SRB’s Clinical Methods in Surgery Sriram Bhat M
Chapter Notes

Save Clear

Introduction on Clinical Examination1

Clinical examination is an art. It is an important basic essential part in surgical learning. Surgery is categorized as clinical surgery; surgical principles and operative surgery. So surgery is not just cutting. It involves proper clinical analysis; and application of principles in treating surgically related patients. All patients in the surgical ward need not undergo or need surgery. Conditions like cellulitis, amebic colitis or acute pancreatitis commonly does not require surgery but treated by surgeons. A surgeon should be a good clinician and physician all together to impart proper treatment to his (surgical) patients. Even though there are many sub-specialties in surgery now, basic clinical surgery remains the same. It is the pillar of surgical basis.
Two important parts in clinical methods are symptoms and signs. Symptom is the one patient complains of. It is the subjective sensation of the patient. Sign is the one which clinician elicits. It is an indication of existence of an objective evidence of a disease.
Clinician is the one who listens patiently; who sees carefully; who feels evidentially; who hears silently.
Clinical methods are schematically divided as:
History taking which is very important part. Careful detail history taking many times gives clue about the exact disease.
Physical examination includes general examination; inspection of the part (diseased or suspected) which is proper observation prior to palpation for specific findings; palpation is done once inspection is completed in detail; followed by percussion done in specific areas like abdomen and chest; later auscultation for altered or specific sounds in particular region.
Case taking or Case analysis includes:
  • Clinical methods.
  • Clinical diagnosis.
Investigations are done to come into final conclusion by various methods like X-ray, CT scan, ultrasound, blood tests and so on. Types of investigations are decided based on the clinical suspicion of the disease.
Final diagnosis is to plan the therapy, predict the outcome.
Treatment plan or protocol often differs for individual patient.
Postoperative/post therapy management.
Progress of the patient.
Follow-up after discharge and further treatment which is often needed after initial management.
History Taking
Clinician should spend adequate time for detailed history taking from the patient. If the patient is a child or patient is dumb, then history is given by the mother or close relative who takes care of the individual. Name and relation of the person who is giving history should be noted down. Patient should be made comfortable while taking history.
General History
Correct name of the patient should be asked and noted down. It is better to remember the patients name while doing rounds at least up to the discharge of the patient. This helps to build a zone of comfort 2with the patient. It may be helpful to keep a pocket note book to write down in short about details of the patient.
Noting the age of the patient is important. Congenital anomalies occur in young age group. Cleft lip and palate; phimosis exists since birth. Branchial cyst even though of congenital origin occurs in later age group in 2nd or 3rd decade. Certain tumors like Wilm's tumor (kidney) and neuroblastoma occur in early childhood. Sarcomas develop in adolescents. Usually carcinomas occur after middle age. But malignancies can occur at any age group. Benign prostatic hyperplasia occurs in old age often causing retention of urine.
Certain diseases occur only in particular sex other than gender specific diseases. Hemophilia occurs only in males but females can be carriers. Thyroid diseases are more common in females. Carcinoma lung, stomach, kidney are more common in males but can occur in females.
Carcinoma penis is not seen in Muslims and Jews due to their religious practice of early circumcision in childhood. Duodenal ulcer perforation is common in Muslims during fasting month of Ramzan.
Residence, complete postal address and method of communication must be taken down: Many diseases have got geographical distribution. Hydatid disease is common in Australia, Iran, Greece, etc; Schistosomiasis is common in Egypt; Trypanosomiasis is common in Africa; amebiasis is common in tropical countries; filariasis is common in Orissa; leprosy in West Bengal; gallstones in Bihar and north east India; peptic ulcer in South India.
Some diseases are common in people with certain occupations. Varicose veins are common in people who stand for long hours like bus conductors, garden workers, watchmen, traffic policemen, surgeons, and nurses, etc. Carcinoma urinary bladder is more common in workers in aniline dye factories. Sportsmen are more prone for injuries to ankle, knee and elbow.
Social status: Tuberculosis is common in low socio-economic group; peptic ulcer disease is common in high socioeconomic group.
Social status is classified as Class I—professionals; Class II—Executive and higher management; Class III—Lower management and clerical; Class IV—Skilled laborers; Class V—Unskilled laborers.
Chief Complaints
Main complaints of the patient are mentioned in the order of occurrence. Complaints of same duration should be narrated in the order of severity. Example–
Lump in the breast-6 months.
Ulcer in the swelling of breast-2 months.
Pain in the breast-1 month.
Fever-1 month.
Often proper leading questions are necessary to elicit clear-cut relevant history. But this should be used only after proper initial detailed history. History should be elicited in language which the patient is comfortable. One should not elicit diagnosis from the patient. Negative reply of the patient is also very relevant and so it should not be ignored.
History of Present Illness
It is detailed history in relation to onset of the present disease until date. It should be in order of occurrence. Each part of the history should be mentioned in detail before going to next part of the history.
Mode of onset of symptom: It may be gradual or sudden or initially slow but later progress rapidly. History suggestive of whether it is related to any trauma or any earlier disease should be asked.
Progress of the disease: Whether the symptoms are decreasing or increasing; gradual or rapid; or waxing and waning (increase-decrease-increase).
Past History
Earlier diseases should be detailed in order. Often patient may not know the name of the disease which he had earlier. History suggestive of specific disease should be elicited like tuberculosis, syphilis, leprosy, 3bronchial asthma, diabetes mellitus, and tropical diseases. When such disease has occurred; detailed history of treatment taken; response to treatment should be asked for. Often patient might have got hospitalised for the treatment which should be asked in detail like place where he was hospitalised; duration; type of treatment (type of drugs, injections, etc). Earlier treatment summary/prescriptions if present should be taken and studied for reference. History of earlier surgery/trauma; its detail like duration of hospital stay, recovery period, any postoperative complications, drain placed or not, response of surgery whether patient is relieved of symptoms completely or partially, any operative notes available for reference should be asked.
Personal History
History of personal habits like smoking beedi or cigarettes with duration/frequency/number of beedi or cigarettes per day; history of drinking alcohol with duration, quantity, whether addicted, whether associated with alcohol induced problems should be noted.
Alcohol Intake
A problem drinker is one whose physical, social and mental well being is harmed by drinking. One unit of alcohol is 8 grams of alcohol in 290 ml of 4% beer. Teetotaler is one who has not taken alcohol in last one year. Occasional drinker is one who has not taken alcohol in last one month. Light drinker who drinks alcohol < 25 units per week in males; < 15 units in females. Moderate drinker who drinks 25-35 units/week in males; 15-25 units in females. Heavy drinker who drinks 36-50 units/week in males; 26-35 units in females. Very heavy drinker is > 50 units/week in males; > 35 units/week in females.
Light smoker smokes one packet of cigarette/day for 2-10 years. Moderate smoker 1-10 packets of cigarettes/day. Chronic heavy smoker smokes 10-20 packets of cigarettes/day for 2-10 years
Type of diet is also important in relation to many diseases. It should be mentioned whether patient is married or not; number of children he/she has.
In females, detailed menstrual history should be noted. Time of menarche/menopause/regularity/presence of pain/dysmenorrhoea/white discharge/date of last menstrual period are noted in detail. Pregnancy history with number of pregnancies/abortions/normal delivery or Caesarean/last child birth should be noted.
Family History and Genetic History
Many diseases run in family. Examples are: piles; breast cancer; diabetes mellitus; tuberculosis, etc. If any of the family member is suffering from any disease; its detail, type, therapy for the same, whether he has underwent any surgery for the same and so on should be mentioned in detail. Number of siblings and their health details should also be taken.
Other Relevant History
In younger age group history of immunization for different diseases; history suggestive of allergy/reactions during earlier drug intake; history of long-term drug therapy like insulin, steroids, antidiabetics, antihypertensives, diuretics, hormones, etc. should be noted.
Pain is a commonest symptom which patient complains to a clinician. Latin word ‘poena’ means penalty/punishment. Pain is the one patient feels; tenderness (sign) is the one surgeon/clinician elicits.
Types of pain:
Superficial pain: It is sharp usually localised pain, due to irritation of peripheral nerve endings in superficial tissues by chemical/mechanical/thermal/electrical injury.
Segmental pain: It occurs due to irritation of particular nerve trunk/root; located in particular dermatome of the body supplied by the sensory nerve trunk or root.
Deep pain: It is due to irritation of deeper structures like muscles/tendons/bones/joints/viscera. It is vague and diffuse when compared to superficial pain. It is often referred to common segmental areas of representation. Often spasm of skeletal muscle of same spinal cord segment can occur.
Psychogenic pain: It may be functional/emotional/hysterical.4
Other types of pain: Like due to thalamic/spinothalamic diseases/causalgia [intense burning pain along the distribution of the partially injured (and healed) nerve].
Specific points in history in relation to pain to be asked are: original site of pain is very important. In acute appendicitis original site of pain is in umbilicus; but later it shifts to right iliac fossa, i.e. shift of pain towards other site.
Time and mode of onset of pain: It is in sudden onset, rapidly progressive in acute appendicitis; it is of insidious onset and of long duration with episodic nature in chronic peptic ulcer; pain after trauma means very important and may be an emergency like internal organ injuries (liver, spleen, and kidney) or due to fracture bone.
Type/nature of pain: It may be superficial/deep; dull ache or sharp severe/pricking/bursting/vague aching (continuous mild pain), throbbing, scalding (burning sensation particularly felt during urination in cystitis, pyelonephritis, urethritis), pins and needles pricking sensation in peripheral nerve injury or irritation, shooting pain (seen in intervertebral disc prolapse and sciatica-pain shoots along the course of nerve), stabbing (sudden, severe, sharp, episodic—seen in perforated duodenal ulcer), distension pain (a feeling of restricted or distended like in paralytic ileus or intestinal obstruction), colicky pain is due to muscular contraction in a hollow tube in an attempt to obviate the obstruction by forcing the content out—griping, episodic pain with vomiting and sweating (seen in intestinal colic, ureteric colic of stone, biliary colic of stone), twisting pain of bowel volvulus/twisted ovarian cyst/torsion testis, constricting pain around the chest by angina, etc.
Severity of the pain: Severe pain is common in acute appendicitis, acute pancreatitis, ureteric colic, perforation of bowel, acute peritonitis, intestinal obstruction, acute abscess.
Progression of pain: It may be persistent and progressive; or initially mild gradually increases, later subsides gradually; or fluctuates in intensity, i.e. increases and decreases in intensity at regular intervals or quickly reaches maximum and remains like that.
Duration of pain: Colicky pain lasts usually for a minute in each episode; anginal pain lasts for 3-5 minutes; an acute pain like of pancreatitis persists.
Periodicity of pain: Pain appears, persists for few weeks and then disappears for few weeks; again reappears. Such periodicity is often observed in chronic peptic ulcer; trigeminal neuralgia.
Precipitating/aggravating factors: Abdominal pain may get worsened by taking food like in gastric ulcer. Pain due to appendicitis, ureteric stone aggravates in change of position, walking, jolting. Pain of urinary bladder stone aggravates in standing position. In reflux oesophagitis pain increases while scooping. Pain in pancreatitis increases on lying down. Pain in intervertebral disc prolapse aggravates by lifting the weight.
Relieving factors of pain: Pain reduces by certain method and patient uses that method to relieve the pain. Hunger pain of early morning in duodenal ulcer is relieved by taking food. Pain of pancreatitis is relieved by sitting and bending forward. Propped up position relieves pain of reflux oesophagitis. In acute peritonitis, pain reduces temporarily by lying still.
Associated symptoms: Acute pain may be associated with pallor, sweating and vomiting. Migraine pain with vomiting and visual disturbances; intestinal/ureteric colic with sweating, vomiting and cold periphery; acute pyelonephritis and urinary infections with chills/rigors and fever; ureteric colic with haematuria; biliary colic with jaundice and pale stool are other examples of such association.
Time of occurrence of pain is often important in diagnosing the condition. In duodenal ulcer, hunger pain occurring in early morning or later evening is typical. Migraine occurs in early morning; frontal sinusitis induced headache occurs few hours after getting up.
Pain may move from one place to other.
Radiation of pain: It is extension of pain from original site to another site with persisting of pain at original site. This radiating pain is of same character of original site. Penetration of duodenal ulcer posteriorly causes pain both in epigastrium and back—is an example. Pain of pancreatitis radiates to back.5
Referred pain: Pain is not felt at the site of the disease but felt at distant site. Diaphragmatic irritation causes referred pain at the tip of shoulder through same segmental supply of diaphragm (phrenic nerve C4, C5) and shoulder (cutaneous supply C4, C5). Hip joint pathology may cause referred pain in knee joint—through articular branches of femoral, obturator and sciatic nerves. Other examples—referred pain in ear from carcinoma tongue through lingual and auriculotemporal nerve; referred pain in the epigastrium from the heart; referred pain in the abdomen from pleura; referred pain over the testis from the ureter.
Shifting/migration of pain: Origin of pain is in one site; later pain shifts to another site and pain at original site disappears. Pain when begins in viscera, is felt at the same somatic segmental area in the body; but once parietal layer is involved by inflammation/pathology pain is felt at the anatomical site. Example is pain of acute appendicitis, where the original visceral pain is at the umbilicus (T9 and T10 segments supply both umbilicus and appendix) which later shifts to right iliac fossa when once the parietal peritoneum of that area is inflamed.
Grading of pain is done using pain scale. It is compared to a 10 cm line numbered 0 to 10. This is called as visual analogue scale (VAS). Minimum is 0 means no pain. 10 is the worst excruciating pain. 2 is mild; 4 is discomforting; 6 is distressing; 8 is intense.
Vomiting is a common symptom heard in clinical practice. It may be due to—pregnancy, travelling sickness, labyrinthitis, gastritis, peptic ulcer, migraine, meningitis, intracranial tumour, ureteric colic, pyloric stenosis, carcinoma stomach (pylorus), intestinal obstruction, intracranial space occupying diseases, acute peritonitis, cholecystitis, pancreatitis, metabolic causes like diabetic ketosis, drug induced. Colour, quantity, smell of the vomitus should be found. Coffee ground coloured vomitus is seen in upper GI bleed. When bled blood comes in contact with gastric juice, hemoglobin forms acid haematin colouring contents blackish or dark brown. Vomitus may contain frank blood/clots. Presence of undigested material should be asked for. Oesophageal obstruction by achalasia cardia or stricture causes regurgitation. Nonbilious vomiting means obstruction proximal to sphincter of Oddi. Bilious vomiting occurs in small bowel obstruction; which may be either yellow or green coloured. Faecal content in the vomitus suggests ileal/large bowel obstruction. Faeculent vomiting is also seen in gastrocolic fistula. Content is brown in colour with faecal odour. Haematemesis should be distinguished from haemoptysis. Vomiting is graded as follows—None (0); one episode of vomiting in 24 hours (1); 2-5 episodes/24 hours (2); > 6 episodes/24 hours (3); needs parenteral fluid/nutrition (4).
It is sense (feel) of vomiting. It may or may not end up with vomiting. It can be none (0); nausea present but able to eat (1); oral intake is reduced (2); No oral intake, on IV fluids (3).
Itching (Pruritus)
It is due to local or general causes. Multiple scratch marks are often obvious. It may be due—Skin diseases: urticaria, eczema, scabies (Psoriasis will not cause itching). Local causes contact dermatitis due to clothing, washing soap, washing powder infection from fungal, parasites like fleas, scabies; vaginal and rectal discharge. Systemic causes are obstructive jaundice due to bile acid irritation, Hodgkin's disease, leukaemia, uraemia, allergy/hypersensitivity, drug reactions, diabetes mellitus, etc.
It is subjective sensation of weakness (asthenia/lethargy). It is graded as none (0); fatigue over baseline (1); moderate fatigue (2); severe (3); bedridden (4).
Anorexia is loss of appetite. It is seen in anorexia nervosa, gastrointestinal cancers, tuberculosis, debilitating illness like sepsis. Anorexia is graded as none (0); loss of appetite (1); significant reduction in oral intake (3); unable to take orally requiring IV fluids (3). Satiety is sense of fullness after completion of meals. It is normal. Early satiety is a feature of GI malignancy.
Flatulence is frequent belching more than normal. Regurgitation is effortless return of food into the 6mouth. It is associated with powerful involuntary contractions of abdominal muscles. It is seen oesophageal/OG junction obstructions like carcinoma and achalasia cardia. Heartburn is burning sensation behind the sternum due to acid reflux into the oesophagus.
Constipation is defined as having bowel movement fewer than three times per week; with hard, dry, small sized stool; difficult to evacuate. It is graded as none(0); needs diet modification (1); needs laxatives (2); needs manual evacuation or enema (3); due to obstruction (4). Constipation can be relative wherein patient can pass flatus but not faeces; or absolute wherein patient neither can pass faeces nor flatus.
Diarrhea is defined as more than 3 stools per day. It is usually soft, often foul smelling. Often it may be associated with incontinence. It is graded as increase of < 4 times/day (1); increase 4-6/day (2); increase > 7/day or with incontinence or need parenteral nutrition (3); needs intensive care with haemodynamic collapse (4).
Physical Examination
It should be done in privacy. Female patients should be examined in presence of a female/nurse. Examination should be done with limited clothing to elicit proper findings. Broad day light is ideal for examination. Usage of other lights may mislead or mimic some clinical findings like jaundice.
General Examination
This part of the examination is essential preliminary step in all patients.
Patient's intelligence level should be assessed while taking history. Uneducated people still can be intelligent.
Mental Status
Mental status and level of consciousness should be assessed in general but in particular in specific clinical situations like head injury, hepatic encephalopathy, septic shock, etc.
Built and Nutritional Status
Built and nutritional status of the patient is important to be assessed. Built is structural organization of underlying skeleton. It is related to age and sex of the patient. Gigantism is height to that age is in excess than normal (in adult more than 6.5 feet). It may be racial; familial; endocrinal (hyperpituitarism, hypogonadism); genetic (Klinefelter's syndrome); metabolic (Marfan's syndrome, homocystinuria); overeating; cerebral causes. Dwarfism is height to that age and sex is far less than normal (below 4.5 feet). It can be hereditary, chromosomal (Turner's syndrome, Down's syndrome); delayed growth; nutritional (Rickets); endocrinal (hypopituitarism, hypothyroidism, excess androgens, congenital adrenal hyperplasia, insulin insufficiency); skeletal (achondroplasia, spinal deformities); systemic diseases (uraemia, cyanotic heart diseases, cirrhosis). In normal adult, height of the person is equal to length of arm span. Upper segment from vertex to pubic symphysis is equal to lower segment from pubic symphysis to heel. In infants upper segment is more than lower segment and height is more than arm span. This infantile body frame persists in achondroplasia, cretinism, and juvenile myxoedema. Greater arm span than height and greater lower segment is observed in Marfan's syndrome, homocystinuria, Klinefelter's syndrome, Frohlich's syndrome.
Nutrition is the proportion of soft tissue structures (muscles, soft tissues, fat) in relation to the bony structure. In gastrointestinal malignancies or in other malignancies with metastases patient will be cachexic. Protein deficiency causes rough skin, brittle hair, and oedema feet. Fat deficiency causes cachexia, hollow cheeks, and loss of fat in hips, abdomen and subcutaneous tissues of elbow. Deficiency of minerals and vitamins has got specific features.7
Weight Gain
Weight gain is increase in weight. It is graded as increase of < 5% (0); increase of 5-10% (1); 10-20% (2); > 20% (3). It is seen in obesity, pregnancy, myxoedema, water retention, Cushing's syndrome.
Weight Loss
Weight loss is graded as loss of < 5% (0); 5-10 % (1); 10-20% (2); > 20 % (3). But time duration of weight loss is also important. Definition of significant weight loss (2009): Weight loss more than 5% (up to 7.5%) in 30 days; weight loss more than 7.5% (up to 10%) in 60 days; weight loss more than 10% in 180 days.
It is obvious on the upper half of the body as there is often oedema due to hypoproteinaemia in lower half of body. By looking at the shoulder girdle, loose skin of arms, trunk and buttocks, severity of wasting can be assessed (Fig. 1.1). It is observed in starvation, severe gastroenteritis, tuberculosis, anorexia nervosa, diabetes mellitus, advanced carcinomas, gastrointestinal malignancies, and old age.
zoom view
Fig. 1.1: Ascites with wasting proximal part probably due to malignancy.
Malignant Cachexia
Malignant cachexia is emaciated (Fig. 1.2), languid, shallow, pale face, loose wrinkled dry skin, loss of fat, lost appetite/weight/energy with oral infection. Profound loss of weight is typical.
zoom view
Fig. 1.2: Typical malignant cachexia.
Attitude of the patient in the bed is good thing to observe. Comatose patient/paraplegic or quadriplegic is silent and immobile. Patient in shock or with peritonitis may not move due to pain. Patient with ureteric stone may be restless and rolling in the bed due to severe colicky pain. Position of the patient in the bed is called as decubitus. It is often typical in certain diseases like cerebral irritation, cerebral palsy, etc. In hemiplegia patient lies with one side immobile, with affected arm flexed and legs externally rotated and extended. In tetanus, patient develops stiff neck. In ureteric colic, patient is restless with rolling and tossing over the bed. In acute peritonitis patient lies in the bed still and motionless. In cardiac diseases, patient is comfortable in sitting up position. In pneumonia, patient lies on the affected side to make that side immobile and restricted so as to reduce the pain.
Stature is the total height from vertex to soles. Posture is positional relationship of different regions of the body. Normal posture is—moderate lordosis of cervical and lumbar spine; kyphosis of thoracic and sacrococcygeal region; forward pelvic inclination 30°; normal rotation of femur; line from the mastoid down passes through the middle of the shoulder and hip, anterior to knee and lateral malleolus.
Face Look
Typical face is diagnostic of some diseases. Hippocratic facies is seen in generalised peritonitis. Face with typical pale look is seen in chronic renal failure, risus sardonicus in tetanus; mask face in Parkinsonism; 8moon face in Cushing's syndrome is to be noted. Acromegaly (due to increased growth hormone in pituitary acidophilic adenoma) shows large face due to overgrowth of soft tissues in face, nose, tongue, air sinuses; large hands (due to enlargement of bones of distal phalanges)—facies of Punch of ‘Punch and Judy’ or an ‘Ape man’. Skin is greasy; mental acumen is normal (in myxoedema skin is dry with decreased mental acumen). In scleroderma, progressively thickened, pale, waxy skin with reduced facial expressions, microstomia, telangiectases on cheeks, mouth and nose, with fine white horizontal scars in the neck in transverse skin creases (with oesophageal stenosis and vasculitis) are seen. In Myasthenia gravis weakness of all muscles is found; in particular of eyelids showing drooping of eyelids with weakness of face muscles and jaw (Fig. 1.3). Cretin is a neonate with deficient thyroid hormone (cured by thyroid hormone supplement); diagnosed at birth; with broad flat face, wide apart eyes, protruded tongue. Down's syndrome/Mongolism is a congenital abnormality with extrachromosome 21 and total chromosomes 47 (instead of 46); males and females and all races are equally affected. Features are—mental retardation, floppiness, short stature, outer ends of the palpebral fissures slanted upwards with prominent epicanthic folds, flat face, protruded tongue and squint.
Klinefelter's syndrome is a congenital abnormality in a male having XXY chromosomes instead of normal XY chromosome. Patient is tall, with female distribution of fat around breast and pelvis but normal hairs in face and pubis. Patient is having small testis without sperms. Turner's syndrome is a congenital abnormality of female, having only one X chromosome, XO instead of XX. Short, webbed shoulder, widened neck with prominently running skin fold from neck to shoulder—are typical.
zoom view
Fig. 1.3: Eyes and face should be examined carefully as part of general examination. Note the visible lower sclera—could be due to exophthalmos.
Pallor is checked in lower palpebral conjunctiva, mucous membrane of lips and cheeks, nailbeds and palmar creases. Causes for pallor are-anaemia, massive bleeding, shock and anxiety status (Figs 1.4A to C).
zoom view
Figs 1.4A to C: Lower eyelid is retracted to see the conjunctiva for pallor. Note the normal conjunctiva and conjunctiva with pallor.
It is due to rise in level of reduced haemoglobin in the blood causing blue/purple discolouration in the skin and mucous membrane. A minimum of 5 gm/dl of reduced 9haemoglobin should be present in the circulation to cause cyanosis. So in severe anaemia (Hb% below 5 gm %), cyanosis is not seen. Two types of cyanosis are observed—peripheral and central. Peripheral cyanosis is due to poor perfusion of peripheral vessels causing reduction in oxyhaemoglobin in the capillaries. It is seen in peripheral vasoconstriction due to any cause like exposure to cold temperature, reduced cardiac output, profound shock where blood is diverted from periphery to vital organs like brain, liver, and kidney. Peripheral cyanosis is checked in nailbed, palm and toes, tip of the nose. Here limb is cold and inhaling pure oxygen may not reduce it. Tongue is not involved in peripheral cyanosis. Central cyanosis occurs due to reduced oxygen saturation of arterial blood due to poor oxygenation in the lungs. It may be due to congenital heart disease with left to right shunt (cyanotic heart disease), congestive cardiac failure, lung diseases, and high altitude due to low oxygen partial pressure. Limb temperature is normal in this type. Clubbing and polycythaemia is common here. Pure oxygen inhalation reduces the central cyanosis. It is confirmed by checking in tongue (Fig. 1.5), nailbed, palms and toes. Methaemoglobinaemia or sulphaemoglobinaemia (abnormal pigments) also causes cyanosis but with normal arterial tension. In carbon monoxide poisoning, carboxyhaemoglobin prevents reduction of oxyhaemoglobin and so there will not be any cyanosis but cherry red discoloration develops.
zoom view
Fig. 1.5: Central cyanosis is checked in the tongue-dorsum.
Differential cyanosis: Patent ductus arteriosus (PDA) with reversal of shunt causes only lower limb cyanosis. PDA with reversal of shunt with transposition of great vessels causes only upper limb cyanosis. PDA with reversal of shunt with preductal coarctation of aorta causes cyanosis of left upper limb and both lower limbs.
Polycythaemia is excess of circulating red blood cells giving patient a purple-red florid appearance; it heightens the colour of all the skin, cheeks, neck, backs of hands and feet whereas cyanosis is limited to tips of hands, feet and nose.
Jaundice is yellowish discoloration of skin and mucous membrane. Tissues and body fluids are also discoloured yellow. Bilirubin has more affinity to elastic tissue, blood vessels and nervous tissue. So it is better seen in sclera and skin. During recovery, bilirubin takes longer time to get cleared from elastic tissue and so clinical jaundice persists for little longer time than biochemical disappearance of jaundice. Initially it is pale lemon yellow colour, later gets darkened becomes yellow-orange, olive greenish yellow as seen in obstructive jaundice. Jaundice is due to deposition of bile pigments with excess of it in plasma. It is checked in upper sclera (better seen against white background; by asking the patient to look at his feet and clinician pulls the upper eyelid upwards). It also can be checked in nailbed, ear lobule, nasal tip, and on under surface of tongue. Greenish colour is due to deposition of biliverdin. Scratch marks observed on the dorsum of the body (forearm, neck, back) is due to deposition of bile acids which releases excess histamine causing itching (Figs 1.6A to C).
Jaundice may be due to pre-hepatic cause (excess haemolysis); hepatic (liver dysfunction—hepatitis, sepsis, drugs, cirrhosis); post-hepatic (CBD stones, carcinoma pancreas, drugs—obstructive); congenital hyperbilirubinaemia (Gilbert's syndrome causing altered bilirubin transport and so increase in unconjugated bilirubin; Criggler-Najjar syndrome causing disturbance in bilirubin conjugation and so increase in unconjugated bilirubin; Dubin-Johnson syndrome and Rotor's syndrome causing disturbance in excretion of bilirubin and so increase in conjugated bilirubin).
zoom view
Figs 1.6A to C: Janudice is checked in sclera by asking the patient to look down on the feet and examiner pulls the upper eyelids upwards. It is also checked in nasal tip, ear lobule, fingertips and under surface of the tongue.
Aged red cells get lysed in the reticuloendothelial cells and breakdown into haem and globin. Haem is divided into globin and bilirubin. Bilirubin is combined with albumin and transported to liver. In the liver bilirubin get separated from albumin and is conjugated to bilirubin glucuronide by glucuronyl transferase. This conjugated bilirubin glucuronide is water soluble and can be excreted in kidney (So in obstructive and hepatic jaundice bile pigment-bilirubin is seen in the urine). This conjugated bilirubin is excreted through biliary canaliculi reaching intestine. In the intestine, it is converted into stercobilinogen and urobilinogen by intestinal bacteria. 70% of this is absorbed in the colon and brought back to liver as enterohepatic circulation (Fig. 1.7). Unabsorbed stercobilinogen colours faeces brown. Circulating urobilinogen is taken up by kidneys for excretion. If direct bilirubin in the serum is more than 0.4 mg%, then bilirubin is seen in urine. Normal urinary urobilinogen is 100-200 mg/day. It is absent in obstructive jaundice. Normal faecal stercobilinogen is 300 mg/day. It is also absent in obstructive jaundice.
Hypercarotinaemia mimics jaundice which is due to increased yellow pigment carotene. It is seen equally in face, palm, sole and skin but not seen in sclera. It is common in vegetarians who eat more raw carrot. Mepacrine therapy also causes yellow discolouration.
It is usually an increase in natural brown pigmentation of the skin. Often pigmentation by other colours like blue/red also can occur. Pigmentation can be generalised or localised.
Generalised: It occurs in Addison's disease (seen in skin and buccal mucosa); arsenic/silver poisoning; haemochromatosis; Gaucher's disease.
Localised: It occurs in pregnancy (around areola, midline abdomen); venous diseases of lower limb (medial third of leg and ankle); erythema eb agne (in the exposed part of leg); ultraviolet and high voltage irradiation; café au lait spots of neurofibromatosis; naevi; melanomas; pellagra (nicotinic acid deficiency); hyperthyroidism (bronzing of eyelids); rheumatoid arthritis.
Examination of Nails
A transverse groove (transverse lines/Bean's lines) seen at similar levels of each nails is suggestive of systemic disease/general debilitating illness.
zoom view
Fig. 1.7: Enterohepatic circulation.
Pallor can be seen in nailbed. In iron deficiency anaemia (Plummer-Vinson syndrome) nails may be brittle/flat (platynychia)/spoon shaped (koilonychia). Splinter haemorrhages are seen in nailbed in bacterial endocarditis and bleeding disorders. Discoloured, deformed, pitted nails are seen in psoariasis. Hypoalbuminaemia causes whitening of the nailbed—Terry's sign. Onychia is deformity of the nail—seen in fungal infection or tuberculosis. Specific discolourations are seen in Raynaud's disease, silver and mercury poisoning. Ribbing, brittleness, falling of nails are seen in syringomyelia, leprosy and tabes dorsalis. Nailbed infarcts are seen in vasculitis due to SLE or polyarteritis. Onychogryphosis (in toe) is heaping up of nail and curling over the end of the toe due to failure of normal sliding mechanism of the nail and is due to trauma or old age. Ingrowing toe nail is common in margins of the nail of great toe where irregular edge of the nail grow beneath the lateral nail fold due to improper trimming of the nail causing repeated pain and infection (Figs 1.8A to 1.10B).
zoom view
Figs 1.8A and B: Nails should be examined in both hands and feet (fingers and toes) for change in colour, splinter haemorrhage, clubbing, pallor, koilonychia and other features.
zoom view
Figs 1.9A and B: Changes in the toe nail also should be observed. Note the pallor and koilonychia in the toe nails.
zoom view
Figs 1.10A and B: Note the change in the great toe nail. It could be onychogryphosis.
It is bulbous enlargement of the soft parts of the terminal phalanges with both transverse and longitudinal curving of the nails. It is due to interstitial oedema and dilatation of the arterioles and capillaries. There is loss of normal angle between surface of the nail and the skin covering the nailbed. When a normal nail is viewed from side, plane of the nail and the plane of the skin covering the base of the nailbed form an angle of 130°-170° (Lovibond angle). In clubbing tissue hypertrophy beneath the nailbed makes the base of the nail bulge upwards distorting the nail growth causing nail to be curved in both directions. So in clubbing plane of the nail and plane of the skin covering the nailbed form an angle which is greater than 180° (Figs 1.11A to D).
Causes: It can be due to pulmonary (Carcinoma bronchus, lung abscess, bronchiectasis, tuberculosis with secondary infection); cardiac (cyanotic congenital heart disease, infective endocarditis); gastrointestinal (ulcerative colitis, Crohn's disease, cirrhosis); endocrinal (myxoedema, acromegaly, exophthalmic ophthalmoplegia—thyroid acropachy); other causes (hereditary, idiopathic), unilateral in Pancoast tumour, subclavian/innominate artery aneurysm:unidigital in trauma or tophi deposition in Gout, only in upper limbs in heroin addicts due to chronic obstructive phlebitis.
Grade I: Softening and fluctuation of nailbed;
Grade II: Obliteration of angle of the nailbed with loss of longitudinal ridges and formation of convexity from above downwards and side-to-side;
Grade III: Swelling of the subcutaneous tissue over the base of the nail causing overlying skin tense, shiny and wet increasing the nail curvature;
Grade IV: Swelling of the fingers occurs in all dimensions, associated with hypertrophic pulmonary osteoarthropathy causing pain and swelling of the hand and radiographic features of subperiosteal new bone formation.
Disappearance of diamond shaped gap between nails when fingers are apposed—Schamroth's sign; Pathogenesis: Hypoxia leads to opening up of deep arteriovenous fistulas which increase the perfusion of the fingers and toes causing its hypertrophy. It may be due to reduced venous blood ferritin which escapes oxygenation in the lungs, which after entering the systemic circulation stimulates dilatation of arteriovenous anastomosis leading to hypertrophy and clubbing of terminal phalanx.
zoom view
Figs 1.11A to D: Typical clubbing. In normal individual angle from skin to nail fold is 130 to 170 degree. In clubbing it is more than 180°. In clubbing both longitudinal and transverse curvatures are increased.
Pseudoclubbing is seen in hyperparathyroidism due to undue bone resorption resulting in disappearance of terminal phalanges causing telescoping of soft tissues into the terminal phalanges which appears like clubbing. Nail is not having curvatures here.
It is the collection of fluid in the interstitial spaces or soft tissues. Oedema will be clinically evident only when fluid accumulates more than 5 litres. Pitting on pressure occurs only when circumference of the limb is increased by 10% (Figs 1.12A and B).
Mechanism: Fluid accumulates in the interstitial space following— Increased capillary permeability like in acute inflammation (cellulitis); increased capillary pressure (cardiac failure); decreased osmotic pressure (hypoproteinaemia); lymphatic block (filariasis). Pitting on pressure is the cardinal sign of oedema. Using pulp of the finger/thumb firm pressure is applied for few seconds over the skin on a bone surface like lower part of medial aspect of leg just above the malleoli. Indentation or pitting is seen on releasing the finger. Slow reaccumulation of fluid in few minutes is observed. Nonpitting oedema is observed in late stage of lymphoedema. Oedema is commonly observed in most dependent part—lower limbs. In bedridden patient, it may be seen on sacral region. Often limb oedema may also be associated with ascites or pleural effusion.
zoom view
Figs 1.12A and B: (A) Pitting oedema in the leg. (B) Note oedema with multiple ulcers.
Oedema can be generalised or localised. Generalised oedema is called as anasarca. It is due to cardiac, renal, hepatic or nutritional causes. Localised oedema is due to cellulitis, lymphatic causes, venous diseases, pretibial myxoedema of thyrotoxicosis. Causes may be classified as bilateral (cardiac, renal, hepatic, IVC obstruction, allergic, nutritional, toxic) or unilateral (lymphatic, traumatic, infection, metabolic like gout, DVT/varicose veins, hereditary). In CCF oedema is in most dependent position—in lower limbs and is more in evening. In LVF pulmonary oedema develops earliest and so dyspnoea, basal crepitations, cough are typical. In pericardial effusion, lower limb oedema, ascites, hepatomegaly—soft smooth liver, raised JVP without pulmonary oedema is observed. In renal cause oedema develops first in eyelids and face, and then it becomes generalised into legs and ascites. In hepatic cause like portal hypertension, ascites develops first due to increased portal pressure and hypoproteinaemia, and then lower limb oedema develops. In myxoedema, oedema is nonpitting. Here oedema over the lateral aspects of the eyelids is typical.
Oedema grading-None (0); asymptomatic, not requires drug therapy (1); symptomatic requires drug therapy (2); symptomatic, with limited function, not responding to therapy (3); anasarca (4).
Visible Veins
Patient should be examined for visible veins. With normal venous pressure external jugular vein is invisible or just visible for short distance. Raised venous pressure causes engorgement of external jugular vein. Bilateral engorgement of external jugular vein/neck veins may be due to myocardial infarction or intravenous fluid infusion or retrosternal goiter/thoracic outlet obstruction. Unilateral engorgement of vein is due to compression by lymph nodes, tumour. In toxic goiter neck veins may be prominent due to increased vascularity. In SVC obstruction, inguinoaxillary veins, chest wall veins, neck veins may be prominent with flow of blood from above downwards and through groin veins (across watershed area) to IVC. In IVC obstruction, veins in the flanks (both sides) will be prominent, with direction of flow from below upwards towards axillary vein along inguinoaxillary vein. Unilateral such flow is observed in unilateral blockage of common or external iliac vein. IVC obstruction is classified as—below the renal vein (standard presentation); at the level of renal vein (lumbar pain, haematuria, proteinuria); above the level of renal vein (like Budd-Chiari syndrome). Caput medusae is visible dilated veins radiating from umbilicus, seen in portal hypertension (Figs 1.13A to 1.14B).15
zoom view
Figs 1.13A to D: Superior vena caval obstruction causing dilated veins in the chest wall. Note the direction of flow from above downwards towards lower abdomen and to inferior vena cava.
zoom view
Figs 1.14A and B: Dilatation of abdominal veins including inguinoaxillary vein and bilateral varicose veins in a patient with IVC obstruction.
Jugular Venous Pulse (JVP)
Normal JVP has got 3 positive waves a, c and v and 2 negative waves x and y. ‘a’ wave is due right atrial contraction (Fig. 1.15). It is absent in atrial fibrillation; prominent in tricuspid/pulmonary stenosis. Cannon a wave is seen in complete heart block, ventricular tachycardia. ‘c’ wave is due to carotid artery impact into jugular vein and right ventricular systole. ‘x’ wave is due to fall in right atrial pressure and atrial relaxation. It is absent in tricuspid regurgitation. It is prominent in constrictive pericarditis. ‘v’ wave is due to right atrial filling. Giant v wave is seen in tricuspid regurgitation. ‘y’ wave is due to opening of tricuspid valve causing rapid inflow of blood from right atrium into the right ventricle. Rapid y descent occurs in constrictive pericarditis, heart failure and tricuspid regurgitation. Jugular venous pressure is 3-4 cm of water. It is elevated in cardiac tamponade, right ventricular failure, tricuspid stenosis, increased blood volume, asthma, emphysema, SVC obstruction. It is reduced in shock, dehydration. During normal inspiration, intrathoracic pressure falls and venous blood flow to thorax increases causing inspiratory collapse of jugular venous pressure. In constrictive pericarditis when intrapericardial pressure rises, there will be paradoxical increase in jugular venous pressure during inspiration—Kussmaul's sign.
zoom view
Fig. 1.15: Normal jugular venous pulse-waves.
Pulse Means Arterial Pulse
Pulse is an ideal indicator of severity of many diseases. It is increased in sepsis, severe pain, shock, fever, toxic thyroid. It is also altered in all cardiac conditions. Rate (count the pulse); rhythm (regularity); tension and force; character; condition of arterial wall should be noted. Pulse felt usually is radial pulse (against head of the radius) but when indicated, other pulses in the body also should be examined. It is felt using three fingers-index, middle and ring. Ring finger is kept distally to obliterate the retrograde pressure transmission; middle finger is over to feel the pulse; index finger is kept proximally to control and fix the artery to reduce the blood flow while checking the vessel wall thickness. Pulse is counted for full one minute. Counting for few seconds and multiplying is wrong. Normal pulse has got a 17small anacrotic wave in the upstroke (which is not felt), a big tidal percussion wave which is felt (Fig. 1.16). During downstroke there is a dicrotic notch with a dicrotic wave (both are not felt). Anacrotic wave pulse is felt in severe aortic stenosis. Pulsus bisferiens is rapid rising, twice beating waves in the systole of the pulse; felt in idiopathic hypertrophic subaortic stenosis, severe aortic incompetence with mitral stenosis. Dicrotic pulse is twice beating pulse with initial normal percussion wave of systole and eventual abnormal prominent dicrotic wave in diastole. It is seen in reduced peripheral resistance like CCF, cardiac tamponade, typhoid fever. Pulsus alterans is alternate strong and weak beats; due to alternate contractions of the cardiac muscle; seen in left ventricular failure, toxic myocarditis. Pulsus paradoxus—During inspiration there is increased venous return to right atrium; lung expansion causes pooling of blood in the pulmonary vessels causing decreased venous return to left atrium and ventricle. It causes decreased left ventricular output and arterial pressure during inspiration by 3-10 mm Hg. When this fall in systolic pressure is exaggerated more than 10 mm Hg, it is called as pulsus paradoxus. It is seen in SVC obstruction, airway obstruction, asthma, pericardial effusion. In immobile thoracic cage pulsus paradoxus does not exists. Pulsus bigeminus with coupling occurs in atrioventricular block. Thready pulse is rapid, small waved pulse seen in shock, cardiac diseases. Waterhammer pulse is large bounding pulse with a forcible jerk, disappearing quickly. It is due to sudden fall in peripheral resistance; seen in thyrotoxicosis, AV fistula, beriberi, aortic regurgitation, PDA. Tachycardia means increased pulse rate more than 100/minute. Bradycardia (Greek-slow) is decreased pulse rate less than 60/minute.
zoom view
Fig. 1.16: Normal arterial pulse wave.
Blood Pressure (BP)
BP is essential part of the general examination in all cases. It gives the idea about the general condition of the patient along with other parameters. BP is lateral pressure exerted by the column of blood on the walls of the arteries. Systolic pressure is due to stroke volume of the heart and stiffness of vessels. It is the maximum pressure produced during (cardiac cycle) systole. Diastolic pressure is due to peripheral resistance. BP varies in phases of respiration. It is the minimum pressure exerted during cardiac cycle (diastole). It is related to emotion, exercise, smoking, alcohol, tobacco, meals, temperature, anxiousness, circadian rhythm, age, race, obesity, etc. BP is recorded by indirect method. Riva Rocci invented sphygmomanometer. It contains mercury manometer, cuff and air pump. Russian surgeon Korotkoff originated the method of placing of stethoscope over cubital fossa to hear sounds of brachial artery. Procedure of taking BP should be meticulous. Patient should be explained about the procedure. Patient should be on rest for 5 minutes prior to checking BP. Patient should avoid exertion or meals 30 minutes prior to checking BP. Clothing of the arm should be removed or kept as it is without folding (folding may cause constriction band). Width of the inflatable bladder cuff should be about 40% of the upper arm circumference (12-14 cm width in average adult); length of the inflatable bladder should be 80% of upper arm circumference, almost long enough to encircle the arm. Standard commonly used is 12 × 23 cm size. In the thigh 18 × 24 cm is used. In obese, 12 × 35 cm sized cuff is used. In children smaller sized cuff (width 3 cm in infants; 8 cm in children) is used. Bladder of the BP cuff should encircle the arm completely; center of the bladder cuff should be over brachial artery; ideally rubber tubes should be placed on the inferior aspect in the line of the brachial artery (eventhough tubes are commonly placed superiorly to make stethoscope placement over cubital fossa easier); though bell of stethoscope gives better sound; diaphragm of the stethoscope is commonly used due to its ability to cover wider area and easier to secure. Usual position is supine lying down with arm supported to heart level. In sitting/standing position arm should be horizontal at 4th intercostals space of the sternum. If arm is not 18supported, arm with isometric contraction will elevate the diastolic BP by 10%. In normal individual, there is not much difference in BP in standing, sitting or lying down positions. BP in right arm is higher by up to 10 mm Hg; if BP is higher by more than 10 mm Hg then it should be analyzed carefully. Repeat inflations of cuff will raise the systolic and diastolic BP and give false readings. So cuff should be inflated rapidly and deflated early and completely; further repeat readings are taken with a gap of 15 seconds.
Phases in BP measurement: Phase I: Appearance of faint clear tapping sound which gradually increases in intensity; Phase II: Softening or swishing sounds; Phase III: Return of sharper crisper sounds; Phase IV: Soft, blowing, muffling of sounds; Phase V: Disappearance of sounds completely. Phase I is systolic BP; Phase V is diastolic BP. Hypertension is persistent raised systolic (above 140 mm Hg) or diastolic (above 90 mm Hg) BP. It is sustained elevation of systemic arterial pressure. It could be—essential HT; renal; vascular; endocrinal; neurological; haematological. Hypotension is diminished BP (systolic pressure less than 90 mm Hg). It could be due to—postural, cardiac, endocrinal like Addison's disease; tuberculosis, malignancy, dehydration, shock, haemorrhage, hypovolaemia, anaemia, anorexia nervosa.
Tachypnoea is rapid breathing seen in fever, shock, hypoxia, acidosis, tetany, hysteria. Gradual deepening of respiration alternating with short periods of apnoea is called as Cheyne-Stokes respiration.
Fever/Rise in Temperature
Normal body temperature is balance between heat gain and loss maintained by hypothalamus. It is the temperature of viscera and body tissues. Normal temperature is 36.7°C-37.5°C (98 to 99°F-98.6°F). A diurnal variation of 1°C is normal; lowest temperature is during morning 2-4 AM highest being in afternoon. Fever is increase in body temperature more than 1°C or more than the maximum range. Hypothermia is 35°C/95°F or below; subnormal temperature is 35°-36.7°C/95°-97°F; normal is 36.7-37.5°C/98° to 99°F (98.6°F); mild fever is 37.2°-37.8°C/99°-100°F; moderate fever is 37.8°-39.4°C/100°-103°F; high fever is 39.4°-40.5°C/103°-105°F hyperpyrexia is more than 40.1°C/106°F.
Types of fever:
Continuous fever: Fever persists throughout the day and does not fluctuate more than 1°C in 24 hours. It is seen in pneumonia, urinary infection, endocarditis.
Remittent fever: Fever is above normal throughout the day but there is fluctuation of more than 1°C in 24 hours. Intermittent fever—temperature is present only few hours a day and reaches to normal. It is observed in malaria, Kala azar. When fever develops daily, it is called as quotidian; when fever develops on alternate days it is called as tertian; when it occurs every third day it is called as quartan.
Pel-Ebstein fever: Recurrent bouts of fever and afebrile periods occur at regular alternations. Fever rises for 3 days, remains high for 3 days, remits in 3 days and goes for an afebrile period of 9 days to develop fever again in the same manner. It observed in brucellosis; earlier also thought to be due to Hodgkin's lymphoma.
Fever with chills is sensation of cold with fever. Rigor is profound chill with piloerection (gooseflesh) with teeth shattering and shivering (Fig. 1.17). Pyrexia Unknown Origin (PUO) is defined as—fever more than 101°F; more than 3 weeks of duration; failure to reach into a diagnosis even after one week of inpatient investigation.
Causes for fever: Infective (bacterial, viral, fungal, parasitic); neoplastic; vascular (myocardial infarction, pulmonary embolism, pontine/subarachnoid haemorrhage); traumatic; collagen diseases; endocrinal; metabolic (Gout, acidosis); haemolytic.
Grading of fever: None (0); 38-39°C (1); 39.1-40° (2); > 40° for 24 hours (3).
Tongue may be large called as macroglossis. It is seen in lymphangioma, haemangioma, acromegaly, myxoedema, critinism, amyloidosis. Tongue tremor is observed in thyrotoxicosis (primary). It is checked with tongue kept inside the oral cavity. If tongue is protruded, tongue twitchings may mimic tremor. Tongue is bright red in colour normally—due to rich blood supply through capillary network. Pallor is seen in anaemia, haemorrhage.
zoom view
Fig. 1.17: Different types of fever.
Discolouration can occur after coloured food intake, tobacco chewing, Addison's disease, iron tablets intake. Central cyanosis is observed in tongue. Tongue is moist normally; dry tongue suggests dehydration, shock. Dry brown tongue is a feature of uraemia, intestinal obstruction. Mouth dryness is graded as normal (0); mild (1); moderate (2). Furring of tongue is seen in smokers, stomatitis, and poor oral hygiene. Black hairy tongue is seen in fungal infection. Bald tongue is due to atrophy of papillae. It is seen in iron deficiency anaemia, vitamin B12 deficiency. Curdy coating is seen in candidiasis infection. Leukoplakia as a whitish opaque thickened epithelium may be seen; it is often associated with superficial glossitis. Congenital fissuring can occur with irregular folds. Fissuring may also be a presentation of carcinoma of tongue. Lozenge shaped loss of papillae and fissuring is seen in midline in front of the foramen caecum. Lingual thyroid may be seen posteriorly in midline. Inability to protrude tongue is seen in ankyloglossia in tongue tie, advanced carcinoma tongue infiltrating the genioglossus muscle. While protruding tongue may deviate towards same side in hypoglossal nerve palsy.
It is spasmodic contraction of diaphragm. It is commonly idiopathic which subsides on its own. Post-operative hiccup is common. It is due to increased abdominal pressure, pushing the diaphragm upwards. There may be paralytic ileus, gastric dilatation, and intestinal obstruction. Peritonitis involving diaphragmatic surface can cause hiccup. Renal failure causes hiccup.
It is crackling or grating sensation felt on palpation of subcutaneous tissue or joint or bone. Crackling sensation is felt when air is under the palpating fingers. Pockets of air moves in between separated subcutaneous or soft tissues causing crackling feel. Grating sensation is felt in bone or joint as crepitus.
Crepitus in subcutaneous (surgical) emphysema: It is crackling sensation felt with gentle pressure under examining fingers similar to a palpating horse hair mattress. It can often be heard by placing a stethoscope over the surface. Subcutaneous emphysema is better felt (often seen as bull neck) in neck, shoulder and chest wall. Causes of subcutaneous emphysema are—traumatic (Fracture ribs, laryngeal injury, tracheostomy, fracture skull with air sinus like frontal sinus injury); after surgery air may get trapped in the subcutaneous plane prior to closure of skin, after 20laparoscopic surgery; infective (in gas gangrene); after oesophageal rupture (Boerhaave's syndrome—here mediastinal emphysema, subcutaneous emphysema, shock, toxicity occurs).
Crepitus of tenosynovitis: It is seen in de Quervain's tenosynovitis. Here hand is laid upon arm above the wrist, and the patient is asked to close and open the hand. Crepitus is felt at the junction of extensor pollicis brevis and abductor pollicis longus crossing the extensor carpi radialis longus and brevis. Crepitus of bursitis is felt when lining is rough or contains loose fibrinous particles.
Joint crepitus: It is felt when affected joint passively moved by one hand, and by placing other hand over the suspected joint. It can be—fine, even crepitations of chronic and subacute joint diseases; coarse, irregular crepitations of osteoarthritis; a click due to loose body or displaced cartilage. Bone crepitus is elicited over the fracture segments of the bone when two fragments are moved against each other. A grating sensation is typical. But this should be elicited with utmost gentleness; only when radiological doubt exists. Crepitus is an unmistakable, diagnostic sign of fracture.
Skin Changes and Eruptions (Figs 1.18 to 1.22)
Macule: It is not raised above the skin; there is alteration in colour of skin; it is seen but not felt; capillary naevi or erythema blanch on pressure, purpuric macules do not blanch on pressure. Macules can be generalised; as seen in typhoid, syphilis, purpura; localised type is called as roseolar.
Papule: It is raised tiny nodule; usually of few mm in size; it may be epidermal or dermal; seen in measles, chickenpox, smallpox, drugs like sulfonamides, occasionally in tuberculosis, sarcoidosis.
Vesicles: They are small blisters; elevations from epidermis containing clear or milk like fluid within; seen in chickenpox, smallpox, herpes.
Pustules: They are epidermal elevations containing pus; due to bacterial like streptococcal infection. Granule is projection of < 2 cm in size. Nodule is large usually solid projection from the skin of more than 2 cm in size.
zoom view
Fig. 1.18: Drug induced allergic rashes on the back extensively involved.
zoom view
Fig. 1.19: Alopecia scalp developed after chemotherapy.
Wheal: It is elevated patch on the skin with centre paler than the periphery; it is oedematous elevation with itching; seen in allergical conditions.
Café au lait spots: They are coffee brown coloured patches in the skin; more than 5 in number with each more than 1.5 cm in size are significant; seen in von Recklinghausen's disease of neurofibromatosis with regular outline and deep indentations; occasionally also seen in Albright's syndrome as irregular outline.
zoom view
Fig. 1.20: Herpes zoster infection.
zoom view
Figs 1.21A and B: Skin rashes and skin vesicles in two different patients.
zoom view
Fig. 1.22: Radiation dermatitis both sides of neck and face.
Petechiae: Tiny haemorrhagic spots less than 1 mm in size.
Purpura: Haemorrhagic spots of 2-5 mm in size.
Ecchymosis: Haemorrhagic spots more than 5 mm in size.
Haematoma: Haemorrhage causing elevation of skin.
Dry skin: Seen in dehydration and myxoedema.
Moist skin: Seen in myocardial infarction, shock of sudden onset (haemorrhage), toxic thyroid.
Thick skin: Seen in myxoedema, acromegaly, and scleroderma.
Thin skin: Seen in old people, and wasting diseases.
Pinched skin a feature of dehydration, malnutrition.
Falling of hair: Seen in infectious fevers like typhoid, chemotherapy for malignancies, drugs and hereditary. Patchy hair loss is seen in alopecia areolata, syphilis. Loss of hair in outer third of eyebrow: Seen in leprosy, myxoedema. Absence of axillary, pubic and facial hairs is seen in hypopituitarism, hypogonadism.
Excessive hair growth in women is seen in Cushing's syndrome, adrenocortical syndrome.
General examination is done for proper diagnosis and differential diagnosis; for selecting the patient for anaesthesia; to decide type of surgery to be done (mesh hernioplasty is done in inguinal hernia if patient is having chronic respiratory disease or if there is poor abdominal muscle tone); to predict the prognosis (patients with gastrointestinal cancer showing palpable supraclavicular lymph node means poor prognosis; patient with carcinoma breast having spread to bones/lungs carry poor prognosis).
Other General Examinations
Other general examinations to be done are:
Head and neck region: Cranial nerve functions; eyes (visual field, pupils for equality and reaction, accommodation reflux, conjunctiva, eyeball movements, 22fundus examination); mouth and pharynx (teeth, gums, soft palate movement, tongue, tonsils, lip); neck (movements of neck, neck veins, neck nodes, carotid pulse, trachea, thyroid).
Upper limbs: General look of hands, forearm, arm (wasting); vascular system; nervous system (sensation, muscle power, muscle tone, reflexes); axillary nodes; joints and movements; fingers and nails.
Thorax: Chest look; dilated veins; swelling (Fig. 1.23); pulsations; breasts; apex beat; lungs and heart.
Abdomen: Abdominal wall (umbilicus, scar, dilated veins); reflexes of abdomen; visible peristalsis; visible pulsation; hernial orifices; palpation; percussion; auscultation; rectal digital examination; per vaginal examination if needed in females; examination after catheterization if needed.
Lower limbs: Examination of feet, legs, thighs; feeling of peripheral pulses; nervous system in the lower limbs; oedema feet; varicose veins; examination in standing position; joints; inguinal nodes.
Examination of genitalia: Testis (its size, texture, presence of hydrocele); epididymis; vas deferens, skin over the scrotum; penis for phimosis, balanoposthitis, chordee, hypospadias.
Skeletal system: spine and skull.
zoom view
Fig. 1.23: Systemic examination is a must. Note the chest wall swelling in this patient. Clothings should be removed properly while examining the patient. This swelling may be secondary in the rib or primary tumour.
Examination of Faeces
It gives indirect evidence of different pathologies in the gastrointestinal tract. The quantity—copious/scanty; consistency—liquid/semisolid/semiformed/formed/hard; colour—black-in upper GI bleed, iron or bismuth intake/pale coloured stool is seen in obstructive jaundice (absence of bile in the bowel), rapid transit of stool in diarrhoea, malabsorption, chronic pancreatitis; odour—offensive in jaundice, semen like odour in acute amebic dysentery, odourless in acute bacillary dysentery; type—slimy stool in carcinoma colon, colitis of different causes; purulent stool in bacterial dysentery; blood in stool in different conditions. Melaena—is black, tarry, foul smelling stool seen in upper GI bleed (Fig. 1.24); red pigmented clots (Maroon coloured) in Meckel's diverticulum; red currant jelly in intussusception; bright red coloured in rectal and anal diseases. Steatorrhoea is large quantity, pale, porridge-like stool that, sticks to lavatory and is difficult to flush. It is due to severe degree of pancreatic insufficiency causing malodourous, voluminous stool which floats on the water. Patient passes quantity of fat that separates from the non-fatty part of the faecal matter that resembles melted butter that become solid again. Pipe stem stool occurs in rectal stenosis usually due to malignant rectal stricture. Toothpaste stool is seen in Hirschsprung's disease. Spurious diarrhea is seen in carcinoma colon.
zoom view
Fig. 1.24: Typical black, foul smelling tarry coloured stool—seen in upper gastrointestinal bleeding.
ECOG performance status (Eastern Cooperative Oncology Group): This performance status is used as a guide to plan the therapy. Other scale used is Karnofsky scale.23
ECOG (Zubroad) scale
Karnofsky score
Fully active and able to carry out work without restriction
Symptoms restrict strenuous physical activity but ambulatory and able to carry light sedentary work
Ambulatory but unable to carry out work; up and about > 50% waking hours
Only limited self care; confined to bed or chair for more than 50% of waking hours
Completely disabled; confined to bed or chair
Local Examination
It is observing the diseased area carefully for clinical features. It should be done with proper complete exposure of the part; compared with normal side.
It is done by feeling of affected part using hand and fingers.
It is tapping of the affected area directly using flexed finger (direct method) or using pleximeter finger and percussion finger (indirect method). Percussion is used over sternum, abdomen (ascites, over mass to find out note, liver dullness), respiratory system (in pleural effusion, pneumothorax).
Stethoscope is used to hear heart sounds, abnormal sounds like adventitious breath sounds, altered bowel or absence bowel sounds; bruit over vessel or organ.
Examination of regional lymph nodes is essential.
Movements and measurements are also often important.
Sequence of events needed in approaching all patients are as follows –
  1. Detailed complete proper history.
  2. Complete clinical examination.
  3. Clinical analysis, diagnosis and differential diagnosis.
  4. Evaluation of the patient routine/general and specific in relation to the patient's probable diagnosis.
  5. Final diagnosis.
  6. Planning the therapy/treatment which are best suitable for the patient.
  7. Implementing the treatment surgical/conservative (like drugs)/radiotherapy, etc.
  8. Follow up of the patient.