions
    • Check vital signs especially temperature.
    • Check stoma for appearance and discharge.
    • 578Provide stoma care.
    • Change and clear the pouch at proper timings.
 
ESOPHAGEAL CANCER
Esophageal cancer is malignancy of the esophagus. Esophageal tumors usually lead to dysphagia (difficulty swallowing), pain and other symptoms. Small and localized tumors are treated surgically with curative intent. Larger tumors tend not to be operable and hence are treated with palliative care; their growth can still be delayed with chemotherapy, radiotherapy or a combination of the two. In some cases chemo- and radiotherapy can render these larger tumors operable. Prognosis depends on the extent of the disease and other medical problems, but is generally fairly poor.
 
Definition
Cancer that forms in tissues lining the esophagus. Two types of esophageal cancer are squamous cell carcinoma (cancer that begins in flat cells lining the esophagus) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids).
 
Causes and risk factors
  • Smoking
  • Heavy drinking
  • Damage from acid reflux.
 
Acid Reflux Raises Risk
This sphincter also prevents stomach contents from refluxing back into the esophagus. If stomach juices with acid and bile come into the esophagus, it causes indigestion or heartburn. e.g. reflux and gastroesophageal reflux disease (GERD).
  • A medical history of other head and neck cancers increases the chance of developing a second cancer in the head and neck area, including esophageal cancer.
  • Plummer–Vinson syndrome (anemia and esophageal webbing)
  • Radiation therapy
  • Celiac disease predisposes towards squamous cell carcinoma
  • Obesity
  • Thermal injury as a result of drinking hot beverages.
 
Esophageal Cancer Types
  • Adenocarcinoma is the most common type especially in white males. It starts in gland cells in the tissue, most often in the lower part of the esophagus near the stomach. The major risk factors include reflux and Barrett's esophagus.
  • Squamous cell carcinoma or cancer, also called epidermoid carcinoma, begins in the tissue that lines the esophagus, particularly in the middle and upper parts. Risk factors include smoking and drinking alcohol.
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Stages of Cancer
Stage 0 (Carcinoma in Situ): In stage 0, abnormal cells are found in the innermost layer of tissue lining the esophagus. These abnormal cells may become cancer and spread into nearby normal tissue. Stage 0 is also called carcinoma in situ.
Stage I: In stage I, cancer has formed and spread beyond the innermost layer of tissue to the next layer of tissue in the wall of the esophagus.
Stage II: Stage II esophageal cancer is divided into stage IIA and stage IIB, depending on where the cancer has spread.
Stage IIA: Cancer has spread to the layer of esophageal muscle or to the outer wall of the esophagus.
Stage IIB: Cancer may have spread to any of the first three layers of the esophagus and to nearby lymph nodes.
Stage III: In stage III, cancer has spread to the outer wall of the esophagus and may have spread to tissues or lymph nodes near the esophagus.
Stage IV: Stage IV esophageal cancer is divided into stage IVA and stage IVB, depending on where the cancer has spread.
Stage IVA: Cancer has spread to nearby or distant lymph nodes.
Stage IVB: Cancer has spread to distant lymph nodes in other parts of the body.
 
Signs and Symptoms
  • Dysphagia
  • Odynophagia (painful swallowing)
  • Pain behind the sternum or in the epigastrium, often of a burning, heartburn.
  • Hoarse-sounding cough, a result of the tumor affecting the recurrent laryngeal nerve.
  • Nausea and vomiting, regurgitation of food, coughing.
  • Cough, fever.
  • If the disease has spread elsewhere, this may lead to symptoms related to this: liver metastasis could cause jaundice and ascites, lung metastasis could cause shortness of breath, pleural effusions, etc.
  • Hemoptysis.
 
Diagnostic Evaluation
  • Esophagoscopy: A procedure to look inside the esophagus to check for abnormal areas. An esophagoscope is inserted through the mouth or nose and down the throat into the esophagus. An esophagoscope is a thin, tube-like instrument with a light and a lens for viewing.
  • Endoscopic ultrasound (EUS): A procedure in which an endoscope is inserted into the body, usually through the mouth or rectum. A probe at the end of the endoscope is used to bounce high-energy sound waves off internal tissues or organs and make echoes. The echoes form a picture of body tissues called a sonogram. This procedure is also called endosonography
  • CT with contrast
  • 580Esophagogastroduodenoscopy (EGD, endoscopy): This involves the passing of a flexible tube down the esophagus and examining the wall.
  • Biopsies taken of suspicious lesions are then examined histologically for signs of malignancy.
  • PET scan (Positron emission tomography scan): A procedure to find malignant tumor cells in the body. A small amount of radionuclide glucose (sugar) is injected into a vein. The PET scanner rotates around the body and makes a picture of where glucose is being used in the body. Malignant tumor cells show up brighter in the picture because they are more active and take-up more glucose than normal cells do.
  • Barium swallow: A series of X-rays of the esophagus and stomach. The patient drinks a liquid that contains barium (a silver-white metallic compound). The liquid coats the esophagus and stomach, and X-rays are taken. This procedure is also called an upper GI series.
 
Management
 
Esophageal Stent
If the patient cannot swallow at all, an esophageal stent may be inserted to keep the esophagus patent;stents may also assist in occluding fistulas.
  • Laser therapy is the use of high-intensity light to destroy tumor cells; it affects only the treated area. This is typically done if the cancer cannot be removed by surgery. The relief of a blockage can help to reduce dysphagia and pain.
  • Photodynamic therapy: A type of laser therapy, involves the use of drugs that are absorbed by cancer cells. When exposed to a special light, the drugs become active and destroy the cancer cells.
  • Chemotherapy
  • Radiotherapy is given before, during or after chemotherapy or surgery.
 
Surgical Management
 
Esophagectomy
Surgery to remove some or most of the esophagus is called an esophagectomy. Often a small part of the stomach is removed as well. The upper part of the esophagus is then connected to the remaining part of the stomach. Part of the stomach is pulled up into the chest or neck to become the new esophagus. It may be done by two approaches:
  • Open esophagectomy: Many different approaches can be used in operating on esophageal cancer. For atransthoracic esophagectomy, the esophagus is removed with the main incisions in the abdomen and the chest. If the main incisions are in the abdomen and neck, it is called a transhiatal esophagectomy. Some approaches use incisions in the neck, chest, and abdomen.
  • Minimally invasive esophagectomy: For some early cancers, the esophagus can be removed through several small incisions instead of 1 or 2 large incisions. The surgeon puts a scope (like a tiny telescope) through one of the incisions to see everything during the operation.
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Fig. 11.2: Esophagogastroduodenoscopy
Fig. 11.3: Esophageal stenting
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Nursing Management
  • Altered nutrition less than body requirement difficulty in swallowing secondary to disease condition.
  • Pain related to disease condition or surgery.
  • Anxiety related to disease condition, its treatment and prognosis.
  • Knowledge deficit related to treatment and prognosis.
  1. Altered nutrition less than body requirement difficulty in swallowing secondary to disease condition.
    Interventions
    • Assess the level of daily nutrition.
    • Assess the likes and dislikes of the patients.
    • Provide small and frequent diet to the patient.
    • If needed provide the food through nesogastric tube.
    • Maintain intake output chart.
  2. Pain related to disease condition or surgery
    Interventions
    • Assess the level of pain.
    • Provide comfortable position to the patient.
    • Provide diversional therapy to the patient.
    • Administed analgesic as per the doctor's order.
  3. Anxiety related to disease condition, its treatment and prognosis
    Interventions
    • Assess the level of anxiety.
    • Diversional therapy provided to the patient.
    • Omfortable environment provided to the patient.
    • Answer each question of the patient.
    • Administer antianxiety drug as order by the doctor.
  4. Knowledge deficit related to treatment and prognosis.
    Interventions
    • Assess the level of knowledge related to disease condition.
    • Answer each question of the patient.
    • Clarify all doubts of the patient.
    • Give information regarding the disease and its treatment.
 
GASTRIC CANCER
Introduction: Gastric cancer was once the second most common cancer in the world. In most developed countries, however, rates of stomach cancer have declined dramatically over the past half century. Men have higher incidence of gastric cancer than women. Most of these deaths occur in people older than 40 years of age.
583Gastric cancer: Tumors in the stomach can be benign or malignant. Gastric cancer is a disease in which tumors are found in the stomach. Stomach cancer is common throughout the world and affects all races, it is more common in men than women, and has its peak age range between 40 and 60 years old. If it is not diagnosed quickly, it may spread to other parts of your stomach as well as to other organs. There are twice as many males with this disease than females.
Stomach cancer usually begins in cells in the inner layer of the stomach. Overtime, the cancer may invade more deeply into the stomach wall. A stomach tumor can grow through the stomach's outer layer into nearby organs, such as the liver, pancreas, esophagus, or intestine.
Fig. 11.4: Gastric cancer
Causes/risk factors of gastric cancer:
  • Helicobacter pylori infection: H. Pylori is a bacterium that commonly infects the inner lining (the mucosa) of the stomach. Infection with H. Pylori can cause stomach inflammation and peptic ulcers.
  • Long-term inflammation of the stomach: People who have conditions associated with long-term stomach inflammation (such as the blood disease pernicious anemia) are at increased risk of stomach cancer.
  • Smoking: Smokers are more likely than nonsmokers to develop stomach cancer. Heavy smokers are most at risk.
  • Family history: Close relatives (parents, brothers, sisters, or children) of a person with a history of stomach cancer are somewhat more likely to develop the disease themselves. If many close relatives have a history of stomach cancer, the risk is even greater.
  • Obesity people who eat a diet high in foods that are smoked, salted, or pickled have an increased risk for stomach cancer.
  • A lack of physical activity may increase the risk of stomach cancer.
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Pathophysiology
 
Signs and Symptoms
Stomach cancer is often either asymptomatic or it may cause only nonspecific symptoms. By the time symptoms occur, the cancer has often reached an advanced stage and may have also metastasized. Stomach cancer can cause the following signs and symptoms:
 
Stage 1 (Early)
  • Indigestion or a burning sensation (heartburn)
  • Loss of appetite, especially for meat
  • Abdominal discomfort or irritation.
 
Stage 2 (Middle)
  • Weakness and fatigue
  • Bloating of the stomach, usually after meals.
 
Stage 3 (Late)
  • Abdominal pain in the upper abdomen
  • Nausea and occasional vomiting
  • Diarrhea or constipation
  • Weight loss
  • Bleeding (vomiting blood or having blood in the stool) which will appear as black. This can lead to anemia.
  • Dysphagia this feature suggests a tumor in the cardiac or extension of the gastric tumor into the esophagus.
 
Diagnosis
  • Physical examination: Abdomen for fluid, swelling, or other changes. Also will check for swollen lymph nodes.
  • 585Endoscopy: Uses a thin, lighted tube (endoscope) to look into your stomach.
  • Biopsy: An endoscope has a tool for removing tissue.
  • Computed tomography or CT scanning of the abdomen may reveal gastric cancer, but is more useful to determine invasion into adjacent tissues, or the presence of spread to local lymph nodes.
  • Gastroscopic examination: This involves insertion of a fiber optic camera into the stomach to visualize it.
Management: Treatment for stomach cancer may include surgery, chemotherapy, and radiation therapy.
Surgery: Surgery is the most common treatment. The surgeon removes part or all of the stomach, as well as the surrounding lymph nodes, with the basic goal of removing all cancer and a margin of normal tissue.
  • Endoscopic mucosal resection (EMR) is a treatment for early gastric cancer (tumor only involves the mucosa. In this procedure, the tumor, together with the inner lining of stomach (mucosa), is removed from the wall of the stomach using an electrical wire loop through the endoscope. The advantage is that it is a much smaller operation than removing the stomach.
  • Endoscopic submucosal dissection (ESD) is a similar technique used to resect a large area of mucosa in one piece. If the pathologic examination of the resected specimen shows incomplete resection or deep invasion by tumor, the patient would need a formal stomach resection.
  • Surgery to remove stomach cancer the types of operation have to remove stomach cancer will depend on which part of the stomach the cancer is in. If cancer is near the area where stomach joins food pipe (esophagus) may need part of food pipe removed as well.
  • Gastric bypass procedures (GBP) in this the stomach is devided into a small upper pouch and a much larger lower ‘remnant’ pouch and then re-arranges the small intestine to connect to both.
  • Radiation therapy is the use of high-energy rays to damage cancer cells and stop them from growing. When used, it is generally in combination with surgery and chemotherapy, or used only with chemotherapy in cases where the individual is unable to undergo surgery.
 
Complications of Abdominal Surgery
  • Infection: Infection of the incisions or of the inside of the abdomen (peritonitis, abscess) may occur due to release of bacteria from the bowel during the operation.
  • Venous thromboembolism: Any injury, such as a surgical operation, causes the body to increase the coagulation of the blood.
  • Hemorrhage: Many blood vessels must be cut in order to divide the stomach and to move the bowel. Any of these may later begin bleeding, either into the abdomen (intra-abdominal hemorrhage), or into the bowel itself (gastrointestinal hemorrhage).
  • Hernia: A hernia is an abnormal opening, either within the abdomen or through the abdominal wall muscles. An internal hernia may result from surgery and re-arrangement of the bowel, and is a cause of bowel obstruction.
  • Bowel obstruction: Abdominal surgery always results in some scarring of the bowel, called adhesions. A hernia, either internal or through the abdominal wall, may also result.
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Preoperative Management
  • Preoperative assessment: The patient's preoperative physiological status is a major factor in determining outcome after major surgery. Although scoring systems including a variety of parameters have been evaluated, the previous medical history and concurrent morbidity remain the strongest predictors.
  • Past medical history: A detailed medical history and physical examination is a prerequisite to the assessment of any anesthetic and operative risk. Cardiorespiratory disease has been identified as the commonest coexisting disease in patients presenting for esophagectomy. Pre-existing ischemic heart disease, poorly controlled hypertension, and pulmonary dysfunction are all associated with increased operative morbidity, particularly in the elderly and following upper abdominal and thoracic surgery. The efficacy of any medication prescribed for cardiorespiratory conditions should be evaluated at an early stage.
  • Social habits: Smoking is a significant etiological factor in preoperative morbidity. All patients must be encouraged to stop smoking preoperatively.
  • Preoperative investigations: The minimum preoperative investigations for all patients undergoing gastric or esophageal surgery should include baseline hematological and biochemical profiles, arterial blood gases on air, pulmonary functions tests, a resting electrocardiogram, and a chest X-ray.
  • Nutritional status: Obesity is associated with increased operative risk.
 
Psychological Preparation
All patients should be counselled about treatment options, paying particular attention to the results and limitations of surgery. A clear description of the preoperative period should be given. An assessment of pretreatment symptoms on quality of life of the patient should be carefully undertaken as there is accumulating evidence of quality of life scores having an independent effect on outcome.
 
Thromboembolic Prophylaxis
Appropriate measures should be taken against the risk of Thromboembolic complications. Antithromboembolic stockings, low molecular weight heparin, and preoperative calf compression should be employed.
  • Antibiotic prophylaxis: Broad spectrum antibiotic prophylaxis should be administered preoperatively.
  • Blood cross match: Four units of blood should be cross matched prior to surgery. Transfusion however should be avoided if at all possible as the immunological suppressive effect can adversely affect survival.
 
Postoperative Management
  • Meticulous attention to the maintenance of fluid balance and respiratory care are essential in the immediate postoperative period.
  • Pain control
  • Pulmonary physiotherapy
  • Early mobilization is important in the prevention of venous thrombosis and pulmonary embolism.
  • 587Promote pulmonary ventilation.
  • Provide adequate analgesic during ist few days.
  • Encourage ambulation
  • Promote nutrition and family education
  • Add food in small amount at frequent interval until well tolerated
  • Monitor weight regularly.
 
Stomach Cancer (Gastric) Prevention
Gastric cancer can sometimes be associated with known risk factors for the disease. Many risk factors are modifiable though not all can be avoided.
  • Dietand lifestyle: Excessive salt intake has been identified as a possible risk factor for gastric cancer. Having a high intake of fresh fruits and vegetables may be associated with a decreased risk of gastric cancer. Studies have suggested that eating foods that contain beta-carotene and vitamin C may decrease the risk of gastric cancer, especially if intake of micronutrients is inadequate.
  • Pre-existing conditions: Infection with a certain bacteria, Helicobacter pylori, is associated with an increased risk of gastric cancer. Long-standing reflux of gastric contents and the development of an abnormal cellular lining is also associated with an increased risk of cancer at the junction of the stomach and esophagus.
  • Cancer-fighting foods
  • Citrus fruits: It is no secret that oranges, tangerines and clementines bring us vitamin C; they are among the richest sources of this critical vitamin.
 
Nursing Management
Nursing assessment: Careful selection of the varying therapeutic modalities is essential. Such selection should consider not only the nature of the symptoms to be relieved but also the general medical and psychological status of the patient. Decisions should be taken in the context of the predicted prognosis and the effect of any treatment intervention on quality of life.
 
Nursing Diagnosis
 
Preoperative
  • Acute pain related to the growth of cancer cells
  • Anxiety related to plan surgery
  • Imbalanced nutrition less than body requirements related to nausea, vomiting and no appetite
  • Activity intolerance related to physical weakness.
 
Postoperative
  • Ineffective breathing pattern related to the influence of anesthesia.
  • Acute pain related to interruption of the body secondary to invasive procedures or surgical intervention.
  • Imbalanced nutrition less than body requirements related to fasting status.
  • Risk for infection related to an increased susceptibility secondary to the procedure.
588Intervention
  • Encourage the patient to eat small and frequent portions of nonirritating foods to decrease gastric irritation
  • Food supplements should be high in calories as well as vitamin A and C and iron to enhance tissue repair
  • The nurse administers analgesic as prescribed
  • A continuous infusion of an opioid may be necessary for severe pain
  • The nurse help the patient express fears, concern grief and diagnosis
  • Encourage the patient to participate in treatment decisions.
 
LIVER CANCER
Definition: Liver cancer or hepatic cancer is a cancer that originates in the liver. Liver cancers are malignant tumors that grow on the surface or inside the liver.
 
Classification
  • Primary liver cancer: It can be benign and malignant
    Origin
    Benign
    Malignant
    Hepatocytes
    Adenoma
    Hepatocellular carcinoma
    Connective tissues
    Fibroma
    Sarcoma
    Blood vessels
    Hemangioma
    Hemangioendothelioma
    Bile ducts
    Cholangioma
    Carcinoma
  • Secondary (metastatic) liver cancer
    Secondary (metastatic) cancer reaches the liver by spreading through the blood system from a primary tumor at a separate site.
  • Mixed tumors: rarer forms of liver cancer include:
    • Mesenchymal tissue
    • Sarcoma
    • Hepatoblastoma, a rare malignant tumor, primarily developing in children. Most of these tumors form in the right lobe.
    • Cholangiocarcinoma
    • Angiosarcomaand hemangiosarcoma
    • Lymphoma of liver.
 
Etiology and Risk Factors
  • Younger population mainly females
  • Chronic liver disease: Cirrhosis, HBV and HCV
  • Chemical toxins such as vinyl chloride
  • Carcinogens in herbal medicines
  • Mycotoxins like aflatoxins
  • Oral contraceptives
  • Metastasis.
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Signs and Symptoms of Primary Liver Cancer
 
Cholangiocarcinoma
  • Sweating
  • Jaundice
  • Abdominal pain
  • Weight loss
  • Hepatomegaly
 
Hepatocellular Carcinoma
  • Abdominal mass
  • Abdominal pain
  • Emesis
  • Anemia
  • Back pain
  • Jaundice
  • Itching
  • Weight loss
 
Signs and Symptoms of Secondary Liver Cancer
  • Tiredness
  • Loss of appetite
  • Nausea
  • A dragging sensation or heaviness felt up under the lower ribs on the right-hand side of the body
  • Pain in the upper part of the belly, particularly on bending forwards.
 
Diagnostic Tests
  • Physical examination and history: The first symptom is usually pain in the right side. Weight loss is common and sometimes patients have episodes of severe pain, fever, and nausea. Rapidly deteriorating health, weakness, swelling, and jaundice.
  • Blood tests: Most useful is AFP (alpha-fetoprotein). AFP is a protein produced by the liver, and an elevated level can indicate tumor growth, though some patients with liver cancer have normal AFP levels.
  • CEA (carcinoembryonic antigen) test.
  • Diagnostic imaging: Ultrasound scan, CT and MRI scans are required-liver imaging may include a four-phase computed tomography (CT), including spiral CT scans obtained during hepatic arterial and portal venous phases following intravenous contrast administration, or magnetic resonance imaging (MRI). These techniques can accurately demonstrate the number of primary tumors within the liver and their relationship to vascular structures.
  • Image-guided biopsy.
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Management
The correct treatment of liver cancer can mean the difference between life and death. Not all patients with cancers in the liver are potentially curable. These are some of the treatments available: surgery, chemotherapy, immunotherapy, photodynamic therapy, hyperthermia, radiation therapy and radiosurgery.
 
Hepatocellular Carcinoma
  • Partial hepatectomy to resect the entire tumor
  • Liver transplantation
  • Cryoablation
  • Chemoembolization
  • Radiotherapy
  • Sorafenib
  • Radiofrequency ablation.
 
Cholangiocarcinoma
  • Photodynamic therapy
  • Brachytherapy
  • Radiotherapy
  • Liver transplantation.
 
Hepatoblastoma
  • Chemotherapy, including vincristine, cyclophosphamide, and doxorubicin
  • Radiotherapy
  • Liver transplantation
  • Surgical resection.
 
PHOTODYNAMIC THERAPY (PDT)
It is a form of phototherapy using nontoxic light-sensitive compounds that are exposed selectively to light, whereupon they become toxic to targeted malignant and other diseased cells. It is used clinically to treat a wide range of medical conditions, including wet age-related macular degeneration and malignant cancers, and is recognized as a treatment strategy which is both minimally invasive and minimally toxic.
 
Transarterial Therapy
Patients with HCC and cirrhosis are frequently treated with transarterial therapy, a technique that delivers treatments directly into the liver. To gain access to the liver, physicians first make a small incision in the patient's leg and then place a long catheter into the femoral artery. Guided by fluoroscopy, the physician then moves the catheter up through the blood vessels to the hepatic artery, one of two blood vessels that feed the liver. These procedures are usually performed in a hospital's radiology suite, and patients remain conscious but sedated throughout the procedures.
591Types of transarterial therapy include:
  • Transarterial chemoembolization (TACE) with lipiodol: Transarterial chemoembolization (TACE) involves delivery of chemotherapy directly to the liver, followed by a process to ‘lock in’ (embolize) the chemotherapy. In this therapy, Lipiodol—a thick, oily sustance— is mixed with chemotherapy (platinol, mitomycin-c, and adriamycin) and injected under radiological guidance directly into the artery supplying the tumor. The Lipiodol acts to contain the chemotherapy within the tumor and blocks further blood flow to the tumor. Blocking the flow of blood to the cancer helps to kill the cancer cells, as it cuts off the tumor's food and oxygen supply.
  • Transarterial chemoembolization (TACE) with Doxorubicin-filled Beads: Doxorubicin is a chemotherapeutic agent that helps stop the growth of tumor cells. In this therapy, doxorubicin-filled beads are delivered directly to the liver, which releases chemotherapy slowly overtime and also blocks the blood flow to the tumor. With doxorubicin-filled beads, the delivery of chemotherapy-filled beads prolongs the dwell time of the chemotherapeutic agent and enhances drug delivery to liver tumors.
  • Radioactive yttrium beads: This therapy uses radioactive yttrium beads delivered via a catheter into the hepatic artery. The beads precisely deliver radiation to the tumor, which kills the tumor cells. The beads are quite small and do not occlude the blood flow, which allows access to the tumor again if further treatment is needed. This therapy can be used in larger tumors than the above therapies, and may also be used if the portal vein is occluded since the arterial flow to the liver is not occluded.
 
Surgical Interventions for Liver Cancer
 
Surgical Resection (Tumor Removal)
If patients can withstand surgery and have sufficient liver function, resection offers an excellent five-year survival rate of more than 50%. Liver cancer can recur after resection, and close surveillance is required. Surgical resection involves the removal of one or more sections of the liver in which a tumor(s) exists. Typically, surgeons can remove up to 70% of a cancerous liver (if there is no or mild fibrosis) and it will regenerate in about two to six weeks following surgery. Unfortunately, less than 10% of patients are candidates for liver resection.
Liver Transplantation
While a liver transplant represents an excellent cure for most patients with HCC, the limited organ supply makes this option unattainable for some. Patients who may benefit from liver transplantation include those with small, unresectable HCC and cirrhosis.
 
Nursing Management
 
For Nonoperative Patients
Assessment: Assess client for:
  • Metabolic malfunctions
  • Pain
  • Bleeding problems
  • Ascites
  • 592Edema
  • Hypoproteinemia
  • Jaundice
  • Endocrine complications
  • Complications of chemotherapy.
 
Common Interventions
  • Take time to prepare client in the diagnostic stage for various procedures.
  • Intervene post procedure complications.
  • Administer analgesics for pain as per prescription.
  • Assist client and family to gain knowledge about the conditions and to offer necessary support to cope with the condition.
 
Nursing Diagnosis
Activity intolerance related to anemia from poor nutrition and bleeding.
Goal: Conservation of energy.
  • Alternate rest and activity.
  • Assist in ADL.
  • Monitor Hb and hematocrit levels.
  • Administer blood transfusion and iron supplements if prescribed.
Imbalanced Nutrition: Less than body requirement related to impaired liver functions.
Goal: Maintain nutritional status.
  • Weigh daily.
  • Monitor nutritional intake.
  • Provide oral hygiene before meals.
  • Provide small and frequent diet.
  • Serve meal in attractive manner considering likes and dislikes of client.
Risk for complications related to chemotherapy.
Goal: Prevent or minimize complications.
  • Monitor for ulcers in mouth, alopecia, photophobia, etc.
  • Weigh daily.
  • Provide oral hygiene.
  • Advice to wear sunglasses when going out.
  • Check for the signs of bleeding.
  • Give psychological support and clear doubts of the client.
    • Acute pain related to tumor
    • Imbalanced fluid and electrolytes related to bleeding and ascites.
 
Nursing Management for Client Undergone Surgery
 
Preoperative Care
  • Do complete physical and psychological assessment.
  • Conduct varies laboratory tests.
  • 593Match donor and recipient blood and tissues reports.
  • Assess clients health needs.
 
Preoperative Care
  • Monitor for signs of rejection, infection and occlusion of blood vessels.
  • Administer prescribed immunosuppressive drugs.
  • Monitor vital signs: Respiration, cardiovascular, neurological and hemodynamic status also.
  • Assess reports of liver function tests.
  • Monitor fluid and electrolyte status.
  • Monitor wound drains and bile drains for patency.
  • Note bile characteristics: Amount, color, consistency.
  • Assess the needs of family.
BIBLIOGRAPHY
  1. Black M. A Textbook of medical surgical nursing, Elsevier.  Noida.  8th ed.
  1. Brunner S. A Textbook of medical surgical nursing, Lippincott Company.  Philadelphia.  5th. ed. 1982.
WEBSITE REFERENCES
  1. Astin M, Griffin T, Neal RD, Rose P, Hamilton W. The diagnostic value of symptoms for colorectal cancer in primary care: a systematic review». The British journal of general practice: the journal of the Royal College of General Practitioners 2011 may;61(586):231–43.
  1. Cancer Genome Atlas Network. ‘Comprehensive molecular characterization of human colon and rectal cancer’. Nature 2012 July 19;487:330–7.
  1. Colorectal Cancer Incidence, Mortality and Prevalence Worldwide in 2008 — Summary.
  1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. (2010) GLOBOCAN 2008 v2.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 10 [Internet]. International Agency for Research on Cancer.  Lyon,  France: Accessed on 11 Oct 2012.
  1. Yamada A. Associate editors, Alpers HD..., et al. (2008). Principles of clinical gastroenterology. Wiley-Blackwell.  Chichester,  West Sussex: 381.

Emergency and Disaster Nursing12

 
DISASTER
  • A disaster can be defined as any occurrence that cause damage, ecological disruption, loss of human life, deterioration of health and health services on a scale sufficient to warrant as extraordinary response from outside the affected community or area.
    – WHO
  • 595An occurrence of a severity and magnitude that normally results in death, injuries and property damage that cannot be managed through the routine procedure and resources of government.
    – Federal Emergency Management Agency
  • A disaster can be defined as an occurrence either nature or manmade that causes human suffering and creates human needs that victims cannot alleviate without assistance.
    – American Red Cross
  • Disaster is the occurrence of a sudden or major misfortune which disrupts the basic fabric and normal functioning of a society or community.
    – United Nations
 
Disaster Nursing
Disaster nursing can be defined as the adaptation of professional nursing skills in recognizing and meeting the nursing physical and emotional needs resulting from a disaster. The overall goal of disaster nursing is to achieve the best possible level of health for the people and the community involved in the disaster.
‘Disaster nursing is nursing practiced in a situation where professional supplies, equipment, physical facilities and utilities are limited or not available’.
DISASTER' alphabetically means:
D—Destructions
I—Incidents
S—Sufferings
A—Administrative, financial failures
S—Sentiments
T—Tragedies
E—Eruption of communicable diseases
R—Research programme and its implementation.
 
Types of Disaster
  • Natural: These are primarily natural events. It is possible that certain human activities could maybe aid in some of these events, but, by and large, these are mostly natural events.
    • Earthquakes
    • Volcanoes
    • Floods
    • Tornado, typhoons, cyclones.
  • Man-made: These are mostly caused due to certain human activities. The disasters themselves could be unintentional, but, are caused due to some intentional activity. Most of these are due to certain accidents which could have been prevented, if sufficient precautionary measures were put in place.
    • Nuclear leaks
    • Chemical leaks/Spill over
    • Terrorist activities
    • Structural collapse
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Principles of Disaster Nursing
  • Make most efficient use of hand, brain, energy and time
  • Make sure that every moment should be counted
  • Expect the unexpected
  • Be economical in use of supply
  • Apply 3 cardinal rules: Assess respiration, stop hemorrhage and care of shock
  • Follow the principal of save the life, preserve the function and provide comfort
  • Speed in the disaster is important but do not be hasty
  • Those who care for themselves but not for others should be removed from the group.
 
Factors Affecting Disaster
 
Host Factors
In the epidemiological frame work as applied to disaster the host is human-kind. Host factors are those characteristics of humans that influence the severity of the disaster effect. Host factors include
  • Age
  • Immunization status
  • Degree of mobility
  • Emotional stability
 
Environmental Factors
  • Physical factors: Weather conditions, the availability of food, time when the disaster occurs, the availability of water and the functioning of utilities such as electricity and telephone service.
  • Chemical factors: Influencing disaster outcome include leakage of stored chemicals into the air, soil, ground water or food supplies, e.g. Bhopal Gas Tragedy.
  • Biological factors: Are those that occur or increase as result of contaminated water, improper waste disposal, insect or rodent proliferations improper food storage or lack of refrigeration due to interrupted electrical services. Bioterrorism: Release of viruses, bacteria or other agents caused illness or death.
  • Social factors: Are those that contribute to the individual social support systems. Loss of family members, changes in roles and the questioning of religious beliefs are social factors to be examined after a disaster.
  • Psychological factors: Psychological factors are closely related to agents, host and environmental conditions. The nature and severity of the disaster affect the psychological distress experienced by the victims.
 
Phases of Disaster
  • Preimpact: Occurs prior to the onset of the disaster. Includes the period of threat and warning.
  • Impact phase: Period of time when disaster occurs, continuing to immediately following disaster. It involves Inventory and rescues period, Assessment of extent of losses, 597Identification of remaining sources, Planning for Use of resource, Rescue of victims, Minimizing further injuries and property damage. May be brief when disasters strike suddenly and is over in minutes (air plane clash, building collapse) or lengthy as incident continues (earthquake, flood, tsunami, etc.).
  • Post impact phase: Occurs when majority of rescue operations are completed. It involves, Remedy and recovery period, Honeymoon phase-feeling of euphoria, appearances of little effect by disaster, Disillusionment phase-feeling of anger, disappointment and resentment. Reconstruction phase-acceptance of loss, copping with stereo, rebuilding.
  • Rehabilitation: The final phase in a disaster should lead to restoration of the pre-disaster conditions. The pattern of healthy needs with change rapidly, moving from casualty treatment to more primary health care.
 
DISASTER CYCLE AND MANAGEMENT
There are three fundamental aspects of disaster management:
  • Disaster response
  • Disaster preparedness and
  • Disaster mitigation.
These three aspects of disaster management correspond to different phases in the so called ‘disaster cycle’
  • Disaster impact
  • Mitigation
  • Preparedness
  • Reconstruction
  • Rehabilitation
  • Response
  • Risk reduction phase before a disaster
  • Recovery phase after a disaster.
598The following table briefly describes each of these phases
The four phases of emergency management
Mitigation
Preventing future emergencies or minimizing their effects
  • Includes any activities that prevent an emergency, reduce the chance of an emergency happening, or reduce the damaging effects of unavoidable emergencies.
  • Buying flood and fire insurance for home is a mitigation activity.
  • Mitigation activities take place before and after emergencies.
Preparedness
Preparing to handle an emergency
  • Includes plans or preparations made to save lives and to help response and rescue operations.
  • Evacuation plans and stocking food and water are both examples of preparedness.
  • Preparedness activities take place before an emergency occurs.
Response
Responding safely to an emergency
  • Includes actions taken to save lives and prevent further property damage in an emergency situation. Response is putting preparedness plans into action.
  • Seeking shelter from a tornado or turning off gas valves in an earthquake are both response activities.
  • Response activities take place during an emergency.
Recovery
Recovering from an emergency
  • Includes actions taken to return to a normal or an even safer situation following an emergency.
  • Recovery includes getting financial assistance to help pay for the repairs.
  • Recovery activities take place after an emergency.
Mitigation
This phase includes any activities that prevent an emergency, reduce the likelihood of occurrence, or reduce the damaging effects of unavoidable hazards. Mitigation activities should be considered long before an emergency. For example, to mitigate fire in home, follow safety standards in selecting building materials, wiring, and appliances. But, an accident involving fire could happen. To protect yourself and animals from the costly burden of rebuilding after a fire, one should buy fire insurance. These actions reduce the danger and damaging effects of fire.
Preparedness
This phase includes developing plans for what to do, where to go, or who to call for help before an event occurs, actions that will improve chances of successfully dealing with an emergency. For instance, posting emergency telephone numbers, holding disaster drills, and installing smoke detectors are all preparedness measures. Other examples include identifying where you would be able to shelter your animals in a disaster. You should also consider preparing a disaster kit with essential supplies for your family and animals.
Response
Your safety and well-being in an emergency depend on how prepared you are and on how you respond to a crisis. By being able to act responsibly and safely, you will be able to protect yourself, your family, others around you and your animals. Taking cover and holding tight in an earthquake, moving to the basement with your pets in a tornado, and safely leading horses away from a wildfire are examples of safe response. These actions can save lives.
Recovery
After an emergency and once the immediate danger is over, your continued safety and well-being will depend on your ability to cope with rearranging your life and environment. During the recovery period, you must take care of yourself and your animals to prevent stress-related illnesses and excessive financial burdens. During recovery, you should also consider things to do that would lessen the effects of future disasters.
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Responsibilities of Various Agencies in Emergency and Disaster Management
Emergency management works when local, State and Federal government fulfill emergency management responsibilities. Voluntary organizations also have important responsibilities during disasters.
Personal responsibilities
Animals owners have the ultimate responsibility for their animals. Community disaster preparedness plans try to incorporate the care of animals and their owners in their plans, but plans can only coordinate care they cannot always provide it. The best way to be prepared is to create a personal emergency plan that includes provisions to care for animals. You can learn how to prepare such a plan from your local Red Cross office, local emergency management agency and numerous other groups. Be prepared to deal with the four phases of most emergencies.
Local government responsibilities
Local governments make plans and provide resources to protect their citizens from the hazards that threaten their communities. This is done through mitigation activities, preparedness plans, response to emergencies, and recovery operations. Wherever you live within the United States, a county or municipal agency has been designated as local emergency management agency.
The local government level is the most important at which to develop emergency management plans because local governments serve as the link between you and the State and Federal agencies in the emergency management network. It includes following responsibilities:
  • Identifying hazards and assessing their potential risk to the community.
  • Determining the community's capability to mitigate against, prepare for, respond to, and recover from major emergencies.
  • Identifying and employing methods to improve the community's emergency management capability through efficient use of resources, improved coordination, and cooperation with other communities and with the State and Federal governments.
  • Establishing mitigation measures such as building codes, zoning ordinances, or land-use management programs.
  • Developing and coordinating preparedness plans.
  • Establishing warning systems.
  • Stocking emergency supplies and equipment.
  • Educating the public and training emergency personnel.
  • Assessing damage caused by the emergency.
  • Activating response plans and rescue operations.
  • Ensuring that shelter and medical assistance are provided.
  • Recovering from the emergency and helping citizens return to normal life as soon as possible.
State government responsibilities
The State emergency management office is responsible for protecting communities and citizens within the State. The State office carries out statewide emergency management activities, helps coordinate emergency management activities involving more than one community, or assists individual communities when they need help. If any community lacks the resources needed to protect itself or to recover from a disaster, the State may help with money, personnel, or other resources.
Federal government responsibilities
At the Federal Level of Government, the Federal Emergency Management Agency (FEMA) is involved in mitigation, preparedness, response, and recovery activities. FEMA helps the States in several ways. FEMA provides the following programs:
  • Training programs and research information on the latest mitigation measures.
  • Review and coordination of State emergency plans.
  • Financial assistance.
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  • Flood insurance to individuals and businesses in communities that join the National Flood Insurance Program (NFIP).
  • Subsidies to State and local offices of emergency management for maintaining emergency management programs.
  • Guidance and coordination for plans to warn and protect the nation in national security emergencies and
  • Coordination of services for disaster response and recovery activities.
Voluntary agencies and organizations
One of the most important voluntary organizations in terms of disasters is the Red Cross Society. The Red Cross provides relief to victims of disasters. Each local agency is responsible for providing disaster relief services in the community. In large-scale disasters, volunteers from across the country may respond. The Red Cross provides individuals and families with food, shelter, first aid, clothing, bedding, medicines and other services.
Emergency management works when Local, State and Federal government fulfill emergency management responsibilities. Voluntary organizations also have important responsibilities during disasters.
Personal responsibilities
Animals owners have the ultimate responsibility for their animals. Community disaster preparedness plans try to incorporate the care of animals and their owners in their plans, but plans can only coordinate care they cannot always provide it. The best way to be prepared is to create a personal emergency plan that includes provisions to care for animals. You can learn how to prepare such a plan from your local Red Cross office, local emergency management agency and numerous other groups. Be prepared to deal with the four phases of most emergencies.
Local government responsibilities
Local governments make plans and provide resources to protect their citizens from the hazards that threaten their communities. This is done through mitigation activities, preparedness plans, response to emergencies, and recovery operations. Wherever you live within the United States, a county or municipal agency has been designated as local emergency management agency.
The local government level is the most important at which to develop emergency management plans because local governments serve as the link between you and the State and Federal agencies in the emergency management network. It includes following responsibilities:
  • Identifying hazards and assessing their potential risk to the community.
  • Determining the community's capability to mitigate against, prepare for, respond to, and recover from major emergencies.
  • Identifying and employing methods to improve the community's emergency management capability through efficient use of resources, improved coordination, and cooperation with other communities and with the State and Federal governments.
  • Establishing mitigation measures such as building codes, zoning ordinances, or land-use management programs.
  • Developing and coordinating preparedness plans.
  • Establishing warning systems.
  • Stocking emergency supplies and equipment.
  • Educating the public and training emergency personnel.
  • Assessing damage caused by the emergency.
  • Activating response plans and rescue operations.
  • Ensuring that shelter and medical assistance are provided.
  • Recovering from the emergency and helping citizens return to normal life as soon as possible.
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State government responsibilities
The State emergency management office is responsible for protecting communities and citizens within the State. The State office carries out statewide emergency management activities, helps coordinate emergency management activities involving more than one community, or assists individual communities when they need help. If any community lacks the resources needed to protect itself or to recover from a disaster, the State may help with money, personnel, or other resources.
Federal government responsibilities
At the Federal level of government, the Federal Emergency Management Agency (FEMA) is involved in mitigation, preparedness, response, and recovery activities. FEMA helps the States in several ways. FEMA provides the following programs:
  • Training programs and research information on the latest mitigation measures.
  • Review and coordination of State emergency plans.
  • Financial assistance.
  • Flood insurance to individuals and businesses in communities that join the National Flood Insurance Program (NFIP).
  • Subsidies to State and local offices of emergency management for maintaining emergency management programs.
  • Guidance and coordination for plans to warn and protect the nation in national security emergencies and
  • Coordination of services for disaster response and recovery activities.
Voluntary agencies and organizations
One of the most important voluntary organizations in terms of disasters is the Red Cross society. The Red Cross provides relief to victims of disasters. Each local agency is responsible for providing disaster relief services in the community. In large-scale disasters, volunteers from across the country may respond. The Red Cross provides individuals and families with food, shelter, first aid, clothing, bedding, medicines and other services.
 
Nursing Responsibilities During Disaster
The nursing management of mass casualties can be divided into search and rescue, first aid, triage and stabilization of victims, hospital treatment and redistribution of patients to other hospitals if necessary.
  1. Search, rescue and first aid: After a major disaster, the need for search, rescue and first aid is likely to be so great that organized relief services will be able to meet only a small fraction of the demand. Most immediate help comes from the uninjured survivors.
  2. Field care: Most injured persons converge spontaneously to health facilities, using whatever transport is available, regardless of the facilities, operating status. Providing proper care to casualties requires that the health service resources be redirected to this new priority. Bed availability and surgical services should be maximized. Provisions should be made for food and shelter. A centre should be established to respond to inquiries from patient's relatives and friends. Priority should be given to victim's identification and adequate mortuary space should be provided.
  3. Triage: When the quantity and severity of injuries overwhelm the operative capacity of health facilities, a different approach to medical treatment must be adopted. The principle of ‘first come, first treated’, is not followed in mass emergencies. Triage consists of rapidly classifying the injured on the basis of the severity of their injuries and the likelihood of their survival with prompt medical intervention. It must be adopted to locally available skills. Higher priority is granted to victims whose immediate or long-term prognosis can be dramatically affected by simple intensive care. Patients who require a great deal of attention, with questionable benefit, have the lowest priority. 602Triage is the only approach that can provide maximum benefit to the greatest number of injured in a major disaster situation.
    Although different triage systems have been adopted and are still in use in some countries, the most common classification uses the internationally accepted four color code system. Red indicates high priority treatment or transfer, yellow signals medium priority, green indicates ambulatory patients and black for dead patients.
    Triage should be carried out at the site of disaster, in order to determine transportation priority, and admission to the hospital or treatment center, where the patient's needs and priority of medical care will be reassessed. Ideally, local health workers should be taught the principles of triage as part of disaster training.
    Persons with minor or moderate injuries should be treated at their own homes to avoid social dislocation and the added drain on resources of transporting them to central facilities. The seriously injured should be transported to hospitals with specialized treatment facilities.
  4. Tagging: All patients should be identified with tags stating their name, age, place of origin, triage category, diagnosis, and initial treatment.
  5. Identification of dead: Taking care of the dead is an essential part of the disaster management. A large number of dead can also impede the efficiency of the rescue activities at the site of the disaster. Care of the dead includes:
    • Removal of the dead from the disaster scene
    • Shifting to the mortuary
    • Identification
    • Reception of bereaved relatives. Proper respect for the dead is of great importance.
  6. Relief phase: This phase begins when assistance from outside starts to reach the disaster area. The type and quantity of humanitarian relief supplies are usually determined by two main factors:
    • The type of disaster and
    • The type and quantity of supplies available locally.
    Immediately following a disaster, the most critical health supplies are those needed for treating casualties, and preventing the spread of communicable diseases. Following the initial emergency phase, needed supplies will include food, blankets, clothing, shelter, sanitary engineering equipment and construction material. A rapid damage assessment must be carried out in order to identify needs and resources. Disaster managers must be prepared to receive large quantities of donations. There are four principal components in managing humanitarian supplies: (a) acquisition of supplies (b) transportation (c) storage and (d) distribution.
  7. Epidemiologic surveillance and disease control: Disasters can increase the transmission of communicable diseases through following mechanisms:
    • Overcrowding and poor sanitation in temporary resettlements. This accounts in part, for the reported increase in acute respiratory infections etc.
    • Population displacement may lead to introduction of communicable diseases to which either the migrant or indigenous populations are susceptible.
    • Disruption and the contamination of water supply, damage to sewerage system and power systems are common in natural disasters.
    • 603Disruption of routine control programmes as funds and personnel are usually diverted to relief work.
    • Ecological changes may favour breeding of vectors and increase the vector population density.
    • Displacement of domestic and wild animals, who carry with them zoonoses that can be transmitted to humans as well as to other animals. Leptospirosis cases have been reported following large floods (as in Orissa, India, after super cyclone in 1999). Anthrax has been reported occasionally.
    • Provision of emergency food, water and shelter in disaster situation from different or new source may itself be a source of infectious disease.
    The principals of preventing and controlling communicable diseases after a disaster are to:
    • Implement as soon as possible all public health measures, to reduce the risk of disease transmission
    • Organize a reliable disease reporting system to identify outbreaks and to promptly initiate control measures
    • Investigate all reports of disease outbreaks rapidly
  8. Vaccination: Health authorities are often under considerable public and political pressure to begin mass vaccination programmes, usually against typhoid, cholera and tetanus.
    • The WHO does not recommend typhoid and cholera vaccines in routine use in endemic areas. The newer typhoid and cholera vaccines have increased efficacy, but because they are multidose vaccines, compliance is likely to be poor.
    • Significant increases in tetanus incidence have not occurred after natural disasters. Mass vaccination of population against tetanus is usually unnecessary. The best protection is maintenance of a high level of immunity in the general population by routine vaccination before the disaster occurs, and adequate wound cleaning and treatment.
    • If tetanus immunization was received more than 5 years ago in a patient who has sustained an open wound, a tetanus toxoid booster is an effective preventive measure.
    • If cold-chain facilities are inadequate, they should be requested at the same time as vaccines.
  9. Nutrition: Natural disaster may affect the nutritional status of the population by affecting one or more components of food chain depending on the type, duration and extent of the disaster, as well as the food and nutritional conditions existing in the area before the catastrophe. Infants, children, pregnant women, nursing mothers and sick persons are more prone to nutritional problems after prolonged drought or after certain types of disasters like hurricanes, floods, land or mudslides, volcanic eruptions and sea surges involving damage to crops, to stocks or to food distribution systems.
    The immediate steps for ensuring that the food relief programme will be effective include:
    • Assessing the food supplies after the disaster
    • Gauging the nutritional needs of the affected population
    • Calculating daily food rations and need for large population groups and
    • Monitoring the nutritional status of the affected population.
  10. Rehabilitation: The final phase in a disaster should lead to restoration of the predisaster conditions. Rehabilitation starts from the very first moment of a disaster. A provision 604by external agencies of sophisticated medical care for a temporary period has negative effects. On the withdrawal of such care, the population is left with a new level of expectation which simply cannot be fulfilled.
    In first weeks after disaster, the pattern of health needs will change rapidly, moving from casualty treatment to more routine primary health care. Services should be reorganized and restructured. Priorities also will shift from health care towards environmental health measures.
  11. Water supply: A survey of all public water supplies should be made. This includes distribution system and water source. It is essential to determine physical integrity of system components, the remaining capacities, and bacteriological and chemical quality of water supplied.
    The main public safety aspect of water quality is microbial contamination. The first priority of ensuring water quality in emergency situations is chlorination. It is the best way of disinfecting water. It is advisable to increase residual chlorine level to about 0.2-0.5 mg/litre. Low water pressure increases the risk of infiltration of pollutants into water mains. Repaired mains, reservoirs and other units require cleaning and disinfection.
    The existing and new water sources require the following protection measures:
    • Restrict access to people and animals, if possible, erect a fence and appoint a guard
    • Ensure adequate excreta disposal at a safe distance from water source
    • Prohibit bathing, washing and animal husbandry, upstream of intake points in rivers and streams
    • Upgrade wells to ensure that they are protected from contamination and
    • Estimate the maximum yield of wells and if necessary. In many emergency situations, water has to be trucked to disaster site or camps. All water tankers should be inspected to determine fitness, and should be cleaned and disinfected before transporting water.
  12. Food safety: Poor hygiene is the major cause of food-borne diseases in disaster situations. Where feeding programmes are used (as in shelters or camps) kitchen sanitation is of utmost importance. Personal hygiene should be monitored in individuals involved in food preparation.
  13. Basic sanitation and personal hygiene: Many communicable diseases are spread through fecal contamination of drinking water and food. Hence, every effort should be made to ensure the sanitary disposal of excreta. Emergency latrines should be made available to the displaced, where toilet facilities have been destroyed. Washing, cleaning and bathing facilities should be provided to the displaced persons.
  14. Vector control: Control programme for vectorborne diseases should be intensified in the emergency and rehabilitation period, especially in areas where such diseases are known to be endemic. Of special concern are dengue fever and malaria, Leptospirosis and rat bite fever, typhus, and plague. Flood water provides ample breeding opportunities for mosquitoes.
 
POST-TRAUMATIC STRESS DISORDER AND REHABILITATION OF DISASTER VICTIMS
PTSD is a set of reactions to an extreme stressor such as intense fear, helplessness, or horror that leads individuals to relieve the trauma.
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Signs and Symptoms
  • Episodes of repeated relieving of the trauma in intensive memories ‘(flashbacks)’ or dreams
  • Flashbacks occurring—against the persisting background of a sense of ‘numbers’ and emotional blunting
  • Detachment from other people
  • Unresponsiveness to surroundings
  • Anhedonia can inability to experience pleasure
  • Avoidance of activities and situations reminiscent of the trauma
  • Fear and avoidance of cues that remind the sufferer of the original trauma
  • May be dramatic, acute bursts of fear, panic or aggression, triggered by stimuli arousing a sudden recollection and re-enactment of the trauma or of the original reaction to it.
 
Predisposing Factors
  • Personality traits—compulsive, asthenic
  • History of neurotic illness childhood abuse, who then suffer subsequent trauma.
 
Etiology
  • Military combat
  • Bombing or war
  • Kidnapping
  • Robbery
  • Abuse—Physical, sexual (e.g. rape) or psychological
  • Terrorist attack
  • Prisoner of war
  • Torture
  • Natural or man-made disasters
  • Witnessing violence (domestic, criminal)
  • Severe automobile accidents
  • Seeing dead body or body parts
  • Serious injury or death of family member or a close friend
  • Diagnosis of life threatening disease in self or child
  • Unexpected death of family member or a close friend.
 
High-Risk Group
  • Children
  • Disabled
  • Elderly
  • Women-young, single, widowed, orphaned, disabled, have lost children
  • Orphans from orphanages
  • Having history of childhood abuse.
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Principles of Nursing Care in PTSD
  • Consistent empathic approach to help the clients tolerate the intense memories and emotional pain
  • Simple reorienting, reassuring statements to prevent suicidal ideation
  • Trusting relationship to covey a sense of respect, acceptance of their distress and belief in the client's reactions
  • Reconnect the individuals with the existing support system
  • Restart activities that provide a sense of mastery
  • Promote independence and the client's highest level of functioning
  • Manager counter transference reactions
  • Group therapies to decrease isolation, to discuss the effect of trauma and develop alternative coping mechanisms
  • Encourage the client to write/verbalize to manage reactions and feelings
  • Help the client identify community resources
  • Teach anxiety management strategies like relaxation, breaking techniques and diverting the individuals mind through involvement inactivities
  • Changes in lifestyle such as following a healthy diet, avoiding stimulants, intoxicants, regular exercise and adequate sleep. Use medication as recommended.
 
REHABILITATION OF DISASTER VICTIMS
In the postdisaster period, along with relief, rehabilitation and the care of physical health and injuries, mental health issues need to be given importance. Apart from material and logistic help, the suffering human beings will require human interventions.
 
Challenges of Rehabilitation
  • Ensuring that people living in the relief camps have access to, Regular food supplies, Additional sets of clothes, Sanitation drinking water, Public health intervention immunization, preventive health care, Heat and rain proof shelters, Child care and education facilities and support.
  • Ensuring access to basic entitlements in terms of their compensation, government schemes and credit institutions so that they can rebuild their homes and livelihood back to the some levels as before the disaster.
  • Ensuring livelihood reintegration.
  • Ensuring legal right and social justice to the disaster victims including filing of FIRs, investigation and contesting cases in the court.
  • Providing psychosocial counseling and support for dealing with loss, betrayal and anger.
  • Community based rehabilitation for widows orphans, elderly, children and physically disabled.
  • Actively rebuilding a culture of communal harmony and trust.
 
Kinds of Reactions Shown by Disaster Victims
  • Physical impact: Stomach aches, diarrohoea, headaches, and body aches, physical impairments (limbs, sight, voice, hearing), injuries, fever, cough, cold, miscarriage, etc.
  • 607Emotional reactions: Anger, betrayal, irritability, revenge-seeking, fear, anxiety, depression, withdrawal, grief, addiction to pan masala, cigarette, beedi, drug abuse (flask backs, numbness, depression).
  • Socioeconomic impact: Loss of trust between communities, lack of privacy, single parent families, widows, orphan state with loss of both parents, discontinuity in educational plans (e.g. loss of employment, homelessness migration, disorganization of life routines, material loss).
 
Psychosocial Interventions
 
Principles
  • Ventilation
  • Empathy
  • Active listening
  • Social support
  • Externalization of interest
  • Lifestyle choice
  • Relaxation and recreation
  • Spirituality
  • Health care
  • Work with individuals (willing to talk immediately Unwilling to talk)
    • For people who are willing to talk immediately
      • Listen attentively
      • Do not interrupt
      • Acknowledge that you understand the pain and distress by learning forward
      • Look into the eyes
      • Console them by patting on the shoulders or touching or holding their hand as they cry
      • Respect the silence during interaction, do not try to fill it in by talking
      • Keep reminding them I am with you. It is good you are trying to release your distress by crying. It will make you feel better.
      • Do not ask them to stop crying.
    • For those unwilling to talk (angry, or remain mute and silent)
      • Do not get anxious or feel rejected, remain calm
      • Maintain regular contact and greet them
      • Maintain interaction
      • Acknowledge that you understand they are not to blame
      • Tell them you will return the next day or in a couple of days
      • Tell them you are not upset or angry because he or she did not talk.
    • Once the person starts talking, maintain a conversation using the following queries like how you are and how are your other family members, what can individuals do to recover?
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Work with Families
  • Share their experience of loss as a family
  • Contact relatives to mobilize support and facilitate reconvey
  • Participate in rituals like prayers, keeping the dead persons photographs
  • Make time for recreation
  • Resume normal activities of the predisaster days with the family
  • Try and do things together as a writ and support one another
  • Be together as a family member. Do not send women and children and the aged to far off places for the sake of safety.
  • Restart activities that are special to your family like having meals together, praying, playing games, etc.
  • Keep touching and comforting your parents, children, spouse, and the aged in your family
  • Keep in constant touch with the family member who is hospitalized.
 
Work with the Community
  • Group mourning
  • Group meetings
  • Supporting group initiatives
  • Cultural aspects
  • Rally
  • Group participation for rebuilding efforts
  • Sensitization process.
 
Rehabilitation of Special Groups
1. Aged people can be helped by
  • Keeping them with their near and dear ones
  • Visiting them regularly and spending time with them
  • Touching them and allowing them to cry
  • Re-establishing their daily routines
  • Making them feel responsible by giving them some work to carry out which is not too difficult
  • Getting them involved in relief work by requesting for their suggestion and advice, etc.
  • Keeping them informed of positive news
  • Attending to their medical ailments
  • Organizing small group prayer meetings.
 
Disabled People
  • Removing them to places of safety
  • Keeping them informed what is happening
  • Getting them involved in activities
  • Integrate them in group discussions
  • 609Attend to their specific needs (wheel chairs, hearing aids)
  • Helping them overcome their feeling of insecurity
  • Taking cognizance of the fact that mentally challenged people, especially the women and children are vulnerable to sexual abuse, and help them.
 
Women
  • Help them to be with their families
  • Keep informing them what is happening
  • Involve them in activities
  • Involving them in relief and rehabilitation activities
  • Initiating self-help formation
  • Involve them in recreation
  • Making them to spend time with young widows or people who have lost their children and supporting them.
 
Children
  • Letting him/her to be close to adults who are loved and familiar
  • Re-establishing some sort of a routine for them like eating, sleeping, Going for programs
  • Actions like touching, hugging, reassuring them verbally
  • Allowing them to take about the event
  • Encourage them to play
  • Involve them in activities like painting and drawing, where then can express their emotions.
  • Organize story telling sessions, singing, songs and games
  • Praising coping behavior
  • Provide referral if required
  • Spending time on their studies once they return to school.
 
Policies Related to Emergency and Disaster Management
This policy aims at:
  • Promoting a culture of prevention, preparedness and resilience at all levels through knowledge, innovation and education
  • Encouraging mitigation measures based on technology, traditional wisdom and environmental sustainability
  • Mainstreaming disaster management into the developmental planning process
  • Establishing institutional and technolegal frameworks to create an enabling regulatory environment and a compliance regime
  • Ensuring efficient mechanism for identification, assessment and monitoring of disaster risks
  • Developing contemporary forecasting and early warning systems backed by responsive and fail-safe communication with information technology support
  • Ensuring efficient response and relief with a caring approach towards the needs of the vulnerable sections of the society
  • 610Undertaking reconstruction as an opportunity to build disaster resilient structures and habitat for ensuring safer living and
  • Promoting a productive and proactive partnership with the media for disaster management.
 
Policy Statement
To develop and implement an integrated action plan that will create an effective disaster management system at local, national and international levels.
 
Focus Areas and Strategies for Intervention
  • Making disaster risk reduction a development priority:
    • To incorporate disaster risk principles in the development agenda and other country programmes.
    • To enhance institutional capacity in disaster risk reduction.
    • To develop national platforms for disaster risk reduction.
  • Improving early warning systems:
    • To monitor continuously the hazard and vulnerability threats.
    • To develop standard risk and monitoring instruments.
    • Do a risk and hazard mapping.
    • To foster an understanding of disaster management mechanisms through dissemination of information and advocacy.
  • Addressing priority development concerns to reduce underlying risk factors:
    • To integrate disaster risk reduction in poverty reduction strategy paper.
    • To address sources of vulnerability especially outbreak of diseases and pests (HIV/AIDS, Avian Flu, locusts, etc).
    • To sensitise both local and traditional authorities with a view to understanding disaster prevention as a development challenge.
    • Mainstream gender and youth policies in the development agenda.
  • Effective disaster response through disaster preparedness:
    • To promote contingency planning in all government departments and all other sectors to ensure alignment of national, local and district disaster management plans.
    • To review and periodically rehearse national preparedness and contingency plans for major hazards.
    • To ensure that operational capacity exists within disaster management systems to enhance community resilience.
 
Policy Implementation Agencies and Structures
The policy will adopt various approaches to ensure that risk reduction in particular and disaster management in general is a national and local priority with strong involvement of local actors, the victims of disaster and institutional basis for implementation.
 
Agencies
  • NGOs
  • Civil Society Organizations
  • 611Government Agencies
  • UN Agencies
  • Private Sector.
 
Functions
  • Identify, assess and monitor disaster risks and enhance early warning systems.
  • Use indigenous knowledge, innovation, practices and education to build a culture of safety and resilience at all levels.
  • Strengthen disaster preparedness for effective response at all levels.
  • Creation of Disaster Prevention Volunteer Corps at local and national levels to be fully trained and equipped to identify, assess and monitor disaster events.
 
Operational Mechanism
This Policy will be implemented through the following strategic actions:
  • Sensitization programmes and advocacy on disaster prevention
  • Mainstreaming disaster prevention and management in school curricula and development programmes.
  • Factor disaster scenarios into economic planning and programmes.
  • Capacity building and information sharing.
  • Monitoring and Evaluation.
 
AGENCIES INVOLVED DURING DISASTER MANAGEMENT
  • The Adventist Community Services (ACS) receives, processes, and distributes clothing, bedding, and food products. In major disasters, the agency brings in mobile distribution units filled with bedding and packaged clothing that is presorted according to size, age, and gender. ACS also provides emergency food and counseling and participates in the cooperative disaster child care program.
  • The Red Cross is required by Congressional charter to undertake disaster relief activities to ease the suffering caused by a disaster. Emergency assistance includes fixed mobile feeding stations, shelter, cleaning supplies, comfort kits, first aid, blood and blood products, food, clothing, emergency transportation, rent, home repairs, household items, and medical supplies.
    Additional assistance for long-term recovery maybe provided when other relief assistance and personal resources are not adequate to meet disaster-caused needs.
  • The Ananda Marga Universal Relief Team (AMURT) renders immediate medical care, food and clothing distribution, stress management, and community and social services. AMURT also provides long-term development assistance and sustainable economic programs to help disaster-affected people. AMURT depends primarily on full- and part-time volunteer help, and has a large volunteer base to draw on worldwide. AMURT provides and encourages disaster services training in conjunction with other relief agencies like the Red Cross.
  • Children's Disaster Services (CDS) provides childcare in shelters and disaster assistance centers by training and certifying volunteers to respond to traumatized children with 612a calm, safe and reassuring presence. CDS provides respite for caregivers as well as individualized consultation and education about their child's unique needs after a disaster. CDS creates a more favorable work environment for the staff and volunteer of their partner agencies. CDS works with parents, community agencies, schools or others to help them understand and meet the special needs of children during or after a disaster.
  • The Friends Disaster Service (FDS) provides clean-up and rebuilding assistance to the elderly, disabled, low income, or uninsured survivors of disasters.
  • The International Relief Friendship Foundation (IRFF) has the fundamental goal of assisting agencies involved in responding to the needs of a community after disaster strikes. When a disaster hits, IRFF mobilizes a volunteer group from universities, businesses, youth groups, women's organizations, and religious groups. IRFF also provides direct support and emergency services immediately following a disaster such as blankets, food, clothing, and relief kits.
  • The National Emergency Response Team (NERT) meets the basic human needs of shelter, food, and clothing during times of crisis and disaster. NERT provides Emergency Mobile Trailer units (EMTUs), which are self-contained, modest living units for up to 8-10 people, to places where disaster occurs. When EMTUs are not in use, they serve as mobile teaching units used in Emergency Preparedness programs in communities.
  • The National Organization for Victim Assistance provides social and mental health services for individuals and families who experience major trauma after disaster, including critical incident debriefings.
 
IMPACT ON HEALTH AND AFTER EFFECTS OF DISASTER
  • Mental health problems have proven to be some of the most common side effects of natural disasters. The great loss and devastation disasters makes mental health problems like post-traumatic stress disorder and depression, rampant among survivors of these horrific acts of nature.
  • Communicable diseases: Communities reeling from natural disasters also tend to become breeding grounds for outbreaks of communicable diseases, which are defined as diseases that easily transfer from person to person or animal to person. Continuing problems with hygiene and diseases related to hygiene are common in refugee camps.
  • Health service system: The real damage in the long-run is done to the health service infrastructure. The physical damage done to the hospitals and health buildings, the loss of medical equipment and medicines, ‘there is the issue of the dysfunction of health facilities.
 
AFTER EFFECTS OF DISASTER
Common reactions to a disaster
Common reactions experienced following a major traumatic event include:
  • Feelings of fear, sadness or anger
  • Feeling overwhelmed
  • Feeling numb, detached or withdrawn
  • Difficulty with focusing attention and concentration
  • 613Difficulty planning ahead
  • Tearfulness
  • Unwanted and recurring memories or bad dreams related to the event
  • Sleep problems
  • Constant questioning – ‘What if I had done x, y or z, instead?’ and ‘What will happen now?’
  • ‘Replaying’ the event and inventing different outcomes in order to be prepared should it happen again.
 
Grief
Grief after the death of a loved one, a pet, or loss of property, can be felt intensely for a long time after the event. Everyone copes differently, but the intensity of the feelings usually diminishes with time. A person may feel one or all of the following:
  • A short-lived sense of unreality or feelings of detachment from the world
  • Numbness, shock, and confusion
  • Anger and self-blame or blaming others for the outcome
  • An inability to find anything meaningful and be able to make sense of the experience— ‘Why has this happened to me?’ and spiritual questions—‘Where is God in this?’
  • Feelings of despair and loneliness
  • Sleep disturbances and changes in appetite
  • Emotional distress so severe it feels like physical pain
  • Fatigue
  • Flooding of memories or preoccupation with thinking about the person who has died
  • Loneliness or longing for the person who has died
  • Stress about financial problems, parenting and practical concerns.
 
Dealing with Emotional Impact of Disaster
Following a disaster, it is important to find ways to regain a sense of safety and control. People often need to have access to a safe and secure environment, to find out what happened to family members and friends and to have access to relevant services. There are steps victims can take to make the situation more manageable.
  • Helping yourself
    • Spend time with family and friends
    • Try to get back to a routine
    • Try to be healthy
    • Take time out
    • Limit the amount of media coverage you watch, listen to, or read. While getting information is important, watching or listening to news bulletins too frequently can cause people who have experienced a disaster to feel distressed.
    • Write down your worries: You may find it helpful to write down your worries and concerns and use the problem-solving worksheet at the back of this booklet to identify some practical steps you can take to address those issues. Identify the 614specific feelings you are experiencing and the concern/worry that maybe underlying each of these feelings.
    • Express your feelings
    • Accept help when it is offered.
    • Do not expect to have the answers.
    • Realise you are not alone: Grief, loss and shock, sadness and stress, can make you feel like isolating yourself from others. It maybe helpful to remember that many people are feeling the same as you and will share your journey of recovery. Shutting yourself off from others is unlikely to make the situation any better.
  • Infectious diseases after disaster
    • Cryptosporidiosis
    • Enteroviruses
    • Escherichia coli (E. coli)
    • Giardiasis
    • Hepatitis B, Hepatitis C, HIV/AIDS
    • Leptospirosis
    • Legionnaires' disease
    • Methicillin-Resistant Staphylococcus aureus (MRSA) Infection
    • Norovirus
    • Rotavirus
    • Shigellosis
    • Skin infections
    • Tetanus
    • Toxoplasmosis
    • Trench Foot or Immersion Foot
    • Tuberculosis (TB)
    • Varicella Disease (Chickenpox)
    • Vibrio cholerae
    • Vibrio parahemolyticus
    • Vibrio vulnificus
    • West Nile Virus.
 
EMERGENCY CONDITIONS
 
Shock
Clinical syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply and demand for oxygen and nutrients.
 
Etiology and Pathophysiology
  • Cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in compromised cardiac output (CO).
    • 615Precipitating causes of Cardiogenic shock include myocardial infarction (MI), cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, cardiac tamponade, and myocardial depression from metabolic problems.
    • Hemodynamic profile will demonstrate an increase in the pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance.
 
Signs and Symptoms
Tachycardia, hypotension, a narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, decreased capillary refill time, anxiety, confusion, and agitation.
  • Hypovolemic shock occurs when there is a loss of intravascular fluid volume.
    • Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g. vomiting, diarrhea), fistula drainage, diabetes insipidus, hyperglycemia, or diuresis.
    • Relative hypovolemia results when fluid volume moves out of the vascular space into extravascular space (e.g., interstitial or intracavitary space) and this is called third spacing.
      • The physiologic consequences of hypovolemia include a decrease in venous return, preload, stroke volume, and CO resulting in decreased tissue perfusion and impaired cellular metabolism.
      • Clinical manifestations depend on the extent of injury or insult, age, and general state of health and may include anxiety, an increase in heart rate, CO, and respiratory rate and depth, and a decrease in stroke volume, PAWP, and urine output.
  • Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or in response to spinal anesthesia.
    • Clinical manifestations include hypotension, bradycardia, temperature dysregulation (resulting in heat loss), dry skin, and poikilothermia (taking on the temperature of the environment).
  • Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g. drug, chemical, vaccine, food, insect venom).
    • Immediate reaction causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability resulting in fluid leaks from the vascular space into the interstitial space.
    • Clinical manifestations can include anxiety, confusion, dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, stridor, flushing, pruritus, urticaria, and angioedema.
  • Septic shock is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of tissue perfusion abnormalities.
    • In severe sepsis and septic shock, the initiated body response to an antigen is exaggerated resulting in an increase in inflammation and coagulation, and a decrease in fibrinolysis.
    • Endotoxins from the microorganism cell wall stimulate the release of cytokines and other proinflammatory mediators that act through secondary mediators such as platelet-activating factor.
    • 616Clinical presentation for sepsis is complex. Patients will usually experience a hyperdynamic state characterized by increased CO. Persistence of a high CO beyond 24 hours is ominous and often associated with hypotension and multiple organ dysfunction syndrome (MODS). Initially patients will hyperventilate as a compensatory mechanism, resulting in respiratory alkalosis followed by respiratory acidosis and respiratory failure. Other clinical signs include alteration in neurologic status, decreased urine output, and GI dysfunction.
 
Stages of Shock
  • Compensatory Stage
    • Decrease in circulating blood volume.
    • Sympathetic nervous system stimulated, release catecholamines (epinephrine and norepinephrine), bronchodilation and increased cardiac output occurs. To maintain blood pressure: increase heart rate and contractility increases in peripheral vasoconstriction due to stimulation of beta adrenergic fibers (cause vasoconstriction of blood vessels of skin and abdominal viscera) and increase in heart rate and contractility.
    • Renin-angiotensin release of aldosterone-reabsorb H2O and sodium, Get fluid shift from interstitial to capillaries due to decrease in hydrostatic pressure in capillaries
    • Shunting blood from the lungs–ventilation–perfusion mismatch.
    • Circulation maintained, but only sustained short time without harm to tissues.
  • Progressive Stage
    • Altered capillary permeability (3rd spacing)
    • In the lungs: Alveolar or pulmonary edema, ARDS, increased pulmonary artery pressures
    • Cardiac output decreases and coronary perfusion is decreased. Decreased myocardial perfusion—arrhythmias and myocardial ischemia
    • Kidneys: Elevated BUN and Creatinine
    • Metabolic acidosis, anaerobic metabolism and kidneys cannot excrete acids and reabsorb bicarbonate
    • GI—ischemia causes ulcers and GI bleed
    • Liver: Cannot eliminate waste products, elevated ammonia and lactate, bilirubin (jaundice) Bacteria released in bloodstream.
    • Hematologic: Disseminated intravascular coagulopathy (DIC).
  • Refractory Stage
    • Anaerobic metabolism starts, Lactic acid build-up
    • Increased capillary blood leak, worsens hypotension and tachycardia, also get cerebral ischemia
    • Get profound hypotension and hypoxemia
    • Cellular death leads, tissue death, vital organs fail and death occurs (lungs, liver and kidneys result in accumulation of waste products. One organ failure leads to another.
    • Recovery unlikely.
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Diagnostic Evaluation
  • Blood: RBC, hemoglobin and hematocrit
  • Arterial Blood Gases: Respiratory alkalosis and metabolic acidosis
  • Electrolytes (Na level increased early, decreased later if hypotonic fluid given) K decrease later increase K with cellular breakdown and renal failure
  • BUN and creatinine increased, specific gravity increased then fixed at 1.010
  • Blood cultures: Identify causative organism in septic shock
  • Cardiac enzymes: Diagnosis of Cardiogenic shock
  • Glucose: Increased early then decreased
  • DIC screen: Fibrinogen level, platelet count, PTT and PT, thrombin time
  • Lactic acid: Increased
  • Liver enzymes, ALT, AST and GGT increased.
 
Management
  • General management strategies for a patient in shock begin with ensuring that the patient has a patent airway and oxygen delivery is optimized. The cornerstone of therapy for septic, hypovolemic, and anaphylactic shock is volume expansion with the administration of the appropriate fluid.
  • It is generally accepted that isotonic crystalloids, such as normal saline, are used in the initial resuscitation of shock. If the patient does not respond to 2 to 3 L of crystalloids, blood administration and central venous monitoring maybe instituted.
  • The primary goal of drug therapy for shock is the correction of decreased tissue perfusion.
    • Sympathomimetic drugs cause peripheral vasoconstriction and are referred to as vasopressor drugs (e.g., epinephrine, norepinephrine).
    • The goals of vasopressor therapy are to achieve and maintain a mean arterial pressure (MAP) of 60 to 65 mm Hg and the use of these drugs is reserved for patients unresponsive to other therapies.
    • The goal of vasodilator therapy, as in vasopressor therapy, is to maintain Mean arterial pressure at 60 to 65 mm Hg or greater.
    • Vasodilator agents most often used are nitroglycerin (in cardiogenic shock) and nitroprusside.
 
Collaborative Care
 
Cardiogenic Shock
  • Overall goal is to restore blood flow to the myocardium by restoring the balance between oxygen supply and demand.
  • Definitive measures include thrombolytic therapy, angioplasty with stenting, emergency revascularization, and valve replacement.
  • Care involves hemodynamic monitoring, drug therapy (e.g. diuretics to reduce preload), and use of circulatory assist devices (e.g. intra-aortic balloon pump, ventricular assist device).
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Hypovolemic Shock
  • The underlying principles of managing patients with hypovolemic shock focus on stopping the loss of fluid and restoring the circulating volume.
  • Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss).
 
Septic Shock
  • Patients in septic shock require large amounts of fluid replacement, sometimes as much as 6 to 10 L of isotonic crystalloids and 2 to 4 L of colloids, to restore perfusion.
  • Vasopressor drug therapy maybe added and vasopressin maybe given to patient's refractory to vasopressor therapy.
  • Intravenous corticosteroids are recommended for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP.
  • Antibiotics are early component of therapy and are started after obtaining cultures.
  • Drotrecogin alpha, a recombinant form of activated protein C, has demonstrated promise in treating patients with severe sepsis.
  • Glucose levels should be maintained at less than 150 mg/dl.
  • Stress ulcer prophylaxis with histamine (H2)-receptor blockers and deep vein thrombosis prophylaxis with low dose unfractionated heparin or low molecular weight heparin are recommended.
 
Neurogenic Shock
  • Treatment of neurogenic shock is dependent on the cause.
    • In spinal cord injury, general measures to promote spinal stability are initially used.
    • Definitive treatment of the hypotension and bradycardia involves the use of vasopressor and atropine respectively.
    • Fluids are administered cautiously as the cause of the hypotension is generally not related to fluid loss.
    • The patient is monitored for hypothermia.
 
Anaphylactic Shock
  • Epinephrine is the drug of choice to treat anaphylactic shock.
  • Diphenhydramine is administered to block the massive release of histamine.
  • Maintaining a patent airway is critical and the use of Nebulization with bronchodilators is highly effective.
  • Endotracheal intubation or cricothyroidotomy maybe necessary.
  • Aggressive fluid replacement, predominantly with colloids, is necessary.
  • Intravenous corticosteroids maybe helpful in anaphylactic shock if significant hypotension persists after 1 to 2 hours of aggressive therapy.
 
Nursing Management
  • Acute Intervention
    • The role of the nurse in shock involves
      • Monitoring the patient's ongoing physical and emotional status to detect subtle changes in the patient's condition.
      • 619Planning and implementing nursing interventions and therapy
      • Evaluating the patient's response to therapy
      • Providing emotional support to the patient and family and
      • Collaborating with other members of the health team when warranted by the patient's condition.
 
Nursing Care
  • Neurologic status, including orientation and level of consciousness, should be assessed every hour or more often.
  • Heart rate, rhythm, BP, central venous pressure, and PA pressures including continuous cardiac output should be assessed at least every 15 minutes.
  • The patient's ECG should be continuously monitored to detect dysrhythmias that may result from the cardiovascular and metabolic derangements associated with shock. Heart sounds should be assessed for the presence of an S3 or S4 sound or new murmurs. The presence of an S3 sound in an adult usually indicates heart failure.
  • The respiratory status of the patient in shock must be frequently assessed to ensure adequate oxygenation, detect complications early, and provide data regarding the patient's acid base status.
  • Pulse oximetry is used to continuously monitor oxygen saturation.
  • Arterial blood gases (ABGs) provide definitive information on ventilation and oxygenation status, and acid base balance.
  • Most patients in shock will be intubated and on mechanical ventilation.
  • Hourly urine output measurements assess the adequacy of renal perfusion and a urine output of less than 0.5 ml/kg/hour may indicate inadequate kidney perfusion.
  • BUN and serum creatinine values are also used to assess renal function.
  • Tympanic or pulmonary arterial temperatures should be obtained hourly if temperature is elevated or subnormal, otherwise every 4 hours.
  • Capillary refill should be assessed and skin monitored for temperature, pallor, flushing, cyanosis, and diaphoresis.
  • Bowel sounds should be auscultated at least every 4 hours, and abdominal distention should be assessed.
  • If a nasogastric tube is inserted, drainage should be checked for occult blood as should stools.
  • Oral care for the patient in shock is essential and passive range of motion should be performed three or four times per day.
  • Anxiety, fear, and pain may aggravate respiratory distress and increase the release of catecholamines.
  • The nurse should talk to the patient, even if the patient is intubated, sedated, and paralyzed or appears comatose. If the intubated patient is capable of writing, a pencil and paper should be provided.
 
SEIZURE OR EPILEPSY
A seizure is a sudden disruption of the brain's normal electrical activity accompanied by altered consciousness and other neurological and behavioral manifestations. Epilepsy is a 620condition characterized by recurrent seizures with symptoms that vary from a momentary lapse of attention to severe convulsions.
 
Types of Seizures
  • Grandmal seizures: This type of seizure presents as a generalized tonic-clonic seizure that often begins with a loud cry before the person having the seizure loses consciousness and falls to the ground. The muscles become rigid for about 30 seconds during the tonic phase of the seizure and alternately contract and relax during the clonic phase, which lasts 30–60 seconds. The skin sometimes acquires a bluish tint and the person may bite his tongue, lose bowel or bladder control, or have trouble breathing.
    A grand mal seizure lasts between two and five minutes, and the person may be confused or have trouble talking when he regains consciousness. The period of time immediately following a seizure is known as the ‘postictal’ state.
  • Primary generalized seizures: This is a primary generalized seizure that occurs when electrical discharges begin in both halves (hemispheres) of the brain at the same time. Primary generalized seizures are more likely to be major motor attacks than to be absence seizures.
  • Absence (petit mal) seizures: This type of seizure generally begins at about the age of four, and usually stops by the time the child becomes an adolescent. Petit mal seizures usually begin with a brief loss of consciousness and last between one and 10 seconds. A person having a petit mal seizure becomes very quiet and may blink, stare blankly, roll his eyes, or move his lips. A petit mal seizure lasts 15–20 seconds. When it ends, the person who had the seizure resumes whatever he was doing before the seizure began. He will not remember the seizure and may not realize that anything unusual has happened.
  • Myoclonic seizures: This type of seizure is characterized by brief, involuntary spasms of the tongue or muscles of the face, arms, or legs. Myoclonic seizures are most likely to occur first thing in the morning.
  • Simple partial seizures: This type of seizure does not spread from the focal area where they arise. Symptoms are determined by what part of the brain is affected. The patient usually remains conscious during the seizure.
  • Complex partial seizures: This type of seizures presents with a distinctive smell, taste, or other unusual sensation (aura) may signal the start of a complex partial seizure. Complex partial seizures start as simple partial seizures, but move beyond the focal area and cause loss of consciousness. Complex partial seizures can become major motor seizures. Although a person having a complex partial seizure may not seem to be unconscious, he does not know what is happening and may behave inappropriately. He will not remember the seizure, but may seem confused or intoxicated for a few minutes after it ends.
 
Etiology
Most cases of epilepsy are of unknown origin. Sometimes, however, a genetic basis is indicated, and other cases maybe traceable to birth trauma, lead poisoning, congenital brain infection, head injury, alcohol or drug addiction, or the effects of organ disease. Known causes of epilepsy and other seizure disorders can include:
  • 621Brain tumor
  • Cerebral hypoxia
  • Cerebrovascular accident
  • Convulsive or toxic agents
  • Alcohol and drug use withdrawal
  • Eclampsia
  • Hormone changes during pregnancy and menstruation
  • Exogenous factors (sound, light, cutaneous stimulation)
  • Fever (especially in children)
  • Head injury
  • Heatstroke
  • Infection (acute or chronic)
  • Metabolic disturbances (diabetes mellitus, electrolyte imbalances)
  • Withdrawal from, or hereditary intolerance of alcohol
  • Kidney failure
  • Degenerative disorders (senile dementia).
 
Diagnostic Evaluation
  • The first step in diagnosing a seizure disorder is to determine whether or not the patient ‘did’ or ‘did not’ actually have seizures. To do this the following is required:
    • Pastmedial history
    • Careful history of clinical presentation and events related to alleged seizure
    • General physical and neurological examination
  • Diagnostic testing which include:
    • Computed Tomography (CT Scan)
    • Magnetic Resonance Imaging (MRI)
    • Electroencephalogram (EEG)
    • Video EEG
    • Single Proton Emission Computerized Tomography.
 
Management
Once a seizure disorder of epilepsy has been diagnosed the first line of treatment is usually medication therapy that focuses on reducing the frequency and severity of the seizures.
The goal is to find a medication that will control the seizures but not produce side effects. Because many people will continue on medication for many years, selection of a good first drug is extremely important.
  • Anticonvulsants and other prescription agents are usually prescribed based on the type of seizures that the patient is experiencing. The following medications are frequently prescribed:
    • Benzodiazepines Examples include:
      • Clonazepam
      • Clorazepate
      • Diazepam
    • 622Phenytoin (Dilantin): A synthetic drug that is classified as a hydantoin. It is used for the treatment of simple partial, complex partial and generalized tonic-clonic seizures.
    • Carbamazepine: Used as a first line agent for the treatment of simple partial, complex partial and generalized tonic-clonic seizures.
    • Lamotrigine: Used when seizures are focal in onset, tonic-clonic, atypical absence or myoclonic in nature.
    • Valproate: Used for the management of myoclonic, tonic, atonic, absence and generalized tonic-clonic seizures especially with patients with one or more type of generalized seizure.
    • Phenobarbital: Once a mainstay in the treatment of seizures (especially status epilepticus), Phenobarbital is now being replaced by other anticonvulsants but can still be used for the treatment of generalized seizures except for absence and partial seizures.
  • Surgical Intervention:
    • The most common surgical areas include:
      • Temporal lobectomy
      • Frontal lobectomy
      • Hemispherectomy
      • Corpus clallostomy (splitting of the two hemispheres of the brain).
  • Placement of a Vagus Nerve Stimulator (VNS): A VNS is an implantable device that is used to decrease seizure frequency. In some cases it eliminates seizure activity altogether. It is a surgically implanted device that is placed in the chest wall (similar to a pacemaker), with a wire that is threaded to the Vagus nerve in the neck. Once in place the Vagus Nerve Stimulator is programmed (using a magnet), to stimulate the Vagus nerve at preset intervals. Patients are sent home with a magnet as well to trigger the device at the onset of a seizure.
 
Nursing Care and Management of Seizures in the Acute Setting
 
Before (and During) Seizure Care
  • If the patient is seated when a major seizure occurs, ease them to the floor
  • Provide privacy if possible
  • If patient experiences an aura, have them lie down to prevent injury
  • Remove eyeglasses and loosen restrictive clothing
  • Do not try to force anything into the mouth
  • Guide the movements to prevent injuries (do not restrain patient)
  • Stay with the patient throughout the seizure to ensure safety
  • Time the seizure
  • Verbalize events as they happen to assist with more accurate recall later
  • If not already available have someone retrieve O2 and suction.
 
Postseizure Care
  • Position patient on their side to facilitate drainage of secretions
  • Provide adequate ventilation by maintaining a patent airway
  • 623Suction secretions if necessary to prevent aspiration
  • Allow the patient to sleep post seizure
Status Epilepticus: Seizures lasting at least 5 minutes or two or more seizures in a row without complete recovery in between is termed as status epilecticus.
 
Initial Nursing Management:
  • ABCs of life support
  • Position patient to avoid aspiration or inadequate oxygenation
  • If possible as soft oral airway can be placed (again do not force teeth apart)
  • Suction and O2 must be available
  • Monitor respiratory function with ongoing pulse oximetry
  • IV access should be secured
  • Frequent monitoring of neurological examination and vital signs
  • Monitor ABGs
  • Monitor Glucose
  • Treat hyperthermia.
 
Anticonvulsant Therapy for Management of Status Epilipticus
The following drug therapy regimen is used to treat status epilepticus
  • Time 0–3 minutes: Lorazepam 4–8 mg IVP (2 mg/min)
  • Time 4–23 minutes: Phenytoin (Dilantin) 20 mg/kg (about 1 gm) in NS at (50 mg/min)
  • Time 22–33 minutes: Phenytoin (Dilantin) 5–10 mg/kg
  • Time 37–58 minutes: Phenobarbital 20 mg/kg IV
  • Time 58–68 minutes: Phenobarbital 5–10 mg/kg
 
Patient and Family Education for Seizures or Epilepsy
 
General Health
  • Trigger signs (patient specific if possible)
  • Regular exercise
  • Regular sleep patterns
  • Showers or bath
  • Good oral hygiene (some anticonvulsant can cause gingival hyperplasia)
  • Eat well rounded meals at routine times
  • Avoid excess sugar, caffeine or other trigger foods
  • Noisy environments should be avoided
  • Avoid bright flashing or fluorescent lights
  • Use a screen filter on the computer screen to avoid glare
  • Do not use recreational or street drugs
  • Avoid work/recreation that could cause injury if a seizure was to occur
  • Swim with a friends only and avoid be alone in pool
  • Avoid contact sports
  • Avoid emotional stress
  • Counselling for stress reduction or depression maybe warranted.
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HEARTSTROKE
Heatstroke is a condition caused by body overheating, usually as a result of prolonged exposure to or physical exertion in high temperatures. This most serious form of heat injury, heatstroke can occur if body temperature rises to 104 °F (40 °C) or higher.
Heatstroke requires emergency treatment. Untreated heatstroke can quickly damage brain, heart, kidneys and muscles. The damage worsens the longer treatment is delayed, increasing risk of serious complications or death.
 
Etiology
Heatstroke can occur as a result of:
  • Exposure to a hot environment: In a type of heatstroke, called nonexertional or classic heatstroke, being in a hot environment leads to a rise in body temperature. This type of heatstroke typically occurs after exposure to hot, humid weather, especially for prolonged periods, such as two or three days. It occurs most often in older adults and in people with chronic illness.
  • Strenuous activity: Exertional heatstroke is caused by an increase in body temperature brought on by intense physical activity in hot weather. Anyone exercising or working in hot weather can get exertional heatstroke.
  • Wearing excess clothing that prevents sweat from evaporating easily and cooling of body
  • Drinking alcohol, which can affect body's ability to regulate the temperature
  • Becoming dehydrated, by not drinking enough water to replenish fluids lost through sweating.
 
Signs and Symptoms
Heatstroke symptoms include:
  • High body temperature: A body temperature of 104 °F (40 °C) or higher is the main sign of heatstroke.
  • Altered mental state or behavior: Confusion, agitation, slurred speech, irritability, delirium, seizures and coma can all result from heatstroke.
  • Alteration in sweating: In heatstroke brought on by hot weather, skin will feel hot and dry to the touch. However, in heatstroke brought on by strenuous exercise, skin may feel moist.
  • Nausea and vomiting
  • Flushed skin
  • Rapid breathing
  • Tachycardia
  • Headache.
 
Risk factors
  • Age: Ability to cope with extreme heat depends of the strength of central nervous system. In the very young, the central nervous system is not fully developed, and in adults over 65, the central nervous system begins to deteriorate, which makes the body less able to cope with changes in body temperature. Both age groups usually have difficulty remaining hydrated, which also increases risk.
  • 625Exertion in hot weather: Military training and participating in sports, such as football, in hot weather are among the situations that can lead to heatstroke.
  • Sudden exposure to hot weather: Such as during an early-summer heat wave or travel to a hotter climate.
  • A lack of air conditioning: Fans may make feel better, but during sustained hot weather, air conditioning is the most effective way to cool down and lower humidity.
  • Certain medications: Beta blockers, diuretics, or reduce psychiatric symptoms (antidepressants or antipsychotics).
  • Certain health conditions: Certain chronic illnesses, such as heart or lung disease, might increase risk of heatstroke.
 
Diagnostic Evaluation
  • A blood test to check blood sodium or potassium and the content of gases in blood to see if there has been damage to central nervous system.
  • A urine test to check the color of urine, because it is usually darker if have a heat-related condition, and to check kidney function, which can be affected by heatstroke.
  • Muscle function tests to check for serious damage to muscle tissue.
  • X-rays and other imaging tests to check for damage to internal organs.
 
Management
  • Immerse in cold water: A bath of cold or ice water can quickly lower temperature.
  • Use evaporation cooling techniques: In this technique, cool water is misted on skin while warm air fanned over body causes the water to evaporate, cooling the skin.
  • Pack with ice and cooling blankets: Another method is to wrap in a special cooling blanket and apply ice packs to groin, neck, back and armpits to lower temperature.
  • Give medications to stop shivering: If treatments to lower body temperature make shiver, muscle relaxant, such as a benzodiazepine can be administered. Shivering increases body temperature, making treatment less effective.
Fig. 12.1: Management of heatstroke
626
 
Prevention
  • Wear loose fitting, lightweight clothing: Wearing excess clothing or clothing that fits tightly would not allow body to cool properly.
  • Protect against sunburn: Sunburn affects body's ability to cool itself, so protect outdoors with a wide-brimmed hat and sunglasses and use a broad-spectrum sunscreen with an SPF of at least 15.
  • Drink plenty of fluid: Staying hydrated will help the body sweat and maintain a normal body temperature.
  • Take extra precautions with certain medications like caffeine.
  • Never leave anyone in a parked car: This is a common cause of heat-related deaths in children. When parked in the sun, the temperature in car can rise 20 degrees F (more than 6.7 C) in 10 minutes.
 
FROSTBITES
It is an emergency condition in with the body fluids freeze because of extreme low temperature. The severity of cold injury depends on the temperature, duration of exposure, environmental conditions, amount of protective clothing, and the patient's general state of health. Exposure to cold can cause localized injury or generalized cooling of the entire body.
 
Risk Factor
  • Lower temperatures—especially windy conditions
  • Dehydration
  • Infancy, elderly age, malnutrition, exhaustion
  • Immobilization
  • Open wounds
  • Prolonged exposure
  • Moisture
  • Peripheral vascular disease
  • Impaired cerebral function: For example, alcohol, other sedatives, psychiatric illnesses, hypoglycemia
  • Smoking, diabetes and Reynaud's disease increase risk due to vasoconstriction
  • Peripheral neuropathy, autonomic neuropathy, head injury, spinal cord damage
  • Body parts previously frostbitten are at increased risk due to damaged microcirculation a summary to use in your appraisal.
 
Management
  • Identify the type and extent of cold injury.
  • Remove jewellery or material that could constrict the body part.
  • Rapidly rewarm in water heated and maintained between 37–39 °C until the area becomes soft and pliable. Allow passive thawing if rapid rewarming is not possible.
  • Give ibuprofen.
  • Air dry the area.
  • 627Apply topical aloe vera cream or gel if available.
  • Protect from refreezing and any direct trauma. Use large, dry, bulky dressings and elevate the body part if possible.
  • Ensure the patient is rehydrated.
  • Avoid walking on a thawed lower limb.
  • Tetanus prophylaxis.
  • Debridement - this may involve selective drainage of clear blisters. Hemorrhagic blisters should be left intact.
  • Systemic hydration with IV fluid.
  • Systemic antibiotics
  • Thrombolytic therapy can be considered.
 
Complications
  • Secondary wound infection.
  • Tetanus
  • Diuresis may cause volume depletion
  • Hyperglycemia, acidosis
  • Dysrhythmias
  • Gangrene
  • Paraesthesias and sensory deficits, tremor
  • Cracking of skin and loss of nails
  • Permanent discoloration
  • Vasospasm, cold sensitivity
  • Joint stiffness
  • Premature closure of epiphyses in children
  • Muscle atrophy.
 
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) provides artificial ventilation and circulation until advanced life support can be provided and spontaneous circulation and ventilation can be restored. CPR can keep oxygenated blood flowing to the brain and other vital organs until more definitive medical treatment can restore a normal heart rhythm.
 
Introduction
In 1954, James Elam was the first to demonstrate experimentally that cardiopulmonary resuscitation (CPR) was a sound technique and, with Dr Peter Safar, he demonstrated its superiority to previous methods. Peter Safar wrote the book ABC of resuscitation in 1957.
 
Definition
  • Cardiopulmonary resuscitation (CPR) is a technique of basic life support for the purpose of oxygenating the brain and heart until appropriate, definitive medical treatment 628can restore normal heart and ventilator action. Management of airway obstruction or cricothyroidotomy maybe necessary to open the airway before CPR can be performed.
  • Cardiopulmonary resuscitation, commonly called CPR, combines rescue breathing (one person breathing into another person) and chest compression in a lifesaving procedure performed when a person has stopped breathing or a person's heart has stopped beating.
 
What is CPR?
  • Emergency lifesaving measure
  • Combination of rescue breathing and chest compressions
  • Done on unconscious/nonbreathing patient
  • Done on persons suffering cardiac arrest
  • Also for near-drowning/asphyxiation/trauma cases
  • CPR conducts defibrillation
  • Supports heart pumping for short duration
  • Allows oxygen to reach brain
  • Buys time till help arrives
  • More effective when done as early as possible.
 
Purpose
  • CPR can save lives in such emergencies as loss of consciousness, heart attacks or heart ‘arrests’, electric shock, drowning, excessive bleeding, drug overdose.
  • The purpose of CPR is to bring oxygen to the victim's lungs and to keep blood circulating so oxygen gets to every part of the body.
 
Indications
  • Cardiac arrest:
    • Ventricular fibrillation
    • Ventricular tachycardia
    • Asystole
    • Pulseless electrical activity.
  • Respiratory arrest:
    • Drowning
    • Stroke
    • Foreign-body airway obstruction
    • Smoke inhalation
    • Drug overdose
    • Electrocution/injury by lighting
    • Suffocation
    • Accident/injury
    • Coma
    • Epiglottitis.
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Complications
  • Postresuscitation distress syndrome (secondary derangements in multiple organs).
  • Neurological impairment, and or brain damage.
 
CHANGES IN BASIC LIFE SUPPORT (BLS) GUIDELINES
New AHA (American Heart Association) Adult Chain of Survival
New 5th link—postcardiac arrest care
  • Immediate recognition and activation of emergency response system
  • Early CPR, w/emphasis on chest compressions
  • Rapid defibrillation
  • Effective advanced life support
  • Integrated postcardiac arrest care
Figure 12.2: Steps of basic life support
 
Key Changes in Revised AHA Guidelines for CPR and ECC
 
The Change From ‘A-B-C’ to ‘C-A-B’
2010 (New): Initiate chest compressions before ventilations.
2005 (Old): The sequence of adult CPR began with opening of the airway, checking for normal breathing, and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths.
Why: To reduce delay to CPR, sequence begins with skill that everyone can perform. Emphasize primary importance of chest compressions for professional rescuers. Starting CPR with 30 compressions rather than 2 ventilations leads to improved outcome, chest compressions provide vital blood flow to the heart and brain, and studies of out-of-hospital adult cardiac arrest showed that survival was higher when bystanders made some attempt rather than no attempt to provide CPR. Chest compressions can be started almost immediately, whereas positioning the head and achieving a seal for mouth-to-mouth or bag-mask rescue breathing all take time.
 
Elimination of ‘Look–Listen–Feel’ in Breathing
2010 (New): ‘Look, listen, and feel’ was removed from the CPR sequence. After delivery of 30 compressions, the lone rescuer opens the victim's airway and delivers 2 breaths.
2005 (Old): ‘Look, listen, and feel’ was used to assess breathing after the airway was opened.
630Why: With the new ‘chest compressions first’ sequence, CPR is performed if the adult is unresponsive and not breathing or not breathing normally (as noted above, lay rescuers will be taught to provide CPR if the unresponsive victim is ‘not breathing or only gasping’). The CPR sequence begins with compressions (C-A-B sequence). Therefore, breathing is briefly checked as part of a check for cardiac arrest; after the first set of chest compressions, the airway is opened, and the rescuer delivers 2 breaths.
 
Chest Compressions Rate: 100/min
2010 (New): It is reasonable for lay rescuers and healthcare providers to perform chest compressions at a rate of at least 100/min.
2005 (Old): Compress at a rate of about 100/min.
Why: The number of chest compressions delivered per minute during CPR is an important determinant of return of spontaneous circulation and survival with good neurologic function. The actual number of chest compressions delivered per minute is determined by the rate of chest compressions and the number and duration of interruptions in compressions (e.g. to open the airway, deliver rescue breaths, or allow AED analysis).
 
Chest Compression Depth
2010 (New): The adult sternum should be depressed at least 2 inches (5 cm).
2005 (Old): The adult sternum should be depressed approximately 1 to 2 inches (approximately 4 to 5 cm).
Why: Compressions create blood flow primarily by increasing intrathoracic pressure and directly compressing the heart. Compressions generate critical blood flow and oxygen and energy delivery to the heart and brain. Confusion may result when a range of depth is recommended, so 1 compression depth is now recommended. Rescuers often do not compress the chest enough despite recommendations to ‘push hard’. In addition, the available science suggests that compressions of at least 2 inches are more effective than compressions of 1½ inches. For this reason the 2010 AHA Guidelines for CPR and ECC recommend a single minimum depth for compression of the adult chest.
 
Cricoid Pressure
2010 (New): Routine use of cricoid pressure during CPR is generally NOT recommended.
Why: Cricoid pressure can interfere with ventilation and advanced airway placement. Not proven to prevent aspiration or gastric insufflation during cardiac arrest.
 
Team Resuscitation
2005 (Old): The steps of BLS consist of a series of sequential assessments and actions. The intent of the algorithm is to present the steps in a logical and concise manner that will be easy for each rescuer to learn, remember, and perform.
2010 (New): The steps in the BLS algorithm have traditionally been presented as a sequence to help a single rescuer prioritize actions. There is increased focus on providing CPR as a team because resuscitations in most EMS and healthcare systems involve teams of rescuers, with rescuers performing several actions simultaneously. For example, one rescuer activates the emergency response system while a second begins chest compressions, a third is either 631providing ventilations or retrieving the bag-mask for rescue breathing, and a fourth is retrieving and setting up a defibrillator.
Why: Some resuscitations start with a lone rescuer who calls for help, whereas other resuscitations begin with several willing rescuers. Training should focus on building a team as each rescuer arrives, or on designating a team leader if multiple rescuers are present. As additional personnel arrive, responsibilities for tasks that would ordinarily be performed sequentially by fewer rescuers may now be delegated to a team of providers who perform them simultaneously. For this reason, BLS healthcare provider training should not only teach individual skills but should also teach rescuers to work in effective teams.
 
Precordial Thump
The precordial thump should not be used for un witnessed out-of-hospital cardiac arrest. The precordial thump maybe considered for patients with witnessed, monitored, unstable VT (including pulseless VT) if a defibrillator is not immediately ready for use, but it should not delay CPR and shock delivery.
 
Simplified ACLS Algorithm and New Algorithm
2005 (Old): ACLS courses focused mainly on added interventions, such as manual defibrillation, drug therapy, and advanced airway management, as well as alternative and management options for special situations.
2010 (New): The conventional ACLS Cardiac Arrest Algorithm has been simplified and streamlined to emphasize the importance of high-quality CPR (including compressions of adequate rate and depth, allowing complete chest recoil after each compression, minimizing interruptions in chest compressions, and avoiding excessive ventilation) and the fact that ACLS actions should be organized around uninterrupted periods of CPR.
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Why: For the treatment of cardiac arrest, ACLS interventions build on the BLS foundation of high-quality CPR to increase CPR Quality
  • Push hard (≥ 2 inches [5 cm]) and fast (≥ 100/min) and allow complete chest recoil
  • Minimize interruptions in compressions
  • Avoid excessive ventilation
  • Rotate compressor every 2 minutes
  • If no advanced airway, 30: 2 compression-ventilation ratio
  • Quantitative waveform capnography – If PETCO2 < 10 mm Hg, attempt to improve CPR quality
  • Intra-arterial pressure – If relaxation phase (diastolic) pressure < 20 mm Hg, attempt to improve CPR quality Return of Spontaneous Circulation (ROSC)
  • Pulse and blood pressure
  • Abrupt sustained increase in PETCO2 (typically ≥ 40 mm Hg)
  • Spontaneous arterial pressure waves with intra-arterial monitoring.
 
Shock Energy
  • Monophasic: 360 J
  • Biphasic: Manufacturer recommendation (e.g. initial dose of 120–200 J); if unknown, use maximum available. Second and subsequent doses should be equivalent, and higher doses maybe considered.
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Drug Therapy
  • Epinephrine IV/IO Dose: 1 mg every 3–5 minutes
  • Vasopressin IV/IO Dose: 40 units can replace first or second dose of epinephrine
  • Amiodarone IV/IO Dose: First dose: 300 mg bolus. Second dose: 150 mg.
 
Advanced Airway
  • Supraglottic advanced airway or endotracheal intubation
  • Waveform capnography to confirm and monitor ET tube placement
  • Eight to ten breaths per minute with continuous chest compressions
 
Reversible Causes
  • Hypovolemia
  • Hypoxia
  • Hydrogen ion (acidosis)
  • Hypo-/hyperkalemia
  • Hypothermia.
 
Capnography
2005 (Old): An exhaled carbon dioxide (CO2) detector or an esophageal detector device was recommended to confirm endotracheal tube placement.
2010 (New): Continuous quantitative waveform capnography is now recommended for intubated patients throughout the periarrest period. When quantitative waveform capnography is used for adults, applications now include recommendations for confirming tracheal tube placement and for monitoring CPR quality and detecting ROSC based on end-tidal carbon dioxide value.
Why: Continuous waveform capnography is the most reliable method of confirming and monitoring correct placement of an endotracheal tube. Although other means of confirming endotracheal tube placement are available, they are not more reliable than continuous waveform capnography. Patients are at increased risk of endotracheal tube displacement during transport or transfer; providers should observe a persistent capnographic waveform with ventilation to confirm and monitor endotracheal tube placement. Because blood must circulate through the lungs for CO2 to be exhaled and measured, capnography can also serve as a physiologic monitor of the effectiveness of chest compressions.
 
Postcardiac Arrest Care
2005 (Old): Therapeutic hypothermia was recommended to improve outcome for comatose adult victims of witnessed out-of-hospital cardiac arrest when the presenting rhythm was VF.
2010 (New): To improve survival for victims of cardiac arrest who are admitted to a hospital after ROSC, a comprehensive, structured, integrated, multidisciplinary system of postcardiac arrest care should be implemented in a consistent manner. Treatment should include 634cardiopulmonary and neurologic support. Therapeutic hypothermia and percutaneous coronary interventions (PCIs) should be provided when indicated. Because seizures are common after cardiac arrest, an electroencephalogram for the diagnosis of seizures should be performed with prompt interpretation as soon as possible and should be monitored frequently or continuously in comatose patients after ROSC.
Why: Postcardiac arrest care with an emphasis on multidisciplinary programmes that focus on optimizing hemodynamic, neurologic, and metabolic function (including therapeutic hypothermia) may improve survival to hospital discharge among victims who achieve ROSC after cardiac arrest either in or out of hospital.
 
Atropine is ‘out’; Adenosine is ‘in’
2005 (Old): Atropine was included in the BLS pulseless Arrest Algorithm: for a patient in asystole, atropine could be considered.
2010 (New): Atropine is not recommended for routine use. Adenosine is recommended in the initial diagnosis and treatment of stable, undifferentiated regular, monomorphic wide-complex tachycardia. It is important to note that adenosine should not be used for irregular wide-complex tachycardias because it may cause degeneration of the rhythm to VF. For the treatment of the adult with symptomatic and unstable.
Bradycardia, chronotropic drug infusions are recommended as an alternative to pacing.
Why: There are several important changes regarding management of symptomatic arrhythmias in adults. Available evidence suggests that the routine use of atropine during pulseless electrical activity (PEA) or asystole is unlikely to have a therapeutic benefit. Adenosine is recommended in the initial diagnosis and treatment of stable, undifferentiated regular, monomorphic wide-complex tachycardia. This is on the basis of new available evidence of its safety and potential efficacy.
 
Automated External Defibrillators (AED) Use in Children Now Includes Infants
2005 (Old): For children 1 to 8 years of age, the rescuer should use a pediatric dose-attenuator system if one is available. If the rescuer provides CPR to a child in cardiac arrest and does not have an AED with a pediatric attenuator system, the rescuer should use a standard AED. There are insufficient data to make a recommendation for or against the use of AEDs for infants < 1 year of age.
2010 (New): For attempted defibrillation of children 1 to 8 years of age with an AED, the rescuer should use a pediatric dose-attenuator system if one is available. If the rescuer provides CPR to a child in cardiac arrest and does not have an AED with a pediatric dose-attenuator system, the rescuer should use a standard AED. For infants (< 1 year of age), a manual defibrillator is preferred.
Why: The lowest energy dose for effective defibrillation in infants and children is not known. The upper limit for safe defibrillation is also not known, but doses > 4 J/kg (as high as 9 J/kg) have effectively defibrillated children and animal models of pediatric arrest with no significant adverse effects. Automated external defibrillators with relatively 635high-energy doses have been used successfully in infants in cardiac arrest with no clear adverse effects.
 
Pediatric Resuscitation
Revised pediatric chain of survival. New postarrest care link
Fig. 12.3: Pediatric chain of survival
 
Pediatric Basic Life Support
  • Similarities in pediatric BLS and adult BLSC-A-B rather than A-B-C sequence
  • Continued emphasis on high-quality CPR
  • Removal of ‘look, listen and feel’
  • De-emphasis of pulse check for HCPs
  • Use AEDs as soon as available
  • AEDs maybe used in infants, although manual defibrillation preferred.
  • Some differences between pediatric BLS and adult BLS
  • Chest compression depth—at least 1/3 of the anterior–posterior diameter of chest infants: about 1½ inches
  • Children: About 2 inches.
  • Lone rescuer provides 2 minutes of CPR before activating emergency response
  • Two rescuers use 15:2 compression to ventilation ratio
  • Traditional CPR (compressions and ventilations) by bystanders associated with higher survival than chest compressions alone.
 
Pediatric Advanced Life Support (PALS)
  • Optimal energy dose for defibrillation of children unknown.
    • Initial dose 2–4 J/kg.
    • Subsequent dose ≥ 4 J/kg.
  • Post-ROSC: Titrate oxygen to limit hyperoxemia.
  • Therapeutic hypothermia (to 32 °C to 34 °C) may be beneficial (studies in progress)
  • 636Young victims of sudden, unexpected cardiac arrest should have a complete autopsy with genetic analysis of tissue to look for inherited channelopathy.
 
Neonatal Resuscitation
  • For babies born at term, begin resuscitation with room air rather than 100% oxygen.
  • Any oxygen administered should be blended with room air, titrated based on oxygen saturation measured from right upper extremity.
  • Suctioning after birth reserved for infants with obvious airway obstruction, those requiring ventilation or nonvigorous babies with meconium.
  • Therapeutic hypothermia recommended for babies near term with evolving moderate to severe hypoxic-ischemic encephalopathy.
 
Ethical Issues
Until recent guidelines, no prognostic indicators had been established for patients undergoing therapeutic hypothermia. According to 2005 guidelines, there were 3 factors associated with poor outcomes:
  • Absence of pupillary response on day 3
  • Absence of motor response on day 3
  • Bilateral absence of somatosensory evoked potentials.
 
STEPS OF BASIC LIFE SUPPORT
 
Step 1
  • Check responsiveness
    • ‘Are you all right’
  • At the same time check for absent/abnormal breathing
    • Scan the chest for movement for 5–10 seconds.
 
Step 2
  • Get Help!!
    • ‘Code blue team’.
  • Send for AED/Defib.
 
Step 3
  • Check the carotid pulse for 5–10 seconds
  • If no pulse (or unsure of pulse) = start chest compressions
    • Compress the lower half of the sternum at a rate of 100/min at a depth of at least 5 cm
    • Allow complete chest recoil after each compression
    • Minimize interruptions in compressions (10 seconds or less)
    • Switch compression providers every 2 minutes
    • 637Give breaths at a rate of 2 breaths for every 30 compressions if no advanced airway is in place or at a rate of 1 breath every 5–6 seconds (8–10 breaths per minute) if advanced airway is in place
    • Avoid excessive ventilation!
  • If pulse present = Give rescue breaths at 1 breath every 5–6 seconds and check pulse every 2 minutes.
 
Step 4
  • No pulse = Check for shockable rhythm with an AED or Defibrillation as soon as it arrives
  • Shock as indicated
  • Follow each shock immediately with CPR, beginning with compressions
  • Check pulse and rhythm after 2 minutes.
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Summary of CPR for adults, children and infants CPR Levels A, B, and C
CPR
Adult
(8 years of age and older)
Child
(1–8 years of age)
Infant
(Less than one year)
Check the scene
Establish unresponsive-ness
Is the Scene safe to help?
Wake and shout—gently squeeze or tap shoulders are you OK?
Activate EMS
and get an AED
Yell for help. If you are alone phone EMS right away
Yell for help. If you are alone phone EMS after giving 5 cycles of CPR
Check for breathing
Open airway using head-tilt/chin-lift, take no more than 5 seconds to look for normal breathing using visual cues such as chest rise. Gasping is not normal breathing
----------------------------------------------------------
Spinal victims: NLS lifeguards attempt jaw thrust to open the airway
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Start CPR
If victims is unresponsive and not breathing normally, immediately start CPR beginning with chest compression (30 compression : 2 breaths)
----------------------------------------------------------
Drowning victims: Start CPR sequence with 2 initial breaths before chest compression
Compression location
Center of chest
Just below nipple line on breastbone
Compression method
2 hands: Heel of 1 hand, other hand on top (or 1 hand for children)
2 fingers middle and ring
Compression depth
5 cm or 2 in
1/3 depth of chest or about (5 cm child or 4 cm infant)
Compression rate
100 per minute
Compression ventilation ratio
30:2
(1 or 2 rescuer CPR)
 
Responder/Rescuer
Everyone can be a lifesaving rescuer for a cardiac arrest victim. CPR skills and their application depend on the rescuer's training, experience, and confidence.
All rescuers, regardless of training, should provide chest compressions to all cardiac arrest victims. Rescuers who are able should add ventilations to chest compressions. Highly trained rescuers working together should coordinate their care and perform chest compressions as well as ventilations in a team-based approach.
 
Precautions
  • Do not leave the victim alone.
  • Do not give chest compressions if the victim has a pulse. Chest compression when there is normal circulation could cause the heart to stop beating.
  • Do not give the victim anything to eat or drink.
  • Avoid moving the victim's head or neck if spinal injury is a possibility. The person should be left as found if breathing freely. To check for breathing when spinal injury is suspected, the rescuer should only listen for breath by the victim's mouth and watch the chest for movement.
  • Do not slap the victim's face, or throw water on the face, to try and revive the person.
  • Do not place a pillow under the victim's head.
  • The description above is not a substitute for CPR training and is not intended to be followed as a procedure.
 
Drugs Used During CPR
Drug
Dose
Indications
Timing of administration
Other
Adrenaline
1 mg IV
(0.01 mg/Kg)
  • Given immediately in nonshockable rhythm.
Repeated every 4 minutes (every other cycle).
Given as a vasopressor for its
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  • Given after the 3rd shock in shockable rhythm (VT/VF).
‘Once adrenaline ALWAYS adrenaline’.
α-adrenergic effect. Not as an inotrope.
Amiodarone
300 mg IV bolus
(5 mg/Kg)
  • Given after the 3rd shock in shockable rhythm.
  • A further dose of 150 mg if VT/VF persists.
If amiodarone is not available Lidocaine can be used instead.
Lidocaine
100 mg IV
(1–1.5 mg/Kg)
  • Given after the 3rd shock in shockable rhythm (if amiodarone is unavailable).
  • A further dose of 50 mg can be given if necessary.
Total dose must not exceed 3 mg/Kg during the 1st hour.
Magnesium
2 g IV
  • VT.
  • Torsade de pointes.
  • Digoxin toxicity with hypomagnesemia
  • May be repeated after 10–15 minutes.
Sodium Bicarbonate
50 mmol IV
  • Routine use is not recommended.
  • Hyperkalemia.
  • Overdose of TCA.
  • May be repeated according to ABG.
Do NOT give calcium solutions and NaHCO3 simultaneously by the same route.
 
Amiodarone
Amiodarone is a membrane-stabilising antiarrhythmic drug that increases the duration of the action potential and refractory period in atrial and ventricular myocardium. Also atrioventricular conduction is slowed, and a similar effect is seen in accessory pathways. The hypotension that occurs with intravenous amiodarone is related to the rate of delivery.
If VF/VT persists, give amiodarone 300 mg by bolus injection (flushed with 20 ml of 0.9% sodium chloride or 5% dextrose) 177 after the third shock. A further dose of 150 mg may be given for recurrent or refractory VF/VT, followed by an infusion of 900 mg over 24 hours.
Lidocaine 1 mg kg-1 may be used as an alternative if amiodarone is not available, but do not give lidocaine if amiodarone has been given already.
 
Magnesium
Give an initial intravenous dose of 2 g (= 8 mmol, 4 ml of 50% magnesium sulfate) for refractory VF if there is any suspicion of hypomagnesemia (e.g. patients on potassium-losing diuretics); it maybe repeated after 10–15 min. Other indications are:
  • Ventricular tachyarrhythmias in the presence of possible hypomagnesemia
  • Torsade de pointes VT
  • Digoxin toxicity.
 
Bicarbonate
Cardiac arrest results in combined respiratory and metabolic acidosis because pulmonary gas exchange ceases and cellular metabolism becomes anaerobic. The best treatment of acidemia in cardiac arrest is chest compression; some additional benefit is gained by ventilation. Bicarbonate causes generation of carbon dioxide, which diffuses rapidly into cells. It has the following effects:
  • 641It exacerbates intracellular acidosis
  • It produces a negative inotropic effect on ischemic myocardium
  • It presents a large, osmotically active, sodium load to an already compromised circulation and brain
  • It produces a shift to the left in the oxygen dissociation curve, further inhibiting release of oxygen to the tissues.
Giving sodium bicarbonate routinely during cardiac arrest and CPR (especially in out-of hospital cardiac arrest), or after ROSC, is not recommended. Give sodium bicarbonate (50 mmol) if cardiac arrest is associated with hyperkalemia or tricyclic antidepressant overdose. Repeat the dose according to the clinical condition of the patient and the results of repeated blood gas analysis.
 
Calcium
Calcium plays a vital role in the cellular mechanisms underlying myocardial contraction. Give calcium during resuscitation only when indicated specifically, i.e. in cardiac arrest caused by hyperkalemia, hypocalcemia, or overdose of calcium channel-blocking drugs.
The initial dose of 10 ml 10% calcium chloride (6.8 mmol Ca2+) maybe repeated if necessary. Calcium can slow the heart rate and precipitate arrhythmias. In cardiac arrest, calcium maybe given by rapid intravenous injection. In the presence of a spontaneous circulation give it slowly. Do not give calcium solutions and sodium bicarbonate simultaneously by the same route.
 
Equipment
  • Oral airway
  • Bag and mask device
  • Oxygen
  • Intravenous (IV) setup
  • Defibrillator
  • Emergency cardiac drugs
  • Cardiac monitor
  • Electrocardiograph machine
  • Intubation equipment
  • Suction.
 
Procedure
Nursing Action
Rationale
Responsiveness/Airway
1. Determine unresponsiveness: tap or gently shake patient while shouting, ‘Are you okay?’
1. This will prevent injury from attempted resuscitation on a person who is not unconscious
Activate Emergency Medical Service
1. Place the patient supine on a firm, flat surface. Kneel at the level of the patient's shoulders. If head or neck trauma is suspected, he should not be moved unless it is absolutely necessary (e.g., at the site of an accident, fire, or other unsafe environment).
1. This enables the rescuer to perform rescue breathing and chest compression without changing position.
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Circulation
Determine presence or absence of pulse
1 While maintaining head-tilt with one hand on the patient's forehead, palpate the carotid or femoral pulse for no more than 10 seconds. If pulse is not palpable, start external chest compressions.
1 Cardiac arrest is recognized by pulselessness in the large arteries of the unconscious, breathless patient. If the patient has a palpable pulse, but is not breathing, initiate rescue breathing at rate of 12 times per minute (once every 5 seconds) after two initial breaths.
This procedure consists of serial, rhythmic applications of pressure over the middle third of the sternum.
1. Kneel as close to side of patient's chest as possible. Place the heel of one hand on the middle third of the sternum. The fingers may either be extended or interlaced but must be kept off the chest.
1. The long axis of the heel of the rescuer's hand should be placed on the long axis of the sternum so that the main force of the compression is on the sternum, thereby decreasing the chance of rib fracture.
2. While keeping your arms straight, elbows locked, and shoulders positioned directly over your hands, quickly and forcefully depress the middle third of the patient's sternum straight down one-third the depth of the chest.
3 Release the external chest compression completely and allow the chest to return to its normal position after each compression. The time allowed for release should equal the time required for compression. Do not lift your hands from the patient's chest or change position.
3. Release of the external chest compression allows blood flow into the heart.
4. For cardiopulmonary resuscitation (CPR) performed by one rescuer, do 30 compressions at a rate of 100 per minute and then perform two ventilations; re-evaluate the patient. After four cycles of 30 compressions and two breaths each, check the pulse; check again every few minutes thereafter. Minimize interruptions of chest compressions.
4. Rescue breathing and external chest compressions must be combined. Check for return of carotid pulse. If absent, resume CPR with two ventilations followed by compressions. For CPR performed by health professionals, mouth-to-mask ventilation is an acceptable alternative to rescue breathing.
5. For CPR performed by two rescuers, the compression rate is 100 per minute. The compression-ventilation ratio is 30:2. Once an advanced airway is in place, the compressing rescuer should give continuous chest compressions at a rate of 100 without pauses for ventilation. The rescuer delivering ventilation provides 8 to 10 breaths per minute.
Open the Airway
1. Head-tilt/chin-lift maneuver:
Place one hand on the patient's forehead and apply firm backward pressure with the palm to tilt the head back. Then, place the fingers of the other hand under the bony part of the lower jaw near the chin and lift up to bring the jaw forward and the teeth almost to occlusion.
1. In the absence of sufficient muscle tone, the tongue or epiglottis will obstruct the pharynx and larynx. This supports the jaw and helps tilt the head back.
2. Jaw-thrust maneuver:
Grasp the angles of the patient's lower jaw, lifting with both hands, one on each side; displacing the mandible forward, while tilting the head backward.
2. The jaw-thrust technique without head tilt is the safest method for opening the airway in the presence of suspected neck injury.
Breathing
1. Place ear over patient's mouth and nose while
observing the chest,
1. To determine presence or absence of spontaneous breathing.
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  • Look for the chest to rise and fall,
  • Listen for air escaping during exhalation,
  • Feel for the flow of air.
2. Perform rescue breathing by mouth-to-mouth, using:
  1. Ventilation barrier device. While keeping the patient's airway open, pinch the nostrils closed using the thumb and index finger of the hand you have placed on his forehead. Take a deep breath, open your mouth wide, and place it around the outside edge of the patient's mouth to create an air tight seal.
  2. Ventilate the patient with two full breaths (each lasting 1 second), taking a breath after each ventilation. If the initial ventilation attempt is unsuccessful, reposition the patient's head and repeat rescue breathing.
2. This prevents air from escaping from the patient's nose. Adequate ventilation is indicated by seeing the chest rise and fall, feeling the air escape during ventilation, and hearing the air escape during exhalation.
Usage of Special Resuscitation Equipment
1. While resuscitation proceeds, simultaneous efforts are made to obtain and use special resuscitation equipment to manage breathing and circulation and provide definitive care.
1. Definitive care includes defibrillation, pharma-cotherapy for dysrhythmias and acid base disturbances, and ongoing monitoring and skilled care in an intensive care unit.
2. Utilize the automated external defibrillator (AED) as soon as possible. Special circumstances affecting use of AEDs include:
  1. AEDs should not be used on children younger than age 8.
  2. The victim should not be lying in water when using an AED. Make sure the patient's chest is dry before attaching the AED.
  3. Do not place the AED electrode directly over an implanted pacemaker.
  4. Remove any transdermal medication patches from the patient before using the AED.
2. The American Heart Association supports the use of AEDs in public places as well as medical centers
  1. The default energy level of AEDs is too high for children younger than age 8.
  2. Using an AED when patients are wet or lying in water may result in burns and shocks to the rescuer.
  3. Placing an AED pad directly over an implanted pacemaker may reduce the effectiveness of the defibrillation.
  4. Placing an AED pad over a transdermal medication patch may make the defibrillation less effective and cause a burn.
3. The four basic steps used in AED operation are:
  1. Turn the power on.
  2. Attach the AED pads to the patient's chest, using the diagrams on the pads to show you exactly where to place them.
  3. Analyze the patient's rhythm by pushing the button on the AED labelled analyzes.
    During this time, no one should touch the patient.
  4. If the machine delivered a shock, anyone touching the patient.
3. The directions provided for operation of the AED were provided by the device manufacturer.
  1. Touching the patient could create artefact and interfere with analysis, tell you what to do.
  2. Charge the AED and deliver the shock if indicated by the AED. Make sure that no one is touching the patient. Push the shock button.
 
Complications
  • Postresuscitation distress syndrome (secondary derangements in multiple organs).
  • Neurological impairment, and or brain damage.
644
 
STRESS
It is an unpleasant psychological and physiological state caused due to some internal and external demands that goes beyond our capacity.
Stress maybe considered as any physical, chemical, or emotional factor that causes bodily or mental unrest and that maybe a factor in causing disease.
Stress is the response of the nervous system to stressors that are too large to handle. It is the internalized result of external overloads. It consists of stored abnormalities that serve to protect us from repeated exposure to the same overloads by limiting our functioning. Meaning of STRESS:
S—Situation
T—That
R—Release
E—Emergency
S—Signal (or)
S—Stimuli.
Stress management: Stress management is a process of learning how to live with the inevitable life stressor of people encounter by learning how to counteract or cope efficiency with counterproductive response to stress through enhanced self-activities.
 
Body Coping Mechanism with Stress
 
General Adaptive Syndrome Model
Hans Selye (1907–1982) explained his stress model based on physiology and psychobiology as General Adaptation Syndrome (GAS). Physiologists define stress as how the body reacts to a stressor, real or imagined, a stimulus that causes stress. Acute stressors affect an organism in the short-term; chronic stressors over the longer term.
  • Alarm stage: It is the first stage, which is divided into two phases: The shock phase and the antishock phase.
    • Shock phase: During this phase, the body can endure changes such as hypovolemia, hypo-osmolarity, hyponatremia, hypochloremia, hypoglycemia—the stressor effect. The organism's resistance to the stressor drops temporarily below the normal range and some level of shock (e.g. circulatory shock) maybe experienced.
    • Antishock phase: When the threat or stressor is identified or realized, the body starts to respond and is in a state of alarm. During this stage, the locus coeruleus/sympathetic nervous system is activated and catecholamines such as adrenaline are being produced, hence the fight-or-flight response. The result is: increased muscular tonus, increased blood pressure due to peripheral vasoconstriction and tachycardia, and increased glucose in blood.
  • Stage 1: Alarm
    • Upon encountering a stressor, body reacts with ‘fight-or-flight’ response and sympathetic nervous system is activated.
    • Hormones such as cortisol and adrenalin released into the bloodstream to meet the threat or danger.
    • The body's resources now mobilized.
645Example
Increased heart rate
Increased RBC production
Increased breathing
  • Resistance stage: It is the second stage and increased secretion of glucocorticoids play a major role, intensifying the systemic response—they have lypolytic, catabolic and antianabolic effects: increased glucose, fat and amino acid/protein concentration in blood. Moreover, they cause lymphocytopenia, eosinopenia, neutrophilia and polycythemia. In high doses, cortisol begins to act as a mineralocorticoid (aldosteron) and brings the body to a state similar to hyperaldosteronism. If the stressor persists, it becomes necessary to attempt some means of coping with the stress. Although the body begins to try to adapt to the strains or demands of the environment, the body cannot keep this up indefinitely, so its resources are gradually depleted.
  • Stage 2: Resistance
    • Parasympathetic nervous system returns many physiological functions to normal levels while body focuses resources against the stressor.
    • Blood glucose levels remain high, cortisol and adrenalin continue to circulate at elevated levels, but outward appearance of organism seems normal.
    • Increase HR, BP, breathing
    • Body remains on red alert.
  • Exhaustion or recovery stage
    • Recovery stage follows when the system's compensation mechanisms have successfully overcome the stressor effect (or have completely eliminated the factor 646which caused the stress). The high glucose, fat and amino acid levels in blood prove useful for anabolic reactions, restoration of homeostasis and regeneration of cells.
    • Exhaustion is the alternative third stage in the GAS model. At this point, all of the body's resources are eventually depleted and the body is unable to maintain normal function. The initial autonomic nervous system symptoms may reappear (sweating, raised heart rate, etc.). If stage three is extended, long-term damage may result (prolonged vasoconstriction results in ischemia which in turn leads to cell necrosis), as the body's immune system becomes exhausted, and bodily functions become impaired, resulting in decompensation.
  • Stage 3: Exhaustion
    • If stressor continues beyond body's capacity, organism exhausts resources and becomes susceptible to disease and death.
 
ADAPTIVE COPING STRATEGIES
  • Awareness: The initial step in managing stress is awareness:
    • To become aware of the factors that creates stress.
    • The feeling associative with a successful response.
    Stress can be controlled only when one recognise that is being experienced as they aware about stressors, they can omitted, avoided, or accepted.
  • Relaxation: Individual relax by engaging in large motor activities such as sports, jogging and physical exercise. Still other techniques such as breathing exercises and progressive relaxation to relieve stress.
  • Meditation: Practiced 20 minutes once or twice daily, meditation has been shown to produce a lasting reduction in blood pressure and other stress related symptoms. Meditation involves assuming a comfortable position, closing eyes, casting off all thoughts and concentrating on a single word, sound that has positive meaning to individual.
  • Interpersonal communication: The strength of one's available support system is an existing condition that put effect in coping with stress. By talking the problem out with other individual helps in reduction of stress.
  • Problem-solving: An extremely adaptive coping strategy is to view the situation objectively as follow:
    • Assess the facts of the situation.
    • Formulate goals for the resolution of the stressful situation.
    • Study the alternatives for dealing with the situation.
    • Determine the risk and benefits of each alternative.
    • Select an alternative.
    • Implement the alternative selected.
    • Evaluate the outcome of the alternative implemented.
    • If the first alternative is ineffective, select and implement a second alternative.
  • Pets: Petting a dog and cat can be therapeutic. It provide cool, calm, warmth, affection and interdependent with a reliable and trusting.
  • 647Music: Creating and listening music stimulate motivation, enjoyment and relaxation. Music can reduce depression and bring measurable changes in mood and general activity.
  • Connect with others: A good way to combat sadness, boredom and loneliness is to see out activities involving others.
  • Take a minute vacation: Imaging a quiet country scene can take you out of the stressful situation. Take a moment to close yours eyes and imagine a place where feel you relaxed and comfortable.
  • Laugh: Maintain your sense of humor including the ability to laugh at yourself.
  • Think positively: Refocus the negative to be positive. Make an effort to stop negative thoughts.
  • Compromise: By cooperation and compromise helps in reduction of strain and help you more comfortable.
  • Have a good cry: A good cry during periods of stress can be a healthy way to bring relief to your anxiety and prevent headache or others physical consequences.
  • Avoid self-medications: Alcohol and other medications do not remove stress. They may provide temporary relief. But it increase more complications.
  • Take care of your body: Healthy eating and adequate sleep fuels your mind as well as your body. Avoid consuming too much caffeine and sugar.
 
Role of Nurse in Stress Management Assessment
 
Nursing Assessment
  • Assessment of the person
    • To much dependence on others for love and affection
    • Inability to change or learn new ways of dealing with frustration.
    • High expectations.
  • Assessment of family
    • Assess the family perception of the problem and it is supportive of the client's efforts at copping.
  • Assessment of environment
    • Occupation with high stress
    • Enviormental factors like lighting and temperature.
 
Nursing Interventions
  • Increasing the client's awareness regarding as an actual health problem.
  • Helping him realize the health problem.
  • To support the client through the process of changes and cooperation with treatment.
  • The client encourage to talk about the losses that have result in behavior changes.
  • Family members also need accurate information about health problem.
 
ICU PSYCHOSIS
ICU psychosis is a disorder in which patients in an intensive care unit (ICU) or a similar setting experience a cluster of serious psychiatric symptoms. Another term that may be 648used interchangeably for ICU psychosis is ICU syndrome. ICU psychosis is also a form of delirium, or acute brain failure. Delirium is often used to refer to drowsiness, disorientation, and hallucination.
 
Etiology
 
Environmental Causes
  • Sensory deprivation: A patient being put in a room that often has no windows, and is away from family, friends, and all that is familiar and comforting.
  • Sleep disturbance and deprivation: The constant disturbance and noise with the hospital staff coming at all hours to check vital signs, give medications, etc.
  • Continuous light levels: Continuous disruption with lights (no reference to day or night).
  • Stress: Patients in an ICU frequently feel the almost total loss of control over their life.
  • Lack of orientation: A patient's loss of time and date.
  • Medical monitoring: The continuous monitoring of the patient's vital signs, and the noise monitoring devices produce can be disturbing and create sensory overload.
 
Medical Causes
  • Pain: Which may not be adequately controlled in an ICU.
  • Critical illness: The pathophysiology of the disease, illness or traumatic event—the stress on the body during an illness can cause a variety of symptoms.
  • Infection: Creating fever and toxins in the body.
  • Metabolic disturbances: Electrolyte imbalance, hypoxia (low blood oxygen levels), and elevated liver enzymes.
  • Heart failure (inadequate cardiac output).
 
Signs and Symptoms
The cluster of psychiatric symptoms of ICU psychosis include:
  • Extreme excitement
  • Anxiety
  • Restlessness
  • Hearing voices
  • Clouding of consciousness
  • Hallucinations
  • Nightmares
  • Paranoia
  • Disorientation
  • Agitation
  • Delusions
  • Abnormal behavior.
 
Diagnostic Evaluation
It is mainly diagnosed with the help of confusion assessment method (CAM). The diagnosis of ICU psychosis can be made only in the absence of a known underlying medical condition 649that can mimic the symptoms of ICU psychosis. A medical assessment of the patient is important to search for other causes of mental status abnormality such as:
  • Stroke
  • Low blood sugar
  • Drug or alcohol withdrawal
  • Any other medical condition that may require treatment.
 
Treatment
  • The treatment of ICU psychosis clearly depends on the cause. Many times the actual cause of the psychosis involves many factors, and many issues will need to be addressed to relieve the symptoms.
  • A first step is a review of the patient's medications. The physician in charge of the patient along with the pharmacist can review each of the patient's medications to determine if they maybe influencing the delirium.
  • Family members, familiar objects, and calm words may help.
  • Sleep deprivation maybe a major contributing factor. Therefore, providing a quiet restful environment to allow the patient optimal sleep is important.
  • Controlling the amount of time visitors are allowed to stimulate the patient can also help. Dehydration is remedied by administering fluids.
  • Heart failure requires treatment with digitalis.
  • Infections must be diagnosed and treated.
  • Sedation with antipsychotic agents may help. A common medication used in the hospital setting to treat ICU psychosis is haloperidol or other medications for psychosis (antipsychotics).
BIBLIOGRAPHY
  1. Joyce BM, Hawks HJ. Medical surgical nursing. 7th ed. Elsevier.  2005; 1906–8.
  1. Perry AG, Potter PA. Potter and Perry's fundamentals of nursing. 6th ed. Elsevier.  2005; 1106–9.

Gastrointestinal Disorders13

 
INTRODUCTION TO THE GASTROINTESTINAL SYSTEM
The gastrointestinal tract (GIT) consists of a hollow muscular tube starting from the oral cavity, where food enters the mouth, continuing through the pharynx, esophagus, stomach and intestines to the rectum and anus, where food is expelled. There are various accessory organs that assist the tract by secreting enzymes to help break down food into its component nutrients. Thus, the salivary glands, liver, pancreas and gallbladder have important functions in the digestive system. Food is propelled along the length of the GIT by peristaltic movements of the oral cavity
The oral cavity or mouth is responsible for the intake of food. It is lined by a stratified squamous oral mucosa with keratin covering those areas subject to significant abrasion, such as the tongue, hard palate and roof of the mouth. Mastication refers to the mechanical breakdown of food by chewing and chopping actions of the teeth. The tongue, a strong muscular organ, manipulates the food bolus to come in contact with the teeth. It is also the sensing organ of the mouth for touch, temperature and taste using its specialized sensors known as papillae.
Salivation refers to the mixing of the oral cavity contents with salivary gland secretions. The mucin (a glycoprotein) in saliva acts as a lubricant. The oral cavity also plays a limited 651role in the digestion of carbohydrates. The enzyme serum amylase, a component of saliva, starts the process of digestion of complex carbohydrates. The final function of the oral cavity is absorption of small molecules, such as glucose and water, across the mucosa. From the mouth, food passes through the pharynx and esophagus via the action of swallowing.
 
Salivary Glands
Three pairs of salivary glands communicate with the oral cavity. Each is a complex gland with numerous acini lined by secretory epithelium. The acini secrete their contents into specialized ducts. Each gland is divided into smaller segments called lobes. Salivation occurs in response to the taste, smell or even appearance of food. This occurs due to nerve signals that tell the salivary glands to secrete saliva to prepare and moisten the mouth. Each pair of salivary glands secretes saliva with slightly different compositions.
 
Esophagus
The esophagus is a muscular tube approximately 25 cm in length and 2 cm in diameter. It extends from the pharynx to the stomach after passing through an opening in the diaphragm. The wall of the esophagus is made up of inner circular and outer longitudinal layers of muscle that are supplied by the esophageal nerve plexus. This nerve plexus surrounds the lower portion of the esophagus. The esophagus functions primarily as a transport medium between compartments.
 
Stomach
The stomach is a J-shaped expanded bag, located just left of the midline between the esophagus and small intestine. It is divided into four main regions and has two borders called the greater and lesser curvatures. The first section is the cardia which surrounds the cardial orifice where the esophagus enters the stomach. The fundus is the superior, dilated portion of the stomach that has contact with the left dome of the diaphragm. The body is the largest section between the fundus and the curved portion of the J.
This is where most gastric glands are located and where most mixing of the food occurs. Finally, the pylorus is the curved base of the stomach. Gastric contents are expelled into the proximal duodenum via the pyloric sphincter. The inner surface of the stomach is contracted into numerous longitudinal folds called rugae. These allow the stomach to stretch and expand when food enters. The stomach can hold up to 1.5 liters of material. The functions of the stomach include:
  • The short-term storage of ingested food
  • Mechanical breakdown of food by churning and mixing motions
  • Chemical digestion of proteins by acids and enzymes
  • Stomach acid kills bugs and germs
  • Some absorption of substances such as alcohol.
 
Small Intestine
The small intestine is composed of the duodenum, jejunum, and ileum. It averages approximately 6 m in length, extending from the pyloric sphincter of the stomach to the ileocecal valve separating the ileum from the cecum. The small intestine is compressed into numerous folds and occupies a large proportion of the abdominal cavity.
652The duodenum is the proximal C-shaped section that curves around the head of the pancreas. The duodenum serves a mixing function as it combines digestive secretions from the pancreas and liver with the contents expelled from the stomach. The start of the jejunum is marked by a sharp bend, the duodenojejunal flexure. It is in the jejunum where the majority of digestion and absorption occur. The final portion, the ileum, is the longest segment and empties into the cecum at the ileocecal junction.
The small intestine performs the majority of digestion and absorption of nutrients. Partly digested food from the stomach is further broken down by enzymes from the pancreas and bile salts from the liver and gallbladder. These secretions enter the duodenum at the Ampulla of Vater. After further digestion, food constituents, such as proteins, fats, and carbohydrates are broken down to small building blocks and absorbed into the body's bloodstream.
The lining of the small intestine is made up of numerous permanent folds called plicae circulares. Each plica has numerous villi (folds of mucosa) and each villus is covered by epithelium with projecting microvilli (brush border). This increases the surface area for absorption by a factor of several hundred. The mucosa of the small intestine contains several specialized cells. Some are responsible for absorption, whilst others secrete digestive enzymes and mucus to protect the intestinal lining from digestive actions.
 
Large Intestine
The large intestine is horse-shoe-shaped and extends around the small intestine like a frame. It consists of the appendix, cecum, ascending, transverse, descending and sigmoid colon, and the rectum. It has a length of approximately 1.5 m and a width of 7.5 cm.
The cecum is the expanded pouch that receives material from the ileum and starts to compress food products into fecal material. Food then travels along the colon. The wall of the colon is made up of several pouches (haustra) that are held under tension by three thick bands of muscle (Taenia coli).
The rectum is the final 15 cm of the large intestine. It expands to hold fecal matter before it passes through the anorectal canal to the anus. Thick bands of muscle, known as sphincters, control the passage of feces.
 
Liver
The liver is a large, reddish-brown organ situated in the right upper quadrant of the abdomen. It is surrounded by a strong capsule and divided into four lobes, namely the right, left, caudate and quadrate lobes. The liver has several important functions. It acts as a mechanical filter by filtering blood that travels from the intestinal system. It detoxifies several metabolites including the breakdown of bilirubin and estrogen. In addition, the liver has synthetic functions, producing albumin and blood-clotting factors. However, its main roles in digestion are in the production of bile and metabolism of nutrients. All nutrients absorbed by the intestines pass through the liver and are processed before traveling to the rest of the body. The bile produced by cells of the liver enters the intestines at the duodenum. Here, bile salts break down lipids into smaller particles so there is a greater surface area for digestive enzymes to act.
 
Gallbladder
The gallbladder is a hollow, pear-shaped organ that sits in a depression on the posterior surface of the liver's right lobe. It consists of a fundus, body and neck. It empties via the 653cystic duct into the biliary duct system. The main functions of the gall bladder are storage and concentration of bile. Bile is a thick fluid that contains enzymes to help dissolve fat in the intestines. Bile is produced by the liver but stored in the gallbladder until it is needed. Bile is released from the gall bladder by contraction of its muscular walls in response to hormone signals from the duodenum in the presence of food.
 
Pancreas
Finally, the pancreas is a lobular, pinkish-grey organ that lies behind the stomach. Its head communicates with the duodenum and its tail extends to the spleen. The organ is approximately 15 cm in length with a long, slender body connecting the head and tail segments. The pancreas has both exocrine and endocrine functions. Endocrine refers to production of hormones which occurs in the Islets of Langerhans. The Islets produce insulin, glucagon and other substances and these are the areas damaged in diabetes mellitus. The exocrine (secretory) portion makes up 80–85% of the pancreas and is the area relevant to the gastrointestinal tract.
It is made up of numerous acini (small glands) that secrete contents into ducts which eventually lead to the duodenum. The pancreas secretes fluid rich in carbohydrates and inactive enzymes. Secretion is triggered by the hormones released by the duodenum in the presence of food. Pancreatic enzymes include carbohydrases, lipases, nucleases and proteolytic enzymes that can break down different components of food. These are secreted in an inactive form to prevent digestion of the pancreas itself. The enzymes become active once they reach the duodenum.
 
GASTROINTESTINAL DISORDERS
 
Gastroesophageal Reflux Disease (GERD)
Gastroesophageal reflux (GER) occurs when stomach contents flow back up into the esophagus. GER is also called acid reflux or acid regurgitation which is characterized by heartburn, burning feeling in the midchest, behind the breastbone, or in the upper part of the abdomen.
Gastroesophageal reflux disease results when the lower esophageal sphincter becomes weak or relaxes when it should not, causing stomach contents to rise up into the esophagus called GERD.
 
Etiology
  • Obesity
  • Pregnancy
  • Certain medications, such as asthma medications, calcium channel blockers, and many antihistamines, pain-killers, sedatives, and antidepressants
  • Smoking, or inhaling second-hand smoke
  • Use of spicy foods
  • Sudden falling to sleep after meal
  • Congenital weakness of LES
654
 
Signs and Symptoms
  • Dry, chronic cough
  • Wheezing
  • Asthma and recurrent pneumonia
  • Nausea
  • Vomiting
  • Sore throat, hoarseness, or laryngitis—swelling and irritation of the voice box
  • Difficulty swallowing or painful swallowing
  • Pain in the chest or the upper part of the abdomen
  • Dental erosion and bad breath
 
Pathophysiology
 
Diagnostic Evaluation
  • Upper GI series: During this procedure, the person will stand or sit in front of an X-ray machine and drink barium, a chalky liquid. Barium coats the esophagus, stomach, and small intestine so the radiologist and gastroenterologist can see theses organs' shapes more clearly on X-rays. The barium shows problems related to GERD, such as hiatal hernias.
  • Upper endoscopy, also known as an esophagogastroduodenoscopy: This procedure involves using an endoscope, a small, flexible tube with a light, to see the upper GI tract. The person may receive a liquid anesthetic that is gargled or sprayed on the back of the throat. After the person receives sedation, the gastroenterologist carefully feeds an endoscope through the mouth and down the esophagus, then into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining.
  • 655Esophageal pH monitoring: The most accurate test to detect acid reflux, esophageal pH monitoring measures the amount of liquid or acid in the esophagus. A gastroenterologist will pass a thin tube, called a nasogastric probe, through the person's nose or mouth to the stomach. The gastroenterologist will then pull the tube back into the esophagus, where it will be taped to the person's cheek and remain in place for 24 hours. The end of the tube in the esophagus has a small probe to measure when and how much liquid or acid comes up into the esophagus. The other end of the tube, attached to a monitor outside the body, shows the measurements taken.
  • Esophageal manometry: Esophageal manometry measures muscle contractions in the esophagus.
 
Management
 
Lifestyle Changes
  • Losing weight
  • Wearing loose-fitting clothing around the stomach area
  • Remaining upright for 3 hours after meals
  • Raising the head of the bed 6 to 8 inches by securing wood blocks under the bedposts
  • Avoiding smoking.
 
Pharmacological Management
  • Antacids, which include over-the-counter medications, recommend relieving heartburn and other mild GERD symptoms
  • H2 blockers, such as cimetidine, famotidine and ranitidine, decrease acid production.
  • PPIs include omeprazole, pantoprazole
  • Prokinetics, which include bethanechol and metoclopramide, help make the stomach empty faster
  • Antibiotics, including one called erythromycin, have been shown to improve gastric emptying.
 
Surgical Management
  • Fundoplication is an operation to sew the top of the stomach around the esophagus to add pressure to the lower end of the esophagus and reduce reflux. A surgeon performs fundoplication using a laparoscope, a thin tube with a tiny video camera attached used to look inside the body.
  • Endoscopic techniques, such as endoscopic sewing and radiofrequency. Endoscopic sewing uses small stitches to tighten the sphincter muscle. Radiofrequency creates heat lesions that help tighten the sphincter muscle.
 
Nursing Intervention
  • Develop a diet for the patient that takes his food preferences into account while helping to minimize reflux symptoms.
  • 656To reduce intra-abdominal pressure, encourage the patient to sleep in reverse Trendelenburg's position with the head of the bed elevated 6” to 12”.
  • Encourage the patent to avoid lying down immediately after meals and late-night snacks.
  • Monitor the patient's response to therapy and compliance with treatment.
  • If surgery was performed, monitor his intake and output and vital signs.
  • Monitor for complication of the disease and of surgery, if appropriate.
  • Teach the patient about the causes of gastroesophageal reflux, and review his antireflux regimen for medication, diet, and positional therapy.
  • Discuss the recommended dietary changes.
  • Instruct the patient to avoid situations or activities that increase intra-abdominal pressure.
  • Encourage the patient's compliance with his drug regimen.
  • Administer the prescribed medications.
  • Avoid aspirin, which is an anticoagulant, and foods and beverages that contain acid-enhancing caffeine (colas, tea, coffee, chocolate), along with decaffeinated coffee.
  • Encourage patient to eat meals at regular intervals in a relaxed atmosphere, obtain regular weights and encourage dietary modifications.
  • Encourage relaxation techniques.
  • Assess what patient wants to know about the disease, and evaluate level of anxiety, encourage patient to express fears openly and without criticism.
  • Explain diagnostic tests and administering medications on schedule.
  • Interact in a relaxing manner, help in identifying stressors, and explain effective coping techniques and relaxation methods.
  • Encourage family to participate in care, and give emotional support.
  • Assess for faintness or dizziness and nausea, before or with bleeding, test stool for occult or gross blood, and monitor vital signs frequently (tachycardia, hypotension, and tachypnea).
  • Insert an indwelling urinary catheter and monitor intake and output, insert and maintain an IV line for infusing fluid and blood.
  • Monitor laboratory values (hemoglobin and hematocrit).
  • Insert and maintain a nasogastric tube and monitor drainage, provide lavage as ordered.
  • Monitor oxygen saturation and administering oxygen therapy.
  • Place the patient in the recumbent position with the legs elevated to prevent hypotension, or place the patient on the left side to prevent aspiration from vomiting.
  • Treat hypovolemic shock as indicated.
 
HIATAL HERNIA
A hiatal hernia occurs when part of stomach pushes upward through diaphragm. Diaphragm normally has a small opening (hiatus) through which esophagus passes on its way to connect to stomach. The stomach can push up through this opening and cause a hiatal hernia.
657
Fig. 13.1: Types of hiatal hernia
 
Etiology
  • Injury to the area
  • Born with an unusually large hiatus
  • Persistent and intense pressure on the surrounding muscles, such as when coughing, vomiting, or straining during a bowel movement or while lifting heavy objects.
 
Signs and Symptoms
  • Most small hiatal hernias cause no signs or symptoms
  • Heartburn
  • Belching
  • Difficulty swallowing
  • Fatigue.
 
Diagnostic Evaluation
  • Barium X-ray: During a barium X-ray, patient is asked to drink chalky liquid containing barium that coats upper digestive tract. This provides a clear view of esophagus, stomach and the upper part of small intestine.
  • Endoscopy: During an endoscopy examination, a thin, flexible tube equipped with a light and video camera (endoscope) is inserted down in throat and into esophagus and stomach to check for inflammation.
 
Management
  • Antacids that neutralize stomach acid, magnesium hydroxide, aluminum hydroxides
  • H-2-receptor blockers, cimetidine, famotidine and ranitidine
  • Proton pump inhibitors block acid production lansoprazole and omeprazole.
 
Surgical Management
Surgery to repair a hiatal hernia, an operation for a hiatal hernia may involve pulling stomach down into abdomen and making the opening in diaphragm smaller, reconstructing a weak esophageal sphincter, or removing the hernia sac (Also see surgical management of GERD).
658
 
Nursing Management
  • Prepare the patient for diagnostic tests, as needed.
  • Administer prescribed antacids and other medications.
  • To reduce intra-abdominal pressure and prevent aspiration, have the patient sleep in a reverse Trendelenburg position with the head of the bed elevated.
  • Assess the patient's response to treatment.
  • Observe for complications, especially significant bleeding, pulmonary aspiration, or incarceration or strangulation of the herniated stomach portion.
  • After endoscopy, watch for signs of perforation, such as falling blood pressure, rapid pulse, shock, and sudden pain caused by endoscope.
  • To enhance compliance, teach the patient about the disorder. Explain significant symptoms, diagnostic tests, and prescribed treatments.
  • Review prescribed medications, explaining their desired actions and possible adverse effects.
  • Teach the patient dietary changes to reduce reflux.
  • Encourage the patient to delay lying down for 2 hours after eating.
 
PEPTIC ULCERS
Peptic ulcers are open sores that develop on the inside lining of esophagus, stomach and the upper portion of small intestine. It is characterized by abdominal pain.
Fig. 13.2: Peptic ulcer
 
Classification of Peptic Ulcer
  • By Region
    • Duodenal ulcer
    • Esophageal ulcer
    • Gastric ulcer
    • Meckel's diverticulum
  • 659Modified Johnson Classification
    • Type I: Ulcer along the body of the stomach, most often along the lesser curve.
    • Type II: Ulcer in the body in combination with duodenal ulcers.
    • Type III: In the pyloric channel within 3 cm of pylorus.
    • Type IV: Proximal gastroesophageal ulcer.
    • Type V: Can occur throughout the stomach.
 
Etiology
  • Lifestyle: These factors include cigarettes, foods and beverages containing caffeine, alcohol, and physical stress.
  • Smoking: Smoking slows the healing of existing ulcers and also contributes to ulcer recurrence.
  • Caffeine: Coffee, tea, colas, and foods that contain caffeine seem to stimulate acid secretion in the stomach, aggravating the pain of an existing ulcer. However, the amount of acid secretion that occurs after drinking decaffeinated coffee is the same as that produced after drinking regular coffee.
  • Alcohol: Ulcers are more common in people who have cirrhosis of the liver.
  • Stress: Emotional stress increases ulcer pain. Physical stress increases the risk of developing ulcers particularly in the stomach.
  • Acid and pepsin: The stomach's inability to defend itself against the powerful digestive fluids, acid and pepsin contributes to ulcer formation.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) make the stomach vulnerable to the harmful effects of acid and pepsin.
  • Helicobacter pylori: H. pylori is a spiral-shaped bacterium found in the stomach and damage stomach and duodenal tissue, causing inflammation and ulcers.
Characteristics
Gastric ulcer
Duodenal ulcer
Incidence
Age = 50 years or above
Male : Female = 1 : 1
15% of peptic ulcers are gastric
Age = 30–60 years
Male : Female = 2–3 : 1
80% of peptic ulcers are duodenal
Definition
Ulcers that occur in the stomach are called gastric ulcers
The duodenum ulcer refers to the upper region of the small intestine
Causes
Helicobacter pylori infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDs).
Excess stomach acid
Helicobacter pylori bacteria
Signs and symptoms
Gastric ulcer causes stomach pain immediate and 1–2 hours after eating
Duodenal ulcer causes pain 3–4 hours later
Gastric ulcer causes hematemesis or vomiting of blood
Duodenal ulcers cause melena or blood in the stool
Located in epigastric area (area between belly button and rib cage)
Pain below the ribs and just below the breastbone
Gastric ulcer causes an aching, burning
Duodenal ulcers cause an aching, burning, hunger-like pain in the upper-middle portion of the abdomen
Vomiting is common
Vomiting is uncommon
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Normal and Hyposecretion of HCl
Hypersecretion of HCl
No Telltale sign of a duodenal ulcer is pain that occurs during the middle of the night
Telltale sign of a duodenal ulcer is pain that occurs during the middle of the night
This pain tends to develop or worsen when the stomach is full
This pain tends to develop or worsen when the stomach is relatively empty
Malignancy possibility
Rare
Occasionally
Risk factors
Alcohol, smoking, cirrhosis, stress
Use of NSAIDs, gastritis, alcohol, smoking
Diet
A gastric ulcer has a special diet
Duodenal ulcers do not have a special diet.
 
Signs and Symptoms
Pain is the Most Common Symptom
Burning pain is the most common peptic ulcer symptom. The pain is caused by the ulcer and is aggravated by stomach acid coming in contact with the ulcerated area. The pain typically may:
  • Be felt anywhere from navel up to breastbone
  • Be worse when stomach is empty
  • Flare at night
  • Often be temporarily relieved by eating certain foods that buffer stomach acid or by taking an acid-reducing medication
  • Disappear and then return for a few days or weeks
  • Blood in vomiting (hemoptysis)
  • Dark blood in stools or stools that are black or tarry (malena)
  • Nausea or vomiting
  • Unexplained weight loss
  • Appetite changes.
 
Pathophysiology
Duodenal ulcer:
661Gastric ulcer:
 
Complications
  • Internal bleeding: Bleeding can occur as slow blood loss that leads to anemia or as severe blood loss that may require hospitalization or a blood transfusion. Severe blood loss may cause black or bloody vomit or black or bloody stools.
  • Infection: Peptic ulcers can create a hole through the wall of stomach or small intestine, putting at risk of serious infection of abdominal cavity (peritonitis).
  • Scar tissue: Peptic ulcers can also produce scar tissue that can block passage of food through the digestive tract, causing to become full easily, to vomit and to lose weight.
 
Diagnostic Evaluation
 
Blood Tests
The body produces antibodies against H. pylori in an attempt to fight the bacteria. The disadvantage is the possibility of false positive results in patients previously treated for ulcers since the levels of H. pylori antibodies fall slowly.
 
Breath Tests
Breath tests measure carbon dioxide in exhaled breath. Patients are given a substance called urea with carbon to drink. Bacteria break down this urea and the carbon is absorbed into 662the bloodstream and lungs and exhaled in the breath. By collecting the breath, doctors can measure this carbon and determine whether H. pylori are present or absent.
 
Tissue Tests
A rapid urease test detects the bacteria's enzyme urease. Histology involves visualizing the bacteria under the microscope. Culture involves specially processing the tissue and watching it for growth of H. pylori organisms.
 
Management
 
Medical Management
  • Antacids: Antacids neutralize existing acid in the stomach. Antacids such as maalox, mylanta, and amphojel are safe and effective treatments. The neutralizing action of these agents is short-lived, and frequent dosing is required. Magnesium containing antacids, such as maalox and mylanta, can cause diarrhea, and aluminum-containing agents like amphojel can cause constipation.
  • H2 Blockers: Histamine antagonists (H2 blockers) are drugs designed to block the action of histamine on gastric cells and reduce the production of acid.
  • Examples of H2 blockers:
    • Cimetidine
    • Ranitidine
    • Nizatidine
    • Famotidine
  • Proton-Pump Inhibitors (PPIs): These are more potent than H2 blockers in suppressing acid secretion. Proton-pump inhibitors are comparable to H2 blockers in effectiveness in treating gastric and duodenal ulcers. They are superior to H2 blockers in treating esophageal ulcers. Esophageal ulcers are more sensitive than gastric and duodenal ulcers to minute amounts of acid. Therefore, more complete acid suppression accomplished by proton-pump inhibitors is important for esophageal ulcer healing. Proton-pump inhibitors do not have any effect on a person's ability to digest and absorb nutrients.
    Example:
    • Omeprazole
    • Pantoprazole
    • Esomeprazole
    • Rabeprazole
  • Sucralfate and misoprostol: Sucralfate coats the ulcer surface and promotes healing. Sucralfate has very few side effects. The most common side effect is constipation and the interference with the absorption of other medications.
    Misoprostol is a prostaglandin-like substance commonly used to counteract the ulcerogenic effects of NSAIDs.
  • H. pylori Treatment: Treatment requires a combination of several antibiotics, sometimes in combination with a proton-pump inhibitor, H2 blockers.
  • Antibiotics: Tetracycline, amoxicillin, metronidazole, clarithromycin and levofloxacin (levaquin). Eradication of H. pylori.
  • 663Probiotic Supplement: (Containing Lactobacillus acidophilus), 5–10 billion CFUs (colony-forming units) a day. Probiotics bacteria may help maintain a balance in the digestive system between good and harmful bacteria such as H. pylori. Probiotics may help suppress H. pylori infection and may also help reduce side effects from taking antibiotics, the treatment for an H. pylori infection.
  • Vitamin C: 500–1,000 mg 1–3 times daily. Taking vitamin C along with triple therapy allowed the dose of one antibiotic to be lower. Vitamin C may also be helpful in treating bleeding stomach ulcers caused by aspirin use.
  • Herbs: Use herbs as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise, make teas with 1 tsp herb per cup of hot water. Steep covered 5–10 minutes for leaf or flowers, and 10–20 minutes for roots. Drink 2–4 cups per day.
  • Cranberry 400 mg twice daily. Cranberry may inhibit H. pylori growth in the stomach. Large amounts of cranberry may be inappropriate for people who are allergic to aspirin due to the fact that cranberry contains salicylic acid. Cranberry extracts also can contain high levels of a chemical called oxalate, which may increase the risk of developing kidney stones.
 
Surgical Management
  • Vagotomy: A vagotomy is a surgical procedure that involves resection of the vagus nerve. Vagus nerve, which transmits messages from the brain to the stomach, is cut. Interrupting these messages reduces acid secretion. However, there can be side effects, such as severe, persistent abdominal pain, vomiting, or diarrhea. The surgery may also interfere with stomach emptying. The newest variation of this surgery involves cutting the only parts of the nerve that control the acid-secreting cells of the stomach. This avoids the parts of the nerve that influence stomach emptying.
 
Types of Vagotomy
  • Truncal vagotomy: It involves division of the anterior and posterior vagal trunks close to the abdominal esophagus and just below the diaphragm. This operation is very successful at reducing acid secretion and, therefore, it promotes ulcer healing.
  • Selective vagotomy: It is an operative means of reducing gastric acid output. Vagal fibers passing to the stomach are divided, whilst those fibers passing to and from the abdominal viscera are preserved. This technique is particularly indicated where gastric drainage has to be employed, e.g. with pyloric stenosis, stenosing or bleeding duodenal ulcers.
  • High selective vagotomy: A vagotomy for peptic ulceration is to reduce parietal cell acid output. Apart from targeting the cells themselves, the easiest way of doing this without disturbing parietal cell function distal to the site is to cut only the closest branches of the nerve. This is done with a highly selective vagotomy.
    • Antrectomy: In this surgery, the lower part of the stomach (antrum) is removed. This section of the stomach produces a hormone that stimulates the stomach to secrete digestive juices. Sometimes a surgeon may also remove an adjacent part of the stomach that secretes pepsin and acid. A vagotomy is usually done in conjunction with an antrectomy.
      1. 664Billroth-I (Gastroduodenostomy): Removal of lower portion of the antrum of the stomach as well as a small portion of duodenum and pylorus. The remaining segment is anatomosed to the duodenum.
      2. Billroth-II (Gastrojejunostomy): Removal of lower portion of the antrum of the stomach as well as a small portion of duodenum and pylorus. The remaining segment is anatomosed to the jejunum.
  • Pyloroplasty: This surgery enlarges the opening to the duodenum and small intestine (pylorus), which enables stomach contents to pass more freely out of the stomach. A vagotomy may also be performed along with a pyloroplasty.
    • Gastrectomy: Gastrectomy is surgery to remove part or all of the stomach.
    1. Partial gastrectomy: Removing part of the stomach is called partial gastrectomy.
    2. Complete gastrectomy: Removing the complete stomach is called gastrectomy.
 
Nutritional Management
  • Foods containing flavonoids, like apples, celery, cranberries (including cranberry juice), onions, garlic, and tea may inhibit the growth of H. pylori.
  • Eat antioxidant-rich foods, including fruits (such as blueberries, cherries, and tomatoes), and vegetables (such as squash and bell peppers).
  • Eat foods high in B vitamins and calcium, such as almonds, beans, whole grains (if no allergy), dark leafy greens (such as spinach and kale), and sea vegetables.
  • Avoid refined foods, such as white breads, pastas, and sugar.
  • Eat fewer red meats and more lean meats, cold water fish, tofu (soy, if no allergy) or beans for protein.
  • Use healthy oils, such as olive oil or vegetable oil.
  • Reduce or eliminate trans-fatty acids, found in commercially baked goods, such as cookies, crackers, cakes, French fries, onion rings, donuts, processed foods, and margarine.
  • Avoid beverages that may irritate the stomach lining or increase acid production including coffee (with or without caffeine), alcohol, and carbonated beverages.
  • Drink 6–8 glasses of filtered water daily.
  • Exercise at least 30 minutes daily, 5 days a week.
 
Prevention
  • Eat a diet rich in fiber, especially from fruits and vegetables. This may reduce risk of developing an ulcer in the first place and speedy recovery.
  • Foods containing flavonoids, like apples, celery, cranberries (including cranberry juice), onions, garlic, and tea may inhibit the growth of H. pylori.
  • Some people may find that spicy foods make existing symptoms worse.
  • Quit smoking.
  • Receive treatment for alcohol abuse.
  • Cut down on coffee, including decaffeinated coffee, as well as carbonated beverages. All can increase stomach acid.
  • Reduce stress with regular use of relaxation techniques, such as yoga, tai chi.
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Complications
  • Gastrointestinal bleeding: It is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
  • Perforation: A hole in the wall often leads to catastrophic consequences. Erosion of the gastrointestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to bleeding due to involvement of gastroduodenal artery that lies posterior to the 1st part of duodenum.
  • Penetration: It is when the ulcer continues into adjacent organs, such as the liver and pancreas.
  • Gastric outlet obstruction: Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting.
  • Cancer: It is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.
  • Dumping syndrome: It occurs after gastrojejunostomy because ingested food rapidly enters the jejunum without proper mixing and without the duodenum digestive process. It is usually subsided within 6–12 months.
 
Nursing Management
  1. Acute pain related to irritation of the mucosa and muscle spasms.
    Interventions
    • Give drug therapy according to the program.
    • Instruct to avoid drugs that are sold freely, especially those containing salicylates. Medicines containing salicylates may irritate the gastric mucosa.
    • Encourage clients to avoid foods and drinks that irritate the gastric mucosa, such as caffeine and alcohol.
    • Encourage clients to use the meals and snacks at regular intervals. Scheduled regular eating helps retain food particles in the stomach that help neutralize the acidity of gastric secretions.
    • Instruct patient to stop smoking. Smoking can stimulate ulcer recurrence.
  2. Anxiety related to the nature of the disease and long-term management.
    Interventions
    • Encourage clients to express their problems and fears and ask questions as needed. Open communication helps clients develop trusting relationships that help reduce anxiety and stress.
    • Explain the reasons for the planned treatment schedule, such as pharmacotherapy, dietary restrictions, modification of activity levels, reducing or stopping smoking.
    • Assist clients to identify situations that cause anxiety. Stressors need to be identified before it can be overcome.
    • 666Teach stress management strategies, e.g. drugs, distraction, and imagination. Decreased anxiety decreases the secretion of hydrochloric acid.
  3. Imbalanced nutrition, less than body requirements related to pain.
    Interventions
    • Encourage eating foods and drinks that do not irritate. Food and drinks are not irritating to help reduce epigastric pain
    • Encourage eating on a regular schedule, avoid snacks before bedtime. Eating regularly helps neutralize gastric acid secretion, snack before bedtime increases the secretion of gastric acid.
    • Encourage eating food in a relaxed environment. Less relaxed environment cause anxiety. Decreased anxiety helps reduce the secretion of hydrochloric acid.
  4. Knowledge deficit: The prevention and treatment of symptoms related to the condition of inadequate information.
    Interventions
    • Assess the level of knowledge and readiness to learn from clients. Desire to learn depends on the physical condition of the client, the level of anxiety and mental readiness.
    • Teach the required information: Use words that correspond with the level of knowledge of the client. Choose a time when most convenient, and interested clients are there. Limit counseling sessions to 30 minutes or less.
    • Assure the client that the disease can be overcome.
 
APPENDICITIS
Appendicitis is an inflammation of the appendix. The inflamed appendix becomes infected with bacteria from the intestine. The inflamed appendix gradually swells and fills with pus. Appendicitis is a medical emergency that requires prompt surgery to remove the appendix. Left untreated, an inflamed appendix will eventually burst, or perforate, spilling infectious materials into the abdominal cavity. This can lead to peritonitis.
 
Etiology
  • An obstruction: Food waste or a hard piece of stool (fecal stone) can block the opening of the cavity that runs the length of appendix.
  • An infection: Appendicitis may also follow an infection, such as a gastrointestinal viral infection, or it may result from other types of inflammation.
 
Signs and Symptoms
  • Aching pain that begins around the navel and often shifts to lower right abdomen (pain usually occurs at McBurney's point over the right side of the abdomen that is one-third of the distance from the anterior superior iliac spine to the umbilicus).
  • Pain that becomes sharper over several hours.
  • Tenderness
  • Sharp pain in lower right abdomen that occurs when the area is pressed on and then the pressure is quickly released (Aure-Rozanova sign).
  • 667Pain that worsens during coughing (Dunphy's sign).
  • Nausea
  • Vomiting
  • Loss of appetite
  • Low-grade fever
  • Constipation
  • Inability to pass gas
  • Diarrhea
  • Abdominal swelling.
 
Diagnostic Evaluation
  • Physical examination: A gentle pressure on the painful area. When the pressure is suddenly released, appendicitis pain will often feel worse, signaling that the adjacent peritoneum is inflamed
  • Blood test: High white blood cell count, which may indicate an infection.
  • Urine test: Urinalysis to make sure that a urinary tract infection or a kidney stone is not causing pain.
  • Imaging tests: An abdominal X-ray, an ultrasound scan or a computerized tomography (CT) scan to help confirm appendicitis.
 
Complications
  • Ruptured appendix: If appendix ruptures, the contents of intestines and infectious organisms can leak into abdominal cavity. This can cause peritonitis.
 
Management
 
Appendectomy
Appendectomy can be performed as open surgery using one abdominal incision that is about 2 to 4 inches long. Or appendicitis surgery can be done as a laparoscopic operation, which involves a few small abdominal incisions. During a laparoscopic appendectomy, the surgeon inserts special surgical tools and a video camera into the abdomen to remove appendix.
 
Lifestyle and Home Remedies
  • Avoid strenuous activity.
  • Support abdomen when coughing.
  • Don't wear tight clothes, like tight belt, etc.
 
Nursing Management
 
Presurgery
  • Installation of nasogastric tube to decompress.
  • Catheters to control urine production.
  • Rehydration
  • Giving antibiotics with broad-spectrum, high doses given intravenously.
  • 668Medicines for fever.
  • If fever, must be lowered before anesthesia.
 
Postsurgery
  • Observation of vital signs.
  • Lift the nasogastric tube; if the patient had been aware of that, aspiration of gastric fluid can be prevented.
  • Put the patient in a semi-Fowler's position.
  • Patients are said to be good when in the last 12 hours without any disturbance, while the patient fasted.
  • When the surgery is greater, for example, on perforation, fasting was continued until bowel function returned to normal.
  • Give the drink starting to 15 ml/h for 4–5 hours and then raise it to 30 ml/hour.
  • One day after surgery patients are encouraged to sit up in bed.
  • On the second day, the patient can stand and sit outside the room.
 
HEMORRHOIDS
Hemorrhoids are enlarged veins in the anus or lower rectum. These comprise the blood supply to the anus and distal rectum.
 
Etiology
  • Constipation
  • Diarrhea
  • Lack of exercise
  • Nutritional factors (low-fiber diets)
  • Increased intra-abdominal pressure
  • Genetics
  • Aging
  • Obesity
  • Prolonged sitting
  • Chronic cough
  • Pregnancy
 
Types
  • External hemorrhoids appear on the outside of the anus, especially around the anal opening. They too can cause a lot of discomfort because of constant friction with clothes, etc.
  • Prolapsed hemorrhoids basically represent a later stage in the development cycle of internal hemorrhoids. When the latter become too bulky due to clogging of the veins with blood, they begin to sag and consequently protrude from the anus.
  • Bleeding hemorrhoids are also a more severe form or stage of internal hemorrhoids characterized by profuse bleeding.
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Pathophysiology
 
Diagnostic Evaluation
  • Examination of anal canal and rectum for abnormalities
  • Visual inspection of anal canal and rectum
 
Management
 
Medications
If hemorrhoids produce only mild discomfort, over-the-counter creams, ointments, suppositories or pads are recommended. These products contain ingredients, such as hydrocortisone, that can relieve pain and itching.
 
Surgical Management
  • Rubber band ligation: One or two tiny rubber bands around the base of an internal hemorrhoid are placed to cut-off its circulation. The hemorrhoid withers and falls off within a week.
  • Sclerotherapy: In this procedure, injection of a chemical solution is introduced into the hemorrhoid tissue to shrink it. While the injection causes little or no pain, it may be less effective than rubber band ligation.
  • Coagulation (infrared, laser or bipolar): Coagulation techniques use laser or infrared light or heat. They cause small, bleeding, internal hemorrhoids to harden and shrivel.
  • Hemorrhoidectomy: During a hemorrhoidectomy, removal of excessive tissue causes bleeding. Various techniques may be used. The surgery may be done with a local anesthetic combined with sedation, a spinal anesthetic or a general anesthetic. Hemorrhoidectomy is the most effective and complete way to treat severe or recurring hemorrhoids.
  • Hemorrhoid stapling: This procedure, called stapled hemorrhoidectomy or stapled hemorrhoidopexy, blocks blood flow to hemorrhoidal tissue. Stapling generally involves less pain than hemorrhoidectomy and allows an earlier return to regular activities.
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Nursing Management
Preoperative Care
  • Give soaking seat.
    Rationalization: Reduce local discomfort, reduce edema and promote healing.
  • Give lubricant during defecation wound.
    Rationalization: Assist in the conduct of defecation so it does not need straining.
  • Give a diet low in residual.
    Rationalization: Reduce stimulation of the anus and weaken the feces.
  • Instruct the patient to do a lot of standing or sitting (must be in balance).
    Rationalization: The force of gravity will affect the incidence of hemorrhoids and sitting can increase intra-abdominal pressure.
  • Observation of patient complaints.
    Rationalization: It helps to evaluate the degree of discomfort and lack of effectiveness of actions or states of complications.
  • Provide an explanation of the emergence of pain and explain briefly.
    Rationalization: Education about it helps in patient's participation to prevent and reduce pain.
  • Give the patient suppository.
    Rationalization: It can soften the stool and can enable the patient to avoid straining during defecation.
Postoperative Care
  • Give the patient a pleasant sleeping position.
    Rationalization: May decrease the pressure on the abdomen and increase the sense of control.
  • Change the bandage every morning according to aseptic techniques.
    Rationalization: Protecting the patient from cross contamination during replacement of bandages. Wet bandage acts as an absorber of external contamination and causes discomfort.
  • Exercise as early as possible.
    Rationalization: It can reduce the problems that occur due to immobilization.
  • Observation of the rectal area if there is bleeding.
    Rationalization: Bleeding on the network may increase the pain.
  • Provide an explanation of the purpose of installation of flue-anus.
    Rationalization: Knowledge of the benefits of the chimney can make the patient understand the anus to funnel anus to cure the wound.
 
Postoperative Complications
Most patients are satisfied with the results of the surgery and recover without any problems. Complications associated with hemorrhoidectomy are rare and include:
  • Anal fistula or fissure
  • Constipation
  • Excessive bleeding
  • 671Excessive discharge of fluid from the rectum
  • Fever of 101°F or higher
  • Inability to urinate or have a bowel movement
  • Severe pain, especially when having a bowel movement
  • Severe redness and swelling in the rectal area.
 
Nursing Diagnosis
  • Ineffective breathing pattern related to decreased pressure inspiration, expiration for anesthetic agent administration.
  • Fluid volume and electrolyte deficit related to lack of or loss of fluid volume during surgery.
  • Risk for injury related to the effects of anesthesia and weakness.
  • Risk for hypothermia related to multiple factors of age, body weight, factors trauma, neuromuscular and environment.
 
Nursing Interventions
  • Administer local anesthetic as prescribed.
  • As needed, provide warm sitz baths or cold compresses to reduce local pain, swelling, and information.
  • Provide the patient with high-fiber diet and encourage adequate fluid intake and exercise to prevent constipation.
  • Monitor the patient's pain level and the effectiveness of the prescribed medications.
  • Check for signs and symptoms of anal infection, such as increased pain and foul-smelling anal drainage.
  • Teach the patient about hemorrhoidal development, predisposing factors, and tests.
  • Encourage the patient to eat high-fiber diet to promote regular bowel movement.
  • Emphasize the need for good anal hygiene. Caution against vigorous wiping with washcloths and using harsh soaps.
  • Encourage the use of medicated astringent pads and toilet paper without dyes or perfumes.
 
GASTROINTESTINAL BLEEDING
Gastrointestinal bleeding or gastrointestinal hemorrhage is a form of hemorrhage in the gastrointestinal tract, from the pharynx to the rectum. The degree of bleeding can range from nearly undetectable to acute or massive, life-threatening bleeding.
 
Etiology
  • Peptic ulcers: Helicobacter pylori (H. pylori) infections and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, are common causes of peptic ulcers.
  • Esophageal varices: Varices, or enlarged veins, located at the lower end of the esophagus may rupture and bleed massively. Cirrhosis is the most common cause of esophageal varices.
  • 672Mallory-Weiss tears: These tears in the lining of the esophagus usually result from vomiting. Increased pressure in the abdomen from coughing, hiatal hernia, or childbirth can also cause tears.
  • Gastritis: NSAIDs and other drugs, infections, Crohn's disease, illnesses, and injuries can cause gastritis, inflammation and ulcers in the lining of the stomach.
  • Esophagitis: Gastroesophageal reflux disease (GERD) is the most common cause of esophagitis.
  • Benign tumors and cancer: A benign tumor is an abnormal tissue growth that is not cancerous. Benign tumors and cancer in the esophagus, stomach, or duodenum may cause bleeding.
  • Diverticular disease: This disease is caused by diverticula, pouches in the colon wall.
  • Colitis: Infections, diseases such as Crohn's disease, lack of blood flow to the colon, and radiation can cause colitis.
  • Hemorrhoids or fissures: Hemorrhoids are enlarged veins in the anus or rectum that can rupture and bleed. Fissures, or ulcers, are cuts or tears in the anal area.
  • Angiodysplasia: Aging causes angiodysplasia, abnormalities in the blood vessels of the intestine.
 
Types of GI Bleeding
  • Upper GI bleeding: Bleeding in the esophagus, stomach, or the beginning of small intestine.
  • Lower GI bleeding: Bleeding in the small intestine, large intestine, rectum, or anus.
  • Frank (obvious) bleeding: Active bleeding that can be easily seen. For example, vomit blood.
  • Occult (hidden) bleeding: Slow bleeding that cannot be seen easily. Tests may be needed to find occult bleeding.
  • Acute GI bleeding: Blood loss that is new or sudden, and lasts for only a short time.
  • Chronic GI bleeding: Blood loss that has been going on for a long time, or that comes back often.
Signs of bleeding in the upper digestive tract include:
  • Bright red blood in vomit.
  • Vomit that looks like coffee grounds.
  • Black or tarry stool.
  • Dark blood mixed with stool.
  • Stool mixed or coated with bright red blood.
Signs of bleeding in the lower digestive tract include:
  • Black or tarry stool.
  • Dark blood mixed with stool.
  • Stool mixed or coated with bright red blood.
Sudden, severe bleeding is called acute bleeding. If acute bleeding occurs, symptoms may include:
  • Weakness
  • Dizziness or faintness
  • 673Shortness of breath
  • Crampy abdominal pain
  • Diarrhea
  • Paleness
Signs and symptoms of losing too much blood may include:
  • Chest pain, or a feeling like heart is beating too fast.
  • Extreme tiredness.
  • Dizziness or fainting, especially after moving from a sitting or lying position.
  • Pale skin or gums, and sweaty or clammy skin.
  • Dry mouth, increased thirst, or passing less urine.
  • Feeling confused or short of breath.
 
Diagnostic Evaluation
 
1. Endoscopy
Endoscopy is the most common method for finding the source of bleeding in the digestive tract. An endoscope is a flexible tube with a small camera on the end. The doctor inserts the endoscope through the patient's mouth to view the esophagus, stomach, and duodenum. This examination is called esophagogastroduodenoscopy (EGD). An endoscope can also be inserted through the rectum to view the colon. This procedure is called colonoscopy.
 
2. Enteroscopy
Enteroscopy is an examination of the small intestine. Because traditional endoscopes cannot reach the small intestine, special endoscopes are used for enteroscopy.
Enteroscopy Procedures Include:
  • Push enteroscopy: A long endoscope is used to examine the upper portion of the small intestine.
  • Double-balloon enteroscopy: Balloons are mounted on the endoscope to help the endoscope move through the entire small intestine.
  • Capsule endoscopy: The person swallows a capsule containing a tiny camera. The camera transmits images to a video monitor as the capsule passes through the digestive tract. This procedure is designed to examine the small intestine.
  • Barium X-rays: Barium is a contrast material that makes the digestive tract visible in an X-ray. Liquid containing barium is either swallowed or inserted into the rectum. Barium X-rays are less accurate than endoscopy and may interfere with other diagnostic techniques.
  • Radionuclide scanning: A small amount of radioactive material is injected into the person's vein. A special camera, similar to an X-ray machine, can detect this radiation and create images of blood flow in the digestive tract. Radionuclide scanning is sensitive enough to detect very slow bleeding, but it is not as accurate as other procedures.
  • Angiography: A dye is injected into the person's vein to make blood vessels visible in X-ray or computerized tomography (CT) scans. Dye leaks out of the blood vessels at the bleeding site.
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Management
 
Pharmacological Management
There are many medicines that may be given to treat bleeding. It includes:
  • Antibiotics: This medicine is given to help treat or prevent an infection caused by bacteria.
  • Antinausea medicine: This medicine may be given to calm the stomach and prevent vomiting.
  • Antiulcer medicine: This medicine helps decrease the amount of acid that is normally made by the stomach.
  • Blood pressure medicine: This medicine may be given in an IV to help improve blood pressure.
  • Pain medicine: Caregivers may give you medicine to take away or decrease your pain.
 
Nursing Management
 
Nursing Diagnosis
  • Nutrition: Imbalanced, less than body requirements related to inadequate diet, inability to process, digest nutrients, anorexia, nausea, vomiting, indigestion.
  • Skin integrity, risk for impaired related to altered circulation, metabolic state and loss of blood.
  • Risk for injury (hemorrhage) related to internal bleeding secondary to other GI problems like portal hypertension, development of esophageal varices, etc.
  1. Nutrition: imbalanced, less than body requirements related to inadequate diet, inability to process, digest nutrients, Anorexia, nausea, vomiting, indigestion.
    Interventions
    • Measure dietary intake by calorie count.
    • Weigh as indicated. Compare changes in fluid status, recent weight history, and skinfold measurement.
    • Encourage patient to eat, explain reasons for the types of diet. Include patient in meal planning to consider his or her preferences in food choices.
    • Encourage patient to eat all meals including supplementary feedings unless contraindicated.
    • Give small, frequent meals.
    • Provide salt substitutes, if allowed, and avoid those containing ammonium.
    • Restrict intake of caffeine, gas-producing or spicy and excessively hot or cold foods.
    • Suggest soft foods, avoiding roughage, if indicated.
    • Encourage frequent mouth care, especially before meals.
    • Promote undisturbed rest periods, especially before meals.
    • Recommend cessation of smoking. Provide teaching on the possible negative effects of smoking.
    • Monitor laboratory studies: serum glucose, prealbumin and albumin, total protein, ammonia.
    • Maintain NPO status when indicated.
    • Provide tube feedings.
    • 675Refer to dietitian to provide diet high in calories and simple carbohydrates, low in fat, and moderate to high in protein, limit sodium and fluid as necessary. Provide liquid supplements as indicated.
  2. Skin integrity, risk for impaired related to altered circulation, metabolic state and loss of blood.
    Interventions
    • Inspect pressure points and skin surfaces closely and routinely. Gently massage bony prominences or areas of continued stress.
    • Use of emollient lotions and limiting use of soap for bathing may help.
    • Encourage and assist patient with reposition on a regular schedule. Assist with active and passive ROM exercises as appropriate.
    • Recommend elevating lower extremities.
    • Keep linens dry and free of wrinkles.
    • Suggest clipping fingernails short, provide mittens, gloves, if indicated.
    • Use calamine lotion and provide baking soda baths.
    • Use alternating pressure mattress, egg-crate mattress, waterbed, sheepskins, as indicated.
    • Provide perineal care following urination and bowel movement.
  3. Risk for injury (hemorrhage) related to internal bleeding secondary to other GI problems like portal hypertension, development of esophageal varices, etc.
    Interventions
    • Closely assess for signs and symptoms of GI bleeding: check all secretions for frank or occult blood. Observe color and consistency of stools, NG drainage, or vomitus.
    • Observe for presence of petechiae, ecchymosis, bleeding from one or more sites.
    • Monitor pulse, BP (and CVP, if available).
    • Note changes in mentation.
    • Avoid rectal temperature and be gentle with GI tube insertions.
    • Encourage use of soft toothbrush, electric razor, avoiding straining for stool, vigorous nose blowing, and so forth.
    • Use small needles for injections. Apply pressure to small bleeding and venipuncture sites for longer than usual.
    • Advice to avoid aspirine-containing products.
    • Monitor Hb/Hct and clotting factors.
    • Supplemental vitamins: vitamins K, D, and C.
    • Administer stool softeners
    • Assist with insertion and maintenance of GI tube.
    • Provide gastric lavage with room temperature and cool saline solution or water as indicated.
 
IRRITABLE BOWEL SYNDROME (IBS)
Irritable bowel syndrome (IBS) is a common disorder that affects large intestine, characterized by cramping, abdominal pain, bloating gas, diarrhea and constipation.
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Etiology and Risk Factors
  • Foods: Carbonated beverages and some fruits and vegetables may lead to bloating and discomfort in some people with IBS.
  • Stress: Signs and symptoms are worse or more frequent during stressful events.
  • Hormones: Because women are more likely to have IBS, many women find that signs and symptoms are worse during or around their menstrual periods.
  • IBS symptoms first appear before the age of 35 for about half of those with the disorder.
  • More women than men are diagnosed with this condition.
  • Have a family history of IBS.
 
Pathophysiology
 
Signs and Symptoms
  • Abdominal pain or cramping
  • A bloated feeling
  • Gas (flatulence)
  • Diarrhea or constipation
  • Mucus in the stool
 
Diagnostic Evaluation
  • Flexible sigmoidoscopy: This test examines the lower part of the colon with a flexible, lighted tube (sigmoidoscope).
  • Colonoscopy: In this, a small, flexible tube is used to examine the entire length of the colon.
  • 677Computerized tomography: CT scans produce cross-sectional X-ray images of internal organs.
  • Lactose intolerance tests: Lactase is an enzyme required to digest the sugar (lactose) found in dairy products.
  • Blood tests: Celiac disease (nontropical sprue) is sensitivity to wheat protein that also may cause signs and symptoms like those of irritable bowel syndrome.
 
Management
  • Fiber supplements: Taking fiber supplements, such as psyllium or methylcellulose with fluids may help control constipation.
  • Anti-diarrheal medications: Over-the-counter medications, such as loperamide can help control diarrhea.
  • Eliminating high-gas foods, especially cabbage, broccoli and cauliflower.
  • Anticholinergic medications: Some people need medications that affect certain activities of the autonomic nervous system (anticholinergics) to relieve painful bowel spasms.
  • Antidepressant medications, such as tricyclic antidepressant or a selective serotonin reuptake inhibitor (SSRI). These medications help relieve depression as well as inhibit the activity of neurons that control the intestines.
  • Alosetron: Alosetron is a nerve receptor antagonist that is designed to relax the colon and slow the movement of waste through the lower bowel.
  • Lubiprostone: Lubiprostone is approved for adult women and men who have IBS with constipation.
 
Nursing Management
 
Nursing Diagnosis
  • Activity intolerance related to fatigue and weakness.
  • Constipation related to immobility, pain, medication, and decreased GI motility.
  • Diarrhea related to acute infectious process.
  • Disturbed body image related to presence of feeding tube.
  • Imbalanced nutrition: Less than body requirements related to enteral feeding problems.
  • Ineffective therapeutic regimen management related to lack of knowledge of long-term management of disease and consequences of not following treatment plan and unwillingness to modify lifestyle.
 
Interventions
  • Change in bowel habit.
  • Lethargy, nausea, backache and bladder symptoms may be used to support diagnosis.
  • Provide information about self-help covering lifestyle, physical activity, diet and symptom-targeted medication.
  • Encourage people to identify and make the most of their leisure time and to create relaxation time.
  • Assess physical activity levels, ideally using the general practice physical activity.
  • Assess diet and nutrition and give general advice.
  • 678Review the person's fiber intake and adjust (usually reduce) according to symptoms. Discourage intake of insoluble fiber (bran). If more fiber is needed, recommend soluble fiber such as ispaghula powder, or foods high in soluble fiber (oats).
  • If the person wants to try probiotics, advise it to take the dose recommended by the manufacturer for at least 4 weeks while monitoring the effect.
  • Discourage use of aloe vera for IBS.
  • Ensuring patients are properly nourished and hydrated will be a priority of nursing care and includes monitoring weight, I and O, provision for adequate fluid intake, monitoring BP, tachycardia.
  • Administration and management of alternative forms of nutrition (TPN, enteral feedings).
  • Assess self-feeding abilities and assist as needed, and administer medications as ordered (appetite stimulants, antiemetic, antidiarrheals, laxatives, stool softeners, antacids, proton pump inhibitors, H2 blockers).
  • Monitoring critical lab values will be ongoing and include potassium, sodium, magnesium, albumin, and CBC with differential WBCs, and BUN/Creatinine.
  • Patient education will include instruction in appropriate fluid intake, appropriate balance of foods, diet planning.
 
ESOPHAGEAL VARICES
Esophageal varices are abnormal, enlarged veins in the lower part of the esophagus. It develops when normal blood flow to the liver is obstructed by scar tissue. Seeking a way around the blockages, blood flows into smaller blood vessels that are not designed to carry large volumes of blood. The vessels may leak blood or even rupture, causing life-threatening bleeding.
 
Etiology
  1. Prehepatic causes:
    • Portal vein thrombosis
    • Portal vein obstruction – congenital atresia or stenosis
    • Increased portal blood flow – fistula
    • Increased splenic flow
  2. Intrahepatic causes:
    • Cirrhosis due to various causes, including alcoholic, chronic hepatitis (e.g. viral or autoimmune)
    • Idiopathic portal hypertension
    • Acute hepatitis
    • Schistosomiasis
    • Congenital hepatic fibrosis
    • Myelosclerosis
  3. Posthepatic causes:
    • Compression (from tumor)
    • Budd-Chiari syndrome
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Signs and Symptoms
  • Hemoptysis
  • Black, tarry or bloody stools
  • Shock
  • Jaundice
  • Spider veins
  • Palmar erythema
  • Dupuytren's contracture
  • Shrunken testicles
  • Swollen spleen
  • Ascites
 
Diagnostic Evaluation
  • Endoscope examination: A procedure called esophagogastroduodenoscopy. It will insert in mouth and into esophagus and small intestine to evaluate the dilated veins, measure their size.
  • Imaging tests: Both CT and MRI scans may be used to diagnose esophageal varices. These tests also allow to examine liver and circulation in the portal vein.
  • Capsule endoscopy: In this test, the patient swallows a vitamin-sized capsule containing a tiny camera, which takes pictures of the esophagus as it passes. This may be an option for people who are unable or unwilling to undergo an endoscope examination.
  • CBC
  • Clotting including INR
  • Renal function
  • LFTs
  • Ascitic tap may be needed if bacterial peritonitis is suspected.
 
Management
  • Beta blocker: It may help reduce blood pressure in portal vein, decreasing the likelihood of bleeding. These medications include propranolol, etc.
  • Band ligation: It is used if esophageal varices appear to have a very high risk of bleeding. Using an endoscope, the varices are wrap with each other with an elastic band, which essentially ‘strangles’ the veins so they cannot bleed. Esophageal band ligation carries a small risk of complications, such as scarring of the esophagus.
  • Transjugular intrahepatic portosystemic shunt (TIPS): The shunt is a small tube that is placed between the portal vein and the hepatic vein, which carries blood from liver back to heart. By providing an additional path for blood, the shunt reduces pressure in the portal vein and often stops bleeding from esophageal varices.
  • Balloon tube tamponade (Sengstaken-Blakemore tube): The Sengstaken tube is inserted through the mouth and into the stomach. The gastric balloon is inflated with air and the gastric balloon in then pulled up against the esophagogastric junction, compressing 680submucosal varices. The Sengstaken tube also contains an esophageal balloon which is only rarely required when the gastric balloon does not work. If bleeding continues, it may be that the tube is wrongly positioned or bleeding is from another source.
Fig. 13.3: Sengstaken-Blakemore tube
 
Nursing Management
 
Nursing Diagnosis
  • Risk for bleeding related to obstruction in blood flow.
  • Imbalanced nutrition: Less than body requirements related to vomiting and jaundice.
 
Interventions
  • Provide ongoing assessment.
  • Assess for ecchymosis, epistaxis, petechiae, and bleeding gums.
  • Monitor level of consciousness, vital signs, and urinary output to evaluate fluid balance.
  • Monitor the client during blood transfusion administration, if prescribed.
  • Use small-gauge needles, and apply pressure or cold for bleeding.
  • Explain the procedure to the client to reduce fear and enhance cooperation with insertion and maintenance of the esophageal tamponade tube.
  • Monitor the client closely to prevent accidental removal or displacement of the tube with resultant airway obstruction.
    • Ensure nasogastric tube patency to prevent aspiration.
      • Observe gastric aspirate for evidence of bleeding.
      • Protect the client from chilling.
    • Administer prescribed vasopressin and vitamin K
    • Closely assess for signs and symptoms of GI bleeding: Check all secretions for frank or occult blood. Observe color and consistency of stools, NG drainage, or vomitus.
    • Observe for presence of petechiae, ecchymosis, bleeding from one or more sites.
    • 681Monitor pulse, BP (and CVP, if available).
    • Note changes in mentation.
    • Avoid rectal temperature and be gentle with GI tube insertions.
    • Encourage use of soft toothbrush, electric razor, avoiding straining for stool, vigorous nose blowing, and so forth.
    • Use small needles for injections. Apply pressure to small bleeding and venipuncture sites for longer than usual.
    • Advise to avoid aspirine-containing products.
    • Monitor Hb/Hct and clotting factors.
    • Supplemental vitamins: Vitamins K, D, and C.
    • Administer stool softeners.
    • Assist with insertion and maintenance of GI tube.
    • Provide gastric lavage with room temperature and cool saline solution or water as indicated.
 
PORTAL HYPERTENSION
Portal hypertension refers to abnormally high pressure in the hepatic portal vein. It is defined as a portal pressure of 12 mm Hg or more (compared with the normal 5–10 mm Hg).
 
Etiology
  • Prehepatic cause
    • Congenital atresia or stenosis.
    • Portal vein thrombosis.
    • Splenic vein thrombosis.
    • Extrinsic compression tumors.
  • Hepatic cause
    • Chronic hepatitis.
    • Myeloproliferative diseases.
    • Idiopathic portal hypertension.
    • Granulomata.
    • Nodular (nodular regenerative hyperplasia, partial nodular transformation).
    • Toxins.
    • Fibropolycystic disease (including congenital hepatic fibrosis).
  • Posthepatic—blockage of hepatic veins or venules
    • Budd-Chiari syndrome (hepatic vein obstruction).
    • Constrictive pericarditis.
    • Right heart failure.
    • Sclerosing hyaline necrosis.
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Pathophysiology
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Signs and Symptoms
  • Dilated veins in the anterior abdominal wall
  • Splenomegaly
  • Ascites
  • Jaundice
  • Spider veins
  • Palmar erythema
  • Confusion
  • Enlarged or small liver
  • Gynecomastia
  • Testicular atrophy
 
Diagnostic Evaluation
  • Blood tests.
  • Abdominal ultrasound—for liver and spleen size, ascites, portal blood flow and thrombosis of the portal or splenic veins.
  • Doppler ultrasound—can show direction of flow in blood vessels.
  • CT scan, especially spiral CT, may show portal vasculature MRI scan—gives similar information to CT.
  • Endoscopy.
  • Portal hypertension measurement: Portal pressure is indirectly measured in clinical practice by the hepatic venous pressure gradient (HVPG).
  • Liver biopsy.
  • Vascular imaging: The site of the portal venous block can be demonstrated by examining the venous phase of a celiac or superior mesenteric arteriogram, by splenic portography following injection of dye into the splenic pulp, or by retrograde portography via a hepatic vein.
  • Hepatic venography is helpful when hepatic vein block or idiopathic portal hypertension is suspected.
 
Complications
  • Bleeding from esophageal or gastric
  • Ascites
  • Spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Hepatic hydrothorax
  • Pulmonary complications
  • Liver failure
  • Hepatic encephalopathy
  • Cirrhotic cardiomyopathy.
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Management
 
Pharmacological Management
  • Beta blockers: Nonselective beta blockers reduce portal pressure in many patients.
  • Nitrates: Added to beta blocker therapy, they contribute to reducing portal pressure and may reduce rates of variceal rebleeding.
  • Vasoactive drugs: Terlipressin and octreotide are used to assist the control of acute variceal bleeding.
 
Surgical Management
  • Transjugular intrahepatic portosystemic shunt (TIPS): It is a radiological procedure, connecting the portal and hepatic veins using a stent. The purpose of TIPS is to decompress the portal venous system, to prevent rebleeding from varices or to reduce the formation of ascites.
  • Surgical portosystemic shunts.
  • Devascularization procedures: These include gastroesophageal devascularization, splenectomy and esophageal transaction.
 
Nursing Management
 
Nursing Diagnosis
  • Risk for infection related to ascites.
  • Activity intolerance related to weakness.
  • Risk for imbalanced fluid volume related to vomiting and edema.
 
Interventions
  • Administer medications, which may include diuretics.
  • Assist the health care provider with paracentesis, which removes the fluid (e.g. ascites) from the peritoneal cavity.
  • Measure and record abdominal girth and body weight daily, assess for abdominal fluid wave.
  • Promote measures to prevent or reduce edema.
  • Encourage the client to elevate the lower extremities and wear support to prevent lower-extremity edema.
  • Administer salt-poor albumin, which temporarily elevates the serum albumin level. This increases serum osmotic pressure, helping to reduce edema by causing ascetic fluid to be drawn back into the bloodstream and eliminated by the kidneys.
  • Measure dietary intake by calorie count.
  • Weigh as indicated. Compare changes in fluid status, recent weight history, and skinfold measurement.
  • Encourage patient to eat, explain reasons for the types of diet. Include patient in meal planning to consider his or her preferences in food choices.
  • Encourage patient to eat all meals including supplementary feedings unless contraindicated.
  • Give small, frequent meals.
  • Provide salt substitutes, if allowed and avoid those containing ammonium.
  • 685Restrict intake of caffeine, gas-producing or spicy and excessively hot or cold foods.
  • Suggest soft foods, avoiding roughage, if indicated.
  • Encourage frequent mouth care, especially before meals.
  • Promote undisturbed rest periods, especially before meals.
  • Measure intake and output chart, weigh daily, and note gain of more than 0.5 kg/day.
  • Monitor BP (and CVP, if available). Note JVD and abdominal vein distension.
  • Assess respiratory status, noting increased respiratory rate, and dyspnea.
  • Auscultate lungs, noting diminished breath sounds and developing adventitious sounds.
  • Monitor for cardiac dysrhythmias. Auscultate heart sounds, noting development of S3/S4 gallop rhythm.
  • Assess degree of peripheral edema.
  • Measure abdominal girth.
  • Encourage bedrest when ascites is present.
  • Provide frequent mouth care, occasional ice chips (if NPO).
  • Monitor serum albumin and electrolytes (particularly potassium and sodium).
  • Monitor serial chest X-rays.
  • Restrict sodium and fluids as indicated.
  • Administer salt-free albumin, plasma expanders, positive inotropic drugs and arterial vasodilators.
  • Administer diuretics: Spironolactone, furosemide, etc.
 
CHOLELITHIASIS AND CHOLECYSTITIS
It refers to presence of stones in gallbladder. A gallstone is a crystalline concretion formed within the gallbladder by accretion of bile components. These calculi are formed in the gallbladder but may distally pass into other parts of the biliary tract and sometimes if the stone may obstruct the flow of bile and will cause inflammation of gallbladder called cholecystitis.
Fig. 13.4: Anatomy of gallbladder
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Types of Gallstones
  • Cholesterol stones: Vary from light yellow to dark green or brown and are oval, between 2 and 3 cm long.
  • Pigment stones: Pigment stones are small and dark and comprise bilirubin and calcium salts that are found in bile.
  • Mixed stones: Mixed gallstones typically contain 20–80% of cholesterol.
 
Etiology
  • Gender: Women are twice as likely as men to develop gallstones. Excess estrogen from pregnancy and hormone replacement therapy can lead to gallstones.
  • Family history: Gallstones often run in families.
  • Obesity: Obesity is a major risk factor for gallstones, especially in women.
  • Diet: Diets high in fat and cholesterol and low in fiber increase the risk of gallstones.
  • Age: People older than age 60 are more likely to develop gallstones than younger people.
  • Hypolipidemic drugs: These drugs increase the amount of cholesterol secreted into bile and contributes to gallstones
  • Hyperglycemia: People with diabetes generally have high levels of fatty acids called triglycerides. These fatty acids may increase the risk of gallstones.
 
Pathophysiology
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Signs and Symptoms
  • Steady pain in the right upper abdomen that increases rapidly and lasts from 30 minutes to several hours
  • Pain in the back
  • Pain under the right shoulder
  • Murphy's sign (guarding type of respiratory pain radiates towards the back and scapula)
  • Prolonged pain—more than 5 hours
  • Nausea and vomiting
  • Fever—even low-grade—or chills
  • Yellowish color of the skin or whites of the eyes
  • Clay-colored stools.
 
Diagnostic Evaluation
  • Computerized tomography (CT) scans: The CT scan is a noninvasive X-ray that produces cross-section images of the body. The test may show the gallstones or complications, such as infection and rupture of the gallbladder or bile ducts.
  • Cholescintigraphy scan: Patient is injected with a small amount of nonharmful radioactive material that is absorbed by the gallbladder, which is then stimulated to contract. The test is used to diagnose abnormal contraction of the gallbladder or obstruction of the bile ducts.
  • Endoscopic retrograde cholangiopancreatography (ERCP): ERCP is used to locate and remove stones in the bile ducts. The doctor inserts an endoscope—a long, flexible, lighted tube with a camera-down the throat and through the stomach and into the small intestine. The endoscope is connected to a computer and video monitor. The doctor guides the endoscope and injects a special dye that helps the bile ducts appear better on the monitor. The endoscope helps the doctor locate the affected bile duct and the gallstone. The stone is captured in a tiny basket and removed with the endoscope.
  • Blood tests: Blood tests may be performed to look for signs of infection, obstruction, pancreatitis, jaundice.
 
Management
 
Pharmacological Management
  • Opoids analgesic like mephridine, morphine
  • Antispasmodic and anticholinergic
  • Antiemetic
  • Bile acid therapy
  • Chenodeoxycholic acid reduces the cholesterol stone by maintaining a normal amount of cholesterol solubility in bile e.g. chenodiol.
  • Anticholelithiotic agents, like ursodiol.
 
Surgical Management
  • Extracorporeal shock wave lithotripsy: It is a noninvasive procedure used as an ambulatory treatment. A machine called lithotreptor generates a powerful shock to shatter the gallstones.
  • 688Percutaneous transhepatic biliary catheter insertion: Insertion of a percutaneous Transbiliary catheter under fluoroscopic guidance. This procedure will decompress obstructed extrahepatic ducts so that the bile can flow.
Other surgical interventions are:
  • Cholecystectomy
  • Laparoscopic laser cholecystectomy
  • Cholecystotomy
  • Choledochotomy (incision of common bile duct)
  • Choledocholithotomy (incision of common bile duct and removal of gallstones)
 
Nonsurgical Treatment
  • Oral dissolution therapy: Drugs made from bile acid are used to dissolve gallstones, e.g. ursodiol and chenodiol.
  • Contact dissolution therapy: This experimental procedure involves injecting a drug directly into the gallbladder to dissolve cholesterol stones. The drug methyl tert-butyl ether can dissolve some stones in 1 to 3 days.
 
CHOLECYSTITIS
Cholecystitis is inflammation of the gallbladder.
 
Etiology
  • Gallstones: The vast majority of cholecystitis cases are the result of gallstones that block the cystic duct, causing bile to build up and resulting in gallbladder inflammation.
  • Tumor: A tumor may prevent bile from draining out of gallbladder properly, causing bile buildup that can lead to cholecystitis.
  • Bile duct blockage: Kinking or scarring of the bile ducts can cause blockages that lead to cholecystitis.
 
Risk Factors
  • Gallstones: Most cases of cholecystitis are linked to gallstones.
  • Sex: Women have a greater risk of gallstones than men do. This makes women more likely to develop cholecystitis.
  • Age: Older people are at high risk of gallstones.
 
Signs and Symptoms
  • Severe, steady pain in the upper right part of abdomen
  • Pain that radiates from abdomen to right shoulder or back
  • Tenderness over abdomen when it is touched
  • Sweating
  • Nausea
  • Vomiting
  • Fever
  • Chills
  • Abdominal bloating.
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Complications
  • Enlarged gallbladder: If gallbladder becomes inflamed due to bile buildup, it may stretch and swell beyond its normal size, which can cause pain and increase the risk of a tear (perforation) in gallbladder, as well as infection and tissue death.
  • Infection within the gallbladder: If bile builds up within gallbladder, causing cholecystitis, the bile may become infected.
  • Gangrene: Untreated cholecystitis can cause tissue in the gallbladder to die (gangrene), which, in turn, can lead to a tear in the gallbladder.
  • Perforation: A tear (perforation) in gallbladder may be caused by an enlarged or infected gallbladder that occurs as a result of Cholecystitis.
 
Diagnostic Evaluation
  • Blood tests: Blood tests are done to look for signs of an infection or of gallbladder problems.
  • Imaging tests: Imaging tests, such as abdominal ultrasound or a computerized tomography (CT) scan can be used to create pictures of gallbladder that may reveal signs of cholecystitis.
  • HIDA: A hepatobiliary iminodiacetic acid (HIDA) scan tracks the production and flow of bile from liver to small intestine and shows if bile is blocked at any point along the way.
 
Management
  • Antibiotics: To treat the infection.
  • Analgesics: To help control pain until the inflammation in gallbladder is relieved.
 
Surgical Interventions
  • Cholecystectomy
  • Laparoscopic laser cholecystectomy
  • Cholecystectomy
  • Choledochotomy (incision of common bile duct)
  • Choledocholithotomy (incision of common bile duct and removal of gallstones).
 
Nursing Management
 
Nursing Assessment
  • Obtain history and demographic data that may indicate risk factors for biliary disease.
  • Assess mental status through interview and interaction with patient.
  • Perform abdominal examination for ascites.
  • Asses the client's bowel elimination pattern, noting the number of stools and their color and also the presence of blood.
  • Assess the client's abdomen for bowel sounds and the location of pain.
  • Assess the complete nutritional status of diseased patient.
  • Observe for any bleeding.
  • Monitor for temperature and WBC counts for indicating inflammation of infection.
  • Assess the emotional status, coping skills, verbal and nonverbal behaviors.
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Nursing Diagnosis
  • Risk for injury related to medication during retrograde endoscopy for stone removal.
  • Knowledge deficit related to oral dissolution agents.
  • Pain related to stone obstruction.
  • Fluid volume deficit related to nausea and vomiting.
  • Activity intolerance related to fatigue, general discomfort.
  • Anxiety-related inflammatory disease of gallbladder.
  • Imbalanced nutrition less than body requirement related to pain.
  • Ineffective coping related to feeling of rejection.
  1. Risk for injury related to medication during retrograde endoscopy for stone removal.
    Interventions
    • Assess for signs and symptoms of GI bleeding, e.g. check all secretions for frank or occult blood. Observe color and consistency of stools, NG drainage, or vomitus.
    • Observe for presence of petechiae, ecchymosis, bleeding from one or more sites.
    • Monitor pulse, BP (and CVP, if available).
    • Note changes in mentation and level of consciousness.
    • Avoid rectal temperature, be gentle with GI tube insertions.
    • Encourage use of soft toothbrush, electric razor, avoiding straining for stool, forceful nose blowing, and so forth.
    • Use small needles for injections. Apply pressure to small bleeding and venipuncture sites for longer than usual.
    • Recommend avoidance of aspirin-containing products.
  2. Knowledge deficit related to oral dissolution agents.
    Interventions
    • Inform patient of altered effects of medications with Cholecystitis and the importance of using only drugs prescribed or cleared by a health care provider who is familiar with patient's history.
    • Assist patient in identifying the support person.
    • Emphasize the importance of good nutrition. Recommend avoidance of high-protein and salty foods, onions, and strong cheeses. Provide written dietary instructions.
    • Discuss sodium and salt substitute restrictions and necessity of reading labels on food and OTC drugs.
    • Encourage scheduling activities with adequate rest periods.
    • Promote diversional activities that are enjoyable to the patient.
    • Recommend avoidance of persons with infections, especially upper respiratory tract infection.
    • Identify environmental dangers, e.g. carbon tetrachloride-type cleaning agents, exposure to hepatitis.
  3. Pain related to stone obstruction.
    Interventions
    • Assess the pain location, severity and characteristics.
    • Administer medications or monitor patient-controlled analgesia.
    • Assist in attaining position of comfort and maintain bed rest.
  4. 691Fluid volume deficit related to nausea and vomiting.
    Interventions
    • Administer IV fluids and electrolytes as prescribed.
    • Administer antiemetic as prescribed to reduce vomiting.
    • Maintain nasogastric decompression until nausea and vomiting subside.
    • Begin food and fluids as tolerated by the client.
    • Observe and record amount of T tube drainage, if applicable.
  5. Activity intolerance related to fatigue, general discomfort.
    Interventions
    • Encouraging alternating periods of rests and ambulation.
    • Maintain some periods of rest.
    • Encourage and assist with gradually increasing periods of exercise.
  6. Imbalanced nutrition less than body requirement related to pain.
    Interventions
    • Encourage a diet that is low in residue fiber and fat and high in calories, protein and carbohydrates with vitamin and mineral supplements.
    • Monitor weight daily.
    • Provide small frequent feeding to prevent distension.
    • Have the patient participate in meal planning to encourage compliance and increased knowledge.
    • Prepare the patient for elementary diet.
    • Restart oral fluid intake gradually. Offer clear liquids hourly; avoid cold fluids.
  7. Ineffective coping related to feeling of rejection.
    Intervention
    • Assess the level of fear and note nonverbal communication.
    • Ask the patient's usual coping pattern.
    • Assure patient he/she will be closely monitored.
    • Allow patient to verbalize fear of dying.
    • Provide diversional materials, such as newspapers, music and television.
    • Offer family support.
 
Complications
  • Acute cholangitis: Acute cholecystitis is a condition indicated by a sudden attack of pain in the upper abdomen that lasts more than 12 hours.
  • Acute biliary pancreatitis: Pancreatitis is a potentially serious disorder that occasionally develops in people with gallstones
  • Gallstone ileus
  • Obstructive jaundice or cholestasis
  • Gallbladder cancer
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LIVER CIRRHOSIS
In cirrhosis of the liver, progressive scarring (fibrosis) of the liver causes scar tissue to replace normal liver tissue. The scar tissue damages the normal structure and function of the liver which affects the normal flow of blood through the liver. The liver itself becomes distorted, hardened and lumpy.
Cirrhosis is a condition in which the liver slowly deteriorates and malfunctions due to chronic injury. Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. Scarring also impairs the liver's ability to:
  • Control infections
  • Remove bacteria and toxins from the blood
  • Process nutrients, hormones, and drugs
  • Make proteins that regulate blood-clotting
  • Produce bile to help absorb fats—including cholesterol—and fat-soluble vitamins
 
Etiology and Pathophysiology
  • Chronic alcoholism: The amount of alcohol intake is broken down act as a toxin, leading to inflammation. With prolonged use, scar tissue develops and the liver is unable to function properly.
  • Viral or autoimmune hepatitis: This disease appears to be caused by the immune system and inflammatory responses by attacking the liver and causing damage, and eventually scarring of the liver tissues.
  • Inherited or genetic disorder: Cystic fibrosis, alpha-1 antitrypsin deficiency, hemochromatosis, Wilson's disease, galactosemia, and glycogen storage diseases are inherited diseases that interfere with how the liver produces, processes, and stores enzymes, proteins, metals, and other substances the body needs to function properly. Cirrhosis can result from these conditions.
  • Bile ducts obstruction: The duct that carries the bile out of the liver is blocked, bile backs up and damages the liver tissue.
  • Drugs and toxins: Prolonged exposure to drugs and environmental toxins can lead to hepatic cell damage.
  • Chronic hepatitis C: The hepatitis C virus is a liver infection that is spread by contact with an infected person's blood. Chronic hepatitis C causes inflammation and damage to the liver over time that can lead to cirrhosis.
  • Chronic hepatitis B and D: The hepatitis B virus is a liver infection that is spread by contact with an infected person's blood, semen, or other body fluid. Hepatitis B, like hepatitis C, causes liver inflammation and injury that can lead to cirrhosis. The hepatitis B vaccine is given to all infants and many adults to prevent the virus. Hepatitis D is another virus that infects the liver and can lead to cirrhosis, but it occurs only in people who already have hepatitis B.
  • Nonalcoholic fatty liver disease (NAFLD): In NAFLD, fat builds up in the liver and eventually causes cirrhosis. This increasingly common liver disease is associated with obesity, diabetes, protein malnutrition, coronary artery disease, and corticosteroid medications.
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Pathophysiology
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Classifications of Cirrhosis
  • Alcoholic cirrhosis: Scar tissue chacteristically surrounds the portal areas. This is the most prevalent type that caused by long history of chronic alcoholism.
  • Postnecrotic cirrhosis: consist broad bands of scar tissue and results from previous acute viral hepatitis or drug-induced massive hepatic necrosis.
  • Biliary cirrhosis: consist of scarring of liver around the bile ducts. This type of cirrhosis usually results from chronic biliary obstruction and infection. It is less common than the other two classifications of cirrhosis.
 
Other Classifications
  • Nonalcoholic fatty liver disease: Scarring occurs when liver cells store excess fatty acids.
  • Hepatitis-related cirrhosis: Scarring results from chronic viral infections of the liver, such as hepatitis B and hepatitis C.
  • Cryptogenic cirrhosis: Scarring has no obvious cause.
  • Nutritional cirrhosis: This is also known as portal cirrhosis. This is the most prevalent type. This type mainly occurs among individuals who have a long history of alcoholism.
  • Pigment cirrhosis: This is also known as hemochromatosis. This type of cirrhosis causes inability to metabolize iron. This is prevalent in 5–10% of the cases.
 
Signs and Symptoms
  • Spider angiomata: Vascular lesions consisting of a central arteriole surrounded by many smaller vessels because of an increase in estradiol. These occur in about 1/3 of cases.
  • Palmar erythema: Exaggerations of normal speckled mottling of the palm, because of altered sex hormone metabolism.
  • Nail changes:
    • Muehrcke's lines: Paired horizontal bands separated by normal color resulting from hypoalbuminemia.
    • Terry's nails: Proximal two-thirds of the nail plate appears white with distal one-third red, also due to hypoalbuminemia.
    • Clubbing: Angle between the nail plate and proximal nailfold > 180 degrees.
  • Hypertrophic osteoarthropathy: Chronic proliferative periostitis of the long bones that can cause considerable pain.
  • Dupuytren's contracture: Thickening and shortening of palmar fascia that leads to flexion deformities of the fingers. Thought to be caused by fibroblastic proliferation and disorderly collagen deposition.
  • Gynecomastia: Benign proliferation of glandular tissue of male breasts presenting with a rubbery or firm mass extending concentrically from the nipples.
  • Hypogonadism: Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy because of primary gonadal injury or suppression of hypothalamic or pituitary function.
  • Liver size: Can be enlarged, normal, or shrunken.
  • Splenomegaly: Caused by congestion of the red pulp as a result of portal hypertension.
  • Ascites: Accumulation of fluid in the peritoneal cavity giving rise to flank dullness (needs about 1500 ml to detect flank dullness).
  • 695Caput medusa: In portal hypertension, periumbilical collateral veins may dilate. Blood from the portal venous system may be shunted through the periumbilical veins and ultimately to the abdominal wall veins, manifesting as caput medusa.
  • Fetor hepaticus: Musty odor in breath as a result of increased dimethyl sulfide.
  • Jaundice: Yellow discoloring of the skin, eye, and mucous membranes because of increased bilirubin (at least 2–3 mg/dl or 30 mmol/l). Urine may also appear dark.
  • Asterixis: Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
  • Others:
    • Weakness, fatigue, anorexia, weight loss
    • Lack of energy (fatigue), which may be debilitating
    • Weight loss or sudden weight gain
    • Bruises
    • Yellowing of skin or the whites of eyes (jaundice)
    • Itchy skin
    • Fluid retention (edema) and swelling in the ankles, legs, and abdomen (often an early sign)
    • A brownish or orange tint to the urine
    • Light-colored stools
    • Confusion, disorientation, personality changes
    • Blood in the stool.
 
Diagnostic Evaluation
  • Physical exam: A cirrhotic liver is bumpy and irregular instead of smooth.
  • Blood tests: Liver function tests
    • International normalized ratio (INR)—tests the clotting tendency of blood
    • Aminotransferases: AST and ALT are moderately elevated.
    • Alkaline phosphatase—usually slightly elevated.
    • Gammaglutamyl transferase—Typically much higher in chronic liver disease from alcohol.
    • Bilirubin may elevate as cirrhosis progresses.
    • Albumin levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver.
    • Prothrombin time – Increases since the liver synthesizes clotting factors.
    • Globulins is increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.
    • Serum sodium: Hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.
    • Thrombocytopenia: This rarely results in platelet count < 50,000/ml.
    • Leukopenia and neutropenia—Due to splenomegaly with splenic margination.
    • Coagulation defects: The liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.
    • Immunoglobulin levels (IgG, IgM, IgA): These are nonspecific but may assist in distinguishing various causes.
    • 696Cholesterol and glucose.
    • Alpha 1-antitrypsin.
  • Computerized tomography (CT scan)
  • Endoscopy: Gastroscopy (endoscopic examination of the esophagus, stomach and duodenum) is performed in patients with established cirrhosis to exclude the possibility of esophageal varices.
  • Ultrasound: It is routinely used in the evaluation of cirrhosis, where it may show a small and nodular liver in advanced cirrhosis along with increased echogenicity with irregular-appearing areas. Other findings suggestive of cirrhosis in imaging are an enlarged caudate lobe, widening of the liver fissures and enlargement of the spleen. An enlarged spleen (splenomegaly), which normally measures less than 11 to 12 cm in adults, is very suggestive of cirrhosis with portal hypertension in the right clinical setting.
  • Biopsy: A liver biopsy can confirm the diagnosis of cirrhosis but is not always necessary. A biopsy is usually done if the result might have an impact on treatment. The biopsy is performed with a needle inserted between the ribs or into a vein in the neck. Precautions are taken to minimize discomfort. A tiny sample of liver tissue is examined with a microscope for scarring or other signs of cirrhosis. Sometimes a cause of liver damage other than cirrhosis is found during biopsy.
 
Management
The goals of treatment include:
  • Treating the cause of cirrhosis to prevent further liver damage.
  • Avoiding substances that may further damage the liver, especially alcohol.
  • Preventing and treating the symptoms and complications of cirrhosis.
 
Treatment
 
Supportive Treatment
If a person has hepatitis, the doctor may prescribe steroids or antiviral drugs to reduce liver cell injury.
  • Eating a nutritious diet: Because malnutrition is common in people with cirrhosis, a healthy diet is important in all stages of the disease. Health care providers recommend a meal plan that is well-balanced. If ascites develops, a sodium-restricted diet is recommended. A person with cirrhosis should not eat raw shellfish, which can contain a bacterium that causes serious infection. To improve nutrition, the doctor may add a liquid supplement taken by mouth or through a nasogastric tube—a tiny tube inserted through the nose and throat that reaches into the stomach.
  • Avoiding alcohol and other substances: People with cirrhosis are encouraged not to consume alcohol or any illicit substances, as these will cause more liver damage. Because many vitamins and medications can affect liver function, a doctor should be consulted before taking them.
 
Medical Treatment
  • Diuretics: For edema and ascites, diuretics are given. This medication removes fluid from the body. Large amounts of ascitic fluid may be removed from the abdomen and checked for bacterial peritonitis.
  • 697Oral antibiotics may be prescribed to prevent infection. Severe infection with ascites will require intravenous (IV) antibiotics.
  • Beta-blocker or nitrate for portal hypertension. Beta-blockers can lower the pressure in the varices and reduce the risk of bleeding.
  • Lactulose: Hepatic encephalopathy is treated by cleansing the bowel with lactulose—a laxative given orally or in enemas.
  • Interferon and other antiviral drugs are prescribed for viral hepatitis, and autoimmune hepatitis requires corticosteroids and other drugs that suppress the immune system.
 
Surgical Treatment
  • Liver transplantation: Liver transplantation is a major operation in which the diseased liver is removed and replaced with a healthy one from an organ donor. A team of health professionals determines the risks and benefits of the procedure for each patient. Survival rates have improved over the past several years because of drugs that suppress the immune system and keep it from attacking and damaging the new liver.
 
Prevention of Cirrhosis of the Liver
  • Do not abuse alcohol. If you do drink alcohol, limit how much you drink and how often. If you drink more than 2 drinks a day, you are increasing your risk. A drink is a 5-oz glass of wine, a 12-oz can of beer, or a 1-1/2 oz portion of hard liquor.
  • Avoid high-risk sexual behavior, such as unprotected sexual contact with multiple partners.
  • Be careful around synthetic chemicals, such as cleaning products and pesticides. If you come into contact with chemicals often, wear protective clothing and a facemask.
  • Get vaccinated against hepatitis B.
  • Eat a well-balanced, low-fat diet and take vitamins.
  • Consume a balanced diet and one multivitamin daily. Patients with PBC with impaired absorption of fat-soluble vitamins may need additional vitamins D and K.
  • Avoid nonsteroidal anti-inflammatory drugs (NSAIDs, e.g. ibuprofen). Patients with cirrhosis can experience worsening of liver and kidney function with NSAIDs.
  • Suppress the immune system with drugs, such as prednisone and azathioprine to decrease inflammation of the liver in autoimmune hepatitis.
  • Immunize patients with cirrhosis against infection with hepatitis A and B to prevent a serious deterioration in liver function. There are currently no vaccines available for immunizing against hepatitis C.
 
Complications
  • Edema and ascites: When liver damage progresses to an advanced stage, fluid collects in the legs, called edema, and in the abdomen, called ascites. Ascites can lead to bacterial peritonitis, a serious infection.
  • Bruising and bleeding: When the liver slows or stops producing the proteins needed for blood clotting, a person will bruise or bleed easily.
  • Portal hypertension: Normally, blood from the intestines and spleen is carried to the liver through the portal vein. But cirrhosis slows down the normal flow of blood, which increases the pressure in the portal vein. This condition is called portal hypertension.
  • 698Esophageal varices and gastropathy: When portal hypertension occurs, it may cause enlarged blood vessels in the esophagus, called varices, or in the stomach, called gastropathy, or both. Enlarged blood vessels are more likely to burst due to thin walls and increased pressure. If they burst, serious bleeding can occur in the esophagus or upper stomach, requiring immediate medical attention.
  • Splenomegaly: When portal hypertension occurs, the spleen frequently enlarges and holds white blood cells and platelets, reducing the number of these cells in the blood. A low platelet count may be the first evidence that a person has developed cirrhosis.
  • Jaundice: Jaundice occurs when the diseased liver does not remove enough bilirubin from the blood, causing yellowing of the skin and whites of the eyes and darkening of the urine. Bilirubin is the pigment that gives bile its reddish-yellow color.
  • Gallstones: If cirrhosis prevents bile from flowing freely to and from the gallbladder, the bile hardens as gallstones.
  • Sensitivity to medications: Cirrhosis slows the liver's ability to filter medications from the blood. When this occurs, medications act longer than expected and build up in the body. This causes a person to be more sensitive to medications and their side effects.
  • Hepatic encephalopathy: A failing liver cannot remove toxins from the blood, and they eventually accumulate in the brain. The buildup of toxins in the brain, called hepatic encephalopathy, can decrease mental function and cause coma. Signs of decreased mental function include confusion, personality changes, memory loss, trouble concentrating, and a change in sleep habits.
  • Insulin resistance and type 2 diabetes: Cirrhosis causes resistance to insulin. With insulin resistance, the body's muscle, fat, and liver cells do not use insulin properly. The pancreas tries to keep up with the demand for insulin by producing more, but excess glucose builds up in the bloodstream causing type 2 diabetes.
  • Liver cancer: Hepatocellular carcinoma is a type of liver cancer that can occur in people with cirrhosis.
  • Other problems: Cirrhosis can cause immune system dysfunction, leading to the risk of infection. Cirrhosis can also cause kidney and lung failure, known as hepatorenal and hepatopulmonary syndromes.
 
Nursing Management
 
Nursing Diagnosis
  1. Nutrition: Imbalanced, less than body requirements related to vomiting secondary to jaundice.
    Interventions
    • Measure dietary intake by calorie count.
    • Weigh as indicated. Compare changes in fluid status, recent weight history, skinfold measurement.
    • Assist and encourage patient to eat and explain reasons for the types of diet.
    • Encourage patient to eat all meals and supplementary feedings.
    • Recommend and provide small, frequent meals.
    • Provide salt substitutes, if allowed; avoid those containing ammonium.
    • 699Restrict intake of caffeine, gas-producing or spicy and excessively hot or cold foods.
    • Suggest soft foods, avoiding roughage if indicated.
    • Encourage frequent mouth care, especially before meals.
    • Promote undisturbed rest periods, especially before meals.
    • Monitor laboratory studies, e.g. serum glucose, prealbumin, albumin, total protein, ammonia.
    • Maintain NPO status when indicated.
    • Consult with dietitian to provide diet that is high in calories and simple carbohydrates, low in fat, and moderate to high in protein, limit sodium and fluid as necessary. Provide liquid supplements as indicated.
  2. Fluid volume excess related to compromised regulatory mechanism or excess sodium and fluid intake.
    Interventions
    • Measure intake and output chart, noting positive balance (intake in excess of output). Weigh daily and note gain more than 0.5 kg/day.
    • Monitor BP (and CVP, if available). Note abdominal vein distension.
    • Assess respiratory status, noting increased respiratory rate or dyspnea.
    • Auscultate lungs, noting diminished or absent breath sounds and developing adventitious sounds (e.g. crackles).
    • Monitor for cardiac dysrhythmias. Auscultate heart sounds, noting development of S3/S4 gallop rhythm.
    • Assess degree of peripheral or dependent edema.
    • Measure abdominal girth.
    • Encourage bed rest when ascites is present
    • Provide frequent mouth care.
    • Monitor serum albumin and electrolytes (particularly potassium and sodium).
    • Monitor serial chest X-rays.
    • Restrict sodium and fluids as indicated.
    • Administer salt-free albumin and plasma expanders as indicated.
    • Administer medications as indicated: Diuretics, e.g. spironolactone, furosemide.
  3. Impaired skin integrity related to altered metabolic state, accumulation of bile salt in skin and edema.
    Interventions
    • Inspect skin surfaces and pressure points routinely.
    • Gently massage bony prominences or areas of continued stress. Use emollient lotions, limit use of soap for bathing.
    • Encourage and assist with repositioning on a regular schedule, while in bed or chair, and active/passive ROM exercises as appropriate.
    • Recommend elevating lower extremities.
    • Keep linens dry and free of winkles.
    • Suggest clipping fingernails short and provide mittens and gloves, if indicated.
    • 700Encourage and provide perineal care following urination and bowel movement.
    • Use alternating pressure mattress, egg-crate mattress, waterbed, sheepskins, as indicated
    • Apply calamine lotion, provide baking soda baths. Administer medications, such as cholestyramine, hydroxyzine, diphenhydramine.
  4. Ineffective breathing pattern related to intra-abdominal fluid collection (ascites), Decreased lung expansion, accumulated secretions and decreased energy, fatigue.
    Interventions
    • Monitor respiratory rate, depth, and effort. Auscultate breath sounds, noting crackles, wheezes, rhonchi.
    • Investigate changes in level of consciousness.
    • Keep the head of bed elevated. Position on sides.
    • Encourage frequent repositioning and deep-breathing exercises and coughing as appropriate.
    • Monitor temperature. Note presence of chills, increased coughing, and changes in color and character of sputum.
    • Monitor serial ABGs, pulse oximetry, vital capacity measurements, chest X-rays.
    • Provide supplemental O2 as indicated.
    • Demonstrate and assist with respiratory adjuncts, e.g. incentive spirometer.
    • Prepare for acute care procedures, e.g. paracentesis.
  5. Risk for injury related to abnormal blood profile and altered clotting factors.
    Interventions
    • Assess for signs and symptoms of GI bleeding, e.g. check all secretions for frank or occult blood. Observe color and consistency of stools, NG drainage, or vomitus.
    • Observe for presence of petechiae, ecchymosis, bleeding from one or more sites.
    • Monitor pulse, BP (and CVP, if available).
    • Note changes in mentation and level of consciousness.
    • Avoid rectal temperature and be gentle with GI tube insertions.
    • Encourage use of soft toothbrush, electric razor, avoiding straining for stool, forceful nose blowing, and so forth.
    • Use small needles for injections. Apply pressure to small bleeding and venipuncture sites for longer than usual.
    • Recommend avoidance of aspirin-containing products.
    • Monitor Hb/Hct and clotting factors.
    • Administer medications as indicated: Supplemental vitamins (e.g. vitamins K, D, and C)
    • Administer Stool softeners.
    • Provide gastric lavage with room temperature and cool saline solution or water as indicated.
    • Assist with insertion of GI or esophageal tube (e.g. Sengstaken-Blakemore tube).
    • Prepare for surgical procedures, e.g. direct ligation (banding) or varices, esophagogastric resection, splenorenal-portacaval anastomosis.
  6. 701Risk for acute confusion related to alcohol abuse or liver encephalopathy.
    Interventions
    • Observe for changes in behavior and mentation, e.g. lethargy, confusion, drowsiness, slowing and slurring of speech, and irritability.
    • Review current medication regimen and schedules.
    • Evaluate sleep and rest schedule.
    • Note development and presence of asterixis, fetor hepaticus, and seizure activity.
    • Have patient write name periodically and keep this record for comparison. Report deterioration of ability. Have patient do simple arithmetic computations.
    • Reorient to time, place, and person as needed.
    • Maintain a pleasant, quiet environment and approach in a slow, calm manner. Encourage uninterrupted rest periods.
    • Provide continuity of care. If possible, assign same nurse over a period of time.
    • Reduce provocative stimuli, confrontation. Refrain from forcing activities. Assess potential for violent behavior.
    • Discuss current situation, future expectation.
    • Maintain bed rest, assist with self-care activities.
    • Identify and provide safety needs, e.g. supervision during smoking, bed in low position, side rails up and pad, if necessary.
    • Investigate temperature elevations. Monitor for signs of infection.
    • Recommend avoidance of narcotics or sedatives, antianxiety agents, and limiting the use of medications metabolized by the liver.
    • Eliminate or restrict protein in diet. Provide glucose supplements, adequate hydration.
    • Assist with procedures as indicated, e.g. dialysis, plasmapheresis, or extracorporeal liver perfusion.
  7. Disturbed body image and self-esteem related to Biophysical changes and altered physical appearance and self-destructive behavior.
    Interventions
    • Discuss situation and encourage verbalization of fears and concerns. Explain relationship between nature of disease and symptoms.
    • Support and encourage patient and provide care with a positive, friendly attitude.
    • Encourage family to verbalize feelings.
    • Assist patient to cope with change in appearance, suggest clothing that does not emphasize altered appearance, e.g. use of red, blue, or black clothing.
    • Refer to support services, e.g. counselors, psychiatric resources, social service, clergy, and/or alcohol treatment program.
  8. Knowledge deficit related to lack of exposure, information misinterpretation and unfamiliarity with information resources.
    Interventions
    • Review disease process and prognosis and future expectations.
    • Stress importance of avoiding alcohol. Give information about community services available to aid in alcohol rehabilitation if indicated.
    • 702Inform patient of altered effects of medications with cirrhosis and the importance of using only drugs prescribed or cleared by a health care provider, who is familiar with the patient's history.
    • Assist the patient in identifying support person.
    • Emphasize the importance of good nutrition.
    • Recommend avoidance of high-protein, salty foods, onions, and strong cheeses. Provide written dietary instructions.
    • Discuss sodium and salt substitute restrictions and necessity of reading labels on food and OTC drugs.
    • Encourage scheduling activities with adequate rest periods.
    • Promote diversional activities that are enjoyable to patient.
    • Recommend avoidance of persons with infections, especially upper respiratory tract infection.
    • Identify environmental dangers, e.g. carbon tetrachloride-type cleaning agents, exposure to hepatitis.
    • Instruct patient of signs and symptoms that warrant notification of healthcare provider, e.g. increased abdominal girth, rapid weight loss or gain, increased peripheral edema, increased dyspnea, fever, blood in stool or urine, excess bleeding, jaundice.
 
Other Nursing Diagnoses
  • Fatigue related to decreased metabolic energy production, states of discomfort, altered body chemistry.
  • Therapeutic regimen: Risk for ineffective management related to perceived benefit, social support deficit, economic difficulties.
  • Family processes, dysfunctional: Alcoholism related to abuse of alcohol, resistance to treatment, inadequate coping or lack of problem-solving skills, addictive personality and codependency.
 
PANCREATITIS
Pancreatitis is an inflammation and potential necrosis of the pancreas. It may be acute or chronic.
 
Types
 
Acute Pancreatitis
  • It ranges from a mild self-limiting disorder to a severe, rapidly fatal disease that does not respond to any treatment.
  • It is very sudden and lasts for a few days.
  • Mild acute pancreatitis is characterized by edema and inflammation confined to the pancreas. Minimal organ dysfunction is present, and return to normal usually occurs within 6 months. Although this is considered the milder form of pancreatitis, the patient is acutely ill and at risk for hypovolemic shock, fluid and electrolyte disturbances, and sepsis.
  • A more widespread and complete enzymatic digestion of the gland characterizes severe acute pancreatitis. The tissue becomes necrotic, and the damage extends into the retroperitoneal tissues.
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Chronic Pancreatitis
  • Chronic pancreatitis is an inflammatory disorder characterized by progressive anatomic and functional destruction of the pancreas.
  • It occurs over many years and has multiple causes and painful symptoms.
  • As cells are replaced by fibrous tissue with repeated attacks of pancreatitis, pressure within the pancreas increases.
  • The end-result is mechanical obstruction of the pancreatic and common bile ducts and the duodenum.
  • Additionally, there is atrophy of the epithelium of the ducts, inflammation, and destruction of the secreting cells of the pancreas.
 
Etiology
There are several possible causes of pancreatitis. The most common are gallstones, which block the duct of the pancreas (for acute pancreatitis), and excessive alcohol consumption (for chronic pancreatitis).
  • Certain drugs, including azathioprine, sulfonamides, corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and antibiotics, such as tetracycline.
  • Infection with mumps, hepatitis virus, rubella, Epstein-Barr virus (the cause of mononucleosis), and cytomegalovirus.
  • Abnormalities in the structure of the pancreas or the pancreatic or bile ducts, including pancreatic cancer.
  • High levels of triglycerides (fats) in the blood.
  • Surgery to the abdomen, heart, or lungs that temporarily cuts off blood supply to the pancreas, damaging tissue.
  • Hereditary diseases, such as cystic fibrosis.
  • Injury to the abdomen.
  • Idiopathic.
There are some less common causes of pancreatitis, such as the adverse effects of some drugs, increased calcium level in the blood, markedly raised triglycerides in blood, trauma, hyperparathyroidism, etc.
 
Pathophysiology
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Signs and Symptoms
 
Acute Pancreatitis
  • Severe abdominal pain: Pain occurs in the mid-epigastrium. Pain is frequently acute in onset, occurring 24 to 48 hours after a very heavy meal or alcohol ingestion, and it may be diffuse and difficult to localize. It is more severe after meals and is unrelieved by antacids.
  • Abdominal tenderness and back pain result from irritation and edema of the inflamed pancreas that stimulate the nerve endings.
  • Abdominal distention: A poorly defined, palpable abdominal mass and decreased peristalsis.
  • Nausea and vomiting: Frequent vomiting that does not relieve the pain or nausea. The emesis is usually gastric in origin but may be bile-stained.
  • Abdominal guarding: The patient appears acutely ill and abdominal guarding is present. The abdomen may remain soft in the absence of peritonitis.
  • Ecchymosis (bruising) in the flank or around the umbilicus may indicate severe pancreatitis.
  • Fever, jaundice, mental confusion, and agitation may also occur.
  • Hypotension: It is typical and reflects hypovolemia and shock caused by the loss of large amounts of protein-rich fluid into the tissues and peritoneal cavity. The patient may develop tachycardia, cyanosis, and cold, clammy skin in addition to hypotension.
  • Acute renal failure is common.
  • Respiratory distress and hypoxia are common, and the patient may develop diffuse pulmonary infiltrates, dyspnea, tachypnea, and abnormal blood gas values.
Myocardial depression, hypocalcemia, hyperglycemia, and disseminated intravascular coagulopathy (DIC) may also occur with acute pancreatitis.
 
Chronic Pancreatitis
  • Severe upper abdominal and back pain: It is recurrent and does not get relief with opioids (even in large dose). As the disease progresses, recurring attacks of pain are more severe, more frequent, and of longer duration. Some patients experience continuous severe pain, others have a dull, nagging constant pain.
  • Nausea and vomiting: It is very severe and patient is unable to take food.
  • Weight loss: It is usually caused by decreased dietary intake secondary to anorexia or fear that eating will precipitate another attack.
  • Malabsorption: It occurs late in the disease, when as little as 10% of pancreatic function remains. As a result, digestion, especially of proteins and fats, is impaired.
  • Steatorrhea: The stools become frequent, frothy, and foul-smelling because of impaired fat digestion, which results in stools with a high fat content.
  • Dependence on opioids: It is increased in pancreatitis because of the chronic nature and severity of the pain.
  • Calcification of the gland may occur, and calcium stones may form within the ducts.
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Diagnostic Evaluation
  • History of abdominal pain and the presence of known risk factors
  • Physical examination
  • Diagnostic findings:
    • Serum amylase and lipase levels are used in making the diagnosis of acute pancreatitis. In 90% of the cases, serum amylase and lipase levels usually raise in excess of three times their normal upper limit within 24 hours. Serum amylase usually returns to normal within 48 to 72 hours. Serum lipase levels may remain elevated for 7 to 14 days.
Urinary amylase levels also become elevated and remain elevated longer than serum amylase levels.
  • The white blood cell count is usually elevated.
  • Hematocrit and hemoglobin levels are used to monitor the patient for bleeding.
  • Hypocalcemia is present in many patients and correlates well with the severity of pancreatitis. Transient hyperglycemia and glucosuria and elevated serum bilirubin levels occur in some patients with acute pancreatitis.
  • The stools of patients with pancreatic disease are often bulky, pale, and foul-smelling. Fat content of stools varies between 50% and 90% in pancreatic disease; normally, the fat content is 20%.
  • Glucose tolerance test is mainly used in chronic pancreatitis.
  • X-ray studies of the abdomen and chest may be obtained to differentiate pancreatitis from other disorders that may cause similar symptoms and to detect pleural effusions.
  • Ultrasonography
  • Contrast-enhanced CT scans and MRI are used to identify an increase in the diameter of the pancreas and to detect pancreatic cysts, abscesses, or pseudocysts.
  • Peritoneal fluid, obtained through paracentesis or peritoneal lavage, may contain increased levels of pancreatic enzymes.
  • ERCP is commonly used in the diagnostic evaluation of chronic pancreatitis because the patient is acutely ill; however, it may be valuable in the treatment of gallstone pancreatitis.
 
Management
 
Medical Management
Management of the patient with acute pancreatitis is directed toward relieving symptoms and preventing or treating complications.
 
Emergency Management
  • Acute pancreatitis may require patient to be admitted to the hospital.
  • Nil per orally is maintained to allow the pancreas to rest and stabilize.
  • Intravenous fluids and nutrition (parenteral nutrition).
  • 707Nasogastric suction may be used to relieve nausea and vomiting, to decrease painful abdominal distention and paralytic ileus, and to remove hydrochloric acid so that it does not enter the duodenum and stimulate the pancreas.
  • If the cause is gallstones, surgery or other procedures to remove them is recommended.
  • People with chronic pancreatitis may require treatment for alcohol addiction.
 
Intensive Care
  • Correction of fluid and blood loss and low albumin levels to maintain fluid volume and prevent renal failure.
  • Monitor in the intensive care unit.
  • Antibiotic agents.
  • Insulin may be required if significant hyperglycemia occurs.
  • Intubation and mechanical ventilation, if required.
 
Pharmacological Management
  • Analgesics: Morphine and morphine derivatives are often avoided because it has been thought that they cause spasm of the sphincter of Oddi. Meperidine is often prescribed because it is less likely to cause spasm of the sphincter.
  • Antiemetic agents.
  • Histamine-2 (H2) antagonists (e.g. Ranitidine).
  • Antibiotics.
  • Enzyme supplements, such as pancrelipase may be prescribed to help body absorb food better.
  • Probiotic supplement (Lactobacillus acidophilus and other beneficial bacteria) for maintenance of gastrointestinal and immune health.
  • Multivitamin daily, containing the antioxidant vitamins A, C, E, D, the B-complex vitamins, and trace minerals, such as magnesium, calcium, zinc and selenium.
  • Omega-3 fatty acids (fish oil: 1–2 capsules or 1–2 tablespoonfuls oil daily) to help decrease inflammation and improve immunity.
 
Nutrition and Supplements
Following nutritional education should be given to the patient:
  • Eliminate all suspected food allergens, including dairy (milk, cheese, eggs, and ice cream), wheat (gluten), soy, corn, preservatives, and chemical food additives.
  • Eat foods high in B-vitamins and iron, such as whole grains, dark-leafy greens (such as spinach and kale), and sea vegetables.
  • Eat antioxidant foods, including fruits (such as blueberries, cherries, and tomatoes), and vegetables (such as squash and bell pepper) as it reduces free radicals.
  • Avoid refined foods, such as white breads, pastas, and sugar.
  • Eat fewer red meat and more lean meats, cold-water fish, tofu (soy) or beans for protein.
  • Use healthy oils for cooking, such as olive oil or vegetable oil.
  • Reduce significantly or eliminate trans-fatty acids (baked goods, such as cookies, crackers, cakes, French fries, onion rings, donuts).
  • 708Avoid coffee and other stimulants, alcohol, and tobacco.
  • Drink 6–8 glasses of filtered water daily.
  • Exercise moderately for 30 minutes daily, 5 days a week.
 
Surgical Management
Surgery is required to:
  • Remove damaged and infected tissue.
  • Drain an abscess.
  • Maintain pancreatic duct patency.
  • Relief pain in chronic pancreatitis.
  • Endoscopic retrograde cholangio-pancreatography (ERCP): In ERCP, a specialist inserts a tube-like instrument through the mouth and down into the duodenum to access the pancreatic and biliary ducts and the gallstones are removed.
  • Biliary drainage: Placement of biliary drains (for external drainage) and stents (indwelling tubes) in the pancreatic duct through endoscopy has been performed to reestablish drainage of the pancreas. This has resulted in decreased pain and increased weight gain.
  • Diagnostic laparotomy: To know the cause of pancreatitis and to establish pancreatic drainage, or to resect or debride a necrotic pancreas. The patient who undergoes pancreatic surgery may have multiple drains in place postoperatively as well as a surgical incision that is left open for irrigation and repacking every 2 to 3 days to remove necrotic debris.
  • Pancreaticojejunostomy: With a side-to-side anastomosis or joining of the pancreatic duct to the jejunum drainage of the pancreatic secretions into the jejunum is allowed. Pain relief occurs by 6 months in more than 80% of the patients who undergo this procedure, but pain returns in a substantial number of patients as the disease itself progresses.
  • Whipple resection (pancreaticoduodenectomy): It has been carried out to relieve the pain of chronic pancreatitis.
  • Pancreatectomy: Total removal or excision of the pancreas.
  • Autotransplantation: Implantation of the patient's pancreatic islet cells has been attempted to preserve the endocrine function of the pancreas in patients who have undergone total pancreatectomy. Testing and refinement of this procedure continue in an effort to improve outcomes.
  • Sphincterotomy: When chronic pancreatitis develops as a result of gallbladder disease, the obstruction is treated by surgery to explore the common duct and remove the stones. Usually, the gallbladder is removed at the same time. In addition, an attempt is made to improve the drainage of the common bile duct and the pancreatic duct by dividing the sphincter of Oddi, a muscle that is located at the ampulla of Vater. A T-tube usually is placed in the common bile duct, requiring a drainage system to collect the bile postoperatively.
 
Postoperative Management
  • Antacids
  • Oral feedings low in fat and protein are initiated gradually
  • 709Caffeine and alcohol are eliminated from the diet
  • If the episode of pancreatitis occurred during treatment with thiazide diuretics, corticosteroids, or oral contraceptives, these medications are discontinued.
 
Preoperative Nursing Management
 
Nursing Assessment
  • Obtain history of gallbladder disease, alcohol use, or precipitating factors.
  • Assess GI distress, including nausea and vomiting, and diarrhea.
  • Assess characteristics and level of abdominal pain.
  • Assess nutritional and fluid status.
  • Assess respiratory rate and pattern and breath sounds.
  • Assess for steatorrhea and malabsorption.
  • Assess for signs and symptoms of diabetes mellitus.
  • Assess current level of alcohol intake and motivation and resources available to abstain from drinking such as alcoholics anonymous.
 
Nursing Diagnosis
  • Acute pain related to disease process.
  • Chronic pain related to chronic and unrelenting insult to pancreas.
  • Risk for fluid and electrolyte imbalance related to vomiting, self-restricted intake, fever, and fluid shifts.
  • Ineffective breathing pattern related to severe pain and pulmonary complications
  • Imbalanced nutrition: Less than body requirements related to fear of eating, malabsorption, and glucose intolerance.
  • Anxiety related to surgical intervention.
 
Nursing Interventions
  1. Acute pain related to disease process.
    Interventions
    • Administer opioid analgesics as ordered to control pain.
    • Assist patient to a comfortable position.
    • Maintain NPO status to decrease pancreatic enzyme secretion.
    • Maintain patency of NG suction to remove gastric secretions and to relieve abdominal distention, if indicated.
    • Provide frequent oral hygiene and care.
    • Administer antacids or H2-receptor antagonists as prescribed.
    • Report increase in severity of pain, which may indicate hemorrhage of the pancreas, rupture of a pseudocyst, or inadequate dosage of the analgesic.
  2. Chronic pain related to chronic and unrelenting insult to pancreas.
    Interventions
    • Assess and record the character, location, frequency, duration of pain.
    • Determine precipitating and alleviating factors of the patient's pain.
    • 710Explore the effect of pain on the patient's lifestyle and eating habits.
    • Administer or teach self-administration of analgesics as ordered to control pain.
    • Use nonpharmacologic methods to promote relaxation, such as distraction, imagery, and progressive muscle relaxation.
    • Assess response to pain control measures, and refer to chronic pain management clinic, if indicated.
  3. Risk for fluid and electrolyte imbalance related to vomiting, self-restricted intake, fever, and fluid shifts.
    Interventions
    • Monitor and record vital signs, skin color, and temperature.
    • Monitor intake and output and weigh daily.
    • Evaluate laboratory data for hemoglobin, hematocrit, albumin, calcium, potassium, sodium, and magnesium levels and administer replacements as prescribed.
    • Observe and measure abdominal girth if pancreatic ascites is suspected.
    • Report trends in falling blood pressure or urine output or rising pulse, because this may indicate hypovolemia and shock or renal failure.
  4. Ineffective breathing pattern related to severe pain and pulmonary complications.
    Interventions
    • Assess respiratory rate and rhythm, effort, oxygen saturation, and breath sounds frequently.
    • Position in upright or semi-Fowler's position to enhance diaphragmatic excursion.
    • Administer oxygen supplementation as prescribed to maintain adequate oxygen levels.
    • Report signs of respiratory distress immediately.
    • Instruct patient in coughing and deep breathing.
  5. Imbalanced Nutrition: Less than body requirements related to fear of eating, malabsorption, and glucose intolerance.
    Interventions
    • Assess nutritional status, history of weight loss, and dietary habits, including alcohol intake.
    • Administer pancreatic enzyme replacement with meals, as prescribed.
    • Administer antacids or H2-receptor antagonists to prevent neutralization of enzyme supplements, as indicated.
    • Monitor intake and output and daily weight.
    • Assess for GI discomfort with meals and character of stools.
    • Monitor blood glucose levels and teach balanced, low concentrated carbohydrate diet and insulin therapy as indicated.
    • Identify foods that aggravate symptoms and teach low-fat diet.
  6. Anxiety related to surgical intervention.
    Interventions
    • Describe planned surgical intervention and the expected results.
      • Decreased pain.
      • Ability to eat better and improve general condition.
    • 711Prepare patient for adverse effects and complications of surgery.
      • Total pancreatectomy will cause permanent diabetes mellitus, dependence on insulin, severe malabsorption, and the need for lifelong pancreatic enzyme replacement.
      • Malnutrition and debility increase a patient's risk for poor healing and complications of surgery.
    • Assist patient to prepare for surgery by encouraging abstinence of alcohol and intake of nutritional and vitamin supplements.
    • Encourage patient to enlist help of support network and strengthen appropriate coping mechanisms.
    • After surgery, provide meticulous care to prevent infection, promote wound healing, and prevent routine complications of surgery.
 
Postoperative Nursing Management
 
Nursing Assessment
  • Postoperatively, the patient is evaluated for:
    • Vital signs, LOC.
    • Level of pain.
    • Wound or puncture sites appearance: wound drain or T-tube patency, security and drainage (if present).
    • Intake and output.
  • Early ambulation is encouraged to prevent thromboembolus, to facilitate voiding, and to stimulate peristalsis.
  • Complications to assess for include incisional infection, hemorrhage, and bile duct injury (persistent pain, fever, abdominal distention, nausea, anorexia, or jaun dice).
 
Potential Complications
  • Deep vein thrombosis or pulmonary embolism
  • Pneumonia or atelectasis
  • Infection, hemorrhage, or bile duct injury
 
Nursing Diagnoses
  • Acute pain related to surgical procedure
  • Risk for infection related to surgical procedure
  • Impaired skin integrity related to poor nutritional status, bed rest, and multiple drains and surgical wound
  • Imbalanced nutrition: Less than body requirements related to surgical procedure, wound pain, or tube drainage.
 
Nursing Interventions
  1. Acute pain related to surgical procedure.
    Interventions
    • Assess pain location, level, and characteristics.
    • Administer prescribed pain medications or monitor patient-controlled analgesia.
    • 712Encourage splinting of incision when moving.
    • Encourage ambulation as soon as prescribed to decrease flatus and abdominal distention and to promote bowel motility.
    • Instruct patient that usual activities can normally be resumed within 5 to 7 days after laparoscopic cholecystectomy or within 4 to 6 weeks of open cholecystectomy.
    • Sexual activity may be resumed when pain has abated.
    • Obtain specific instructions for wound care, activity, such as heavy lifting, strenuous activity, showers and tub baths, and driving per surgeon's protocol.
  2. Risk for infection related to surgical procedure.
    Interventions
    • Assess wound dressings for any increased or purulent drainage.
    • Assess wound drain or T-tube site for drainage, and note amount, color, and odor.
    • Assess bile drainage from T-tube into bile bag:
      • Report decrease in drainage.
      • Maintain T-tube patency and security.
    • Report right upper quadrant pain, abdominal distention, fever, chills, or jaundice, as these may indicate a bile duct injury.
    • Administer antibiotics as prescribed.
    • Encourage use of incentive spirometer, coughing and deep breathing, and ambulation.
  3. Impaired skin integrity related to poor nutritional status, bed rest, and multiple drains and surgical wound.
    Interventions
    • Carefully assess the wound, drainage sites, and skin for signs of infection, inflammation, and breakdown.
    • Wound care as prescribed and take precautions to protect intact skin from contact with drainage.
    • Consulting with an enterostomal therapist is often helpful in identifying appropriate skin care devices and protocols.
    • Change the patient's position every 2 hours. Use of specialty beds may be indicated to prevent skin breakdown.
    • Provide skin care and back care.
  4. Imbalanced nutrition: Less than body requirements related to surgical procedure, wound pain, or tube drainage
    Interventions
    • Assess for nausea and vomiting and administer antiemetics as prescribed.
    • Encourage fluid intake and advance to regular diet as tolerated.
    • Administer replacement fluids for bile drainage from T-tube.
    • Encourage small frequent diet.
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Patient Education and Health Maintenance
  • Teach patient and family that rapid postoperative recovery should be expected.
  • Advise patient and family to notify the surgeon immediately of any subtle change in postoperative course or persistent symptoms.
  • Advise patient to advance diet as tolerated. Fats can be taken as tolerated because the bile ducts dilate to accommodate storage of bile as needed.
 
Complications
 
Acute (Early) Complications
  • Shock
  • Hypocalcemia
  • High blood glucose
  • Dehydration, and kidney failure (from inadequate blood volume)
  • Respiratory complications, such as pleural effusion, atelectasis, pneumonitis and acute respiratory distress syndrome
  • Systemic inflammatory response syndrome (SIRS)
  • Hemorrhagic pancreatitis
  • Pancreatic acitis.
 
Late Complications
  • Pancreatic pseudocysts
  • Pancreatic abscess.
 
INTESTINAL OBSTRUCTION
Intestinal obstruction is an interruption in the normal flow of intestinal contents along the intestinal tract. The obstruction may occur in small intestine or colon and can be partial or complete, may be mechanical or may be paralytic, may or may not comprise of the vascular supply.
Intestinal obstruction exists when there is blockage, mechanical or functional, that prevents the normal flow of the intestinal contents through the intestinal tracts. It can occur at any level distal to the small intestine or large intestine and is a medical emergency.
 
Etiology
  • Obstructions of the small intestine may be caused by narrowing of the intestinal lumen as a result of inflammation, neoplasms, adhesions, hernia, volvulus, intussusceptions, food blockage or compression from outside the intestine.
  • Paralytic ileus, vascular problems, such as mesenteric embolus and thrombus, hypokalemia from diuretics or antihypertensive agents also may result in small bowel obstructions.
  • Cancer accounts for about 80% of obstructions of the large intestine, with mostly occurring in the sigmoid colon. Other causes are diverticulitis, ulcerative colitis, and previous abdominal surgery. Factors that are caused are mechanical, neurogenic or vascular.
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Risk Factors
  • Mechanical factors: A physical block to passage of intestinal contents without disturbing blood supply of bowel. High small bowel, or low small bowel obstructions occur four times more frequently than chronic obstructions. These includes:
 
Extrinsic
  • Adhesions: These fibrous bands of scar tissue can become looped over a portion of the bowel. The loops then can become either the focus around which the bowel can twist or the band that mechanically obstructs the bowl by external pressure. The presence of multiple adhesions increases the risk of obstruction.
  • Hernia: An incarcerated hernia may or may not cause obstruction, depending on the size of the hernia ring. However, the potential for obstruction is always present in any hernia. A strangulated hernia is always obstructed because the bowel cannot function when its blood supply is cut-off.
  • Volvulus: Volvulus is a twisting of the bowel that commonly occurs about a stationary focus in the abdominal cavity. It can cause infraction of the bowel and can occur in either the large or small bowel. Volvulus sometimes can be corrected without surgical interventions. Successful decompression of the bowel with a long tube releases pressure against the proximal end of the loop, thus allowing bowel volvulus to relax.
 
Intrinsic
Hematoma, tumor, intussusception (relescoping of intestinal wall inside itself), stricture or stenosis, congenital (artesia, imperforate anus), trauma, inflammatory disease (ulcerative colitis, diverticulum).
 
Nonmechanical Factor
  • Neurologic factors: Neurogenic factors are responsible for a dynamic obstruction, also called paralytic ileus, which is caused by lack of peristaltic activity and commonly occurs after abdominal surgery. Extensive surgical procedures in the bowel and in the retroperitoneal area may cause a postoperative neurologic problem. Treatment involves aspiration of secretions by NG suction until the bowel begins to function.
  • Vascular factors: When the blood supply to any part of the body is interrupted, the part ceases to function and pain occurs. Blood is supplied by way of the celiac and superior and inferior mesenteric arteries. These vessels have autosomotic intercommunications at the head of the pancreas and along the transverse bowel. Obstruction of blood flow can arise as a result of complete occlusion (mesenteric infarction) or partial occlusion (abdominal angina).
  • Intraluminal: Foreign body, fecal or barium impaction, polyp, gallstones, meconium in infants. In postoperative patients, approximately 90% of mechanical obstructions are due to adhesion.
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Other Causes
  • Spinal cord injuries, vertebral fractures
  • Postoperatively after any abdominal surgery
  • Peritonitis, pneumonia
  • Wound dehiscence
  • GI tract surgery
  • Strangulation—obstruction comprises blood supply, leading to gangrene of the intestinal wall, caused by the prolonged mechanical obstruction.
 
Types
It is a series that depends on the region of bowel that is affected, the degree to which the lumen is occluded and the degree to which the blood circulation in the bowel wall is disturbed. Treatment involves aspiration of the secretion which involves aspiration of the secretion by gastric suction until the bowel begins to function.
  • Partial occlusion
  • Complete occlusion
Complete occlusion: An occlusion of arterial blood supply to the bowel as in mesenteric thrombosis effectively stops bowel function. The usual cause is an embolus. The extent of the resulting symptoms is determined by:
  • Size of the vessels that is occluded
  • The length of the bowel that is without a supply of blood
  • The rapidity with which the occlusion occurs.
 
Signs and Symptoms
  • Crampy pain that is wave-like and colicky in character
  • The patient may pass blood and mucus but no fecal matter and no flatus.
  • Vomiting
  • Obstruction
  • Crampy, lower abdominal pain
  • Fecal vomiting
  • Shock
  • Constipation
  • Abdominal distension.
 
Diagnostic Evaluation
  • X-ray studies: Abdominal X-ray will show abnormal qualities of gas or fluid in the bowel.
  • Lab studies: Complete blood cell count, electrolytes, and blood urea nitrogen will reveal dehydration and loss of plasma volume and possibly infection. An elevated WBC count will indicate strangulation or perforation.
  • Hematocrit: This will indicate hemoconcentration, decreased hemoglobin and HCT values indicate bleeding from neoplasm or strangulation with necrosis. Increased BUN will indicate dehydration, stool to be checked for occult blood.
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Pathophysiology
 
Management
 
Assessment
  • Assess the signs and symptoms of abdominal pain, indigestion, nausea and vomiting.
  • Take the history of prolonged constipation and complaint of dysphagia and abdominal pain.
  • Assess for the diagnostic studies of the radiography of the flat and upright abdomen.
  • Assess for the abdominal distension through bowel sounds.
Decompression of the bowel through a nasogastric tube by the removal of gas, and fluid, correction and relief of the obstruction. Decompression of the bowel is done by inserting the NG tube or intestinal tube.
 
Surgical Management
Surgical treatment involves resection of the obstructed segment of bowel anastomosing the remaining healthy bowel. Partial or total colectomy, colostomy or ileostomy may be required when extensive obstruction or necrosis is present, e.g. hernia and adhesions.
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Nonsurgical Treatment
  • Introducing colonoscope for the removal of polyps, dilated strictures, and removing necrotic tumors with laser.
  • Correction of fluid and electrolyte imbalances with normal saline or Ringer's solution with potassium as required.
  • NG suction to decompress bowel.
  • Treatment of shock and peritonitis.
  • TNP may be necessary to correct protein deficiency from chronic obstruction, paralytic ileus, or infection.
  • Analgesics and sedatives, avoiding opiates due to GI mobility inhibition.
  • Ambulation for the patients with paralytic ileus to encourage return of the peristalsis.
 
Nursing Management
 
Nursing Diagnosis
  • Ineffective breathing pattern related to abdominal distension, interfering with normal lung expansion.
  • Acute pain related to obstruction, distension, and strangulation.
  • Risk of fluid deficit volume related to impaired fluid intake, vomiting, and diarrhea from intestinal obstruction.
  • Risk for electrolyte imbalance related to suctioning.
  • Diarrhea related to obstruction.
  • Risk of injury related to complication and severity of illness.
  • Fear related to life-threatening symptoms of intestinal obstruction.
  1. Ineffective breathing pattern related to abdominal distension, interfering with normal lung expansion.
    Interventions
    • Keep the patient in Fowler's position to promote ventilation.
    • Provide oxygenation to the patient.
    • Monitor ABG level for oxygenation to decompress.
  2. Acute pain related to obstruction, distension, and strangulation
    Interventions
    • Provide supportive care during NG intubation to assist with discomfort.
    • To relieve air-fluid syndrome, turn the patient from supine to prone position every 10 minutes until enough flatus is passed to decompress the abdomen.
    • A rectal tube may be indicted.
    • Administer prescribed analgesics.
  3. Risk of fluid deficit volume related to impaired fluid intake, vomiting, and diarrhea from intestinal obstruction.
    Interventions
    • Measure and record all intake and output.
    • Administer IV fluid and parental nutrition as prescribed.
    • 718Monitor electrolytes, urine analysis, haemoglobin and blood cells count and report any abnormalities.
    • Monitor renal output to assess the renal function and to detect urine retention due to bladder compression by the distended intestine.
    • Monitor vital signs, a drop in BP may indicate decrease circulatory volume due to blood loss from strangulated hernia.
  4. Risk for electrolyte imbalance related to suctioning.
    Interventions
    • Monitor electrolyte values to identify imbalances.
    • Monitor vital signs and watch for signs of electrolyte for imbalances such as weakness accompanied by low potassium levels to identify imbalances for prompt treatment.
    • Give ice chips sparingly if ordered by the physician melted ice increases electrolyte and hydrochloric acid removal when suctioned from the stomach, and electrolyte imbalance and metabolic alkalosis occur.
  5. Diarrhea related to obstruction.
    Interventions
    • Collect stool sample for test for occult blood if occur.
    • Maintain adequate fluid balance.
    • Record and amount of consistency of stools.
    • Maintain NG tube as prescribed to decompress bowel.
  6. Fear related to life threatening symptoms of intestinal obstruction.
    Interventions
    • Recognize the patient's concerns and initiate measures to provide emotional support.
    • Encourage the presence of support person.
 
Complications
  • Dehydration due loss of water, sodium, and chloride.
  • Peritonitis.
  • Shock due to loss of electrolyte and dehydration.
  • Death due to shock.
 
Health Education
  • Explain the rational for NG suction, NPO status, and IV fluids initially. Advise the patient to progress diet slowly as tolerated once home.
  • Advise plenty of rest and slow progression of activity as directed by surgeon or other health care provider.
  • Teach wound care, if indicated.
  • Encourage the follow-up directed and to call surgeon or health care provider, if increasing abdominal pain, vomiting, or few occur prior to follow-up.
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CROHN'S DISEASE
Crohn's disease is a chronic idiopathic inflammatory disease that can affect any part of GI tract, usually the small intestine and large intestines that characterized by ulceration, swelling and scarring of the part of intestine. It is also known as regional enteritis.
 
Etiology
IBD most commonly begins during adolescence and early adulthood (usually between the ages of 15 and 35). There is a small second peak of newly diagnosed cases after age 50. Although the reason for this is not completely understood.
  • The exact cause of Crohn's disease is unknown.
  • Family history of inflammatory bowel disease.
  • Immune system problems: For some reason, people with Crohn's disease have an immune system that reacts inappropriately.
  • Genetics: Brothers, sisters, children, and parents of persons with IBD, including Crohn's disease, are slightly more likely to develop the disease themselves.
  • Environmental factors: Environmental factors may help trigger Crohn's disease. Associated environmental factors may include any of the following:
    • Substances from something you have eaten
    • Microbes such as bacteria or viruses
    • Cigarette smoke
    • Other substances that are yet unknown.
 
Types
  • Crohn's colitis
  • Crohn's enteritis
  • Crohn's terminal ileitis
  • Crohn's enterocolitis and ileocolitis
    • Crohn's colitis is inflammation that is confined to the colon. Abdominal pain and bloody diarrhea are the common symptoms. Anal fistulae and perirectal abscesses can also occur.
    • Crohn's enteritis refers to inflammation confined to the small intestine (the first part, called the jejunum or the second part, called the ileum). Involvement of the ileum alone is referred to as Crohn's ileitis. Abdominal pain and diarrhea are the common symptoms. Obstruction of the small intestine can also occur.
    • Crohn's terminal ileitis is inflammation that affects only the very end of the small intestine (terminal ileum), the part of the small intestine closest to the colon. Abdominal pain and diarrhea are the common symptoms. Small intestinal obstruction can also occur.
    • Crohn's enterocolitis and ileocolitis are terms to describe inflammation that involve both the small intestine and the colon. Bloody diarrhea and abdominal pain are the common symptoms. Small intestinal obstruction can also occur.
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Pathophysiology
 
Signs and Symptoms
Common symptoms of Crohn's disease include abdominal pain, diarrhea, and weight loss. Less common symptoms include poor appetite, fever, night sweats, rectal pain, and occasionally rectal bleeding. The symptoms of Crohn's disease are dependent on the location, the extent, and the severity of the inflammation.
  • Swelling of the tissue of the anal sphincter, the muscle at the end of the colon that controls defecation.
  • Development of ulcers and fissures (long ulcers) within the anal sphincter. These ulcers and fissures can cause bleeding and pain with defecation.
  • Development of anal fistulae (abnormal tunnels between the anus or rectum and the skin surrounding the anus). Mucus and pus may drain from the openings of the fistulae on the skin.
  • Development of perirectal abscesses (collections of pus in the anal or rectal area). Perirectal abscesses can cause fever, pain and tenderness around the anus.
721
 
Diagnostic Evaluation
The diagnosis of Crohn's disease is suspected in patients with fever, abdominal pain and tenderness, diarrhea with or without bleeding, and anal diseases.
  • Laboratory blood tests may show elevated white blood cell counts and sedimentation rates, both of which suggest infection or inflammation.
  • Other blood tests may show low red blood cell counts (anemia), low blood proteins, and low body minerals, reflecting loss of these minerals due to chronic diarrhea.
  • Colonoscopy: It is more accurate than barium X-rays in detecting small ulcers or small areas of inflammation of the colon and terminal ileum. Colonoscopy also allows for small tissue samples to be taken and sent for examination under the microscope to confirm the diagnosis of Crohn's disease. Colonoscopy also is more accurate than barium X-rays in assessing the degree (activity) of inflammation.
  • Computerized axial tomography (CAT) or (CT): Scanning is a computerized X-ray technique that allows imaging of the entire abdomen and pelvis. It can be especially helpful in detecting abscesses.
  • Video capsule endoscopy (VCE): VCE has also been added to the list of tests for diagnosing Crohn's disease. For video capsule endoscopy, a capsule containing a miniature video camera is swallowed. As the capsule travels through the small intestine, it sends video images of the lining of the small intestine to a receiver carried on a belt at the waist. The images are downloaded and then reviewed on a computer.
  • Stool specimens: Mainly composed of mucus, blood, pus, and intestinal organisms, especially Entamoeba histolytica (active stage). Fecal leukocytes and RBCs indicate inflammation of GI tract. Stool positive for bacterial pathogens, ova and parasites or clostridium indicates infections. Stool positive for fat indicates malabsorption.
  • Barium enema: May be performed after visual examination has been done, although rarely done during acute, relapsing stage, because it can exacerbate condition.
  • Electrolytes: Decreased potassium, magnesium, and zinc are common in severe disease.
 
Complications
  • Bowel strictures
  • Nutritional deficiencies
  • Loss of weight
  • Anemia
  • Growth retardation
  • Delayed puberty
  • Formation of fistulas
  • Massive intestinal bleeding.
Management: The aim of the management is:
  • To understand the natural history and prognostic factors of Crohn's disease.
  • To understand when to use early combination therapy with an anti-TNF agent and an immunomodulator in moderate to severe Crohn's patients.
  • 722To understand the side effects of anti-TNF therapy.
  • To understand when to administer appropriate vaccinations to inflammatory bowel disease patients both before and during immunosuppressive therapy.
 
Medical Management
  1. Immunosuppressant – to reduce the inflammation. This drug includes:
    • Azathioprine
    • Cyclosporine
    • Infliximab
    • Tacrolimus
    • Mycophenoate mofetil.
  2. Aminosalicylates (oral)
    • Olsalazine: antibacterial action
    • Balsalazine
    • Mesalamine.
  3. Corticosteroids (oral)
    • Prednisolone
    • Prednisone.
  4. Corticosteroids (rectal)
    • Hydrocortisone intrarectal form
    • Retention enema.
  5. Immune modifiers
    • 6-mercaptourine
    • Azathioprine
    • Cyclosporine.
  6. Monoclonal antibodies
    • Infiximab reduces inflammation.
  7. Antibiotics
    • Metronidazole IV
    • Ciprofloxacin.
      These drugs are helpful to reduce harmful intestinal bacteria and suppress the intestine's immune system.
  8. Iron supplements should also be prescribed to restore the iron level to normal.
 
Surgical Management
Surgery plays important but different roles in management of Crohn's disease and ulcerative colitis. Surgery is indicated for patients whose disease is refractory to medical therapy and for the management of complications. It plays a curative role in ulcerative colitis.
Surgical intervention is avoided whenever possible in Crohn's disease because of high rates of recurrence of disease process in the same area. Surgical approaches to Crohn's disease focus on sparing and conserving as much of the bowel as possible, particularly when the small bowel is involved.
723
 
Preparation for Surgery
In some cases, surgery will be an emergency procedure and there will be little time to prepare.
  • Try to be in the best possible physical and mental shape prior to the procedure. Nutrition is extremely important because when you are well-nourished, your immune system is strong, which lessens the likelihood of surgical complications, such as infection.
  • Prepare yourself mentally for surgery and recovery. If the procedure will result in an ostomy, there will be much to learn. It is best to start preparing in advance by consulting with a wound-ostomy care nurse (a health care provider who specializes in ostomies).
  • Build a support team of family, friends, and others who can assist you before and after surgery with transportation, meal preparation, and other daily tasks.
  • Try to resolve work, family, and school obligations in advance. Speak with your employer about taking time off from work or ask about the company's Family Medical Leave policy. Check into temporary disability, social security, or other appropriate programs. For children, try to schedule procedures when school is not in session. If this is not possible, secure a tutor for your child and make other school accommodations.
  • Segmental resection with anastomosis has been the primary surgical approach. Surgeons typically resect the bowel 5 to 10 cm above and below the macroscopically visible disease.
  • Ileocolostomy.
 
Common Procedures for Crohn's Disease
  • Different types of surgical procedures may be performed for Crohn's disease, depending on the complication, severity of the illness, and location of the disease in the intestines. In many cases, surgery is performed to remove a diseased portion of the gastrointestinal tract. This surgery may involve removal of a section of an intestine, or it may mean removing an entire organ (such as the colon and/or rectum).
  • Unlike ulcerative colitis, Crohn's disease cannot be cured with surgery, except in some instances where only the colon, rectum, and anus are affected. If the diseased portion of the intestine is removed, the inflammation can reappear adjacent to the site of the surgery, even if that part of the intestine was normal prior to the surgery. The primary goals of surgery for Crohn's disease are to conserve as much bowel as possible, alleviate complications, and to help the patient achieve the best possible quality of life.
 
A. Small Bowel Disease
When Crohn's disease affects the small intestine, areas of diseased bowel may alternate with areas of normal bowel. The areas of active disease may narrow, forming strictures, which can block the passage of digested food. The sections of normal bowel compensate by pushing against this strictured area, causing severe crampy pain. There are two surgical procedures for strictures: strictureplasty and small bowel resection.
  • Strictureplasty: In a strictureplasty, the narrowed area of intestine is widened without removing any portion of the small intestine. The surgeon makes a lengthwise incision along the narrowed area and then sews it up crosswise. This shortens and widens the segment of bowel. Several strictures may be treated in one surgical procedure. Strictureplasty is most effective in the lower sections of the small intestine (ileum and jejunum), and is less effective in the upper section (duodenum). 724Performing strictureplasty avoids the need of the removal of a section of the small intestine, which can sometimes lead to a condition called short bowel syndrome. Strictureplasty is generally safe and effective, but about half of the people who have this procedure will require subsequent surgery.
  • Small bowel resection: Strictures may also be treated with a small bowel resection. In this procedure, a segment of the small intestine is removed and the two ends of healthy intestine are joined together. Small bowel resection may also be required if a hole develops in the wall of the small intestine.
    A bowel resection may offer patients many years of symptom relief. However, about 50 percent of adult patients will have a recurrence of symptomatic Crohn's disease within five years after having a resection. The disease usually recurs at the site of the anastomosis. Recurrent Crohn's disease can often be successfully treated with medications, such as immunomodulator or biologics. However, about one-half of people with recurrent symptoms will need a second surgery.
 
B. Colonic Disease
Some people have severe Crohn's disease that affects the colon or rectum. Surgery may be needed to remove the entire colon (colectomy), the colon and rectum (proctocolectomy), or a portion of the colon (resection).
  • Large bowel resection: In a large bowel resection, the diseased portion of the colon is removed and the healthy intestine on either side of the removed area is sewn together. This is similar to a small bowel resection. As with that procedure, Crohn's disease recurs about 50 percent of the time, usually at the site where the intestine was connected.
  • Colectomy and proctocolectomy: If the colon needs to be removed entirely but the rectum is unaffected by the disease, a colectomy will be performed. Once the colon is taken out, the ileum will be joined to the rectum. This allows the person to continue to pass stool through the anus.
    If the rectum is affected and needs to be removed along with the colon, the surgeon will perform a proctocolectomy with end ileostomy. Unlike ulcerative colitis patients, Crohn's disease patients generally do not undergo the variation of the procedure that eliminates the need to wear an external ostomy bag (proctocolectomy with ileal pouch-anal anastomosis). This is because the disease frequently recurs in the internal pouch, making pouch excision more common.
 
C. Perianal Disease and Intestinal Fistulas
About 35 to 50 percent of adults with Crohn's disease will develop a fistula during their lifetime. A fistula usually starts as an infection. A collection of pus, intestinal bacteria, and fluids penetrates through the wall of an intestinal organ, and a channel forms to another loop of intestine or organ (bladder, vagina, or skin). Because they contain infected material, fistulas may initially be treated with antibiotics. Surgery for a fistula may be necessary if its symptoms do not respond to medications. In some cases, emergency surgery is necessary to prevent the spread of infection.
An anal fistula is a tunnel that forms between the inside of the anus and the skin surrounding the anus. In a surgical procedure called fistulotomy, the goal is to cure the fistula 725without damaging the anal sphincter muscles, which are necessary for fecal continence. For these fistulas, the recurrence rate is fairly low following surgery and there is little impact on continence. Complications from this procedure are rare.
Women with Crohn's disease can develop a fistula between the rectum and vagina, which may be difficult to treat. The procedure that is performed will depend on the individual circumstances.
Total Proctocolectomy: In this surgery, the colon and rectum are removed and the anus is closed.
 
Dietary Recommendations
  • Eat regularly, do not skip meals. Empty bowels produce gas.
  • When adding new foods to your diet, try a little bit with other foods you know will be easy to digest.
  • Small, frequent meals are best, always chew thoroughly.
  • Rice, potatoes, or pasta once daily may reduce bowel frequency and irritation.
  • High potassium foods will help offset the side effects of diarrhea.
  • Limit foods containing simple sugars. They aggravate diarrhea.
The following are potential anal irritants:
  • Coconut
  • Dried fruits (raisins, figs)
  • Foods with seeds or nuts
  • Raw fruits (oranges, apples)
  • Raw vegetables (celery, corn, coleslaw)
  • Spicy foods
 
Nursing Management
The goal of nursing management is:
  • To control the inflammatory process.
  • To relieve symptoms.
  • To correct metabolic and nutritional problems and promote healing.
  • To achieve the previous health status.
 
Nursing Diagnosis
  • Diarrhea related to inflamed intestinal mucosa.
  • Deficit fluid volume related to diarrhea.
  • Chronic pain-related inflammatory disease of small intestine.
  • Imbalanced nutrition less than the body requirement related to pain.
  • Ineffective coping related to feeling of rejection.
  1. Diarrhea related to inflamed intestinal mucosa.
    Interventions
    • Antidiarrheal medications are commonly used to treat diarrhea.
    • Nurse monitors the number and consistency of stools.
    • 726Perineal area must be clean with antiseptic solution and then with water.
    • Perineal area must be clean in every evacuation.
    • Report reduction in frequency of stools, return to more normal stool consistency.
    • Identify and avoid contributing factors.
    • Promote bed rest, provide bedside commode.
  2. Deficit fluid volume related to diarrhea.
    Interventions
    • Monitor intake and output chart.
    • Provide fluids as prescribed by the doctor to maintain hydration.
    • Monitor electrolytes and acid base balance because diarrhea can lead to metabolic acidosis.
    • Watch for cardiac dysrhythmias and muscular weakness due to loss of electrolytes.
  3. Chronic pain-related inflammatory disease of small intestine.
    Interventions
    • Administer medications for control of inflammatory process as prescribed.
    • Observe and record changes in pain, frequency, location, characteristics, precipitating events and duration.
    • Monitor for distension, increased temperature, hypotension and rectal bleeding—all signs of obstruction due to inflammation.
    • Clean the rectal area and apply ointments as necessary to decrease discomfort from skin breakdown.
    • Prepare the patient for surgery if response to medical and drug therapy is unsatisfactory.
  4. Imbalanced nutrition less than the body requirement related to pain.
    Interventions
    • Encourage a diet that is low in residue fiber and fat and high in calories, protein and carbohydrates with vitamin and mineral supplements.
    • Monitor weight daily.
    • Provide small frequent feeding to prevent distension.
    • Have the patient participate in meal planning to encourage compliance and increased knowledge.
    • Prepare the patient for elemental diet.
    • Restart oral fluid intake gradually. Offer clear liquids hourly, avoid cold fluids.
  5. Ineffective coping related to feeling of rejection.
    Interventions
    • Offer understanding concern and encouragement.
    • Facilitate supportive psychological counseling, if appropriate.
    • Encourage the patients' usual support by people to be involved in management of disease.
    • Encourage health-promoting behavior.
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Health Education
  • Provide comprehensive education about anatomy and physiology of GI system, the chronic disease process, drug therapy, potential complications and potential surgery.
  • Instruct patient about all prescribed medications including the purpose, dosage and adverse effects.
  • Encourage regular follow-up and report signs of complications.
    • Increasing abdominal distension.
    • Cramping pain.
    • Diarrhea, malaise, fever.
  • Explain the importance of adequate hydration and nutrition monitoring weight.
  • Encourage the patient to participate in stress-reducing activities, such as exercise, relaxation techniques, music therapy.
  • For further information and support.
  • Information about IBD must be given in a way that promotes positivity and reassurance.
  • Nutrition and dietary considerations need to be discussed.
  • If the patient is on medications, instruct regarding the dose, when and how to take the drug, why it is ordered and also about the side effects.
  • Instructions regarding the daily care provided if patient has an ileostomy or colostomy.
  • Encourage regular follow-up and to report signs of complications
  • Encourage the patient to participate in stress-reducing activities, such as exercise, relaxation techniques, etc.
 
ABDOMINAL HERNIA
In general, hernia refers to a condition that arises when an organ pushes through a weak area in the muscles or tissue that surrounds and contains it.
An abdominal hernia occurs when there is a tear in the inner lining of the abdominal wall (the outer layer of muscle, fat and tissue that extends from the bottom of the ribs to the top of the thighs), causing a bulge in the abdominal wall where the organs protrude.
The bulge can be either reducible, which means that by applying slight pressure to the area, the organs are being pushed back into the abdominal cavity and the hernia will flatten and disappear, or nonreducible, which means the fat or tissue cannot be pushed back into the abdomen and the hernia will not flatten.
 
Etiology and Risk Factors
A hernia can develop in anyone, from a newborn baby to a senior citizen. The following may increase risk of developing a hernia by increasing pressure on the abdominal wall:
  • A chronic cough, such as smoker's cough
  • Obesity
  • Straining during bowel movements or while urinating
  • Pregnancy
  • Straining to lift heavy objects
  • Persistent sneezing, such as that caused by allergies
  • 728Prolonged seating or standing
    The risk of having an abdominal hernia increases with age because the older you get, the weaker your abdominal wall muscles become.
 
Signs and Symptoms
  • The main sign of an abdominal hernia is having a bulge or swelling appear on a part of abdomen. Often, the bulge will disappear in lying down position or push on it and then reappear during standing, cough or sneeze. This is called a reducible hernia.
  • Other symptoms are burning, slight discomfort and a feeling of heaviness or aching in abdomen.
 
Types of Abdominal Hernias
The following are different types of abdominal hernia:
 
Inguinal Hernia
When a male's testicles descend into the scrotum, this causes a naturally weakened area in the wall of the abdomen, called the internal ring. This weakened area makes men more susceptible to a hernia at this location.
It is of two types:
  • Indirect inguinal hernia: An indirect inguinal hernia is the most common type of inguinal hernia. It occurs at the internal ring in the groin area. The intestine drops down into the internal ring and can extend down into the scrotum in men or to the outer folds of the vagina in women. An indirect inguinal hernia can be the result of an inherited weakness at the internal ring or one that occurs later in life. The latter is known as an acquired hernia.
  • Direct inguinal hernia: Less common than an indirect inguinal hernia, a direct inguinal hernia occurs near the internal ring instead of within it. They are acquired hernias that usually occur after age 40 as a result of aging or injury.
 
Epigastric Hernia
This type of hernia occurs as a result of a weakness in the muscles of the upper-middle abdomen, above the navel. Men are about three times more likely to have an epigastric hernia than women.
 
Umbilical Hernia
They involve protrusion of intra-abdominal contents through a weakness at the site of passage of the umbilical cord through the abdominal wall. These hernias often resolve spontaneously. Umbilical hernias in adults are largely acquired, and are more frequent in obese or pregnant women. Abnormal decussation of fibers at the linea alba may contribute. These hernias can occur in babies, children and adults.
 
Femoral Hernia
Femoral hernias occur just below the inguinal ligament, when abdominal contents pass into the weak area at the posterior wall of the femoral canal. They can be hard to distinguish from the inguinal type. It occurs in the area between the abdomen and the thigh, and appears as a bulge on the upper thigh. This type of hernia is more common in women than men.
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Incisional Hernia
An incisional hernia occurs when the defect is the result of an incompletely healed surgical wound. It can occur at the site of an incision from a previous surgery. The fat or tissue pushes through a weakness created by the surgical scar. An incisional hernia can occur months or years after the initial surgery.
 
Diaphragmatic Hernia
Higher in the abdomen, diaphragmatic hernia results when part of the stomach or intestine protrudes into the chest cavity through a defect in the diaphragm. A hiatus hernia is a particular variant of this type, in which the normal passageway through which the esophagus meets the stomach (esophageal hiatus) serves as a functional ‘defect’, allowing part of the stomach to herniate into the chest.
 
Diagnosis of Abdominal Hernia
  • By taking history
  • Physical examination
  • Examine the bulge or swelling
  • Ultrasound scan
  • X-rays
  • CT scan
 
Management
 
Nonsurgical Treatment
Treatment for hernias can be surgical or nonsurgical, depending on their severity. Non-surgical treatments usually help ease pain and discomfort caused by a hernia but do not correct the problem.
 
Trusses
There are two kinds of trusses for hernias, the spring truss and the umbilical truss. The spring truss is worn around the waist and acts as a support, while the umbilical truss is worn around the midsection. Trusses also come in different sizes and are usually worn under briefs.
 
Hernia Belts
Hernia belts are lightweight and made in such a way that movement is not restricted while you are recovering. These belts were designed to be worn over briefs, are made with adjustable straps and are lined with foam for extra comfort. The foam compression pads provide gradual pressure and support to the weakened muscles.
 
Bindings
Abdominal bindings are made of elastic and provide uniform compression and support of the abdominal muscles. They can be fastened around the waist.
 
Hernia Briefs
Hernia briefs look like regular briefs except they are made with spandex and foam pads for extra support and are designed to provide rupture relief. The material is convenient because it is lightweight, cool and washable and is easy to wear. It is important to remember that these nonsurgical treatments for hernias are not meant to correct the problem. They are only 730meant to provide comfort and pain-relief for those engaged in physically demanding tasks.
Surgical treatment: Surgery of hernia can be performed through various approaches:
  • Herniotomy (removal of the hernial sac only) alone is adequate for an indirect inguinal hernia in children in whom the abdominal wall muscles are normal.
  • Herniorrhaphy (herniotomy plus repair of the posterior wall of the inguinal canal) may be suitable for a small hernia in a young adult with good abdominal wall musculature.
  • Hernioplasty (reinforcement of the posterior inguinal canal wall with a synthetic mesh) is required for large hernias and hernias in the middle-aged and elderly with poor abdominal wall musculature.
  • Laparoscopic hernia repair surgery: During a laparoscopic hernia repair, a surgeon makes small incisions in the abdominal wall, and the abdomen is inflated with carbon dioxide. A laparoscope (a thin, tube-like instrument with a small video camera) and surgical instruments are then inserted through the incisions. While viewing a monitor, the surgeon pushes the herniated intestine back into place and repairs the hernia opening with surgical staples. Mesh is then placed over the defect to reinforce the abdominal wall.
 
Nursing Interventions
  • Find out the recurrent coughing or sneezing causing symptoms and treat them.
  • Encourage not to strain too much on the toilet. Encourage to eat enough fruit and vegetables and increase fiber intake.
  • Also encourage to drink enough fluids.
  • Encourage to maintain a healthy weight.
  • Encourage exercising to tone the muscles of the abdomen.
  • Provide medical help for chronic constipation, allergies or a chronic cough.
  • Encourage not to do heavy work that will increase the intra-abdominal pressure.
  • Prepare the patient for diagnostic tests as needed.
  • Administer prescribed antacids and other medications.
  • To reduce intra-abdominal pressure and prevent aspiration, have the patient sleep in a reverse Trendelenburg position with the head of the bed elevated.
  • Assess the patient's response to treatment.
  • Observe for complications, especially significant bleeding, pulmonary aspiration, or incarceration or strangulation of the herniated stomach portion.
  • After endoscopy, watch for signs of perforation such as falling blood pressure, rapid pulse, shock, and sudden pain caused by endoscope.
  • To enhance compliance, teach the patient about the disorder. Explain significant symptoms, diagnostic tests, and prescribed treatments.
  • Review prescribed medications, explaining their desired actions and possible adverse effects.
  • Teach the patient dietary changes to reduce reflux.
  • Encourage the patient to delay lying down for 2 hours after eating.
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HEPATITIS
Hepatitis is a viral infection of the liver associated with a broad spectrum of non-symptom producing infection through icteric hepatitis to hepatic necrosis.
Viral hepatitis is a systemic, viral infection in which necrosis and inflammation of liver cells produce a characteristic cluster of clinical, biochemical and cellular changes. There are five definite types of viral hepatitis which have been identified, hepatitis A, B, C, D and E. Hepatitis A and E are similar in mode of transmission, whereas Hepatitis B, C and D share many characteristics.
 
Pathophysiology
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Types of Hepatitis
 
1. Type A hepatitis
It is caused by RNA virus of the enterovirus family. Hepatitis A is a liver disease caused by the hepatitis A virus. The virus is primarily spread when an uninfected (and unvaccinated) person ingests food or water that is contaminated with the feces of an infected person. The disease is closely associated with a lack of safe water, inadequate sanitation and poor personal hygiene.
Unlike hepatitis B and C, hepatitis A infection does not cause chronic liver disease and is rarely fatal, but it can cause debilitating symptoms and fulminant hepatitis (acute liver failure), which is associated with high mortality.
Hepatitis A occurs sporadically and in epidemics worldwide, with a tendency for cyclic recurrences. Every year there are an estimated 1.4 million cases of hepatitis A worldwide.
Mode of transmission
  • It is primarily fecal-oral, usually through ingestion of food or liquid contaminated with virus.
  • The virus has been found in the stool of infected patient.
  • Children acquire the infection at school by poor hygiene, hand-to-mouth contact.
Risk factors
  • As in overcrowding and poor sanitation and infected food handlers
  • Poor sanitation
  • Lack of safe water
  • Injecting drugs
  • Living in a household with an infected person
  • Being a sexual partner of someone with acute hepatitis A infection
  • Travelling to areas of high endemicity without being immunized.
Etiology
  • Prevalent in underdeveloped countries or overcrowding and poor sanitation.
  • Infected food handlers, people can contract it by consuming water or shellfish from contaminated water.
  • Commonly spread by person to person and rarely by blood transfusion.
Clinical manifestation
  • Prodromal symptom, fatigue, anorexia, malaise, headache, low-grade fever, nausea and vomiting, jaundice.
  • Icteric phase—jaundice, tea-colored urine, clay-colored stool and right upper quadrant tenderness.
 
2. Type B Hepatitis
It is double-shelled particle containing DNA. This particle is composed of hepatitis B core antigen, hepatitis B surface antigen and independent protein circulating in the blood. Hepatitis B is an infection of the liver caused by the hepatitis B virus (HBV). It is estimated that 350 million individuals worldwide are infected with the virus, which causes 620,000 733deaths worldwide each year. The major modes of hepatitis are sexual illicit, drug use and expose to infected blood.
Risk factors
  • Hemodialysis, male homosexual and bisexual activity.
  • Close contact with carrier of HBV, multiple sexual partner.
  • Receipt of blood or blood products, recent history of sexual transmitted disease.
  • Frequent exposure to blood or blood products.
Mode of transmission
  • It is primarily through blood. Oral route through saliva or through breastfeeding.
  • Sexual activity through blood. Semen saliva or vaginal secretions.
  • Gay men are high at risk.
  • Multiple sexual partners.
Clinical manifestation
  • One week to 2 months of prodromal symptoms appears.
  • Extrahepatic manifestation may include photophobia, arthritis, urticaria, maculopapular eruptions, skin rashes and vacuities.
  • Jaundice in icteric phase.
  • In rare cases, it may progress to fulminant hepatitis of hepatic failure.
  • May become chronic active or chronic persistent hepatitis.
 
3. Type C Hepatitis
It was formerly called non-A, non-B hepatitis, an RNA virus.
Risk factors
  • Receipt of blood product, health care and safety workers after needle stick injury.
  • Children born to women infected with hepatitis C virus.
  • Past treatment with chronic hemodialysis, sex with infected partners, history of STD.
  • Unprotected sex.
Mode of transmission
  • In most cases through blood or blood product, as through blood transfusion.
  • IV drug users and renal dialysis patients, sexual intercourse.
  • Through piercing and tattooing and ink.
Clinical manifestation
Similar to those associated with HBV but usually less severe. Symptom usually occurs 6 to 7 weeks after transfusion but may be attributed to another viral infection and not diagnosed as hepatitis.
 
4. Type D Hepatitis (Delta Hepatitis)
Hepatitis D virus is a defective RNA agent that appears to replicate only with the hepatitis B virus. It requires HBsAg to replicate.
  • 734Occurs along with HBV, or may superinfect a chronic HBV carrier.
  • Cannot outlast a Hepatitis B infection.
  • May be acute or chronic.
Hepatitis D or delta hepatitis is caused by the hepatitis delta virus (HDV), a defective RNA virus.
Risk factors
  • Chronic HBV carriers are at risk for infection with HDV.
  • Individuals who are not infected with HBV, and have not been immunized against HBV, are at risk of infection with HBV with simultaneous or subsequent infection with HDV.
  • Since HDV absolutely requires the support of a hepadnavirus for its own replication, inoculation with HDV in the absence of HBV will not cause hepatitis D. Alone, the viral genome indeed replicates in a helper-independent manner, but virus particles are not released.
Mode of transmission
Transmission is similar to that of HBV:
  • Blood-borne and sexual
  • Percutaneous (injecting drug use)
  • Permucosal (sexual)
  • Perinatal
Clinical manifestation
Similar to HBV but more severe.
With superinfection of chronic HBV carriers, it causes sudden worsening of condition and rapid progression of cirrhosis.
 
5. Type E Hepatitis
A single identified nonenveloped single-stranded RNA virus.
Mode of transmission
The hepatitis E virus is transmitted mainly through the fecal-oral route due to fecal contamination of drinking water. Other transmission routes have been identified, which include:
  • Foodborne transmission from ingestion of products derived from infected animals.
  • Zoonotic transmission from animals to humans.
  • Transfusion of infected blood products.
  • Vertical transmission from a pregnant woman to her fetus.
Although humans are considered the natural host for the hepatitis E virus, antibodies to the hepatitis E virus or closely related viruses have been detected in primates and several other animal species.
Hepatitis E is a waterborne disease, and contaminated water or food supplies have been implicated in major outbreaks. The ingestion of raw or uncooked shellfish has also been identified as the source of sporadic cases in endemic areas.
735The risk factors for hepatitis E are related to poor sanitation in large areas of the world and shedding of the hepatitis E virus in feces.
 
COMPARISON OF MAJOR FORMS OF VIRAL HEPATITIS
Previous name
Hepatitis A
Infectious hepatitis
Hepatitis B
Serum hepatitis
Hepatitis C
Non-A, Non-B
Hepatitis
Hepatitis D
Hepatitis E
Cause
HAV
HBV
HCV
HDV
HEV
Mode of transmission
Fecal-oral route, poor sanitation, contact, water and food-borne, during sex.
Oral and sexual contact, contact with acute disease, perinatal, and an occupational hazard for health care.
Blood products, contaminated drug and blood. sex with infected partners, STD.
Same as HBV, HVB, HBV surface. Antigen necessary for replication.
Fecal-oral route, person-to-person contact
Incubation
15–50 days
28–160 days
15–160 days
21–140 days
15–65 days
Immunity
30 days
70–80 days
50 days
35 days
42 days
Signs and symptoms
Fluelike illness, preicteric phase headache, malaise
Fatigue, anorexia, fever, dark urine, jaundice of sclera
and skin.
May develop arthralgias, rash
Similar to HBV, less severe
Similar to HBV
Similar to HAV
Very severe in
pregnant women.
Outcome
Usually mild with recovery.
Fatality < 1%. No carrier state or increased risk of chronic hepatitis, cirrhosis, cancer
May be severe.
Fatality—1–10%.
Increased risk of
chronic hepatitis,
cirrhosis and
hepatic cancer.
Frequent occurrence
of chronic carrier
state and chronic
liver disease.
Increased risk of
hepatic cancer.
Similar to HBV
but greater
likelihood of
carrier state, chronic
Active hepatitis
and cirrhosis.
Similar to HAV
except very severe
in pregnant women.
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Signs and Symptoms
Typical signs and symptoms of hepatitis include:
  • Jaundice (yellow discoloration of the skin and sclera of the eyes, dark urine and pale stools)
    • Anorexia
    • Hepatomegaly
    • Abdominal pain and tenderness
    • Nausea and vomiting
    • Fever
 
Diagnostic Evaluation
  • Elevated serum transferase levels (aspartate transaminase) AST, alanine transaminase of all forms of hepatitis.
  • Radioimmunoassay: That reveal immunoglobulin M antibodies to hepatitis virus in the acute phase of HAV.
  • Radioimmunoassay to include HBsAg, anti-HBc, anti-HBsAg detected in various stages of HBV.
  • Hepatitis C antibody—may not be detected for 3 to 6 months after onset of HCV illness, antibody test used for screening purpose.
  • Polymerase chain reaction test to confirm viral activity in HIV illness.
  • Antidelta antibodies of HBsAg for HDV or detection of IgM in acute disease and IgG in chronic disease.
  • Hepatitis E antigen.
  • Liver biopsy to detect chronic active disease, progression and response to therapy.
Hepatitis B infection is diagnosed with blood tests. These tests can detect pieces of the virus in the blood (antigens), antibodies against the virus, and viral DNA (viral load). Blood tests for HBV are often done when routine blood work shows abnormal liver function tests or in patients who are at an increased risk for exposure. If a patient has had a large amount of vomiting or has not been able to take in liquids, blood electrolytes may also be checked to ensure that the patient's blood chemistry is in balance.
  • X-rays and other diagnostic images are needed only in very unusual circumstances.
  • CT scan or ultrasound: These diagnostic imaging tests are used to detect the extent of liver damage and may also detect cancer of the liver caused by chronic hepatitis B.
  • Liver biopsy: This involves removal of a tiny piece of the liver. It is usually done by inserting a long needle into the liver and withdrawing the tissue. The tissue is examined under a microscope to detect changes in the liver. A biopsy may be done to detect the extent of liver damage or to evaluate how well a treatment is working.
 
Self-care at Home
The goals of self-care are to relieve symptoms and prevent worsening of the disease.
  • Drink plenty of fluids to prevent dehydration. Although broth, sports drinks, gelatin, frozen ice treats and fruit juices may be better because they also provide calories.
  • Ask your physician before taking any medications, even those that are over-the-counter. Some medications depend on the liver, and liver damage may impair the body's 737ability to metabolize these drugs. If you are on prescription medications, check with your physician to see if the doses should be adjusted or if the medication should be temporarily discontinued.
  • Avoid drinking alcohol until your health care practitioner allows it. Individuals with chronic HBV should avoid alcohol for the rest of their lives.
  • Try to eat a diet that provides adequate nutrition. Take it easy. It may take some time for your energy level to return to normal.
  • Avoid prolonged, vigorous exercise until symptoms start to diminish.
  • Call your health care practitioner for advice if your condition worsens or new symptoms appear.
  • Avoid any activity that may spread the infection to other people (sexual intercourse, sharing needles, etc.).
 
Management
  • Rest according to patient's level of fatigue.
  • Therapeutic measures to control dyspeptic symptom and malaise.
  • Hospitalization for protracted nausea and vomiting.
  • Small frequent feeding of high calories, low-fat diet, and proteins are restricted when liver cannot metabolize protein byproducts.
  • Vitamin K-injected SC if PT is prolonged.
  • IV fluids and electrolyte replacement is indicated.
  • Antiemetic drugs are administered.
  • After jaundice has cleared, gradual increase in physical activity.
  • For HBV patients—for those patients who have active viral replication treatment with nucleoside analogue (epivir) and have shown some efficacy.
Active immunization: A hepatitis B vaccine prepared from plasma of humans chronically infected with HBV is used only rarely and in patients who are immunodeficient or allergic to recombinant yeast-derived vaccines. It provides active immunity. The need for booster doses may be revisited if reports of hepatitis B increase, prevalence of carrier state develops, indicating the protection is declining.
Vaccines are administered IM in three doses, the second and third doses 1 and 6 months after the first dose. The third dose is very important in providing long immunity. It should be administered in deltoid muscle in adults. Antibody response may be measured by anti-HBs levels 1 to 3 months after completing the basic course of vaccine.
Passive immunity: Hepatitis B immune globulin provides passive immunity to hepatitis B and is indicated for people exposed to HBV who have never had hepatitis B and have never received Hepatitis B vaccine.
Indications: Inadvertent exposure to HBAg-positive blood through percutaneous or transmural routes, Sexual contact with people positive for HBAg, perinatal exposure.
HBIG, which provides passive immunity, is prepared from plasma selected from high titers of anti-HBs. Both active and passive immunization are recommended for people exposed to hepatitis B through sexual contact or through percutaneous routes.
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Pharmacological Intervention
 
Hepatitis B Medications
All of the following medications described that are used to treat chronic hepatitis B are antiviral medications. They reduce the ability of the virus to reproduce in the body and give the liver a chance to heal it. These drugs are not a cure for hepatitis B, but they do reduce the damage caused by the virus.
a. Pegylated interferon alfa-2b
Pegylated interferon is used alone or in combination with other medications.
  • Pegylated interferon slows the replication of the virus and boosts the body's immune system to fight the infection.
  • It works best in people who have relatively low levels of HBV DNA (low viral load).
  • Pegylated interferon usually is not given to people whose liver damage has progressed to cirrhosis, because it can make the liver damage worse.
  • Treatment is often given for 48 weeks, which is shorter than for other medications, but pegylated interferon requires regular shots (injections) while other medications are taken orally.
  • Pegylated interferon has unpleasant side effects in many people. The side effects are similar to having the flu. For many people, side effects are so severe that they cannot continue taking the medication.
  • Liver function tests and HBV DNA tests are used to check how well the treatment is working.
  • Interferon appears to stop the liver damage in up to 40% of people, although relapse is possible.
b. Nucleoside/nucleotide analogues (NAs)
Nucleoside/nucleotide analogues (NAs) are compounds that mimic normal building blocks for DNA. When the virus tries to use the analogues, it is unable to make new viral particles. Examples of these agents include adefovir (Hepsera), entecavir (Baraclude), lamivudine (Epivir-HBV, Heptovir, Heptodin), telbivudine (Tyzeka) and tenofovir (Viread).
  • NAs reduce the amount of virus in the body. Between 20% and 90% of patients may have levels reduced so far that they become undetectable. Obviously, this is a broad range. The higher success rates are achieved in patients who do not have ‘hepatitis B e antigen’ (HBeAg). HBeAg is detected by a blood test and indicates that the virus is actively multiplying.
  • Side effects are less common than with pegylated interferon. NAs have been associated with changes in body fat distribution, reduced blood cell counts, and increased levels of lactic acid in the blood. Rarely, NAs are associated with a severe flare of hepatitis that can be serious or fatal.
  • HBV may become resistant to NAs overtime.
  • NAs do not cure the infection. Relapse is possible even in patients who have had a good response to treatment.
 
Dietary Management of Viral or Drug-induced Hepatitis
  • Recommend small, frequent meals.
  • Provide intake of 2000 to 3000 kcal/day during acute illness.
  • 739High-protein, high-calorie diet may be beneficial. Advise patient not to force food and to restrict fat intake.
  • Carefully monitor fluid balance.
  • If anorexia and nausea and vomiting persist, enteral feedings may be necessary.
  • Instruct patient to abstain from alcohol during acute illness and for 6 months after recovery.
  • Advise patient to avoid substances (medication, herbs, drugs and toxins) which may affect liver function.
 
Preventive Measures
  • Hepatitis A
    • Wash your hands with soap after going to the toilet
    • Only consume food that has just been cooked
    • Only drink commercially bottled water, or boiled water if you are unsure of local sanitation
    • Only eat fruits that you can peel if you are somewhere where sanitation is unreliable
    • Only eat raw vegetables if you are sure they have been cleaned/disinfected thoroughly
    • Get a vaccine for Hepatitis A if you travel to places where hepatitis may be endemic.
  • Hepatitis B
    • Tell the partner if you are a carrier or try to find out whether he/she is a carrier.
    • Practice safe sex.
    • Use only clean syringes that have not been used by anyone else.
    • Do not share toothbrushes, razors, or manicure instruments.
    • Have a Hepatitis B series of shots if you are at risk.
    • Only allow well-sterilized skin-perforating equipment (tattoo, acupuncture, etc.)
  • Hepatitis C
    • If you are infected, do not let others share your toothbrush, razor, manicure equipment.
    • If you are infected, cover the open wounds.
    • Do not share needles, toothbrushes, or manicure equipment.
    • If your skin is to be pierced, make sure the equipment is well-sterilized (tattoo, etc.).
    • Go easy on the alcohol.
    • Do not share drug equipment.
  • Hepatitis D
    Use the same guidelines as for Hepatitis B. Only a person who is infected with Hepatitis B can become infected with Hepatitis D.
  • Hepatitis E
    Do the same as you would to protect yourself from Hepatitis A infection
    The risk of infection and transmission can be reduced by:
    • Maintaining quality standards for public water supplies.
    • Establishing proper disposal systems to eliminate sanitary waste.
    • 740Maintaining hygienic practices, such as handwashing with safe water, particularly before handling food.
    • Avoid drinking water or ice of unknown purity.
    • Avoid eating uncooked shellfish, and uncooked fruits or vegetables that are not peeled or that are prepared by people living in or travelling in highly endemic countries.
 
NONVIRAL HEPATITIS
Certain chemicals have toxic effects on the liver and produce acute liver cell necrosis or toxic hepatitis when inhaled, injected parenterally or are taken by mouth. The chemicals most commonly implicated in this disease are carbon tetrachloride, phosphorus, choloroform and gold compounds. These substances are true hepatotoxins.
 
Toxic Hepatitis
It resembles the viral hepatitis. Obtaining the history of exposure to hepatotoxic chemicals, medications or other toxic agents assists in early treatment and removal of causative agents.
Symptoms: Anorexia, nausea, vomiting are usual symptoms. Jaundice and hepatomegaly are noted in physical assessment, fever.
Treatment: Therapy as to maintain fluid and electrolyte balance, blood replacement, comfort and supportive measures.
 
Drug-induced Hepatitis
This liver disease is the most common cause of acute liver failure.
Symptoms: Chills, fever, rash, pruritus, arthralgia, anorexia and nausea. Later may produce symptoms like jaundice, dark urine, or enlarged or tender liver.
Treatment: Stop the use of medication. A short course of high-dose corticosteroids may be used in patients with severe hypersensitivity reactions. Liver transplantation is an option for drug-induced hepatitis, but outcomes may not be as successful as with other causes of liver failure.
 
Fulminant Hepatitis
Acute liver failure or fulminant hepatitis is a rare but potentially fatal disease. Fulminant liver failure is acute necrosis of liver cell without pre-existing liver disease, resulting in inability of liver to perform its many functions.
Etiology: Viral hepatitis is a common cause. Poisons, chemicals, such as acetaminophen, tetracycline, isoniazid, methyldopa, etc. may cause liver disease.
  • Ischemia and hypoxia because of hepatic vascular occlusion, hypovolemic shock, acute circulatory failure, septic shock, heat stroke.
  • Other causes includes: Hepatic vein obstruction, acute fatty liver of pregnancy, autoimmune hepatitis, partial hepatectomy, complication of liver transplantation.
  • Progression of hepatocellular injury and necrosis with development of encephalopathy.
 
Clinical Features
  • Malaise, anorexia, nausea, vomiting, fatigue, jaundice, urine is tea-colored and frothy when shaken.
  • 741Purities caused by bile salts are deposited in the skin.
  • Steatorrhea and diarrhea because of decrease of fat absorption, peripheral edema as fluid move from intravascular to interstitial spaces, secondary to hypoproteinemia.
  • Ascites from hypoproteinemia or portal hypertension.
  • Easy bruising, petechiae, overt bleeding because of clotting deficiency.
  • Altered LOC, ranging from irritability and confusion to stupor, somnolence and coma.
  • Change in tendon reflexes—initially hyperactive, become flaccid, tremor.
  • Breath odor of acetone and portal systemic encephalopathy, also known as hepatic coma.
  • Cerebral edema as a cause of death because of brainstem herniation.
 
Diagnostic Evaluation
  • Prolonged PT, decreased platelet counts.
  • Elevated ammonia, amino acid levels.
  • Hypoglycemia or hyperglycemia.
 
Management
  • Oral or rectal administration of lactulose to minimize formation of ammonia and other nitrogenous byproducts in the bowel.
  • Rectal administration of neomycin to suppress urea-splitting enteric bacteria in the bowel and decrease ammonia formation.
  • Low molecular weight or albumin followed by potassium sparing diuretic (spironolactone) to enhance fluid shift from interstitial back to intravascular spaces.
  • Pancreatic enzymes, if diarrhea and steatorrhea.
 
Complications
  • Encephalopathy and cerebral edema.
  • Sepsis
  • Gastrointestinal bleeding
  • Renal failure
  • Hemodynamic complications
 
Nursing Management
 
Nursing Assessment
  • Assess for systemic and liver-related symptoms.
  • Obtain history, such as IV drug use, sexual activity, ingestion of possible contaminated food or water to assess for any mode of transmission of virus.
  • Assess size and shape of liver to detect enlargement or characteristics of cirrhosis.
  • Obtain vital history, including temperature.
 
Nursing Diagnosis
  • 742Imbalanced nutrition less than body requirement related to effects of liver dysfunction.
  • Deficient fluid volume related to nausea and vomiting.
  • Activity intolerance related to anorexia and liver dysfunction.
  • Deficient knowledge related to transmission.
  1. Imbalanced nutrition less than body requirement related to effects of liver dysfunction.
    Interventions
    • Encourage frequent small feedings of high-calorie, low-fat diet.
    • Encourage eating meal in sitting position to decrease pressure in liver.
    • Encourage taking pleasing meal in the environment with noxious stimuli.
    • Administer antiemetic drug to patient.
  2. Deficient fluid volume related to nausea and vomiting.
    Interventions
    • Provide frequent oral fluid as tolerated.
    • Administer IV fluids for patient with inability to maintain oral fluids.
    • Monitor intake and output.
  3. Activity intolerance related to anorexia and liver dysfunction.
    Interventions
    • Promote periods of rest during symptom-producing phase.
    • Promote comfort by administering the analgesic to the patient.
    • Provide emotional support and diversional activities when recovery is prolonged.
    • Encourage gradual resumption of activities and mild exercise during convalescent period.
  4. Knowledge deficit regarding transmission of disease related to lack of exposure of health services and information.
    Interventions
    • Encourage specific protection for close contacts, immune globin and hepatitis B immune globin, followed by HBV vaccine series.
    • Explain precautions to patient and family about transmission and prevention of transmission to others.
    • Good handwashing and maintain hygiene.
    • Avoidance of sexual activity.
    • Avoidance of sharing needles and toothbrushes to prevent blood or body fluid contact.
BIBLIOGRAPHY
  1. Black M. A textbook of medical surgical nursing. Elsevier.  Noida.  8th ed.
  1. Brunner S. A textbook of medical surgical nursing. Lippincott Company.  Philadelphia.  10th ed. 2007.
  1. Chintamani. Lewis textbook of medical surgical nursing. Elsevier.  1070–5.
  1. Hopper P, William L. Understanding of medical surgical nursing. Devis.  2nd ed. 2003.
  1. Lemone P, Burke K. A textbook of medical surgical nursing. Dorling Kindersely.  South Asia.  4th ed. 2007.
  1. Siddarth and Brunner. Textbook of medical surgical nursing. 2010; 1263–71.
  1. Wilkins and William L. Mannual of nursing practice. Elsevier.  Noida.  8th ed.
  1. Wilkins and Williams. Textbook of Lippincott mannual of nursing practice. Wolters Kulwers health.  9th ed. 687–9.

Musculoskeletal Disorders14

The musculoskeletal system provides support to the body and gives humans, the ability to move. The body's bones (the skeletal system), muscles (muscular system), cartilage, tendons, ligaments, joints, and other connective tissue that supports and binds tissues and organs together comprise the musculoskeletal system.
Most importantly, the system provides form, support, stability, and movement to the body. For example, the bones of the skeletal system protect the body's internal organs and support the weight of the body. The skeletal portion of the system serves as the main storage depot for calcium and phosphorus. It also contains critical components of the hematopoietic system (blood cell production). The muscles of the muscular system keep bones in place; they also play a role in movement of the bones by contracting and pulling on the bones, allowing for movements as diverse as standing, walking, running, and grasping items. To allow motion, different bones are connected by joints. Within these joints, bones are connected to other bones and muscle fibers via connective tissue such as tendons and ligaments. Cartilage prevents the bone ends from rubbing directly on each other. Muscles contract to move the bone attached at the joint.
744
Fig. 14.1: Anatomy of joint
Fig. 14.2: Major muscles of the body. Right side: superficial; Left side: deep (anterior view)
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Fig. 14.3: Major muscles of the body. Right side: superficial; Left side: deep (posterior view)
 
OSTEOARTHRITIS
Osteoarthritis (OA), which is also known as degenerative joint disease. It is the degenerative disorder caused by gradual loss of cartilage and resulting in bony spurs and cysts at the margins of the joints.
Fig. 14.4: Osteoarthritis
746Risk Factors: Risk factors are categorized into modifiable and nonmodifiable causes:
 
Modifiable Factors
  • Excess body mass.
  • Joint injury (sports, work, trauma).
  • Knee pain.
  • Occupation (due to excessive mechanical stress: hard labor, heavy lifting, knee bending,
  • Men: Often due to work that includes construction, mechanics, agriculture, laborers and engineers
  • Women: Often due to work that includes cleaning, construction, agriculture, and small business and retail.
  • Muscle weakness.
 
Nonmodifiable
  • Gender (women higher risk).
  • Age (increases with age and levels around age risk) increasing age directly relates to degenerative process of joints because the ability of the articular cartilage to resist microfracture with repetitive low loads diminished with age.
  • Genetic predisposition.
 
Other Possible Factors
  • High bone density may increase risk of knee.
  • Race.
 
Pathophysiology
Pathophysiology of osteoarthritis is explained in 6 stages
  • Build-up: The surface cartilage starts to show signs of weakness due to life time and excessive use. In this stage no symptoms appear in body.
  • Cartilage swelling: Weight bearing activity causes the weekend cartilage to start swelling. In this stage, mild pain which appears during activity but disappears during rest period.
  • Joint narrowing: Swollen, weakened cartilage starts to wear causing the joint space to decrease. In this stage pain and stiffness are main symptoms.
  • Breakdown: Continued wearing away the cartilage leads to irregular joint surface. In this stage swelling and joint clicking are main signs .
  • Compensation: As the joint becomes more painful, this leads to new bone growth on the joint margins. During this phase deep ache and night pain is present.
 
Signs and Symptoms
  • Pain: Pain is the most common symptom of osteoarthritis. It is usually made worse by moving the joints or placing weight on it, and it is usually relieved by rest. As the condition progresses and inflammation develops, pain may become constant.
  • Stiffness: Stiffness of the affected joint is often noticed first time in the morning and after resting.
  • Swelling: Swelling, which sometimes warm to touch, may be noticeable in an arthritic joint.
  • 747Deformity: Deformity can occur with osteoarthritis due to bone growth and cartilage loss. Bone growths in the end joints of the fingers are called Heberden's nodes. Bouchard's nodes are bone growths in the middle joints of the fingers. Degeneration of knee cartilage can result in the outward curvature of knees.
  • Crepitus: A crackling sound or granting feeling may be noticed when an arthritic joint is moved. This is caused by bone rubbing against bone or roughened joint is moved.
 
Diagnostic Evaluation
  • Plain radiography: The imaging method of choice because radiographs are cost-effective and can be readily and quickly obtained, in the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis and cyst formation.
  • Computed tomography (CT) scanning: Rarely used in the diagnosis of primary osteoarthritis; however, it may be used in the diagnosis of OA of the foot and ankle joints.
  • Magnetic resonance imaging (MRI): Not necessary in most patients with osteoarthritis unless additional pathology amenable to surgical repair is suspected; unlike radiography, MRI can directly visualize articular cartilage and other joint tissues.
  • Ultrasonography: No role in the routine clinical assessment of patients with osteoarthritis; however, it is being investigated as a tool for monitoring cartilage degeneration, and it can be used for guided injections of joints not easily accessed without imaging
  • Bone scanning: Maybe helpful in the early diagnosis of osteoarthritis of the hand; bone scans also can help differentiate osteoarthritis from osteomyelitis and bone metastases
  • Arthrocentesis: The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of joint pain. Other synovial fluid findings that aid in the differentiation of osteoarthritis from other conditions are negative Gram stains and cultures, as well as the absence of crystals when fluid is viewed under a polarized microscope.
 
Management
 
Nonpharmacological Intervention
  • Heat and cold
  • Weight loss
  • Exercise
    748
    Fig. 14.5: Management of osteoarthritis
  • Physical therapy
  • Occupational therapy
  • Unloading in certain joints (e.g. knee, hip).
 
Nonpharmacolological Management and Lifestyle Changes
Staying active and getting exercise can maintain joint and overall movement. The health care provider should recommend an exercise routine. Water exercises, such as swimming, are helpful. Other lifestyle tips include:
  • Applying heat and cold to the joint
  • Eating healthy foods
  • Getting enough rest
  • Losing weight if you are overweight
  • Protecting joints from injury.
 
Healthy Body Weight
Maintaining a healthy body weight will reduce stress on the arthritic joints. A physiatrist may help in formulating a nonpharmacologic management plan for the patient with osteoarthritis, and a nutritionist may help the patient to lose weight. A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical management plan.
  • Exercise: Exercise can assist with weight loss, the maintenance of muscle strength and mobility of arthritic joints. Activity at a level that does not cause pain is not thought to worsen OA. Nonweight bearing exercises such as swimming or aqua jogging in a heated pool may be beneficial.
  • 749Physiotherapy: Physiotherapists can advise on appropriate exercises to improve mobility, increase muscle strength and decrease pain with the aim of improving function.
  • Synovial fluid supplements (viscosupplements), when medications, exercise or physiotherapy do not provide adequate relief of symptoms, a synovial fluid supplement may be injected into the joint. Synovial fluid is a clear, sticky, viscous solution that lubricates, protects and supports joints. In osteoarthritis this fluid does not function effectively. Synovial fluid supplements can reduce joint cartilage damage and delay the need for joint replacement, e.g. glucosamine.
  • Massage therapy: Massage therapy may provide short-term pain relief, but it should be taken from licensed massage therapist who is experienced in working on sensitive joints.
  • Braces: Splints and braces may help support weakened joints. Some types prevent the joint from moving. Others allow some movement. Use a brace only when doctor or therapist recommends one. Using a brace the wrong way can cause joint damage, stiffness, and pain.
  • Acupuncture: Acupuncture is a traditional Chinese treatment. It is thought that when acupuncture needles stimulate certain points on the body, chemicals that block pain are released. Acupuncture may provide short term pain relief.
  • Pharmacological management: The goal of medical treatment for osteoarthritis (OA) is to reduce joint pain and stiffness and to prevent complications. There is no known cure for OA, but there are many medications available to helps maintain or improve joint mobility and feel better.
    • Medicines for osteoarthritis may be taken by mouth, injection, or applied directly to the skin. They include:
      • Analgesics
      • Nonsteroidal anti-inflammatory drugs (NSAIDs)
      • Topical pain relievers
      • Corticosteroid injections
      • Hyaluronic acid injections.
 
Analgesics
Analgesics are drugs designed to relieve pain, including pain from osteoarthritis and related conditions, e.g. acetaminophen, opioids (narcotics) and an atypical opioid called tramadol.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs): NSAIDs are the mostly commonly used drugs for arthritis-related pain, swelling and stiffness. They interfere with the body's production of hormone-like chemicals called prostaglandins. Prostaglandins are one of the biggest contributors to inflammation in the body. NSAIDs are available over-the-counter or with a prescription. They include aspirin, ibuprofen, naproxen, etc.
  • Topical pain relievers: Topical pain relievers are creams, ointments or salves that are applied directly to the skin on the painful area to help relieve mild joint and muscle aches.
  • Corticosteroids: Corticosteroids are powerful anti-inflammatory medicines. Doctors prescribe corticosteroids for people with arthritis who need quick relief from severe inflammation acetaminophen. Patient can have corticosteroid injections in the same joint three to four times per year.
  • 750Hyaluronic Acid: Hyaluronic acid occurs naturally in joint fluid, acting as a shock absorber and lubricant. However, the acid appears to breakdown in people with osteoarthritis. Injecting hyaluronic acid into a joint may lessen pain and inflammation.
 
Nursing Management
 
Nursing Diagnosis
Nursing diagnosis for osteoarthritis
  • Acute pain related to distention of tissue by the accumulation of fluid inflammatory process.
  • Impaired physical mobility related to skeletal deformities, pain, discomfort, decreased muscle strength.
  • Disturbed body image related to physical and psychological changes and dependency imposed by chronic illness.
  • Ineffective coping related to perceived lifestyle or role changes.
  • Knowledge deficit related to disease condition and treatment plan.
  1. Acute pain related to distention of tissue by the accumulation of fluid/inflammatory process.
    Intervention
    • Assess pain the location and intensity of pain.
    • Assess the factors that accelerate and signs of nonverbal pain.
    • Provide hard mattress and small pillow.
    • Elevate bed when a client needs to rest or sleep.
    • Provide a comfortable position when sleeping or sitting in a chair.
    • Monitor the use of a pillow.
    • Advice clients to frequently change positions.
    • Provide clients to a warm compress on the sore joints several times a day.
    • Monitor temperature compress.
    • Give a massage. Encourage the use of stress management.
    • Give the drugs before activity, exercise that is planned as directed.
    • Assist clients with physical therapy.
  2. Impaired Physical Mobility related to skeletal deformities, pain, discomfort, decreased muscle strength.
    Intervention
    • Monitor the level of inflammation and pain in joints
    • Provide safe techniques
    • Engage in activities of entertainment that is suitable for individual situations.
    • Assist in daily living activities.
 
OSTIOMYLITIS
Osteomyelitis is an infection of a bone caused by Staphylococcus aureus. Infection with a fungus is a rare cause.
751
Fig. 14.6: Osteomylitis
 
Modes of Transmission
If some bacteria settle on a small section of bone, they can multiply and cause infection. Bacteria can get to bone:
  • Via the bloodstream: This is the common cause in children. Bacteria sometimes get into the blood from an infection in another part of the body and then travel to a bone.
  • Following an injury: Bacteria can spread to bone if you have a deep cut on the skin. In particular, if you have a broken bone which you can see through the cut skin.
 
Pathophysiology
752
 
Causes and Risk Factors
Anyone at any age can develop osteomyelitis. However, one have an increased risk if:
  • Have recently fractured (broken) a bone.
  • Have bone prosthesis (an artificial hip, a screw in a bone following surgery, etc).
  • Have recently had surgery to a bone.
  • Have a poor immune system. For example, AIDS, taking chemotherapy, seriously ill with another disease, etc.
  • Have had a previous episode of osteomyelitis.
  • Have reduced skin sensation. This can lead to damage and infection of the skin which can spread to the blood or to local bone. For example, some people with diabetes have reduced sensation in their feet.
  • Have regular kidney dialysis.
 
Signs and Symptoms
  • Pain and tenderness over an area of bone.
  • A lump may develop over a bone, which is usually very tender.
  • Redness of overlying skin may then develop.
  • Feeling generally unwell with fever (high temperature) as the infection develops.
 
Diagnostic Evaluation
  • X-ray
  • CT scan
 
Medical Treatment
 
Antibiotics
An antibiotic is usually started as soon as possible. The initial antibiotic chosen is one that is likely to kill the bacteria which commonly cause osteomyelitis. However, the antibiotic is sometimes changed to a different one when the results of the tests confirm which bacterium is causing the infection. The symptoms may settle quite quickly after taking an antibiotic. Penicillin and cephalosporin are the drug of choices.
To control pain you may be given painkillers.
 
Surgical Management
Surgery is Required if
  • An abscess develops. The pus in an abscess needs to be drained.
  • 753The infection presses on other important structures. For example, an infection in the spine may press on the spinal cord.
  • The infection has become chronic (persistent) and some bone has been destroyed. Dead and infected bone may need to be removed to allow the infection to clear. Sometimes plastic surgery is needed at the same time to cover any wound to give the best chance of cure.
Rarely, amputation of a foot or leg is needed if infection persists in a leg bone.
 
Nursing Management
  1. Acute pain related to inflammation and swelling.
    • Assess the level of pain
    • The affected part may be immobilized with a splint to decrease pain and muscle spasm.
    • Elevation reduces swelling and associated discomfort.
    • Comfortable position is given
    • Analgesic given to treat pain.
  2. Impaired physical mobility related to pain, use of immobilization devices, and weight-bearing limitations.
    • Assess the normal level of activity
    • The joints above and below the affected part should be gently placed through their range of motion.
    • The nurse encourages full participation in ADLs within the physical limitations to promote general well-being.
    • Analgesics are given.
  3. Deficient knowledge related to the treatment regimen.
    • Assess the level of knowledge by verbalization with the patient
    • Answer each question of the patient
    • Clarify all doubts of the patient.
 
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a chronic inflammatory disorder that typically affects the small joints in hands and feet.
It is an autoimmune disorder, it occurs when immune system mistakenly attacks own body's tissues. In addition to causing joint problems, rheumatoid arthritis sometimes can affect other organs of the body — such as the skin, eyes, lungs and blood vessels.
 
Etiology and Risk Factors
  • The causes of rheumatoid arthritis are unknown.
  • It is believed that the tendency to develop rheumatoid arthritis may be genetically inherited (hereditary).
 
Risk Factors
  • Age: Risk increases with age.
  • Gender: Women are more affected than men.
  • Genetic risk: There is a strong familial link in some cases.
754
 
Pathophysiology
 
Clinical Manifestations
  • Fatigue
  • Anorexia
  • Weight loss
  • Stiffness
  • Lack of appetite
  • Low-grade fever
  • Muscle and joint aches.
 
Specific Aarticular Involvement is Manifested
  • Pain stiffness limitation of motion and signs of inflammation (heat swelling tenderness).
 
Extra-articular Manifestations
  • Peripheral edema
  • Peripheral neuropathy
  • Myositis
  • Tenocynovitis
  • Rheumatoid vasculitis
  • Sjorgen's syndrome
  • Amyloidosis
  • Fetly syndrome.
755
 
Complications
  • Osteoporosis: Rheumatoid arthritis itself, along with some medications used for treating rheumatoid arthritis, can increase the risk of osteoporosis — a condition that weakens bones and makes them more prone to fracture.
  • Carpal tunnel syndrome: If rheumatoid arthritis affects wrists, the inflammation can compress the nerve that serves most of hand and fingers.
  • Heart problems: Rheumatoid arthritis can increase risk of hardened and blocked arteries, as well as inflammation of the sac that encloses heart.
  • Lung diseases: People with rheumatoid arthritis have an increased risk of inflammation and scarring of the lung tissues, which can lead to progressive shortness of breath.
 
Diagnostic Evaluation
  • History collection
  • Physical examination: Check joints for swelling, redness and warmth. Also check reflexes and muscle strength.
  • Laboratory tests
    • Complete blood count (CBC): People with rheumatoid arthritis tend to have an elevated erythrocyte sedimentation rate (ESR), which indicates the presence of an inflammatory process in the body.
  • Radiographic studies of joint: X-rays help to track the progression of rheumatoid arthritis in your joints overtime.
  • Synovial fluid analysis.
 
Treatment
  • NSAIDs: Are medications that can reduce tissue inflammation, pain, and swelling, e.g. brufen, etc.
  • Steroids: Corticosteroid medications such as prednisone reduce inflammation and pain and slow joint damage.
  • Disease-modifying antirheumatic drugs (DMARDs): These drugs can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage. Common DMARDs include methotrexate, leflunomide, hydroxychloroquine and sulfasalazine.
  • Calcium and vitamin D supplements: To prevent thinning of the bones due to osteoporosis.
 
Surgical Management
If medications fail to prevent or slow joint damage, surgery may help to restore ability to use joint.
Rheumatoid arthritis surgery may involve one or more of the following procedures:
  • Total joint replacement: During joint replacement surgery, surgeon removes the damaged parts of joint and inserts a prosthesis made of metal and plastic.
  • Tendon repair: Inflammation and joint damage may cause tendons around joint to loosen or rupture. Repair the tendons around joint.
  • Joint fusion: Surgically fusing a joint may be recommended to stabilize or realign a joint and for pain relief when a joint replacement is not an option.
756
 
Nursing Management
 
Nursing Diagnosis
  1. Chronic pain related to joint inflammation and overuse.
    Interventions
    • Perform a comprehensive assessment of pain to include location characteristics, onset, duration, frequency, severity.
    • Evaluate with patient and health care team, effectiveness of past pain control measures that have been used.
    • Reduce or eliminate the factors that increase the pain experience (e.g. fear fatigue lack of knowledge).
    • Teach use of nonpharmacological techniques (relaxation, distraction, massage).
    • Provide optimal pain relief with prescribed analgesics.
  2. Impaired physical mobility related to joint pain and stiffness.
    Interventions
    • Determine the limitations of joint movement and affect on function to establish baseline plan of care.
    • Collaborate with physical therapy into establish exercises program to improve the joint function.
    • Explain the plan and purpose of exercises to the patient and family.
    • Initiate pain control measures before beginning of joint exercises (hot packs, warm shower.
    • Assist patient to do active, passive joint movements (selection of proper footwear use of assistive devices).
  3. Self-care deficit related to disease progression, weakness.
    Interventions
    • Monitor patient's ability for independent self-care
    • Monitor patients need for hygiene, dressing grooming, eating.
    • Establish a routine for self-care activities assist patient in accepting dependency needs to ensure all needs are meet.
    • Teach family to encourage independence and to intervene only when patient is unable.
 
OSTEOMALACIA
Osteomalacia refers as a metabolic disease of bones, often caused by a vitamin D deficiency. Metabolic disorder characterized by inadequate or delayed mineralization of bone and it results from a defect in the bone-building process.
 
Etiology
Body uses calcium and phosphate to build strong bones. Osteomalacia may occur if bodies do not get enough of these minerals in diet or if body does not absorb them properly. These problems may be caused by:
  • Vitamin D deficiency: People who live in areas where sunlight hours are short or eat a diet low in vitamin D can develop osteomalacia. Vitamin D deficiency is a common cause of Osteomalacia
  • 757Certain surgeries: Normally, the stomach breaks down food to release vitamin D and other minerals that are absorbed in the intestine. This process is disrupted if one have surgery like gastrectomy, and may result in osteomalacia. Surgery to remove or bypass small intestine also can lead to Osteomalacia.
  • Celiac disease: In this autoimmune disorder, the lining of small intestine is damaged by consuming foods containing gluten, a protein found in wheat, barley and rye. A damaged intestinal lining does not absorb nutrients, such as vitamin D, as well as a healthy one does.
  • Kidney or liver disorders: Problems with kidneys or liver can interfere with ability to process vitamin D.
  • Drugs: Some drugs used to treat seizures, including phenytoin and phenobarbital, can cause Osteomalacia.
 
Signs and Symptoms
  • Bone pain
  • Tenderness
  • Difficulty in changing position
  • Muscle weakness
  • Bowing of bones
  • Pathologic fractures.
 
Pathophysiology
758
 
Diagnostic Evaluation
  • Physical examination: Check for skeletal deformity like spinal kyphosis, bowed legs.
  • Blood and urine tests: In cases of osteomalacia caused by vitamin D deficiency or by phosphorus loss, abnormal levels of vitamin D and the minerals calcium and phosphorus are often detected.
  • X-ray: Slight cracks in bones that is visible on X-rays.
  • Bone biops: During a bone biopsy, doctor inserts a slender needle through skin and into bone to withdraw a small piece of bone for viewing under a microscope. This procedure is done after using a local anesthetic and takes only about a half-hour. Although a bone biopsy is very accurate in detecting osteomalacia.
 
Management
  • Vitamin D, phosphorus, calcium supplements are prescribed.
  • Exposure to sunlight is also advised to patient (for short period of time).
  • Vitamin D rich diet (fortified milk and milk products, cereals, egg, etc.) is given to the patient.
 
Nursing Management
 
Nursing Diagnosis
  1. Impaired physical mobility related to decalcification and stretching of the muscles.
    Interventions
    • Encourage patient to do the daily activities.
    • If person is not able to perform daily routine then assist him.
    • Ask patient for some exercises but also ready with some pain control measures.
    • Provide supplements of calcium as prescribed by the physician.
  2. Bone pain related to weakness and stretching of muscles.
    Interventions
    • Assess the intensity, duration, onset of the pain.
    • Assess the measures use by the health care time previously.
    • Provide comfort devices.
    • Provide medications as prescribed by the physician.
    • Provide psychological support and assist while changing the position.
  3. Risk for fractures related to calcium deficiency and muscle weakness.
    Interventions
    • Assess for any cracks on the bones.
    • Encourage for vitamin D rich diet.
    • Provide calcium supplements to the patient as prescribed by physician.
 
POTT'S DISEASE
Pott disease, also called tuberculous spondylitis or tuberculosis of the spine that is caused by infection of the spinal column, or vertebral column, by the tuberculosis bacillus 759(Mycobacterium tuberculosi). Pott disease is characterized by softening and collapse of the vertebrae, often resulting in a hunchback curvature of the spine. Pott's spine is a major complication of extrapulmonary tuberculosis.
Etiology and pathophysiology, the four primary patterns of involvement in adults are as follows:
  • Paradiscal
    • Most common, comprising 50% of all cases
    • Primary focus of infection in the vertebral metaphysis
    • The granuloma erodes the cartilaginous endplate and narrows the disk space
  • Anterior Granuloma
    • Granulomas develop underneath the anterior longitudinal ligament
    • Less bony destruction but increased bone devascularization
    • Further development of abscess, necrosis and deformity
  • Central Lesions
    • Involves entire vertebral body.
    • 2–3 vertebrae are often affected.
    • Results in significant deformities and pathological fractures.
  • Appendiceal Type Lesions
    • Lamina, pedicles, articular facets and spinous processes.
    • Initial expansion followed by rupture and failure.
 
Signs and symptoms
  • Spinal Involvement
    • Lower thoracic vertebrae are the most common area of involvement followed by the lumbar spine.
    • Approximately 10% of Pott's disease cases involve the cervical spine.
    • The thoracic spine is involved in about 65% of cases, and the lumbar, cervical and thoracolumbar spine in about 20%.
    • The atlantoaxial region may also be involved in less than 1% of cases
    • Localized Tenderness
    • Muscle spasms
    • Restricted spinal motion
    • Spinal deformity
    • Neurological deficits
    • Back pain
  • Neurological Signs
    • Neurologic abnormalities occur in 50% of cases and can include spinal cord compression with the following:
      • Paraplegia
      • Paresis
      • Impaired sensation
      • Nerve root pain
      • Cauda equina syndrome
  • 760Spinal Deformities
    • Almost all patients with Pott's disease have some degree of spine deformity with thoracic kyphosis being the most common.
  • Constitutional Symptoms
    • Fever
    • Night sweats
    • Weight loss
    • Malaise
  • Cervical spinal TB
    • This condition is characterized by:
      • Cervical pain and stiffness
      • Torticollis
      • Hoarseness
      • Neurological deficits
      • Single nerve palsy hemiparesis or quadriplegia
      • Retropharyngeal abscesses
      • In lower cervical spine insults, the patient can present with dysphagia or stridor.
Systemic Signs and Symptoms of Pott's Disease
Musculoskeletal
Neurological
Cardiovascular
Integumentary
Urogenital
Constitutional symptoms
Vertebral fractures
Paresthesia
Spinal artery infarction
Pressure ulcers (secondary)
Bowel dysfunction
Fever
Vertebral Collapse
Paralysis
Avascularity of intervertebral disks
Sinus (secondary to abscess rupture)
Bladder dysfunction
Night sweats
Spinal ligament destruction
Paresis
Thrombosis
Cutaneous fungal infections
Malaise
Intervertebral disk destruction
Abnormal muscle tone
Weight loss
Paravertebral abscess
Abnormal reflexes
Osteopenia/osteoporosis
Cauda equina syndrome
Bone sequestrations
Myelomalacia
Dislocated vertebrae
Gliosis
Kyphotic deformity
Syringomyelia
Muscle atrophy
Torticollis
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Diagnostic Evaluation
  • The Mantoux Test (Tuberculin Skin Test): Injection of a purified protein derivative (PPD) is injected interadermaly to check the presence of bacilli's, Results are positive in 84–95% of patients with Pott's disease who are not infected with HIV.
  • Erythrocyte Sedimentation Rate (ESR): ESR may be markedly elevated (> 100 mm/h)
  • Microbiology studies: Microbiology studies are used to confirm diagnosis. Bone tissue or abscess samples are obtained to stain for acid-fast bacilli (AFB), and organisms are isolated for culture and susceptibility.
  • Radiography: Radiographic changes associated with Pott's disease present relatively late. The following are radiographic changes characteristics of spinal tuberculosis on plain radiography:
    • Lytic destruction of anterior portion of vertebral body
    • Increased anterior wedging
    • Collapse of vertebral body
    • Reactive sclerosis on a progressive lytic process
    • Vertebral end plates may be osteoporotic
    • Intervertebral disks may be shrunk or destroyed
    • Vertebral bodies show variable degrees of destruction
    • Fusiform paravertebral shadows suggest abscess formation
    • Bone lesions may occur at more than one level.
  • CT scanning: CT scanning provides much better bony detail of irregular lytic lesions, sclerosis, disk collapse, and disruption of bone circumference. Low contrast resolution provides a better assessment of soft tissue, particularly in epidural and paraspinal areas. CT scanning reveals early lesions and is more effective for defining the shape and calcification of soft tissue abscesses which is common in TB lesions.
  • MRI: MRI is the criterion gold standard for evaluating disk-space infection and osteomyelitis of the spine and is most effective for demonstrating the extension of disease into soft tissue and the spread of tuberculous debris under the anterior and posterior longitudinal ligaments. MRI is also called the most effective imaging study for demonstrating neural compression. MRI findings useful to differentiate tuberculosis spondylitis from pyogenic spondylitis.
  • Biopsy: Use of a percutaneous CT-guided needle biopsy of bone lesions can be used to obtain tissue samples. This is a safe procedure that also allows therapeutic drainage of large paraspinal abscesses.
  • Polymerase Chain Reaction (PCR): PCR techniques amplify species-specific DNA sequences which is able to rapidly detect and diagnose several strains of mycobacterium without the need for prolonged culture. They have also been used to identify discrete genetic mutations in DNA sequences associated with drug resistance.
 
Management
 
Physical Therapy Management
Patients with Pott's disease often undergo spinal fusion or spinal decompression surgeries to correct their structural deformity and prevent further neurological complications:
  • 762Spinal stabilization exercises
  • Maitland surgery
  • Exercise and strengthening.
 
Postspinal Fusion Surgery
  • TENS (Transcutaneous Electrical Neuromuscular Stimulation)
  • Aquatic therapy
  • Overground training (Walking Program)
  • Aerobic exercise.
 
Pharmacological Management
The duration of treatment is somewhat 6 to 9 month course, traditional courses range from 9 months to longer than 1 year. The duration of therapy should be individualized and based on the resolution of active symptoms and the clinical stability of the patient.
The main drug class consists of agents that inhibit growth and proliferation of the causative bacteria. Isoniazid and rifampin should be administered during the whole course of therapy. Additional drugs are administered during the first two months of therapy and these are generally chosen among the first-line drugs which include pyrazinamide, ethambutol, and streptomycin. The use of second-line drugs is indicated in cases of drug resistance.
  • Isoniazid: Highly active against Mycobacterium tuberculosis. Has good GI absorption and penetrates well into all body fluids and cavities.
  • Rifampin: For use in combination with at least one other antituberculous drug; inhibits DNA-dependent bacterial.
  • Pyrazinamide: Bactericidal against M tuberculosis in an acid environment. Has good absorption from the GI tract and penetrates well into most tissues, including CSF.
  • Ethambutol: Has bacteriostatic activity against M tuberculosis. Has good GI absorption. CSF concentrations remain low, even in the presence of meningeal inflammation.
  • Streptomycin: Bactericidal in an alkaline environment. Because it is not absorbed from the GI tract, must be administered parenterally.
 
Nursing Management
 
Nursing Priorities
  • Support psychological and physiological adjustment.
  • Alleviate pain.
  • Prevent complications.
  • Promote mobility and functional abilities.
  • Provide information about surgical procedure, prognosis and treatment needs.
 
Nursing Management
  1. Acute pain related to inflammation and swelling
    • Assess the level of pain
    • The affected part may be immobilized with a splint to decrease pain and muscle spasm.
    • Elevation reduces swelling and associated discomfort.
    • Comfortable position is given
    • Analgesic given to treat pain.
  2. 763Impaired physical mobility related to pain, use of immobilization devices, and weight-bearing limitations
    • Assess the normal level of activity
    • The joints above and below the affected part should be gently placed through their range of motion.
    • The nurse encourages full participation in ADLs within the physical limitations to promote general well-being.
    • Analgesics are given.
  3. Deficient knowledge related to the treatment regimen.
    • Assess the level of knowledge by verbalization with the patient
    • Answer each question of the patient
    • Clarify all doubts of the patient.
 
AMPUTATION AND PROSTHESIS
The surgical removal of a partial or entire limb. It can result from injury, disease, or loss of circulation.
 
Types of Amputation
  • Acquired amputation: The surgical removal of a limb associated with complications of disease or trauma
  • Vascular amputation: The surgical removal of a limb associated with tissue ischemia
  • Traumatic amputation: The surgical removal of a limb associated with traumatic injury
  • Bilateral amputee: Removal of both limbs on one side.
 
Levels of Amputation
  • Transhumeral amputation (AE): An amputation performed at the above the elbow
  • Transfemoral amputation (AK): An amputation performed at the level above the knee
  • Transtibial amputation (BK): An amputation performed at the level below the knee
  • Partial foot amputation: An amputation performed at the level of the foot
  • Wrist disarticulation (WD): An amputation performed at the level of the wrist
  • Symes amputation: An amputation performed at the level of the ankle joint that retains the fatty heel pad portion intended to preserve weight bearing function.
 
Amputation Recovery
 
Prostatic Devices for Amputation
  • The goal is to form a round numb so it can be fitted well into a prostatic
  • 2–3 weeks following removal, replacement limb planning occurs
  • The prostatic is fitted to the residual limb.
 
Potential Complications Associated with Amputation
  • Infection
  • Acute pain and chronic pain
  • 764Abdominal aortic aneurysm (AAA)
  • Emotional issues such as depression and impaired body image.
 
Pain Complications
  • Phantom pain is a painful sensation in the area where the limb once was; it is believed to be related to neural memory—the nerves have memory of those feelings
  • Adherent scar tissue grows in the area where the removal took place; it often causes pain
  • Causalgia: A persistent pain with a burning sensation that results from injury to a peripheral nerve
 
Phantom Pain
Phantom pain is the neurological interpretation of noxious stimuli that is commonly associated with amputation. The pain is felt in the region in which the body part was removed. It occurs from nerve damage in the residual limb and is associated with muscle and neural memory. This form of pain is common in veterans who experienced a traumatic injury that resulted in amputation.
 
Neuroplasticity and Phantom Pain
Limb amputation and injuries to the spinal cord injury result in major trauma to the nervous system. This damage has been linked to reorganization of neural responses that occur in the cortical level of the central nervous system. In parts of the body that have been denervated, the section of the cortical homunculus that responds to input remains in communication to the adjacent region of the sensory cortex that is normally activated by stimulus in the region of the body part or tissue that is missing. Even though the region on which the stimulus is interpreted to be originated from is longer present, such as an amputated calf, a response still occurs to perceived stimulus. For instance, consider an individual who had a calf amputated just below the knee. While moving the remaining portion of the leg to put on a pair of pants, stimulus can be activated that is associated with movement the brain has come to expect from this common activity. A sensation may be felt as if the calf was moving up off of the floor to accommodate the pants leg.
 
Prosthesis
Prosthesis is an artificial extension that replaces a missing body part. It is part of the field of biomechatronics, the science of fusing mechanical devices with human muscle, skeleton, and nervous systems to assist or enhance motor control lost by trauma, disease, or defect.
An artificial limb is a type of prosthesis that replaces a missing extremity, such as arms or legs. The type of artificial limb used is determined largely by the extent of an amputation or loss and location of the missing extremity. Artificial limbs may be needed for a variety of reasons, including disease, accidents, and congenital defects.
 
Types of Prosthesis
There are four main types of artificial limbs. These include the transtibial, transfemoral, transradial, and transhumeral prostheses.
  • Transradial prosthesis: A transradial prosthesis is an artificial limb that replaces an arm missing below the elbow. Cable operated limbs work by attaching a harness and cable765 around the opposite shoulder of the damaged arm. The other form of prosthetics available are myoelectric arms. These work by sensing, via electrodes, when the muscles in the upper arm moves, causing an artificial hand to open or close.
  • Transhumeral prosthesis: A transhumeral prosthesis is an artificial limb that replaces an arm missing above the elbow. Transhumeral amputees experience some of the same problems as transfemoral amputees, due to the similar complexities associated with the movement of the elbow. This makes mimicking the correct motion with an artificial limb very difficult.
  • Transtibial prosthesis: A transtibial prosthesis is an artificial limb that replaces a leg missing below the knee. Transtibial amputees are usually able to regain normal movement more readily than someone with a transfemoral amputation, due in large part to retaining the knee, which allows for easier movement.
  • Transfemoral prosthesis: A transfemoral prosthesis is an artificial limb that replaces a leg missing above the knee. Transfemoral amputees can have a very difficult time regaining normal movement. In general, a transfemoral amputee must use approximately 80% more energy to walk than a person with two whole legs. This is due to the complexities in movement associated with the knee. In newer and more improved designs, after employing hydraulics, carbon fiber, mechanical linkages, motors, computer microprocessors, and innovative combinations of these technologies to give more control to the user.
Fig. 14.7: Prosthesis
 
Nursing Management
 
Nursing Interventions
  • Pain: Assess and treat pain.
  • Determine the risk of suicide and provide an environment that is safe.
  • Altered functioning: Assist the patient in performing activities of daily living, which may be altered due to depression.
  • Social functioning: Assist the patient in identifying new ways to function socially.
  • 766Ineffective coping patterns for enhanced coping patterns: assess the patient's coping style and provide education.
  • Knowledge deficit for enhanced learning: Educate the patient on the healing process, including anticipatory grieving to be expected from the situation, and provide information about limb replacement prostatic and adaptive devices.
  • Assess the patient's pain, including location, onset, characteristics (such as dull, stabbing, or throbbing), and level, preferably using a measurable scale such as 0–10.
  • If assessing the patient after the acute post-amputation period, determine what factors worsen pain or relieves pain.
  • Administer pain medications as ordered.
  • To determine efficacy of the therapeutic regimen, reassess pain levels 30–60 minutes after administering pain medication by mouth and 15 minutes following intravenous administration.
  • Phantom pain can be an extremely isolating and frustrating experience. Acknowledge the individual's pain in order to validate the experience of phantom pain.
  • Assess the patient for suicidal ideation by using an assessment tool such as SAD PERSONS.
  • Inquire about family history, cohabiting mental health conditions such as depression, and if the patient has ever made any previous suicide attempts.
  • Determine if there is a suicide plan in place.
  • If a suicide plan is in place, inquire to learn about the lethality of the plan and availability to carry it through (such access to a gun or high ledge of a building).
  • If the patient is deemed to be suicidal, immediately institute suicide watch—do not leave the patient unattended, ensure that a competent staff member remains no more than an arm's reach away from the patient at all times, remove any potentially harmful objects out of the room, and facilitate referral to the appropriate team members.
  • Ask open ended questions to determine the patient's coping style.
  • Learn if the patient was experiencing any other extremely stressful experiences prior to the current crisis.
  • Determine what coping patterns the patient is currently using to manage the present crisis.
  • Determine if any maladaptive or potentially dangerous coping patterns are being used, which could place the patient at risk for injury.
  • Ask about previous coping patterns ones used successfully to manage past crises or stressful situations.
 
Nursing Diagnosis
  1. Impaired physical mobility related to pain and discomfort and loss of body part.
    Interventions
    • Encourage him to perform prescribes exercises.
    • Provide stump care on a routine basis: inspect area, cleanse and dry thoroughly, and rewrap stump with elastic bandage or air splint, or apply a stump shrinker (heavy stockinette sock), for ‘delayed’ prosthesis.
    • 767Measure circumference periodically.
    • Rewrap stump immediately with an elastic bandage, elevate if ‘immediate or early’ cast is accidentally dislodged. Prepare for reapplication of cast.
    • Assist with specified ROM exercises for both the affected and unaffected limbs beginning early in postoperative stage.
    • Instruct patient to lie in prone position as tolerated at least twice a day with pillow under abdomen and lower-extremity stump.
    • Maintain knee extension.
    • Provide trochanter rolls as indicated.
    • Encourage active and isometric exercises for upper torso and unaffected limbs.
    • Demonstrate and assist with transfer techniques and use of mobility aids like trapeze, crutches, or walker.
    • Assist with ambulation.
    • Instruct patient in stump-conditioning exercises.
  2. Risk for infection related to inadequate primary defenses (broken skin, traumatized tissue), invasive procedures; environmental exposure.
    Interventions
    • During emergency treatment, monitor vital signs (especially in hypovolemic shock), clean the wound and give tetanus prophylaxis, and antibiotics as ordered.
    • After a complete amputation, wrap the amputated part in wet dressing soaked in normal saline solution. Label the part, seal it in a plastic bag, and float the bag in ice water.
    • Inspect dressings and wound; note characteristics of drainage.
    • Maintain aseptic technique when changing dressings and caring for wound.
    • Flush the wound with sterile saline solution, apply a sterile pressure dressing.
    • Maintain patency and routinely empty drainage device.
    • Cover dressing with plastic when using the bedpan or if incontinent.
    • Expose stump to air; wash with mild soap and water after dressings are discontinued.
    • Monitor vital signs.
    • Administer antibiotics as indicated.
    • Obtain wound and drainage cultures and sensitivities as appropriate.
  3. Risk for ineffective tissue perfusion related to reduced arterial or venous blood flow, tissue edema, hematoma formation or hypovolemia.
    Interventions
    • Inspect dressings and drainage device, noting amount and characteristics of drainage.
    • Perform periodic neurovascular assessments (sensation, movement, pulse, skin color, and temperature).
    • Monitor vital signs. Palpate peripheral pulses, noting strength and equality.
    • Apply direct pressure to bleeding site if hemorrhage occurs. Contact physician immediately.
    • 768If the patient experiences throbbing after the stump is wrapped, the bandage may be too tight. Remove the bandage and reapply.
    • Check the bandage regularly.
    • Investigate reports of persistent or unusual pain in operative site.
    • Administer IV fluids and blood products as indicated.
    • Encourage and assist with early ambulation.
    • Evaluate nonoperated lower limb for inflammation, positive Homans' sign.
    • Monitor laboratory studies: Hb and Hct. etc.
  4. Situational low self-esteem related to Loss of body part or change in functional abilities
    Interventions
    • Encourage participation in ADLs. Provide opportunities to view and care for stump, using the moment to point out positive signs of healing.
    • Help the amputee cope with his altered body image.
    • Encourage expression of fears, negative feelings, and grief over loss of body part.
    • Reinforce preoperative information including type and location of amputation, type of prosthetic fitting if appropriate (immediate, delayed), expected.
    • Ascertain individual strengths and identify previous positive coping behaviors.
    • Assess and consider patient's preparation for and view of amputation.
    • Encourage and provide for visit by another amputee, especially one who is successfully rehabilitating.
    • Note withdrawn behavior, negative self-talk, use of denial, or over concern with actual and perceived changes.
    • Provide open environment for patient to discuss concerns about sexuality.
    • Discuss availability of various resources: psychiatric and sexual counselling, occupational therapist.
 
OSTEITIS DEFORMANS (PAGET'S DISEASE)
Paget's disease of bone disrupts the body's normal bone recycling process, in which old bone tissue is gradually replaced with new bone tissue. Overtime, the affected bones may become fragile and week. Paget's disease of bone most commonly occurs in the pelvis, skull, spine and legs. The involved bone can be soft, leading to weakness and bending of the pelvis, low back (spine), hips, thighs, head and arms.
 
Etiology and Pathophysiology
  • Both genetic and environmental factors are thought to play a role.
  • About 15% of people with Paget's disease have a family history.
  • Autosomal dominant inheritance has also been described in some families.
  • Mutations have been identified in four genes that cause Paget's disease.
  • Mechanical stress may play a role.
  • Paramyxovirus infection (including measles and respiratory syncytial virus) has been suggested as a possible trigger but this has been disputed.
769
 
Pathophysiology
 
Paget's Disease Evolves Through three Distinct Phases
  1. An initial, short-lived burst of multinucleate osteoclastic activity causing bone resorption
  2. A mixed phase of both osteoclastic and osteoblastic activity, with increased levels of bone turnover leading to deposition of structurally abnormal bone
  3. A final chronic sclerotic phase, during which bone formation outweighs bone resorption.
 
Signs and Symptoms
Most people who have Paget's disease of bone experience no symptoms. When symptoms do occur, the most common complaint is bone pain which may includes:
  • Pelvis: Paget's disease of bone in the pelvis can cause hip pain.
  • Skull: An overgrowth of bone in the skull can cause hearing loss or headaches.
  • Spine: If spine is affected, nerve roots can become compressed. This can cause pain, tingling and numbness in an arm or leg.
  • Leg: As the bones weaken, they may bend. Enlarged and misshapen bones in legs can put extra stress on nearby joints, which may cause wear-and-tear arthritis in knee or hip.
 
Diagnostic Evaluations
  • Bone-specific alkaline phosphatase (BSAP) levels are raised.
  • Urinary excretion of deoxypyridinoline and N-telopeptide are elevated.
  • Serum calcium, phosphorus, and parathyroid hormone levels are usually normal but immobilization may lead to hypercalcemia.
  • 770X-rays may show a number of signs of both osteolysis and excessive bone formation occur.
  • Radionuclide bone scans can show the extent of the disease.
  • Bone biopsy may be needed if malignant change is suspected.
 
Management
Treatment approaches can focus on providing physical assistance, including the addition of wedges in the shoe, walking aids and the administration of physical therapy and pharmaco-therapy.
 
Pharmacotherapy
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) and paracetamol may be effective for pain.
  • Anti-resorptive therapy is with either bisphosphonates or calcitonin.
  • Bisphosphonates:
    • Oral or intravenous bisphosphonates are the mainstay of treatment.
    • They are thought to reduce bone turnover, improve bone pain, promote healing of osteolytic lesions and restore normal bone histology.
    • Newer bisphosphonates such as zoledronic acid may help to better achieve metabolic control of the disease and so improve these statistics.
    • Pamidronate, risedronate, and zoledronic acid are preferred.
    • Any calcium and vitamin D deficiency needs to be corrected before starting a bisphosphonate to avoid hypocalcemia.
All oral medications should be taken with a large glass of water (6–8 oz) upon arising in the morning. Patients should remain upright for the next 30 minutes and not eat until that time has passed. Any of these treatments can be repeated if necessary. Side effects of these medicines may involve heartburn and sometimes increasing bone pain for a short period of time.
There are also injectable medications. Injectable medications that can be given for Paget's include:
  • Pamidronate: Which is injected in the vein once a month or once every few months? The injection takes a few hours. Unusually, there can be inflammation of the eye or loss of bone around the teeth (osteonecrosis).
  • Zoledronate: This is injected in the vein once a year.
  • Calcitonin, a hormone that is injected under the skin several times a week.
 
Complications
Complications from Paget's disease depend on the site affected and the activity of the disease:
  • Bone pain.
  • Bone deformity, kyphosis, frontal bossing of the skull, an enlarged maxilla, an increase in head size.
  • Pathological fractures.
  • Osteoarthritis.
  • Deafness and tinnitus may be due to compression of cranial nerve VIII.
  • Spinal stenosis.
  • Nerve compression syndromes.
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Nursing Management
  1. Acute pain related to nerve compression, muscle spasm.
    Interventions
    • Assess complaints of pain, location, duration of attacks, precipitating factors which aggravate
    • Maintain bedrest, semi-Fowler position to the spinal bones, hips and knees in a state of flexion, supine position
    • Use logroll (board) during a change of position
    • Auxiliary mounting brace.
    • Limit activity during the acute phase according to the needs
    • Teach relaxation techniques
    • Collaboration: Analgesics, traction, physiotherapy.
  2. Impaired physical mobility related to pain, muscle spasms, and damage neuro-muskulus restrictive therapy.
    Interventions
    • Give patients to perform passive range of motion exercises and active
    • Assist patients in ambulation activity progressively
    • Provide good skin care, massage point pressure after rehap change of position. Check the state of the skin under the brace with a specific time period
    • Note the emotional responses and behaviors in immobilizing
    • Demonstrate the use of auxiliary equipment such as a cane
    • Collaboration: Analgesic.
 
PROLAPSED LUMBAR DISK (HERNIATED RUPTURED DISK)
A prolapsed lumbar disk is a spinal condition that can cause lower back pain, as well as numbness, tingling, a ‘pins and needles’ feeling and muscle weakness in the lower body. This condition is also referred to as a herniated or ruptured disk, and usually is caused by normal, age-related deterioration.
Fig. 14.8: Herniated ruptured disk
772
 
Etiology and Pathophysiology
A prolapsed cervical disk is another name for a herniated, or ruptured, disk in the neck or upper back. It occurs among the seven top-most vertebrae of the spine, known as the cervical vertebrae (C1 to C7). Although disc herniation is more common in the lower back, the C4 to C7 levels of the cervical spine are also vulnerable to disc prolapse as the body ages.
 
Pathophysiology
 
Signs and Symptoms
A prolapsed cervical disk can produce symptoms in the following areas of the body:
  • Shoulders
  • Upper back
  • Deltoid muscles
  • Biceps
  • Triceps
  • Forearms
  • Wrists
  • Hands
  • Fingers
  • Head (migraine symptoms)
 
Prolape Thoracic Disk
A thoracic disk prolapse is another way of referring to a herniated disk located in the region of the 12 thoracic vertebrae (T1 to T12), which form the central portion of the spine.
The relatively rigid thoracic vertebrae: which serve as a base for the ribcage are less vulnerable to disk prolapse than the more flexible and weight-bearing cervical and lumbar 773spine regions. However, thoracic disk prolapse does occur occasionally, normally in association with degenerative disk disease or traumatic spinal injury.
Because the symptoms associated with a prolapsed disk in the thoracic spine can resemble other conditions—including heart, lung, kidney or gastrointestinal disorders—a thorough diagnosis will be necessary if experience the following:
  • Chest pain
  • Upper back pain
  • Abdominal pain
  • Numbness or tingling below the pinched nerve
  • Loss of balance
  • Lower body muscle weakness.
 
Pathophysiology
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Diagnostic Evaluation
  • Diagnosis is made on the basis of the history, symptoms, and physical examination. At some point in the evaluation, tests may be performed to confirm or rule out other causes of symptoms such as spondylolisthesis, degeneration, tumors, metastases and space-occupying lesions, as well as to evaluate the efficacy of potential treatment options.
 
Imaging
  • X-ray: Although traditional plain X-rays are limited in their ability to image soft tissues such as disks, muscles, and nerves, they are still used to confirm or exclude other possibilities such as tumors, infections, fractures, etc. In spite of these limitations, X-ray can still play a relatively inexpensive role in confirming the suspicion of the presence of a herniated disk. If a suspicion is thus strengthened, other methods may be used to provide final confirmation.
  • Computed tomography scan: It can show the shape and size of the spinal canal, its contents, and the structures around it, including soft tissues.
  • Magnetic resonance imaging: A diagnostic test that produces three-dimensional images of body structures using powerful magnets and computer technology. It can show the spinal cord, nerve roots, and surrounding areas, as well as enlargement, degeneration, and tumors.
  • Myelogram: An X-ray of the spinal canal following injection of a contrast material into the surrounding cerebrospinal fluid spaces. By revealing displacement of the contrast material, it can show the presence of structures that can cause pressure on the spinal cord or nerves, such as herniated discs, tumors, or bone spurs.
  • Electromyogram and nerve conduction studies: These tests measure the electrical impulse along nerve roots, peripheral nerves, and muscle tissue. This will indicate whether there is ongoing nerve damage.
 
Pharmacological Management
  • Anti-inflammatory painkillers: They include ibuprofen, diclofenac or naproxen need. Some people with asthma, high blood pressure, kidney failure, or heart failure may not be able to take anti-inflammatory.
  • A stronger painkiller such as codeine is an option if anti-inflammatory do not suit or do not work well. Codeine is often taken in addition to paracetamol. Constipation is a common side effect from codeine. This may make back pain worse if you need to strain to go to the toilet. To prevent constipation, have lots to drink and eat foods with plenty of fiber.
  • A muscle relaxant such as diazepam is sometimes prescribed for a few days if the back muscles become very tense and make the pain worse.
 
Nursing Management
  1. Acute pain related to nerve compression, muscle spasm.
    Interventions
    • Assess complaints of pain, location, duration of attacks, precipitating factors which aggravate.
    • 775Maintain bedrest, semi-Fowler position to the spinal bones, hips and knees in a state of flexion, supine position
    • Use logroll (board) during a change of position
    • Auxiliary mounting brace.
    • Limit activity during the acute phase according to the needs
    • Teach relaxation techniques
    • Collaboration: Analgesics, traction, physiotherapy.
  2. Impaired physical mobility related to pain, muscle spasms, and damage neuro-muskulus restrictive therapy.
    Interventions
    • Give patients to perform passive range of motion exercises and active
    • Assist patients in ambulation activity progressively
    • Provide good skin care, massage point pressure after rehab change of position. Check the state of the skin under the brace with a specific time period.
    • Note the emotional responses and behaviors in immobilizing
    • Demonstrate the use of auxiliary equipment such as a cane.
    • Collaboration: Analgesic.
  3. Anxiety related to ineffective individual coping.
    Interventions
    • Assess the patient's anxiety level
    • Provide accurate information
    • Give the patient the opportunity to reveal problems such as the possibility of paralysis, the effect on sexual function, changes in roles and responsibilities.
    • Review of secondary problems that may impede the desire to heal and may hinder the healing process.
    • Involve the family members in care.
  4. Knowledge deficient related to the lack of information about the condition, prognosis.
    Interventions
    • Explain the process of disease and prognosis, and restrictions on activities
    • Give information about own body mechanics to stand, lift and use the shoes backer
    • Discuss about treatment and side effects.
    • Suggest to use the board or mat, a small pillow under neck a little flat, bed side with knees flexed.
    • Avoid the use of heaters for a long-time
    • Give information about the signs that need attention such as puncture pain, loss of sensation and ability to walk.
 
Types of Surgeries in Muscular Skeleton System
Various types of total and partial knee replacement surgery:
 
Total Knee Replacement
Total Knee Replacement (TKR), also referred to as Total Knee Arthroplasty (TKA), is a surgical procedure where worn, diseased, or damaged surfaces of a knee joint are removed and776 replaced with artificial surfaces. It is a common surgical procedure most often performed to relieve the pain and disability from degenerative arthritis, meniscus tears, osteoarthritis, cartilage defects, and ligament tears.
The most common cause for knee pain which needs Knee Replacement Surgery is osteoarthritis. In Total Knee Replacement, the surgeon removes damaged cartilage and bone from the surface of your knee joint and replaces them with a prosthesis or implant of metal and plastic. Total knee replacement can help put an end to arthritic pain in knee and enable to resume a functional and active lifestyle.
Fig. 14.9: Total knee transplant
 
Partial Knee Replacement
Most people are aware of the total knee replacement surgery. This involves replacing the unhealthy surface of the entire knee joint with metal and plastic implants. It is a very successful operation with good long-term results. However a large percentage of patients have arthritis limited to one part of the joint alone.
Replacing the whole joint in these patients is overkill and unnecessary. Many middle aged men and women develop osteoarthritis of the knee. Osteoarthritis of the knee affects the inner half or medial compartment to start with and then proceeds to affect the outer half or lateral compartment. In this operation only that part of the knee, which is unhealthy, is replaced. The normal surfaces are left alone. This operation has several advantages over total knee replacement surgery like small incision, longer life of implant and postoperative hospitalization is reduced and return to normal is much faster than total knee replacement surgery.
Fig. 14.10: Partial knee replacement
 
Simultaneous Bilateral Knee Replacement—Both Knee Replacement Surgery
A simultaneous procedure means that both knees are replaced at the same surgery, in one day. The benefit of simultaneous knee replacement is that both problems are taken care of777 at one time. The overall stay and rehabilitation can be done in a shorter time, and there is only one hospitalization. Patients also only require one anesthesia.
Fig. 14.11: Bilateral knee replacement
 
Revision Knee Replacement
Total Knee Replacements that need to be revised after 15–20 years (postprimary surgery) are also done. The most advanced prosthesis and Computer Assisted Surgery (CAS) is also used for Revision Knee Replacements.
 
Knee Arthroscopic Surgery
Knee arthroscopic surgery is a procedure performed through small incisions in the skin to repair injuries to tissues such as ligaments, cartilage, or bone within the knee joint area. The surgery is conducted with the aid of an arthroscope, which a very small instrument is guided by a lighted scope attached to a television monitor.
Knee arthroscopy has in many cases replaced the classic arthrotomy that was performed in the past. Today knee arthroscopy is commonly performed for treating meniscus injury, reconstruction of the anterior cruciate ligament and for cartilage microfracturing. Many knee joint problems are amenable to arthroscopic surgery like:
  • Trimming a torn meniscus of the knee
  • Repairing a torn meniscus of the knee
  • Treatment of cartilage damage in the knee.
Arthroscopic surgery is a ‘less invasive’ procedure and being a surgical procedure involves risks, but when performed for the right problem it is often very successful.
 
Anterior Cruciate Ligament (ACL) Reconstruction
The Anterior Cruciate Ligament (ACL) keeps the shin bone (tibia) in place. A tear of this ligament can cause Knee and Hip to give way during physical activity. ACL reconstruction surgery is done to replace the ligament in the center of Knee and Hip with a new ligament.
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Arthroscopic Meniscectomy
Meniscectomy is the surgical removal of all or part of a torn meniscus (rupturing of one or more of the fibrocartilage strips in the Knee and Hip called menisci). A meniscus tear is a common Knee and Hip joint injury and can lead to pain and swelling of the Knee and Hip joint. Menisci can also be torn during innocuous activities such as walking or squatting. Depending on the location of the tear, a repair may be possible. The outer third of the meniscus, an adequate blood supply exists and a repair will likely heal. Usually younger patients are more resilient and respond well to this treatment, while older, more sedentary patients do not have a favorable outcome after a repair.
 
Total Hip Replacement Surgery (THR)
Total Hip Replacement (THR) is a treatment to all kinds of hip arthritis, improving the quality of life of patients who undergo the operation. The trouble causing hip is surgically removed and replaced with an artificial one. In Total Hip Replacement, the entire femoral head is removed. A new ball and socket is placed as an implant or prosthesis. The new hip ball is attached to a stem which gets machined inside the hip bone. Hip Replacement Implant can wear out over a period of time due to various reasons.
There are two major types of artificial hip replacements—Cemented Prosthesis and the Uncemented Prosthesis. Both types of prosthesis are widely used. Each prosthesis is made up of two parts:
  1. The acetabular component, or socket portion, which replaces the acetabulum.
  2. The femoral component or stem portion, which replaces the femoral head.
The femoral component is made of a metal stem with a metal ball on the end. Some prosthesis have a ceramic ball attached to the metal stem. The acetabular component is a metal shell with a plastic inner socket liner that acts like a bearing. The type of plastic used is highly cross linked ultra high molecule weight Polyethylene which is wear resistant.
A cemented prosthesis is held in place by Poly Metha Acrylate (PMMA) cement that attaches the metal to the bone. An uncemented prosthesis has a fine mesh of holes on the surface area that touches the bone. The mesh allows the bone to grow into the mesh and ‘become part of’ the bone.
 
Indications of Hip Replacement Surgery
  • Progressively worsening severe arthritis in the hip joint
  • Common hip problems resulting into osteoarthritis
  • Bony fractures of the hip joint, rheumatoid arthritis, and death (aseptic necrosis) of the hip bone.
  • Dependency on Anti-inflammatory and pain medications.
  • Benign and malignant bone tumors.
  • Paget's disease occurs mainly in the elderly. Bones become enlarged and weakened, with the potential of a fracture or deformity of the hip bones.
 
Advantages of Hip Replacement Surgery
  • Hip replacement improves quality of life.
  • Age is no barrier to hip replacement benefits.
  • 779Hip replacement is cost effective.
  • High rate of patient satisfaction associated with hip replacement.
  • The artificial hip often improves the movements in a hip joint that has become increasingly stiff from the effects of long-term arthritis and this permits the patient to resume at first gentle activity and then their favorite leisure hobbies.
  • Improves mobility.
  • Independence of arthritis sufferers.
 
Types of Shoulder Surgery
  • Arthroscopic acromioplasty: This is an arthroscopic procedure to widen the space between the upper arm and the shoulder blade so that the rotator cuff tendons do not get stuck between them. Arthroscopy with shoulder instability—In case of dislocation of the shoulder, it is normal to have an arthroscopy. It is often possible to repair damage to the shoulder but sometimes a separate operation is needed.
  • Rotator cuff repair: Arthroscopic repair of the shoulder tendons. The goal of these procedures is to minimize the pain, restore strength and functionality.
  • Total shoulder replacement: Shoulder arthroplasty with loss of cartilage the patient will suffer severe shoulder arthritis. This will eventually make surgical treatment is necessary.
BIBLIOGRAPHY
  1. Alexandersen P, Peris P, Guanabens N, et al. Non-isomerized C-telopeptide fragments are highly sensitive markers for monitoring disease activity and treatment efficacy in Paget's disease of bone. J Bone Miner Res. 2005 Apr;20(4):588–95.
  1. Eekhoff EW, Karperien M, Houtsma D, et al. Familial Paget's disease in the Netherlands: occurrence, identification of new mutations in the sequestosome 1 gene, and their clinical associations. Arthritis Rheum. 2004 May;50(5):1650–4.
  1. Hess LM, Jeter JM, Benham-Hutchins M, et al. Factors associated with osteonecrosis of the jaw among bisphosphonate users. Am J Med. 2008 Jun;121(6):475–83.
  1. Hosking D, Lyles K, Brown JP, et al. Long-term control of bone turnover in Paget's disease with zoledronic acid and risedronate. J Bone Miner Res. 2007 Jan;22(1):142–8.
  1. Juvenile Paget Disease. Online Mendelian Inheritance in Man (OMIM).
  1. Karaoglan A, Akdemir O, Erdogan H, et al. A rare emergency condition in neurosurgery: foot drop due to Paget's disease. Turk Neurosurg. 2009 Apr;19(2):208–10.
  1. Langston AL, Campbell MK, Fraser WD, et al. Clinical determinants of quality of life in Paget's disease of bone. Calcif Tissue Int. 2007 Jan;80(1):1–9.
  1. Mackenzie I, Young C, Fraser WD. Tinnitus and Paget's disease of bone. J Laryngol Otol. 2006 Nov;120(11):899–902.
  1. Paget Disease of Bone (PDB). Online Mendelian Inheritance in Man (OMIM).
  1. Ralston SH. Clinical practice. Paget's disease of bone. N Engl J Med. 2013 Feb 14; 368(7):644–50.
  1. Ralston SH, Langston AL, Reid IR. Pathogenesis and management of Paget's disease of bone. Lancet. 2008 Jul 12;372(9633):155–63.
  1. Van Staa TP, Selby P, Leufkens HG, et al. Incidence and natural history of Paget's disease of bone in England and Wales. J Bone Miner Res. 2002 Mar;17(3):465–71.

Genitourinary Disorders15

 
INTRODUCTION
Anatomy and physiology of kidney: The urinary system is the main excretory system and consists of following structures:
  • Two kidneys, which secrete urine.
  • Two ureters, which conveys the urine from kidney to the urinary bladder.
  • The urinary bladder where urine collects and is temporarily stored.
  • The urethra through which the urine passes from the urinary bladder to the exterior.
The urinary system plays a vital part in maintaining homeostasis of water and electrolyte concentrations within the body.
  • The kidney produce urine that contains metabolic waste products, including nitrogenous compounds urea and uric acid, excess ions, and some drugs.
  • Urine is stored in the bladder and excreted by the process of micturition.
  • The kidneys lie on the posterior abdominal wall, one on each side of the vertebral column. Behind the peritoneum and below the diaphragm.
  • The right kidney is usually slightly lower than the left, probably, because of the considerable space occupied by the liver.
  • 781Kidneys are bean shaped organs, about 11 cm long, 6 cm wide, 3 cm thick and 150 gm weight.
  • A sheath of fibrous connective also known as renal fascia encloses the kidney and the renal fat.
Organs associated with the kidneys: As the kidneys lie on either side of the vertebral column, each is associated with a different group of structures.
 
Right Kidney
  • Superiorly: The right adrenal gland.
  • Anteriorly: The right lobe of the liver, the duodenum, and the hepatic flexure of the colon.
  • Posteriorly: The diaphragm and the muscles of the posterior abdominal wall.
  • Left kidney: Superiorly: The left adrenal gland.
  • Anteriorly: The spleen, stomach, pancreas, jejunum, and splenic, flexure of the colon.
  • Posteriorly: The diaphragm and muscle of the posterior abdominal wall.
Gross structure of the kidney: There are three areas of tissue that can be distinguished when a longitudinal section of kidney is viewed with the naked eye.
  • An outer fibrous capsule, surrounding the kidney.
  • The cortex, a reddish brown layer of tissue immediately below the capsule and outside the pyramids.
  • The medulla, the inner most layer, consisting of pale conical shaped striations, the renal pyramids.
  • The hilum is the concave medial border of the kidney where the renal blood and lymph vessels, the ureter and nerves enter.
  • The renal pelvis is the funnel structure that collects urine formed by the kidney.
    Fig. 15.1: Human kidney
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GENITOURINARY DISORDERS
 
ACUTE RENAL FAILURE
Introduction of Topic: Renal failure results when the kidneys cannot remove the body's metabolic waste or perform their regulatory functions. The substances normally eliminated in the urine accumulate in the body result fluids as a result of impaired renal excretion, leading to a disruption in endocrine as well as fluid, electrolyte and acid base disturbances.
Definition: Renal failure is a systemic disease and is a final common pathway of many different kidney and urinary tract diseases. Acute renal failure is a sudden and almost complete loss of kidney function (decreased GFR) over a period of hour to days.
 
Etiology
There are many possible causes of kidney damage:
  • Acute tubular necrosis.
  • Autoimmune kidney disease.
  • Blood clot from cholesterol.
  • Decreased blood flow due to very low blood pressure which can result from:
    • Burns
    • Dehydration
    • Hemorrhage
    • Injury
    • Septic shock.
  • Urinary tract blockage.
  • Calculi (stones)
  • Tumor
  • Infectious processes such as acute pyelonephritis, acute glomerulonephritis.
  • Advanced age.
    Fig. 15.2: Causes of acute renal failure
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Prerenal Causes
Prerenal causes interfere with renal perfusion. The kidney depends on an adequate delivery of blood to a filtered by the glomeruli. Therefore a reduce blood flow obviously decreases the GFR conditions that contribute to decreased renal blood flow include:
  • Decreased output
  • Increased vascular resistance
  • Fluid volume shifts
  • 784Vascular obstruction
  • Renal losses.
 
Intrarenal Causes
Renal causes refer to parechymal changes from disease or nephrotoxic substances. Acute tubular necrosis is the most frequent renal cause of ARF. This destruction of tubular epithelial cells in the result of impaired renal perfusion or direct damage from nephrotoxins. Acute tubular necrosis may also be caused by the presence of heme pigments such as myogloben and hemoglobin. Which are liberated from damaged tissue. This may result from trauma surgery, crush injury and electrical shock or from no traumatic conditions (infectious disease and metabolic condition, diabetes mellitus and malignant hyperthermia and diabetes mellitus).
  • Prolonged renal ischemia, resulting from pigment nephropathy
  • Acute pyelonephritis
  • Nephrotoxic agent.
 
Postrenal Causes
Postrenal causes leading to ARF arise from obstruction in the urinary tract, anywhere from the tubles to the urethral meatus. Common source of obstruction include prostatic, hyperplasia, calculi, invading, tumors, surgical accident.
In managing the client with ARF, it is important to determine. Whether the disorder is originates from prerenal, renal, postrenal intervention.
 
Types of Acute Renal Failure
There are two varities of ARF: Nonoliguric and oliguric
  • Nonoligouric renal failure: Although nonoligouric or polyuric, ARF is being recognized more often wheather it an entity in and overall in and of itself a phase of oligouric.
  • ARF remain controversial clients with nonoligouric renal failure may excrete as much 2 L/day and this recognized as possible sign of ARF. Hypertension and tacypenia with sign of fluid overload are frequently found.
  • Oligouric renal failure: In oligouric renal failure, urine production is usually falls below 400 ml/day. However, it is remembered the aging kidney normally loses of concentrating ability and renal function are more susceptible to insult. Therefore the older client develop a oliguria at urine volume at 600 to 700 ml/day.
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Pathophysiology
786
 
Signs and Symptoms
There are four clinical phases of acute renal failure:
  1. Initiation phase: It begins with the initial insult and ends when oliguria develops and can last hours to days.
  2. Oliguria phase: Usually caused by a reduction in the GFR. The minimum amount of urine needed to rid the body of normal metabolic waste products is 400 ml. In this phase uremic symptoms first appear and life threatening conditions such as hyperkalemia develops.
  3. Diuresis phase: In this phase patient experiences gradually increasing urine output of 1 to 3L/day, but may reach 3 to 5 L or more, which signals that glomerular filtration has started to recover. Volume of urine output may reach normal or elevated levels, renal function may still be abnormal. Because uremic symptoms may still be present, the patient must be observed closely for dehydration during this phase. If dehydration occurs uremic symptoms are likely to increase.
  4. Recovery phase: The recovery phase signals the improvement of renal function and take 3 to 12 months.
  • Signs and Symptoms: In acute renal failure patient may appear critically ill, lethargic, with nausea and vomiting, and diarrhea.
  • The skin and mucous membrane are dry from dehydration
  • Drowsiness, headache
  • Decreased appetite, shortness of breath
  • Fatigue, slow, sluggish movements
  • Flank pain, high blood pressure
  • Decreased sensation in hand and feet
  • Nose bleeds, bleeding, anemia, seizures
  • Swelling due to body keeping in fluid usually in ankle, feet and legs
  • Urination changes-little or no urine.
  • Excessive urine.
  • Diarrhea.
 
Diagnostic Evaluation
  • Urinalysis
  • Urine specific gravity
  • Sodium levels
  • Serum creatinine
  • Urea nitrogen
  • The amount of urine in relation to intake is also important in formulating the diagnosis.
    To measure the exact amount of urine output or obtain a specimen for culture and sensitivity, a straight catheter may need to be inserted.
Urinalysis may reveal the following:
  • A fixed specific gravity of 1.010 as the tubules loses the ability to concentrate the filtrate.
  • The presence of abnormal protein if glomerular damage is the cause of ARF
  • Microscopic examination of the urine sediment may show red blood cells, indicating glomerular dysfunction; white blood cells, indicating an inflammatory process.
  • 787Cell casts are protein and cellular debris moulded in the shape of the tubular lumen.
  • In the acute renal failure, RBC, WBC, and renal tubular epithelial casts maybe absorbed.
  • Brownish pigmented casts together with positive tests for occult tests for occult blood in the absence of hematuria are indicate of either moglobinuria or myoglobinuria.
    • Serum creatinine and BUN are determined to evaluate renal function and the presence of azotemia, serum creatinine levels increase rapidly within 24 to 48 hours of the onset
    • Serum electrolyte are monitored to evaluate the fluid and electrolyte status of the client in ARF. The serum potassium rises at a moderate rate. The serum potassium rises at a moderate rate and is indicate the need to dialysis
    • Arterial blood gases show a metabolic acidosis
    • Complete blood count demonstrates reduced RBCs and moderate anemia, with a hematocrit of 25 to 35%
    • Bladder catheterization is performed to rule out urethral obstruction as cause of renal function and obtain urine specimen for culture. The presence of urinary tract infection is suggestive of a post renal cause of ARF
    • Renal ultrasonography is useful to identify obstructive cause of renal failure
    • Computed tomography provide other mean of evaluating kidney size and possible urinary tract obstruction
    • A renal biopsy may necessary when other diagnostic studies do not provide a clear differentiation between acute and chronic renal failure. Microscopic examination of kidney tissue can provide a definitive diagnosis.
 
Management
  • Medical management: Goal is to prevent complications and restoration of renal function.
  • Over all medical management includes maintaining fluid balance, avoiding fluid excesses.
  • Collaborative therapy: Goal is to eliminate cause and manage signs and symptoms, [prevent complications].
  • It includes treatment of precipitating causes.
  • Fluid restriction.
  • Nutritional therapy: Adequate protein intake.
  • Potassium restriction.
  • Calcium supplements because of decreased level of calcium.
  • Initiation of dialysis if necessary. If the patient do not respond to treatment and adequate kidney function does not return, they will need to undergo dialysis.
  • Be active, eat balanced diet and avoid alcohol and cigarette smoking.
  • The amount of liquid client eat (such as soup) or drink will be limited to the amount of urine produce.
  • Provide diet high in carbohydrates, low in protein, salt, potassium.
 
Medical Management
The medical management of ARF is largely based on preventing and treating its effects. As with any disease process, prevention is the primary intervention. Attaining and maintaining adequate hydration and diuresis in high-risk client is crucial, as is the prevention of contributing factors. Once ARF has developed, prompt recognition and action facilitate restoration of optimal renal function. Correction of the underlying condition maybe all that 788is necessary in ARF due to prerenal disorders. Postrenal cause must be rectified. Treatment involves dialysis and early identification and treatment of infection.
 
Pharmacologic Management
Fluid replacement must be done very carefully to prevent fluid overload. Fluid overload. Fluid replacement volumes are usually calculated on the basis of some fraction of the pervious day's urine output plus an amount to account for the usual insensible loss that occurs during a 24-hour period. Diuretic therapy maybe used, although it remains controversial, furosemide and mennitol, the most commonly used pharmacologic agents, must be administered cautiously.
Electrolyte replacement is based primary on urine and serum electrolyte concentrations. Hyperkalemia is probably the most dangerous imbalance because of its probably the most dangerous imbalance because of its contribution to cardiac arrhythmias and arrest.
  • Dialysis is usually used for severe acidosis
  • Calcium and phosphorus binders
  • Antihypertensive and cardiovascular agent
  • Antiseziure agent
  • Erythropoietin.
 
Calcium and Phosphate Binder
Hyperphosphatemia and hypocalcemia are treated with medication that binds dietary phosphorus in the GI tract. Binder such as calcium carbonate or calcium acetate is prescribed, but there is a risk of hypercalcemia. If calcium is high or calcium phosphate is exceeds more than 55 mg/dl, a polymeric phosphate binder such as sevelamer hydrochloride (Renagel) maybe prescribed.
 
Antihypertensive and Cardiovascular Agent
Hypertension is managed by intravascular volume control and a variety of antihypertensive agents. Heart failure and pulmonary edema may also require treatment with fluid restriction, low sodium, diuretic agents such as digoxin and doubtamine. Sodium bicarbonate and dialysis may needed for the treatment to correct the acidosis.
 
Antiseizure Agents
Neurological abnormalities may occur so the patient must be observed for early evidence of slight twitching, headache delirium or seizure activity. The physician is notified immediately IV diazepam and phenytoin is usually administration to control the seizure.
 
Erythropoietin
Patients with anemia hematocrit less than 30% present with nonspecific symptoms such as malaise, decrease activity tolerance. Erythropoietin therapy is initiated to achieve a hematocrit of 33 to 38% and target hemoglobin 12 g/dl. it is administrated IV and SC three times a week.
 
Dietary Management
Dietary intervention is necessary with the deterioration of renal function and careful regulation of protein intake, fluid intake to balance fluid losses, sodium intake to balance sodium losses or some restriction of potassium. Vitamin supplements is necessary because protein restriction diet does not completion the necessary compliment of vitamin. Protein is restricted urea, uric acid, and organic acids are the breakdown product of dietary and tissue protein accumulate rapidly in blood when there is impaired renal clearance.
789The protein must contain the essential amino acid to reduce the nitrogen product low potassium liquid supplements maybe used. If oral intake is not sufficient to meet the daily requirements, tube feeding and parental nutrition maybe instituted. Usually the fluid allowance per day is 500 to 600 ml more than previous day 24 hours urine output.
 
Hemodialysis
The patient with increasing symptoms of renal failure is referred to dialysis and transplantation center early in the course of progressive renal disease. Dialysis is usually initiated when the patient cannot maintain a reasonable lifestyle with conservative treatment. It prevents the death but not cure renal disease and does not compensate for the loss of endocrine and metabolic activities of the kidneys.
The objectives of the hemodialysis are to extract toxic nitrogenous substance from the blood and remove the excess water, a dialyzer serve as synthetic semipermeable membrane replacing the renal glomeruli and tubules as the filter for the impaired kidneys. In hemodialysis blood laden with toxic and nitrogenous wastes is diverted from the patient to a machine, a dialyzer, when toxins are filtered out and removed and blood is return to patient. Diffusion, osmosis and ultra filtration are the principles on which hemodialysis is base. The toxins and waste in blood are removed by diffusion that moves from the higher concentration in the blood to an area of lower concentration. Excess water is removed from the blood by the blood by osmosis, in which water moves from an area of low concentration potential to an area higher concentration potential. In ultrafiltration, water moves under higher pressure to an area of lower pressure. This process is much more efficient than the osmosis at water removal and accomplished by negative pressure or a suction forces to the dialysis membrane.
 
Nutritional Therapy
The challenge of nutritional management in renal failure is to provide adequate calories to prevent catabolism. Acute renal failure causes nutritional imbalances because nausea and vomiting contribute to inadequate dietary intake.
  • Foods and fluid that contain potassium or phosphorus (bananas, citrus fruit, juices, coffee) are restricted. The patient may require parenteral nutrition when the GI tract is not functional.
  • Monitor daily weight and record the changes in weight.
  • Avoid the products with added salts including foods such as canned soups and fast foods, salty snacks.
  • Provide food with patient preferences with in dietary restrictions.
  • Provide high calorie, low protein, low sodium, and low potassium snacks between meals.
  • Provide food with a pleasant surroundings.
 
Home Care
Recovery from ARF is highly depends on condition and age of patient and severity of nephron damage.
  • Advise patient for good nutrition, rest, protein and potassium intake should be according to renal function.
  • Advise for regular follow up and care and regular evaluation of treatment is necessary.
  • Taught patient about the signs and symptoms of kidney disease.
  • Advise to avoid use of alcohol, smoking.
  • Advise to avoid spicy food.
  • The kidney do not recover the patient will eventually need dialysis or transplantation.
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Nursing Management
  • It is important to monitor the vital signs and fluid intake and output. The urine should be examined for blood, protein, color.
  • Assess the general appearance of patient including skin color, edema.
  • If patient is receiving dialysis observe or access the site for signs of inflammation.
  • Assess the mucous membrane for dryness and inflammation.
  • Nurse should monitor client for any complications, fluid and electrolyte imbalance, assess progress and response to treatment.
  • Provide psychological and emotional support to patient and family members.
  • It is a duty of nurse to keep informed family members about the patient condition and helps them to understand the treatment.
  • It is a duty of a nurse to maintain fluid and electrolyte balance, monitor fluid intake (IV medications should be administered), urine output, edema.
  • Provide skin care because the skin maybe dry and susceptible to breakdown as a result of edema.
  • Massaging the bony prominences, changing positions frequently.
 
Nursing Diagnosis
  • Excess fluid volume related to renal failure and fluid retention.
  • Risk for infection related to altered immune responses secondary to kidney failure.
  • Imbalanced nutrition pattern less than body requirement related to dietary restrictions.
  • Impaired skin integrity related to edema.
  • Anxiety related to disease process and uncertainty of prognosis.
  • Deficient knowledge regarding disease condition and treatment.
  • Activity intolerance related to fatigue, retention of waste products.
  1. Excess fluid volume related to renal failure and fluid retention
    Interventions
    • Assess the fluid status of the patient.
    • Monitor daily weight of patient.
    • Assess the skin turgor and presence of edema.
    • Monitor vital signs.
    • Limit fluid intake to prescribed volume.
    • Assist patient to cope with the discomforts resulting from fluid retention.
    • Provide frequent oral care and maintain oral hygiene.
    • Administer medications and fluids as prescribed by the doctor.
  2. Imbalance nutrition pattern less than body requirement related to dietary restrictions.
    Interventions
    • Assess the nutritional status of patient.
    • Monitor daily weight and record the weight changes.
    • Provide patient's food preferences within dietary restrictions.
    • Promote intake of high protein foods, e.g. Eggs, dairy products, meats.
    • Encourage high calorie, low protein, low potassium snacks in between meals.
    • Provide pleasant surrounding at meal times.
    • Maintain intake output chart.
  3. 791Deficient knowledge regarding disease condition and treatment.
    Interventions
    • Assess the knowledge of patient.
    • Assess the understanding of cause of renal failure and its treatment.
    • Provide explanations of renal function and consequences of renal failure at patient's level of understanding and guided by the patient's readiness to learn.
    • Assist patient to identify ways to incorporate changes related to illness and its treatment into lifestyle.
    • Provide oral and written information about disease, fluid and dietary restrictions, medications, follow-up schedule.
    • Provide psychological support to the patient.
 
CHRONIC RENAL FAILURE (CRF) OR END STAGE RENAL DISEASE (ESRD)
Chronic renal failure or ESRD is a progressive, irreversible deterioration in renal function in which the body's ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia, or azoremia (retention of urea and other nitrogenous wastes in the blood).
 
Definition
Chronic renal failure is a progressive, irreversible deterioration in renal function in which the body's ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia (retention of urea and other nitrogenous wastes in the blood) in such a extent the GFR < 60 ml/min for longer. ERDS is caused by systemic disease such as:
  • Diabetes mellitus
  • Hypertention
  • Chronic glomerulonephritis
  • Pylonephritis
  • Obstruction in urinary tract
  • Hereditary lesions
  • Polycystic kidney disease
  • Vascular disorder
  • Toxic agents
  • Infections
 
Stages of Chronic Renal Failure
Stages
Description
GFR (ml/min/1.73 m
Action
Stage 1
At increased risk for CKD
Kidney damage with normal or ↑GFR
≥90(with CKD risk factor)
≥90
Screening CKD risk reduction
Diagnosis and treatment
Stage 2
Kidney damage with mild ↓GFR
60-89
Estimation of progression
Stage 3
Moderate ↓GFR
30-59
Evaluation and treatment of complications
Stage 4
Severe ↓GFR
15-29
Preparation for renal replacement therapy
Stage 5
Kidney failure
< 15 (or dialysis)
Renal replacement (if uremia present)
* All GFR values are normalized to an average surface area (size) of 1.73 m2
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Pathophysiology
 
Signs and Symptoms
  • Neurologic system
    • Lethargy
    • Apathy
    • 793Decreased ability to concentrate
    • Altered mental ability fatigue confusion.
      Fig. 15.3: Pathophysiological changes in CRF
  • 794Integumentary
    • Grey bronze skin color.
    • Dry pruritus
    • Echymosis
    • Brittle nails
    • Thinning hairs.
      Fig. 15.4: Pathophysiological changes in CRF
  • Cardiovascular disease
    • Hypertension
    • Pitting edema (feet, hands)
    • Periorbital edema
    • Pericarditis
    • Acceleration of atherosclerotic vascular disease
    • Congestive heart failure.
  • Respiratory system
    • Dyspnea
    • Tachypnea
    • Kussmual-type respiration
    • Uremic pneumonitis.
  • Gastrointestinal system
    • Ammonia odor to breath
    • Metallic taste
    • Mouth ulceration and bleeding
    • 795Anorexia
    • Nausea and vomiting
    • Inflammation of GI tract
  • Hematologic
    • Anemia
    • Thrombocytopenia.
  • Reproductive system
    • Amenorrhea
    • Testicular atrophy
    • Infertility
    • Decreased libido.
  • Musculoskeletal system
    • Muscle cramp
    • Loss of muscle strength
    • Ostetis fibrosa
    • Osteomalacia.
 
Diagnostic Evaluation
  • Glomerular filtration rate: Decreased glomerular filtration rate is obtaining a 24 hour urinalysis for creatinine clearance. As GFR decreases the value of creatinine clearance decreases and the value of creatinine and BUN increases. Serum creatinine is the most sensitive indicator of the renal function.
  • Sodium and water retention: The kidney cannot concentrate or dilute the urine normally in ESRD. Appropriate response by the kidney to change in daily intake of water and electrolytes, therefore do not occur. Some patient retains sodium and water that increases the risk of edema, heart failure and hypertension. Hypertension may also result from activation of rennin-angiotensin mechanism. Some patients have tendancy to loss salts and run the risk of developing hypotention and hypovolemia.
  • Acidosis: With the advanced renal disease the metabolic acidosis occurs because the kidney cannot excrete increased load of acids. Decreased acid secretion primirly caused by the inability of the kidney tubules to excrete ammonia and to reabsorb sodium bicarbonate. There is also decreased secretion of phosphate and other organic aids.
  • Anemia: Anemia develops as a result of inadequate erythropoietin production, the shortened life span of RBCs, nutritional deficiencies, and the patient tendency to bleed.
  • Calcium and phosphorus imbalance: The serum calcium and phosphorus level have a reciprocal relationship in the body, the one rise the other decreases. With decreases in filtration of GFR the serum phosphorus increases and calcium decreases. The decreased calcium level increased the secretion of parathormone from the parathyroid glands. Uremic disease is also known as osteodystrophy, develops from the complex changes in calcium, phosphate and parathormone balance.
 
Complication
  • Hyperkalemia: Due to decrease excretion, metabolic acidosis, catabolism, and excessive intake.
  • Pericarditis, Pericardial effusion, Pericardial tamponade due to retention of uremic waste products and inadequate dialysis.
  • 796Hypertention due to sodium and water retention and malfunction of rennin angiotensin aldosterone system.
  • Anemia due to decreased erythropoietin production.
  • Bone disease and metastatic calcification due to retention of phosphorus, low serum calcium level.
 
Medical Management
Goal: The goal of management is to maintain the kidney function and homeostasis for as long as possible. The management is divided into three categories:
  1. Pharmacologic therapy
  2. Nutrition therapy
  3. Other therapy.
 
Pharmacologic Therapy
The complication can be prevented by administering antihypertensives, erythropoietin, iron supplement, phosphate binding agent, and calcium supplements.
  • Antacids: Hyperphosphatemia and hypocalcemia are treated with aluminium based antacids that bind dietary phosphorus in the GI tract. Magnesium based antacids must be avoided to prevent magnesium toxicity.
  • Antihypertensive and cardiovascular agents: Hypertension is managed by intravascular volume control and a varity of antihypertensive. Heart failure and pulmonary edema may also require treatment with the fluid restriction, low sodium diet, diuretic agent, Inotropic agent such as digitalis, dobutamine.
  • Antiseizure agents: Neurologic abnormalities can occur. If seizer occur, the onset of seizer is recorded along with the type, duration, general effect on the patient. The physician is notified immediately. Intravenous diazepam or phenytoin is usually administered to control seizure. The side rail of the bed should be padded to protect the patient.
  • Erythropoitin: Anemia associated with renal failure is treated with the recombinant human erythropoietin. It is either administered intravenously or subcutaneously three times a week. It may take 2-6 weeks to rise the hematocrit. The adverse effect of this maybe hypertension, seizure, etc.
 
Nutritional Therapy
The dietary intervention is very necessary for these patients. It includes the careful intake of protein, fluid intake, sodium and potassium intake. At the same time calorie intake and vitamin supplement must be ensured. Calories are supplied by carbohydrates and fat to prevent wasting. Vitamin supplementation is necessary because a protein restricted diet does not provide the necessary complement of vitamin.
797
 
Other Therapy
 
Dialysis
  • Indication: The decision to initiate dialysis or hemofiltration in patients with renal failure depends on several factors. These can be divided into acute or chronic indications.
    • Acidemia from metabolic acidosis in situations in which correction with sodium bicarbonate is impractical or may result in fluid overload
    • Electrolyte abnormality, such as severe hyperkalemia, especially when combined with AKI
    • Intoxication, that is, acute poisoning with a dialyzable substance. These substances can be represented by the mnemonic Slime: salicylic acid, lithium, isopropanol, Magnesium-containing laxatives, and ethylene glycol
    • Overload of fluid not expected to respond to treatment with diuretics
    • Uremia complications, such as pericarditis, encephalopathy, or gastrointestinal bleeding.
  • Chronic indications for dialysis:
    • Symptomatic renal failure
    • Low glomerular filtration rate (GFR) (RRT often recommended to commence at a GFR of less than 10-15 ml/min/1.73 m2). In diabetics, dialysis is started earlier.
    • Difficulty in medically controlling fluid overload, serum potassium, and/or serum phosphorus when the GFR is very low.
 
Nursing Management
Nurse should obtain a complete history of any existing renal disease or family history of renal disease because some kidney disorders have a hereditary basis. Nursing is directed toward assessing fluid status and identifying potential sources of imbalance, implementing a dietary program to ensure proper nutritional intake within the limit of the treatment regimen and promoting positive feelings by encouraging increased self-care and greater independence.
 
Nursing Diagnosis
  • Excess fluid volume related to decreased urine output, dietary excesses, and retention of sodium and water.
  • Imbalance nutrition less than body requirement related to anorexia, nausea, vomiting, dietary restrictions, and altered oral membrane.
  • Fatigue related to anemia, metabolic state and dietary restriction.
  • Activity intolerance related to fatigue, retention of waste products, and dialysis procedure.
  • Grieving related to loss of kidney function as evidenced by expression of feelings of sadness, anger, inadequacy hopelessness.
  • Anxiety related to disease process therapeutic interventions and uncertainty of prognosis.
  • Deficient knowledge regarding condition and treatment.
  • Risk of infection related to suppressed immune system, access sites and malnutrition secondary to dialysis and uremia.
  1. 798Excess fluid volume related to decreased urine output, dietary excesses, and retention of sodium and water
    Interventions
    • Assess fluid status:
      • Daily weight
      • Intake output balance
      • Skin turgor and presence of edema
      • Blood pressure, pulse rate.
    • Limit fluid intake
    • Identify potential sources of fluid:
      • Medications and fluids used to take or administer medications foods.
    • Explain to patient and family rational for fluid restriction.
    • Assist the patient to cope with the discomfort resulting from fluid restriction.
    • Provide or encourage frequent oral hygiene.
  2. Imbalance nutrition less than body requirement related to anorexia, nausea, vomiting, dietary restrictions, and altered oral mucous membranes
    Interventions
    • Assess nutritional status
      • Weight changes
      • Laboratory values (serum electrolyte, BUN, creatinine, protein)
    • Provide patient's food preferences within dietary restrictions
    • Promote intake of high biologic value protein foods eggs, dairy products, meats.
    • Provide written list of foods allowed and suggestions for improving their taste without use of sodium or potassium.
    • Weigh patient daily.
  3. Activity intolerance related to fatigue, anemia, retention of waste products and dialysis procedure
    Interventions
    • Assess factors contributing to activity intolerance:
      • Fatigue
      • Anemia
      • Fluid and electrolyte imbalance
      • Retention of waste products
      • Depression
    • Promote independence in self-care activities as tolerated assist if fatigued
    • Encourage altering activity with rest
    • Encourage patient to rest after dialysis treatment.
799
 
DIALYSIS
Definitions: It is a process used to remove fluid and uremic waste products from the body when kidneys cannot do so.
Or
It refers to the diffusion of solute molecules through a semipermeable membrane, passing form higher concentration to lower concentration.
 
Basic Goals
  • To remove the end products of protein metabolism, such as urea and creatinine, from the blood.
  • To maintain a safe concentration of serum electrolytes.
  • To correct acidosis and replenish the bicarbonate levels of the blood.
  • To remove access fluid from the body.
  • To keep the client alive until a suitable donor is found.
  • To maintain functions until the newly transplanted kidney starts functioning properly.
 
Principles of Dialysis
  • Ultrafiltration: It refers to removal of fluid from blood using either osmotic or hydrostatic pressure to produce the necessary gradient.
  • Diffusion: It is the process of passage of particles from an area of higher concentration to lower concentration occurs through a semipermeable membrane.
  • Osmosis: It is the process of passage of particles from an area of lower concentration to higher concentration occurs through a semipermeable membrane.
Methods include
  • Peritoneal dialysis
    • Intermittent peritoneal dialysis.
    • Intermittent peritoneal dialysis.
    • Continuous ambulatory peritoneal dialysis.
    • Continuous cycling peritoneal dialysis.
    • Automated peritoneal dialysis.
  • Hemodialysis
  • Continuous Renal Replacement Therapies (CRRT).
 
Hemodialysis
It is the process of cleansing the blood of accumulated wastes. It is the most commonly used method of dialysis. It is used for patients who are at ESRF or for acutely ill and require short-term dialysis (days to weeks).
 
Principle
  • Diffusion
  • Osmosis
  • Ultrafilteration.
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Procedure
 
Requirements for Hemodialysis
  • Access to the patient's circulation.
  • Dialysis machine and dialyser with semipermeable membrane.
  • Appropriate dialysate bath.
  • Time—approximately 4 hours, 3 times weekly.
  • Place—dialysis center or home (if feasible).
 
Components to Dialysis
There are three essential components to dialysis:
  • The dialyzer
  • The composition and delivery of the dialysate
  • The blood delivery system.
 
DIALYZER
  • The dialyzer consists of a plastic device with the facility to perfuse blood and dialysate compartments at very high flow rates.
  • There are currently two geometric configurations for dialyzers: hollow fiber and flat plate.
  • These dialyzers are composed of bundles of capillary tubes through which blood circulates while dialysate travels on the outside of the fiber bundle. In contrast, the less frequently utilized flat plate dialyzers are composed of sandwiched sheets of membrane in a parallel plate configuration. The advantage of the hollow fiber dialyser is easier reprocessing of the filter for reuse in future dialysis treatments. Reprocessing and reuse of hemodialyzers are employed for patients on chronic hemodialysis.
801There are four categories of dialysis membranes:
  1. Cellulose
  2. Substituted cellulose
  3. Cellulosynthetic
  4. Synthetic.
 
Dialysate
  • Dialysis in the Treatment of Renal Failure 1665
  • Composition of Commercial Dialysate for Hemodialysis is:
  • Solute Bicarbonate Dialysate
  • Sodium (meq/L) 137–143
  • Potassium (meq/L) 0–4.0
  • Chloride (meq/L) 100–111
  • Calcium (meq/L) 0–3.5
  • Magnesium (meq/L) 0.75–1.5
  • Acetate (meq/L) 2.0–4.5
  • Bicarbonate (meq/L) 30–35
  • Glucose (g/L) 0–0.25.
 
Blood Delivery System
  • The blood delivery system is composed of the extracorporeal circuit in the dialysis machine and the dialysis access. The dialysis machine consists of a blood pump, dialysis solution delivery system, and various safety monitors. The blood pump, using a roller mechanism, moves blood from the access site, through the dialyzer, and back to the patient. The blood flow rate may range from 250 to 500 mL/min.
  • Dialysis Access: The fistula, graft, or catheter through which blood is obtained for hemodialysis is often referred to as a dialysis access. A native fistula created by the anastomosis of an artery to a vein. This facilitates its subsequent use in the placement of large needles (typically 15 gauge) to access the circulation.
 
Methods of Circulatory Access
  • Arteriovenous Fistula (AVF): Creation of a vascular communication by suturing a vein directly to an artery.
    • Usually, radial artery and cephalic vein are anastomosed in nondominant arm
    • After the procedure, the superficial venous system of the arm dilates.
    • By means of two large-bore needle inserted into the dilated venous system, blood maybe obtain and passed through the dialyzer. The arterial end is used for arterial flow and the distal end for reinfusion of dialyzed blood.
    • Healing of AVF requires several weeks; a central vein catheter is used in the interim.
  • Arteriovenous graft: Arteriovenous connection consisting of a tube graft made from autologous saphenous vein or from polytetrafluoroethylene. Ready to use in 2 to 3 weeks.
  • Central vein catheters: Direct cannulation of vein (subclavain, internal jugular, femoral);
  • May be used as temporary or permanent dialysis access.
802
 
Complications of Vascular Access
  • Infection
  • Catheter clotting
  • Central vein thrombosis or stricture
  • Stenosis and thrombosis
  • Ischemia of the hand (steal syndrome)
  • Aneurysm or pseudoaneurysm.
 
LIFESTYLE MANAGEMENT FOR CHRONIC HEMODIALYSIS
  • Dietary management: Restriction or adjustment of protein, sodium, potassium or fluid intake.
  • Protein is restricted to 1 g/kg of body weight.
  • Sodium is restricted to 2–3 g/kg.
  • Fluids are restricted to an amount equal to daily urine output plus 500 ml/day.
  • Potassium is restricted to 1.5–2.5 g/day.
 
Pharmacological Therapy
All medications (Antihypertensives, cardiac glycosides, antibiotics, antiarrhythmic drugs) and their dosage must be carefully evaluated.
 
Peritoneal Dialysis
It is type of dialysis which involves repeated cycles of instilling dialysate into the peritoneal cavity, allowing time for substance exchange an then removing the dialysate.
 
Indications
  • ARF, ESRD and sever cardiovascular disease.
  • To treat overdose of drugs and toxins.
 
Contraindications
  • Hypercatabolism (uremic toxins are not cleared properly because of poor scarred condition of peritoneal membrane)
  • History of ruptured diverticulum
  • Abdominal disease
  • Respiratory disease
  • Peritonitis
  • Abdominal malignancy
  • Abdominal surgery.
 
Types of Peritoneal Dialysis
  • Continuous ambulatory peritoneal dialysis (CAPD): It is a form of intracorporeal dialysis that uses the peritoneum for the semipermeable membrane.
803
 
Procedure
 
Complications
  • Infectious peritonitis
  • Catheter malfunction, obstruction, dialysate leak.
  • Hernia formation
  • Distension
  • Nausea
  • Bleeding at catheter site.
 
Patient Education
  • Use strict technique when performing bag exchanges
  • Perform bag exchange in clean, closed-off area without pets, etc.
  • Inspect bag, tubing for defects and leaks
  • Check weight because therapy cause weight gain.
  • Report signs and symptoms of peritonitis (cloudy peritoneal fluid, abdominal pain or tenderness, malaise and fever).
  • Continues cycle peritoneal dialysis (CCPD): In this type there are usually three cycles at night and one cycle with an 8 hour dwell in the morning. The advantage of this procedure is that the peritoneal catheter is opened only for the on-and-off procedures, which reduces the risk of infection. Another advantage is that the client does not require exchanges at work or school.
  • Intermittent peritoneal dialysis: Dialysis is performed for 10–14 hours, 3–4 times/week.
  • 804Automated peritoneal dialysis: It requires use of a peritoneal cycling machine. This method can be performed as continuous cyclic, intermittent or nightly intermittent peritoneal dialysis.
  • Night intermittent peritoneal dialysis: Dialysis is performed for 8–12 hours each night with no daytime dwells.
 
CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT)
These are various therapies that maybe indicated for the patients who have acute or chronic renal failure. These use extracorporeal blood circulation through a small-volume, low-resistance filter to provide continuous removal of solutes and fluid in intensive care settings.
 
Indications
  • Those who are too clinically unstable for traditional hemodialysis.
  • Renal failure
  • Pulmonary edema
  • Cerebral edema
  • Acute electrolyte disorders—metabolic crisis
  • Septic shock.
 
Types
  • Continuous Arteriovenous Hemofiltration (CAVH): Blood is circulated through a small-volume. Low-resistance filter using the patient's arterial pressure rather than that of the blood pump as is used in hemodialysis. Blood flows from an artery to a hemofilter. After filtration the blood return to body through vein.
  • Continuous Arteriovenous Hemodialysis (CAVHD): It has many of the characteristics of CAVH but offers the advantage of a concentration gradient for faster clearance of urea. This is accomplished by the circulation of the dialysate on one side of a semipermeable membrane.
  • Continuous Venovenous Hemofiltration (CVVH): Here blood from a double-lumen venous catheter is pumped through a hemofilter and returned to the patient through the same catheter. Here the filteration occurs slowly so the hemodynamic effects are mild and better tolerated by patients with unstable conditions.
  • Continuous Arteriovenous Hemodialysis (CVVHD): It is similar to CVVH. Blood is pumped from a double-lumen venous catheter through a hemofilter and returned to the patient through the same catheter. Here concentration gradients are required to remove the uremic toxins. So no arterial access is required.
 
Nursing Management
 
Assessment
  • Assess the client for multiple effects of chronic renal disease on all body systems.
  • Assess the clients understanding of his/her disease condition, diagnostic tests, treatment.
  • Assess the client and family understands about dialysis and diet management.
  • Assess for any sign and symptom of complications.
805
 
Nursing Diagnosis
  1. Altered fluid volume (can be deficient or excess) related to impaired renal functions, fluid shift between dialysate and blood.
    Interventions
    • Monitor fluid volume status by daily weighting
    • Monitor BP regularly
    • Maintain input/output chart
    • Follow the strict diet plan focusing on fluid restrictions.
  2. Imbalanced nutrition less than body requirement related to anorexia and nausea.
    Interventions
    • Assess the clients status for persistent nausea and vomiting
    • Help to stimulate client's appetite
    • Give dietary counselling to the client
    • Involve the client in planning his diet
    • Give written diet plan to client
    • Serve the diet attractively.
  3. Risk for impaired skin integrity related to edema, dry skin and pruritus.
    Interventions
    • Assess the skin condition of the client
    • Assess the pressure site frequently
    • Avoid use of soap
    • Apply moisturizers to prevent dryness
    • Teach the client about foot care, etc.
  4. Risk for infections related to presence on indwelling catheter.
    Interventions
    • Check the vital signs of patient
    • Check the insertion sight of catheter for presence of any redness, etc.
    • Follow strict aseptic techniques
    • Soak the catheter in disinfectant solution if it is needed next time
    • Change the dressings on time.
 
NEPHROTIC SYNDROME
 
Introduction
It is an indication that something is wrong with the kidney function. It is usually caused by damage to the clusters of the small blood vessels in the kidneys that filter waste and excess water from the blood. In nephrotic syndrome, the body excretes more protein in the urine and also results in low blood protein levels, high cholesterol levels, low levels of albumin and high triglyceride levels in the blood which leads to swelling of feet, ankles and sometimes in the face. A person suffering from nephrotic syndrome excretes 20 times more protein in the urine than the healthy person.
 
Definition
Nephrotic syndrome is a kidney disease characterized by:
  • A marked increase in protein in the urine (proteinuria)
  • A decrease of albumin the blood (hypoalbuminemia)
  • 806Edema (swelling, especially around the eyes, feet, and hands)
  • High cholesterol and low density lipoproteins (hyperlipidemia).
 
Etiology
The cause of nephrotic syndrome can be divided in three types:
  1. Primary
  2. Secondary
  3. Congenital
  • Primary cause of nephrotic syndrome is the disease that affects only the kidneys. Diseases like minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, diabetic kidney disease. About 75% of nephrotic syndrome cases result from primary causes.
  • Secondary cause of nephrotic syndrome is diabetes, systemic lupus erythematosus, amyloidosis (abnormal protein called amyloid builds up in tissue and organs), blood clot in kidney vein and heart failure, infection and some medicines that can cause damage of glomeruli. More than 50% of the adult cases of nephrotic syndrome are associated with diabetes as a common secondary cause.
  • Congenitally weak spleen and kidney, or weak physique due to the improper nursing after a chronic disease resulting asthenia of the lung, spleen and kidney and this is supposed to be the internal causes of the nephrotic syndrome.
  • In children, the most common cause of nephrotic syndrome is minimal change disease and in adult it is membranous glomerulo nephritis.
807
 
Pathophysiology
 
Signs and Symptoms
The major manifestation of nephrotic syndrome is edema. It is usually soft and pitting, and is most commonly found around the eyes (periorbital), in dependent areas (sacrum, ankles and hands) and in the abdomen (ascites). Other
  • Massive proteinuria, hyperlipidemia, hypoalbuminenia
  • Foamy appearance of the urine due to excess protein excreted in the urine
  • High blood pressure
  • Weight gain due to excess fluid retention in the body
  • Poor appetite
  • Malaise
  • Headache
  • Irritability
  • Fatigue.
 
Diagnostic Evaluation
  • Urinalysis: Shows microscopic hematuria, urinary casts, large amounts of protein and other abnormalities.
  • Needle biopsy of the kidney: For histological examination of renal tissue to confirm the diagnosis.
  • Blood analysis: Creatinine clearance, BUN, creatine blood test, albumin blood test. Often shows high cholesterol levels and low albumin. BUN and Creatinine may or may not be elevated. If BUN and Creatinine are elevated the patient has renal failure and the prognosis is worse.
 
Complications
Complication of the nephrotic syndrome includes:
  • Infection (due to a deficient immune response)
  • Thromboembolism (especially of the renal vein)
  • Pulmonary emboli
  • ARF (due to hypovolemia)
  • Accelerated atherosclerosis (due to hyperlipidemia).
 
Management
 
Medical Management
  • Keep the patient on bedrest for a few days to promote diuresis, thereby, reducing edema.
  • Low-sodium diet (for severe edema).
  • Prednisone (adrenocorticosteroids)—to reduce proteinuria.
  • Diuretics—for severe edema.
  • ACE inhibitors or angiotensin receptor blockers–to control hypertension.
  • ACE inhibitors may also help decrease the amount of protein loss in the urine.
  • Lipid-lowering agents may result in moderate decreases in serum cholesterol levels.
  • If thrombosis is detected, anticoagulant therapy may necessary for up to 6 months.
808
 
Nursing Management
Assessment
  • Collect the history of the patient.
  • Identify the past medical history of the patient.
  • Assess the pattern of the daily habit: Eating, drinking hygiene patterns etc.
  • Assess the vital signs, weight and height of the patient.
  • Examine the breathing pattern of the patient.
  • Assess the level of the consciousness.
  • Assess the bowel habit of the patient.
  • Assess the frequency, color and amount of the urine.
 
Nursing Diagnosis
  • Risk of fluid overload related to sodium retention.
  • Imbalanced nutrition less than body requirements related to damaged protein metabolism.
  • Ineffective breathing pattern related to suppression of the diaphragm due to ascites.
  • Anxiety related to the deficient knowledge regarding the disease process or hospitalization.
  • Ineffective therapeutic regimen management related to lack of knowledge regarding disease process.
 
Nursing Intervention
  • Balance the body fluid volume
    • Monitor intake and output, and measuring body weight everyday
    • Monitor blood pressure
    • Assessing respiratory status including breath sounds
    • Giving diuretics, as prescribed by physician
    • Measure and record the abdominal girth.
  • Balance the body fluid
    • Monitor intake and output of the patient
    • Monitor vital signs
    • Monitor lab test (electrolytes)
    • Assess the oral mucous membrane and elasticity of the skin turgor.
  • Maintenance of adequate nutritional intake
    • Assess the nutritional status of the patient
    • Assess patient's nutritional dietary pattern
    • Encourage high-calorie, low protein, low-sodium, and low-potassium snacks between meals
    • Weigh patient daily
    • Assess for evidence of inadequate protein intake
    • Edema formation, decreased serum albumin levels.
809
 
Health Education
  • Done kidney functions test regularly as prescribed by doctor.
  • Take all your medicines as prescribed, even after you start to feel better.
  • Make sure your doctor knows about all the medicines, vitamins, or herbal supplements which patient take. This means anything you take with or without a prescription.
  • Cut down on salt. This can reduce the amount of water your body retains.
  • Choose foods low in saturated fat and cholesterol. This can help prevent and reduce high cholesterol.
  • Weight gain may be a sign that you are retaining fluid. Told doctor if patient gaining weight or have other problems, such as trouble breathing.
  • Be gentle with patient skin. Nephrotic syndrome may cause skin to be dry and fragile. It also increases risk of skin infections. So maintain the personal hygiene of the patient.
 
GLOMERULONEPHRITIS
  • Introduction: Immunlogical processes involving the urinary tract predominantly affect the renal glomerulus, the disease process results in glomerulo nephritis. It means inflammation of glomeruli, which affects both kidneys equally. It is a type of kidney disease in which the part of kidney (glomeruli) that helps in filter waste and fluids from blood is damaged.
  • Definition: Glomerulonephritis means inflammation of glomeruli. It is an inflammation of tiny filters of kidney (glomeruli) that helps to remove excess fluid, and waste from bloodstream and pass them into the urine.
  • Types: It is of two types acute glomerulonephritis and chronic glomerulonephritis.
    • Acute glomerulonephritis.
    • Chronic glomerulonephritis.
  • Acute Glomerulonephritis: It means active inflammation in glomeruli. Acute glomerulonephritis is most common in children and young adults, but all ages can be affected.
    • Each kidney is composed of about 1 million filtering screens called glomeruli that remove uremic waste products. The inflammatory process usually begins with the immune system fights off the infection scars tissue forms.
    • There are many diseases that cause an active inflammation within glomeruli. When there is active inflammation occur within the kidney scar tissue may replace normal functional kidney tissue and cause irreversible renal impairment.
  • Etiology: It is caused when there is problem with immune system or diseases like HIV and lupus that affect immune system. Disorders that attack several organs and can cause glomerulonephritis.
    • It occurs after an infection elsewhere in the body or may develop secondary to systemic disorders.
    • An infection with group A streptococci bacteria.
810
 
Pathophysiology
 
Signs and Symptoms
The primary presenting feature of acute glomerulonephritis is hematuria. The urine may be cola, coffee colored because of RBCs and protein plugs.
  • Proteinuria and elevated (BUN) Blood urea and nitrogen and serum creatinine.
Other manifestations:
  • Oliguria
  • Edema, fever
  • Shortness of breath or dyspnea. Possible flank pain
  • Nausea and vomiting
  • Abdominal pain
  • Back pain, fatigue, weight gain
  • Headache, loss of appetite
  • Weakness, fatigue
  • High blood pressure.
 
Diagnostic Evaluation
  • History: Assess and collect history from patient regarding change in pattern of urination frequency, color, or volume
    • Ask patient for signs and symptoms like headache, nausea, vomiting, and loss of appetite.
    • 811Ask for any history of flank pain.
    • Physical examination: In physical examination assess for adequate intake output .
    • Check vital signs.
    • Monitor weight of patient.
    • Assess patient for edema and any signs and symptoms of infection.
  • Urinalysis: For the presence of hematuria. A urinalysis may show red blood cells in urine an indicator of damage to the glomeruli. Urinalysis results may also show white blood cells, a common indicator of infection and inflammation and increased protein which results nephron damage.
  • Check patient BUN and serum creatinine level. There is an increase in BUN and serum creatinine level.
  • Needle biopsy: It reveals obstruction of glomerular capillaries from proliferation of endothelial cells. It is a diagnostic test that involves collecting small pieces of tissue, usually through a needle, for examination with a microscope. In this we collect a sample of kidney tissue, to check any unusual deposits, scarring, or infecting organisms that would explain a person's condition.
 
Management
  • Management includes:
    • Antihypertensive's, to treat high blood pressure and diuretics, they increase the renal blood flow by decreasing renal vascular resistance.
    • Provide antibiotics if infection is still present usually Pencillin. Helps to reduce infection and prevent further spread of infection.
    • Steroids and other medicines that suppress the immune system. Prednisolone and methylprednisolone is useful and most commonly prescribed drug. It can suppress the inflammatory response in kidney and reduce the permeability of renal blood vessels. And reducing the proteinuria.
 
Nutritional Therapy
Dietary protein should be restricted if BUN level is increased.
  • Potassium and sodium should be avoided if edema is present.
  • Dietary protein should be restricted if there is evidence of an increase in nitrogenous wastes.
  • Fluid intake should be restricted.
  • Provide low protein diet to the patient.
  • Provide vegetables, rice, cereals, dried beans, breads.
  • Advise to avoid animal products they are rich source of protein.
  • Eat healthy foods.
  • Get proper rest and sleep.
 
CHRONIC GLOMERULONEPHRITIS
Chronic glomerulonephritis is a kidney disorder caused by slow, cumulative damage and scaring of tiny blood filters in the kidneys. These filters known as glomeruli, remove waste products from the blood.
  • 812In chronic glomerulonephritis, scarring of glomeruli impedes the filtering process, trapping waste products in the blood while allowing red blood cells or protein to escape into the urine, eventually producing the characteristic signs of high blood pressure and swelling in legs and ankles.
  • The disorder may first come to one's attention because of high blood pressure. In other, fluid retention or urine maybe first signs. Long-term inflammation and scarring of the kidneys may lead to kidney failure in severe cases. Damage may progress without symptoms for months or years by the months or year, by the time symptoms appear, the course of the disorder maybe irreversible.
 
Etiology
Specific cause is unknown.
  • Viral infections such as hep B, C, HIV, and AIDS may leads to chronic glomerulonephritis.
  • Autoimmune disorder such as systemic lupus erythematosus, vasculitis may cause chronic glomerulonephritis.
  • Acute glomerulonephritis may after a symptom less period of many years, reappear as chronic glomerulonephritis.
 
Pathophysiology
 
Signs and Symptoms
Patient with severe disease has no symptoms at all for many years. There condition maybe detected when BUN Level and serum creatinine level are detected.
  • Blood or protein in the urine
  • Swelling of legs or ankle and other parts of body due to fluid accumulation (edema).
  • Shortness of breath due to less blood.
  • Headache or blood pressure high.
  • Fatigue, nausea, vomiting, loss of appetite, abdominal pain.
  • 813Nocturia (increased need to urinate at night).
  • Crackles sound in the lungs, poorly nourished, pale skin color.
 
Diagnostic Evaluation
  • History: Collect any history of acute glomerulonephritis if present.
    • Ask patient for the history of urination changes in patient.
    • Ask for the presence of signs and symptoms.
    • Ask patient for history of abdominal pain, etc.
    • Physical examination: Assess patient for edema and swelling, check patient body weight.
    • Monitor patient blood pressure.
  • Urinalysis and blood tests to know about the elevated level of for the presence of hematuria. A urinalysis may show red blood cells in urine an indicator of damage to the glomeruli. Urinalysis results may also show white blood cells, a common indicator of infection and inflammation and increased protein which results nephron damage.
  • A blood test to measure protein and creatinine level. Level of creatinine and protein is elevated.
  • An ultrasound of kidneys maybe performed to evaluate the size of kidneys and any blockages.
  • CT scan or abdominal ultrasound can be performed to show the damage to the glomeruli.
  • Renal biopsy maybe performed, under local anesthesia, to extract a small sample of tissue from kidney, to determine the exact cause and the nature of the glomerulonephritis.
 
Management
  • Antihypertensive drugs (propranol) maybe prescribed to reduce high blood pressure.
  • Diuretics (frusemide) may be prescribed to reduce excess fluid excess fluid retention and increase urine production.
  • Steroid medications, if immunosuppressive drugs (prednisolone and methyl prednisolone), maybe prescribed for some patients. Prednisolone and methylprednisolone are useful and most commonly prescribed drug. It can suppress the inflammatory response in kidney and reduce the permeability of renal blood vessels. And reducing the proteinuria.
  • In severe cases where kidney failure occurs, dialysis maybe necessary. Dialysis performs the function of the kidney by removing waste products and excess fluid from the blood when kidney cannot.
  • A kidney transplant is also an alternative in case of kidney failure. A kidney transplant is a surgical procedure performed to replace a diseased kidney with a healthy kidney from another person.
 
Diet Management
  • Provide low salt diet and provide low protein diet, because it reduces the workload on the kidney.
  • Nuts, dried beans, cereals, vegetables, rice, breads are low in protein.
  • 814Limit the amount of animal products.
  • Take vitamin supplements.
  • Fluid intake should be restricted.
  • Provide adequate diet and fruits.
  • Get proper rest.
  • Take medication regularly.
 
Prevention
  • In prevention it can be prevented by limit the salts, fluids, protein.
  • Control blood pressure, controlling high blood pressure is the most important part of treatment.
  • Maintain good hygiene practices.
  • Practicing safe sex helps in preventing the viral infection such as HIV infection and hepatitis which leads to this illness.
  • Take calcium supplements.
 
Nursing Management
 
Nursing Assessment
  • Observe patient for changes in fluid and electrolyte status and for the signs and symptoms.
  • Monitor vital signs of patient blood pressure.
  • Anxiety levels are often extremely high for both the patient and family.
  • Throughout the course of disease and treatment, the nurse should gives emotional support by providing opportunities for the patient and family to verbalize their concerns, have their questions answered, and explore their options.
 
Nursing Diagnosis
  • Ineffective renal tissue perfusion related to damage of glomerular infiltration.
  • Excess fluid volume related to compromised renal function.
  • Imbalanced nutrition less than body requirement less than body requirements related to anorexia, nausea, vomiting.
  • Deficient knowledge regarding condition and treatment.
  • Activity intolerance related to fatigue, retention of waste products.
  1. Excess fluid volume related to compromised renal function, decreased urine output, retention of sodium and water.
    Interventions
    • Assess the fluid status of patient.
    • Check weight daily and record.
    • Maintain intake output chart.
    • Monitor vital signs.
    • Limit fluid intake to the patient.
    • Explain the rationale for restriction of fluid.
    • 815Assist patient to cope up with the discomforts results from fluid restriction.
    • Provide and encourage oral hygiene, it minimizes the dryness of oral membranes.
  2. Imbalanced nutrition pattern less than body requirements related to anorexia, nausea, vomiting.
    Interventions
    • Assess the nutritional status of the patient.
    • Monitor weight of patient daily and record it.
    • Assess the patient nutritional dietary patterns- diet history, food preferences.
    • Provide patients food preference within dietary restrictions.
    • Provide, low salt and protein diet.
    • Restrict fluids rich diet to the patient.
    • Provide adequate diet to patient.
    • Encourage for proper rest.
    • Provide pleasant surroundings at the meal time.
  3. Deficient knowledge related to disease condition and treatment
    Interventions
    • Assess the understanding of patient regarding disease condition and treatment.
    • Provide explanation regarding renal function and consequences of disturbed renal function at the level of patient understanding and guided by patient's readiness to learn.
    • Assist patient to identify ways to incorporate changes related to illness and its treatment into lifestyle.
    • Provide oral and written information as appropriate about: renal function, fluid and dietary restrictions.
    • Clear all the doubts of the patient.
    • Provide psychological support to the patient.
 
NEPHROLITHIASISX
Nephrolithiasis also called the renal calculi, are hard, usually small stones that form somewhere in the renal structure. The stones are masses of crystals and protein that form when the urine became supersaturated with a salt capable of forming solid crystals.
Symptoms occur when the stone become impacted in the urinary tract. When stones are found in the kidneys, the condition is called nephrolithiasis.
 
Etiology
  • Hypercalcemia and hypercalciuria caused by hyperparathyroidism
  • Chronic dehydration, poor fluid intake and immobility
  • Chronic infection with urea-splitting bacteria (proteus vulgaris)
  • Chronic obstruction with stasis of urine, foreign bodies within the urinary tract.
 
Risk Factors
  • Metabolic: Abnormalities that result in increased urine levels of calcium, oxaluric acid, uric acid, or citric acid.
  • 816Climate: Warm climate that cause increased fluid loss, low urine volume and increased solute concentration in the urine.
  • Diet
    • Large intake of dietary proteins that increases uric acid excretion
    • Excessive amounts of tea or fruit juices that elevate urinary oxalate level
    • Large intake of calcium and oxalate
    • Low fluid intake that increases urinary concentration.
  • Genetic factors: Family history of stone formation, cystinuria, gout, or renal acidosis
  • Lifestyle: Sedentary occupation, immobility.
 
Pathophysiology
 
Types
  • Calcium oxalate, calcium phosphate, or mixture.
    • Incidence: 90%
    • Feature: Account for two-third of stones. Small, rough, and hard. Shaped like needles. Colors vary from gray to white.
    • Possible causes:
    • Excessive calcium. Excessive urea. Hyperparathyroidism, Cushing's disease, immobility, etc.
    • Predisposing factors: Idiopathic hypercalciuria, hyperoxaluria, independent of urinary pH, family history.
  • Struvite—magnesium ammonium phosphate
    • Incidence: x 2%
    • Features: Second most common type of stone. Calculi crumble easily. Stones have a yellow color.
    • Causes: Infection by urea splitting microbes, usually Proteus. May cause abscess formation in the kidney.
    • Predisposing factors: Urinary tract infection.
  • Uric acid stones
    • Incidence: 2%
    • Features: Dye enhancement needed for x-ray visualization. Small, hard and color varies from yellow to red.
    • 817Causes: Gout, high uric acid levels, decreased fluid intake.
    • Predisposing factors: Gout, acid urine, inherited condition.
  • Cystine stones:
    • Incidence: Rare.
    • Feature: Small, smooth calculi, waxy stones.
    • Causes: Cystine-containing crystals appear in the urine.
    • Predisposing factors: Acid urine.
 
Signs and Symptoms
  • Costovertebral angle pain
  • Groin pain
  • Renal colic because renal stones produce an increase in hydrostatic pressure and distention of the renal pelvis and proximal ureters causing renal colic. Pain relief is immediate after stone passage.
  • Flank pain radiating to genitalia
  • Hematuria
  • Anuria
  • Restlessness
  • Pallor
  • Temperature
  • Nausea vomiting, diarrhoea, abdominal discomfort due to renointestinal reflexes.
 
Diagnostic Evaluation
  • History collection
  • Physical examination
  • Kidney radiography may show stone
  • IVP (intravenous pyelogram), retrograde pyelogram is used to localize the degree and site of obstruction or to confirm the presence of a radiolucent stones, such as a uric acid or Cystine calculus.
  • Urinalysis: May indicate gross or microscopic hematuria and could indicate abrasion of the urinary tract.
  • Ultrasonography can be used to identify a radiopaque or radiolucent calculus in the renal pelvis, calyx, or proximal ureters. But it is less useful when attempting to locate stones trapped in the midureter.
  • A CT scan may be used to differentiate a nonopaque stone from the tumor.
  • Lab test: Serum calcium, phosphorus, sodium, potassium, bicarbonate, uric acid, BUN and Creatinine levels are also measured.
 
Management
 
Medical Management
  • The goals of management are to eradicate the stone, determine the stone type, prevent nephrons destruction, control infection, and relieve any obstruction that may be present.
  • 818The immediate objective of treatment of renal colic is to relieve the pain until its cause can be eliminated.
  • Opioid analgesic agents are administered to prevent shock and syncope that may result from the excruciating pain.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in treating renal stone pain because they provide specific pain relief. They also inhibit the synthesis of prostaglandin E, reducing swelling and facilitating passage of the stone.
  • Hot baths or moist heat to the flank areas may also be helpful.
 
Nutritional Therapy
  • Nutritional therapy plays an important role in preventing renal stones.
  • Fluid intake is the mainstay of most medical therapy for renal stones.
  • Patient with renal stones should drink eight to ten ounce glasses of water daily or have IV fluids prescribed to keep the urine dilute.
  • A urine output exceeding 2 L/day is advisable.
 
International Procedures
If the stone does not pass spontaneously if complications occur, common interventions include endoscopic or other procedure. For example:
  • Ureteroscopy
  • Extracorporeal shock wave lithotripsy (ESWL)
  • Endourologic (percutaneous) stone removal.
Ureteroscopy
  • It involves first visualizing the stone and then destroying it.
  • In this inserting an ureteroscope into the ureter and then inserting a laser, electrohydraulic lithotripter, or ultrasound device through the ureteroscope to fragment and remove the stones.
Extracorporeal shock wave lithotripsy
  • It is used for most symptomatic, nonpassable upper urinary stones. Electromagnetically generated shock waves are focused over the area of the renal stone.
  • The high energy dry shock waves pass through the skin and fragment the stone.
Endourologic (Percutaneous) stone removal
  • It is used to treat the larger stones.
  • A percutaneous tract is formed and a nephroscope is inserted through it. Then the stone extracted or pulverized.
Electrohydraulic lithotripsy
  • It is a similar method in which an electrical discharge is used to create a hydraulic shock wave to break up the stone.
  • A probe is passed through the cystoscope and the tip of lithotripter is placed near the stone.
  • This procedure is performed under topical anesthesia.
  • The most common complications are hemorrhage, infection and urinary extravasations.
819Chemolysis
  • Stone dissolution using infusions of chemical solutions (e.g. alkylating agents, acidifying agents).
 
Surgical Management
  • Today surgery is performed in only 1 to 2% of patients. It is indicated if the stone does not respond to other forms of treatment.
  • If the stone is in kidney, the surgery performed maybe a nephrolithotomy (incision into the kidney with removal of the stone) or a nephrectomy, if the kidney is nonfunctional secondary to infection.
  • Stones in the kidney pelvis are removed by a pyelolithotomy.
 
Complication
  • Obstruction: From remaining stone fragments.
  • Infection: From dissemination of infected stone particles or bacteria resulting from obstruction.
  • Impaired renal function: From prolonged obstruction before treatment and removal.
  • Perirenal hematoma: From bleeding around the kidney caused by trauma of shock waves or laser treatments.
 
Nursing Management
 
Nursing Assessment
  • Obtain history focusing on family history of calculi, episodes of dehydration, prolonged immobility, UTI, dietary, bleeding history, and medication history.
  • Assess pain location and radiation; assess level of pain using a scale of 1 to 10. Observe for presence of associated symptoms: nausea, vomiting, diarrhoea, abdominal distension.
  • Monitor for signs and symptoms of UTI, such as chills, fever, Dysuria, frequency. Examine urine for hematuria.
  • Observe for signs and symptoms of obstruction, such as frequent urination of small amounts, oliguria, anuria.
 
Nursing Diagnosis
  • Acute pain related to the presence of, obstruction or movement of a stone with in urinary system.
  • Impaired urinary elimination related to blockage of urine flow by stones.
  • Risk for infection related to obstruction of urine flow and instrumentation during treatment.
  • Anxiety related to hospitalization.
  • Fear related to deficient knowledge regarding the disease.
  • Deficient knowledge related to lack of knowledge about prevention of recurrence, diet and symptoms of renal calculi.
  1. 820Acute pain related to the presence of obstruction or movement of a stone with in urinary system
    Interventions
    • Ask severity, location, and duration of pain using a pain scale. Pain is typically in the flank or Costovertebral angle and may radiate to the pelvic, groin, or abdominal area.
    • Encourage fluid intake, unless contraindicated, to promote the passage of stone, dilute the urine, and reduce the risk of further stone formation.
    • Administer pain medication as ordered to promote comfort.
    • Apply heat to flank pain area to reduce pain and promote comfort.
  2. Impaired urinary elimination related to blockage of urine flow by stones
    Interventions
    • Monitor total urine output and pattern of voiding. Report Oliguria or Anuria.
    • For outpatient treatment, patient may use a coffee filter to strain urine.
    • Help patient to walk, if possible because ambulation may help move the stone through the urinary tract.
    • Teach patient to drink eight ounces of liquid with meals, between meals and in early evening to provide fluids for hydration but not to an excess that may increase renal colic.
  3. Risk for infection related to obstruction of urine flow and instrumentation during treatment
    Interventions
    • Administer parenteral or oral antibiotics, as prescribed during treatment, and monitor for adverse effects.
    • Assess urine for color, cloudiness, and odor.
    • Obtain vital signs, and monitor for fever and symptoms of impending sepsis (tachycardia, hypotension).
 
Health Education
  • Encourage fluids to accelerate passing of stone particles.
  • Teach about analgesics that still maybe necessary for colicky pain, which may accompany passage of stone debris.
  • Warn that some blood may appear in urine for several weeks.
  • Encourage frequent walking to assist in passage of stone fragments.
  • Teach patient to strain urine through a coffee filter or stone strainer and to save for analysis.
  • Teach patient to take alpha-adrenergic blockers to help dilate ureters, thus improve stone passage.
 
BENIGN PROSTATIC HYPERPLASIA (BPH)
  • Introduction: Benign prostatic hyperplasia is also called BPH is a condition in men in which the prostate glands becomes enlarged and not cancerous. It is also called benign prostate hypertrophy or benign prostatic obstruction.
    • The prostrate goes through two main growth periods as a man ages. The first occurs early in puberty when the male prostate doubles in size. The second phase 821of growth begins around age 25 years and continues during most of a man's life. It often occurs with the second growth phase. As the prostate enlarges the gland presses against and pinches the urethra.
    • The bladder wall become thicker eventually the bladder may weaken and lose the ability to empty completely, leaving some urine in bladder, narrowing of urethra and inability to empty the bladder completely causes many problems associated with benign prostate hyperplasia.
Benign prostate hyperplasia means it is an enlargement of the prostate gland resulting from increase in number of epithelial cells and stromal tissue. It is probably a normal part of the aging process in men, caused by changes in hormones balance and in cell growth.
 
Etiology
The cause of benign prostrate hyperplasia is not understood, however it occurs mainly in older men.
  • Throughout their lives men produce testosterone male hormone, and small amount of estrogen, female hormone. As men age the amount of active testosterone in their blood decreases, which leaves a higher proportion of estrogen. So that estrogen within the prostrate increases the activity of substances that promote prostate cell growth.
  • Some risk factors: Age 40 years and older.
  • Family history of benign prostatic hyperplasia.
  • Medical conditions such as Obesity, lack of physical exercise.
  • Erectile dysfunction.
 
Pathophysiology
 
Signs and Symptoms
Symptoms of BPH patient result from urinary obstruction. Symptoms fall into two groups:
  1. Obstructive Symptoms: Caused by prostate enlargement include a decrease in the caliber and force of urine, difficulty in initiating voiding, dribbling at the end of urine.
    • Weak and interrupted urine stream, smelly urine. These symptoms due to urinary retention.
  2. 822Irritative Symptoms
    • It includes urinary frequency, urgency, dysuria, bladder pain, nocturia
    • Incontinence are associated with inflammation or infection.
 
Diagnostic Evaluation
  • History: Take personal and family history. Ask the client about the symptoms that is present, when symptoms began, ask about any history of UTI ask about general medical history.
  • Physical examination: Examine patient for discharge from urethra.
  • Enlarged or tender lymph nodes in groin.
  • Swelling or tenderness in scrotum.
  • Urine analysis: Examination of a urine sample under a microscope is performed in all patients who are having lower urinary tract symptoms. It can indicate the signs of infection in urine.
  • Prostate specific antigen blood test: Prostate cells create a protein called PSA. Men with prostate cancer, prostate infection, in case of BPH may have a higher amount of PSA in their blood.
  • Uroflowmetry: It is a test that helps to know that how well the bladder and urethra store and release urine. It also helps to know about the urethral blockage.
  • Cystourethroscopy: It is a procedure allowing internal visualization of the urethra and bladder, used to see any blockage in urinary tract.
  • Trans rectal ultrasound: It is used to examine the prostate and shows any abnormalities in prostate
  • Biopsy: It is a procedure that involves taking a small piece of prostate tissue for examination with a microscope, used to diagnose cancer of prostate.
 
Management
Collaborative care: The goals of collaborative care is to restore bladder drainage, relieve the patient's symptoms, and to prevent or treat the complications.
  • Management of BPH includes: Men with mildly enlarged prostate need no treatment, unless their symptoms affecting their quality of life.
    • Pharmacological management: Medications is used to shrink or stop the growth of prostate and reduce symptoms.
      • Drugs used 5-reductase inhibitors
      • Alpha-adrenergic receptors blockers
      • Phosphodiesterase-5 inhibitors
      • Combinations medication.
    • Combination therapy: Combination therapy using both types of drugs has been shown to be more effective in reducing symptoms than using one drug alone, combination includes: Finasteride and doxazosin.
      • Dutasteride and tamsulosin.
      • Alpha blockers and antimuscarinics for patient with overactive bladder symptoms, means where bladder muscles contract uncontrollably and cause urinary frequency, and incontinence.
      • 823Alpha-adrenergic blockers: These are most widely prescribed drugs for patient with BPH who is experiencing mild symptoms without presence of other complications. It includes drugs doxazosin, terazosin, tamsulosin, alfuzosin.
      • 5-alpha reductase inhibitors: Used to reduce and shrink the size of prostate gland. Drugs finasteride, dutasteride.
      • Phosphodiesterase-5 inhibitors: Used to reduce the lower urinary tract symptoms by relaxing smooth muscles in lower urinary tract.
    • Intensive management: It is indicated when there is decrease in urine flow, urinary retention because of obstruction.
      • Transurethral resection of prostate: In this rectoscope is inserted through urethra into prostate and cut pieces of enlarged prostate. It also treats the blockage of urethra.
      • Transurethral incision of prostate: Used to widen the urethra by making a small cuts in prostate and in the bladder neck.
      • Open prostatectomy: In this procedure a cut or incision is make through the skin to reach the prostate. Urologist removes all parts of prostate through the incision. It is done when prostate is greatly enlarged, complications occur or bladder is damaged and needs repair.
    • Lifestyle changes:
      • Reducing intake of liquids, particularly before going out or before sleep periods.
      • Avoiding or reducing intake of caffeine, alcohol. Because these substances make the body to get rid of water.
      • Avoiding and monitoring the use of medications such as diuretics.
      • Training the bladder to hold more urine for longer periods of time.
      • Exercising pelvic floor muscles.
      • Preventing or treating constipation.
      • Eat healthy and adequate diet.
 
Prevention
  • Urinate as much as possible, relax for few moments and then urinate again.
  • Relax before urinate.
  • Take plenty of time to urinate. Do not take stress about symptoms.
  • Do not limit fluid intake because client is dehydrated, which can further leads to other problems.
  • Empty the bladder before bedtime.
  • Take adequate diet.
 
Diet Management
  • Eat fruits and vegetables daily.
  • Limit the consumption of red meat because it is high in fat.
  • Advice to take egg, fish, beans rich in protein.
  • Eat slowly and do not eat when stomach is full.
  • 824Avoid caffeine, because it is a diuretic and it increases the urine output.
  • Avoid spicy food.
 
Nursing Management
 
Nursing Assessment
  • Assess the condition of client.
  • Monitor vital signs of patient and record.
  • Maintain intake output chart.
  • Monitor daily weight and record.
  • If patient is having urinary retention then insert catheter.
  • Obtain urine culture if UTIs suspected.
  • Prepare patient for diagnostic tests and surgery as appropriate.
 
Nursing Diagnosis
  • Acute pain related to bladder distension secondary to enlarged prostate.
  • Urinary retention related to urethral obstruction and loss of bladder tone due to prolonged distension/retention.
  • 825Anxiety related to concern and lack of knowledge about the diagnosis, treatment plan and prognosis.
  • Deficient knowledge related to disease condition, urinary difficulties, and treatment modalities.
  • Disturbed sleeping pattern related to the bladder pain, urinary urgency.
1. Acute pain related to bladder distension secondary to enlarged prostate
Interventions
  • Assess the level, location, intensity of pain by using pain relating scale.
  • Avoid the activities that increase the pain.
  • Provide comfortable bed, position to the patient.
  • Initiate bowel to prevent constipation.
  • Provide opioid analgesics to constipation as prescribed by doctor.
  • Administer analgesics as prescribed by doctor.
2. Urinary retention related to urethral obstruction secondary to prostatic enlargement and loss of bladder tone due to prolonged distension/retention.
Interventions
  • Assess the patient usual pattern of urinary function.
  • Assess for sign of urinary retention, amount and frequency of urination, urgency and discomfort.
  • Initiate measures to treat retention; encourage assuming normal position for voiding.
  • Administer cholinergic agent as prescribed by doctor, helps to stimulate bladder contraction.
  • Monitor the effect of medication.
3. Anxiety related to concern and lack of knowledge about the diagnosis, treatment and prognosis.
Interventions
  • Obtain the history to determine the patients concerns.
  • Ask questions regarding disease to check his understanding and knowledge of his health problem.
  • Provide education about diagnosis and treatment.
  • Allow the patient to ask questions.
  • Provide psychological support to the patient.
  • Answer all the questions asked by the patient.
  • Provide comfortable environment.
 
Preoperative Care if Patient is Having Surgery
  • Urinary drainage must be restored before surgery. Prostatic obstruction results into acute retention or inability to void.
  • A urethral catheter such as coude (curved tip) catheter maybe needed to restore drainage.
  • If there is any infection treat before surgery.
  • All type of prostate surgery results into some degree of retrograde ejaculation.
  • Patient should be informed that the ejaculate maybe decreased in amount or totally absent.
  • Postoperative care
  • After surgery patient may will have catheter. Bladder irrigation is done to remove clotted blood from bladder and ensure drainage of urine.
  • Careful septic technique should be maintained when irrigating the bladder because bacteria can easily enter into urinary tract.
  • Blood clots are expected after surgery for the first 24–36 hours.
  • If large amount of bright red color is present in urine it indicates hemorrhage.
  • Activity that increases abdominal pressure such as walking for long periods should be avoided.
  • Sphincter tone maybe poor after catheter removal that results in continence so educate about kegel exercises, pelvic floor muscle technique.
  • Patient should be observed for signs of infection.
  • Dietary intervention stool softeners should be given to prevent from straining while bowel movements.
 
Complications
  • Urinary retention: Client can feel sudden inability to urinate.
  • Urinary tract infection: Inability to empty the bladder can increase the risk of infection in urinary tract .
  • Bladder stones: It can caused by an inability to completely empty the bladder. Bladder stones can cause infection, bladder irritation, and obstruction in urine flow.
  • Kidney damage: Pressure in the bladder from urinary retention can directly damage the kidneys or allow bladder infection to reach the kidneys.
826
BIBLIOGRAPHY
  1. Black JM, Howks JH. Medical surgical nursing. South Asia, 8th ed. 822–34.
  1. Brunner, Sidharth. Textbook of medical surgical nursing, 12th ed. Vol. 2, Wolters Kluwer;  1317–8.
  1. Brunner, Sidharth. Textbook of medical surgical nursing. Lippincott William and Wilkins.  10th ed. 1285–300.
  1. Burkart JM. Peritoneal dialysis in Brenner and Rector's The Kidney. Saunders,  2004. 7th ed. 233–45.
  1. Chintamani. Lewis's medical surgical nursing, Elsevier.  1179–80.
  1. Chintamani. Lewis's medical surgical nursing. 7th ed. Elsevier Limited;  New Delhi:  2010. 1207–21.
  1. Hauser K. Longo B. Jameson F. Harrison's principle of internal medicine. McGraw Hill. 2005.16th ed. 1663–70.
  1. Manahan S. Phipps' medical surgical nursing, 8th ed. Elsevier.  970–2.
  1. Smeltzer CS, Brunner Bare B, Suddarth's textbook of medical surgical nursing. 10th ed. Lippincott Publishers;  Philadelphia (PA):  2006. 1326–35.
  1. Suddarth B. Medical surgical nursing. SAE.  12th ed. 1320–34.
  1. Wilkins. w. Manual of nursing practice. JP.  ed .8th.771–775
  1. Williams L. Medical surgical nursing F.A. Davis.  2nd ed. 601–4.
  1. Wilson R. Anatomy and physiology evolve. 10th ed. 335–7.

Integumentary Disorders16

 
INTRODUCTION TO SKIN
The skin is far more than just the outer covering of human beings, it is an organ just like the heart, lung, or liver. Besides providing a layer of protection from pathogens, physical abrasions, and radiation from the sun, the skin serves many functions. It plays a vital role in homeostasis by maintaining a constant body temperature via the act of sweating or shivering and by making you aware of external stimuli through information 828perceived within the touch receptors located within the integumentary system. It only takes one visit to a burn unit to see the value of skin and the many complications that arise when this organ is compromised.
Fig. 16.1: The skin
The skin, or integument, is considered an organ because it consists of all four tissue types. The skin also consists of accessory organs, such as glands, hair, and nails, thus making up the integumentary system.
 
Functions of Skin
The skin performs a variety of functions:
  • Protection is provided against biological invasion, physical damage, and ultraviolet radiation.
  • Sensation is provided by nerve endings for touch, pain, and heat.
  • Thermoregulation is supported through the sweating and regulation of blood flow through the skin.
  • Synthesis of vitamin D occurs in the skin.
  • Blood within the skin can be shunted to other parts of the body when needed.
  • Excretion of salts and small amounts of wastes (ammonia and urea) occurs with the production of sweat.
 
PEMPHIGUS
  • Pemphigus vulgaris is a rare autoimmune disease that causes painful blistering on the skin and the mucous membranes that is characterized by the location where the blisters form. Pemphigus vulgaris affects the mucous membranes of mouth, throat, nose, eyes, genitals, and lungs. This disease usually starts with blisters in the mouth and then on the skin.
Fig. 16.2: Pemphigus
 
Etiology
Autoimmunity: The immune system produces proteins called antibodies. Antibodies normally attack harmful foreign substances such as bacteria and viruses. Pemphigus vulgaris 829occurs when the immune system mistakenly makes antibodies against proteins in healthy skin and mucous membranes. The antibodies breakdown the bonds between the cells, and fluid collects between the layers of the skin. This leads to blisters and erosions on the skin. The precise cause of the attack by the immune system is not known.
 
Signs and Symptoms
The signs and symptoms of pemphigus is depending on the type:
  • Pemphigus vulgaris: The most common form of pemphigus vulgaris usually begins with blisters in mouth, which then erupt on skin. Blisters can also break out on the mucous membranes of genitals. The blisters typically are painful, but do not itch. Blisters in mouth or throat may make it hard to swallow and to eat.
  • Pemphigus foliaceus: This type does not usually affect mucous membranes. The blisters, which usually begin on face and scalp and later erupt on chest and back, usually are not painful. They tend to be crusty and itchy.
  • Pemphigus Vegetans: The blisters appear on the groin and under the arms and on the feet.
  • Paraneoplastic Pemphigus: A very rare type of pemphigus that occurs in people with some cancers is called paraneoplastic pemphigus. The blisters and sores may appear in the mouth, on the lips, and on the skin. This type may also cause scars on the eyelids and eyes and lung problems.
 
Diagnostic Evaluation
The diagnosis may not be clear at first. There are other causes of mouth ulcers and skin blisters. Tests are usually done to confirm the diagnosis. These include:
  • Biopsy: A small sample of skin may be taken. This is looked at under the microscope and tested to confirm that the blisters are due to Pemphigus vulgaris.
  • Blood test for antibodies: This uses methods called immunofluorescence or ELISA to measure the level of the antibody that causes Pemphigus.
 
Management
  • Steroids: The usual treatment is to take steroid tablets such as prednisolone. Steroids reduce inflammation (redness and soreness) and suppress the immune system. A high dose is usually needed at first and this may be given by injection. Steroid treatment can work fairly quickly. Symptoms may start to improve within a few days. New blisters may stop in 2–3 weeks and old blisters may heal in 6–8 weeks.
  • Immunosuppressant: An immunosuppressant medicine may be advised. Example, cyclophosphamide, azathioprine, ciclosporin, methotrexate or mycophenolate mofetil. Immunosuppressants usually take longer to work than steroids (about 4-6 weeks).
  • Skin and mouth treatments (topical treatments):
    • A steroid cream is sometimes used on the skin blisters in addition to other treatments. This may keep the dose of steroid tablets lower than would otherwise be needed. Steroid mouthwashes or sprays may be used to help treat mouth blisters and erosions.
    • Mouthwashes containing antiseptic or local anesthetic can also help.
    • Wound care treatments such as dressings help raw areas to heal.
    • 830Compresses or soaks using saline (sterile salt water) or certain antiseptics may be advised if there are large areas of raw skin. This is to reduce the chance of infection and to stop raw skin from becoming too dry.
    • Patient may be advised to protect the skin and mouth from roughness as much as possible. For example, avoid contact sports; eat soft bland food, and use cream or ointment to protect skin from friction.
    • Antifungal medication helps if thrush infects the mouth, throat or gullet area.
 
Other Treatments
Plasmapheresis, intravenous immunoglobulin and rituximab (a monoclonal antibody) may be tried if patient does not respond to high doses of steroids. Sometimes they may also be tried in combination with steroid tablets.
 
PSORIASIS
Psoriasis is a chronic, autoimmune skin disease characterized by red patches on the skin, often accompanied by silvery-white scales of dead skin cells. It is not contagious.
 
Etiology
  • Skin infections
  • Injury to the skin, such as a cut or scrape, bug bite, or a severe sunburn
  • Stress
  • Cold weather
  • Smoking
  • Heavy alcohol consumption
  • Certain medications including lithium, which is prescribed for bipolar disorder; high blood pressure medications such as beta blockers; antimalarial drugs; and iodides.
 
Signs and Symptoms
Psoriasis signs and symptoms can vary from person to person but may include one or more of the following:
  • Red patches of skin covered with silvery scales
  • Small scaling spots
  • Dry, cracked skin that may bleed
  • Itching, burning or soreness
  • Thickened, pitted or ridged nails
  • Swollen and stiff joints
Psoriasis patches can range from a few spots of dandruff-like scaling to major eruptions that cover large areas. Most types of psoriasis go through cycles, flaring for a few weeks or months, then subsiding for a time or even going into complete remission.
 
Types of Psoriasis
  • Plaque psoriasis: The most common form, plaque psoriasis causes dry, raised, red skin lesions (plaques) covered with silvery scales. The plaques itch or may be painful and can occur anywhere on body, including genitals and the soft tissue inside mouth.
  • 831Nail psoriasis: Psoriasis can affect fingernails and toenails, causing pitting, abnormal nail growth and discoloration. Psoriatic nails may become loose and separate from the nail bed (onycholysis). Severe cases may cause the nail to crumble.
  • Scalp psoriasis: Psoriasis on the scalp appears as red, itchy areas with silvery-white scales. The red or scaly areas often extend beyond the hairline. Dead skin in hair or on shoulders, especially after scratching scalp.
  • Guttate psoriasis: This primarily affects young adults and children. It is usually triggered by a bacterial infection. It is marked by small, water-drop-shaped sores on trunk, arms, legs and scalp. The sores are covered by a fine scale and are not as thick as typical plaques are.
  • Inverse psoriasis: Mainly affecting the skin in the armpits, in the groin, under the breasts and around the genitals, inverse psoriasis causes smooth patches of red, inflamed skin. It is worsened by friction and sweating. Fungal infections may trigger this type of psoriasis.
  • Pustular psoriasis: This uncommon form of psoriasis can occur in widespread patches (generalized pustular psoriasis) or in smaller areas on hands, feet or fingertips. It generally develops quickly, with pus-filled blisters appearing just hours after skin becomes red and tender. The blisters may come and go frequently. Generalized pustular psoriasis can also cause fever, chills, severe itching and diarrhea.
  • Erythrodermic psoriasis: The least common type of psoriasis, erythrodermic psoriasis can cover entire body with a red, peeling rash that can itch or burn intensely.
  • Psoriatic arthritis: In addition to inflamed, scaly skin, psoriatic arthritis causes pitted, discolored nails and the swollen, painful joints that are typical of arthritis. Symptoms range from mild to severe and psoriatic arthritis can affect any joint.
 
Risk Factors
Anyone can develop psoriasis, but these factors can increase risk of developing the disease:
  • Family history: Perhaps the most significant risk factor for psoriasis is having a family history of the disease. Having one parent with psoriasis increases risk of getting the disease, and having two parents with psoriasis increases risk even more.
  • Viral and bacterial infections: People with HIV are more likely to develop psoriasis than people with healthy immune systems. Children and young adults with recurring infections.
  • Stress: Because stress can impact immune system, high stress levels may increase risk of psoriasis.
  • Obesity: Excess weight increases the risk of psoriasis. Plaques associated with all types of psoriasis often develop in skin creases and folds.
  • Smoking: Smoking tobacco not only increases risk of psoriasis but also may increase the severity of the disease. Smoking may also play a role in the initial development of the disease.
 
Diagnostic Evaluation
  • Physical exam and medical history: Usually can diagnose psoriasis by taking medical history and examining skin, scalp and nails.
  • Skin biopsy: A small sample of skin (biopsy) that is examined under a microscope to determine the exact type of psoriasis and to rule out other disorders.
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Management
Psoriasis treatments aim to:
  • Stop the skin cells from growing so quickly, which reduces inflammation and plaque formation
  • Remove scales and smooth the skin.
Psoriasis treatments can be divided into three main types: topical treatments, light therapy and oral or injected medications.
 
Topical Treatments
  • Topical corticosteroids: These powerful anti-inflammatory drugs are the most frequently prescribed medications for treating mild to moderate psoriasis. They slow cell turnover by suppressing the immune system, which reduces inflammation and relieves associated itching. Topical corticosteroids range in strength, from mild to very strong.
  • Vitamin D analogous: These synthetic forms of vitamin D slow down the growth of skin cells. Calcipotriene is a prescription cream or solution containing a vitamin D analog that may be used alone to treat mild to moderate psoriasis or in combination with other topical medications or phototherapy.
  • Anthralin: This medication is believed to normalize DNA activity in skin cells. Anthralin also can remove scale, making the skin smoother.
  • Topical retinoids: These are commonly used to treat acne and sun-damaged skin.
  • Calcineurin inhibitors: Calcineurin inhibitors, tacrolimus and pimecrolimus, are approved only for the treatment of atopic dermatitis. Calcineurin inhibitors are thought to disrupt the activation of T cells, which, in turn, reduces inflammation and plaque build-up.
  • Salicylic acid: Available over-the-counter, salicylic acid promotes sloughing of dead skin cells and reduces scaling. Sometimes it is combined with other medications, such as topical corticosteroids or coal tar, to increase its effectiveness. Salicylic acid is available in medicated shampoos and scalp solutions to treat scalp psoriasis.
  • Coal tar: A thick, black byproduct of the manufacture of petroleum products and coal, coal tar is probably the oldest treatment for psoriasis. It reduces scaling, itching and inflammation.
  • Moisturizers: Moisturizing creams would not heal psoriasis, but they can reduce itching and scaling and can help combat the dryness that results from other therapies.
 
Light therapy (Phototherapy)
  • Sunlight: Ultraviolet (UV) light is a wavelength of light in a range too short for the human eye to see. When exposed to UV rays in sunlight or artificial light, the activated T cells in the skin die. This slows skin cell turnover and reduces scaling and inflammation.
  • UV phototherapy: Controlled doses of UV light from an artificial light source may improve mild to moderate psoriasis symptoms. UV phototherapy, also called broadband UV, can be used to treat single patches, widespread psoriasis.
  • Narrow band UV therapy: A newer type of psoriasis treatment, narrow band UV therapy may be more effective than broadband UV treatment. It is usually administered two or three times a week until the skin improves, then maintenance may require only weekly sessions.
  • 833Goeckerman therapy: Combination of UV treatment and coal tar treatment, which is known as Goeckerman treatment. The two therapies together are more effective than either alone because coal tar makes skin more receptive to UV light.
  • Photochemotherapy or psoralen plus ultraviolet A (PUVA): Photochemotherapy involves taking a light-sensitizing medication (psoralen) before exposure to UVA light. UVA light penetrates deeper into the skin, and psoralen makes the skin more responsive to UVA exposure. This more aggressive treatment consistently improves skin and is often used for more-severe cases of psoriasis. PUVA involves two or three treatments a week for a prescribed number of weeks. Short-term side effects include nausea, headache, burning and itching. Long-term side effects include dry and wrinkled skin, freckles, and increased risk of skin cancer, including melanoma, the most serious form of skin cancer.
  • Excimer laser: This form of light therapy, used for mild to moderate psoriasis, treats only the involved skin. A controlled beam of UV light of a specific wavelength is directed to the psoriasis plaques to control scaling and inflammation.
 
Oral or Injected Medications
  • Retinoids: Related to vitamin A, this group of drugs may reduce the production of skin cells. Signs and symptoms usually return once therapy is discontinued, however. Side effects may include lip inflammation and hair loss. And because retinoids such as acitretin can cause severe birth defects, women must avoid pregnancy for at least three years after taking the medication.
  • Methotrexate: Taken orally, Methotrexate helps psoriasis by decreasing the production of skin cells and suppressing inflammation. It may also slow the progression of psoriatic arthritis in some people. Methotrexate is generally well-tolerated in low doses but may cause upset stomach, loss of appetite and fatigue. When used for long periods, it can cause a number of serious side effects, including severe liver damage and decreased production of red and white blood cells and platelets.
  • Cyclosporine: Cyclosporine suppresses the immune system and is similar to methotrexate in effectiveness.
  • Drugs that alter the immune system (biologics): Several immunomodulator drugs are approved for the treatment of moderate to severe psoriasis. They include etanercept, infliximab, adalimumab and ustekinumab. These drugs are given by intravenous infusion, intramuscular injection or subcutaneous injection and are usually used for people who have failed to respond to traditional therapy or who have associated psoriatic arthritis.
  • Other medications: Thioguanine and hydroxyurea are medications that can be used when other drugs cannot be given.
 
Complications
  • Psoriatic arthritis: This complication of psoriasis can cause joint damage and a loss of function in some joints.
  • Eye conditions: Certain eye disorders—such as conjunctivitis, blepharitis and uveitis are more common in people with psoriasis.
  • Obesity: The inflammation linked to obesity may play a role in the development of psoriasis. Or it may be that people with psoriasis are more likely to gain weight, possibly because they are less active because of their psoriasis.
  • 834Type 2 diabetes: The risk of type 2 diabetes is upped in people with psoriasis. The more severe the psoriasis, the greater the likelihood of type 2 diabetes.
  • High blood pressure: The odds of having high blood pressure are higher for people with psoriasis.
  • Cardiovascular disease: For people with psoriasis, the risk of heart attack is almost three times greater than for those without the disease. The risk of irregular heartbeats and stroke is also higher in those with psoriasis. This could be due to excess inflammation or to an increased risk of obesity and other risk factors for cardiovascular disease.
  • Metabolic syndrome: This is a cluster of conditions—including high blood pressure, elevated insulin levels and abnormal cholesterol levels.
  • Other autoimmune diseases: Celiac disease, sclerosis and the inflammatory bowel disease called Crohn's disease are more likely to strike people with psoriasis.
  • Parkinson's disease: This chronic neurological condition is more likely to occur in people with psoriasis.
  • Kidney disease: Moderate to severe psoriasis has been linked to a higher risk of kidney disease.
 
Nursing Management
 
Nursing Interventions
  • Administer antimicrobial agents if ordered to treat cutaneous infections
  • Apply topical corticosteroids if ordered to treat inflammatory skin conditions
  • Cleanse infected lesions with antibacterial or antifungal solutions if ordered
  • Assist and prepare client for procedures such as cryotherapy, electrocautery, curettage, incision and drainage, phototherapy, and radiation that may be performed to remove or reduce the size of cutaneous lesion
  • Assist client to turn at least every 2 hours
  • Position client properly, use pressure-reducing or pressure-relieving devices (e.g. pillows, gel or foam cushions, alternating pressure mattress, air-fluidized bed) if indicated
  • Gently massage around reddened areas at least every 2 hours
  • Apply a thin layer of a dry lubricant such as powder or cornstarch to bottom sheet or skin and to opposing skin surfaces (e.g. axillae, beneath breasts) if indicated to reduce friction
  • Lift and move client carefully using a turn sheet and adequate assistance, perform actions to keep client from sliding down in bed (e.g. gatch knees slightly when head of bed is elevated 30° or higher, limit length of time client is in semi-Fowler's position to 30-minute intervals) in order to reduce the risk of skin surface abrasion and shearing.
  • Keep client's skin clean
  • Keep bedlinens dry and wrinkle-free
  • Thoroughly dry skin after bathing and as often as needed, paying special attention to skin folds and opposing skin surfaces (e.g. axillae, perineum); pat skin dry rather than rub
  • Provide elbow and heel protectors if indicated
  • Increase activity as allowed and tolerated
  • Perform actions to maintain an adequate nutritional status
  • 835Implement measures to relieve pruritus (e.g. use a mild soap for bathing, add cornstarch or baking soda to bath water, and administer prescribed antihistamines)
  • Keep nails trimmed and apply mittens if necessary
  • Instruct client to apply firm pressure to pruritic areas rather than scratching
  • Apply a protective covering such as a hydrocolloid or transparent membrane dressing to areas of the skin susceptible to breakdown (e.g. coccyx, elbows, and heels).
 
DERMATITIS (ECZEMA)
  • Dermatitis is inflammation of the skin characterized by red and itchy skin with some acute attacks causing crusty scales or blisters that ooze fluid.
 
Etiology
This depends on the type of dermatitis:
  • Contact dermatitis: Contact dermatitis typically causes the skin to develop a pink or red rash, which usually itches. Contact dermatitis may be irritant or allergic. Common chemical irritants include detergents, soaps, some synthetic fibers, nail polish remover, anti-perspirants, and formaldehyde. Some plants, in particular primula, chrysanthemums, daffodils and tulips, irritate some people. Wearing rubber gloves, or nickel or cobalt in jewelry can cause contact allergic dermatitis if the person is allergic to these substances. Both types of contact dermatitis may be caused by cosmetics, perfumes, hair dyes, and skin-care products.
  • Nummular dermatitis: Nummular dermatitis consists of distinctive coin-shaped red plaques that are most commonly seen on the legs, hands, arms, and torso. It is more common in men than women and the peak age of onset is between 55 and 65. Living in a dry environment or having very hot showers can cause this condition.
  • Atopic dermatitis: Atopic dermatitis, or eczema, causes the skin to itch, scale, swell, and sometimes blister. This type of eczema usually runs in families and is often associated with allergies, asthma, and stress.
  • Seborrheic dermatitis: Seborrheic dermatitis consists of greasy, yellowish, or reddish scaling on the scalp and other hairy areas, as well as on the face or genitals, and in skin creases along the nose and under the breasts. This condition is called cradle cap in infants and is likely to be related to maternal hormonal changes affecting the sebaceous glands.
  • Stasis dermatitis: Stasis dermatitis is caused by poor circulation and can happen in people with varicose veins, congestive heart failure, or other conditions. Veins in the lower legs fail to return blood efficiently, causing pooling of blood and fluid build-up and edema. This leads to irritation, especially round the ankles.
 
Signs and Symptoms
Dry, reddish, itchy skin indicates some kind of dermatitis, or skin inflammation, of which there are many types:
  • A red rash that is limited to the area of skin exposed to an irritant is probably contact dermatitis.
  • Red, itchy, circular patches of weeping, scaly, or encrusted skin suggest nummular dermatitis, common in older people who have dry skin or live in dry environments.
  • 836Greasy, yellowish scales on the scalp and eyebrows, behind the ears, and around the nose indicate Seborrheic dermatitis, in infants it is called cradle cap.
  • Scaling, sometimes ulcerated skin appearing inside the lower legs and around the ankles, may indicate stasis dermatitis.
  • Extreme, persistent itchiness may signal atopic dermatitis (eczema). Very often, however, itchiness results simply from dry skin.
 
Diagnostic Evaluation
  • Identifying allergens and irritants
  • Patch testing: The best way to test for a reaction to allergens is by patch testing. During a patch test, tiny amounts of known allergens are applied to the skin. The substances are attached the back using a special kind of nonallergic tape. Sometimes, they may be attached to the upper arms. After two days, the patches are removed and the skin is assessed to check if there has been any reaction. Skin will usually also be examined after four to six days as most allergic contact dermatitis reactions will take this long to develop.
  • Open application testing: Open application testing is used to assess potential irritants. In an open patch test, the substance is applied to the skin of forearm or inner elbow and left uncovered, and then the skin will initially be checked for a reaction and again after a few days.
 
Management
There are several ways to treat contact dermatitis, including:
  • Avoiding the cause
  • Emollients
  • Topical corticosteroids
  • Oral corticosteroids
  • Avoiding the cause: One of the most important steps in treating contact dermatitis is identifying and avoiding the allergens or irritants.
    Diet: The allergen nickel may rarely cause some cases of contact dermatitis. This is a trace element found in foods such as lentils, nuts and oats. There is limited evidence that people who are sensitive to nickel might benefit from following a diet low in nickel.
  • Emollients: Emollients are substances that help soften and smooth skin to keep it supple and moist.
As contact dermatitis can cause skin to be dry and cracked, it is important to keep it moisturized to prevent it from becoming further irritated. Emollients prevent water being lost from the outer layer of the skin and add water to the skin. They act as a protective barrier to keep the moisture in and the irritants out.
To apply the emollient:
  • Use a large amount
  • Smooth the emollient into the skin in the same direction that the hair grows
  • Do not rub the emollient in
  • For very dry skin, apply the emollient every three to four hours
  • 837After a bath or shower, gently dry the skin and then immediately apply the emollient while the skin is still moist
  • Do not share emollients with other people
  • Topical corticosteroids: Corticosteroids are any type of medication that contains steroids, a type of hormone. Hormones are groups of powerful chemicals that have a wide range of effects on the body. It will reduce the inflammation of the skin, e.g. hydrocortisone, prednisolone, etc.
Treatments from a dermatologist could include:
  • Phototherapy, where contact dermatitis is exposed to ultraviolet (UV) light—this may be ultraviolet A or ultraviolet B, and may also involve a medicine containing psoralen, which makes skin more sensitive to light
  • Steroid-sparing immunosuppressant therapy—Immunosuppressant medicines suppress immune system, e.g. cyclophosphamide, methotrexate.
 
Nursing Management
 
Nursing Diagnosis
  1. Impaired skin integrity related to inflammation, contact with irritants or allergens.
    Intervention
    • Assess skin, noting color, moisture, texture, temperature; note erythema.
    • Assess skin, noting color, moisture, texture, temperature; note erythema, edema, tenderness.
    • Identify signs of itching and scratching
    • Encourage the patient to adopt skin care routines to decrease skin irritation
    • Bath or shower using lukewarm water and mild soap or nonsoap cleansers
    • After bathing, allow the skin to air dry or gently pat the skin dry. Avoid rubbing or brisk drying
    • After bathing, allow the skin to air dry or gently pat the skin dry. Avoid rubbing or brisk drying.
    • After bathing, allow the skin to air dry or gently pat the skin dry. Avoid rubbing or brisk drying.
    • Apply topical lubricants immediately after bathing.
    • Apply topical immunomodulator: Tacrolimus, Pimecrolimus
    • Prepare the patient for phototherapy or photochemotherapy.
  2. Disturbed body image related to visible skin lesions.
    Interventions
    • Assess the patient's perception of changed appearance
    • Assess the patient's behavior related to appearance
    • Assist the patient in articulating responses to questions from others regarding lesions and contagion.
    • Allow patients to verbalize feelings regarding their skin condition.
    • Assist patients in identifying ways to enhance their appearance, clothing, cosmetics, and accessories may direct attention away from the skin lesions
  3. 838Risk for infection related to severe inflammation excoriation.
    Interventions
    • Assess skin for severity of skin integrity compromise
    • Apply topical antibiotics
    • Administer oral antibiotics
    • Encourage the patient to use appropriate hygiene methods.
 
CELLULITIS
Cellulitis is an infection of the skin and the tissues just below the skin surface. Any area of the skin can be affected but the leg is the most common site. Cellulitis is an infection of the deep layer of skin (dermis) and the layer of fat and tissues just under the skin (the subcutaneous tissues). Erysipelas is an infection of the skin which is nearer to the skin surface (more superficial) than cellulitis.
Fig. 16.3: Cellulitis
 
Etiology and Risk Factors
The skin is a good barrier against infection. Any break in the skin from a cut, skin ulcer, injection, athlete's foot, scratch, etc, is a way in which bacteria can get into and under the skin. Cellulitis is a common problem. It can affect anyone. For example:
  • Athlete's foot
  • Skin abrasions (cuts)
  • Swollen legs or are overweight
  • Previous episode of cellulitis
  • Poor immune system
  • Poorly controlled diabetes
  • An intravenous drug user
  • An insect bite
  • Skin problems such as eczema.
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Signs and Symptoms
  • The lower part of the leg is the most common site for cellulitis to develop. However, cellulitis can affect any area of the skin. Affected skin feels warm, may look swollen, and looks red and inflamed.
  • The infected area may spread and is usually tender. Sometimes blisters occur on the skin.
  • The nearest glands may swell and become tender. This is because they are fighting off the infection to stop it spreading to other parts of the body. For example, the glands in the groin may swell during cellulitis of the leg.
  • Patient may feel unwell and have a fever. Indeed, the first symptom is often to feel feverish and shivery for up to 24 hours before any changes to the skin appear.
  • With erysipelas, the face or a leg is commonly affected. If erysipelas affects the face, infection has often travelled from the nasal passages from a recent infection of the nasal passages. On the face, infection typically spreads from the nose area across both cheeks. Infection elsewhere produces similar symptoms to cellulitis.
 
Management
There are several ways to treat contact dermatitis, including:
  • Avoiding the cause
  • Emollients
  • Topical corticosteroids
  • Oral corticosteroids
  • Maintain personal hygiene
 
Nursing Interventions
  • Assess skin, noting color, moisture, texture, temperature; note erythema.
  • Assess skin, noting color, moisture, texture, temperature; note erythema, edema, tenderness.
  • Identify signs of itching and scratching
  • Encourage the patient to adopt skin care routines to decrease skin irritation
  • Bath or shower using lukewarm water and mild soap or nonsoap cleansers
  • After bathing, allow the skin to air dry or gently pat the skin dry. Avoid rubbing or brisk drying
  • After bathing, allow the skin to air dry or gently pat the skin dry. Avoid rubbing or brisk drying.
  • After bathing, allow the skin to air dry or gently pat the skin dry. Avoid rubbing or brisk drying.
  • Apply topical lubricants immediately after bathing.
 
ACNE
Acne is a very common skin condition which affects most people at some stage in their life. Acne spots can be blackheads and whiteheads (called comedones) characterized by, papules and pustules, nodules and cysts. Acne can be mild or the spots can be inflamed and filled with pus.
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Etiology
  • Puberty
  • Hormonal changes
  • Excessive use of oily and fatty food
  • Stress
  • Poor personal hygiene
  • Manipulating acne lesions
  • Clothing (for example, hats and sports helmets) and headgear
  • Air pollution and certain weather conditions, especially high humidity
  • Fluctuating hormone levels around the time of periods in women.
 
Signs and Symptoms
  • Whiteheads (closed plugged pores)
  • Blackheads (open plugged pores—the oil turns brown when it is exposed to air)
  • Small red, tender bumps (papules)
  • Pimples (pustules), which are papules with pus at their tips
  • Large, solid, painful lumps beneath the surface of the skin (nodules)
  • Painful, pus-filled lumps beneath the surface of the skin (cystic lesions).
 
Nursing Care
  • Teach good skin care
  • Wash skin with mild soap and water twice a day
  • Do not use astringents
  • Avoid vigorous scrubbing
  • Praise good habits
  • Advise the adolescent to wash hair with antiseborrheic shampoo, avoid oil-based cosmetics or lotions
  • Encourage a balanced diet, adequate fluids, exercise, and adequate rest
  • Encourage the adolescent to keep a diary of health and diet habits
  • Educate the adolescent about medications (action, side effects, dosage, method of application)
  • Encourage application of tretinoin at night
  • Encourage use of nonoil sunscreens of at least SPF 15
  • Educate the adolescent about time needed for response and importance of daily compliance.
 
Management
  • Only wash areas of the skin affected by acne twice a day. Too frequent washing may irritate the skin making the symptoms worse.
  • Use a mild soap or cleanser and lukewarm water. Water that's too hot or cold water can make acne worse.
  • Do not squeeze the spots or try to clean out blackheads. This can make things worse or lead to scars.
  • 841Do not use too much make-up or cosmetics.
  • Remove all make-up before bed.
  • Use a water-based emollient that is fragrance-free for any dry skin.
  • Shower after a workout or exercise to stop sweat irritating acne.
  • Regular hair washing and keeping hair off the face can also help.
 
Medical Management
  • Benzoyl peroxide: This cream or gel helps prevent dead skin blocking follicles and kills bacteria on the skin. This treatment may have side-effects, including dry skin, burning, itching, redness and extra sensitivity to sunlight.
  • Topical retinoids: Treatments such as tretinoin cream or gels reduce the production of fatty secretions called sebum and stop dead skin cells blocking hair follicles.
  • Azelaic acid: This cream or gel may be used to remove dead skin and bacteria if benzoyl peroxide or topical retinoids cause troubling side-effects.
  • Antibiotics: Either applied to the skin (clindamycin, erythromycin), or taken as tablets (tetracycline and its derivatives) control surface bacteria, which aggravate and often foster acne. Antibiotics are more effective when combined with benzoyl peroxide or retinoids.
 
SHINGLES (VARICELLA-ZOSTER)
The varicella-zoster virus is responsible for causing chickenpox and shingles. Both chickenpox and shingles, herpes zoster, are characterized by an outbreak of rash or blisters on the skin. People who have had chickenpox in the past are at risk of developing shingles because the virus remains inactive in certain nerve cells of the body and can become active later in life.
 
Etiology and Risk Factors
  • Weak immune system (such as people with cancer or HIV)
  • Age over 50
  • Chronic ill patient
  • Trauma
  • Are under significant stress
 
Signs and Symptoms
  • Pain that is itching, stabbing or shooting
  • Tingling feeling in or under the skin, which is red in the affected area
  • High temperature, chills, and headache.
 
Diagnostic Evaluation
  • Physical examination of rashes
  • Swab of the fluid.
Fig. 16.4: Shingles
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Management
There is no cure for shingles, but treatments for the condition can help ease the associated pain and discomfort. Treatments can also help the healing of blisters and rash.
  • Antiviral medication such as aciclovir, famciclovir and valaciclovir can ease discomfort and reduce the duration of symptoms.
  • Painkillers can also offer relief. Over-the-counter paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen can be effective in relieving mild pain.
 
SCABIES
Scabies is a contagious and itchy skin condition caused by microscopic mites (Sarciotes scabiei) that burrow into the skin. An allergic reaction and rash usually appear within a few weeks of the mite burrowing into the skin.
Fig. 16.5: Scabies
 
Etiology
Scabies mites, called Sarciotes scabiei, can be picked up through having sex, close contact with another person or sharing bedding, clothes or towels.
 
Signs and Symptoms
  • The primary symptom of scabies is severe itching which is often so bad that it keeps people awake at night.
  • Small red bumps (resembling tiny bites or pimples) can form on the skin.
  • The most common areas for scabies to develop on the body are warmer sites such as skin folds, areas where clothing is tight, near the belt line or buttocks, on the penis, and around the breasts.
  • Excessive scratching may lead to bacterial infections of the skin in people who have scabies.
 
Diagnostic Evaluation
A skin scraping may be taken to look for mites, eggs, or mite faecal matter to confirm the diagnosis.
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Management
  • Scabies is treated with a lotion or cream that is applied to the body.
  • The person with scabies should put on clean clothes.
  • All clothing, bedding, and towels used by the person in the preceding 24 hours should be washed in hot water and dried in a hot dryer.
  • Seven days after the first treatment, a second treatment of the body with the same treatment is usually necessary.
  • Medication may be prescribed to relieve itching such as corticosteroid topical drugs, emollients and cleansing lotion for sensitive skin.
 
COLD SORE
  • Cold sores are common and painful blisters around the lips and mouth caused by the herpes simplex virus. The blisters will eventually break and ooze before crusting over and clearing up on their own after around seven to 10 days.
 
Etiology
  • Cold sores are usually caused by the herpes simplex virus (HSV) type 1, which is transmitted by such forms of contact as kissing an infected person or sharing eating utensils, towels or razors.
  • Genital herpes is usually caused by herpes simplex virus type 2 but can also be caused by HSV type 1.
  • Sores may develop as late as 20 days after exposure to the virus. Once the virus enters the body, it may emerge years later at or near the original site of entry. About two days before an attack patient may experience itching or sensitivity at the site.
  • The virus may be triggered by certain foods, stress, fever, colds, allergies, sunburn and menstruation.
 
Signs and Symptoms
  • Fluid-filled blisters or red, painful sores on or near the mouth.
  • Swollen, sensitive gums of a deep red color.
  • A fever, flu-like symptoms and swollen lymph nodes in the neck often accompanying the first attack.
  • Tingling and itching in the affected area.
 
Management
  • Avoiding spicy or acidic foods, applying ice and using over-the-counter remedies.
  • Look for medicines that contain numbing agents such as phenol and emollients to reduce cracking and soften scabs.
  • Over-the-counter topical remedies can be used to help speed healing and minimize pain from a cold sore. Antiviral cream such as acyclovir which may reduce the length of the outbreak.
  • If cold sore is especially painful or irritating, an anesthetic gel to alleviate pain or an antiviral oral medication is prescribed to help speed healing or prevent recurrence.
  • 844Wash hands after touching a cold sore.
  • Do not rub eyes after touching cold sore.
  • Do not touch genitals after touching cold sore.
  • Replace your toothbrush.
  • Do not kiss someone who has a cold sore or use the same utensils, towels or razors.
  • Use sunscreen to the face and lips before exposure to the sun.
 
IMPETIGO
  • Impetigo is a highly contagious bacterial skin infection characterized blisters and sores. Impetigo mainly affects children, often on the face, especially around the nose and mouth, and sometimes on the arms or legs.
 
Etiology
  • The most common cause of impetigo is Staphylococcus aureus. However, another bacterial cause is the group A streptococcus. These bacteria lurk everywhere. It is easier for a child with an open wound or fresh scratch to contract impetigo.
  • Other skin-related problems, such as eczema, body lice, insect bites, fungal or bacterial infections, and various forms of dermatitis can make a person susceptible to impetigo.
  • Most people get this highly infectious disease through physical contact with someone who has it, or from sharing the same clothes, bedding, towels, or other objects. The very nature of childhood, which includes much physical contact and large-group activities, makes children the primary victims and carriers of impetigo.
  • In extreme cases, the infection invades a deeper layer of skin and develops into ecthyma, a deeper form of the disease. Ecthyma forms small, pus-filled ulcers with a crust much darker and thicker than that of ordinary impetigo. Ecthyma can be very itchy, and scratching the irritated area spreads the infection quickly. The gravest potential complication of impetigo is poststreptococcal glomerulonephritis.
Fig. 16.6: Impetigo
 
Signs and Symptoms
  • Symptom may varies on the basis of type of impetigo:
  • The two types of impetigo are: Bullous impetigo and nonbullous impetigo.
    1. Bullous impetigo causes large fluid-filled blisters that are painless.
    2. Nonbullous impetigo is the more contagious form of the condition causing sores that burst leaving a yellow-brown crust.
845Other signs are:
  • A small patch of blisters that after a few hours break into red, moist areas that ooze or weep fluid, appears mainly on the face, but also on exposed areas of the arms and legs.
  • In a few days, the formation of a golden or dark-yellow crust resembling grains of brown sugar occurs.
 
Management
  • The key to treating and preventing of impetigo is good personal hygiene and a clean environment. Once the infection occurs, prompt attention will keep it under control and prevent its spread.
  • Even if only one family member has impetigo, everyone in the household should follow the same hygiene regime.
  • Regular washing with soap and water can clear up mild forms.
  • A topical antibiotic cream is highly successful in treating routine cases.
  • Do not try over-the-counter antibacterial ointments they are too weak to kill the bacteria responsible, and applying the ointment carelessly may actually spread the impetigo.
  • If one have only a few small impetigo sores, simply bathing them regularly with soap and warm water.
  • Anyone in a household who develops impetigo should use a clean towel each time they wash. Do not share towels or sheets with infected people.
  • Always wash those towels and sheets separately. Toys should also be washed where possible.
  • Wash hands often particularly after touching infected skin.
  • Children should stay off school or nursery until sores have dried up and crusted over, or until 48 hours after commencing treatment.
 
WARTS
Warts are skin growths, that are usually fairly small and rough, and are caused by the human papillomavirus. HPV causes an excess amount of keratin that stimulates rapid growth of cells on the skin's outer layer.
Fig. 16.7: Warts
846
 
Types of Warts
  • Plantar warts: This type of wart usually appears as flesh-colored or light brown lumps that are flecked with small clotted blood vessels that appear as tiny black dots. Plantar warts appear on the soles of the feet.
  • Genital warts: Genital warts can appear in the pubic area, on the genitals, in the anus, and in the vagina.
  • Flat warts: This type of wart is more common in teens and children than in adults. Flat warts are smoother and smaller than other warts and they generally occur on the face. Flat warts also can appear on the legs, especially among females.
 
Management
In most cases, warts found on the skin are harmless and can disappear without treatment. Treatments may include:
  • Freezing (cryotherapy): A liquid nitrogen is used to freeze the wart. This helps to kill the cells of the wart.
  • Salicylic acid: The acid ‘burns’ off the top layer of the wart. Every few days the dead tissue can be rubbed away with emery paper, so the wart is removed bit by bit.
  • Minor surgery: When warts cannot be removed by other therapies, surgery may be used to cut away the wart. The base of the wart will be destroyed using an electric needle or by cryosurgery.
  • Laser surgery: This procedure uses an intense beam of light to burn and destroy wart tissue. It may be used for warts that are difficult to treat.
 
ALOPECIA
  • Alopecia simply means ‘hair loss’. It is the medical term for hair loss and there are numerous forms of alopecia.
  • Alopecia is the partial or complete loss of hair, especially on the scalp, either in patches (alopecia areata), on the entire head (alopecia totalis), or over the entire body (alopecia universalis).
 
Etiology
Etiology of alopecia is based on its type:
  • Alopecia Totalis
  • Alopecia Universalis
  • Androgenetic Alopecia
 
Alopecia Totalis
Alopecia Totalis is thought to be an autoimmune disorder that causes loss of all head hair. Unlike androgenetic alopecia (male or female pattern baldness), there are no remaining patches or areas with hair on the scalp once alopecia totalis has run its course.
847
 
Alopecia Universalis
Alopecia universalis is the term used to describe rapid loss of hair all over the body. It includes head hair, eyebrows, and even eyelashes. It is the most severe form of hair loss and is believed to be an autoimmune disorder.
 
Androgenetic Alopecia
Androgenetic alopecia is the most common type of hair loss. It is also referred to as male or female pattern hair loss. Heredity and hormones are the two major factors that can cause this type of hair loss. Androgenetic alopecia causes more than 95% of hair loss in men. Women are greatly affected by it as well, due to contributing factors like ovarian cysts, high androgen index birth control pills, pregnancy, and menopause.
 
Diagnostic Evaluation
  • Because hair loss is caused by a variety of conditions, a physician diagnoses the cause of the child's hair loss based on medical history, family history of hair loss, medications (including vitamins), nutritional status, hair-care habits, and a physical examination.
  • If the physician suspects a fungal infection of the scalp, a hair sample may be tested by microscopic examination in the laboratory. Microscopic examination of a hair plucked at the periphery of the hair loss area often reveals a characteristic disruption of the integrity of the hair shaft. The infection may be confirmed by culturing the scalp for fungal organisms.
  • Blood tests or a scalp biopsy may be required if a medical condition—such as lupus erythematosus, thyroid dysfunction, iron deficiency, or hormonal imbalance is suspected.
 
Treatment
Alopecia cannot be cured, however, it can be treated and hair can grow back. In many cases, alopecia is treated with drugs that are used for other conditions. Treatment options for alopecia include:
  • Corticosteroids: Anti-inflammatory drugs that are prescribed for autoimmune diseases. Corticosteroids can be given as an injection into the scalp or other areas, orally, or applied topically as an ointment, cream, or foam.
  • Topical contact allergens or sensitizers: This type of therapy may be used if the hair loss is widespread or if it recurs. The inflammation that the treatments cause may promote hair re growth. Another name for this treatment is topical immunotherapy.
  • Rogaine (minoxidil): This topical drug is already used as a treatment for pattern baldness. It usually takes about 12 weeks of treatment with Rogaine before hair begins to grow.
 
Nursing Management
  • Explain that alopecia and physiologic hair loss are usually only temporary and self-limiting.
  • For alopecia due to chemotherapy, assure the client that the hair will eventually grow back a few months after the treatment.
  • Encourage the client to verbalize his fears and body-image concerns regarding alopecia, especially if the client is a teenager or a young adult.
  • 848For females, encourage them to change their hairstyle or to wear head pieces or beautiful head scarfs until their hair grows back.
  • Counsel male patients on the slow and limited effects of minoxidil and stress that when treatment is stopped, the effects are reversed.
  • Encourage to eat a well-balanced diet, especially rich in protein and iron to promote hair growth.

Occupational Health Hazards17

 
OCCUPATIONAL HEALTH DISORDERS
Occupational disease, any illness associated with a particular occupation or industry. Such diseases result from a variety of biological, chemical, physical, and psychological factors that are present in the work environment or are otherwise encountered in the course of employment. Occupational nursing is concerned with the effect of all kinds of work on health and the effect of health on a worker's ability and efficiency and its treatment.
 
Effects of Occupational Health Disorders
Occupational diseases are essentially preventable and can be ascribed to faulty working conditions. The control of occupational health hazards decreases the incidence of work-related diseases and accidents and improves the health and morale of the work force, leading to decreased absenteeism and increased worker efficiency. In most cases the moral and economic benefits far outweigh the costs of eliminating occupational hazards.
 
TYPES OF OCCUPATIONAL AND INDUSTRIAL DISORDERS
 
Disorders Due to Chemical Agents
Hazardous chemicals can act directly on the skin, resulting in local irritation or an allergic reaction, or they may be absorbed through the skin, ingested, or inhaled. In the workplace ingestion of toxic chemicals is usually accidental and most commonly results from handling contaminated food, drink, or cigarettes. Substances that occur as gases, vapors, aerosols, and dusts are the most difficult to control, and most hazardous chemicals are therefore absorbed through the respiratory tract. If inhaled, airborne contaminants act as irritants to the respiratory tract or as systemic poisons. Toxicity in such cases depends on the contaminant's 850concentration, particle size, and physicochemical properties, particularly its solubility in body fluids. An individual's reaction to any hazard depends primarily on the length, pattern, and concentration of exposure but is also affected by such factors as age, sex, ethnic group, genetic background, nutritional status, and coexistent disease, concomitant exposure to other toxic agents, lifestyle, and history of previous exposure to the agent in question. The wide range of both naturally occurring and synthetic chemical compounds that can give rise to adverse health effects can be roughly organized into four major categories: gases, metals, organic compounds, and dusts.
 
Gases
  • Gases may act as local irritants to inflame mucous surfaces. Common examples include sulfur dioxide, chlorine, and fluorine, which have pungent odors and can severely irritate the eyes and the respiratory tract. Some gases, such as nitrogen oxides and phosgene, are much more insidious. Victims may be unaware of the danger of exposure because the immediate effects of these gases may be mild and overlooked. Several hours after exposure, however, breathlessness and fatal cardiorespiratory failure due to pulmonary edema may develop.
  • Gases that interfere with oxygen supply to the tissues are known as asphyxiates. Simple asphyxiants are physiologically inert gases that act by diluting atmospheric oxygen. If the concentration of such gases is high enough, hypoxia may develop. Victims of mild hypoxia may appear to be intoxicated and may even resist rescue attempts. Common examples of simple asphyxiants are methane and carbon dioxide.
  • In contrast to simple asphyxiants, chemical asphyxiants, such as carbon monoxide and hydrogen sulfide, are highly reactive. They cause a chemical action that either prevents the blood from transporting oxygen to the tissues or interferes with oxygenation in the tissues. For example, carbon monoxide, a frequently encountered gas produced by incomplete combustion, combines with hemoglobin in the blood and reduces its oxygen-carrying capacity. In low concentration carbon monoxide poisoning can cause symptoms of fatigue, headache, nausea, and vomiting, but heavy exposure leads to coma and death. It is especially dangerous because it is both colorless and odorless. Hydrogen sulfide, acts by inhibiting the respiratory enzyme cytochrome oxidase, thus giving rise to severe tissue hypoxia. In addition to its asphyxiant properties, hydrogen sulfide also acts as an irritant to the eyes and mucous membranes.
 
Prevention
Preventing gas poisoning involves preventing exposure. Workers should never enter enclosed spaces that have suspect atmospheres alone, workplaces should provide adequate ventilation, and air should be regularly tested for contamination. If exposure does occur, treatment involves the removal of the victim from the contaminated atmosphere, artificial respiration, and administration of oxygen or recommended antidotes. Victims exposed to gases with insidious delayed effects should be kept under medical observation for an appropriate period.
 
Metals
  • Metals and their compounds are among the poisons most commonly encountered in the home and workplace. Even metals essential for life can be toxic if they are 851present in excessive amounts. Iron, e.g. is an essential element and is sometimes given therapeutically, if taken in overdose, however, it can be lethal.
  • Mercury poisoning, one of the classic occupational diseases, is a representative example of metal poisoning. Exposure to mercury can occur in many situations, including the manufacture of thermometers, explosives, fungicides, drugs, paints, batteries, and various electrical products. The disorders it can cause vary depending on the type of mercury compound and the method of exposure.
  • Ingestion of mercury salts such as mercuric chloride leads to nausea, vomiting, and bloody diarrhea. Kidney damage resulting in death may follow in extreme cases. Inhalation or absorption through the skin of mercury vapor causes salivation, loosening of the teeth, and tremor, it also affects the higher centers of the brain, resulting in irritability, loss of memory, depression, anxiety, and other personality changes. Poisoning with organic mercury compounds (used in fungicides and pesticides) results in permanent neurological damage and can be fatal.
  • Other hazardous metals commonly encountered in industry include arsenic, beryllium, cadmium, chromium, lead, manganese, nickel, and thallium. Some have been shown to be carcinogenic, including certain compounds of nickel (linked to lung and nasal cancer), chromium (lung cancer), and arsenic (lung and skin cancer).
 
Organic Compounds
  • The organic compounds that pose the greatest occupational hazards are various aromatic, aliphatic, and halogenated hydrocarbons and the organophosphates, carbamates, organochlorine compounds, and bipyridylium compounds used as pesticides.
  • Pesticides are used the world over and even though precautionary measures (such as using protective clothing and respirators, monitoring contamination of equipment and clothing, keeping workers out of recently sprayed areas, and requiring workers to wash thoroughly after exposure) can be instituted, poisoning not infrequently occurs in agricultural communities. The organophosphates and the generally less toxic carbamates exert their effects by inhibiting cholinesterase, an enzyme that prevents stimulation from becoming too intense or prolonged by destroying the acetylcholine involved in the transmission of impulses in the autonomic nervous system. Cholinesterase inhibitors allow the accumulation of acetylcholine, causing symptoms related to parasympathetic overactivity, such as chest tightness, wheezing, blurring of vision, vomiting, diarrhea, abdominal pain, and in severe cases respiratory paralysis. Atropine and certain oximes counteract their effects.
 
Dusts
The inhalation of a variety of dusts is responsible for a number of lung and respiratory disorders, whose symptoms and severity depend on the composition and size of the dust particle, the amount of dust inhaled, and the length of exposure. The lung diseases known as the pneumoconioses result when certain inhaled mineral dusts are deposited in the lungs, where they cause a chronic fibrotic reaction that leads to decreasing capacity for exercise and increasing breathlessness, cough, and respiratory difficulty. No specific treatment is known, but as with all respiratory disorders patients are urged to quit smoking, which aggravates the condition. Suggested measures for limiting exposure include using water and exhaust 852ventilation to lower dust levels and requiring workers to wear respirators or protective clothing, but such procedures are not always feasible. Coal worker's pneumoconiosis, silicosis, and asbestosis are the most common pneumoconioses.
 
DISORDERS DUE TO PHYSICAL AGENTS
 
Temperature
When working in a hot environment, humans maintain normal body temperature by perspiring and by increasing the blood flow to the surface of the body. The large amounts of water and salt lost in perspiration then need to be replaced. In the past, miners who perspired profusely and drank water to relieve their thirst experienced intense muscular pain, a condition known as miner's cramps, as a result of restoring their water but not their salt balance. When salt in the requisite amount was added to their drinks, workers no longer developed miner's cramps. Heat exhaustion is characterized by thirst, fatigue, giddiness, and often muscle cramps, fainting can also occur. Heatstroke, a more serious and sometimes lethal condition, results when prolonged exposure to heat and high humidity prevents efficient perspiration, causing the body temperature to rise above 106 °F (41 °C) and the skin to feel hot and dry. If victims are not quickly cooled down, coma, convulsions, and death can follow. To prevent heat exhaustion or heatstroke, workers unaccustomed to high temperatures should allow adequate time (ranging from days to weeks) for their bodies to become acclimatized before performing strenuous physical tasks.
Work in cold environments may also have serious adverse effects. Tissue damage that does not involve freezing can cause inflammatory swelling known as chilblains. Frostbite, or the freezing of tissue, can lead to gangrene and the loss of fingers or toes. If exposure is prolonged and conditions (such as wet or tight clothing) encourage heat loss, hypothermia, a critical fall in body temperature, may result. When body temperature falls below 95 °F (35 °C), physiological processes are slowed, consciousness is impaired, and coma, cardiorespiratory failure, and death may ensue. Workers exposed to extreme cold require carefully designed protective clothing to minimize heat loss, even though a degree of acclimatization occurs with time.
 
Atmospheric Pressure
Decompression sickness can result from exposure to high or low atmospheric pressure. Under increased atmospheric pressure (such as that experienced by deep-sea divers or tunnel workers), fat-soluble nitrogen gas dissolves in the body fluids and tissues. During decompression the gas comes out of solution and, if decompression is rapid, forms bubbles in the tissues. These bubbles cause pains in the limbs (known as the bends), breathlessness, angina, headache, dizziness, collapse, coma, and in some cases death. Similarly, the gases in solution in the body tissues under normal atmospheric pressure form bubbles when pressure rapidly decreases, as when aviators in unpressurized aircraft ascend to high altitudes too quickly. Emergency treatment of decompression sickness consists of rapid recompression in a compression chamber with gradual subsequent decompression. The condition can be prevented by allowing sufficient decompression time for the excess nitrogen gas to be expelled naturally.
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Noise
Exposure to excessive noise can be unpleasant and can impair working efficiency. Temporary or permanent hearing loss may also occur, depending on the loudness or intensity of the noise, its pitch or frequency, the length and pattern of exposure, and the vulnerability of the individual. Prolonged exposure to sound energy of intensity above 80 to 90 decibels is likely to result in noise-induced hearing loss, developing first for high frequencies and progressing downward. The condition can be prevented by enclosing noisy machinery and by providing effective ear protection. Routine audiometry gives an indication of the effectiveness of preventive measures.
 
Vibration
Whole-body vibration is experienced in surface and air transport, with motion sickness its most familiar effect. A more serious disorder, known as Raynaud's syndrome or vibration white finger (VWF), can result from the extensive use of vibratory hand tools, especially in cold weather. The condition is seen most frequently among workers who handle chain saws, grinders, pneumatic drills, hammers, and chisels. Forestry workers in cold climates are particularly at risk. Initial signs of VWF are tingling and numbness of the fingers, followed by intermittent blanching, redness and pain occur in the recovery stage. In a minority of cases the tissues, bones, and joints affected by the vibration may develop abnormalities; even gangrene may develop. VWF can be prevented by using properly designed tools, avoiding prolonged use of vibrating tools, and keeping the hands warm in cold weather.
 
Other Mechanical Stresses
Muscle cramps often afflict workers engaged in heavy manual labor as well as typists, pianists, and others who frequently use rapid, repetitive movements of the hand or forearm. Tenosynovitis, a condition in which the sheath enclosing a tendon to the wrist or to one of the fingers becomes inflamed, causing pain and temporary disability, can also result from prolonged repetitive movement. When the movement involves the rotation of the forearm, the extensor tendon attached to the point of the elbow becomes inflamed, a condition commonly known as tennis elbow.
 
Ionizing Radiation
Ionizing radiation damages or destroys body tissues by breaking down the molecules in the tissues into positively or negatively charged particles called ions. Radiation that is capable of causing ionization may be electromagnetic (X-rays and gamma rays) or particulate (radiation of electrons, protons, neutrons, alpha particles, and other subatomic particles) and has many uses in industry, medicine, and scientific research.
Ionizing radiation injury is in general dose-dependent. Whole-body exposure to doses in excess of 1,000 rads results in acute radiation syndrome and is usually fatal. Doses in excess of 3,000 rads produce cerebral edema (brain swelling) within a matter of minutes, and death within days. Lesser doses cause acute gastrointestinal symptoms, such as severe vomiting and diarrhea, followed by a week or so of apparent well-being before the development of the third toxic phase, which is characterized by fever, further gastrointestinal symptoms, ulceration of the mouth and throat, hemorrhages, and hair loss. There is an immediate drop in the white-cell elements of the blood, affecting the lymphocytes first and then the 854granulocytes and platelets, with a slower decline in the red cells. If death does not occur, these symptoms may last for many months before slow recovery begins.
Delayed effects of exposure to radiation include the development of leukemia and other cancers. Examples include the skin cancers that killed many of the pioneering scientists who worked with X-rays and radioactive elements, the lung cancer common among miners of radioactive ores, and the bone cancer and aplastic anemia that women who painted clock dials with a luminous mixture containing radium and mesothorium developed as a result of ingesting small amounts of paint when they licked their paintbrushes to form a point.
 
Nonionizing Radiation
Nonionizing forms of radiation include electromagnetic radiation in the radiofrequency, infrared, visible light, and ultraviolet ranges. Exposure to radiation in the radiofrequency range occurs in the telecommunications industry and in the use of microwaves. Microwaves produce localized heating of tissues that may be intense and dangerous. Various other disorders, mainly of a subjective nature, have been reported in workers exposed to this frequency range. Infrared radiation can be felt as heat and is commonly used in industry in drying or baking processes. Prolonged exposure to the radiation can result in severe damage to the skin and especially to the lens of the eye, where cataracts may be produced. Working under poor lighting conditions can adversely affect worker efficiency and well-being and may even cause temporary physical disorders, such as headache or dizziness. Proper lighting should provide adequate, uniform illumination and appropriate contrast and color, without any flickering or glare. Exposure to ultraviolet radiation from the Sun or such industrial operations as welding or glassblowing causes erythema of the skin, skin cancer, and inflammation of the conjunctiva and cornea. Pigmentation offers natural protection against sunburn, and clothing and glass can also be used as effective shields against ultraviolet radiation. Lasers emit intense infrared, visible, or ultraviolet radiation of a single frequency that is used in surgery, for scientific research, and for cutting, welding, and drilling in industry. Exposure to these beams can burn the skin and cause severe damage to the eye.
 
Disorders Due to Infectious Agents
A large number of infectious diseases are transmitted to humans by animals. Many such diseases have been largely eliminated, but some still pose hazards. Anthrax for example, can be acquired by workers handling the unsterilized hair, hide, and bone of infected animals and slaughterhouse workers, farmers, veterinarians, and others in contact with infected animals, milk, and milk products still frequently contract brucellosis.
 
Disorders Due to Psychological Factors
Psychological factors are important determinants of worker health, well-being, and productivity. Studies have shown the benefits to workers who feel satisfied and stimulated by their jobs, who maintain good relationships with their employers or supervisors and with other employees, and who do not feel overworked. Such workers have lower rates of absenteeism and job turnover and higher rates of output than average.
The two psychological hazards commonly encountered at work are boredom and mental stress. Workers who perform simple, repetitious tasks for prolonged periods are subject to 855boredom, as are people who work in bland, colorless environments. Boredom can cause frustration, unhappiness, inattentiveness, and other detriments to mental well-being. More practically, boredom decreases worker output and increases the chances of error and accident. Providing refreshment and relaxation breaks or other outside stimulus can help relieve boredom.
Mental stress often results from overwork, although nonoccupational factors, such as personal relationships, lifestyle, and state of physical health, can play a major role. Job dissatisfaction, increased responsibility, disinterest, competition, feelings of inadequacy, and bad working relationships can also contribute to mental stress. Stress affects both mental and physical health, causing anger, irritation, fatigue, aches, nausea, ulcers, migraine, asthma, colitis, and even breakdown and coronary heart disease. Moderate exercise, meditation, relaxation, and therapy can help workers to cope with stress.
 
Common Occupational and Industrial Health Hazards
  • Acute and chronic intoxications with chemical substances and their sequels
  • Metallic fever
  • Pneumoconioses (Refer respiratory system)
  • Silicosis (Refer respiratory system)
  • Coal workers' pneumoconiosis (Refer respiratory system)
  • Pneumoconiosis associated with tuberculosis
  • Welders' pneumoconiosis
  • Asbestosis and other pneumoconioses due to silicates (Refer respiratory system)
  • Pneumoconiosis due to talc
  • Graphite fibrosis
  • Pneumoconioses due to metal dusts
  • Allergic contact dermatitis
  • Irritant contact dermatitis
  • Oil acne, chloroacne, coal tar acne of diffuse nature
  • Candida infections: hand intertrigo, nail dystrophy with paronychia due to working conditions
  • Dermatophyte infections due to contact with biological material from animals
  • Contact urticaria
  • Occupational photodermatoses.

Immunological Disorders18

 
IMMUNODEFICIENCY DISORDERS
Immunodeficiencies disorders involve malfunction of the immune system, resulting in infections that develop and recur more frequently, are more severe, and last longer than usual.
Immunodeficiency disorders impair the immune system's ability to defend the body against foreign or abnormal cells that invade or attack it (such as bacteria, viruses, fungi, and cancer cells). As a result, unusual bacterial, viral, or fungal infections or lymphomas or other cancers may develop. Another problem is that up to 25% of people who have an immunodeficiency disorder also have an autoimmune disorder (such as immune thrombocytopenia). In an autoimmune disorder, the immune system attacks the body's own tissue. Sometimes the autoimmune disorder develops before the immunodeficiency causes any symptoms.
There are two types of immunodeficiency disorders:
 
Primary Immunodeficiency Disorders
  • X-linked agammaglobulinemia
  • Severe combined immunodeficiency
  • 857Common variable immunodeficiency
  • Alymphocytosis
 
Primary Immunodeficiency Syndromes
  • Mostly these are inherited single-gene disorders that present in infancy in early childhood with the exception of common variable immunodeficiency which usually occurs in adults.
  • Mutations or deletions of genes governing stem-cell differentiation.
  • They are sometimes classified according to which component is faulty (T cells, B cells, phagocytic cells or complement) or according to individual clinical syndromes.
  • About 80% of patients are less than 20 years old when diagnosed, because the majority of cases are inherited or congenital. 70% occur in males due to X-linked inheritance in many syndromes.
  • B-cell defects account for 50% of primary immunodeficiency.
  • T-cell defects account for 30%, phagocytic deficiencies 18% and complement deficiencies 2%.
  • Antibody deficiency syndromes: This is a group of conditions characterized by an inability to produce antibodies in sufficient quantity or of sufficient quality.
  • Common variable immunodeficiency: This is a heterogeneous syndrome characterized by various degrees of hypogammaglobulinemia, commonly associated with autoimmunity. Thymoma and hypogammaglobulinemia: this is characterized by low numbers of B cells and a distinctive T-cell type.
  • X-linked (Bruton's agammoglobulinemia): The agammaglobulinemia is an X-linked immunodeficiency in which there is a failure to produce mature B lymphocyte cells. The defect in this disorder is a fault in the enzyme in Bruton's tyrosine kinase, a key regulator in B-cell development.
  • Cell-mediated immunity can be subject to a number of genetic defects affecting the function of the T-cells.
  • Thymic aplasia (DiGeorge's syndrome): There are genetic defects of the thymus and often the parathyroid glands and heart, associated with T-cell dysfunction and significant immune deficiency.
  • Severe combined immunodeficiency disease: This is in fact a group of rare congenital diseases in which there is severe and usually fatal immune deficiency.
  • Inherited syndromes associated with immunodeficiency: A wide range of inherited immunodeficiency conditions has been identified, many involving a single gene.
 
Congenital Immune Disorders
Secondary disorders happen when body is attacked by an outside source, such as a toxic chemical or an infection. Severe burns and radiation also can cause secondary disorders. Secondary disorders include:
  • AIDS
  • Cancers of the immune system, such as leukemia
  • Immune complex diseases, such as viral hepatitis
  • Multiple myeloma
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Secondary Immunodeficiencies
There are many possible causes and so it is difficult to obtain exact epidemiological data. It is known that the current epidemics of AIDs and tuberculosis have caused global increases in the condition.
Secondary immunodeficiency is common in people who are hospitalized for:
  • Lymphoreticular malignancy
  • Drugs: particularly cytotoxic drugs and immunosuppressant
  • Viruses, e.g. HIV
  • Malnutrition
  • Metabolic disorders, e.g. renal disease requiring peritoneal dialysis
  • Trauma or major surgery
  • Protein loss, e.g. due to nephrotic syndrome.
 
Presentation of Secondary Immunodeficiencies
The most common presenting feature is frequent infections. Recurrent respiratory infections are common.
  • The development of severe, persistent recurrent bacterial infection is a better indicator. A common scenario is repeated episodes of sore throat or upper respiratory tract infection which lead to sinusitis, chronic otitis and bronchitis. Another feature is the ease with which complications develop, e.g. bronchitis progresses to pneumonia, bronchiectasis and respiratory failure.
  • Opportunistic infections are common, such as Pneumocystis jirovecii or cytomegalovirus, especially in patients with T-cell deficiencies. Infection of the skin and mucous membranes occurs frequently, including resistant thrush, oral ulcers and periodontitis. Conjunctivitis, pyoderma, severe warts, alopecia, eczema and telangiectasia are also prominent features.
  • Common gastrointestinal symptoms include diarrhea, malabsorption and failure to thrive or losing weight. The diarrhea is usually noninfectious, although a range of organisms, including rotavirus, Giardia lamblia, Cryptosporidium and cytomegalovirus may be involved.
  • Less commonly, hematological abnormalities such as autoimmune hemolytic anemia, leukopenia, or thrombocytopenia can occur.
  • Neurological problems, such as seizures and encephalitis, and autoimmune conditions, such as vasculitis and arthritis, are also sometimes seen. There is also a higher incidence of gastric carcinoma and liver disease.
  • Paradoxically, autoimmune diseases can be associated with primary immunodeficiencies.
 
Diagnostic Evaluation
  • Family history: There may be a familial tendency to early death, similar disease, autoimmunity, allergy, early malignancy or intermarriage.
  • Check for risk factors: Diabetes, medications, illicit drug use and sexual history.
  • A history of adverse reactions to immunizations or complications of viral infections may be significant.
  • 859Enquiry should be made about the frequency of previous antibiotic prescriptions and any history of relevant surgery, e.g. splenectomy, tonsillectomy, adenoidectomy.
  • A history of radiation therapy to the thymus or nasopharynx may also be a pointer to the diagnosis.
 
Examination
  • Patients with immunodeficiency often look ill, with pale skin, general malaise, cachexia and a distended abdomen. Various skin manifestations may be apparent, such as rashes, vesicles, pyoderma, eczema and telangectasia.
  • The eyes may be inflamed and infected.
  • Signs of chronic ENT disease, such as scarred eardrums, encrusted nostrils and postnasal drip may be evident.
  • There may be a chronic cough with crepitations in both lungs.
  • Hepatomegaly and splenomegaly may be detected in the abdomen.
  • In infants, crusting around the anus may be a sign of chronic diarrhea. Delayed developmental milestones or ataxia may be evident.
 
Investigation
Specialist tests are often required to elucidate the exact diagnosis, but screening tests can be done in primary care. These should include:
  • FBC, IgG, IgM and IgA levels and tests to confirm the presence and type of any infection. A systematic review called for screening in patients with recurrent infections, irrespective of age.
  • An elevated ESR may indicate chronic infection and CXR and sinus X-ray may confirm the source.
  • Appropriate microbiological swabs should be taken, as dictated by the clinical picture.
  • More advanced investigations include assays of lymphocyte response, antibody response to immunization of diphtheria, tetanus and pneumococcal polysaccharides, phagocytosis assay.
 
Management
  • General measures include making sure that patients have a healthy lifestyle and are protected as far as possible from infection. This includes having regular dental checks and their own accommodation. There may be an element of social isolation and psychological issues may need to be addressed.
  • If there is any evidence of antibody response, the standard regime of killed vaccines should be given. Live vaccines are contraindicated in T-cell deficiency.
  • Bacterial and fungal infection should be recognized and treated early. Swabs should be taken before treatment so that empirical treatment failures can be rectified rapidly. Continuous prophylactic antibiotics may be appropriate in some circumstances. Chest infections may require physiotherapy and lung exercises.
  • Antiviral therapies such as amantidine and ramantadine may be lifesaving in the management of viral infections.
  • 860Intravenous or subcutaneous immunoglobulin replacement is the first-line treatment for most immunoglobulin deficiency states. Subcutaneous therapy is preferred by many patients because it is more convenient and they can be more independent. The best treatment for T-cell deficiency conditions is bone marrow transplant, if a donor can be found.
  • Other treatment options, some of which are still in the experimental phase, include cytokines, thymic transplants, gene therapy, and stem-cell transplantation.
 
Prevention and Treatment
Some of the disorders that can cause immunodeficiency can be prevented and treated, thus helping prevent immunodeficiency from developing. The following are examples:
  • HIV infection: Following safe sex guidelines and not sharing needles to inject drugs can reduce the spread of this infection. Also, antiretroviral drugs can usually treat HIV infection effectively.
  • Cancer: Successful treatment usually restores the function of the immune system unless people need to continue taking immunosuppressant.
  • Diabetes: Good control of blood sugar levels can help white blood cells function better and thus prevent infections.
Strategies for preventing and treating infections depend on the type of immunodeficiency disorder. For example, people who have an immunodeficiency disorder due to a deficiency of antibodies are at risk of bacterial infections. The following can help reduce the risk:
  • Being treated periodically with immune globulin (antibodies obtained from the blood of people with a normal immune system) given intravenously or under the skin
  • Practicing good personal hygiene (including conscientious dental care)
  • Not eating undercooked food
  • Not drinking water that may be contaminated
  • Avoiding contact with people who have infections:
    • Antibiotics are given as soon as a fever or another sign of an infection develops and before surgical and dental procedures, which may introduce bacteria into the bloodstream. If a disorder (such as severe combined immunodeficiency) increases the risk of developing serious infections or particular infections, people may be given antibiotics to prevent these infections.
    • Antiviral drugs are given at the first sign of infection if people have an immunodeficiency disorder that increases the risk of viral infections (such as immunodeficiency due to a T-cell abnormality). These drugs include amantadine and acyclovir.
    • Vaccines are given if the specific immunodeficiency disorder does not affect antibody production. Vaccines are given to stimulate the body to produce antibodies that recognize and attack specific bacteria or viruses. If the person's immune system cannot make antibodies, giving a vaccine does not result in the production of antibodies and can even result in illness. For example, if a disorder does not affect production of antibodies, people with that disorder are given the influenza vaccine given once a year. Doctors may also give this vaccine to the person's immediate family members and to people who have close contact with the person. Generally, 861live-virus vaccines are not given to people who have a B- or T-cell abnormality because these vaccines may cause an infection in such people. Live-virus vaccines include rotavirus vaccines, measles-mumps-rubella vaccine, chickenpox (varicella) vaccine, varicella-zoster (shingles) vaccine, bacille Calmette-Guérin (BCG) vaccine, and influenza vaccine given as a nasal spray.
    • Stem cell transplantation can correct some immunodeficiency disorders, particularly severe combined immunodeficiency. Stem cells are usually obtained from bone marrow but occasionally from blood (including umbilical cord blood). Transplantation of thymus tissue is sometimes helpful. Gene therapy for a few congenital immunodeficiency disorders has been successful.
 
HUMAN IMMUNODEFICIENCY VIRUS (HIV)
‘HIV’ stands for Human Immunodeficiency Virus.
  • HHuman: This particular virus can only infect human beings.
  • IImmunodeficiency: HIV weakens immune system by destroying important cells that fight disease and infection. A ‘deficient’ immune system cannot protect you.
  • VVirus: A virus can only reproduce itself by taking over a cell in the body of its host.
 
Acquired Immunodeficiency Syndrome (AIDS)
‘AIDS’ stands for Acquired Immunodeficiency Syndrome.
  • AAcquired: AIDS is not something inherited from parents. You acquire AIDS after birth.
  • IImmuno: Body's immune system includes all the organs and cells that work to fight off infection or disease.
  • DDeficiency: You get AIDS when the immune system is ‘deficient’, or is not working the way it should.
  • SSyndrome: A syndrome is a collection of symptoms and signs of disease. AIDS is a syndrome, rather than a single disease, because it is a complex illness with a wide range of complications and symptoms.
As noted above, AIDS is the final stage of HIV infection, and not everyone who has HIV advances to this stage. People at this stage of HIV disease have badly damaged immune systems, which put them at risk for opportunistic infections (OIs).
 
Cycle of HIV Virus
HIV can infect multiple cells in body, including brain cells, but its main target is the CD4 lymphocyte, also called a T-cell or CD4 cell. When a CD4 cell is infected with HIV, the virus goes through multiple steps to reproduce itself and create many more virus particles.
The process is broken up into the following steps:
  • Binding and fusion: This is the process by which HIV binds to a specific type of CD4 receptor and a coreceptor on the surface of the CD4 cell. This is similar to a key entering a lock. Once unlocked, HIV can fuse with the host cell (CD4 cell) and release its genetic material into the cell.
  • Reverse transcription: A special enzyme called reverse transcriptase changes the genetic material of the virus, so it can be integrated into the host DNA.
  • 862Integration: The virus' new genetic material enters the nucleus of the CD4 cell and uses an enzyme called integrase to integrate itself into own genetic material, where it may ‘hide’ and stay inactive for several years.
  • Transcription: When the host cell becomes activated, and the virus uses its own enzymes to create more of its genetic material—along with a more specialized genetic material which allows it make longer proteins.
  • Assembly: A special enzyme called protease cuts the longer HIV proteins into individual proteins. When these come together with the virus' genetic material, a new virus has been assembled.
  • Budding: This is the final stage of the virus' life cycle. In this stage, the virus pushes itself out of the host cell, taking with it part of the membrane of the cell. This outer part covers the virus and contains all of the structures necessary to bind to a new CD4 cell and receptors and begin the process again.
These steps of the life-cycle of HIV are important to know because the medications used to control HIV infection act to interrupt this replication cycle.
 
Stages of HIV
Below are the stages of HIV infection. People may progress through these stages at different rates, depending on a variety of factors.
 
Acute Infection Stage
Within 2 to 4 weeks after HIV infection, many, but not all, people develop flu-like symptoms, often described as ‘the worst flu ever’. Symptoms can include fever, swollen glands, sore throat, rash, muscle and joint aches and pains, fatigue, and headache. This is called ‘acute retroviral syndrome’ (ARS) or ‘primary HIV infection’, and it is the body's natural response to the HIV infection.
During this early period of infection, large amounts of virus are being produced in body. The virus uses CD4 cells to replicate and destroys them in the process. Because of this, CD4 count can fall rapidly. Eventually immune response will begin to bring the level of virus in body back down to a level called a viral set point, which is a relatively stable level of virus in body. At this point, CD4 count begins to increase, but it may not return to preinfection levels. It may be particularly beneficial to health to begin ART during this stage.
  • It is important to be aware that you are at particularly high-risk of transmitting HIV to your sexual or drug using partners during this stage because the levels of HIV in bloodstream are very high. For this reason, it is very important to take steps to reduce risk of transmission.
 
Clinical Latency Stage
After the acute stage of HIV infection, the disease moves into a stage called the ‘clinical latency’ stage. ‘Latency’ means a period where a virus is living or developing in a person without producing symptoms. During the clinical latency stage, people who are infected with HIV experience no HIV-related symptoms, or only mild ones. (This stage is sometimes called ‘asymptomatic HIV infection’ or ‘chronic HIV infection’).
During the clinical latency stage, the HIV virus continues to reproduce at very low levels, although it is still active. If patient takes ART, he may live with clinical latency for 863several decades because treatment helps keep the virus in check. For people who are not on ART, the clinical latency stage lasts an average of 10 years, but some people may progress through this stage faster.
It is important to remember that people in this symptom-free stage are still able to transmit HIV to others, even if they are on ART, although ART greatly reduces the risk of transmission.
  • If you have HIV and you are not on ART, then eventually your viral load will begin to rise and your CD4 count will begin to decline. As this happens, you may begin to have constitutional symptoms of HIV as the virus levels increase in your body.
 
AIDS
This is the stage of HIV infection that occurs when immune system is badly damaged and become vulnerable to infections and infection-related cancers called opportunistic infections. When the number of CD4 cells falls below 200 cells per cubic millimeter of blood (200 cells/mm3), you are considered to have progressed to AIDS. (In someone with a healthy immune system, CD4 counts are between 500 and 1,600 cells/mm3.)
  • Without treatment, people who progress to AIDS typically survive about 3 years. Once you have a dangerous opportunistic illness, life-expectancy without treatment falls to about 1 year. However, if you are taking ART and maintain a low viral load, then you may enjoy a near normal life span. You will most likely never progress to AIDS.
 
Factor Affecting the HIV Progression
  • People living with HIV may progress through these stages at different rates, depending on a variety of factors, including their genetic make-up, how healthy they were before they were infected, how soon after infection they are diagnosed and linked to care and treatment, whether they see their health care provider regularly and take their HIV medications as directed, and different health-related choices they make, such as decisions to eat a healthful diet, exercise, and not smoke.
  • Factors that may shorten the time between HIV and AIDS:
    • Older age
    • HIV subtype
    • Coinfection with other viruses
    • Poor nutrition
    • Severe stress
    • Genetic background.
  • Factors that may delay the time between HIV and AIDS:
    • Taking antiretroviral therapy
    • Staying in HIV care
    • Closely adhering to doctor's recommendations
    • Eating healthful foods
    • Taking care of yourself
    • Genetic background.
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Symptoms of Acute Infection
When a person first becomes infected with HIV, they are said to be in the acute stage of infection. The acute stage is a time when the virus is multiplying very rapidly. At this stage, the immune system actively tries to fight off the infection and body will show following symptoms:
  • Tiredness
  • Weight loss
  • Frequent fever and sweats
  • Lymph node enlargement
  • Yeast infections
  • Persistent skin rashes or flaky skin.
 
Symptoms of AIDS
AIDS does not cause many symptoms itself. With AIDS you will suffer symptoms from opportunistic infections. These are infections that take advantage of decreased immune function. Symptoms and signs of common opportunistic infections include:
  • Dry cough or shortness of breath
  • Difficult or painful swallowing
  • Diarrhea lasting for more than a week
  • White spots or unusual blemishes in and around the mouth
  • Pneumonia-like symptoms
  • Fever
  • Vision loss
  • Nausea, abdominal cramps, and vomiting
  • Red, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or eyelids
  • Seizures or lack of coordination
  • Neurological disorders such as depression, memory loss, and confusion
  • Severe headaches and neck stiffness
  • Coma
  • Development of various cancers.
Opportunistic infections are signs of a declining immune system. Most life-threatening opportunistic infections occur when CD4 count is below 200 cells/mm3. Opportunistic infections are the most common cause of death for people with HIV/AIDS.
The CDC developed a list of more than 20 opportunistic infections that are considered AIDS-defining conditions—if one have HIV and one or more of these opportunistic infections, you will be diagnosed with AIDS, no matter what CD4 count happens to be:
  • Candidiasis of bronchi, trachea, esophagus, or lungs
  • Invasive cervical cancer
  • Coccidioidomycosis
  • Cryptococcosis
  • Cryptosporidiosis, chronic intestinal (greater than 1 month duration)
  • 865Cytomegalovirus disease (particularly CMV retinitis)
  • Encephalopathy, HIV-related
  • Herpes simplex: Chronic ulcer (greater than 1 month's duration); or bronchitis, pneumonitis, or esophagitis
  • Histoplasmosis
  • Isosporiasis, chronic intestinal (greater than 1 month's duration)
  • Kaposi's sarcoma
  • Lymphoma, multiple forms
  • Mycobacterium avium complex
  • Tuberculosis
  • Pneumocystis carinii pneumonia
  • Pneumonia, recurrent
  • Progressive multifocal leukoencephalopathy
  • Salmonella septicemia, recurrent
  • Toxoplasmosis of brain
  • Wasting syndrome due to HIV.
 
Opportunistic Infections Symptoms on the Basis of CD4 Count
Opportunistic infections can occur all over the body and be relatively localized or systemic or disseminated. Whether and when you become susceptible to opportunistic infections is often related to CD4 count.
 
Greater than 500 cells/mm3
  • Opportunistic infections: In general, people with CD4 counts greater than 500 cells/mm3 are not at risk for opportunistic infections. For people with CD4 counts around 500, however, the daily fluctuations in CD4 cell levels can leave them vulnerable to minor infections, such as candidal vaginitis or yeast infections.
 
500 cells/mm3 to 200 cells/mm3
Opportunistic infections
  • Candidiasis (Thrush): This is a fungal infection that is normally seen in patients with CD4 counts in this range. It is treatable with antifungal medications. A trained provider can usually diagnose thrush with a visual examination.
  • Kaposi's Sarcoma (KS): KS is caused by Human Herpes Virus-8. Before the introduction of antiretroviral therapy, as many as 1 in 5 patients with AIDS had KS. It can cause lesions on the body and in the mouth. In addition, this virus can affect internal organs and disseminate to other parts of the body without any external signs.
Symptoms
Oral symptoms include:
  • White patches on gums, tongue or lining of the mouth
  • Pain in the mouth or throat
  • Difficulty swallowing
  • Loss of appetite.
866Vaginal symptoms include:
  • Vaginal irritation
  • Itching
  • Burning
  • Thick, white discharge
Signs and symptoms of KS can include:
  • Appearance of a purplish lesion on skin
  • Appearance of a purplish lesion in the mouth
  • Occasionally gastrointestinal complaints with disseminated KS.
 
200 cells/mm3 to 100 cells/mm3
Opportunistic infections
  • Pnuemocystis Jirovecii (Carinii) Pneumonia (PCP): PCP is a fungal infection and is the opportunistic infections that most often causes death in patients with HIV. It is treatable with antibiotic therapy and close monitoring. If necessary, prophylaxis is available for patients who are at risk for PCP. Diagnosing PCP usually involves a hospital stay to ensure proper testing and treatment without complications.
Signs and symptoms of PCP can include:
  • Shortness of breath
  • Fever
  • Dry cough
  • Chest pain
  • Histoplasmosis and Coccidioidomycosis
  • These are fungal infections. They often present as severe, disseminated illnesses in patients with low CD4 counts. Diagnosis consists of blood tests and evaluation for possible exposures related to geographical areas.
Signs and symptoms of histoplasmosis and coccidioidomycosis can include:
  • Fever
  • Fatigue
  • Weight loss
  • Cough
  • Chest pain
  • Shortness of breath
  • Headache
  • Progressive Multifocal Leukoencephalopathy (PML): PML is a severe neurological condition and typically occurs in patients with CD4 counts below 200. While there is no definitive treatment for this disease, it has been shown to be responsive to antiretroviral therapy. In some cases, the disease resolves without any treatment.
Signs and symptoms of PML can include:
  • Dementia
  • Seizures
  • Difficulty Speaking
  • 867Confusion
  • Difficulty walking.
 
100 cells/mm3 to 50 cells/mm3
Opportunistic infections
  • Toxoplasmosis: Toxoplasmosis is caused by the parasite Toxoplasma gondii that can cause encephalitis and neurological disease in patients with low CD4 counts. The parasite is carried by cats, birds, and other animals and is also found in soil contaminated by cat feces and in meat, particularly pork. Toxoplasmosis is treatable with aggressive therapy, and prophylaxis is recommended for patients with low CD4 counts (usually less than 200).
Signs and symptoms of toxoplasmosis can include:
  • Headache
  • Confusion
  • Motor weakness
  • Fever
  • Seizures
  • Cryptosporidiosis: Cryptosporidiosis is a diarrheal disease caused by the protozoa Cryptosporidium, and it can become chronic for people with low CD4 counts. Symptoms include abdominal cramps and severe chronic diarrhea. Infection with this parasite can occur through: swallowing water that has been contaminated with fecal material (in swimming pools, lakes, or public water supplies); eating uncooked food (like oysters) that are infected; or by person-to-person transmission, including changing diapers or exposure to feces during sexual contact.
    Signs and symptoms of cryptosporidiosis can include:
    • Chronic watery diarrhea
    • Stomach cramps
    • Weight loss
    • Nausea
    • Vomiting
  • Cryptococcal infection or cryptococcosis: Cryptococcal infection is caused by a fungus that typically enters the body through the lungs and can spread to the brain, causing cryptococcal meningitis. In some cases, it can also affect the skin, skeletal system, and urinary tract. This can be a very deadly infection if not caught and properly treated with antifungal medication. Although this infection is found primarily in the central nervous system, it can disseminate to other parts of the body, especially when a person has a CD4 count of less than 50.
    Signs and symptoms of cryptococcal meningitis include:
    • Fever
    • Fatigue
    • Headache
    • Neck stiffness
    • Some patients can have memory loss or mood changes.
868
 
50 to 100 Cells/mm3
Opportunistic infections
  • Cytomegalovirus (CMV): CMV is an extremely common virus that is present in all parts of the world. It is estimated that a majority of the population have had CMV by the time they are 40 years old. CMV can be transmitted by saliva, blood, semen and other bodily fluids. It can cause mild illnesses when first contracted and many people may never have symptoms. However, it does not leave the body when someone is infected with CMV. In patients with HIV and low CD4 counts it can cause infections in the eye and gastrointestinal system.
Signs and symptoms of CMV:
  • Sore throat
  • Swollen glands
  • Fatigue
  • Fevers
In people with low CD4 counts it can cause:
  • Blurred vision (if there is CMV infection is in the eye)
  • Painful swallowing
  • Diarrhea
  • Abdominal pain
 
Less than 50 Cells/mm3
Opportunistic infections
  • Mycobaterium Aviam Complex (MAC): MAC is a type of bacteria that can be found in soil, water, and many places in the environment. These bacteria can cause disease in people with HIV and CD4 Counts less that 50. The bacteria can infect the lungs or the intestines, or in some cases, can become ‘disseminated’. This means that it can spread to the blood stream and other parts of the body. If this occurs, it can be a life-threatening infection.
Signs and symptoms of MAC:
  • Fevers
  • Night sweats
  • Abdominal Pain
  • Fatigue
  • Diarrhea
 
Diagnostic Evaluation
  • Confirming diagnosis: Signs and symptoms may occur at anytime after infection, but AIDS is not officially diagnosed until the patient's CD4+ T-cell count falls below 200 cells/mcl or associated clinical conditions or disease.
  • CBC: Anemia and idiopathic thrombocytopenia (anemia occurs in up to 85% of patients with AIDS and may be profound). Leukopenia may be present; differential shift to the left suggests infectious process (PCP).
  • 869PPD: Determines exposure or active TB disease. Of AIDS patients, 100% of those exposed to active Mycobacterium tuberculosis will develop the disease.
  • Serologic: Serum antibody test: HIV screen by ELISA. A positive test result may be indicative of exposure to HIV but is not diagnostic because false-positives may occur.
  • Western blot test: Confirms diagnosis of HIV in blood and urine.
  • Viral load test:
    • RI-PCR: The most widely used test currently can detect viral RNA levels as low as 50 copies/ml of plasma with an upper limit of 75,000 copies/ml.
    • bDNA 3.0 assay: Has a wider range of 50–500,000 copies/ml. Therapy can be initiated, or changes made in treatment approaches, based on rise of viral load or maintenance of a low viral load. This is currently the leading indicator of effectiveness of therapy.
    • T-lymphocyte cells: Total count reduced.
    • CD4+ lymphocyte count (immune system indicator that mediates several immune system processes and signals B cells to produce antibodies to foreign germs): Numbers less than 200 indicate severe immune deficiency response and diagnosis of AIDS.
    • T8+ CTL (cytopathic suppressor cells): Reversed ratio (2:1 or higher) of suppressor cells to helper cells (T8+ to T4+) indicates immune suppression.
    • Polymerase chain reaction (PCR) test: Detects HIV-DNA; most helpful in testing newborns of HIV-infected mothers. Infants carry maternal HIV antibodies and therefore test positive by ELISA and Western blot, even though infant is not necessarily infected.
  • STD screening tests: Hepatitis B envelope and core antibodies, syphilis, and other common STDs may be positive.
  • Cultures: Histologic, cytologic studies of urine, blood, stool, spinal fluid, lesions, sputum, and secretions may be done to identify the opportunistic infection.
  • Neurological studies, e.g. electroencephalogram (EEG), magnetic resonance imaging (MRI), computed tomography (CT) scans of the brain; electromyography (EMG)/nerve conduction studies: Indicated for changes in mentation, fever of undetermined origin, and changes in sensory or motor function to determine effects of HIV infection or opportunistic infections.
  • Chest X-ray: May initially be normal or may reveal progressive interstitial infiltrates secondary to advancing PCP (most common opportunistic disease) or other pulmonary complications disease processes such as TB.
  • Pulmonary function tests: Useful in early detection of interstitial pneumonias.
  • Gallium scan: Diffuse pulmonary uptake occurs in PCP and other forms of pneumonia.
  • Biopsies: May be done for differential diagnosis of Kaposi's sarcoma (KS) or other neoplastic lesions.
  • Bronchoscopy or tracheobronchial washings: May be done with biopsy when PCP or lung malignancies are suspected.
  • Barium swallow, endoscopy, colonoscopy: May be done to identify opportunistic infection (e.g. Candida, CMV) or to stage KS in the GI system.
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HOW HIV VIRUS TRANSFERS
Certain body fluids from an HIV infected person can transmit HIV
These body fluids are:
  • Blood
  • Semen
  • Preseminal fluid
  • Rectal fluids
  • Vaginal fluids
  • Breast milk
These body fluids must come into contact with a mucous membrane or damaged tissue or be directly injected into bloodstream (by a needle or syringe) for transmission to possibly occur. Mucous membranes are the soft, moist areas just inside the openings to body. They can be found inside the rectum, the vagina or the opening of the penis, and the mouth.
 
How the HIV Spread
  • Having sex with someone who has HIV. In general:
    • Anal sex is the highest-risk sexual behavior. Receptive anal sex (bottoming) is riskier than insertive anal sex (topping).
    • Vaginal sex is the second highest-risk sexual behavior.
    • Having multiple sex partners or having sexually transmitted infections can increase the risk of HIV infection through sex.
    • Sharing needles, syringes, rinse water, or other equipment (works) used to prepare injection drugs with someone who has HIV.
  • Less commonly, HIV may be spread by:
    • Being born to an infected mother. HIV can be passed from mother to child during pregnancy, birth, or breastfeeding.
    • Being stuck with an HIV-contaminated needle or other sharp object. This is a risk mainly for health care workers.
    • Receiving blood transfusions, blood products, or organ transplants that are contaminated with HIV.
    • Eating food that has been prechewed by an HIV-infected person. The contamination occurs when infected blood from a caregiver's mouth mixes with food while chewing, and is very rare.
    • Being bitten by a person with HIV. Each of the very small number of documented cases has involved severe trauma with extensive tissue damage and the presence of blood. There is no risk of transmission if the skin is not broken.
    • Oral sex, giving fellatio (mouth to penis oral sex) and having the person ejaculate in mouth is riskier than other types of oral sex.
    • Contact between broken skin, wounds, or mucous membranes and HIV-infected blood or blood-contaminated body fluids. These reports have also been extremely rare.
    • 871Deep, open-mouth kissing if the person with HIV has sores or bleeding gums and blood is exchanged. HIV is not spread through saliva. Transmission through kissing alone is extremely rare.
 
HIV is NOT Spread by
  • Air or water
  • Insects, including mosquitoes or ticks
  • Saliva, tears, or sweat
  • Casual contact, like shaking hands, hugging or sharing dishes, drinking glasses
  • Drinking fountains
  • Toilet seats
However, a person with HIV can still potentially transmit HIV to a partner even if they have an undetectable viral load, because:
  • HIV may still be found in a person's genital fluids (e.g. semen, vaginal fluids). The viral load test only measures virus in a person's blood.
  • A person's viral load may go up between tests. When this happens, they may be more likely to transmit HIV to partners.
  • Sexually transmitted diseases (STDs) increase viral load in a person's genital fluids.
 
Signs and Symptoms of HIV
  • The symptoms of HIV vary, depending on the individual and what stage of the disease are in.
 
Early Stage
Within 2–4 weeks after HIV infection, many, but not all, people experience flu-like symptoms, often described as the ‘worst flu ever’. This is called ‘acute retroviral syndrome’ (ARS) or ‘primary HIV infection,’ and it is the body's natural response to the HIV infection.
Symptoms can include:
  • Fever (this is the most common symptom)
  • Swollen glands
  • Sore throat
  • Rash
  • Fatigue
  • Muscle and joint aches and pains
  • Headache
These symptoms can last anywhere from a few days to several weeks.
 
Clinical Latency Stage
  • After the early stage of HIV infection, the disease moves into a stage called the ‘clinical latency’ stage. ‘Latency’ means a period where a virus is living or developing in a person without producing symptoms. During the clinical latency stage, people who are infected with HIV experience no HIV-related symptoms, or only mild ones. (This stage is sometimes called ‘asymptomatic HIV infection’ or ‘chronic HIV infection’).
  • 872During the clinical latency stage, the HIV virus reproduces at very low levels, although it is still active. If you take antiretroviral therapy (ART), you may live with clinical latency for several decades because treatment helps keep the virus in check.
    • It is important to remember that people in this symptom-free period are still able to transmit HIV to others even if they are on ART, although ART greatly reduces the risk of transmission.
 
PROGRESSION FROM HIV TO AIDS SYMPTOMS
The onset of symptoms signals the transition from the clinical latency stage to AIDS (Acquired Immunodeficiency Syndrome).
During this late stage of HIV infection, people infected with HIV may have the following symptoms:
  • Rapid weight loss
  • Recurring fever or profuse night sweats
  • Extreme and unexplained tiredness
  • Prolonged swelling of the lymph glands in the armpits, groin, or neck
  • Diarrhea that lasts for more than a week
  • Sores of the mouth, anus, or genitals
  • Pneumonia
  • Red, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or eyelids
  • Memory loss, depression, and other neurologic disorders.
 
Management and Prevention From HIV
There are several steps can be taken to reduce the risk of getting HIV through sexual contact, and the more of these actions you take, the safer you can be. These actions include:
  • Choose less risky sexual behaviors: Oral sex is much less risky than anal or vaginal sex. Anal sex is the highest-risk sexual activity for HIV transmission. HIV can be sexually transmitted via blood, semen, preseminal fluid, rectal fluid, and vaginal fluid. Sexual activities that do not involve the potential exchange of these bodily fluids (e.g. touching) carry no risk for getting HIV.
  • Use condoms consistently and correctly: When used consistently and correctly, condoms are highly effective in preventing HIV.
  • Reduce the number of sexual partners: The number of sex partners can affects HIV risk. The more partners you have, the more likely you are to have a partner with HIV whose viral load is not suppressed or to have a sex partner with a sexually transmitted disease. Both of these factors can increase the risk of HIV transmission.
  • Talk to doctor about pre-exposure prophylaxis (PrEP): PrEP is taking HIV medicine daily to prevent HIV infection. PrEP should be considered if you are HIV-negative and in an ongoing sexual relationship with an HIV-positive partner. PrEP also should be considered if you are HIV-negative and have had a sexually transmitted disease (STD) or any anal sex (receptive or insertive) with a male partner without condoms in the past six months and are not in an exclusive relationship with a recently tested, HIV-negative partner.
  • 873Talk to doctor right away (within 3 days) about post-exposure prophylaxis (PEP) if you have a possible exposure to HIV: An example of a possible exposure is if you have anal or vaginal sex without a condom with someone who is or may be HIV-positive and you are HIV-negative and not taking PrEP. Your chance of exposure to HIV is lower if your HIV-positive partner is taking antiretroviral therapy (ART) consistently and correctly, especially if his/her viral load is undetectable. Starting PEP immediately and taking it daily for 4 weeks reduces chance of getting HIV.
  • Get tested and treated for other sexually transmitted diseases (STDs) and encourage your partners to do the same.
 
Management of HIV
 
Preexposure Prophylaxis
  • ‘PrEP’ stands for Preexposure Prophylaxis. The word ‘prophylaxis’ means ‘to prevent or control the spread of an infection or disease’. PrEP is a way for people who do not have HIV to prevent HIV infection by taking a pill everyday. The pill contains two medicines that are also used to treat HIV. If you take PrEP and are exposed to HIV through sex or injection drug use, these medicines can work to keep the virus from taking hold in body.
  • Along with other prevention methods like condoms, PrEP can offer good protection against HIV if taken everyday.
 
Postexposure Prophylaxis (PEP)
  • Postexposure Prophylaxis (PEP) involves taking anti-HIV medications as soon as possible after being exposed to HIV to reduce the chance of becoming HIV positive. These medications keep HIV from making copies of itself and spreading through body.
There are two types of PEP:
  1. Occupational PEP (‘oPEP’), taken when someone working in a healthcare setting is potentially exposed to material infected with HIV.
  2. Nonoccupational PEP (‘nPEP’), taken when someone is potentially exposed to HIV outside the workplace (e.g. from sexual assault, or during episodes of unprotected sex or needle-sharing injection drug use).
  • To be effective, PEP must begin within 72 hours of exposure, before the virus has time to make too many copies of itself in body. PEP consists of 2–3 antiretroviral medications and should be taken for 28 days. PEP is not 100% effective; it does not guarantee that someone exposed to HIV will not become infected with HIV.
 
Antiretroviral Therapy (Art)
In 1987, a drug called AZT became the first approved treatment for HIV disease. Since then, approximately 30 drugs have been approved to treat people living with HIV/AIDS.
It includes:
  • ‘The Cocktail’
  • Antiretrovirals (ARVs)
  • Highly Active Antiretroviral Therapy (HAART or ART): Each HIV medication is pretty powerful by itself—and the key to treating HIV disease successfully is to pick the right 874combination of drugs from the different classes of HIV medicines. Antiretrovirals are separated into different classes, The classes include:
    • Nucleoside or Nucleotide Reverse Transcriptase Inhibitors (NRTIs): Sometimes called ‘nukes’. These drugs work to block a very important step in HIV's reproduction process. Nukes act as faulty building blocks in production of viral DNA production. This blocks HIV's ability to use a special type of enzyme (reverse transcriptase) to correctly build new genetic material (DNA) that the virus needs to make copies of itself, e.g. Lamivudine, Zidovudine, Emtricitabine, Abacavir.
    • Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs): These are called ‘non-nukes’. They work in a very similar way to ‘nukes’. Non-nukes also block the enzyme, reverse transcriptase, and prevent HIV from making copies of its own DNA. But unlike the nukes (which work on the genetic material), non-nukes act directly on the enzyme itself to prevent it from functioning correctly, e.g. Delavirdine, Efavirenz, Rilpivirine, Etravirine.
    • Protease Inhibitors (PIs): When HIV replicates inside cells, it creates long strands of its own genetic material. These long strands have to be cut into shorter strands in order for HIV to create more copies of itself. The enzyme that acts to cut up these long strands is called protease. Protease inhibitors (stoppers) block this enzyme and prevent those long strands of genetic material from being cut up into functional pieces, e.g. Amprenavir, Saquinavir, Indinavir, Tipranavir.
    • Entry or Fusion Inhibitors: These medications blocks the virus from entering in cells. HIV needs a way to attach and bond to CD4 cells, and it does that through special structures on cells called receptor sites. Receptor sites are found on both HIV and CD4 cells. Fusion inhibitors can target those sites on either HIV or CD4 cells and prevent HIV from ‘docking’ into healthy cells, e.g. Enfuvirtide, T-20, Maraviroc.
    • Integrase Inhibitors: HIV uses cells' genetic material to make its own DNA (a process called reverse transcription). Once that happens, the virus has to integrate its genetic material into the genetic material of body cells. This is accomplished by an enzyme called integrase. Integrase inhibitors block this enzyme and prevent the virus from adding its DNA into the DNA of CD4 cells. Preventing this process prevents the virus from replicating and making new viruses, e.g. Raltegravir, Dolutegravir.
    • Fixed-dose combinations: These are not a separate class of HIV medications but combinations of the above classes and a great advancement in HIV medicine. They include antiretrovirals which are combinations of 2 or more medications from one or more different classes. These antiretrovirals are combined into one single pill with specific fixed doses of these medicines, e.g. Efavirenz, Emtricitabine, Tenofovir, Disoproxil, Fumarate.
 
Nursing Management
 
Nursing Priorities
  • Prevent or minimize development of new infections.
  • Maintain homeostasis.
  • Promote comfort.
  • Support psychosocial adjustment.
  • Provide information about disease process, prognosis and treatment needs.
875
 
Discharge Goals
  • Infection prevented and resolved.
  • Complications prevented and minimized.
  • Pain and discomfort alleviated or controlled.
  • Patient dealing with current situation realistically.
  • Diagnosis, prognosis, and therapeutic regimen understood.
  • Plan in place to meet needs after discharge.
 
Nursing Diagnosis
  1. Imbalanced Nutrition: Less than Body Requirements related to Inability or altered ability to ingest, digest metabolize nutrients, nausea, vomiting, hyperactive gag reflex, intestinal disturbances, GI tract infections, fatigue.
    Possibly evidenced by:
    • Weight loss, decreased subcutaneous fat or muscle mass
    • Lack of interest in food, aversion to eating, altered taste sensation
    • Abdominal cramping, hyperactive bowel sounds, diarrhea
    • Sore, inflamed buccal cavity
    • Abnormal laboratory results: Vitamin, mineral and protein deficiencies, electrolyte imbalances.
    Desired outcomes:
    • Maintain weight or display weight gain toward desired goal.
    • Demonstrate positive nitrogen balance, be free of signs of malnutrition, and display improved energy level.
Interventions
  • Assess patient's ability to chew, taste, and swallow.
  • Auscultate bowel sounds.
  • Weigh as indicated. Evaluate weight in terms of premorbid weight. Compare serial weights and anthropometric measurements.
  • Note drug side effects.
  • Plan diet with patient, suggesting foods from home if appropriate. Provide small, frequent meals and snacks of nutritionally dense foods and nonacidic foods and beverages, with choice of foods palatable to patient. Encourage high-calorie and nutritious foods, some of which may be considered appetite stimulants. Note time of day when appetite is best, and try to serve larger meal at that time.
  • Limit food that induce nausea and vomiting or are poorly tolerated by patient because of mouth sores or dysphagia. Avoid serving very hot liquids and foods. Serve foods that are easy to swallow like eggs, ice cream, cooked vegetables.
  • Schedule medications between meals (if tolerated) and limit fluid intake with meals, unless fluid has nutritional value.
  • Encourage as much physical activity as possible.
  • Provide frequent mouth care, observing secretion precautions. Avoid alcohol-containing mouthwashes.
  • 876Provide rest period before meals. Avoid stressful procedures close to mealtime.
  • Remove existing noxious environmental stimuli or conditions that aggravate gag reflex.
  • Encourage patient to sit up for meals
  • Record ongoing caloric intake.
  • Administer, appetite stimulants: Dronabinol, Megestrol, Ooxandrolone
    • Antibiotic therapy: Ketoconazole, Fluconazole
    • Antidiarrheals: Diphenoxylat, Loperamide, Octreotide.
  1. Fatigue relate to decreased metabolic energy production, increased energy requirements or hypermetabolic state or altered body chemistry: side effects of medication, chemotherapy.
    Possibly evidenced by:
    • Unremitting lack of energy, inability to maintain usual routines, decreased performance, impaired ability to concentrate, lethargy
    • Disinterest in surroundings.
    Desired outcomes:
    • Report improved sense of energy.
    • Perform ADLs, with assistance as necessary.
    • Participate in desired activities at level of ability.
Intervention
  • Assess sleep patterns and note changes in thought processes and behavior.
  • Recommend scheduling activities for periods when patient has most energy. Plan care to allow for rest periods. Involve patient in schedule planning.
  • Establish realistic activity goals with patient.
  • Encourage patient to do whatever possible: Self-care, sit in chair, short walks. Increase activity level as indicated.
  • Identify energy conservation techniques: Sitting, breaking ADLs into manageable segments. Keep travel ways clear of furniture. Provide or assist with ambulation and self-care needs as appropriate.
  • Monitor physiological response to activity: Changes in BP, respiratory rate, or heart rate.
  • Encourage nutritional intake.
  • Refer to physical and occupational therapy.
  • Provide supplemental O2 as indicated.
  1. Acute or Chronic Pain related to tissue inflammation, infections, internal or external cutaneous lesions, rectal excoriation, malignancies, necrosis.
    Possibly evidenced by:
    • Reports of pain
    • Self-focusing; narrowed focus, guarding behaviors
    • Alteration in muscle tone; muscle cramping, ataxia, muscle weakness, paresthesias, paralysis
    • Autonomic responses; restlessness.
    877Desired outcomes:
    • Report pain relieved or controlled.
    • Demonstrate relaxed posture or facial expression.
    • Be able to sleep or rest appropriately.
Interventions
  • Assess pain reports, noting location, intensity (0–10 scale), frequency, and time of onset. Note nonverbal cues like restlessness, tachycardia, grimacing.
  • Instruct and encourage patient to report pain as it develops rather than waiting until level is severe.
  • Encourage verbalization of feelings.
  • Provide diversional activities: Provide reading materials, light exercising, visiting, etc.
  • Perform palliative measures: Repositioning, massage, ROM of affected joints.
  • Instruct and encourage use of visualization, guided imagery, progressive relaxation, deep-breathing techniques, meditation, and mindfulness.
  • Apply warm or moist packs to pentamidine injection and IV sites for 20 min after administration.
  • Administer analgesics or antipyretics, narcotic analgesics. Use patient-controlled analgesia (PCA).
  1. Impaired Skin Integrity related to decreased level of activity, altered sensation, skeletal prominence, changes in skin turgor.
    May be related to:
    • Immunologic deficit: AIDS-related dermatitis; viral, bacterial, and fungal infections (e.g. herpes, Pseudomonas, Candida); opportunistic disease processes.
    Possibly evidenced by:
    • Skin lesions; ulcerations; decubitus ulcer formation.
    Desired outcomes:
    • Improvement in wound or lesion healing.
    • Demonstrate behaviors or techniques to prevent skin breakdown and promote healing.
Interventions
  • Assess skin daily. Note color, turgor, circulation, and sensation.
  • Describe and measure lesions and observe changes. Take photographs if necessary.
  • Maintain and instruct in good skin hygiene: Wash thoroughly, pat dry carefully, and gently massage with lotion or appropriate cream.
  • Reposition frequently. Use turn sheet as needed.
  • Encourage periodic weight shifts. Protect bony prominences with pillows, heel and elbow pads.
  • Encourage ambulation as tolerated.
  • Cleanse perianal area by removing stool with water and mineral oil or commercial product.
  • Avoid use of toilet paper if vesicles are present. Apply protective creams: zinc oxide, A and D ointment.
  • 878File nails regularly.
  • Cover open pressure ulcers with sterile dressings or protective barrier. Tegaderm, DuoDerm, as indicated.
  • Provide foam, flotation, alternate pressure mattress or bed.
  • Obtain cultures of open skin lesions.
  • Apply and administer medications as indicated.
  1. Impaired oral mucous membrane related to immunologic deficit and presence of lesion-causing pathogens, dehydration, malnutrition, ineffective oral hygiene and side effects of drugs, chemotherapy.
    Possibly evidenced by:
    • Open ulcerated lesions, vesicles
    • Oral pain or discomfort
    • Stomatitis; leukoplakia, gingivitis, carious teeth.
    Desired outcomes:
    • Display intact mucous membranes, which are pink, moist, and free of inflammation and ulcerations.
    • Demonstrate techniques to maintain integrity of oral mucosa.
Intervention
  • Assess mucous membranes and document all oral lesions. Note reports of pain, swelling, difficulty with chewing and swallowing.
  • Provide oral care daily and after food intake, using soft toothbrush, nonabrasive toothpaste, nonalcohol mouthwash, floss, and lip moisturizer.
  • Rinse oral mucosal lesions with saline and dilute hydrogen peroxide or baking soda solutions.
  • Suggest use of sugarless gum and candy.
  • Encourage oral intake of at least 2500 ml/day.
  • Encourage patient to refrain from smoking.
  • Obtain culture specimens of lesions.
  • Administer medications, as indicated: nystatin, ketoconazole.
  • Refer for dental consultation, if appropriate.
  • Plan diet to avoid salty, spicy, abrasive, and acidic foods or beverages. Check for temperature tolerance of foods. Offer cool or cold smooth foods.
  1. Disturbed thought process related to hypoxemia, CNS infection by HIV, brain malignancies and disseminated systemic opportunistic infection.
    Possibly evidenced by:
    • Altered attention span; distractibility
    • Memory deficit
    • Disorientation, cognitive dissonance, delusional thinking
    • Sleep disturbances.
    Desired outcomes:
    • Maintain usual reality orientation and optimal cognitive functioning.
879Intervention
  • Assess mental and neurological status using appropriate tools.
  • Consider effects of emotional distress. Assess for anxiety, grief, and anger.
  • Monitor medication regimen and usage.
  • Investigate changes in personality, response to stimuli, orientation and level of consciousness; or development of headache, nuchal rigidity, vomiting, fever, seizure activity.
  • Maintain a pleasant environment with appropriate auditory, visual, and cognitive stimuli.
  • Provide reorientation by putting on radio, television, calendars, clocks, room with an outside view if necessary. Use patient's name. Identify yourself. Maintain consistent personnel and structured schedules as appropriate.
  • Encourage family to socialize and provide reorientation with current news, family events.
  • Encourage patient to do as much as possible: dress and groom daily, see friends, and so forth.
  • Discuss use of datebooks, lists, and other devices to keep track of activities.
  • Encourage discussion of concerns and fears.
  • Provide information about care on an ongoing basis. Answer questions simply and honestly. Repeat explanations as needed.
  • Reduce provocative and noxious stimuli. Maintain bedrest in quiet, darkened room if indicated.
  • Decrease noise, especially at night.
  • Discuss causes or future expectations and treatment if dementia is diagnosed.
  • Maintain safe environment: Excess furniture out of the way, call bell within patient's reach, bed in low position and rails up, restriction of smoking, seizure precautions, etc.
  1. Anxiety and fear related to threat to self-concept, threat of death, and change in health, separation from support system and fear of transmission of the disease to family and loved ones.
    Possibly evidenced by:
    • Increased tension, apprehension, feelings of helplessness and hopelessness
    • Expressed concern regarding changes in life
    • Fear of unspecific consequences
    • Somatic complaints, insomnia; sympathetic stimulation, restlessness.
    Desired outcomes:
    • Verbalize awareness of feelings and healthy ways to deal with them.
    • Display appropriate range of feelings and lessened fear and anxiety.
    • Demonstrate problem-solving skills.
    • Use resources effectively.
Intervention
  • Assure patient of confidentiality within limits of situation.
  • Maintain frequent contact with patient. Talk with and touch patient. Limit use of isolation clothing and masks.
  • 880Provide accurate, consistent information regarding prognosis. Avoid arguing about patient's perceptions of the situation.
  • Be alert to signs of withdrawal, anger, or inappropriate remarks as these can be signs of indenial or depression. Determine presence of suicidal ideation and assess potential on a scale of 1–10.
  • Provide open environment in which patient feels safe to discuss feelings or to refrain from talking.
  • Permit expressions of anger, fear, despair without confrontation. Give information that feelings are normal and are to be appropriately expressed.
  • Recognize and support the stage patient and family is at in the grieving process.
  • Explain procedures, providing opportunity for questions and honest answers. Arrange for someone to stay with patient during anxiety-producing procedures and consultations.
  • Identify and encourage patient interaction with support systems. Encourage verbalization and interaction with family.
  • Discuss advance directives, end-of-life desires or needs. Review specific wishes and explain various options clearly.
  • Provide contact with other resources as indicated: Spiritual advisor or hospice staff.
  • Refer to psychiatric counseling (psychiatric clinical nurse specialist, psychiatrist, social worker).
  1. Social isolation related to altered state of wellness, changes in physical appearance, alterations in mental status, perceptions of unacceptable social or sexual behavior and values.
    Possibly evidenced by:
    • Expressed feeling of aloneness imposed by others, feelings of rejection
    • Absence of support from partner, family, acquaintances and friends.
    Desired outcomes:
    • Identify supportive individual
    • Use resources for assistance
    • Participate in activities.
Intervention
  • Ascertain patient's perception of situation.
  • Spend time talking with patient during and between care activities. Be supportive, allowing for verbalization. Treat with dignity and regard for patient's feelings.
  • Limit or avoid use of mask, gown, and gloves when possible and when talking to patient.
  • Identify support systems available to patient, including presence of and relationship with immediate and extended family.
  • Explain isolation precautions and procedures to patient and family.
  • Encourage open visitation, telephone contacts, and social activities within tolerated level.
  • Develop a plan of action with patient: Look at available resources, support healthy behaviors.
  • Help patient problem-solve solution to short-term or imposed isolation.
  • 881Be alert to verbal or nonverbal cues: withdrawal, statements of despair, sense of aloneness. Ask patient if thoughts of suicide are being entertained.
  1. Powerlessness related to confirmed diagnosis of a potentially terminal disease, incomplete grieving process, Social ramifications of AIDS and alteration in body image.
    Possibly evidenced by:
    • Feelings of loss of control over own life
    • Depression over physical deterioration that occurs despite patient compliance with regimen
    • Anger, apathy, withdrawal, passivity
    • Dependence on others for care/decision-making, resulting in resentment, anger, guilt.
    Desired outcomes:
    • Acknowledge feelings and healthy ways to deal with them.
    • Verbalize some sense of control over present situation.
    • Make choices related to care and be involved in self-care.
Intervention
  • Identify factors that contribute to patient's feelings of powerlessness: diagnosis of a terminal illness, lack of support systems and lack of knowledge about present situation.
  • Assess degree of feelings of helplessness: Verbal or nonverbal expressions indicating lack of control, flat affect and lack of communication.
  • Encourage active role in planning activities, establishing realistic and attainable daily goals.
  • Encourage patient control and responsibility as much as possible. Identify things that patient can and cannot control.
  • Encourage living will and durable medical power of attorney documents, with specific and precise instructions regarding acceptable and unacceptable procedures to prolong life.
  • Discuss desires and assist with planning for funeral as appropriate.
  1. Deficient knowledge related to lack of exposure, information misinterpretation, cognitive limitation and unfamiliarity with information resources.
    Possibly evidenced by:
    • Questions and request for information
    • Inaccurate follow-through of instructions, development of preventable complications.
    Desired outcomes:
    • Verbalize understanding of condition and disease process and potential complications.
    • Identify relationship of signs and symptoms to the disease process and correlate symptoms with causative factors.
    • Verbalize understanding of therapeutic needs.
    • Correctly perform necessary procedures and explain reasons for actions.
    • Initiate necessary lifestyle changes and participate in treatment regimen.
882Intervention
  • Review disease process and future expectations.
  • Determine level of independence or dependence and physical condition. Note extent of care and support available from family and need for other caregivers.
  • Review modes of transmission of disease, especially if newly diagnosed.
  • Instruct patient and caregivers concerning infection control, using good handwashing techniques for everyone (patient, family, caregivers), using gloves when handling bedpans, dressings or soiled linens, wearing mask if patient has productive cough, placing soiled or wet linens in plastic bag and separating from family laundry, washing with detergent and hot water, cleaning surfaces with bleach and water solution of 1:10 ratio, disinfecting toilet bowl and bedpan with full-strength bleach, preparing patient's food in clean area, washing dishes and utensils in hot soapy water.
  • Stress necessity of daily skin care, including inspecting skin folds, pressure points, and perineum, and of providing adequate cleansing and protective measures: ointments, padding.
  • Ascertain that patient can perform necessary oral and dental care. Review procedures as indicated. Encourage regular dental care.
  • Review dietary needs (high-protein and high-calorie) and ways to improve intake when anorexia, diarrhea, weakness, depression interfere with intake.
  • Discuss medication regimen, interactions, and side effects.
  • Provide information about symptom management that complements medical regimen with intermittent diarrhea, take diphenoxylate before going to social event.
  • Stress importance of adequate rest.
  • Encourage activity and exercise at level that patient can tolerate.
  • Stress necessity of continued health care and follow-up.
  • Recommend cessation of smoking.
  • Identify signs and symptoms requiring medical evaluation: Persistent fever and night sweats, swollen glands, continued weight loss, diarrhea, skin blotches and lesions, headache, chest pain and dyspnea.
  • Identify community resources: Hospice and residential care centers, visiting nurse, home care services, meals on wheels, peer group support.
  1. Risk for injury related to abnormal blood profile, decreased vitamin K absorption, alteration in hepatic function, and presence of autoimmune antiplatelet antibodies, malignancies, and circulating endotoxins.
    Desired outcomes:
    • Display homeostasis as evidenced by absence of bleeding.
Intervention
  • Avoid injections, rectal temperatures and rectal tubes. Administer rectal suppositories with caution.
  • Maintain a safe environment. Keep all necessary objects and call bell within patient's reach and place bed in low position.
  • Maintain bedrest or chair rest when platelets are below 10,000 or as individually appropriate.
  • 883Hematest body fluids: Urine, stool, vomitus, for occult blood.
  • Observe for or report epistaxis, hemoptysis, hematuria, nonmenstrual vaginal bleeding, or oozing from lesions or body orifices or IV insertion sites.
  • Monitor for changes in vital signs and skin color: BP, pulse, respirations, skin pallor and discoloration.
  • Evaluate change in level of consciousness.
  • Avoid use of aspirin products and NSAIDs, especially in presence of gastric lesions.
  • Administer blood products as indicated.
  • Review laboratory studies: PT, aPTT, clotting time, platelets, Hb/Hct.
  1. Risk for deficient fluid volume related to copious diarrhea, profuse sweating, vomiting and hypermetabolic state.
    Desired outcomes:
    • Maintain hydration as evidenced by moist mucous membranes, good skin turgor, stable vital signs, and individually adequate urinary output.
Intervention
  • Monitor vital signs, including CVP if available. Note hypotension, including postural changes.
  • Note temperature elevation and duration of febrile episode. Administer tepid sponge baths as indicated. Keep clothing and linens dry.
  • Maintain comfortable environmental temperature.
  • Assess skin turgor, mucous membranes, and thirst.
  • Measure urinary output and specific gravity. Measure and estimate amount of diarrheal loss.
  • Weigh as indicated.
  • Monitor oral intake and encourage fluids of at least 2500 ml/day.
  • Make fluids easily accessible to patient; use fluids that are tolerable to patient and that replace needed electrolytes
  • Eliminate foods potentiating diarrhea
  • Encourage use of live culture yogurt or Lactobacillus acidophilus.
  • Administer fluids and electrolytes via feeding tube and IV, as appropriate.
  • Monitor laboratory studies as indicated: Serum or urine electrolytes; BUN, stool specimen collection.
  • Maintain hypothermia blanket if used.
  1. Risk for infection related to inadequate primary defenses: broken skin, traumatized tissue, stasis of body fluids, depression of the immune system, chronic disease, environmental exposure and invasive techniques.
    Desired outcomes:
    • Achieve timely healing of wounds
    • Be afebrile and free of purulent drainage or secretions and other signs of infectious conditions.
    • Identify participate in behaviors to reduce risk of infection.
884Intervention
  • Assess patient knowledge and ability to maintain opportunistic infection prophylactic regimen.
  • Wash hands before and after all care contacts. Instruct patient and family to wash hands as indicated.
  • Provide a clean, well-ventilated environment. Screen visitors and staff for signs of infection and maintain isolation precautions as indicated.
  • Discuss extent and rationale for isolation precautions and maintenance of personal hygiene.
  • Monitor vital signs, including temperature.
  • Assess respiratory rate and depth, note dry spasmodic cough on deep inspiration, changes in characteristics of sputum, and presence of wheezes or rhonchi. Initiate respiratory isolation when etiology of productive cough is unknown.
  • Investigate reports of headache, stiff neck, and altered vision. Note changes in mentation and behavior. Monitor for nuchal rigidity and seizure activity.
  • Examine skin and oral mucous membranes for white patches or lesions.
  • Clean patient's nails frequently. File, rather than cut, and avoid trimming cuticles.
  • Monitor reports of heartburn, dysphagia, and retrosternal pain on swallowing, increased abdominal cramping, and profuse diarrhea.
  • Inspect wounds and site of invasive devices, noting signs of local inflammation and infection.
  • Wear gloves and gowns during direct contact with secretions and excretions or any-time there is a break in skin of caregiver's hands. Wear mask and protective eyewear to protect nose, mouth, and eyes from secretions during procedures (suctioning) or when splattering of blood may occur.
  • Dispose of needles and sharps in rigid, puncture-resistant containers.
  • Label blood bags, body fluid containers, soiled dressings and linens, and package appropriately for disposal per isolation protocol.
  • Clean-up spills of body fluids and blood with bleach solution (1:10), add bleach to laundry.

Reproductive Disorders19

 
INTRODUCTION
The vagina is an elastic, muscular tube connecting the cervix of the uterus to the vulva and exterior of the body that is located between the bladder and the rectum. Measuring around 3 inches in length and less than an inch in diameter, the vagina stretches to become several inches longer and many inches wider during sexual intercourse and childbirth.
 
Size
In its normal state, there is anatomical variation in the length of the vagina of a woman of child-bearing age. The length is approximately 7.5 cm (2.5 to 3 in) across the anterior wall (front), and 9 cm (3.5 in) long across the posterior wall (rear), making the posterior fornix deeper than the anterior. During sexual arousal, the vagina expands in both length and width.
 
Layers
  • Epithelial layer: Deep to the epithelial layer is the lamina propria, a layer of connective tissue with many elastin fibers that allow the vagina to stretch.
  • 886Lamina propria: A layer of smooth muscle tissue located deep to the lamina propria allows the vagina to expand and contract during sexual intercourse and childbirth.
  • Tunica externa: Surrounding the smooth muscle is the outermost layer of the vagina known as the tunica externa. The tunica externa is a layer of dense irregular connective tissue that forms the outer protective shell of the vagina.
 
Functions
The vagina provides the passageway for childbirth and menstrual flow. It also receives the penis and semen during sexual intercourse. The inner surface of the vagina is folded to provide greater elasticity and to increase friction during sexual intercourse. Watery secretions produced by the vaginal epithelium lubricate the vagina and have an acidic pH to prevent the growth of bacteria and yeast. The acidic pH also makes the vagina an inhospitable environment for sperm, which has resulted in males producing alkaline seminal fluid to neutralize the acid and improve the survival of sperm.
 
Uterus
  • Uterus is a hollow muscular pear-shaped organ, flattened anteroposteriorly. It lies in the pelvic cavity between the urinary bladder and the rectum. It is about 7.5 cm long, 5 cm wide and its walls are about 2.5 cm thick. It weighs about 30 to 40 gm.
  • The parts of the uterus are the fundus, body, and cervix.
    • Fundus: This is the dome-shaped part of the uterus above the openings of the uterine tubes.
    • Body: This is the main part. It is narrowest inferiorly at the internal os, where it is continuous with the cervix.
    • Cervix (neck of uterus): This protrudes through the anterior wall of the vagina, opening into it at the external os.
 
Structure
The walls of the uterus are composed of three layers of tissue:
  • Perimetrium: This is peritoneum, which is distributed differently on the various surfaces of the uterus. Anteriorly, it lies over the fundus and the body where it is folded on the upper surface of the urinary bladder. This fold of peritoneum forms the vesicouterine pouch. Posteriorly, the peritoneum covers the fundus, the body and the cervix, then it folds back on the rectum to form the rectouterine pouch.
  • Myometrium: It is the thickest layer of tissue in the uterine wall. It is a mass of smooth muscle fibers interlaced with areolar tissue, blood vessels and nerves.
  • Endometrium: It consists of columnar epithelium containing a large number of mucus-secreting tubular glands. It is divided functionally into two layers:
    • The functional layer is the upper layer and it thickens and becomes rich in blood vessels in the first half of the menstrual cycle. If the ovum is not fertilized and does not implant, this layer is shed during menstruation.
    • The basal layer lies next to the myometrium and is not lost during menstruation. It is the layer from which the fresh functional layer is regenerated during each cycle.
887
 
Functions of Uterus
The uterus is a dynamic female reproductive organ that is responsible for several reproductive functions, including menstruation, implantation, gestation, labor, and delivery. It is responsive to the hormonal milieu within the body, which allows adaptation to the different stages of a woman's reproductive life. The uterus adjusts to reflect changes in ovarian steroid production during the menstrual cycle and displays rapid growth and specialized contractile activity during pregnancy. It serves two important functions: It is the organ of menstruation and, during pregnancy, it receives the fertilized ovum, retains and nourishes it until it expels the fetus during labor.
 
Terminology
  • Premenstrual syndrome: Emotional and physical manifestations that occur cyclically in the female before menstruation.
  • Dysmenorrhea: Characterized by severe and frequent menstrual cramps and pain associated with menstruation.
  • Amenorrhea: It is the medical term used for the absence of menstrual periods.
  • Fistula: It is an abnormal opening between two internal organs and exterior of the body.
  • Vaginitis: It is an inflammation of vagina.
  • Cryptorchidism: It is also called undescended testis.
  • Epispadias: It is congenital anomaly in males, the urethra is on the upper surface of the penis.
FEMALE REPRODUCTIVE DISORDERS
 
PREMENSTRUAL SYNDROME
It is defined as a combination of emotional and physical manifestations that occur cyclically in the female before menstruation and regress or disappear during menstruation.
 
Etiology
The cause of PMS is unclear. However, neuroendocrine mechanisms appear to be involved. It is not clear whether PMS is a single syndrome or a group of separate disorders. Some suggested causes of PMS are as follows:
  • Estrogen progesterone imbalance, especially in estrogen excess and a progesterone deficiency or estrogen deficiency.
  • Interaction among estrogen, progesterone, and aldosterone.
  • Excess of prolactin, hypothyroidism or hypoglycemia.
  • Dietary factors, such as deficiency of vitamin B6, magnesium.
  • Lifestyle factors, such as increased stress and poor diet.
888
 
Pathophysiology
 
Clinical Manifestations
 
Physical Symptoms
  • Fluid retention
  • Sensation of weight gain
  • Episodes of binge-eating
  • Breast discomfort
  • Headache
  • Peripheral edema
  • Abdominal cramp
  • Sleep disturbance
  • Joint or muscle pain.
 
Affective Symptoms
  • Depression
  • Anger
  • Anxiety
  • Irritability
  • Confusion
  • Insomnia
  • Tendency to cry easily
  • Poor concentration.
 
Diagnostic Evaluation
There is no objective of diagnosing PMS. Diagnosis is usually made by documenting the cyclic nature of the symptoms on a menstrual calendar. A diagnosis of PMS requires a 889recurrence of symptoms for a minimum of three menstrual cycles. Diagnosis is made at the time of symptoms rather than on the presence of particular symptoms.
 
Management
Vitamins and minerals: Daily intake of vitamin B6 and elimination of caffeine have improved some premenstrual manifestations.
 
Medications
  • Spironolactone is a synthetic steroid aldosterone antagonist that inhibits the physiologic effect of aldosterone on the distal tubules. It is commonly used to treat the edema associated with excessive aldosterone secretions.
  • Progesterone may relieve physiologic and psychological manifestations.
  • Bromocriptine reduces serum prolactin concentrations by inhibiting prolactin release from the anterior pituitary gland. It has been used successfully to reduce breast pain in some cases of PMS.
  • Antidepressants: Selective serotonin reuptake inhibitors, which include fluoxitine, paroxetine and sertraline and others, have been successful in reducing symptoms and first-line agents for treatment of premenstrual syndrome.
  • Analgesic: These are commonly given for menstrual cramps, headache and pelvic discomfort. The most effective group of analgesic appears to be the nonsteroidal anti-inflammatory medications, e.g. ibuprofen.
 
Health Education
  • Avoid salt before menstrual period.
  • Reduce caffeine intake.
  • Quit smoking.
  • Reduce alcohol intake.
  • Increase fiber intake.
  • Adequate rest and sleep.
  • Eat smaller quantity but more frequent diet to reduce fluid retention.
 
DYSMENORRHEA
It is a menstrual condition characterized by severe and frequent menstrual cramps and pain associated with menstruation. The degree of pain and discomfort varies with the individual.
 
Types
  • Primary dysmenorrhea: It is believed to be caused by either a prostaglandin excess or an increased sensitivity to prostaglandins with no underlying pathologic pelvic disorders.
  • Secondary dysmenorrhea: It has caused other than menstruation and natural production of prostaglandins. The cramps caused by another medical problem, such as endometriosis, uterine fibroid, pelvic inflammatory disease, etc.
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Etiology
 
Primary Dysmenorrhea
  • Early age of menarche (< 12 years)
  • Nulliparity
  • Heavy and prolonged menstrual flow
  • Smoking
  • Alcohol
  • Family history
 
Secondary Dysmenorrhea
  • Pelvic inflammatory disease
  • Endometriosis
  • Uterine prolapse
  • Uterine myomas
  • Polyps
 
Pathophysiology
 
Clinical Manifestations
  • Pain: Concentrated in lower abdomen in umbilical region or the suprapubic region of abdomen. May radiate to thighs and lower back.
  • Nausea, vomiting
  • 891Headache
  • Dizziness
  • Fainting
  • Fatigue
  • Diarrhea
  • Back pain
 
Diagnostic Evaluation
  • History and physical examination.
  • Physical examination: Manual vaginal examination to examine for masses, tenderness or enlarged uterus. Examine for discharge coming from the cervix which suggests pelvic inflammatory disease.
  • Pelvic ultrasound: To reveal function of internal organ if there is an enlarged uterus or fallopian tube or ovarian mass found on physical examination or if suspect ectopic pregnancy.
  • Blood test: Full blood count and ESR.
  • Thyroid function test.
  • Pregnancy test: If suspect an ectopic pregnancy.
  • Hysteroscopy: A visual examination of the canal of the cervix and the interior of the uterus using an instrument (hysteroscope) inserted through the vagina.
 
Management
  • Administer prostaglandin synthesis inhibitors: Prostaglandin synthesis inhibitors may provide relief by decreasing prostaglandin activity, even in the presence of ovulatory cycle. Some commonly prescribed medications in this group are ibuprofen, indomethacin.
  • Analgesics, such as aspirin and paracetamol, may be useful as a starting point, especially when NSAIDs are contraindicated.
  • Administer oral contraceptives: If contraception as well as relief of dysmenorrheal is desired, combination of oral contraceptives may relieve menstrual pain. The combination inhibits ovulation, resulting in decreased endometrial prostaglandin production and a concurrent reduction in uterine activity.
 
Nonpharmacological Treatment
  • Women should be advised that during acute pain, relief may be obtained by lying down for short period.
  • Drinking hot beverages such as herbal teas.
  • Applying heat to the abdomen or back.
  • Taking warm tub bath.
  • Regular exercise is thought to be beneficial because it may reduce endometrial hyperplasia and subsequently reduce prostaglandin production.
  • Acupuncture and transcutaneous nerve stimulation also provide varying degree of relief.
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Nursing Management
 
Nursing Assessment
  • Assess the general condition of the patient. Assess the level of discomfort and vital signs of the patient.
  • Obtain full history of illness.
 
Nursing Diagnosis
  • Acute pain related to increased uterine contractility, hypersensitivity.
  • Imbalanced nutrition less than body requirement related to nausea, vomiting.
  • Ineffective individual coping related to emotional excess.
  • Activity intolerance related to pain.
  • Disturbed sleeping pattern related to discomfort.
  1. Acute pain related to increased uterine contractility
    Interventions
    • Assess the level and severity of pain.
    • Provide warm application to the patient, like hot water bottle.
    • Massage the abdominal area to reduce the pain due to the stimulus of therapeutic touch.
    • Provide diversional therapy to the patient, like music, meditation, etc.
    • Provide comfort devices to the patient.
    • Administer analgesic to the patient.
  2. Imbalance nutrition less than body requirement related to nausea and vomiting
    Interventions
    • Assess the condition of the patient.
    • Provide small and frequent diet to the patient.
    • Maintain intake and output of the patient.
    • Provide liquid diet to the patient.
  3. Ineffective individual coping related to emotional related to emotional excess
    Interventions
    • Assess the patient's understanding of her illness.
    • Determine additional symptoms that accompany it.
    • Provide an opportunity to the patient to discuss about the pain.
    • Provide relaxation therapy and deep breathing exercise to the patient.
    • Give the period of sleep and rest.
    • Provide psychological support to the patient.
    • Counsel the patient.
 
AMENORRHEA
  • Amenorrhea is the medical term used for the absence of menstrual periods, either on a permanent or temporary basis in women of reproductive age.
  • Physiological state of amenorrhea is seen during pregnancy and lactation.
  • Other than reproductive years, menses is absent during childhood and after menopause.
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Classification of Amenorrhea
  • Primary amenorrhea: It is the absence of menstrual bleeding and secondary sexual characteristics (e.g. Breast development, pubic hair) in a girl by age of 14 years or the absence of menstrual bleeding with normal development of secondary sexual characteristics in a girl by age of 16 years. It may be caused by:
    • Congenital absence of uterus
    • Failure of ovary to receive or maintain egg cells
    • Delay in pubertal development.
  • Secondary amenorrhea: It is the absence of menstrual bleeding in a woman who had been menstruating but later stop menstruating 3 or more months in the absence of pregnancy, lactation and menopause. It may be caused by:
    • Hormonal disturbance
    • Premature menopause
    • Intrauterine scar formation
 
Etiology
 
Lifestyle Factors
  • Sometimes lifestyle factors contribute to amenorrhea, for instance:
  • Low body weight: Excessively low body weight, about 10 percent under normal weight interrupts many hormonal functions in our body, potentially halting ovulation. Women who have an eating disorder, such as anorexia or bulimia, often stop having periods because of these abnormal hormonal changes.
  • Excessive exercise: Women who participate in activities that require rigorous training, such as ballet, may find their menstrual cycles interrupted. Several factors combine to contribute to the loss of periods in athletes, including low body fat, stress and high energy expenditure.
  • Stress: Mental stress can temporarily alter the functioning of hypothalamus, an area of brain that controls the hormones that regulate menstrual cycle. Ovulation and menstruation may stop as a result. Regular menstrual periods usually resume after stress decreases.
    • Hormonal imbalance
    • Many types of medical problems can cause hormonal imbalance, including:
  • Polycystic ovary syndrome (PCOS): PCOS causes relatively high and sustained levels of hormones, rather than the fluctuating levels seen in the normal menstrual cycle.
  • Thyroid malfunction: An overactive thyroid gland (hyperthyroidism) or underactive thyroid gland (hypothyroidism) can cause menstrual irregularities, including amenorrhea.
  • Pituitary tumor: A noncancerous (benign) tumor in pituitary gland can interfere with the hormonal regulation of menstruation.
  • Premature menopause: Menopause usually begins around age 50. But, for some women, the ovarian supply of eggs diminishes before age 40 and menstruation stops.
    • Structural problems
894Problems with the sexual organs themselves also can cause amenorrhea. Examples include:
  • Uterine scarring: Asherman's syndrome, a condition in which scar tissue builds up in the lining of the uterus, can sometimes occur after a dilation and curettage (D & C), cesarean section or treatment for uterine fibroids. Uterine scarring prevents the normal buildup and shedding of the uterine lining.
  • Lack of reproductive organs: Sometimes problems arise during fetal development that lead to a girl being born without some major part of her reproductive system, such as her uterus, cervix or vagina. Because her reproductive system did not develop normally, she cannot have menstrual cycles.
  • Structural abnormality of the vagina: An obstruction of the vagina may prevent visible menstrual bleeding. A membrane or wall may be present in the vagina that blocks the outflow of blood from the uterus and cervix.
 
Clinical Manifestations
Symptoms of primary amenorrhea may include:
  • Headache
  • Galactorrhea
  • Acne
  • Excessive hair growth (hirsutism)
  • Excessive anxiety
Symptoms of secondary amenorrhea may include:
  • Nausea
  • Breast tenderness
  • Headache
  • Being very thirsty
  • Weight gain or weight loss may be present
  • Goiter (an enlarged thyroid gland)
  • Darkening skin
  • Vaginal dryness
  • Hot flashes
  • Night sweats
  • Mood changes
 
Diagnostic Evaluation
  • History and physical examination
  • Lab tests:
    • Pregnancy test: This will probably be the first test doctor suggests, ruling out or confirming a possible pregnancy.
    • Thyroid function test: Measuring the amount of thyroid-stimulating hormone (TSH) in blood can determine if thyroid is working properly.
    • Ovary function test: Measuring the amount of follicle-stimulating hormone (FSH) in blood can determine if ovaries are working properly.
    • 895Prolactin test: Low levels of the hormone prolactin may be a sign of a pituitary gland tumor.
    • Male hormone test: If someone is experiencing increased facial hair and a lowered voice, doctor may assess the level of male hormones in blood.
  • Ultrasound: This test uses sound waves to produce images of internal organs. Ultrasound test is used to check for any abnormalities in reproductive organs.
  • Computerized tomography (CT): CT scans combine many X-ray images taken from different directions to create cross-sectional views of internal structures. A CT scan can indicate whether uterus, ovaries and kidneys look normal.
  • Magnetic resonance imaging (MRI): MRI uses radiowaves with a strong magnetic field to produce exceptionally detailed images of soft tissues within the body.
  • Hysteroscopy: A test in which a thin, lighted camera is passed through vagina and cervix to look at the inside of the uterus.
 
Management
Treatment of both primary and secondary amenorrhea is determined by the precise cause of amenorrhea.
 
Goals
  • To relieve symptoms of hormonal imbalance
  • To establish menstruation
  • To prevent complications associated with amenorrhea
  • To achieve fertility.
 
Drug Therapy
  • Dopamine agonists, such as bromocriptine or pergolide are effective in treating hyperprolactinemia. In most women, treatment with dopamine agonists restores normal ovarian endocrine function and ovulation.
  • Hormonal replacement therapy, consisting of an estrogen—a progestin, is needed for women with estrogen deficiency.
  • Metformin is a drug that has been successfully used in women with polycystic ovary syndrome to induce ovulation.
 
Surgical Management
  • Some pituitary and hypothalamic tumours may require surgery and, in some cases, radiation therapy.
  • Women with intrauterine adhesions require dissolution of the intrauterine adhesions.
  • Surgical procedures required for other genital tract abnormalities depend on the specific clinical situation.
 
VAGINAL FISTULA
A fistula is an abnormal opening between two internal organs and exterior of the body. Fistula indicates the two areas that are connected abnormally. It may occur congenital as well as due to tissue damage of the particular areas.
A fistula is an abnormal connection between the two different organs. Vaginal fistula is of four types:
  • Rectovaginal fistula: It is an opening between rectum and vagina.
  • Vesicovaginal fistula: It is an opening between the bladder and the vagina.
  • 896Uterovaginal fistula: It is an opening between the ureter and the vagina.
  • Urethrovaginal fistula: It is an opening between the urethra and vagina.
  • Vaginoperineal fistula: Vaginoperineal fistula is an opening between the vagina and the perineum.
 
Etiology
  • A vaginal fistula starts with some kind of tissue damage. After days to years of tissue breakdown, a fistula opens up. Vaginal fistulas are not a common problem in developed countries.
  • A vaginal fistula may result from an injury during childbirth.
  • Crohn's disease or other inflammatory bowel disease can cause vaginal fistula.
  • Radiation treatment for pelvic cancer.
  • Surgery of the back wall of the vagina, the perineum, anus, or rectum.
  • A deep tear in the perineum or an infected episiotomy after childbirth.
 
Pathophysiology
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Signs and Symptoms
Depending on the size and location of the fistula, the patient may have minor symptoms or significant problems with continence and hygiene. Signs and symptoms of a rectovaginal fistula may include:
  • A vaginal fistula is painless. But a fistula lets urine or feces pass into the vagina. This is called incontinence.
  • Passing stool via the vagina
  • Inability to control bowel movements
  • Foul-smelling vaginal discharge
  • Pain during sexual intercourse
  • Persistent pain in the pelvic area
  • The symptoms of a rectovaginal fistula often cause emotional distress as well as physical discomfort, which can impact self-esteem and intimate relationships.
 
Diagnostic Evaluation
Often a fistula is not found during the physical examination. The doctor may recommend other tests, such as those below, to locate and evaluate a vaginal fistula. These tests can also help medical team in planning for surgery.
  • Contrast tests: A vaginogram or a barium enema can help identify a fistula located in the upper rectum. These tests use a contrast material to show either the vagina or the bowel on an X-ray image.
  • Blue dye test: This test involves placing a tampon into vagina, then injecting blue dye into the rectum. Blue staining on the tampon shows the presence of a fistula.
  • Computerized tomography (CT) scan: A CT scan of abdomen and pelvis provides more detail than a standard X-ray does. The CT scan can help locate a fistula and determine its cause.
  • Magnetic resonance imaging (MRI): This test creates images of soft tissues in the body. MRI can show the location of a fistula, as well as involvement of pelvic organs or the presence of a tumor.
  • Anorectal ultrasound: This procedure uses sound waves to produce a video image of anus and rectum. The doctor inserts a narrow, wand-like instrument into the anus and rectum. Anorectal ultrasound can evaluate the structure of anal sphincter and may show injury caused during childbirth.
  • Anorectal manometry: This test measures the sensitivity and functions of the rectum and can provide useful information about rectal sphincter and ability to control stool passage. This test does not locate fistulas, but it can help in planning to repair the fistula.
  • Urinalysis: To check for infection and blood test (complete blood count) to check for signs of infection in the body.
 
Complications
Physical complications of rectovaginal fistula may include:
  • Incontinence
  • Problems with hygiene
  • 898Recurrent vaginal or urinary tract infections
  • Irritation or inflammation of the vagina, perineum or the skin around anus
  • Infected fistula that forms an abscess, a problem that can become life-threatening if not treated
  • Fistula recurrence.
 
Management
  • Education: The majority of patients with fistula are from rural areas, where there are low literacy levels and a lack of physical and economic access to medical care. Since many expectant mothers do not attend antenatal clinics, exposure to high-risk conditions, medical and obstetric complications which endanger the life or harm the health of the mother and her baby, will not be detected early enough for precautionary measures to be taken. So, education should be given to the pregnant women specially.
  • Health care facilities: In the short term, better use of existing obstetric services and increased provision of effective health services in rural areas will lower the incidence of fistula. Such improvements would lead women to seek safer obstetric practices, including the use of family planning, delayed childbearing, and prenatal and antenatal care during pregnancy. Good hygiene can help ease discomfort and reduce the chance of vaginal or urinary tract infections while waiting for repair.
 
Personal Hygiene
  • Wash with water: Gently wash the outer genital area with warm water each time when vaginal discharge or passage of stool is experienced.
  • Avoid irritants: Soap can dry and irritate skin, but a gentle unscented soap may be necessary in moderation. Avoid harsh or scented soap and scented tampons. Vaginal douches can increase chance of infection.
  • Dry thoroughly: Allow the area to air-dry after washing, or gently pat the area dry with toilet paper or a clean washcloth.
  • Avoid rubbing with dry toilet paper: Premoistened, alcohol-free wipes or moistened cotton balls may be a good alternative for cleaning the area.
  • Use a cold compress: Apply a cold compress, such as a washcloth, to the folds at the opening of the vagina.
  • Apply a cream or powder: Moisture-barrier creams help keep irritated skin from having direct contact with liquid or stool. Nonmedicated talcum powder or cornstarch also may help relieve discomfort. Be sure the area is clean and dry before applying any cream or powder.
  • Wear loose clothing: Tight clothing can restrict airflow, making skin problems worse. Products such as absorbent pads, disposable underwear or adult diapers can help if patient is passing liquid or stool.
 
Pharmacological Management
Depending on the circumstances, the doctor may recommend medications, such as:
  • Antibiotics: Antibiotics may also be recommended for women with Crohn's disease who develop a fistula.
  • 899Nonsteroidal anti-inflammatory drugs (NSAIDs): NSAIDs are the mostly commonly used drugs for arthritis-related pain, swelling and stiffness. They interfere with the body's production of hormone-like chemicals called prostaglandins. Prostaglandins are one of the biggest contributors to inflammation in the body. NSAIDs are available over-the-counter or with a prescription. They include aspirin, ibuprofen, naproxen, etc.
 
Surgical Management
  • The main treatment for all types of fistulas needs surgical repair. The success and recovery rate from an operation to correct simple fistula is very high, almost 90%. However, the success of the repair is not only dependent on good surgery, but also on excellent nursing care and the prevention of complications. Sometimes fistulas heal on their own, but most people need surgery to close or repair the abnormal connection. Before an operation can be done, the skin and other tissue around the fistula must be healthy, with no signs of infection or inflammation.
  • Urinary or colorectal bypass surgery: This essentially involves repairing a hole in the bladder or rectum and can usually take place through the vagina without the need for major incision. The operation is delicate and specially trained surgeons and support staff are required.
    • Sewing an anal fistula plug or patch of biologic tissue into the fistula to allow the tissue to grow into the patch and heal the fistula.
    • Using a tissue graft taken from a nearby part of the body or folding a flap of healthy tissue over the fistula opening.
    • Doing more complicated surgical repair if the anal sphincter muscles also are damaged or if there is scarring or tissue damage from radiation or Crohn's disease.
    • Performing a colostomy before repairing a fistula in more complex or recurrent cases to divert stool through an opening into the abdomen instead of through rectum. This may be needed if patient had tissue damage or scarring from previous surgery or radiation treatment, an ongoing infection or significant fecal contamination, a cancerous tumor, or an abscess. If a colostomy is needed, the surgeon may wait 8 to 12 weeks before repairing the fistula. Usually after about three to six months and confirmation that the fistula has healed, the colostomy can be reversed and normal bowel function is restored.
 
Nursing Management
  • History taking: The nurse will first consider history of vaginal infections or sexually transmitted infections and perform a physical or pelvic examination. If women have a discharge from vagina, a sample will be sent to a lab for analysis to determine whether there is an infection or not.
  • Psychological assessment: Psychosocial assessment should include evaluation of the patient's home situation and a sexual history. Ask the patient about the type of contraception she and her partner use. Provide a private environment to allow the patient to answer questions without being embarrassed.
 
Nursing Diagnoses
  • Risk for infection related to contamination of urinary tract by flora or contamination of the vagina by rectal organisms.
  • 900Impaired urinary elimination related to fistula.
  • Anxiety related to the diagnosis of fistula, surgery and possible loss of femininity.
  • Sexual dysfunction related to change in vaginal structure.
  • Self-care deficit related to lack of understanding of perineal care and general health status.
  1. Risk for infection related to contamination of urinary tract by flora or contamination of the vagina by rectal organisms.
    Interventions
    • Encourage frequent sitz baths.
    • Perform vaginal irrigation as ordered, and teach patient the procedure.
    • Before repair surgery, administer prescribed antibiotics to reduce pathogenic flora in the intestinal tract.
    • Maintain patient on clear liquids as prescribed to limit bowel activity for several days.
    • Encourage rest because of debilitation.
    • Administer warm perineal irrigations to decrease healing time and increase comfort.
  2. Impaired urinary elimination related to fistula.
    Interventions
    • Suggest the use of perineal pads or incontinence products preoperatively.
    • Maintain proper drainage from indwelling catheter to prevent pressure on newly sutured tissue.
    • Administer vaginal or bladder irrigations gently because of tenderness at operative site.
    • Maintain strict intake and output records.
    • Encourage patient to express feelings about her altered route of elimination and share them with significant others.
    • Prevention: Prevention of fistulas requires skilled attendants at birth and a swift surgical intervention if obstructed labor occurs. The pressure of the fetal head during obstructed labor causes ischemia to the pelvic organs, and a spectrum of injuries follows as a consequence.
  3. Patient education and health maintenance
    • Teach patient to report signs of infection early.
    • Teach patient to clean perineum gently and to follow surgeon's instructions on when to resume sexual intercourse and strenuous activity.
    • Advise patient to keep regular follow-up appointments.
 
VAGINITIS
It is an inflammation of vagina.
 
Etiology and Types
There are many different causes and types of vaginitis. These are:
  • Noninfectious vaginitis: It refers to vaginal inflammation that is due to chemical irritants or allergies. Spermicides, douches, detergents, fabric softeners, and latex condoms can 901all irritate the vaginal lining. Also, some sanitary napkins can cause irritation at the entrance to the vagina.
  • Atrophic vaginitis: It may occur after a woman has reached menopause. It results from lower hormone (estrogen) levels and the thinning of the vaginal lining caused by them. This makes the vagina more prone to irritation.
  • Infectious vaginitis: It is caused by an infection with bacteria or yeast. Trichomoniasis is caused by a parasite called trichomonas vaginalis and spreads through unprotected sex with an infected partner. Other types of vaginal infections can occur when a woman has a fistula, an abnormal passage connecting the intestine to the vagina. This allows stool to enter the vaginal area, greatly increasing the risk of infections.
  • Bacterial vaginitis: It may be due to an imbalance between normally occurring bacteria that protect the vagina and potentially infectious ones. Cigarette smoking, using intrauterine devices, douching, and having multiple sexual partners—these all have been increasing the risk of infection. Bacterial vaginitis is not considered a sexually transmitted infection, however, since it can occur in women who have never had vaginal intercourse.
  • Yeast infection: Also known as vaginal candidiasis, occurs when there is an overgrowth of the yeast called Candida that normally lives in the vagina. Anything that changes the type and amount of bacteria normally present in the vagina, such as douching or irritation from inadequate vaginal lubrication can increase risk. An yeast infection can be sexually transmitted, especially through oral-genital sexual contact. However, yeast infection is not considered a sexually transmitted infection because it happens in women who are not sexually active and the candida fungus is naturally present in the vagina. Newborns can also have vaginal inflammation and discharge for the first couple of weeks of life, caused by exposure to the mother's estrogen just prior to birth.
 
Pathophysiology
The vagina is protected against infection by its normal pH 3.5–4.5 which is maintained by the actions of Lactobacillus Acidophilus, which maintains normal vaginal ecosystem. These bacteria suppress growth of anerobes and produce lactic acid which maintains normal pH.
 
Signs and Symptoms
  • Bacterial infection: In some cases, women have no symptoms even if they have a bacterial infection. Generally, bacterial vaginitis causes itching and burning during urination or after sexual intercourse. There may also be whitish discharge with an unpleasant (fishy) odor. The discharge may be more noticeable after sex.
  • 902Trichomoniasis infection: It can be quite severe for some women, whereas others may have no symptoms at all. Trichomoniasis causes vaginal soreness and, sometimes, abdominal discomfort. It can lead to heavy yellow-green or grey discharge accompanied by an unpleasant odor. Urination and sexual intercourse can be painful. If left untreated during pregnancy, trichomoniasis can lead to premature labor.
  • Yeast infections: These include vaginal itching and painful urination. The labia often swell and can be quite sore. There may be a thick and whitish discharge that can look like cottage cheese.
  • Irritant or allergic vaginitis: It can cause mild-to-severe itching or burning of the vagina, which often becomes swollen and red. This type of vaginitis does not cause a vaginal discharge.
  • Atrophic vaginitis often causes no symptoms. However, some women have dry, sore vaginas, which may be red and irritated. Sexual intercourse is painful and is often followed by a burning feeling. Occasional spotting and watery discharge are common with the rectovaginal fistula.
 
Diagnostic Evaluation
  • Wet mount: A vaginitis test called a wet mount is used to help diagnose vaginal infections that do not affect the urinary tract. It is also called a ‘wet prep’. The doctor will lie down the patient on an examination table, with her feet in stirrups, like a regular gynecologic exam. He or she will insert a speculum into the vagina to help him or her see the area. A sterile, moist cotton swab is inserted into the vagina to obtain a sample of vaginal discharge. The swab is then used to transfer the sample onto a slide. The slide can then be examined under a microscope to check for infection.
  • pH test: The pH of the vaginal secretions can be obtained by placing a sample from the lateral wall of the vagina on pH paper. The paper should include a range of pH from 4.0 to above 5.0. The normal pH is 4.5 or less.
  • Whiff test: It is a test for the fishy odor that occurs in bacterial vaginitis (previously called Gardnerella vaginitis and nonspecific vaginitis). A drop of KOH is mixed with some vaginal discharge. A positive test is abnormal and consists of a characteristic fishy odor.
  • Gram staining: Gram stain of the endocervical mucus may be helpful in the evaluation of cervicitis. An excess of leukocytes (more than 10/hpf) in the endocervical mucus suggests chlamydial cervicitis, and appropriate studies should be obtained.
  • Pap smear: In addition to information about cervical cytology, the Pap smear will often add information regarding possible vaginal and cervical pathogens.
  • Cultures test: Depending on the results of a vaginal culture without microscopic examination of the secretions, it will result in frequent errors in treatment. Nevertheless, cervical cultures may be especially helpful in some cases.
 
Management
 
Nonpharmacological Management
History taking: The nurse will first consider history of vaginal infections or sexually transmitted infections and perform a physical or pelvic examination. If women have a discharge from vagina, a sample will be sent to a lab for analysis to determine whether there 903is an infection or not. If an infection is ruled out, ask questions about what chemicals or irritants (e.g. douches or latex condoms) vagina has been exposed to. In some cases, vaginitis can be diagnosed simply by considering a woman's age, as postmenopausal women are prone to irritation of the vaginal lining.
Treatment of vaginitis depends on the cause
  • Tablets, gels, or creams are used to treat bacterial vaginitis: Some treatments might not be safe to use with alcohol or during pregnancy. Talk to doctor or pharmacist about how to safely use the medication prescribed. Trichomoniasis requires a single dose of prescription antibiotics, and sexual partners should be treated at the same time to prevent them from reinfecting each other.
  • Antifungal pills or cream are available for vaginal yeast infections: It is a good idea to seek doctor's opinion before purchasing nonprescription products. It is especially important to detect if:
    • It is the first yeast infection
    • Woman is pregnant or breastfeeding
    • The treatments tried earlier but have not worked
    • The infection keeps recurring
    • Other signs like pelvic pain, fever, or a colored or unpleasant-smelling vaginal discharge
  • Steroid ointments: The doctor can also recommend a steroid ointment or cream to reduce the redness, swelling, and itching that can be caused by irritative or allergic vaginitis. 4 to 5 tablespoons of baking soda in a lukewarm water bath can provide some relief. It is important to identify the cause of the vaginitis so that irritants can be avoided in the future.
Tips to keep vaginal skin healthy and prevent noninfectious vaginitis include the following:
  • Avoid prolonged moisture and friction; for instance, rubbing vigorously with a towel.
  • Do not wear bathing suits or exercise clothes for long period of time.
  • Wear cotton underwear which provides some air-flow.
  • Wear loose-fitting slacks.
  • Find alternative contraceptives if skin is irritated by lubricated condoms, jellies, creams, or sponges.
  • Keep the area around the genitals clean and dry.
  • Avoid irritants, such as douches, feminine hygiene sprays, deodorized sanitary pads or tampons, and colored or perfumed toilet paper.
 
Pharmacological Management
The goals of pharmacotherapy in vaginitis are to reduce morbidity, prevent complications, and eradicate the infection. Drugs used for infectious causes of vaginitis may be applied topically or may require oral or parenteral administration.
  • Antibiotics: It may inhibit bacterial protein synthesis. The antibiotics metronidazole, clindamycin and tinidazole are used to treat bacterial vaginosis. Depending on the antibiotic which is prescribed, patient may take it by mouth or use it vaginally.
  • 904Antifungals: Believed to bind to sterol in fungal cells membrane, thereby altering cell permeability. Some of the antifungals are fluconazole, clotrimazole, miconazole, etc.
  • Antiprotozoal: They act by entering into cells of microorganisms containing nitroreductase, interfering and finally causing cell death, .e.g. mitronidazole. Avoid drinking alcohol during treatment with metronidazole or tinidazole. These medicines can cause severe nausea and vomiting if drinking alcohol when taking one of them.
 
Surgical Management
  • Radial hysterectomy: Radical hysterectomy includes removal of the uterus with parametrial and paracervical tissue, proximal vagina, and proximal uterosacral ligaments. The uterine artery is transected at its origin, lateral to the ureter. In order to complete this dissection, the ureter is unroofed from the paracervical tunnel until the point of entry into the bladder. In order to resect the parametrial and paracervical tissue and unroof the ureter, the paravesical and pararectal spaces must be developed.
  • Vaginectomy: Partial and total vaginectomy refer to procedures in which the vaginal epithelium is removed without disruption of the adjacent tissues of the paracolpium. Partial vaginectomy may also be utilized to biopsy large vaginal lesions of unknown etiology. Radical vaginectomy is performed for pelvic malignancy involving or encroaching upon the vagina. It is rarely indicated. More commonly, at the time of radical hysterectomy for early cervix cancer or endometrial cancer involving the cervix, the upper third (2 to 3 cm) of the vagina is removed.
 
Nursing Management
 
Nursing Assessment
  • History taking
    • Elicit a history of the onset and description of symptoms, with particular attention to the nature and amount of vaginal discharge, which may be frothy, thick, or malodorous.
    • Question the patient to determine if she is experiencing discomfort, such as external inflammation and pain, and pruritus.
    • Patients may describe exertional dysuria, dyspareunia, and valvular inflammation. Determine the medications that the patient is taking, with particular attention to antibiotics, hormone replacement therapy, and contraceptives.
    • Ask about the patient's rest, sleep, and nutrition, exercise, and hygiene practices. Ask the patient if she is pregnant or a diabetic, both of which place the patient at risk for vaginitis.
  • Vaginal examination
    • Vaginal examination should take place under the following conditions: not on menses, no douching or vaginal sprays for 24 hours prior to exam, no sexual intercourse without a condom for 24 hours prior to the exam. Physical examination generally reveals some type of discharge, such as frothy, malodorous, greenish-yellow, purulent vaginal discharge (trichomoniasis), thick, cottage cheese-like discharge (candidiasis) or malodorous, thin, grayish-white, foul, fishy odor discharge.
  • Psychological assessment
    • Psychosocial assessment should include evaluation of the patient's home situation and a sexual history. Ask the patient about the type of contraception her or his 905partner use. Provide a private environment to allow the patient to answer questions without being embarrassed.
 
Nursing Diagnosis
  • Risk for infection related to invasion or proliferation of microorganisms.
  • Acute pain related to inflammation and subsequent wound care.
  • Impaired skin integrity related to the inflammation and drainage from vagina.
  • Sexual dysfunction related to change in vaginal structure.
  • Self-care deficit related to lack of understanding of perineal care and general health status.
  1. Risk for infection related to invasion or proliferation of microorganisms
    Interventions
    • Encourage the patient to get adequate rest and nutrition.
    • Encourage the patient to use appropriate hygiene techniques by wiping from front to back after urinating or defecating.
    • Teach the patient to avoid wearing tight-fitting clothing (pantyhose, tight pants or jeans) and to wear cotton underwear rather than synthetic.
    • Explain to the patient that the risk of getting vaginal infections increases if one has sex with more than one person.
    • Teach the patient to abstain from sexual intercourse until the infection is resolved.
  2. Acute pain related to inflammation and subsequent wound care.
    Interventions
    • Assess the level, intensity and severity of pain by pain scale.
    • Provide wet compresses, and then using a hair dryer on a cool setting several times a day provides some relief of itching.
    • Suggest the patient for sitz bath as it provides comfort.
    • For yeast infections, tepid sodium bicarbonate baths and dry the area may increase comfort during treatment.
    • Be informed about which sexually transmitted diseases need to be reported to the local health department.
  3. Impaired skin integrity related to the inflammation and drainage from vagina
    Interventions
    • Assess the condition of the skin.
    • A pressure-reducing mattress may be used to prevent pressure ulcers.
    • Change the position of the patient frequently.
    • Clothes should be changed everyday.
    • The wound is cleaned everyday with normal saline, antiseptic solutions, etc.
 
Health Education
Home health care guidelines involve teaching the patient how to maintain lifestyle changes with regard to rest, nutrition, and medication management. Make sure that the patient understands all aspects of the treatment regimen with particular attention to taking the 906full course of medication therapy. Make sure the patient understands the necessity of any follow-up visits.
 
PELVIC ORGAN PROLAPSE
Common prolapse are: Cystocele, urethrocele, enterocele, rectocele.
These disorders involve protrusion of an organ into the vaginal canal: Cystocele (bladder), urethrocele (urethra), enterocele (small intestine and peritoneum), and rectocele (rectum).
 
 
Types of Prolapse
  • Anterior: Cystocele, urethrocele
  • Posterior: Enterocele, rectocele
 
Cystocele
Ii is a downward displacement of the bladder toward the vaginal orifice, resulting from the damage to the anterior vaginal support structures. Cystocele and cystourethrocele commonly develop when the pubocervical vesical fascia is weakened.
 
Etiology
  • It usually results from injury and strain during childbirth
  • Being overweight or obese
  • Repeated heavy-lifting
  • Straining with bowel movements
  • A chronic cough or bronchitis.
 
Risk Factors
  • Childbirth: Women who have vaginally delivered one or more children have a higher risk of anterior prolapse.
  • Aging: Risk of anterior prolapse increases as you age. This is especially true after menopause, when body's production of estrogen, which helps keep the pelvic floor strong, decreases.
  • Hysterectomy
  • Obesity: Women who are overweight or obese are at a higher risk of anterior prolapse.
 
Clinical Manifestation
  • Feeling of fullness or pressure in pelvis and vagina
  • Discomfort when you strain, cough, bear down or lift
  • A feeling that you have not completely emptied your bladder after urinating
  • Repeated bladder infections
  • Pain or urinary leakage during sexual intercourse.
 
Rectocele
It is an upward pouching of the rectum that pushes the posterior wall of the vagina forward. The thin wall of fibrous tissue that separates the rectum from the vagina weakens, allowing the vaginal wall to bulge.
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Etiology
  • Weight on pelvic floor
  • Constipation
  • Chronic cough or bronchitis
  • Repeated heavy-lifting
  • Being overweight or obese
  • Pregnancy and childbirth.
 
Risk Factors
  • Genetics: Some women are born with weaker connective tissues in the pelvic area, making them naturally more likely to develop posterior prolapse.
  • Childbirth: If women have vaginally delivered multiple children, you have a higher risk of developing posterior prolapse.
  • Aging: Risk of posterior prolapse increases with age because you naturally lose muscle mass, elasticity and nerve function as you grow older, causing muscles to stretch or weaken.
  • Obesity: A high body mass index is linked to an increased risk of posterior prolapse. This is likely due to the chronic stress that excess body weight places on pelvic floor tissues.
 
Clinical Manifestation
  • A soft bulge of tissue in vagina that may or may not protrude through the vaginal opening
  • Difficulty having a bowel movement with the need to press
  • Sensation of rectal pressure or fullness
  • A feeling that the rectum has not completely emptied after a bowel movement.
 
Enterocele
Occurs when the small intestine descends into the lower pelvic cavity and pushes at the top part of the vagina, creating a bulge.
 
Etiology
  • Pregnancy and childbirth
  • Aging
  • Chronic constipation or straining with bowel movements
  • Chronic cough or bronchitis
  • Repeated heavy-lifting
  • Being overweight or obese.
 
Risk Factors
  • Pregnancy and childbirth: Vaginal delivery of one or more children contributes to the weakening of pelvic floor support structures, increasing the risk of prolapse. The more pregnancies you have, the greater your risk of developing any type of pelvic organ prolapse.
  • 908Age: As a person gets older, he tends to lose muscle mass and muscle strength in pelvic muscles as well as other muscles.
  • Pelvic surgery: Removal of uterus (hysterectomy) or surgical procedures to treat incontinence may increase the risk of developing small bowel prolapse.
  • Increased abdominal pressure: Being overweight increases pressure inside the abdomen, which increases the risk of developing small bowel prolapse.
  • Smoking: Smoking is associated with developing prolapse because smokers frequently cough, increasing abdominal pressure. Also, smokers may have problems with healing of damaged connective tissues, which can contribute to prolapse.
  • Family history.
 
Clinical Manifestation
  • Feeling of pelvic fullness, pressure or pain
  • Low back pain that eases when lie down
  • A soft bulge of tissue in vagina
  • Vaginal discomfort and painful intercourse
 
Urethrocele
It is the prolapse of urethra into the vagina.
 
Etiology
  • Multiple pregnancies and deliveries
  • Obesity
  • Aging related to muscle changes
  • Pelvic tumor
  • Excessive strain during bowel movement.
 
Risk Factors
  • Multiple pregnancies and vaginal deliveries: Women mostly at risk for this condition are those who have had multiple pregnancies and deliveries.
  • Age: Decreased muscle tone due to aging, excessive strain during bowel movement and complications of pelvic surgery have also been associated with prolapse of the uterus.
  • Chronic coughing
  • Heavy-lifting.
 
Clinical Manifestations
  • Backache
  • Perineal pain
  • Sense of ‘heaviness’ in the vaginal area
  • Pain
  • Urinary incontinence.
 
Diagnostic Evaluation
  • History: Pregnancies, any surgical procedure, family history.
  • Pelvic examination: During the exam, look for a tissue bulge into the vagina to check the strength of pelvic floor muscles.
  • 909Bladder and urine tests: To see how well and completely bladder empties. Run a test on a urine sample to look for signs of a bladder infection
  • Imaging test: X-ray or MRI to determine the size of tissue bulge.
  • Defecography: To know how efficiently bladder empties.
 
Management
  • Pessary: This device is inserted into the vagina and positioned to keep an organ properly aligned.
  • Colpexin sphere: It is an intrauterine device similar to pessary, and it supports the pelvic floor muscles.
  • Kegel exercises: It involves contracting or tightening of the vaginal muscles, prescribed to help strengthen these weakened muscles.
 
Surgical Management
  • Anterior colporrhaphy: Procedure to repair anterior vaginal wall.
  • Perineorrhaphy: To repair perineal lacerations.
 
Nursing Management
 
Nursing Diagnosis
  1. Acute pain related to pelvic pressure.
    Interventions
    • Encourage period of rest with legs elevated to relieve strain on pelvis.
    • Psychologically support the patient.
    • Check for proper placement of pessary.
    • Advise mild analgesics as prescribed by the physician.
    • Encourage fluid intake and void frequently to prevent bladder infection.
  2. Urinary retention related to displaced organ.
    Interventions
    • Encourage fluid to decrease bacterial flora in bladder.
    • Catheterize the patient if retention is suspected.
    • Obtain urine sample if infection is suspected.
  3. Constipation related to displaced rectum or bowel.
    Interventions
    • Patients to increase fluid and fiber in diet.
    • Use stool softeners or bulk laxatives to make passage of stool easier.
    • Use of enema may be necessary to prevent staining.
 
Male Reproductive System
 
Anatomy and Physiology
In male reproductive system, male urethra is a tube that connects the lower end of urinary bladder to the exterior, urine stored in the bladder is passed out through it.
910The male urethra is divisible into three parts:
  • First part is prostatic part
  • Second part is sphincter urethra externus
  • Third part is spongiose part.
    • The male gonads are the right and left testes. They produce the male gametes which are called spermatozoa.
    • From each testis, the spermatozoa pass through a complicated system of genital ducts. The most obvious of these are the epididymis and the ductus deferens. Tests are surrounded by three layers of tissue:
      • Tunica vaginalis: This is a double membrane forming the outer covering of the testes and is down growth of the abdominal and pelvic peritoneum.
      • Tunica albuginea: This is a fibrous covering beneath the tunica vaginalis that surrounds the testes.
      • Tunica vasculosa: This consists of a network of capillaries supported by delicate connective tissue.
  • Scrotum: The scrotum is a pouch of deeply pigmented skin, fibrous and connective tissue and smooth muscle. It is divided into two compartments, each of which contains one testis, one epididymis and the testicular end of the spermatic cord. It lies below the symphysis pubis in front of the upper parts of the thighs and behind the penis.
 
Functions of Testes
  • Spermatozoa (sperm) are produced in the semniferous tubules of the testes, and mature as they pass through the epididymis, where they are stored. The hormone controlling sperm production is FSH from the anterior pituitary.
 
Spermatic Cords
  • The spermatic cords suspend the testes in the scrotum. Each cord contains a testicular artery, veins, lymphatics, deferent duct and testicular nerves, which come together to form the cord from their various origins in the abdomen.
  • The cord which is covered in a sheath of smooth muscle and connective and fibrous tissues extends through the inguinal canal and is attached to the testis on the posterior wall.
MALE REPRODUCTIVE DISORDERS
 
CRYPTORCHIDISM
Cryptorchidism is the most common congenital abnormality of the genitourinary tract. Most cryptorchid testes are undescended, but some are absent (due to atrophy). Undescended testes are the failure of one or both testes to reach the normal position in the scrotum through the inguinal canal.
Cryptorchidism is also called undescended testis. In this a baby boy is born without both the testicles in his scrotum.
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Etiology
The most probable cause is an impairment of the hypothalamus pituitary gonadal axis that is blocked in the hormonal pathway to stimulate the testes to descend or the testes may fail to respond to stimulus due to some inherited deficit.
  • Hereditary and chromosomal abnormalities: It can further occur from one generation to next generation due to hereditary or chromosomal factors.
  • One or both testes (anorchia) can be the cause of undescended testis.
  • Short spermatic cord and artery mechanically prevent the descend of small and ill-formed immobile testes, which may fail to descent below the external inguinal ring. There are ectopic attachments of the testes which prevent the abdominal cavity near the pubic tubercle, in the inguinal canal and retroperineal space.
 
Risk Factors
  • Low birth weight: Boys with a birth weight of less than 2.5 kg are more likely to be born with undescended testicles than those with a normal birth weight.
  • Being born prematurely: The earlier a boy is born, the likely he will be born with undescended testicles (premature labor and birth).
  • Having a family history of undescended testicles: Having an older brother with undescended testicles means that a boy is more likely born with the condition compared with the general population.
 
Types
  • Retractile testis and pseudocryptorchidism: It is because of cremasteric reflex, testis may be temporarily pulled up from the scrotum into the inguinal canal or abdomen, especially in cold environment and during examination that can be coaxed back into the scrotum by sliding the fingers from the internal inguinal ring towards the scrotum.
  • This condition can be prevented by placing the fingers first across the upper portion of the inguinal canal. This condition is termed as retractile testis or pseudocryptorchidism.
  • True cryptorchidism: It occurs when the testis is located in the abdominal cavity or inguinal canal, also called intraabdominal testes. Rarely, it can be found in perineum, femoral area or in front of symphysis pubis at the base of the penis as ectopic testis. Scrotum of the affected side may be smaller or flat in bilateral type. It may be associated with inguinal hernia.
It can be described as follows:
  • Arrested descent: Descent may stop anywhere along the normal pathway. The subtypes are intra-abdominal, canalicular, emergent and high scrotal.
  • Deviated or ectopic testis: Testes are found away from the normal line of descent. The subtypes are superficial, inguinal, pubopenile, perineal.
  • Absence of testis: It can associate with or without the intersex and destruction of testis following any mumps and torsion. Absence of testis is called anorchia.
 
Clinical Manifestations
  • Undescended testis can be unilateral and bilateral. The child presents with the absence of testis in the scrotum showing the scrotum empty.
  • 912There may be a sign of complications, like torsion, tumor, trauma and hernia which is usually associated with 60 to 70% cases.
  • If the problem is not treated, it can be complicated with impaired testicular function leading to sterility, as the sperm-forming cells are damaged when testes remain in higher temperature in abdominal cavity than the scrotal temperature.
  • Dysgenesis of sperms may cause malignancy.
  • Psychological problems may be found in some children with this condition.
 
Diagnostic Evaluation
  • History: Ask the family history of the client related to undescended testis. Ask for the childbirth history related to preterm labor or birth, ask for the birthweight of the child.
  • Physical examination: In physical examination, undescended testicles usually have no symptoms other than not being able to feel the testicles in the scrotum. Physical examination helps to determine whether the testicles are:
    • Palpable: Can be felt just above the scrotum.
    • Unpalpable: Cannot be felt because they are higher up in the groin or abdomen.
  • Ultrasound: Ultrasound is the most heavily used imaging modality to evaluate undescended testis. It helps to detect the palpable testis and helps to localize the nonpalpable testes.
  • Laparoscopy: It is needed to find an unpalpable testicle. A laparoscope is a small tube containing a light source and a camera that helps to monitor inside. Laparoscope is inserted through a small incision usually made in child abdomen. When procedure is complete, the incisions are usually closed with dissolvable stitches.
  • MRI: In this, contrast agent dye is injected in bloodstream which helps to locate the testicles if it is in the groin region or abdomen.
 
Management
  • Undescended testicles usually move down into the scrotum naturally by the time when child is three to six months old. In some cases, this does not happen until child is six to twelve months old.
  • If the testicles do not descend spontaneously and naturally, then further action for treatment should be taken.
  • The best time for the therapy is from 1 to 12 years of age to prevent further complications.
  • Administration of hormonal therapy: Administer hormonal therapy with hCG (human chorionic gonadotropin). hCG also results in enlargement of the testis. It is administered as 250 units below one year, 500 units between one and five years and 1,000 units above 5 years, twice a week for 5 to 6 weeks. Usually good response is found with in one month.
 
Surgical Management
  • Orchiopexy: It is the surgery to reposition the testicle from his abdomen into the scrotum. It should be done early by 2 years of age for good result. It is performed to fix the testis, In this, the small incision is made in the groin and the testicle is located. Then second incision is made in the scrotum to make a pocket under the scrotal skin and place the testicle into the scrotum. If there is an associated hernia, then herniotomy along with orchidopexy is indicated at the same time.
  • 913Herniotomy: It is a simple precise surgery that can be performed under the sedation and an inhalational anesthesia. In this, a small cut in the groin region at the natural skin creases the contents of hernia sac which are emptied back into the abdomen and the sac is tied off. The wound is closed with dissolvable stitches that will not need to be removed.
  • In case of absence of testes, silastic prosthesis can be inserted at 8 to 10 years of age to overcome the emotional problems. Silastic prosthesis is a type of testicular prosthesis made up of silastic with an elliptical shape to mimic a normal shape of testis.
 
Preoperative Management
  • Explain the whole procedure to the parents of the child.
  • Clear all the doubts of parents regarding surgery.
  • Take consent from the client; in case of a child, take consent from the parents.
  • Tell the parents that child surgery will be done under general anesthesia, which means child will be asleep during surgery.
  • Follow the rules for eating or drinking that must be followed in hours before surgery.
  • Tell that surgery will take about 45 minutes, but recovery from anesthesia will take several hours.
 
Postoperative Management
  • In postoperative management, educate the parents about the diet after the surgery.
  • Advise to restrict the clear liquids, such as water, for a couple of hours to ensure his stomach is settled after the surgery.
  • Child should avoid fast food.
  • Advise them to maintain hygiene.
  • If there is any swelling or redness, pain occurs at the incision site, then report to the doctor.
  • Advise for the follow-up visits at least 4 to 6 weeks after surgery.
 
Family Teaching
  • Nurses are helpful in teaching and preparing both the child and caregivers for surgery.
  • Caregivers should be reassured that these side effects will dissipate after the therapy is discontinued.
  • They should also be instructed that their child will have discomfort postoperatively.
  • Loose clothing is recommended so as not to apply pressure to the wounds immediately after surgery.
  • The child may appear to have difficulty in walking related to tenderness, but this will resolve in a few days.
  • Caregivers need reassurance that all these are expected because of the surgery but will resolve in a few days to several weeks.
  • Nurses must teach the caregiver to observe for the signs of infection including increased pain, swellings, drainage from the incisions along with the fever.
  • Frequent diaper changes and proper hygiene will reduce the risk of infections. Lastly, caregivers should be instructed to help the child avoid strenuous activity, sports, and riding toys.
  • 914Nurses should provide assistance to the caregiver to develop a supportive environment in which the child has opportunities to ask the questions regarding sexuality and fertility as he becomes an adolescent.
 
Nursing Management
 
Nursing Assessment
  • In nursing assessment at the time of birth, the nurses have to evaluate for the presence of both testes.
  • She can evaluate by gently compressing both inguinal canal, small nodule which should be felt on both the sides.
  • The nurses should assess the caregivers understanding of disease condition and the importance of timely surgical incision.
 
Nursing Diagnosis
  • Deficient knowledge (caregiver) related to cryptorchidism and its treatment.
  • Anxiety (caregiver) related to the possible decreased fertility and increased risk of malignancy.
  • Disturbed body image related to appearance of genitalia.
  • Low self-esteem related to the disease condition.
  • Risk for infection related to surgical incision.
  1. Deficient knowledge (caregiver) related to cryptorchidism and its treatment.
    Interventions
    • Assess the knowledge of the caregivers regarding the disease condition and home care needs of a child.
    • Educate them regarding the disease condition and its treatment.
    • Listen to the caregivers regarding all their doubts.
    • Clear all the doubts of caregivers regarding the care needs and disease condition.
    • Provide written and verbal instructions to the caregivers.
  2. Anxiety (caregiver) related to the possible decreased fertility and increased risk of malignancy.
    Interventions
    • Assess the level of anxiety in the caregivers.
    • Educate the caregivers regarding the treatment of the disease that early treatment can prevent infertility.
    • Clear the doubts of the caregivers related to the disease.
    • Provide them the psychological support.
    • Educate them regarding the early treatment.
  3. Disturbed body image related to the appearance of genitalia (if the client is younger)
    Interventions
    • Assess the conditio n of the client.
    • Provide emotional support regarding the appearance of the genitalia.
    • Encourage visits by loved ones and understanding friends.
    • Confirm with the doctor the nature of the treatment anticipated.
    • 915Promote the positive acceptance of the condition.
    • Provide positive reinforcement to the client.
    • Promote the realistic adaptation to the condition.
 
Complications
  • Testicular cancer: Men who were born with undescended testicles have a higher risk of developing testicular cancer, compared to other men.
  • Fertility problems: Men who were born with this have a high risk of having low sperm counts, poor sperm quality and poor fertility.
 
EPISPADIAS
  • It is a rare type of malformation, and a congenital abnormality of the location of urethra. It is the congenital abnormal urethral opening on the dorsal aspect of the penis. In this, urethra is displaced dorsally due to the abnormal development of the infraumbilical wall and upper wall of the urethra.
  • It is a rare type of malformation of penis in which the urethra ends in an opening on the upper aspect (the dorsum) of the penis.
  • It is congenital anomaly in males in which the urethra is on the upper surface of the penis. Classification: Epispadias in a male child can be classified as:
    • Anterior epispadias: Anterior epispadias with normal continence.
      • Glandular
      • Balanitic or penile
    • Posterior epispadias: Associated with incomplete bladder neck and incontinence of urine.
      • Penopubic
      • Subsymphyseal
  • In males, infants with epispadias are having short and broad penis with dorsal curvature.
  • In females a cleft extends along the roof or entire urethra involving the bladder neck; urethra is short.
It is classified as:
  • Bifid clitoris with no incontinence of urine: It is incomplete epispadias in a female with the urethra opening superior to the clitoris or into it.
  • Subsymphyseal with incontinence of urine: It is incomplete epispadias in a female with the urethral opening beneath the symphysis pubis.
 
 
In a male
  • In anterior:
    • Glandular epispadias: It is also called blanic epispadias in which incomplete epispadias in a male with the urethral opening above and behind the glans, the dorsum of the penis is usually intended to its tip, but the opening may end at the corona or proximal to it.
    • Penile epispadias: Also called blanitic epispadias in which the proximal position of urethral meatus on the dorsum of the penile shaft.
  • 916In posterior:
    • Penopubic epispadias: Penopubic epispadias means proximal position of urethral meatus at the junction of base of penis and lower abdominal wall.
    • Subsymphyseal epispadias: In subsymphseal epispadias in which bladder does not entirely open to the outside designated according to the location of urethral opening in the male, also called incomplete epispadias.
 
Etiology
The causes of epispadias are not known. It may occur because the pubic bone does not develop properly. It can occur with a birth defect.
 
Risk Factors
  • Family history: About 6% of patients with this condition have children with epispadias and 12% of male siblings of the index patient with epispadias.
  • Increased maternal age above 32 years have greater risk in the child.
  • Low birth weight babies also have a risk of having this condition.
  • Environmental factors: A variety of substances with estrogenic activity contaminate the environment and are enriched through the food chain. Substances with estrogen activity are insecticides, chemical from plastics industry.
  • Exposure to smoking and drugs: There is some speculation about an association between a mother exposures to pesticides, smoking, in that case, there is risk in child with epispadias.
 
Clinical Features
 
In a male
  • Male usually has a short, wide penis with an abnormal curve.
  • The urethra usually opens on the top or side of the penis instead of the tip.
  • The urethra may be open along the whole length of the penis.
  • Urinary incontinence, involuntary urine loss.
  • Enlarged pubic bone.
  • Urinary tract infection.
  • Bladder exstrophy means an open, inside-out bladder (inner surface exposed) and exposed dorsal urethra on the surface of the lower abdominal wall.
  • Reflux nephropathy, in which there is backward flow of urine into the kidney.
 
In a female
  • Female has an abnormal clitoris and labia.
  • The opening is usually between the clitoris and the labia, but it may be in the belly area.
  • Trouble in controlling urination, urinary incontinence.
  • Urinary tract infection.
  • Enlarged pubic bone.
  • Backward flow of urine is present.
917
 
Diagnostic Evaluation
  • History: Collect the family history medical history, birth history of the client.
  • Physical examination: Assess the child-voiding pattern.
  • If the child is not voiding normally, report to the physician.
  • Assess the child's ability to stand during urinating in case of a boy.
  • Blood test: Blood test is used to check the level of electrolytes.
  • Intravenous pyelogram: It is an X-ray test in which a contrast agent called dye is injected into a patient's vein. The contrast agent acts to outline the client's kidneys, ureter and bladder when X-rays are subsequently taken. It helps to detect the abnormalities of upper urinary tract and also the bladder capacity. The patient will commonly be placed on a restricted diet 24 hours prior to the test and will be asked to urinate before the test to ensure the bladder is empty.
  • MRI/CT scan: It depends upon the client's condition. MRI and CT scan of the upper urinary tract is done to detect or to evaluate the abnormalities of upper urinary tract.
  • Pelvic MRI also helps to detect or provide adequate information about internal genitalia before and after surgery.
  • Pelvic X-ray: Pelvic X-ray is used to detect any abnormalities in the pelvic area like widened and enlarged pelvic bone. Pelvic X-ray is a painless test that uses a small amount of radiation to take a picture of the pelvic bones, which surrounds the hip area. Procedure takes usually 10 minutes or longer from start to finish, and exposure to the radiation usually less than a few seconds.
  • Ultrasound of urinary system: Ultrasound of urinary system helps to detect the main cause of problems, like involuntary urination, urinary incontinence, and backward flow of the urine. Ultrasound is a noninvasive diagnostic examination that produces the images and helps to detect the problems. In ultrasound, we use a transducer that sends out ultrasound waves at a frequency too high to be heard.
 
Management
Main goal of the management is to maximize penile length and function by correcting dorsal bend and chordee.
Management is done by surgical correction usually in three stages:
  • Bladder exotrophy:
    • First stage: Operation is done at 1.5 to 2 years' age for penile lengthening, elongation of urethral strip and chordee correction.
    • Second stage: Operation is done at least 6 months after the first stage for urethral reconstruction.
    • Third stage: Operation is done at about 3 to 4 years of age for the bladder neck reconstruction and the correction of vesicoureteric reflux.
  • Cystoplasty: It can be done to enhance the bladder capacity after 2 to 3 years of the third stage of the operation. It is a surgical repair of a defect in the urinary bladder and improves the bladder function and capacity.
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Nursing Management
 
Preoperative Care
  • Prepare the child's parents and the child for surgery.
  • The parents must be assured that if surgery is done early in a child's life, there will be no influence on his self-image.
  • They should also be prepared for appearance of surgical area postoperatively.
  • Explain the procedure to the parents.
  • Take a written consent from the client and parents.
 
Postoperative Care
  • If the surgery is done, the nurse must also help the child to handle the anxiety.
  • It is important that the nurse helps both the parents and child to relieve their anxieties so that they are not transmitted from one family member to the other family members.
  • Keep the operated area clean and dry to prevent from infection and urinary tract infection.
  • Provide play therapy to child to divert the mind.
  • Be with the client.
Other supportive nursing care includes:
  • Provide more emphasis on the prevention of infection.
  • Provide emotional support for long-term management schedule.
  • Maintain health of the child by giving more emphasis on the child's growth and development.
  • Provide adequate, balanced diet and healthy nutrition to the child.
  • Maintain hygiene.
 
HYPOSPADIAS
Hypospadias is the most common congenital anomaly of the penis and also a malformation of male children. Undescended testis and inguinal hernia or upper urinary tract anomalies may be associated with hypospadias. It may be found in females as an urethral opening with dribbling of urine.
Hypospadias is a condition in which the opening of the urethra is on the underside of the penis instead of the tip. Hypospadias is a congenital defect that involves an abnormally placed urinary hole in both female and male.
 
Classification
Hypospadias can be classified as follows depending upon the sites of the urethral metus:
  • Anterior hypospadiasis: It occurs in 60–70%. It may be found as glandular or coronal or on distal penile shaft. In this the opening of urethra is located somewhere near the head of the penis.
  • Middle penile shaft hypospadias: It occurs in 10–15%. In this, the opening of the urethra is located along the shaft of the penis.
  • Posterior hypospadias: It occurs in 20%. It may be found in proximal penile shaft, or as penoscrotal, scrotal or perineal type, in which the opening of the urethra is located where the penis and scrotum meet.
919
 
Etiology
Hypospadias is present at birth but the exact cause is unknown. It results when a malfunction occurs in the action of hormones causing the urethra to develop abnormally.
Some risk factors include:
  • Family history: About 7% of patients with this condition have children with hypospadias and 14% of male siblings of the index patient with hypospadias.
  • Increased maternal age above 32 years have greater risk in the child.
  • Low birth weight babies also have a risk of having this condition.
  • Androgen deficiency: An absolute or relative decreased sensitivity of the target tissue androgen deficiency is a major cause for the development of hypospadias.
  • Environmental factors: A variety of substances with estrogenic activity contaminates the environment and is enriched through the food chain. Substances with estrogen activity are insecticides, chemicals from plastics industry.
  • Exposure to smoking and drugs: There is some speculation about an association between mother exposures to pesticides, smoking. In that case, there is risk in children with hypospadias.
 
Clinical Manifestations
  • Presence of the painful downward curvature of the penis during erection as chordee.
  • Due to chordee, there is presence of deflected stream of urine and the child wets his thigh during urination.
  • Inability to void urine while standing.
  • If the appropriate management is not done in early life, then, in later stage of life, it interferes with the sexual intercourse with difficulty in penetration due to presence of chordee.
  • Severe forms interfere with the reproductive ability.
  • There can be fistula, urethral stricture.
  • Abnormal spraying during urination.
  • Hooded appearance of penis because only the top half of the penis is covered by foreskin.
  • Having to sit down to urinate.
 
Diagnostic Evaluation
 
History
  • Collect the history related to exposure to any chemicals, smoking.
  • Ask the clients for their family history.
  • Collect the maternal history related to age.
 
Physical Examination
  • Assess the children for their urinary pattern.
  • Assess the children for difficulty during urinating.
  • In cases of severe hypospadias, there is absence of testicles in the scrotum. So, sex determination evaluation may be performed.
  • Assess the children's ability to stand during urination in case of a boy.
  • 920Ultrasound imaging: Ultrasound of urinary system helps to detect the main cause of problems like involuntary urination, urinary incontinence, and backward flow of the urine. Ultrasound is a noninvasive diagnostic examination that produces the images and helps to detect the problems. In ultrasound, we use a transducer that sends out ultrasound waves at a frequency too high to be heard.
  • Intravenous urography: It is an X-ray test in which a contrast agent called dye is injected into a patient's vein. The contrast agent acts to outline the client's kidneys, ureter and bladder when X-ray are subsequently taken. It helps to detect the abnormalities of upper urinary tract and also the bladder capacity.
  • Cystourethrogram: It is an X-ray test that takes pictures of bladder and urethra, in which a thin flexible tube (urinary catheter) is inserted through urethra into bladder, and a contrast material is injected into bladder through catheter. Then X-ray is taken in bladder with contrast material. It helps to detect the cause of urinary incontinence, urinary tract infections, and to detect the problems of bladder and urethra.
  • Cystoscopy: It is used to examine inside the bladder using instrument cystoscope, and also used to detect problems related to urinary bladder.
 
Management
If hypospadias is in mild form, no treatment is required, but if in severe form, management is done by surgical reconstruction. The main goal of the treatment is to obtain straight erectile penis, and to form urethral tube or urethral meatus at the tip of glans penis.
  • Meatotomy: It can be done at any age after birth of the child. Chordee correction and advancement of prepuce can be done at the age of 2 to 3 years.
  • Meatoplasty and Glanuloplasty: It is a reconstruction of meatus and glans to achieve meatus at the tip of penis.
  • Urethroplasty: It can be done 3 to 4 months after chordee correction. The surgical repair should be completed before school admission. It is a reconstruction of the missing distal urethra.
 
Nursing Management
 
Preoperative Care
  • Prepare the child's parents and the child for the surgery.
  • The parents must be assured that if surgery is done in an early stage in child's life, there will be no influence on his self-image.
  • They should also be prepared for appearance of surgical area postoperatively.
  • Explain the procedure to the parents.
  • Take written consent from client and parents.
 
Postoperative Care
  • If the surgery is done, the nurse must also help the child to handle the anxiety.
  • It is important that the nurse help both the parents and child to relieve their anxieties so that they are not transmitted from one family member to the other family members.
  • Keep the operated area clean and dry to prevent from urinary tract infection.
  • Provide play therapy to the child to divert the mind.
  • Be with the client.
921
 
Other Supportive Nursing Care
  • Provide more emphasis on the prevention of infection.
  • Provide emotional support for long-term management schedule.
  • Maintain health of the child by giving more emphasis on child's growth and development.
  • Provide adequate, balanced diet and healthy nutrition to child.
  • Maintain hygiene.
  • Provide parental guidance and educate them how to cope with the problem.
 
Nursing Management
 
Nursing Assessment
  • In nursing assessment, nurse has to assess the condition of the child.
  • Nurse has to do the inspection of genitalia of child that helps to show the location of abnormal urethra and other problems associated with these conditions.
  • Assess that baby or a boy cannot urinate at a normal position.
 
Nursing Diagnosis
  • Acute pain related to physical factors (damage to the tissue), incision.
  • Impaired skin integrity related to surgical trauma.
  • Altered urinary elimination related to disease condition.
  • Risk of infection related to contamination of catheter.
  • Altered family process related to the diagnosis of disease condition.
  • Knowledge deficit related to the disease condition, prognosis.
  1. Acute pain related to physical factors (damage to tissue), incision.
    Interventions
    • Assess the level of pain in the client.
    • Provide diversional therapy to the client, like play and music therapy.
    • Provide comfortable environment to the client.
    • Monitor the vital signs.
    • Provide emotional support to the clients and their parents.
  2. Altered family process related to the diagnosis of disease conditions.
    Interventions
    • Assess the anxiety of parents and fear level of the child by asking questions.
    • Provide emotional support to the child.
    • Allowing parents' involvement in the treatment.
    • Allowing play and self-care as tolerated by the child.
    • Encouraging child interaction with other child.
    • Answering the questions asked by the parents and allowing expressing their frustration.
  3. Knowledge deficit related to the disease condition and prognosis.
    Interventions
    • Assess the ability of the parents to take care of the child.
    • Discussing about the care after discharge from the hospital, regarding rest, diet, hygiene, continuation of medication, need for medical help and follow-up.
    • 922Teaching about features of infections, signs of relapse and precautions to prevent complications.
    • Provide parental guidance and educate them how to cope with the problem.
 
INFERTILITY
According to the WHO, infertility is a disease of the reproductive system defined by the failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercourse.
Infertility is the inability of a sexually active, noncontracepting couple to achieve pregnancy in one year. The male partner can be evaluated for infertility using a variety of clinical interventions and also from a laboratory evaluation of semen.
 
Types of Infertility
  • Primary infertility: Primary infertility means when someone who has never conceived a child in the past has difficulty in conceiving.
  • Secondary infertility: When a person has had one or more pregnancies in the past, but is having difficulty in conceiving again.
 
Etiological factors
  • Infertility may be caused by many factors.
 
In females
  • Ovulation disorders: Infertility is most commonly caused by problems with ovulation. Some problems stop women releasing eggs at all and some cause an egg to be released during some cycles but not others. Ovulation problems can occur as a result of many problems.
  • Polycystic ovary syndrome: A condition that makes it more difficult for ovaries to produce an egg.
  • Thyroid problems: Both an overactive thyroid gland (hyperthyroidism) and hypothyroidism can prevent ovulation.
  • Premature ovarian failure: Where a woman's ovaries stop working before she is 40.
  • Womb and fallopian tubes: The fallopian tubes are the tubes along which an egg travels from the ovary to the womb. The egg is fertilized as it travels down the fallopian tubes, where it reaches the womb. It is then implanted into womb lining, where it continues to grow. If the womb or the fallopian tubes are damaged or stop working, it may be difficult to conceive.
  • Scarring from surgery: Pelvic surgery can sometimes cause damage and scarring to the fallopian tubes. Cervical surgery can also cause scarring or shortening of the cervix.
  • Cervical mucus defect: At the time of ovulation, mucus in the cervix becomes thinner so that sperm can swim through it more easily. If there is a problem with mucus, it can make it harder to conceive.
  • Endometriosis: It is a condition where small pieces of the womb lining, known as the endometrium, start growing in other places, such as ovaries. This can cause infertility because the new growths form adhesions or cysts that block the pelvis.
  • 923Pelvic inflammatory disease: It is an infection of the upper female genital tract. It is often the result of a sexually transmitted infection which can damage fallopian tubes.
  • Medicines and drugs: Nonsteroidal inflammatory drugs' long-term use cause difficulty in conceiving, like aspirin, ibuprofen.
  • Chemotherapy: They make ovaries weak and unable to function properly.
  • Other drugs like marijuana and cocaine can affect fertility.
  • Age: It is also linked to age, the biggest decrease in fertility begins during the mid-thirties among women who are 35.
 
In males
  • Due to abnormal semen
  • Decreased number of sperms
  • Decreased sperm mobility
  • Abnormal sperm, abnormal shape
  • If testicles are damaged, these affect semen
  • An infection in testicles (orchitis)
  • Testicular cancer
  • Testicular surgery
  • Congenital defect in testicles (cryptorchidism)
  • Trauma to testicles
  • Sterilization: Vasectomy involves cutting and sealing of vas deferens so that semen will no longer contain sperm.
  • Hypogonadism: It is an abnormal low level of testosterone that is involved in making sperm.
  • Alcohol: Damages the quality of sperm.
  • Smoking: It can adversely affect fertility.
  • Stress: If either one partner is in stress, it affects the relationship by decreasing sex drive.
 
Clinical Manifestations
  • The main symptom of infertility is not getting pregnant.
 
In females
  • In females, changes in the menstrual cycle and ovulation may be a symptom of infertility.
  • Abnormal periods, bleeding may be heavy or low.
  • Acne.
  • Change in sex drive and desire.
  • Weight gain.
  • Milky discharge from nipples but unrelated to breastfeeding.
  • Pain during sex.
 
In males
  • In males, it includes problems with the sexual functions, i.e. difficulty in ejaculation, reduced desire, and erectile dysfunction.
  • Pain and swelling in testicles.
  • Having a lower normal sperm count.
924
 
Diagnostic Evaluation
  • History
    • Collect the history related to irregular menstruation.
    • Collect the history related to the known problems with uterus, tubes or other problems like endometriosis.
    • Collect history related to male infertility problems.
    • Ask about the history of drug use and about the alcohol and smoking use.
    • Ask the couple about their relationship.
  • Physical examination: In physical examination, assess patient for any abnormalities like abnormalities of penis, vas deferens, testicles.
    • Assess the client for skin changes.
    • Check the weight of the patient.
    • Ask the client for her menstrual history.
  • Male partner semen analysis: It provides information related to the number, movement, shape of the sperm. It is an essential part of infertility evaluation.
  • Hysterosalpingogram: This is an X-ray procedure to see if the fallopian tubes are open and to see the shape of uterine cavity. A catheter is inserted into opening of the cervix through the vagina. A liquid containing iodine contrast is injected through catheter.
  • Transvaginal ultrasonography: An ultrasound probe placed in vagina allows to check uterus and ovaries for abnormalities.
  • Other blood tests: Thyroid-stimulating hormone and prolactin levels are useful to identify thyroid disorders, which may cause infertility, menstrual irregularities and repeated miscarriages. A blood progesterone level drawn in the second half of the menstrual cycle can help to document whether ovulation has occurred.
  • Sonohysterography: This procedure uses transvaginal ultrasound after filling the uterus with saline. This improves detection of intrauterine problems, such endometrial polyps, fibroids.
  • Hysteroscopy: This is a surgical procedure in which hysteroscope is passed through the cervix to view the inside of uterus. It helps to diagnose or treat problems inside the uterine cavity, such as fibroids, polyps and adhesions.
  • Laparoscopy: This is a surgical procedure in which laparoscope is inserted through the wall of the abdomen into the pelvic cavity. It is used to evaluate pelvic cavity for endometriosis, pelvic adhesions.
 
Management
In management, limited numbers of medical treatments are aimed at improving chances of conception for patients with known cause of infertility.
  • Endocrinopathies: A number of patients with hypogonadotropic hypogonadism respond to gonadotropin replacement.
  • Artificial insemination: Depositing semen into the female genital tract by artificial insemination. If the sperm cannot penetrate the cervical canal normally, artificial insemination using the partner's semen may be considered.
  • 925Indications for using artificial insemination: The inability to deposit semen in the vagina which may be due to premature ejaculation, due to hypospadiasis or dyspareunia.
  • Inability of semen to be transported from the vagina to uterine cavity: This is usually due to faulty chemical conditions and may occur with an abnormal cervical discharge.
  • During insemination, women may have received clomiphene and menotropins to stimulate ovulation.
  • The success rate for artificial insemination varies, three to six inseminations may be required over 2 to 4 months, because artificial insemination is likely to be a stressful and difficult situation for couples. Nursing support should be provided.
  • Insemination with donor semen: When the sperm of the woman's partner is defective or absent or when there is a risk of transmitting a genetic disease, donor sperm may be used. Written consent is obtained from patient.
  • In vitro fertilization: It involves ovarian stimulation, egg retrieval, fertilization and embryo transfer. This procedure is accomplished by first stimulating the ovary to produce multiple eggs, or ova, usually with medications.
  • Most common indications are irreparable tubal damage, endometriosis, immunologic problems, unexplained infertility, and inadequate sperm.
 
Pharmacological Therapy
  • Pharmacologically induced ovulation is undertaken when the female does not ovulate. There are various medications depending upon the primary cause of infertility. These all medications induce ovulation.
  • Clomiphene is used when hypothalamus does not stimulate pituitary gland to release FSH and LH.
  • Menotropin is a combination of FSH or LH is used for women with deficiencies in these hormones.
  • Urofollitropin containing FSH with a small amount of LH is used in polycystic ovarian syndrome to stimulate follicle growth.
  • Chronic gonadotropin is used to stimulate release of egg from the ovary.
 
Lifestyle Modifications
  • Healthy lifestyle and daily exercise may restore fertility.
  • Body weight or underweight can affect the chances of ovulating normally in women who have less or more body fat, may hinder menstrual cycle, make conception difficult. So, it is a must to maintain a healthy body weight before conception.
  • Avoid smoking and alcohol. It affects the conception and in males, it decreases the sperm count.
  • Caffeine and drugs should be avoided because it affects the sperm count and also interferes with the menstrual cycle.
  • Take a healthy diet rich in antioxidants, vitamin C and certain minerals. It helps to maintain ideal body weight.
  • A high intake of vitamin C and E increases sperm count and motility of sperm or in women, it can reduce stress on eggs or reproductive organs.
926
 
Nursing Management
 
Nursing Assessment
  • Nursing interventions are appropriate when working with couples during fertility evaluations include the following:
    • Assist the client in reducing stress in the relationship.
    • Encourage cooperation, protect privacy, foster understanding and refer the couple to appropriate resources when necessary.
    • Infertility work-ups are expensive, time-consuming, stressful. So couples need support in working together to deal with these problems.
 
Nursing Diagnosis
  • Anticipatory grieving related to the loss of pregnancy.
  • Anxiety related to the diagnosis of infertility.
  • Disturbed body image related to altered fertility and fears about sexuality and relationships with partner and family.
  • Deficient knowledge related to the disease process.
  • Community coping impairment related to the diagnosis of infertility.
  1. Anticipatory grieving related to loss of pregnancy.
    Interventions
    • Assess the client's condition.
    • Client's distress may not be expressed verbally, and not by partner.
    • So nurse should be present to listen and provide support.
    • The client's partner should also participate in this process.
    • If the client is having severe distress, refer her for counseling.
  2. Anxiety related to the diagnosis of fertility.
    Interventions
    Assess the level of anxiety in client:
    • The patients must be allowed to talk and ask questions.
    • Assist the patients in expressing their feelings.
    • Provide support.
    • Educate them about the disease condition and also about the treatment.
    • Tell the client's partner to be with the patient.
  3. Disturbed body image related to the altered fertility and fears about sexuality and relationship between partner and family.
    Interventions
    • Assess the condition of the patient.
    • The patient may have strong emotional reactions related to the diagnosis of infertility, view the others who may be involved (family, partner, religious beliefs, and fears about prognosis).
    • Provide reassurance to the client.
    • Provide psychological support.
    • If the fear or stress level is high, then refer the patient for counseling.
927
BIBLIOGRAPHY
  1. Chintamanni. Textbook of medical surgical nursing. 1123–7.
  1. Lippincott. Textbook of manual of nursing practice. 6th ed. 767–75.
  1. Luckman. Textbook of medical surgical nursing. 2230–4.
  1. Polakshi, Arlene L. Luckmann's core principle and practice medical surgical nursing, Elsevier. 
  1. Smeltzer CS, Bare B. Brunner and Sidharth's Textbook of medical surgical nursing, Lippincott publisher,  10th ed. 1449–52.
928
929Index
Page numbers followed by ‘f’ indicate figures respectively.
A Abdominal compartment syndrome Abdominal discomfort Abdominal hernia diagnosis of abdominal hernia CT scan etiology and risk factors allergies chronic cough pregnancy straining to lift heavy objects management nursing interventions signs and symptoms types of abdominal hernias Acellular human dermal allograft Acetylsalicylic acid Acidosis Acne etiology medical management nursing care signs and symptoms Acute myelogenous leukemia Acute renal failure antihypertensive and cardiovascular agent dialysis digoxin low sodium sodium bicarbonate antiseizure agents IV diazepam phenytoin calcium and phosphate binder calcium carbonate calcium phosphate sevelamer hydrochloride (Renagel) causes of definition diagnostic evaluation serum creatinine urine specific gravity dietary management fluid allowance per day 500 to 600 ml protein intake erythropoietin etiology hemodialysis home care intrarenal causes medical management nursing diagnosis nursing management nutritional therapy pathophysiology pharmacologic management postrenal causes prerenal causes signs and symptoms Acute respiratory distress syndrome assessment and diagnostic findings ABG chest X-ray CT scan of thorax echocardiography pulmonary artery catheterization sputum culture clinical manifestations decreased mental status dyspnea hypotension increased pulse rates low blood oxygen levels low PaO2 lung inflammation marked restlessness sudden breathlessness tachycardia tachypnea management complications nutritional therapy pharmacological management treatment of ARDS nursing diagnosis nursing intervention maintain airway clearance reducing anxiety relieving pain pathophysiology acute lung injury release of mediators Acute retroviral syndrome Adaptive coping strategies awareness compromise connect with others 930interpersonal communication laugh meditation music nursing interventions pets problem-solving relaxation assessment of environment assessment of family assessment of person take a minute vacation think positively Addison's disease diagnostic evaluation ACTH stimulation test blood test imaging tests insulin-induced hypoglycemia test etiology primary adrenal insufficiency secondary adrenal insufficiency glucocorticoids management of Addisonian crisis (treatment typically) hydrocortisone saline solution sugar (dextrose) mineralocorticoids nursing management assessment diagnosis pathophysiology ACTH secretion aldosterone deficiency androgen deficiency cortisol deficiency signs and symptoms body hair loss depression hyperkalemia hyperpigmentation Adenoidectomy Adhesions Adrenal insufficiency primary secondary After effects of disaster common reactions grief Agencies involved during disaster management Children's Disaster Services The Adventist Community Services The Ananda Marga Universal Relief Team The Friends Disaster Service The International Relief Friendship Foundation The National Emergency Response Team The National Organisation for Victim Assistance The Red Cross Air embolism diagnostic evaluation etiology signs and symptoms areas of abnormal sensation bloody sputum cessation of breathing treatment Alcoholic cirrhosis Alkylating agents nursing management treatment corticosteroids rogaine (minoxidil) topical contact allergens or sensitizers Amantidine Ambulatory monitors Amenorrhea classification of drug therapy etiology management surgical management Aminotransferases Amputation and prosthesis amputation recovery levels of nursing diagnosis nursing management types of Anemia classification of anemia etiology , iron deficiency anemia management medical management morphologic classification Angina accelerating angina CABG pre- and post-operative care coronary arteriography coronary artery bypass graft surgery off-pump procedure on-pump procedure decubitus angina diagnostic evaluation imaging studies etiology history 931laboratory studies lifestyle modification microvascular angina nursing care pathophysiology percutaneous transluminal coronary angioplasty pharmacologic therapy physical examination Angioplasty and stents Angiotensin-converting enzyme captopril enalapril (Vasotec) lisinopril ramipril Anosmia Anterior cruciate ligament Anthracyclines Antibody deficiency syndromes Antimicrobial dressing Antitumor antibiotics Aortic aneurysm causes clinical manifestations definition diagnostic evaluation etiology incidence 932management pathophysiology , risk factors , shapes types , Aortic valve stenosis Aphakia Aplastic anemia clinical manifestation diagnostic evaluation etiology management Appendicitis complications diagnostic evaluation etiology management nursing management signs and symptoms Aqueous shunt devices Arrhythmia classification signs and symptoms Arteriosclerosis Arteriosclerotic vascular disease complications of atherosclerosis diagnostic evaluation intervention and rational nursing management pathology of atherosclerosis pathophysiology of atherosclerosis physical examination prevention risk factors for atherosclerosis signs and symptoms treatment Arteriovenous fistula graft Arthroscopic acromioplasty meniscectomy Asbestosis diagnosis etiology pathophysiology symptoms of treatment Assess signs of wound infection Asterixis Asthma diagnostic evaluation etiology lifestyle management management nursing management pathophysiology risk factors signs and symptoms Asymmetric septal hypertrophy Asystole , Atelectrauma Atheroma in coronary artery Atherosclerosis Atrial fibrillation flutter Audiometry Auditory brainstem response audiometry Augmentative and alternative communication Automated external defibrillators peritoneal dialysis Autotransplantation B Bacille Calmette-Guérin (BCG) vaccine Barium swallow, endoscopy Barotrauma , Basal ganglia , Basic sanitation and personal hygiene Bell's palsy complications diet and nutrition etiology management surgical management teaching about maintaining muscle tone teaching eye care Benign prostatic hyperplasia complications diagnostic evaluation diet management etiology management preoperative care prevention signs and symptoms Biguanides Bilateral knee replacement Biliary cirrhosis Binds hemoglobin Biological therapy cetuximab Biotrauma Bland dressings Blepharitis signs and symptoms treatment Blood disorders Bone marrow biopsy Bone-specific alkaline phosphatase Bradycardia , Bronchiectasis diagnostic evaluation etiology and types management Bronchitis clinical manifestations complications diagnostic evaluation etiology management nursing management pathophysiology Brugada syndrome Bruton's tyrosine kinase Bundle branch block anatomy and physiology normal conduction system types Burns according to burn severity depth the extent of body surface area airway breathing chemical circulation clinical manifestation bacterial contamination of tissues definition depth of burn diagnostic studies arterial blood gases blood urea nitrogen carboxyhemoglobin complete blood count urine electrical inhalational injury management and plastic surgeries pathophysiology wound coverage skin substitutes and skin replacements temporary wound coverage wound dressings antimicrobial salves antimicrobial soaks C Cancer according to American Cancer Society recommendations caution characteristics of cancer cells classification of cancer clinical staging detection and prevention of known chemical carcinogens in humans secondary prevention surgical techniques surgical therapy terminology related to cancer tertiary prevention tumors according to histological analysis various treatment modalities of cancer Capacity of metastasis Capnography Caput medusa Cardiac temponade diagnostic evaluation etiology signs and symptoms treatment Cardiomyopathy diagnostic evaluation etiology interventions management nursing management signs and symptoms surgical management treatment Cardiopulmonary arrest classification of nonshockable shockable arrest diagnosis and treatment 933resuscitation complications definition Cardiovascular emergencies stress testing Care of burn wounds unrelated to previously operated wounds Care of patient on ventilator basics of mechanical ventilation breath types care essential -, - complications of mechanical ventilation cycle variables limit variables nursing care of ventilated patients nursing care plan for the ventilated patient other care essentials care of the airway eye care genital/urinary tract GIT monitors oral care repositioning and pressure area care suction of an artificial airway ventilation trigger variables vili and other complications Cataract diagnostic evaluation management nursing management nursing assessment nursing intervention postoperative assessment pathophysiology , pharmacologic therapy risk factors and etiology signs and symptoms surgical management extracapsular cataract extraction surgery intracapsular cataract surgery phacoemulsification types of cataract Catecholamines Celiac disease Cellulitis etiology and risk factors management nursing interventions signs and symptoms Central nervous system medulla midbrain pons spinal cord Cerebral hemispheres Cerebrovascular accident diagnostic evaluation etiology and types hemorrhagic stroke ischemic stroke management nursing management pathophysiology risk factors signs and symptoms Chalazion (meibomian cyst) Changes in basic life support (BLS) guidelines advanced airway drug therapy reversible causes shock energy Chemotherapy antimetabolites antitumor antibiotics classification of chemotherapeutic drugs extravasation management at peripheral site focus of chemotherapy treatment hormone therapy mechanism of action of chemotherapeutic drugs prevention of extravasation role of nurse in side effects of long-term side effects short-term side effects Chest compartment syndrome Chest compression depth rate Chest injuries blunt trauma classification crush injury diagnostic evaluation general management management penetrating injuries postoperative intensive care signs and symptoms Chest X-ray after heart surgery Children's disaster services Cholecystitis complications enlarged gallbladder gangrene infection within the gallbladder perforation diagnostic evaluation etiology bile duct blockage gallstones tumor 934management nursing diagnosis management risk factors age gallstones signs and symptoms surgical interventions Cholelithiasis and cholecystitis diagnostic evaluation etiology management nonsurgical treatment pathophysiology signs and symptoms types of gallstones Choose less risky sexual behaviors Chronic glomerulonephritis diagnostic evaluation diet management etiology management nursing management pathophysiology prevention signs and symptoms Chronic obstructive pulmonary disease (COPD) alpha1-antitrypsin deficiency treatment complications component 1: assess and monitor disease component 2: reduce risk factors component 3: manage stable COPD component 4: manage exacerbations diagnostic evaluation etiology management of sputum viscosity and secretion clearance mechanism of pathophysiology nursing management pathophysiology pharmacological therapy risk factors schematic diagram of signs and symptoms Chronic pericarditis causes clinical features common causes of chronic pericarditis common treatment of chronic pericarditis definition diagnostic evaluation nursing management pathophysiology treatment types Chronic renal failure complication definition diagnostic evaluation acidosis anemia calcium and phosphorus imbalance glomerular filtration rate sodium and water retention dialysis medical management nursing diagnosis nursing management nutritional therapy signs and symptoms stages of Chronic respiratory failure Chronic venous insufficiency clinical manifestation diagnostic evaluation Doppler study physical examination tourniquet test etiology invasive testing management Cigarette smoking Clubbing Cluster headache etiology management symptoms Coagulation defects Coal worker's pneumoconiosis causes complications diagnostic evaluation management nursing management pathophysiology prevention and control signs and symptoms Cochlear implant advantages of disadvantages of functioning of otosclerosis Coiling (endovascular embolization) Cold sores etiology management signs and symptoms Colonic disease colectomy and proctocolectomy large bowel resection Colonoscopy for colon cancer Colorectal cancer cause definition diagnostic tests 935medical management alternative treatment chemotherapy radiation therapy targeted drug therapy pathophysiology signs and symptoms surgery for Colostomy or ileostomy Common variable immunodeficiency Compartment syndrome, complications of over-resuscitation Complications of surgeries for burn management Conduction block pathway Confusion assessment method Congestive heart failure categories of heart failure compensatory mechanism during complications diagnostic evaluation major criteria minor criteria etiology cardiomyopathy conditions that overwork the heart coronary artery disease heart attack management nursing management pathophysiology pharmacological management signs and symptoms congested lungs surgical management biventricular pacing stem cell transplantation Conjunctival disorders conjunctivitis management prevention signs and symptoms types of conjunctivitis pterygium prevention symptoms treatment subconjunctival hemorrhage causes treatment and management Constipation or diarrhea Continuous renal replacement therapy indications nursing diagnosis nursing management types Contracture prevention Cor pulmonale clinical manifestations complications diagnostic evaluation etiology management nursing management pathophysiology Corneal disorders Corneal dystrophies management medical management surgical management Coronary artery bypass graft disease etiology and risk factors pathophysiology signs and symptoms Cortical hormones glucocorticoids mineralocorticoids sex hormone Corticosteroids Cranial ganglia Cretinism Creutzfeldt–Jacob disease Cricoid abscess pressure Crohn's disease common procedures for colonic disease perianal disease and intestinal fistulas small bowel disease diagnostic evaluation barium enema colonoscopy computerized axial tomography electrolytes laboratory blood tests stool specimens video capsule endoscopy dietary recommendations etiology environmental factors genetics immune system problems health education medical management aminosalicylates antibiotics nursing diagnosis nursing management pathophysiology preparation for surgery signs and symptoms surgical management 936types Crohn's colitis Crohn's enteritis Cryopexy Cryosurgery (cryotherapy) Cryptogenic cirrhosis Cryptorchidism clinical manifestations complications diagnostic evaluation etiology surgical management types Cryptosporidiosis Cryptosporidium Cultured epidermal autograph Cushing syndrome diagnostic evaluation etiology management Cycle of HIV virus assembly binding and fusion budding integration reverse transcription transcription Cytomegalovirus D Dawn phenomenon Debridement of burn wounds definition purpose technique Deep vein thrombosis clinical manifestation diagnostic evaluation etiology management anticoagulation graduated compression stockings and walking nursing diagnosis nursing management pathophysiology surgical management inferior vena cava filters mechanical thrombectomy thrombolysis Dependence on opioids Dermal regenerative template Dermatitis (eczema) diagnostic evaluation etiology management nursing management signs and symptoms Dexamethasone suppression test Diabetes mellitus complications diagnostic evaluation gestational diabetes lifestyle and home remedies management Dialysis basic goals components definitions hemodialysis Dialyzer blood delivery system complications of vascular access dialysate methods of circulatory access Diencephalon Differential diagnosis (cardiovascular disorders) avoid (irregular heartbeat) alcohol appetite suppressants diagnostic evaluation electrophysiology study stress test tilt table test drug history manage your risk factor management , cardioversion defibrillation electrical cautery medications (goals of management) anticoagulants other drugs physical maneuvers normal electrical activity bradycardias in SADS tachycardias nursing management (nursing assessment) general complaints physical examination Dilated cardiomyopathy Direct brow lift visualization of the endocrine glands Disaster cycle and management environmental factors factors affecting nursing nursing responsibilities during disaster phases of principles of Disorders due to physical agents atmospheric pressure 937common occupational and industrial health hazards disorders due to infectious agents psychological factors ionizing radiation noise nonionizing radiation other mechanical stresses temperature vibration Dissection/dissecting aorta aortogram assessment and diagnostic tests classification clinical manifestations definition etiology incidence magnetic resource imaging medical management pathophysiology risk factors surgical management transesophageal echocardiography Disseminated intravascular coagulation clinical manifestation diagnostic evaluation dietary management etiology health education management nursing diagnosis nursing management pathophysiology prevention risk factors types Dupuytren's contracture Dysmenorrhea diagnostic evaluation etiology management nonpharmacological treatment nursing diagnosis nursing management pathophysiology types primary dysmenorrhea secondary dysmenorrhea Dysrhythmias E Ear disorders Ear, nose and throat disorders Eardrum perforation Ectropion Electrical conduction signals and blood flow Electrocardiography augmented limb leads axis determination characteristics of the normal basic ECG clinical lead groups ECG paper estimation of heart rate normal ECG waveforms and intervals normal Q-wave placement of electrodes precordial leads precordial placement of unipolar electrodes right axis deviation (RAD) Electrochemical mechanism Elimination of ‘look–listen–feel’ in breathing Emergency and disaster nursing Emergency conditions collaborative care diagnostic evaluation etiology and pathophysiology Emotional impact of disaster Endocarditis diagnostic evaluation etiology management nursing management pathophysiology risk factors signs and symptoms Endocrine disorders Endolymphatic sac procedures Entropion Eosinopenia Epidemiologic Surveillance and Disease Control Epispadias clinical features female male diagnostic evaluation etiology management bladder exotrophy cystoplasty nursing management postoperative care risk factors Epistaxis diagnostic evaluation history investigation etiology management nursing management Erythrocytes 938Escharotomy definition technique Esophageal cancer diagnostic evaluation management nursing management signs and symptoms stages of cancer surgical management tumors acid reflux raises risk causes and risk factors definition varices diagnostic evaluation etiology management nursing management signs and symptoms Esophagectomy Esophagogastroduodenoscopy Esophagus Ethanol (alcohol) ablation Ethical issues Excision of burn wounds definition purpose technique full thickness excision tangential excision Eye banking and corneal transplantation after surgery contraindications for donation functions of eye bank home care instructions retrieval procedure role of nurse during corneal transplantation disorders F Facial nerve grafting Fasting blood sugar test Feeling of fullness in the ear Fegan's test Female reproductive disorders Fingolimod Flail chest characteristics etiology signs and symptoms surgical fixation treatment Flank pain Folic acid deficiency clinical manifestation diagnostic evaluation etiology management Food safety Foreign bodies Free flap procedure Friends disaster service Frostbites complications management risk factor Functions of skin testes G Gallbladder cancer Gallium scan Gallstone ileus Gamma knife Gammaglutamyl transferase Gangrene Gastric cancer causes/risk factors of family history Helicobacter pylori infection long-term inflammation of the stomach obesity poor diet, lack of physical activity smoking complications of abdominal surgery diagnosis biopsy computed tomography endoscopy gastroscopic examination physical examination management nursing diagnosis nursing management pathophysiology postoperative management preoperative management psychological preparation signs and symptoms stomach cancer (gastric) prevention surgery endoscopic mucosal resection endoscopic submucosal dissection gastric bypass procedures radiation therapy surgery to remove stomach cancer thromboembolic prophylaxis 939Gastroesophageal reflux disease etiology management lifestyle changes pharmacological management surgical management nursing intervention pathophysiology signs and symptoms Gastrointestinal bleeding diagnostic evaluation etiology management nursing management types of GI bleeding disorders , hemorrhage system Genitourinary disorders , Giardia lamblia Giardiasis Glaucoma complications diagnostic evaluation etiology and risk factors intervention management nursing management pathophysiology signs and symptoms stages of glaucoma types angle-closure glaucoma exfoliation syndrome low-tension glaucoma open-angle glaucoma pigmentary glaucoma Glomerulonephritis definition diagnostic evaluation etiology management nutritional therapy pathophysiology signs and symptoms types acute glomerulonephritis chronic glomerulonephritis Glucocorticoids Glucose-6-phosphate dehydrogenase deficiency clinical manifestations medical management Glycated hemoglobin test Grandmal seizures Graves' disease Guillain-Barré syndrome diagnostic evaluation emergency symptoms etiology management nursing management pathophysiology signs and symptoms Gynecomastia H Hair loss Hashimoto's thyroiditis Head injuries causes of assault falling and hitting head gunshot wounds vehicle accidents violent shaking nursing management assessment interventions nursing diagnosis pharmacological management analgesic anesthetic anticonvulsant treatment of acute head injury types of head injuries closed injury open injury Headache chronic tension headache etiology and risk factors management symptoms types of headache Hearing aids assistive technology systems loss Heart blocks definition etiology prognosis of patients with complete heart block types AV nodal block first-degree AV block infra-hisian bundle block SA nodal block second-degree AV block third-degree AV blocks Heart murmur Heart valve disease Heart's pumping Heatstroke diagnostic evaluation etiology management prevention risk factors signs and symptoms 940Hematochromatosis Hemolytic anemia clinical manifestation medical management pathophysiology types of hemolytic anemia Hemolytic-uremic syndrome Hemophilia (factor VIII deficiency) clinical manifestation complications etiology incidence Hemorrhoids diagnostic evaluation etiology management nursing diagnosis nursing interventions postoperative complications types Hemothorax complications diagnostic evaluation etiology management pathophysiology signs and symptoms Hepatitis diagnostic evaluation dietary management of viral or drug-induced hepatitis management pathophysiology pharmacological intervention preventive measures hepatitis A, B, C, D, E types of hepatitis type A, B, C, D, hepatitis type E hepatitis Herbs Hereditory hemochromatosis clinical manifestation management nursing management spherocytosis Herniated ruptured disk Hertoghe Hiatal hernia diagnostic evaluation etiology management signs and symptoms Hippocampus and amygdala Holter monitor recordings How HIV virus transfers Human immunodeficiency virus (HIV) acquired immunodeficiency syndrome cycle of HIV virus diagnostic evaluation factor affecting the HIV progression opportunistic infections symptoms on the basis of CD4 count stages of HIV symptoms of acute infection aids Human kidney Hyperaldosteronism Hypercapnic respiratory failure Hyperkalemia Hyperparathyroidism complications diagnostic evaluation drugs bisphosphonates calcimimetics hormone replacement therapy etiology lifestyle and home remedies management nursing management risk factors signs and symptoms surgical management Hypertension classification of clinical manifestation etiology hypertensive crisis nonpharmacologic intervention nursing diagnosis intervention management pathophysiology pharmacological management risk factors treatment of types of blood pressure Hypertensive emergency etiology signs and symptoms treatment enalaprilat fenoldopam labetalol nitroprusside Hyperthyroidism clinical features complications diagnostic evaluation etiology management nursing management pathophysiology symptoms 941Hypertrophic cardiomyopathy osteoarthropathy Hypoglossal-facial nerve anastomosis Hypogonadism Hypokalemia Hypoparathyroidism complication diagnostic evaluation etiology management nursing management risk factors Hypospadias classification clinical manifestations diagnostic evaluation etiology management nursing diagnosis management , Hypotension according to diseases condition clinical manifestation diagnostic evaluation etiology adrenal insufficiency anaphylaxis bradycardia dehydration drug toxicity weakened heart muscle medium-term treatments of pathophysiology prevention treatment management Hypothyroidism according to system causes congenital hypothyroidism iodine deficiency mood stabilizers postpartum thyroiditis temporary hypothyroidism classification complication diagnostic evaluation management nursing management pathophysiology signs and symptoms supportive management Hypovolemic Hypoxemic respiratory failure I Identification of dead Immune hemolytic anemia classification clinical manifestation diagnostic evaluation etiology management Immunodeficiency disorders congenital immune disorders diagnostic evaluation examination investigation management prevention and treatment Immunoglobulin levels Immunological disorders Impact on health and after effects of disaster communicable diseases health service system mental health problems Impaired cerebral function Impetigo etiology management signs and symptoms Infectious diseases after disaster polyneuritis Infertility clinical manifestations females males diagnostic evaluation etiological factors females males lifestyle modifications management artificial insemination endocrinopathies in vitro fertilization indications for using artificial insemination insemination with donor semen nursing diagnosis management pharmacological therapy types of Inflammation and infection of the eye assessment interventions nursing management nursing process Inherited syndromes associated with immunodeficiency Inner ear cochlea vestibular or balance system Insulin therapy Insulin-dependent diabetes mellitus Integumentary disorders 942Intensive care unit psychosis diagnostic evaluation etiology medical causes critical illness heart failure signs and symptoms treatment International Relief Friendship Foundation Interstitial lung disease complications definition diagnostic evaluation etiology management pathophysiology risk factors signs and symptoms surgical management Interventricular septum Intestinal obstruction diagnostic evaluation etiology health education management nonmechanical factor nonsurgical treatment nursing management other causes types Irritable bowel syndrome (IBS) diagnostic evaluation etiology and risk factors management nursing management pathophysiology signs and symptoms Ischemic heart disease clinical manifestation coronary artery bypass graft surgery diagnostic evaluation etiology and pathophysiology management nursing management pathophysiology pharmacological treatment procedure completion, both methods surgical management J Janeway lesions Jaundice , , Jejunum drainage Joint stiffness K Kaposi's sarcoma Keratitis causes treatment types Ketoconazole Kidney anatomy and physiology of damage , failure , gross structure of right kidney stones Kiesselbach's plexus Kiwi also found vitamin C Knee arthroscopic surgery Kussmaul's sign L Labyrinthectomy Labyrinthitis diagnostic evaluation etiology management nursing management risk factors signs and symptoms Lactobacillus acidophilus , Lagophthalmos Lamina propria , Laparoscopic-assisted colectomy Large intestine Laryngeal or tracheal stenosis Larynx cancer types of cancers that start in gland cells connective tissue cancers diagnostic evaluation etiology and risk factors management radiotherapy signs and symptoms stages of cancer surgery hemilaryngectomy partial laryngectomy (also called cordotomy) supraglottic laryngectomy total laryngectomy Left bundle branch block causes characteristics characteristics of QRS complex classification clinical manifestations Leukemia classification clinical manifestation , complication diagnostic evaluation etiology and pathophysiology 943health education other management chronic phase supportive care symptom control pathophysiology risk factors treatment , Lhermittes's sign Lifestyle management for chronic hemodialysis complications contraindications indications patient education peritoneal dialysis pharmacological therapy procedure types of peritoneal dialysis Liver cancer cholangiocarcinoma classification diagnostic tests etiology and risk factors hepatoblastoma hepatocellular carcinoma management signs and symptoms of primary liver cancer secondary liver cancer cirrhosis classifications of cirrhosis complications diagnostic evaluation etiology and pathophysiology management signs and symptoms treatment transplantation Lung transplant Lyme disease Lymphomas clinical manifestation , diagnostic evaluation , etiology , Hodgkin's lymphoma management , non-hodgkin lymphoma nursing management pathophysiology risk factors stages of Hodgkin's lymphoma M Malabsorption Male reproductive disorders system anatomy and physiology Mallory-Weiss tears Mantoux test (tuberculin skin test) McBurney's point Megaloblastic anemias clinical manifestation cobalamine (vit B12) deficiency diagnostic evaluation etiology folic acid deficiency vitamin B12 deficiency management types Meglitinide derivatives Meniere's disease diagnostic evaluation etiology management nursing management signs and symptoms Middle ear eustachian tube middle ear cavity ossicular chain tympanic membrane Migraines etiology management symptoms Minimally invasive esophagectomy Mitotic inhibitors Mitoxantrone Mitral valve prolapse regurgitation stenosis Mucosal lesions Mucous membrane Muehrcke's lines Multifocal atrial tachycardia Multiple myeloma clinical manifestation diagnostic evaluation etiology management nursing management pathophysiology , Multiple sclerosis complications diagnostic evaluation etiology and risk factors management nursing management pathophysiology signs and symptoms Multiple-stage excision and grafting Musculoskeletal disorders Myasthenia gravis diagnostic evaluation 944etiology autoimmunity genetic factors thymus gland management nursing management signs and symptoms surgical management Mycobacterium tuberculosis Mycobaterium aviam complex Myelosuppressive drugs Myocarditis and pericarditis complications definition of diagnostic evaluations etiology immunological causes physical agents toxins pathophysiology prevention signs and symptoms treatment N Narcolepsy diagnostic evaluation etiology management avoid caffeine break up larger tasks into small pieces medical management nursing management signs and symptoms Natalizumab National Emergency Response Team National Organization for Victim Assistance Nausea and vomiting Neonatal resuscitation Nephrolithiasis complication diagnostic evaluation etiology health education management nursing diagnosis management pathophysiology risk factors signs and symptoms surgical management types Nephrotic syndrome complications definition diagnostic evaluation etiology health education management nursing diagnosis intervention Neurodegenerative disorder Neurological disorders Neutrophilia Night intermittent peritoneal dialysis Nonnucleoside reverse transcriptase inhibitors Nonviral hepatitis clinical features diagnostic evaluation drug-induced hepatitis fulminant hepatitis management nursing management toxic hepatitis Normal electrical conduction of the heart Nosocomial pneumonia causes treatment Nucleotide reverse transcriptase inhibitors Nutritional management aggressive nutritional support is often required assessment energy requirements are elevated by the burn injury enteral feeding should be commenced early goals of objectives of protein requirements are substantially increased O Obesity Obstructive jaundice or cholestasis Occupational health hazards Oliguric Oncological conditions Open colectomy esophagectomy Oral glucose tolerance test Organs associated with the kidneys Osteitis deformans Osteoarthritis analgesics diagnostic evaluation healthy body weight management modifiable factors nonmodifiable nonpharmacolological nursing management 945other possible factors pathophysiology signs and symptoms Osteomalacia diagnostic evaluation etiology management nursing management pathophysiology signs and symptoms Osteomyelitis causes and risk factors diagnostic evaluation medical treatment modes of transmission nursing management pathophysiology signs and symptoms surgical management Otitis media agents used in the treatment of otitis media acetaminophen amoxicillin antipyrine augmentin azithromycin benzocaine complications diagnostic evaluation etiology management nursing management signs and symptoms types Otosclerosis complications of surgery diagnostic evaluation etiology fluorides nursing management treatment of otosclerosis types of hearing impairment Outer ear ear canal pinna Oxymetazoline P Paget's disease diagnostic evaluations etiology and pathophysiology management pathophysiology signs and symptoms Palmar erythema Pancreas Pancreatectomy Pancreaticoduodenectomy Pancreaticojejunostomy Pancreatitis complications acute (early) complications late complications diagnostic evaluation management patient education and health maintenance postoperative nursing management preoperative nursing management signs and symptoms acute pancreatitis chronic pancreatitis types acute pancreatitis chronic pancreatitis etiology pathophysiology Parkinson's disease diagnostic evaluation etiology and risk factors management nursing management pathophysiology secondary symptoms Parkinson's disease bradykinesia parkinsonian gait postural instability rigidity tremors stages Parkland formula Paroxysmal atrial tachycardia Partial knee replacement nerve section Pediatric advanced life support basic life support resuscitation Pegylated interferon alfa-2b Pelvic organ prolapse types of prolapse cystocele enterocele rectocele urethrocele management Pemphigus diagnostic evaluation etiology management other treatments signs and symptoms Peptic ulcers classification of peptic ulcer complications , diagnostic evaluation 946etiology management nursing management nutritional management pathophysiology prevention signs and symptoms surgical management types of vagotomy Percutaneous ethanol injection transluminal coronary angioplasty Perfusion and circulation after cosmetic surgery Perianal disease and intestinal fistulas Pericarditis causes classification on the basis of etiological factors definition diagnostic evaluations infective pathophysiology signs and symptoms surgical management Peripheral nervous system Peripheral vascular disease classification clinical manifestation diagnostic evaluation etiology management medical management surgical management Permanent wound coverage Perthe's test Petrosal sinus sampling Phagocytosis assay Photochromic lens therapy nursing diagnosis management Physiology of hearing sound transmission through the brain inner ear middle ear outer ear Pigment cirrhosis Pituitary gland tumor Plaque in coronary artery Plastic surgery for burns or wounds Pleural effusion complications diagnostic evaluation etiology management nursing interventions nursing management signs and symptoms Plummer–Vinson syndrome Pneumococcal polysaccharides Pneumocystis jirovecii Pneumonia according to location and radiologic appearance organism site diagnostic evaluation etiology and risk factors health education management monitoring and preventing complications nursing management other risk factors other types of pneumonia pathophysiology of pneumonia signs and symptoms Pneumothorax classification of pneumothorax diagnostic evaluation etiology management pathophysiology risk factors signs and symptoms Pnuemocystis jirovecii (carinii) pneumonia Polycarbonate lens Polycythemia assessment clinical manifestation diagnostic evaluation etiology medical management aspirin interferon marrow hyperplasia phlebotomy radioactive phosphorus nursing management pathophysiology risk factors types of primary relative secondary stress Polymerase chain reaction Polypectomy and local excision Portal hypertension complications diagnostic evaluation etiology management nursing management pathophysiology signs and symptoms 947Positron emission tomography scan Postcardiac arrest care Post-discharge burn wound management Postnecrotic cirrhosis Post-traumatic stress disorder and rehabilitation of disaster victims etiology high-risk group predisposing factors principles of nursing care signs and symptoms Posturography Pott disease diagnostic evaluation management nursing management pharmacological management postspinal fusion surgery signs and symptoms systemic signs and symptoms of Precordial thump Premature supraventricular contraction or premature atrial contraction ventricular contraction Premenstrual syndrome clinical manifestations diagnostic evaluation etiology health education management pathophysiology Primary immunodeficiency disorders Probiotic supplement Progression from HIV to AIDS symptoms discharge goals interventions management and prevention from HIV management of HIV nursing diagnosis nursing management Progressive multifocal leukoencephalo-pathy , Prolapsed lumbar disk advantages of hip replacement surgery diagnostic evaluation etiology and pathophysiology indications of hip replacement surgery nursing management Prostate Prosthesis types of transfemoral prosthesis transhumeral prosthesis transradial prosthesis transtibial prosthesis Protease inhibitors Proton-pump inhibitors Pruritus Psoriasis complications diagnostic evaluation etiology light therapy (phototherapy) management nursing management oral or injected medications risk factors signs and symptoms topical treatments types of psoriasis Pulmonary contusion complications acute respiratory distress syndrome pneumonia pulmonary edema diagnostic evaluation computed tomography ultrasound X-ray etiology pathophysiology prevention signs and symptoms treatment fluid therapy supportive care ventilation Pulmonary embolism clinical manifestation complications diagnostic evaluation etiology management Pulmonary function tests Pulmonary hematoma Pulmonary hypertension clinical manifestations complications diagnostic tests etiology management nursing management pathophysiology types of pulmonary hypertension Pulmonary laceration classification complications diagnostic evaluation etiology management pathophysiology surgical treatment 948Pulmonary valve stenosis balloon valvuloplasty diagnostic evaluation etiology management nursing management nursing diagnosis nursing interventions Pulmonary valve stenosis open-heart surgery other contributing conditions carcinoid syndrome other contributing conditions rheumatic fever risk factors sign and symptoms surgical management Pulseless electrical activity Purkinje fibers , Pyothorax or empyema etiology and risk factors signs and symptoms stages of pyothorax treatment options types Q QRS shape and duration QRS wider Quarrying R Radiation therapy beta radiation gamma and X-radiation new in radiation therapy nursing management side effects of radiation therapy treatment types of ionizing radiation nonionizing radiation Radioactive yttrium beads Radiofrequency ablation Ramantadine Random blood sugar test Raynaud's phenomenon causes clinical manifestation types types of Raynaud's disease Rectal surgery abdominoperineal (AP) resection local transanal resection (full thickness resection) low anterior resection pelvic exenteration polypectomy and local excision proctectomy with coloanal anastomosis transanal endoscopic microsurgery Refractive error astigmatism hypermyopia myopia presbyopia treatment of refractive errors eyeglass frames eyeglass lenses Rehabilitation of disaster victims agencies challenges of rehabilitation children disabled people functions kinds of reactions shown by disaster victims operational mechanism policies related to emergency and disaster management policy implementation agencies and structures policy statement psychosocial interventions women Reinke's edema Reproductive disorders Respiratory disorders Respiratory failure administration of oxygen airway obstruction chest wall dysfunction and neuromuscular factor classification of clinical manifestations management mechanism of pathophysiology medical management Restrictive cardiomyopathy lung diseases corticosteroids (such as prednisone) cytotoxic therapy definition diagnostic evaluation management pathophysiology signs and symptoms Resuscitation formulas Retinal detachment diagnostic evaluation interventions nursing management risk factors signs and symptoms surgical management types and causes Retinoblastomas Retinopexy Revision knee replacement Reyes syndrome Rheumatic heart disease diagnostic evaluation etiology management nursing management pathophysiology Rheumatoid arthritis clinical manifestations 949complications diagnostic evaluation etiology and risk factors extra-articular manifestations nursing management risk factors specific aarticular involvement is manifested surgical management treatment Rib fracture definition etiology signs and symptoms treatment Right bundle branch block causes characteristics of QRS complex Ringing in the ear (tinnitus) Rogaine clearly speak at a moderate pace do not shout do not talk from another room face the client directly get attention first give clues when changing subjects keep your hands away from your face pay attention to the listener Rotary-chair testing Rotator cuff repair S SA nodal block atrioventricular block characteristics diagnostic test first-degree atrioventricular block prognosis treatment Salivary glands Scabies diagnostic evaluation etiology management signs and symptoms Scar prevention Schwartz test Scleral buckling Scrotum Second-degree atrioventricular block causes characteristics , , etiology , second-degree av block , third-degree atrioventricular block treatment , types Seizure or epilepsy anticonvulsant therapy diagnostic evaluation etiology initial nursing management management patient and family education types of seizures Semifowler position Semisolid Serum sodium Severe combined immunodeficiency disease upper abdominal and back pain Sexual function and fertility after colorectal surgery Sexually transmitted diseases Shin bone Shingles (varicella-zoster) diagnostic evaluation etiology and risk factors management signs and symptoms Sick sinus syndrome Sickle cell anemia Sigmoidoscopy for colorectal cancer screening Signs of infection at the surgical site Silicosis classification of accelerated silicosis acute silicosis chronic silicosis complications diagnostic test etiology experimental treatments pathophysiology prevention signs and symptoms silica treatment Simultaneous bilateral knee replacement Single-and multiple-stage excision and grafting Single-stage excision and grafting Sinus tachycardia Sinusitis and nasal injury Skin changes after cosmetic surgery Skin grafts Small bowel disease stricture plasty Small intestine Special burns Speech disorders advantages of hearing aids clinical manifestations aphasia apraxia of speech dysarthria stuttering daily care for the hearing aid direct audio input 950disadvantages of hearing aids etiology aphasia dysarthria spasmodic dysphonia vocal disturbances features available in hearing aids management types of speech impairment Spermatic cords Spermatozoa Sphincterotomy Spider angiomata Spinal injury etiology hemiplegia types of management nursing intervention signs and symptoms types of paralysis types of spinal injuries Splenectomy Stapedial otosclerosis Steatorrhea Stem cell transplantation Steps of basic life support amiodarone bicarbonate calcium Sternal fracture diagnostic test etiology signs and symptoms treatment Stomach Stress body coping mechanism with stress Stress general adaptive syndrome model Stress management Stress stages Stye (external and internal hordeolum) causes prevention signs and symptoms treatment Sucralfate and misoprostol Sudden arrhythmic death syndrome etiology signs and symptoms Sudden cardiac death , Sulfonylureas Supraventricular tachycardia Surgery and other local treatments for colorectal cancer metastases Swimmer's ear symptoms Syphilitic aortitis clinical manifestation pathophysiology T Tachycardic Taenia coli Takayasu's disease clinical manifestation diagnostic evaluation etiology management pathophysiology surgical management Taste disturbance and mouth dryness Team resuscitation Techniques for burn reconstruction Teriflunomide Terms of total body surface area Terry's nails Thalassemia complication diagnostic evaluation management medical therapy nursing interventions nursing management standard treatments types of thalassemia Thoracic aortic aneurysm abdominal aortic aneurysm assessment and diagnostic tests , causes clinical manifestations , endovascular surgery open surgery prevention risk factors surgical management , treatment (medical management) , Thoracic trauma Thromboangiitis obliterans (Buerger's disease) clinical manifestation diagnostic evaluation etiology pathophysiology prevention Thrombocytopenia Thymic aplasia (DiGeorge's syndrome) Thyroiditis diagnostic evaluation etiology management signs and symptoms Thyroxine Tic douloureux Tilt-table tests Tissue expansion Tonsillectomy Topoisomerase inhibitors Total body irradiation Total hip replacement surgery Total knee replacement 951Total shoulder replacement Toxoplasma gondii Toxoplasmosis of brain Tracheobronchial injury clinical manifestations complications bronchial stenosis bronchiectasis pneumonia diagnostic evaluation etiology Tracheobronchial injury prevention treatment endotracheal tube mechanical ventilation tracheotomy Tracheobronchial washings Tracheoesophageal fistula Transarterial chemoembolization with doxorubicin-filled beads with lipiodol Transient ischemic attack Transposition flaps Transposition of temporalis Trendelenburg test Trichiasis Tricuspid and pulmonic stenosis Trigeminal neuralgia etiology management deep brain stimulation medical management nursing management signs and symptoms surgical management types of tic douloureux Troubleshooting ventilator alarms Tubbing Tuberculosis complications diagnostic evaluation etiology chemical industries immunocompromised person mycobacterium tuberculosis health education intervention activity intolerance deficient knowledge ineffective airway clearance ineffective therapeutic regimen management risk for infection medical management pathophysiology and clinical manifestations risk factors types Tunica albuginea externa vaginalis vasculosa Tuning fork test Tympanic membrane perforation diagnostic evaluation etiology management signs and symptoms surgical management Types of occupational and industrial disorders disorders due to chemical agents dusts gases metals organic compounds U Unaided communication systems Upper endoscopy GI series Ureteroscopy Urinary retention Urine glucose and ketone levels Uterus cervix V Vaccination Vaginal fistula complications Vaginal fistula diagnostic evaluation etiology management nursing diagnoses Vaginal fluids Vaginitis diagnostic evaluation etiology and types health education management Vagus nerve Valvular heart disease diagnosis etiology and pathophysiology health education management nursing diagnosis types Varicose veins clinical manifestation clinical manifestation complications , diagnostic evaluation , etiology etiology health education 952management nursing diagnosis other diagnostic tests pathophysiology risk factors stages , treatment management types Vascular disease common vascular disorders arotic aneurysm Buerger's disease deep vein thrombosis Vascular disorders of heart Vasovagal reaction Vector control Vein wall weakness Venous thromboembolism Ventricular dysrhythmias fibrillation , myocardium repolarization tachycardia tachycardia or ventricular fibrillation Vestibular evoked myogenic potentials nerve section Video capsule endoscopy Videonystagmography Vinca alkaloids Viral load test Visual acuity test Vitrectomy Vocal cord and tracheostomy Volutrauma W Warts management freezing (cryotherapy) Wasting syndrome due to HIV Water supply Waves and intervals Weakness of the face Weaning procedure Wear a medical alert bracelet or necklace Wear loose fitting, lightweight clothing Weight gain and water retention West Nile virus Western blot test Wet mount Whiff test Whipple resection White patches in patient's mouth Witnessing violence Wolff-Parkinson-White syndrome Women with Cushing syndrome Worsening constipation Wound care daily treatment Wound care first aid healing phase in children initial treatment other wound care methods Wrap alcohol wipe X Xanthine derivatives Xenograft (Pigskin) X-linked (Bruton's agammoglobulinemia) X-ray studies Y Yeast infection , Yellowing of skin , Z Zestril Zinc Zoledronate Zoonotic transmission Z-plasty and modifications