Emergencies for Medicine Table viva : Snake bite DKA MI OP poisoning Status epilepticus (SE) Anaphylaxis Status asthmaticus Acute LVF Hypoglycemia Tension pneumothorax Describe these questions in detail

Reading File

Finding Sources

Reading File

I now have substantial textbook material. Let me compile the full comprehensive viva answer from the textbook data I've retrieved, supplemented by my medical knowledge.

🏥 Medical Emergencies - Table Viva: Complete Guide

1. 🐍 SNAKE BITE

Definition

Envenomation by venomous snakes causing local and systemic toxic effects. Medically significant snakes in India: Cobra (Naja naja), Krait (Bungarus caeruleus), Russell's Viper (Daboia russelii), Saw-scaled Viper (Echis carinatus) - the "Big Four."

Classification of Venom

Type	Snake	Effect
Neurotoxic	Cobra, Krait	Descending flaccid paralysis, respiratory failure
Hemotoxic/Vasculotoxic	Russell's viper, Saw-scaled viper	Coagulopathy, bleeding, renal failure
Cytotoxic	Cobra	Local tissue necrosis
Cardiotoxic	Russell's viper	Direct myocardial depression

Clinical Features

Local: Pain, swelling, erythema, blistering, necrosis (viper > cobra), fang marks (may be absent with krait)
Neurotoxic: Ptosis (earliest sign), ophthalmoplegia, dysphagia, dysarthria, respiratory paralysis (death from respiratory failure)
Hemotoxic: Bleeding from bite site, hematuria, hematemesis, epistaxis, 20-Minute Whole Blood Clotting Test (20WBCT) - incoagulable blood
Systemic: Hypotension, tachycardia, rhabdomyolysis, acute renal failure (viper)

20WBCT (20-Minute Whole Blood Clotting Test)

Place 2 mL fresh venous blood in a clean glass tube, leave undisturbed for 20 minutes
If blood is NOT clotted → systemic envenomation (viper)
Cheap, bedside, reliable indicator of coagulopathy

Management

First Aid (Field):

Immobilize limb (splint like a fracture) - reduces lymphatic spread
Remove constricting items (rings, watches)
Avoid: Tourniquets, incision, suction, electric shock (harmful)
Transport urgently to hospital

Hospital Management:

Airway/Breathing/Circulation - secure IV access, monitor vitals
Anti-Snake Venom (ASV) - cornerstone of treatment
- Polyvalent ASV (covers all 4 Indian snakes)
- Indications: Neurotoxicity, coagulopathy (20WBCT positive), hemoglobinuria/myoglobinuria, hypotension, local swelling crossing 2 joints
- Dose: 8-10 vials IV initially; repeat 8-10 vials every 6 hours till improvement; up to 50+ vials may be needed
- Dilute in 100 mL NS, give over 30-60 minutes
- Premedicate with adrenaline 0.25 mg SC + antihistamine + hydrocortisone to prevent anaphylaxis
Neostigmine for neurotoxic (cobra) envenomation: 0.5-1 mg IV + Atropine 0.6 mg IV (anticholinesterase - reverses post-synaptic block of cobra venom; ineffective for krait)
Tetanus prophylaxis
Monitor urine output - catheterize; dialysis if ARF develops
FFP/blood products if coagulopathy

2. 🩸 DIABETIC KETOACIDOSIS (DKA)

Definition

Life-threatening acute metabolic complication of diabetes characterized by the triad:

Hyperglycemia (glucose >200 mg/dL, usually >300)
Ketosis (ketonemia/ketonuria)
Metabolic acidosis (pH <7.3, HCO₃ <15 mmol/L, anion gap >12)

Precipitating Factors (6 I's)

Infection (most common - pneumonia, UTI)
Insulin omission (missed doses)
Infarction (MI, stroke)
Inflammation (pancreatitis)
Intoxication (alcohol)
Iatrogenic (steroids, thiazides)

Pathophysiology

Insulin deficiency + glucagon excess → unopposed lipolysis
Free fatty acids → hepatic ketogenesis (acetone, acetoacetate, β-hydroxybutyrate)
80% of ketones are β-hydroxybutyrate (not detected well by nitroprusside/urine dipstick)
Osmotic diuresis → fluid & electrolyte loss
Total body K⁺ depleted despite initially normal or elevated serum K⁺ (due to acidosis-driven K⁺ shift out of cells)

Clinical Features

Early: Polyuria, polydipsia, nausea, vomiting, abdominal pain
Late: Kussmaul breathing (deep, sighing respiration - compensatory hyperventilation), fruity/acetone breath, dehydration, altered mental status, coma
Signs of precipitant (fever = infection)

Diagnosis

Parameter	DKA
Blood glucose	>200 mg/dL
pH	<7.30
HCO₃	<15 mmol/L
Anion gap	>12 (elevated)
Ketones	Positive in blood and urine
Serum K⁺	Normal or ↑ initially (but total body depleted)

Severity: Mild (pH 7.25-7.30), Moderate (pH 7.10-7.24), Severe (pH <7.10)

Management (FLUID-INSULIN-K⁺)

1. Fluids (aggressive rehydration):

0.9% Normal Saline: 1 L in first hour, then 500 mL/hr x 4 hrs, then 250 mL/hr
Switch to 0.45% NS if Na⁺ corrected; add 5% Dextrose when glucose <200 mg/dL

2. Insulin:

Start insulin ONLY after K⁺ >3.5 mEq/L (insulin drives K⁺ into cells → can cause fatal hypokalemia)
Regular insulin IV infusion: 0.1 unit/kg/hr
Target glucose reduction: 50-75 mg/dL/hour
Do NOT stop insulin until ketosis cleared (anion gap normalized)

3. Potassium:

If K⁺ <3.5: Give K⁺ first, hold insulin
If K⁺ 3.5-5.5: Add 20-40 mEq/L K⁺ to IV fluids
If K⁺ >5.5: Hold K⁺, monitor

4. Bicarbonate: Only if pH <6.9 (controversial; risk of paradoxical CSF acidosis)

5. Monitor: Hourly glucose, electrolytes every 2-4 hrs, urine output, anion gap

Resolution criteria: Glucose <200, HCO₃ ≥15, pH ≥7.3, anion gap normalized

Key pitfall in viva: "Why does apparent ketosis increase initially on treatment?" - Because β-hydroxybutyrate converts to acetoacetate (nitroprusside-detectable) during recovery.

3. ❤️ MYOCARDIAL INFARCTION (MI) - Acute STEMI

Definition

Myocardial necrosis due to sustained ischemia from coronary artery occlusion, confirmed by rise/fall of cardiac biomarkers + ≥1 of: symptoms, ECG changes, imaging evidence.

Types

STEMI: ST elevation - complete occlusion - requires immediate reperfusion
NSTEMI: No ST elevation - partial occlusion - biomarker positive
Unstable Angina: No biomarker rise

Clinical Features

Classic: Central crushing chest pain radiating to left arm/jaw, lasting >20 minutes, not relieved by nitrates
Associated: Sweating, nausea, vomiting, breathlessness, sense of impending doom
Atypical (diabetics, elderly, women): Epigastric pain, fatigue, dyspnea only ("silent MI")
Signs: Pallor, diaphoresis, hypotension (cardiogenic shock), S3/S4, new MR murmur (papillary muscle rupture)

ECG Changes

Time	ECG
Minutes	Hyperacute T waves (tall peaked)
Hours	ST elevation (>1mm in 2 contiguous limb leads, >2mm precordial)
6-24 hrs	T-wave inversion, Q waves develop
Days-weeks	Persistent Q waves (marker of necrosis)

Reciprocal ST depression in opposite leads confirms STEMI.

Biomarkers

Marker	Rise	Peak	Normalize
Troponin I/T	3-4 hrs	18-24 hrs	7-10 days
CK-MB	4-6 hrs	18-24 hrs	48-72 hrs
Myoglobin	1-2 hrs	6-9 hrs	24 hrs (earliest but non-specific)

Immediate Management - MONABASH / BATMAN

M - Morphine 2-4 mg IV (pain/anxiety) O - Oxygen (only if SpO₂ <94%) N - Nitrates - Sublingual GTN (avoid if hypotension, RV infarct, sildenafil use) A - Aspirin 325 mg chewed immediately + P2Y12 inhibitor (Clopidogrel 300 mg or Ticagrelor 180 mg) B - Beta-blocker (oral, after stabilization; not in acute heart failure/shock) A - Anticoagulation (Heparin UFH or LMWH) S - Statin (high intensity - Atorvastatin 80 mg) H - Hospital/reperfusion

Reperfusion (TIME IS MYOCARDIUM):

Primary PCI (PPCI): Door-to-balloon time <90 minutes - preferred if available
Thrombolysis (fibrinolysis): If PPCI not available within 120 min - Door-to-needle <30 min
- Agents: Streptokinase, Alteplase (rtPA), Tenecteplase
- Contraindications: Prior hemorrhagic stroke, active bleeding, recent major surgery, severe hypertension

Complications: Arrhythmias (VF - most common cause of early death), cardiogenic shock, cardiac failure, papillary muscle rupture, VSD, free wall rupture, Dressler's syndrome (weeks later)

4. ☠️ ORGANOPHOSPHORUS (OP) POISONING

Mechanism

OP compounds (insecticides, nerve agents) irreversibly inhibit acetylcholinesterase → accumulation of acetylcholine at all cholinergic synapses → overstimulation of muscarinic and nicotinic receptors.

Clinical Features - SLUDGE / DUMBELS / Day vs. Night

MUSCARINIC effects (SLUDGE/DUMBELS):

Salivation, Lacrimation, Urination, Defecation
Gastrointestinal cramps, Emesis
- Bronchospasm, Bronchorrhea (most life-threatening), Bradycardia, Miosis ("pinpoint pupils"), Diaphoresis

NICOTINIC effects:

Muscle fasciculations (early), weakness, flaccid paralysis
Tachycardia (can mask bradycardia), hypertension
Intermediate syndrome (IMS): Proximal limb weakness + respiratory failure 24-96 hrs after apparent recovery

CNS: Anxiety, restlessness, seizures, coma

Miosis + bronchorrhea + bradycardia + fasciculations = classic OP triad

Diagnosis

Plasma/RBC cholinesterase level (low) - best confirmation
Clinical diagnosis is primary; do not wait for lab

Management

1. Remove/Decontaminate:

Remove contaminated clothing, wash skin with soap and water (protect rescuers - gloves!)
Gastric lavage if oral ingestion (within 1 hr, airway secured)

2. Atropine (ANTIDOTE for muscarinic effects):

2-4 mg IV bolus immediately, double dose every 5 minutes until "atropinization"
End point of atropinization: Dry secretions (no bronchorrhea), HR >80, pupils dilate (do NOT aim for pupil dilation alone - use secretions as endpoint)
Massive doses may be required (hundreds of mg in severe poisoning)
Atropine does NOT treat nicotinic (muscle) effects

3. Pralidoxime (2-PAM) / Oximes (antidote for nicotinic effects + regenerates cholinesterase):

1-2 g IV over 15-30 minutes, then infusion
Must be given EARLY (before "aging" of enzyme-OP complex - irreversible binding within hours)
Pralidoxime reactivates cholinesterase - treats muscle paralysis, reduces atropine requirement
Controversial: Some studies question benefit; use based on clinical judgment/local guidelines

4. Benzodiazepines for seizures (diazepam)

5. Ventilator support if respiratory failure (succinylcholine may have prolonged action due to cholinesterase inhibition)

5. ⚡ STATUS EPILEPTICUS (SE)

Definition

Seizure lasting ≥5 minutes OR
Two or more seizures without return to baseline consciousness between them (Old definition was 30 min; changed to 5 min because seizures rarely stop spontaneously after 5 min and neuronal damage begins)

Types

Convulsive SE (CSE): Most common and most dangerous - tonic-clonic movements
Non-convulsive SE (NCSE): Subtle or no motor activity - requires EEG; suspect in persistent altered consciousness after convulsions stop
Refractory SE: Fails two adequate antiepileptic drugs
Super-refractory SE: Continues despite anesthesia for 24 hours

Causes

In known epileptics: Medication non-compliance (most common)
Acute symptomatic: Hyponatremia, hypoglycemia, hypocalcemia, CNS infection (meningitis/encephalitis), stroke, head injury, drug toxicity, alcohol withdrawal

Management (TIME-BASED PROTOCOL)

0-5 min: Stabilize (ABCDE)

Position, O₂, IV/IO access
Labs: Glucose (bedside), electrolytes, CBC, LFT, toxicology, antiepileptic levels
Correct hypoglycemia (50 mL 50% Dextrose IV + Thiamine 100 mg IV in alcoholics/malnourished)

5-20 min: FIRST-LINE - Benzodiazepines (70% success rate)

Lorazepam 0.1 mg/kg IV (preferred - longest CNS duration) OR
Diazepam 0.15-0.2 mg/kg IV (faster but shorter action) - rectal/IM if no IV access
Midazolam 0.2 mg/kg IM/intranasal/buccal (if no IV - IM midazolam = IV lorazepam in efficacy)
Wait 5 min - if seizure persists, give 2nd benzodiazepine dose
Delays >10 min before benzodiazepines → higher mortality

20-40 min: SECOND-LINE (if benzodiazepines fail)

Levetiracetam 60 mg/kg IV (max 4500 mg) - preferred (no drug interactions, safe in liver disease)
Fosphenytoin 20 mg PE/kg IV (water-soluble prodrug of phenytoin, safer than phenytoin - can give IM)
Valproate 40 mg/kg IV (contraindicated: liver disease, thrombocytopenia, pregnancy)
Phenytoin 20 mg/kg IV at ≤50 mg/min (causes hypotension, arrhythmias - monitor ECG)

>40 min: REFRACTORY SE - THIRD-LINE (ICU intubation + anesthesia)

Propofol 1-2 mg/kg IV then infusion
Midazolam infusion 0.2 mg/kg then 0.05-0.5 mg/kg/hr
Thiopental/phenobarbitone (barbiturate coma)
Ketamine - NMDA antagonist, evidence as add-on in refractory SE
EEG monitoring for burst suppression pattern as endpoint

6. 💉 ANAPHYLAXIS

Definition

Severe, life-threatening, generalized hypersensitivity reaction. Rapid-onset multi-system reaction involving mast cell and basophil degranulation, releasing histamine, tryptase, leukotrienes, prostaglandins.

Mechanism

IgE-mediated (Type I hypersensitivity): Prior sensitization → re-exposure → IgE cross-linking → mast cell degranulation
Non-IgE mediated (anaphylactoid): Direct mast cell activation (contrast media, opioids, NSAIDs) - clinically identical, treated identically

Common Triggers

Foods: Peanuts, shellfish, tree nuts, milk, eggs (most common overall)
Drugs: Beta-lactam antibiotics, NSAIDs, contrast media, chemotherapy
Insect stings: Hymenoptera (bee, wasp)
Latex
Exercise-induced, idiopathic (~60% adults)

Clinical Features

Diagnostic criteria: Sudden onset affecting skin/mucosa PLUS at least one of:

Respiratory compromise (bronchospasm, stridor, hypoxia)
Reduced BP or end-organ dysfunction

System	Features
Skin (80-90%)	Urticaria, angioedema, flushing, pruritus
Respiratory (50-70%)	Bronchospasm, wheeze, stridor (laryngeal edema), hoarseness
Cardiovascular	Hypotension, tachycardia, cardiac arrest
GI	Nausea, vomiting, abdominal cramps, diarrhea
CNS	Anxiety, dizziness, syncope

Note: Absence of skin findings does NOT exclude anaphylaxis (occurs in ~20%)

Management

1. EPINEPHRINE (ADRENALINE) - THE DRUG OF CHOICE - GIVE IMMEDIATELY

0.5 mg (1:1000) IM into outer thigh (mid-anterolateral)
NOT IV unless cardiac arrest
Can repeat every 5-15 minutes if no improvement
Acts on α1 (vasoconstriction, reduces angioedema), β1 (inotropic/chronotropic), β2 (bronchodilation)
No absolute contraindications in anaphylaxis

2. Position:

Lay flat + elevate legs (if hypotensive) - sudden standing can cause cardiac arrest ("empty heart" syndrome)
Sit up if respiratory distress

3. O₂: High-flow 15 L/min via non-rebreather mask

4. IV Access + Fluids: 1-2 L crystalloid bolus for hypotension

5. Secondary treatments (AFTER epinephrine - do NOT delay epi for these):

Antihistamines (H1 + H2 blockers - cetirizine/chlorphenamine + ranitidine): treat skin symptoms, do NOT treat cardiovascular collapse
Corticosteroids (hydrocortisone 200 mg IV): prevent biphasic reaction (up to 20% of cases; delayed reaction 8-72 hrs later)
Salbutamol inhaler/nebulizer for bronchospasm
Glucagon 1-2 mg IV if beta-blocker use (bypasses blocked beta-receptors)

6. Disposition: Observe 6-12 hours for biphasic reaction; discharge with epinephrine auto-injector (EpiPen) + allergy referral

7. 🌬️ STATUS ASTHMATICUS

Definition

Severe acute asthma that is life-threatening and unresponsive to standard bronchodilator therapy (beta-agonists + steroids given in the first 30-60 minutes).

Risk Factors for Near-Fatal Asthma

Previous near-fatal attack (intubation history)
Nocturnal attacks
Poor perception of bronchoconstriction
Psychosocial problems, non-compliance
Brittle asthma

Clinical Features

Severity	Features
Mild	Can speak in sentences, RR <25, HR <110, PEFR >50% predicted
Severe	Can't speak, RR >25, HR >110, PEFR 33-50%, accessory muscle use
Life-threatening	Silent chest, cyanosis, bradycardia, exhaustion, PEFR <33%, SpO₂ <92%
Near-fatal	Hypercapnia (PaCO₂ >45 mmHg), altered consciousness

"Silent chest" = no wheeze = near-total airway obstruction = MOST DANGEROUS SIGN

ABG interpretation: Initially respiratory alkalosis (hyperventilation) → Normal PaCO₂ is a WARNING sign (patient tiring) → Respiratory acidosis (PaCO₂ rising) = impending respiratory arrest

Management

Immediate:

O₂ - target SpO₂ 93-95% (not 100% - hyperoxia may worsen V/Q mismatch)
Salbutamol (albuterol) - continuous nebulization 2.5-5 mg or MDI with spacer (4-8 puffs)
Ipratropium bromide (Atrovent) 0.5 mg nebulized - add to salbutamol (synergistic)
Corticosteroids - Hydrocortisone 200 mg IV or Prednisolone 40-50 mg oral (take 4-6 hours to work)
Magnesium Sulfate 2g IV over 20 min - if poor response to above; bronchodilates by blocking Ca²⁺ channels in smooth muscle; reduces admission rate; give even in severe cases

If inadequate response: 6. IV Salbutamol or IV Aminophylline (loading dose 5 mg/kg over 20-30 min, avoid if on oral theophylline) 7. Heliox (helium-oxygen mixture) - reduces turbulent flow, less work of breathing 8. NIV (BiPAP) - reduces work of breathing, may defer intubation

Intubation (Last resort):

Indications: Altered consciousness, apnea, exhaustion, PaCO₂ rising despite treatment, SpO₂ <90%
Induction agent: KETAMINE (1.5 mg/kg IV) - best choice as it is a bronchodilator
Succinylcholine for rapid sequence intubation
Ventilation strategy: Low RR (8-12/min), low tidal volume (6-8 mL/kg IBW), HIGH inspiratory flow rate (to maximize expiratory time), low PEEP - to prevent auto-PEEP/breath stacking
Permissive hypercapnia acceptable if hemodynamically stable

8. 🫀 ACUTE LVF (Acute Pulmonary Edema)

Definition

Sudden failure of the left ventricle to maintain adequate cardiac output, causing acute rise in pulmonary venous pressure, fluid transudation into alveoli, and acute pulmonary edema.

Causes

Acute MI (most common)
Hypertensive emergency
Acute valvular failure (MR, AR)
Arrhythmias (AF with rapid ventricular rate)
Flash pulmonary edema (renal artery stenosis)
Volume overload (ESRD, over-transfusion)

Clinical Features - "Drowning from Inside"

Symptoms: Sudden severe breathlessness, orthopnea, PND, pink frothy sputum, extreme anxiety
Signs:
- Tachycardia, hypertension or hypotension (cardiogenic shock)
- Tachypnea, use of accessory muscles
- Bilateral fine basal crepitations (crackles) + wheeze ("cardiac asthma")
- S3 gallop (heart failure sign)
- Elevated JVP
- Pink frothy blood-tinged sputum (frank pulmonary edema)

CXR Findings (ABCDE)

Alveolar shadowing (bat-wing / butterfly pattern)
B lines / Kerley B lines (interstitial edema, horizontal lines at bases)
Cardiomegaly
Diversion of blood flow to upper zones (upper lobe blood diversion)
Effusion (pleural)

Management - LMNOP / UNLOAD

Position: Sit patient upright (legs dangling) - reduces venous return O₂: High flow; consider NIV (CPAP/BiPAP) - first-line non-invasive support; reduces preload, increases FRC, improves oxygenation; avoids intubation in many patients Morphine 2-5 mg IV - reduces anxiety and venodilates (reduces preload); use cautiously (respiratory depression)

Nitrates (vasodilators) - KEY DRUG:

IV GTN (Glyceryl Trinitrate) infusion - powerful vasodilator (venodilates = reduces preload; arterodilates at higher doses = reduces afterload)
Sublingually (GTN 0.5 mg SL) if BP allows
Avoid if SBP <90 mmHg, RV infarct, or phosphodiesterase inhibitor use

Furosemide (Frusemide) 40-80 mg IV:

Rapid venodilation within minutes (before diuresis starts)
Then diuresis 30-60 min later
Monitor urine output, electrolytes

Additional:

Dobutamine (inotrope) if cardiogenic shock (BP <90, cold peripheries, oliguria)
ACE inhibitor/ARB - not in acute phase
Treat underlying cause (PPCI for MI, cardioversion for AF, etc.)
Intubation if CPAP/BiPAP fails: PEEP improves oxygenation and reduces left ventricular afterload

9. 🍬 HYPOGLYCEMIA

Definition

Blood glucose <70 mg/dL (3.9 mmol/L) in diabetic patients; <55 mg/dL in non-diabetics. Severe hypoglycemia = requires external assistance.

Causes

Diabetics: Excess insulin dose, missed meal, exercise, alcohol, renal failure (decreased insulin clearance)
Non-diabetics: Insulinoma, Addison's disease, severe liver disease, sepsis, reactive hypoglycemia, factitious (surreptitious insulin)

Clinical Features (Whipple's Triad: symptoms + low glucose + relief with glucose)

Adrenergic/Autonomic (early, glucose 50-70)	Neuroglycopenic (late, glucose <50)
Sweating, tremor, palpitations	Confusion, cognitive impairment
Anxiety, hunger	Bizarre behavior, aggression
Pallor, tachycardia	Seizures
Nausea	Focal neurological deficits (hemiplegia - can mimic stroke)
	Coma, death

"Hypoglycemia unawareness" - in long-standing diabetes/repeated episodes, autonomic symptoms blunted; patient goes directly to neuroglycopenia without warning

Management

Conscious patient:

15-20 g fast-acting oral carbohydrates: 4-5 glucose tablets / 150-200 mL fruit juice / regular soda
Recheck glucose in 15 minutes; repeat if still <70 (Rule of 15)
Follow with a snack (complex carbohydrate + protein) to prevent recurrence

Unconscious/unable to swallow:

50 mL of 50% Dextrose (D50) IV - immediate effect
OR Glucagon 1 mg IM/SC - if no IV access (mobilizes hepatic glycogen; ineffective in starvation/liver disease/alcohol-induced hypoglycemia)
10% Dextrose infusion to maintain glucose after reversal

In malnourished/alcoholics: Give Thiamine 100 mg IV BEFORE glucose to prevent precipitating Wernicke's encephalopathy

After recovery:

Identify and treat underlying cause
If sulfonylurea-induced: Prolonged effect - admit, sustained dextrose infusion, consider Octreotide (inhibits insulin secretion)
If insulin overdose: Calculate timing of insulin action; extended monitoring

10. 💨 TENSION PNEUMOTHORAX

Definition

Air accumulates under pressure in the pleural space due to a one-way valve mechanism, causing progressive mediastinal shift, compression of contralateral lung, impaired venous return, and cardiovascular collapse - a true life-threatening emergency.

Mechanism - One-Way Valve

Injured lung/chest wall acts as flap valve: air enters pleural space on inspiration, cannot exit on expiration → pressure builds progressively → mediastinum shifts away from affected side → kinks SVC/IVC → reduces cardiac output → cardiovascular collapse

Causes

Barotrauma (most common in ventilated patients - positive pressure ventilation)
Traumatic (rib fractures, penetrating chest injury)
Spontaneous (tall young males with bullae - Marfan's syndrome)
Central line insertion complication
CPR (rib fractures + PPV)

Clinical Features - "5Ts" + Classic Triad

Classic Triad (late, not always present):

Absent breath sounds (one side)
Tracheal deviation (AWAY from lesion - late sign)
Elevated JVP (obstructive shock)

Plus:

Sudden respiratory distress, cyanosis
Hypotension, tachycardia → cardiovascular collapse
Hyper-resonant percussion on affected side
Distended neck veins
In ventilated patient: Rising airway pressures, falling SpO₂, hemodynamic deterioration

DIAGNOSIS IS CLINICAL - DO NOT WAIT FOR CXR

Feature	Tension Pneumothorax	Cardiac Tamponade
Trachea	Deviated away	Midline
Breath sounds	Absent (one side)	Present (bilateral)
Percussion	Hyper-resonant	Dull
JVP	Raised	Raised
ECG	Tachycardia	Low voltage, alternans

Management - IMMEDIATE NEEDLE DECOMPRESSION

DIAGNOSIS IS CLINICAL - TREAT IMMEDIATELY - DO NOT WAIT FOR X-RAY

Step 1: Needle Thoracostomy (Emergency decompression)

2nd intercostal space, mid-clavicular line (MCL), affected side (traditional)
OR 4th/5th intercostal space, anterior axillary line (recommended - better success rate as chest wall thinner here)
Large-bore needle (14-16G), ≥5 cm length - insert over UPPER BORDER of rib (to avoid neurovascular bundle)
Successful: Rush of air + hemodynamic improvement
Converts tension pneumothorax → simple pneumothorax
Temporary measure only

Step 2: Tube Thoracostomy (Chest Drain) - Definitive Treatment

4th/5th intercostal space, anterior/mid-axillary line
Insert after needle decompression
Connect to water-seal drain (underwater seal)
In the ED, "finger thoracostomy" (blunt dissection, finger in, then tube) is preferred as faster

Post-stabilization:

CXR to confirm lung re-expansion
Assess for underlying cause
Surgery (VATS/pleurodesis) for recurrent pneumothorax

Quick Summary Table for Viva

Emergency	Key Drug	Dose	Antidote/Specific Rx
Snake bite	ASV (polyvalent)	8-10 vials IV	Neostigmine (cobra)
DKA	Insulin (regular)	0.1 U/kg/hr IV	Fluids + K⁺ first
STEMI	Aspirin + reperfusion	325 mg + PPCI	Door-to-balloon <90 min
OP poisoning	Atropine	2-4 mg IV; repeat to dry secretions	Pralidoxime (early)
Status epilepticus	Lorazepam/Diazepam	0.1 mg/kg IV	Fosphenytoin/Levetiracetam
Anaphylaxis	Epinephrine IM	0.5 mg (1:1000) IM thigh	None (epi IS the antidote)
Status asthmaticus	Salbutamol + steroids	Continuous nebs + MgSO₄ 2g IV	Ketamine for intubation
Acute LVF	GTN (nitrates) + furosemide	IV GTN + 40-80 mg frusemide IV	CPAP/BiPAP
Hypoglycemia	50% Dextrose	50 mL IV (conscious: oral glucose)	Glucagon 1 mg IM (if no IV)
Tension pneumothorax	Needle decompression	14G needle, 2nd ICS MCL	Chest tube (definitive)

Sources: Rosen's Emergency Medicine (9th ed.), Goldman-Cecil Medicine, Harriet Lane Handbook (23rd ed.), Quick Compendium of Clinical Pathology (5th ed.) - compiled for table viva preparation.

This is a shared conversation. Sign in to Orris to start your own chat.