General Medicine
Final Professional MBBS — General Medicine. Long Questions (10 marks) and Short Notes (5 marks) across 15 systems, exam-formatted with clinical pearls, drug doses and mnemonics.
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MECHANISM
Organophosphate (OP) compounds = irreversible inhibitors of acetylcholinesterase (AChE) → excess acetylcholine (ACh) accumulation at all cholinergic synapses → cholinergic toxidrome . Sources: insecticides (parathion, malathion, chlorpyrifos ), nerve agents (sarin, VX ). Most common cause of poisoning death in India/developing world.
CLINICAL FEATURES — CHOLINERGIC SYNDROME
◆ SLUDGE + BBB — Muscarinic effects ▸ S = Salivation (excessive — hallmark) ▸ L = Lacrimation (watering eyes) ▸ U = Urination (involuntary urination — incontinence) ▸ D = Defecation/Diarrhoea (gut hypermotility) ▸ G = GI cramps (nausea + vomiting + abdominal pain) ▸ E = Emesis (vomiting) ▸ B = Bradycardia + Bronchoconstriction (wheeze; most dangerous — respiratory failure) ▸ B = Bronchorrhoea (excess airway secretions — 'wet lung'; leading cause of death ) - Nicotinic effects (NMJ + autonomic ganglia): Fasciculations (earliest muscle sign); muscle weakness → paralysis (respiratory failure from diaphragm + intercostal weakness); tachycardia (often predominates over bradycardia); hypertension; mydriasis (can be variable)
- CNS effects: Anxiety; agitation; seizures; coma; central respiratory failure ; miosis (pupil constriction — muscarinic)
- Intermediate Syndrome (IMS): Weakness of proximal limbs + neck flexors + respiratory muscles + CN palsies occurring 24–96 hrs after OP exposure (after cholinergic crisis resolves); mechanism: NMJ dysfunction post-crisis; may require prolonged ventilation
INVESTIGATIONS
- Plasma cholinesterase (PChE) — falls early; RBC cholinesterase (AChE) — more specific for OP toxicity; both ↓ confirm OP poisoning; also used to monitor atropine adequacy
- ECG (bradycardia/QTc prolongation ); ABG (respiratory failure, metabolic acidosis ); CBC; electrolytes; blood glucose; amylase (pancreatitis )
MANAGEMENT
- Remove from exposure — decontaminate skin/eyes (water; remove clothing ); healthcare workers wear PPE
- Airway — suction secretions; O2; intubate if respiratory failure (GCS drop, ↓ SpO2, respiratory distress); NO suxamethonium (AChE inhibition → prolonged neuromuscular blockade; use atracurium )
- ATROPINE (antidote for MUSCARINIC effects) — cornerstone:
▶ IV Atropine 1.8–3 mg (2–4 mg if severe) STAT → double dose every 5–10 min until atropinisation: Dry secretions (bronchorrhoea resolved) + HR > 80/min + dry skin; then maintenance infusion (10–20% of loading dose/hr)
Total doses can be VERY HIGH (up to 100s of mg in severe cases)
DO NOT target pupils or HR alone — target is DRY LUNGS- PRALIDOXIME (2-PAM / P2AM) — reactivates AChE IF given within 48 hours (before 'ageing'/irreversible phosphonylation ); 1–2 g IV loading over 30 min → 0.5 g/hr infusion × 48 hrs; treats NICOTINIC effects (fasciculations, weakness, paralysis) — atropine does NOT treat nicotinic effects
- Benzodiazepines (diazepam 10 mg IV) — for seizures; DO NOT use phenytoin (less effective for OP seizures)
💡CLINICAL PEARL: Atropine treats MUSCARINIC effects (SLUDGE, bradycardia, bronchospasm/bronchorrhoea). Pralidoxime treats NICOTINIC effects (muscle weakness, fasciculations). BOTH needed in moderate-severe OP poisoning.INTRODUCTION
Aluminium phosphide (AlP — 'Celphos' ') = grain fumigant and rodenticide; widely available in India and South Asia. Exposure to moisture → phosphine gas (PH₃) releases → cytochrome c oxidase inhibition (inhibits mitochondrial electron transport chain — same mechanism as cyanide ) → cellular asphyxia → multi-organ failure. NO specific antidote ; fatality 50–100% depending on dose; highly lethal suicidal poisoning in India.
CLINICAL FEATURES
- GI (immediate) — garlic/fish-like smell of vomitus/breath (phosphine odour — characteristic ); nausea; severe retching and vomiting; abdominal pain; diarrhoea
- Cardiovascular (most fatal) — refractory hypotension (from myocardial toxicity + peripheral vasodilation); cardiogenic shock ; severe bradycardia → VF/VT; ↑ QTc ; ST changes; myocarditis; pulmonary oedema
- Respiratory — ARDS; pulmonary oedema; respiratory failure (phosphine directly toxic to lung)
- Metabolic — severe metabolic acidosis (lactic; from cellular hypoxia); hypoglycaemia; hypomagnesaemia; hypokalaemia
- CNS — restlessness; agitation; altered sensorium → coma
INVESTIGATIONS
- Silver nitrate test — breath/gastric sample + silver nitrate paper → black discolouration (silver phosphide) = confirms phosphine exposure
- ABG (severe metabolic acidosis + hypoxia ); ECG (↑ QTc, arrhythmias ); cardiac enzymes (troponin ↑); echo (LV dysfunction); blood glucose; electrolytes
MANAGEMENT — PURELY SUPPORTIVE
- Safety: Phosphine gas released from vomitus — resuscitators use PPE; do NOT perform mouth-to-mouth (rescuer at risk ); well-ventilated area
- Airway: O2; intubate if respiratory failure; MV with PEEP for ARDS
- GI decontamination: DO NOT induce emesis (risk of aspiration + pharyngeal burns); Gastric lavage (potassium permanganate 1:10,000 to oxidise phosphine OR plain water) if < 1–2 hours and intubated; CHARCOAL NOT effective
- Cardiovascular support (most critical):
▶ IV fluids cautiously (pulmonary oedema risk )
Vasopressors: Noradrenaline + Adrenaline infusion for refractory shock
Intra-aortic balloon pump (IABP) or ECMO — for refractory cardiogenic shock (bridge therapy)
Antiarrhythmic therapy (amiodarone for VT; NO digoxin )- Metabolic: Correct acidosis (IV NaHCO₃); glucose; Mg²⁺ replacement; IV antioxidants (NAC, Vitamin E, Vitamin C — reduce free radical injury from phosphine ); Melatonin (some evidence)
- NO specific antidote — management entirely supportive; mortality very high (50–100%)
⚠️DANGER / REMEMBER: AlP poisoning (Celphos) — key points: Most lethal suicidal poisoning in India. Phosphine gas = cytotoxic (same as cyanide). Cardiogenic shock = main killer. No antidote. Early IABP/ECMO may be life-saving. Do NOT attempt mouth-to-mouth.Snake Venom Type Clinical Features Treatment Cobra (Naja) Neurotoxic (postsynaptic — blocks ACh-R) Neurotoxicity: Ptosis → diplopia → facial palsy → dysphagia → respiratory paralysis; local minimal; no haemorrhage ASV + ventilatory support; neostigmine may help (cobra postsynaptic block ) Krait (Bungarus) Neurotoxic (presynaptic — blocks ACh release) Severe neurotoxicity ; minimal local; abdominal pain; often bites at night (nocturnal ); can be painless ASV + ventilation; neostigmine less helpful (presynaptic ) Viper (Russell's, Saw-scaled) Haemotoxic + cytotoxic Haemotoxicity: bleeding (haemoptysis, haematuria, gingival); DIC; local tissue destruction (painful swelling, necrosis, blistering); AKI (tubular necrosis); VT/VF (Russell's viper) ASV (most important); FFP + blood products; dialysis for AKI King Cobra Neurotoxic Most potent; large venom volume; rapid paralysis ASV + ventilation urgently - Anti-Snake Venom (ASV) — indications: Neurotoxicity (ANY); haemotoxicity; local necrosis > 5 cm; coagulopathy; AKI; cardiovascular involvement
- 20-min Whole Blood Clotting Test (WBCT20) — place 2 mL blood in glass tube; if no clot at 20 min = coagulopathy → ASV needed; repeat q1h to monitor response
- Dosing: 8–10 vials (polyvalent ASV) IV initially; repeat based on clinical response; premedicate with SC adrenaline and IV antihistamine
- DO NOT: Incise/suck the wound; tourniquet; electric shock therapy; traditional remedies
- Classification of venom effects: neurotoxic (cobra, krait) - ptosis, diplopia, bulbar palsy, respiratory paralysis, minimal local effects; haemotoxic (viper) - local swelling, blistering, necrosis, spontaneous bleeding, coagulopathy, AKI; cytotoxic - local tissue destruction.
- Clinical features: local - pain, swelling, fang marks, blistering, necrosis; systemic - neurotoxicity (descending paralysis starting with ptosis), coagulopathy (spontaneous bleeding, non-clotting blood), AKI, hypotension, rhabdomyolysis.
- Investigations: WBCT20 (whole blood clotting test - primary field test); PT/APTT, fibrinogen and D-dimer (coagulopathy); serum creatinine and urine for haemoglobinuria (AKI); neostigmine test (reverses cobra neurotoxicity post-synaptic).
- ASV - administration and monitoring: dilute 8-10 vials in 250 mL saline over 1 hour IV; premedicate with SC adrenaline 0.25 mg + chlorpheniramine; repeat every 6 h if WBCT still abnormal; give neostigmine + atropine for neurotoxicity.
Stage/Time Features Treatment < 12 hrs (Minor withdrawal) Tremor; anxiety; diaphoresis; tachycardia; HTN; nausea/vomiting; insomnia Oral Diazepam 10 mg q1–2h (symptom-triggered) or Lorazepam (hepatic impairment — not metabolised by liver ) 12–24 hrs — Hallucinosis Visual/auditory/tactile hallucinations WITH normal orientation (unlike DT) + intact sensorium Benzodiazepines; thiamine; reassurance 12–48 hrs — Withdrawal seizures Generalised tonic-clonic seizures ; usually single; brief; rarely status epilepticus IV Diazepam/Lorazepam; IV thiamine before any dextrose 48–72 hrs — Delirium Tremens (DT) Delirium (confusion + disorientation) + Autonomic hyperactivity (fever, tachycardia, hypertension, diaphoresis); agitation; visual hallucinations (bugs crawling on skin — Lilliputian hallucinations); mortality 5–15% (untreated) IV Diazepam (5–10 mg q5 min until sedated) + Thiamine + fluids + electrolytes; ICU; high-dose BZ may be needed CIWA-Ar score (Clinical Institute Withdrawal Assessment for Alcohol) — symptom-triggered benzodiazepine protocol; reduces total BZ use; preferred over fixed dosing. - Pathophysiology: chronic alcohol upregulates NMDA glutamate receptors and downregulates GABA receptors; abrupt cessation → CNS hyperexcitability, catecholamine excess, autonomic instability.
- Delirium tremens (DTs): peaks 48-72 h after last drink; confusion, vivid hallucinations, extreme agitation, hyperthermia, profuse diaphoresis, autonomic instability; mortality 5-15% if untreated.
- Treatment in detail: long-acting benzodiazepines (diazepam or chlordiazepoxide) titrated to CIWA-Ar score; IV thiamine before any dextrose; correct electrolytes (Mg, K, PO4 are typically depleted); phenobarbital or propofol for refractory DTs; consider ICU for severe withdrawal.
- Long-term management: motivational interviewing, alcohol liaison nurse referral, and pharmacotherapy for relapse prevention - naltrexone (blocks reward), acamprosate (reduces craving), disulfiram (aversion).
Feature Opiate Intoxication Opiate Withdrawal Pupils Miosis (pinpoint) Mydriasis (dilated) CNS CNS depression; drowsiness → stupor → coma Insomnia; anxiety; agitation; restlessness Respiratory Respiratory depression (rate ↓; irregular; most dangerous ) Yawning; rhinorrhoea; lacrimation GI Constipation; nausea/vomiting Diarrhoea + vomiting ; GI cramps Autonomic Bradycardia; hypotension; hypothermia Tachycardia; hypertension; sweating; piloerection ('goose flesh' — cold turkey ) Drug test Urine positive opioids Urine positive (clearance varies) ▶ Intoxication treatment: IV Naloxone (μ-opioid receptor antagonist) 0.4–2 mg IV/IM/IN every 2–3 min until RR > 12 and GCS improves; SHORT half-life (30–60 min) — may need infusion for long-acting opioids (fentanyl, methadone ); monitor for re-narcotisation; O2; airway management
▶ Withdrawal treatment: Methadone substitution (opioid maintenance therapy); Buprenorphine + Naloxone (Suboxone) (partial agonist — safer; preferred); Clonidine (α2 agonist — suppresses autonomic symptoms ); symptomatic (loperamide, NSAIDs)
- Opiate toxidrome recognition: miosis (pinpoint pupils), respiratory depression and coma are the classic triad; bradycardia and hypotension may also occur; check oxygen saturations and respiratory rate.
- Naloxone - practical: short half-life (30-90 min) much shorter than most opioids; repeat doses or infusion needed to avoid re-narcotisation; titrate to respiratory rate > 12 breaths/min without fully reversing analgesia; IM or intranasal routes available for community use.
- Opioid use disorder: buprenorphine/naloxone (Suboxone) is the preferred maintenance therapy; methadone is an alternative under supervised dispensing; psychosocial support is essential for relapse prevention.
- Pharmacology of opioids: activate mu, kappa, and delta opioid receptors; mu-receptor activation mediates analgesia, euphoria, respiratory depression, miosis, constipation, and physical dependence; tolerance develops rapidly to the euphoric effect but more slowly to respiratory depression.
- Opioid-induced respiratory depression: the most life-threatening effect; mediated by mu-receptors in the pre-Botzinger complex; respiratory rate falls before consciousness; give naloxone promptly; buprenorphine (partial agonist) causes a ceiling effect on respiratory depression unlike full agonists.
CARBON MONOXIDE POISONING
CO poisoning = odourless, colourless gas (silent killer); CO binds Hb with 240× affinity compared to O2 → COHb (carboxyhaemoglobin) → impaired O2 delivery + cytochrome c oxidase inhibition. Sources: car exhaust, generators, heaters, fires.
- Clinical: Headache (most common + earliest); nausea/vomiting; confusion; cherry-red discolouration of skin (classic but rare in real life); coma; pulse oximetry NORMAL (false negative ) — SpO2 reads COHb as oxyhaemoglobin; ABG COHb level is diagnostic; cardiac arrhythmias; delayed neurological syndrome
▶ 100% O2 via non-rebreather mask — reduces COHb half-life from 5 hours (room air) to 1 hour; Hyperbaric O2 (HBO) (if available: COHb > 25%, cardiac complications, neurological symptoms, pregnancy; reduces half-life to 20 min); continue until COHb < 5%
- CO poisoning - pathophysiology: CO binds Hb with 240x greater affinity than O2 forming carboxyhaemoglobin (COHb) which neither carries oxygen nor releases it (left shift of dissociation curve); also binds myoglobin and cytochrome oxidase causing cellular hypoxia.
- CO investigations: ABG (co-oximetry measures COHb - pulse oximetry falsely normal because SpO2 cannot distinguish oxHb from COHb); ECG (ischaemia, arrhythmia); troponin and CK; neurological assessment; head CT if altered consciousness.
- Hyperbaric oxygen indications: COHb > 25%, any loss of consciousness, neurological deficit, ECG changes/cardiac involvement, pregnancy; reduces risk of delayed neuropsychiatric sequelae.
- Salicylate - investigations and monitoring: plasma salicylate level (4-6 h post-ingestion for peak); ABG showing the characteristic mixed respiratory alkalosis and metabolic acidosis; glucose (hypoglycaemia); INR and LFTs for hepatotoxicity with large doses.
SALICYLATE (ASPIRIN) POISONING
- Mechanism: Uncouples oxidative phosphorylation; stimulates respiratory centre → hyperventilation → respiratory alkalosis (initially); then metabolic acidosis (salicylic acid) + lactic acidosis → mixed disorder
- Clinical: Tinnitus (earliest; pathognomonic ); hyperventilation (compensatory); hyperthermia; non-cardiogenic pulmonary oedema; bleeding (antiplatelet); hypoglycaemia
▶ Activated charcoal (if < 1 hr); IV fluids; urinary alkalinisation (IV NaHCO₃ — maintains urine pH 7.5–8.5; ↑ ionisation of salicylate in tubule → ↓ reabsorption → ↑ excretion ); Haemodialysis (salicylate > 700 mg/L; coma; pulmonary oedema; severe acidosis; renal failure)
Ethylene glycol = antifreeze; toxic metabolites: glycolaldehyde → glycolate → oxalate (by alcohol dehydrogenase ) → oxalate nephropathy + CNS toxicity + cardiac toxicity. Osmolar gap ↑ (early) → Anion gap metabolic acidosis (late).
- Phases:
- Phase 1 (0–12 hrs): Inebriation without odour of alcohol ; nausea; vomiting; CNS depression
- Phase 2 (12–24 hrs): Cardiopulmonary failure (tachycardia, hypertension, CHF, pulmonary oedema)
- Phase 3 (24–72 hrs): AKI (oxalate crystals in renal tubules → flank pain + haematuria); calcium oxalate crystals in urine (monohydrate — needle-shaped; dihydrate — envelopes )
- Investigations: Anion gap metabolic acidosis; ↑ osmolar gap; hypocalcaemia (oxalate binds Ca²⁺); urine oxalate crystals; serum ethylene glycol level; urine fluorescence (car antifreeze contains fluorescein )
▶ Fomepizole (4-MP; alcohol dehydrogenase inhibitor) — antidote of choice ; 15 mg/kg IV loading → 10 mg/kg q12h; blocks conversion to toxic metabolites; preferred over ethanol
▶ Ethanol (competitive ADH inhibitor — if fomepizole unavailable); Haemodialysis (for severe AKI, acidosis, ethylene glycol > 8 mmol/L); Thiamine + Pyridoxine (cofactor supplementation)
- Source and mechanism: antifreeze (ethylene glycol) and brake fluid; metabolised by alcohol dehydrogenase to glycolaldehyde, glycolate (causes acidosis) and finally oxalate (forms calcium oxalate crystals in renal tubules).
- Investigations: anion gap metabolic acidosis with raised osmolar gap (early, before metabolism); urine fluorescence under Wood lamp (fluorescein additive in some antifreeze); urine oxalate crystals; hypocalcaemia; serum ethylene glycol level.
- Fomepizole: the antidote of choice - blocks alcohol dehydrogenase and prevents formation of toxic metabolites; given as loading dose 15 mg/kg IV then 10 mg/kg every 12 h; haemodialysis removes ethylene glycol and corrects acidosis.
Methaemoglobinaemia (MetHb) = iron in Hb oxidised from Fe²⁺ (ferrous) → Fe³⁺ (ferric) → Hb cannot carry O2 + left shift of O2-dissociation curve (↑ affinity for remaining O2 → impaired O2 delivery to tissues). Normal MetHb < 1%.
- Causes: Drugs — Dapsone (#1 drug cause ); nitrites (amyl nitrite; nitroglycerin); metoclopramide ; primaquine; sulphonamides; benzocaine (topical anaesthetic); nitrates in well water (infant metHbaeaemia — 'blue baby syndrome ')
- Clinical: Cyanosis not relieved by O2 (pathognomonic — most important clinical clue); headache; dyspnoea; confusion; chocolate-brown blood (venous blood appears brown — pathognomonic ); pulse oximetry reads ~85% regardless of true SpO2 (SpO2 spuriously normal or ~85%; does NOT correlate with severity )
- Diagnosis: Co-oximetry on ABG (directly measures MetHb fraction ); levels: 10–20% = symptomatic; > 30% = severe (coma/seizures); > 70% = fatal
▶ Methylene blue 1–2 mg/kg IV over 5 min — antidote ; cofactor for NADPH-methaemoglobin reductase → reduces Fe³⁺ back to Fe²⁺; repeat at 30 min if inadequate response; CONTRAINDICATED in G6PD deficiency (may cause haemolysis; use ascorbic acid instead )
- O2 by non-rebreather mask; treat underlying cause; exchange transfusion (severe MetHb + G6PD deficiency); hyperbaric O2 (if no response to methylene blue )
- Normal physiology: methaemoglobin is produced at a low rate normally and reduced back to haemoglobin by cytochrome b5 reductase (NADH pathway, major) and NADPH-methaemoglobin reductase (minor; activated by methylene blue).
- Congenital causes: cytochrome b5 reductase deficiency (autosomal recessive); haemoglobin M variants.
- Management nuances: methylene blue requires G6PD activity to work (NADPH-dependent); it will NOT work and may worsen methaemoglobinaemia in G6PD-deficient patients - use high-dose ascorbic acid or exchange transfusion instead.
Heat stroke = life-threatening hyperthermia (core temp > 40°C ) with CNS dysfunction (distinguishes from heat exhaustion where CNS intact); failure of thermoregulation. Two types: Exertional (young, healthy athletes in hot weather); Classic (non-exertional) (elderly, infants, chronically ill, drugs impairing sweating ).
- Clinical: Hyperthermia > 40°C (rectal temperature); anhidrosis (classic type; exertional may have diaphoresis); CNS — confusion, agitation, seizures, coma; tachycardia; hypotension; hot, dry skin (classic)
- Complications: Rhabdomyolysis (CK ↑↑↑; myoglobinuria → AKI); DIC; hepatic failure; ARDS; multi-organ failure
- Investigations: Core temp (rectal); CK (rhabdo ); coagulation (DIC ); ABG; LFT; RFT; blood glucose; electrolytes
◆ Heat Stroke Management — COOL THE PATIENT RAPIDLY ▸ Remove from hot environment; undress; lay flat ▸ Ice packs (neck, axilla, groins — major vessels ) + cool water spray + fans ▸ Cooled IV fluids (cold saline 0.9% 1 L over 30 min) ▸ Immersion in ice water bath (most effective — exertional heat stroke); target core temp < 38.5°C ▸ Cold wet towels; cooling blankets ▸ Monitor temperature q5 min; STOP cooling at 38.5°C to avoid overshoot hypothermia ▸ Treat complications: hydrate aggressively for rhabdomyolysis; benzodiazepines for shivering/seizures; no antipyretics (not effective ) - Heat exhaustion vs heat stroke: heat exhaustion - normal or mildly elevated temperature, normal CNS, profuse sweating, responds to rest and fluids; heat stroke - core temp > 40 C, CNS dysfunction (confusion/coma), medical emergency requiring immediate cooling.
- Cooling methods: ice-water immersion (most effective, fastest cooling), evaporative cooling (fans + misted water), ice packs to groin/axillae/neck; target core temp < 39 C within 30 min; avoid antipyretics (not effective, hepatic damage risk in rhabdomyolysis).
- Complications and monitoring: rhabdomyolysis (CK, urine for myoglobinuria, treat with aggressive IV fluids to protect kidneys); DIC (clotting screen); AKI (U&E, creatinine); hepatic failure (LFTs rise after 24-48 h); multi-organ failure - ICU care.
Type Mechanism Key Features Treatment Organophosphate AChE inhibition SLUDGE + fasciculations; bradycardia; miosis Atropine + Pralidoxime Carbamate (e.g. carbaryl) Reversible AChE inhibition Like OP but milder, shorter duration; self-limiting 4–6 hrs Atropine ONLY (NO pralidoxime — ineffective/harmful in carbamate ) Pyrethroid (e.g. cypermethrin) Na⁺ channel prolongation Paraesthesia (skin tingling — pathognomonic ); seizures in severe; NO cholinergic syndrome Benzodiazepines (seizures); symptomatic Organochlorine (e.g. DDT, lindane) CNS stimulation (GABA antagonism) Seizures; tremor; confusion; hepatotoxicity; bioaccumulates in fat Benzodiazepines; cholestyramine (↑ elimination) - Organophosphate management summary: decontaminate (gloves, remove clothing, wash skin); secure airway (avoid suxamethonium - AChE-dependent); IV atropine (treat until bronchial secretions dry - not until pupils dilate) + pralidoxime (within 48 h to reactivate AChE); benzodiazepines for seizures.
- Carbamate vs organophosphate: carbamates (carbofuran, aldicarb) also inhibit AChE but the inhibition is spontaneously reversible; treat with atropine and supportive care; pralidoxime is NOT needed for carbamate poisoning.
- Pyrethroid poisoning: sodium channel toxins; cause paraesthesia, tremor, salivation and in severe cases seizures; treat supportively with vitamin E and phenobarbitone for seizures; no specific antidote.
- Organophosphate - intermediate syndrome: occurs 24-96 hours after cholinergic crisis resolves; weakness of proximal limb muscles, neck flexors, and respiratory muscles; cranial nerve palsies; caused by persistent AChE inhibition at NMJ; supportive (ventilatory support); pralidoxime less effective at this stage.
- Management priorities: decontamination and airway protection are the most urgent steps; avoid succinylcholine (prolonged paralysis due to AChE inhibition); use non-depolarising NMJ blockers if intubation needed; document the time and dose of atropine given for handover.
Barbiturate poisoning = CNS depression from excess GABA-A receptor activation; now less common (benzodiazepines largely replaced). Common in elderly/chronic users (phenobarbitone); suicidal overdose.
- Clinical: CNS depression → coma; respiratory depression (most dangerous — main cause of death ); hypothermia (severe cases); bullous skin lesions (pressure blisters — 'barb blisters' ); hypotension; cardiac arrhythmias; absent reflexes (severe)
- Investigations: Serum barbiturate level; ABG (respiratory acidosis + hypoxia); urine drug screen; ECG
▶ NO SPECIFIC ANTIDOTE (unlike benzodiazepines where flumazenil is partial antidote)
Supportive care: Airway (intubate early ) + O2 + MV for respiratory failure; IV fluids + vasopressors for hypotension; maintain body temperature
Decontamination: Activated charcoal (within 1–4 hrs ); multiple-dose charcoal (MDAC ) for phenobarbitone (enterohepatic recirculation )
Alkalinisation of urine (NaHCO₃ ) for phenobarbitone (↑ ionisation → ↑ excretion )
Haemodialysis/haemoperfusion for severe/refractory phenobarbitone poisoning- Mechanism: barbiturates enhance GABA-A receptor activity (increase duration of Cl- channel opening), causing CNS and respiratory depression; in overdose they also directly open the channel.
- Clinical grading (Reed): Grade I - drowsy but rousable; Grade II - unconscious, rousable; Grade III - unconscious, not rousable, reflexes present; Grade IV - unconscious, absent reflexes, apnoea.
- Treatment: airway protection and mechanical ventilation is the cornerstone; multiple-dose activated charcoal for phenobarbitone (enterohepatic recirculation); urinary alkalinisation increases excretion of phenobarbitone (weak acid); haemodialysis for severe phenobarbitone poisoning.
- Phenobarbitone vs short-acting: phenobarbitone has a longer half-life and more prolonged toxicity; short-acting barbiturates (thiopentone, secobarbital) cause deeper but more transient coma.
NEAR DROWNING
- Near drowning = survival (at least temporarily) after submersion/immersion; ARDS (secondary drowning ) main complication (pulmonary surfactant destruction); hypoxia; hypothermia; acidosis
- Management: Rescue; ABC; CPR if arrested; ALL should be hospitalised (secondary drowning up to 24 hrs later ); warm IV fluids (hypothermia); PEEP/CPAP for pulmonary oedema; antibiotics only if infection evidence; do NOT use prophylactic antibiotics (fresh vs salt water — similar management now)
LATHYRISM
- Lathyrism = neurotoxic disease from prolonged consumption of Lathyrus sativus (chickling vetch/khesari dal) — contains BOAA (beta-oxalyl-amino-alanine ) — excitotoxin → spastic paraparesis (UMN); irreversible; common in famine/drought conditions (India, Ethiopia, Bangladesh )
- Prevention: Avoid khesari dal; dehusk before cooking (removes BOAA); nutritional supplements (antioxidants); no effective treatment once established
BIOTERRORISM AGENTS
- Category A (highest priority — greatest public health impact):
- Near drowning - pathophysiology: aspiration of even small volumes causes surfactant washout, atelectasis and ARDS (secondary drowning - can be delayed up to 24 h); hypoxia and hypothermia drive cardiac arrest; fresh vs salt water aspiration has less clinical relevance than previously thought.
- Resuscitation: standard CPR; do NOT delay for "drainage manoeuvres"; warm the patient (remove wet clothing, warm IV fluids, warm humidified O2); treat hypothermia if present; admit all patients even if initially asymptomatic.
- Lathyrism: caused by beta-N-oxalyl-amino-L-alanine (BOAA) in Lathyrus sativus (khesari dal); neurolathyrism presents as spastic paraplegia in adults who consumed the dal excessively during famine; endemic in India, Ethiopia and Bangladesh.
- Bioterrorism - key agents: anthrax (cutaneous - painless black eschar, pulmonary - widened mediastinum, treat with ciprofloxacin); plague (bubonic/pneumonic - streptomycin/doxycycline); smallpox (deep synchronous rash on palms/soles - vaccinate contacts); botulinum toxin (descending flaccid paralysis - antitoxin).
- Anthrax (*B. anthracis*) — cutaneous (black eschar ), pulmonary (widened mediastinum ), GI; treat with ciprofloxacin/doxycycline
- Smallpox (Variola) — eradicated; deep synchronous rash involving palms/soles; highly contagious; vaccine stockpiles
- Plague (*Y. pestis*) — bubonic (bubo ); pneumonic (most contagious); treat streptomycin/gentamicin/doxycycline
- Botulinum toxin — descending flaccid paralysis; antitoxin
- Ebola/VHF