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Emergency Medicine
RK Singal, AK Agarwal, DG Jain, Rajesh Upadhyay
1:
ABC of Emergency Room Management
Organisation of emergency service
The chain of care
Initial evaluation
Primary survey
Resuscitation
Secondary survey
Definitive care
Conclusions
2:
Basics of Emergency Room Management
Primary assessment and management of the patient
A – Airway
Foreign body obstruction may present as a distressed, very agitated, or cyanosed patient
Signs of partial upper airway obstruction
Clearance and maintenance of the airway
Protection of the airway
Total airway management consists of opening, securing, and maintaining the patency of the airways. This will help you achieve the following:
B – Breathing
C – Circulation
D – Disability
E – Environment and exposure
F – Fits
G – Glucose
H – History
I–Immediate analgesia and investigations
Secondary assessment and management
Management rather than diagnosis
3:
Management of Paediatric Problems in the Emergency Room
Anticipate
Activate
Act
Record keeping
Cardiac arrest
Collapsed patient
Very ill child with or without rash
Diabetes
Poisoning
Child with seizures
Acute respiratory distress
Thermal injuries
Foreign bodies
Trauma
Chest injuries:
4:
Acute Coronary Syndrome
Pathophysiology
Mismatch between supply and demand
Plaque disruption
Thrombosis
Embolisation
Clinical evaluation
Risk stratification in acute coronary syndromes
Clinical risk stratification
Electrocardiogram
Cardiac markers
TIMI score
Treatment
General measures
Antiplatelet agents
GP IIb/IIIa receptor antagonists
Antithrombin treatment
Nitrates
Beta-blockers
Calcium channel blockers
Lipid lowering therapy
ACE-inhibitors
Invasive versus non-invasive strategy
Dedicated randomised control trials
Conclusion (see flowchart for details)
5:
Acute Myocardial Infarction and its Early Complications
Pathophysiology
Risk factors
Conventional risk factors
A. Dyslipidaemia
B. Smoking
C. Hypertension
D. Diabetes mellitus and insulin resistance syndromes
E. Obesity
F. Alcohol
G. Lifestyle factors
Emerging risk factors
A. Lipoprotein (a)
B. Homocysteine
C. Fibrinogen
D. High sensitivity C-reactive protein (hs-CRP)
E. Other inflammatory markers
Clinical features of AMI
History and prodrome
Physical findings
Diagnosis of acute myocardial infarction
Electrocardiography
Areas of infarction
Serum cardiac markers in AMI
A. Creatine kinase
B. Cardiac troponins
C. Myoglobin
D. Lactate dehydrogenase
Serum cardiac markers and the temporal profile of AMI
Echocardiography
Radionuclide imaging
A. For assessment of patients presenting with chest pain to the emergency department
B. For detection of AMI when conventional measures are non-diagnostic
C. For risk assessment: prognosis and assessment of therapy after STEMI
D. Radionuclide testing in risk assessment: prognosis and assessment of therapy after NSTEMI or UA
Management of AMI
ECG
Cardiac markers and laboratory investigations
Cardiac imaging
Routine measures
a. Oxygen
b. Nitroglycerin (NTG)
c. Analgesia
d. Aspirin
e. Beta-blockers
f. Angiotensin converting enzyme inhibitors (ACEI)
g. Antiplatelet therapy
h. Antithrombotics
Reperfusion therapy
Pharmacological reperfusion
Alteplase
Reteplase
Streptokinase
Urokinase
Percutaneous coronary intervention (PCI)
Primary PCI in STEMI
Facilitated PCI in STEMI
Rescue PCI in STEMI
PCI after fibrinolysis
Acute surgical reperfusion
Early complications of AMI
Haemodynamic disturbances
a. Haemodynamic assessment
b. Hypotension
c. Pulmonary oedema
d. Cardiogenic shock
e. Right ventricular infarction
f. Mechanical causes of heart failure/low-output syndrome
Mitral valve regurgitation
Ventricular septal rupture (VSR) after AMI
Left ventricular free wall rupture
Arrhythmias after AMI
1. Ventricular arrhythmias
a. Ventricular fibrillation
b. Ventricular tachycardia
c. Ventricular premature beats
d. Accelerated idioventricular rhythms and accelerated/junctional rhythms
Implantable cardioverter-defibrillator implantation in patients after AMI
2. Supraventricular arrhythmias/atrial fibrillation
3. Ventricular asystole
4. Permanent pacemakers
5. Sinus node dysfunction after AMI
Recurrent chest pain after STEMI
Recurrent ischaemia
Pericarditis
Other complications
Ischaemic stroke
Haemorrhagic stroke
DVT and pulmonary embolism
6:
Management of Hypertensive Crises
Definitions and terminology
Pathophysiology
Patients at risk
Signs, symptoms, and diagnosis
History and physical examination
Laboratory studies
Immediate management and goals of therapy
Treatment
Treatment of hypertensive emergency
Treatment of hypertensive urgency
Special clinical situations
Summary and conclusions
7:
Congestive Heart Failure
Definition
Aetiology and pathophysiology
Neurohumoral mechanisms in congestive heart failure
Sympathetic nervous system
Renin-angiotensin-aldosterone system (RAAS)
Natriuretic peptides
Remodelling
Diagnosis and evaluation of patients with heart failure
History
Physical findings
Laboratory investigations
Roentgenogram of the chest
Electrocardiogram
Echocardiography
Radionuclide studies
Cardiac catheterisation
BNP and CHF diagnosis: A new paradigm
Differential diagnosis
Management of heart failure in the emergency room
Acute pulmonary oedema
Acutely decompensated heart failure
General measures
Specific measures
Nesiritide in acute decompensated heart failure
Management of heart failure
Diuretics
ACE-inhibitors
Beta-adrenergic receptor blockers
Digitalis compounds
Inotropic support
Hydralazine and isosorbide dinitrate
Antiarrhythmic drugs and device therapy
Cardiac resynchronisation therapy
Cardiac transplantation and cellular cardiomyoplasty
Conclusions
8:
Narrow Complex Tachycardia
Narrow QRS complex tachycardia (NCT):
Irregular narrow QRS complex tachycardia
Atrial fibrillation
Diagnosis
Treatment
Ventricular rate control
Other irregular arrhythmias
Atrial flutter
PSVT? But what is the mechanism?
AV nodal re-entrant tachycardia
ECG
Characteristics
Clinical features
Treatment
Atrioventricular re-entrant tachycardia
Atrial tachycardias
Treatment
9:
Wide Complex Tachycardia
Regular wide complex tachycardia
SVT with aberrancy
Certain features which when present support VT
AVRT with a manifest accessory pathway
ECG
Treatment
Wide QRS complex tachycardia of uncertain origin
Ventricular tachycardia
Monomorphic ventricular tachycardia
Treatment
Lidocaine
Procainamide
Amiodarone
Irregular polymorphic WCT
Polymorphic ventricular tachycardia with normal QT
Polymorphic ventricular tachycardia with long QT
Treatment
Cardioversion
Beta-blockers
Other therapies
Ventricular fibrillation
Amiodarone
Magnesium
Beta-blockers
WPW with atrial fibrillation/flutter
Conclusion
10:
Complete Heart Block
Cardiac conduction system
Definitions
Heart block
Complete heart block (CHB)
High-grade AV block
Electrocardiographic recognition
‘Giant’ T wave inversion
Ventriculophasic sinus arrhythmia
Bradycardia-induced ventricular arrhythmias
Causes of complete heart block
1. Degenerative diseases
2. Coronary artery disease
3. Myocardial diseases
4. Valvular heart diseases
5. Drug toxicity
6. Congenital heart disease
7. Intracardiac surgery
8. Miscellaneous
Symptoms and their underlying pathophysiology
Syncope
Stokes-Adams attacks
Approach to patients with CHB
Physical examination
Pulse and blood pressure
The jugular venous pressure (JVP)
Cardiac examination
12-lead ECG
Ambulatory ECG monitoring
Event monitoring
Electrophysiological testing
Management
Asymptomatic AV block
Symptomatic AV block
Medical management
Temporary pacing
Transcutaneous pacing
Temporary transvenous pacing
Permanent pacing
Special situations
Acute mycocardial infarction
CHB in inferior wall MI
CHB in anterior wall MI
Use of pacemakers in AMI
Temporary pacing
Anterior wall MI
Inferior wall MI
Fascicular blocks
Asystole
Permanent pacing
Vagotonic block
Features of vagally-mediated bradyarrhythmias
Treatment
Congenital CHB
Paroxysmal AV block
Inducible AV block
CHB in presence of AF
11:
Cardiac Tamponade
Pathophysiology
Aetiology
Clinical features
Variants of cardiac tamponade
Diagnosis
Other investigations
Management
Conclusion
12:
Diabetic Coma
Diabetic ketoacidosis
Pathogenesis of DKA
Clinical features
Diagnosis
Laboratory abnormalities
Treatment
Antibiotics
Frequency of monitoring in DKA
Complications of DKA therapy
Hyperglycaemic hyperosmolar state (HHS)
Precipitating and predisposing factors
Pathogenesis
Diagnosis
Treatment strategies
Prevention
Complications
Lactic acidosis
Causes:
Clinical features
Lab. investigation
Management
Hypoglycaemia
Clinical features
Management of hypoglycaemia
a) The conscious patient
b) The unconscious patient
c) Prevention of hypoglycaemia
13:
Thyroid Emergencies
Thyroid endocrine basics
Evaluation of thyroid function (laboratory and imaging)
Thyroid storm
Precipitating factors
Pathogenesis
Laboratory findings
Treatment
Anti-thyroid therapy
Iodides
Thionamide plus iodide combo
Lithium
Others: Dialysis, cholestyramine
Therapy to block peripheral effects of thyroid hormone
Supportive measures and therapy against the precipitating illness
Long-term treatment considerations
Myxoedema coma
Precipitating factors
Clinical features
Laboratory abnormalities
Treatment
Thyroid hormone therapy
Hypothermia
Hypoventilation
Hyponatraemia and hypoglycaemia
Hypotension
Conclusion
Suggested Reading
Thyroid storm
14:
Other Endocrinal Emergencies
Addisonian crisis
Pathophysiology
Common causes
Clinical presentation
Investigations
Treatment
Hypercalcaemia
Pathophysiology
Common causes
Clinical presentation
Investigations
Treatment
Hypocalcaemia
Pathophysiology
Common causes
Clinical presentation
Investigations
Treatment
Hypoglycaemia
Pathophysiology
Common causes
Clinical presentation
Investigations
Treatment
15:
Acute Upper Gastrointestinal Bleeding
Clinical presentation
Causes of UGI bleed
Principles of management
Resuscitation
Assessment
Evaluation of blood loss
Assessment of patient's risk
Clinical assessment for aetiology of bleed
Investigations
Stabilisation of the patient
High risk patient
Low risk patient
Specific diagnosis and therapy
Treatment of peptic ulcer bleed
Pharmacotherapy
Endoscopic therapy
Other therapies
Treatment of variceal haemorrhage
Pharmacotherapy of variceal bleed
Balloon tamponade
Endoscopic therapy
Other therapies
UGI bleed due to other causes
16:
Acute Liver Failure
Definitions
Complications and sequelae of ALF
Cerebral oedema
Encephalopathy
Immunologic breakdown, and infectious complications
Metabolic dysfunction
Coagulopathy
Cardiovascular effects
Renal failure
Hematologic disturbances
Aetiology
Hepatitis A (HAV)
Hepatitis B (HBV)
Hepatitis B mutants
Reactivation of hepatitis B
Hepatitis D (HDV) super-infection/co-infection
Hepatitis C
Hepatitis E
Mushrooms
Wilson's disease
Other viruses
Drugs
ALF in pregnancy
Prognostic criteria
Management
Neurologic support
Intracranial pressure monitoring
Reverse jugular venous monitoring
Osmotherapy
Thiopentone
Hypothermia
Prophylactic phenytoin
Hyperventilation
Ammonia lowering measures
Other therapies
Prevention and treatment of infection
Haemodynamic support
Coagulopathy
Mechanical ventilation of patients with liver failure
Microcirculation
Renal support
Nutritional and metabolic support
Liver transplantation
Non-transplant therapies for liver support
Molecular adsorbent recirculating system (MARS)
17:
Management of Acute Pancreatitis
Terminology and definitions
Aetiology
Gallstones
Alcohol
Metabolic causes
Structural Abnormalities
Post-endoscopic retrograde cholangio-pancreatography (ERCP) pancreatitis
Drugs
Clinical presentation
Investigations to establish diagnosis
Serum pancreatic enzymes
Imaging
Investigations to establish severity
CT Staging
Investigations to establish aetiology
Treatment
Resuscitation
Analgesia
Antibiotic prophylaxis
Nutritional support
Specific management of gallstone pancreatitis
Endoscopic treatment of acute biliary pancreatitis
Timing of cholecystectomy
Late complications
Fistulae
Pseudocyst
Pancreatic abscess
Vascular complications
Recognition of infected necrosis
Surgery in necrotising acute pancreatitis
Clinical course and outcome
18:
Approach to Bleeding Disorders
Basic pathophysiology
Investigations which are not helpful in excluding a bleeding disorder
Precautions in interpreting laboratory values, and special requests to the laboratory
Important causes of bleeding seen in medical practice
Platelet disorders
Thrombocytopenia
Reduced Platelet Production
Increased platelet destruction
Idiopathic thrombocytopenic purpura (ITP)
HIV and thrombocytopenia
Post-transfusion purpura
Thrombotic thrombocytopenic purpura (TTP)
Platelet function defects
Acquired platelet function defects
Drugs
Uraemia
Myeloproliferative disorders
Dysproteinaemias
Inherited platelet function defects
Bernard-Soulier syndrome
Glanzmann thromboasthenia
VWD (von Willebrand's disease)
Coagulation disorders
Hereditary or acquired
Value of initial laboratory tests (Table 3)
Acquired coagulation disorders
Liver disease
Vitamin K deficiency
Oral anticoagulant overdose (Warfarin)
Heparin overdose
Bleeding after fibrinolytic therapy
Bleeding after massive blood transfusion
Bleeding after cardio-pulmonary bypass
Acquired inhibitors
Inherited disorders
Haemophilia
von Willebrand's disease (VWD)
Treatment of VWD:
Combined disorders
Vascular disorders
Summary of management in case of emergency bleeding
General measures
Stop that which is aggravating the bleeding
Replace what is low
Optimise production of clotting factors and platelets
Consult experts in the field.
19:
Severe and Complicated Malaria
Complicated malaria
Pathophysiology
Clinical features
Cerebral malaria
Acute renal failure
Hypoglycaemia1, 6, 21
Hypotension/Shock (algid malaria)1, 6
Anaemia1, 6, 21
Jaundice
Coagulopathy and thrombocytopenia
Black water fever
Metabolic acidosis
Hyperpyrexia
Hyperparasitaemia
Malaria in special situations
HIV
Children
DiagnosiS
Treatment
Antimalarial drugs
Preventing drug-resistance
Other treatment measures
Conclusion
20:
Dengue Haemorrhagic Fever and Dengue Shock Syndrome
Dengue fever
Dengue haemorrhagic fever (DHF)
(a) One or more signs of haemorrhagic tendency
(b) Evidence of plasma leakage due to increased capillary permeability manifested by one or more of the following
(c)Hepatomegaly
Dengue shock syndrome
Disease course
Laboratory confirmation of diagnosis
Investigations
Treatment of DF and DHF
Management of dengue shock syndrome (Gr. III, IV DHF)
Correction of electrolyte and metabolic disturbances
Blood transfusion
Unusual manifestations of DHF and DSS
CNS involvement
Liver involvement
Renal involvement
Cardiac involvement
Differential diagnosis
Monitoring of anti-shock therapy
Fluids required for intravenous therapy
What not to do
Signs of recovery
Criteria for discharging patients
Prevention of death
21:
Acute Meningitis
Bacterial meningitis
Pathogenesis
Epidemiology and causes
Clinical features
Prognostic factors
Diagnosis
Management
Pre-hospital antibiotic
Antimicrobial treatment
Duration of antimicrobial theapy
Adjunctive therapy
Tuberculous meningitis
Viral meningitis
22:
Septic Shock
Definitions
Epidemiology
Aetiology
Pathophysiology of septic shock
Organ dysfunction
Cardiovascular dysfunction6, 7
Pulmonary dysfunction
Central nervous system dysfunction
Gastrointestinal dysfunction
Renal dysfunction
Haematological changes
Skin changes
Clinical presentation
Symptoms
Physical signs
Differential diagnosis
Laboratory investigations
Management
I. Initial resuscitation
Fluid therapy
SCCM recommendation
Vasopressors
SCCM recommendations
Inotropic therapy
SCCM recommendation
Packed cell transfusion
SCCM recommendation
Early goal-directed therapy
II. Diagnostic evaluation
SCCM recommendations
Assessing organ function
III. Antibiotic therapy
SCCM recommendations
IV. Source control
SCCM recommendations
V. Corticosteroids
SCCM recommendations
VI. Blood product administration
SCCM recommendations
VII. Mechanical ventilation
SCCM recommendations
VIII. Sedation, analgesia, and neuromuscular blockade
SCCM recommendation
IX. Glucose control
SCCM recommendations
X. Renal replacement
SCCM recommendation
XI. Bicarbonate therapy
SCCM recommendation
XII. Deep vein thrombosis (DVT) prophylaxis
SCCM recommendation
XIII. Stress ulcer prophylaxis
SCCM recommendation
XIV. Newer therapies
Drotrecogin alfa (activated) (recombinant human activated protein C: rhAPC)
SCCM recommendation
Prognosis
Conclusions
23:
Management of Needle Stick Injuries
Conclusion
24:
Acute Renal Failure
Aetiology
Pre-renal causes
Post-renal causes
Intrinsic causes
Spectrum of acute renal failure
Pathogenesis
Clinical features
Diagnosis of ARF
Pre-renal azotaemia versus ATN
ARF versus acute-on-chronic renal failure
Urinalysis
Role of renal biopsy
Prevention of ARF
Resuscitation
Role of reno-protective drugs
Low-dose dopamine
Mannitol
Loop diuretics
Newer agents
Management of ARF
Fluid and electrolyte balance
Hyperkalaemia
Metabolic acidosis
Nutrition
Bleeding
Infection
Modification of drug dosage
Role of dialysis
Role of continuous renal replacement therapy
Prognosis
Acute cortical necrosis
Summary
25:
Rapidly Progressive Glomerulonephritis
Epidemiology
Process of crescent formation
Clinical features
Classification
Anti-glomerular basement membrane disease
Pathology
Pathogenesis
Treatment
Outcome
Immune complex-mediated crescentic glomerulonephritis
Pathology
Pathogenesis
Treatment
Special situations
Post-streptococcal nephritis
Infective endocarditis
Lupus nephritis
Henoch-Schonlein purpura
Pauci-immune crescentic glomerulonephritis
Pathology
Pathogenesis
Treatment
Summary
26:
Raised Intracranial Pressure
Aetiology
Clinical features
Effects of raised ICP
Management
Diagnosis
Treatment
Treatment of primary cause
Treatment of raised ICP
General measures and monitoring in a critically ill patient with raised ICP
Specific measures
Osmotic agents
Role of Surgery
Monitoring of ICP
27:
Stroke Management in the first Six Hours
Pathophysiology
Diagnostic modalities
Pre-hospital management
Stroke units
Management in hospital/emergency unit
General measures
Patients with underlying pulmonary disease
Patients with hypertension
Patients with hyperthermia
Patients with hyperglycaemia
Cerebral oedema
Thrombolysis or reperfusion therapy
Patients who are eligible for thrombolytic therapy with rt-PA20
Intra-arterial thrombolytic therapy
Anticoagulation
Anti-platelet agents
Neuronal protection
Management of intracerebral haemorrhage
Conclusions
Key points
Time is brain, evaluate quickly and confirm by CT at the earliest.
28:
Status Epilepticus
Definition
Epidemiology
Aetiology
Classification
Clinical features
Pathogenesis of status epilepticus
Anatomical localisation
CNS injury
Systemic pathophysiology
Differential diagnosis
Diagnostic workup
Electroencephalography
Blood investigations
Neuro-imaging
Management
Hospital management
Intravenous antiepileptic drugs
Benzodiazepines
Phenytoin and Phosphenytoin
Barbiturates
Choice of antiepileptic drug
Follow-up treatment
Refractory status epilepticus
Prognosis
Conclusion
29:
Acute Idiopathic Inflammatory Neuropathies (AIINs)
GBS subtypes1–3
Incidence
Antecedent events
Pathology
Immunopathogenesis
Clinical features
Signs and symptoms
Special features
The axonal forms of GBS
Miller-Fisher syndrome (MFS)
Pure sensory syndrome
Acute pandysautonomia
Recurrent GBS
Differential diagnosis
Course and prognosis
Common complications of GBS5
Diagnosis of GBS
Diagnosis of GBS is based on:
Clinical profile
CSF examination
Electrophysiological studies
Electrodiagnostic criteria of demyelination7
Electrodiagnostic criteria of axonal GBS
Other tests
Management
Specific therapy
Selection of patients for PE / IVIg therapy
Selection criteria are based on14
PE or IVIg should be considered in all patients who:
Plasma exchange (PE)
Treatment protocols and number of sittings of PE
Volume of PE
Other therapeutic modalities akin to plasma exchange
Intravenous immune globulin (IVIg) therapy
Dose and mode of administration of IVIg
Side effects of IVIg
Efficacy of IVIg
Plasma exchange vs. IVIg therapy
Combined use of PE and IVIG
Combined therapy of IVIg with steroids
Steroid therapy in GBS
General measures or supportive therapy in GBS
Assessment of respiratory function
Cardiovascular monitoring
Management of pain
Prophylaxis of deep vein thrombosis (DVT)
Physiotherapy
Future therapies
30:
Hypokalaemic Paralysis
Familial (primary) hypokalaemic periodic paralysis (Hypo KPP)
Thyrotoxic periodic paralysis (TPP)
Barium poisoning
Renal potassium loss
Endocrine causes
Gastrointestinal potassium loss
Hypokalaemic paralyses – An Indian experience
31:
Myasthenic Crisis
Clinical features
Management
Prognosis
32:
Oncologic Emergencies
Spinal cord compression
Epidemiology
Pathophysiology
Clinical presentation
Diagnostic evaluation
Treatment
Corticosteroids
Surgery
Radiation therapy
Chemotherapy
SVC syndrome
Presentation
Aetiology
Diagnosis
Treatment
Small cell lung cancer
Non-Hodgkin's lymphoma
Catheter-induced obstruction
Radiation therapy
General measures
Tumour lysis syndrome
Pathophysiology
Signs and symptoms
Management(Figure 4)
Hypercalcaemia of malignancy
Epidemiology
Differential diagnosis
Signs and symptoms
Pathophysiology
Evaluation of the patient
Treatment
General measures
Specific measures
Intravenous fluids and diuretics
Bisphosphonates
Gallium nitrate
Calcitonin
Corticosteroids
Phosphates
Plicamycin
Approach to treatment of hypercalcaemia
Hyperuricaemia
Treatment
Lactic acidosis
Hypoglycaemia
Pathophysiology
Therapy
Adrenal failure
Clinical manifestations and management
33:
Management of Acute Poisoning
Resuscitation and initial stabilisation
Dextrose
Naloxone
Flumazenil
Diagnosis of type of toxin
History
Examination
Simple laboratory investigations
Non-specific treatment
Gut decontamination
Induction of emesis
Contraindications
Complications
Gastric lavage
Contraindications
Complications
Cathartics
Contraindications
Complications
Activated charcoal
Contraindications
Whole bowel irrigation (WBI)
Contraindications
Miscellaneous methods for gut decontamination
Forced diuresis
Alkaline diuresis
Contraindications
Acid diuresis
Multiple-dose activated charcoal (MDAC)
Dialysis
Pre-requisites for dialysis
Contraindications
Haemoperfusion
Specific therapy
Supportive therapy
Indications for admission
Legal responsibilities of physicians
34:
Common Poisonings in North India
Aluminium phosphide
Availability
Mechanism of toxicity
Clinical features of phosphine inhalation
Clinical features of aluminium phosphide intoxication
Diagnosis
Silver nitrate test on gastric aspirate
Silver nitrate test on breath
Management
Prevention of absorption of phosphine through gut
Enhancing phosphine excretion
Reducing organ toxicity
Supportive measures
Organophosphates and carbamates
Availability
Mechanism of toxicity
Clinical features
Muscarinic features
Nicotinic features
CNS features
Other features
Intermediate syndrome
Delayed neuropathy
Diagnosis
Severity of poisoning
Management
Removal of unabsorbed poison from gut
Prevention of absorption from other sites
Administration of specific antidote
Supportive measures
Organochlorines
DDT and analogs
Clinical features
Management
Kerosene oil
Clinical features
Management
Phenol
Clinical features
Management
Rodenticides
Barium carbonate
Zinc phosphide
Sodium fluoroacetate
Super-warfarins
Benzodiazepines
Clinical features
Treatment
Ethylene dibromide
Clinical features
Laboratory features
Management
Methanol (Methyl alcohol)
Mechanism of toxicity
Clinical and laboratory features
Management
Ethanol
Haemodialysis
4-methylpyrazole or fomepizole
Folinic acid or leucovorin
Ethyl alcohol
Strength of alcohol
Metabolism
Toxic quantity
Clinical features
Laboratory features
Management
Methaemoglobinaemia-producing chemicals
Mechanism of toxicity
Clinical features
Laboratory diagnosis
Management
Datura
Clinical features
Management
Cannabis
Clinical features
Management
Oleander
Clinical features
Treatment
Opium
Clinical features
Management
35:
Snake Bite
Clinical features
Laboratory investigations
Management of snake bites
Elapid bites
Viperine bites
Anti-snake venom (ASV)
Which ASV?
When to start ASV treatment?
Dose of ASV to be given
Duration of ASV treatment
Adverse effects of ASV
Prognosis and mortality
36:
Massive Haemoptysis
Definition
Aetiology
Clinical assessment
History
Physical examination
Management
Resuscitation
Protection of the airway
Laboratory investigations
Sputum
Chest radiograph
Computed tomographic scan
Bronchoscopy
Bronchial artery embolisation
Surgery
Other treatment options
Outcome
Conclusions
37:
Acute Severe Asthma
Acute severe asthma
Clinical presentation
Assessment of severity of illness
Management
Aim
Oxygen therapy
Bronchodilators
Corticosteroids
Doses
Adjuvant treatment
Intubation and mechanical ventilation
Indications for intensive care and for mechanical ventilation in acute severe asthma
Indications for intensive care
Indications for intubation
Indications for intermittent positive pressure ventilation (IPPV)
Instructions on discharge and follow-up
38:
Acute and Acute‒on‒Chronic Respiratory Failure
Classification
Aetiology and pathophysiology
Clinical presentation
Acute respiratory failure
History and physical examination
Manifestations of hypoxaemia
Manifestations of hypercapnia
Manifestations due to aetiological cause
Management
Diagnosis
Laboratory investigations
Arterial blood gas analysis
Acute respiratory distress syndrome (ARDS)
Electrocardiogram
Chest radiograph
Computerised tomography
CT pulmonary angiography
Pulmonary function testing
Echocardiography
Tests for pulmonary thromboembolism
Other tests
Principles of treatment
General therapeutic measures
Poisoning and overdosage
Antibiotics
Bronchodilator therapy
Corticosteroids
Intensive care and monitoring
Type I respiratory failure
Type II respiratory failure
Respiratory stimulants
Ventilatory support
Non-invasive ventilation
Mechanical ventilation
Modes of ventilation
Pressure support ventilation
Intermittent mandatory ventilation
Assist-control ventilation
Volume-control ventilation
Pressure-control ventilation
Positive end-expiratory pressure
Mechanical ventilation strategies in specific diseases
Acute respiratory distress syndrome
Other strategies
Obstructive airways disease
Weaning from mechanical ventilation
Complications
Acute-on-chronic respiratory failure
Acute vs. acute-on-chronic respiratory failure
Principles of treatment
Chronic respiratory failure
History and physical examination
Manifestations of chronic hypoxaemia
Manifestations of chronic hypercapnia
Management
Diagnosis
Principles of treatment
Outcome
Conclusions
39:
Acute Respiratory Distress Syndrome (ARDS)
ARDS?
What is acute lung injury and what are the major conditions and causative factors, which are responsible for most of the episodes of ALI/ ARDS in clinical practice?
Mortality/morbidity
Age
What are the stages of ARDS?
What are the clinical and laboratory derangements of early and advanced ARDS?
Is pulmonary artery catheterisation required for the diagnosis of ARDS?
How does mechanical ventilation worsen pre-existing lung injury and produce VILI, i.e., ventilator-induced lung injury? What is the concept of epithelial cell apoptosis and organ dysfunction?
ARDS treatment – Salient features
Nutrition in ARDS
What is required?
How is the goal achieved?
What are the potential salutary and counter-productive effects of mechanical ventilation in patients with ARDS?
Application of lung protective ventilation with small tidal volume
Application of prone position
Volume cycled versus pressure controlled ventilation in ARDS – which applications is beneficial?
Lung protective ventilation with higher PEEP
PaCO2 and pH in critically ill patients
What are the newer treatment strategies for ARDS/ALI?
High frequency ventilation (HFV)
Tracheal gas insufflation (TGI)
Inverse ratio ventilation and airway pressure release ventilation
Surfactant replacement therapy
Extra-corporeal gas exchange
Fluorocarbon liquid assisted gas exchange
Other measures
Conclusion
40:
Venous Thromboembolism (VTE), Deep Venous Thrombosis (DVT), and Pulmonary Embolism (PE)
Diagnostic approach
DVT
Physical examination
Differential diagnosis
Non-invasive testing for DVT
Impedance plethysmography (IPG)
Magnetic resonance imaging (MRI)
Invasive contrast venography (CV)
Other tests
Pulmonary embolism
The diagnostic approach to acute pulmonary embolism
Differential diagnoses
Pre-test probability for PE
Diagnostic studies for PE
Electrocardiogram (ECG)
Arterial blood gas
V/Q scan
Magnetic resonance imaging (MRI)
Pulmonary angiography
Pitfalls in diagnosis of VTE
Treatment of VTE
Pulmonary embolectomy
Venacaval filters
Prophylaxis of VTE
41:
Tension Pneumothorax
Definition
Predisposing factors
Classification of pneumothorax
A. Classification by ‘Aetiology’ :
B. Classification by ‘Extent’:
C. Classification by ‘Mechanism’:
D. Classification by ‘Duration’:
Aetiological factors6, 1
Pathophysiology
Clinical manifestations of tension pneumothorax
Striking clinical features
ECG changes
Radiological appearances
Diagnosis
Clinical confirmation of diagnosis
Differential diagnosis
Treatment
Principles of management12:
The goal of treatment
Treatment options
Tube thoracostomy
Open thoracotomy
Pneumothorax in patients on mechanical ventilation16
Recurrence
Prevention of recurrence
Complications3
Treatment of other complications1
Follow-up
42:
Emergencies in Rheumatology
Classification of rheumatological emergencies
Acute low backache
Acute gout
Acute arthritis
Lupus flare
Systemic vasculitides
Scleroderma renal crisis
Catastrophic antiphospholipid syndrome (CAPS)
Erythema nodosum (EN)
Reflex sympathetic dystrophy syndrome (RSDS)
Conclusions
43:
Severe Dehydration
Causes of dehydration
Types of dehydration
Isotonic dehydration
Hypotonic dehydration
Hypertonic dehydration
Assessment of dehydration
Laboratory investigations
General principles of management
Fluid resuscitation in dehydration
Intravenous rehydration therapy
Indications
Vascular access
Fluids used for intravenous therapy in dehydration
Fluid resuscitation of hypovolaemic shock
WHO Regimen for management of severe dehydration
Correction of deficit according to type of dehydration
Isonatraemic dehydration
Sample correction of 10% isonatraemic dehydration in a 10 kg child
Initial findings
Requirements for 24 hours
Resuscitation fluids
Net deficit
Fluid schedule
Hyponatraemic dehydration
Hypernatraemic dehydration
Oral rehydration therapy
Role of antibiotics
Other metabolic derangements
Hypokalaemia
Metabolic acidosis
Metabolic alkalosis
44:
Acute Abdomen in Non-Surgical Disorders
Definition of the acute abdomen
Types of abdominal pain
History
Laboratory evaluation
Diagnostic imaging
Acute myocardial infarction
Pneumonia
Primary adrenocortical deficiency (Addison's disease)
Diabetic ketoacidosis
Acute intermittent porphyria
Uraemia
Hypercalcaemia
Neurogenic causes of acute abdominal pain
Psychogenic pain
Abdominal wall syndromes
45:
Heat-related Illness
Physiology
Classification
Heat cramps
Heat exhaution
Heat stroke
Pathogenesis
Thermoregulation and acclimatisation
Acute-phase response
Heat shock response
Progression from heat stress to heat stroke
Pathophysiology
Heat
Cytokines
Clinical features
Treatment
Prevention
46:
Acute Transfusion Reactions
Aetiopathogenesis
Approach
Investigations
Management
Deterrence/prevention
Prognosis
Medical/legal pitfalls
47:
The Physician and An Emergency Patient
Medico-legal emergency patient
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