IM21.1-9 | Envenomation — Graded Quiz

Correct. A repeat dose of ASV is indicated when the 20WBCT remains non-clotting 6 hours after the initial dose. The initial 10 vials were insufficient to neutralise the circulating venom. ASV is the only definitive treatment — blood products (FFP, platelets, cryoprecipitate) do not work in VICC until all circulating venom is neutralised (giving clotting factors in the presence of active venom simply provides more substrate for depletion). A further 10 vials should be given.

ASV response monitoring: Repeat 20WBCT at 6 hours after ASV — if still non-clotting, give further 10 vials. Continue until 20WBCT normalises. Blood products for VICC are NOT first-line — venom must be neutralised first. After WBCT normalises, clotting factors recover within 6 hours as the liver synthesises them (provided liver function is intact).

Persistent non-clotting 20WBCT at 6 hours post-ASV = inadequate venom neutralisation = repeat ASV dose (10 more vials). Blood products (FFP, platelets) are INEFFECTIVE in VICC while free venom is still circulating — the venom will consume the transfused factors immediately. Blood products are only given once ASV has neutralised all circulating venom and WBCT normalises.

Correct. This is systemic neurotoxic envenomation (ptosis, dysphagia, neck weakness, falling SpO2) — an absolute ASV indication regardless of 20WBCT result. Additionally, a neostigmine test/trial is indicated for post-synaptic neurotoxicity (cobra-type): neostigmine 1.5 mg IV (or 0.04 mg/kg) PLUS atropine 0.6 mg IV (to block muscarinic side effects). If there is improvement in ptosis/power within 30 min, continue neostigmine. Pre-synaptic toxins (krait) do not respond to neostigmine.

Neostigmine in snakebite: Indicated for post-synaptic neurotoxic envenomation (cobra). Dose: neostigmine 1.5 mg IV + atropine 0.6 mg IV — ALWAYS together. Assess for improvement in ptosis and respiratory function at 30 minutes. Pre-synaptic neurotoxins (krait) do not respond. In clinical practice, a test dose is given and response determines continued use.

Neurotoxic envenomation with systemic signs = ASV indication (neurotoxic envenomation is systemic envenomation). Plus: a neostigmine/atropine trial is indicated as some cobras have predominantly post-synaptic toxins that are reversible by acetylcholinesterase inhibition. Atropine must always accompany neostigmine (blocks excessive muscarinic secretions). Never give neostigmine without atropine.

Correct. This is severe krait envenomation (nocturnal bite on sleeping person, painless, minimal local signs, pure neurotoxic). Common krait uses pre-synaptic neurotoxins (beta-bungarotoxin) that deplete acetylcholine from the neuromuscular junction — these do NOT respond reliably to neostigmine. The patient will require prolonged mechanical ventilation. ASV reduces further venom burden but cannot reverse established neurological damage quickly. Recovery takes days to weeks as nerve terminals regenerate.

Pre-synaptic neurotoxins (krait: beta-bungarotoxin) versus post-synaptic (cobra: alpha-bungarotoxin / alpha-cobratoxin). Pre-synaptic: deplete ACh from nerve terminal, established paralysis does not respond to neostigmine, prolonged ventilation needed. Post-synaptic: competitively block nicotinic receptor, may respond to neostigmine — test dose 1.5 mg with atropine 0.6 mg and assess in 30 min.

Krait envenomation uses predominantly PRE-synaptic neurotoxins — they irreversibly prevent acetylcholine release. ASV is indicated and important, but established paralysis will not reverse quickly. Neostigmine is unlikely to help (works on post-synaptic toxins). Prolonged mechanical ventilation is the cornerstone of treatment. A normal 20WBCT with neurotoxicity does not mean dry bite — krait is purely neurotoxic.

Correct. This is Grade I scorpion envenomation — local pain only with normal vital signs. Grade I is managed with analgesia (paracetamol or NSAIDs) and observation for progression to systemic features. Prazosin is indicated only for Grade II or III (systemic autonomic features). Giving prazosin to a Grade I patient may cause hypotension without benefit. Propranolol is absolutely contraindicated at any grade.

Scorpion management by grade: Grade I (local only) = analgesia + observation 4-6 hours; Grade II (systemic autonomic features) = prazosin 250-500 mcg orally + observation + repeat dose every 3h if features persist; Grade III (pulmonary oedema, cardiogenic shock) = ICU, dobutamine for cardiogenic shock, prazosin, ventilatory support. Propranolol ALWAYS contraindicated — causes unopposed alpha vasoconstriction.

Grade I scorpion envenomation (local pain only) = analgesia + observation. Prazosin is only for Grade II (systemic autonomic features: hypertension, diaphoresis, tachycardia, cold extremities) or Grade III (pulmonary oedema, shock). Giving prazosin without systemic features is inappropriate. Propranolol is ALWAYS contraindicated in scorpion envenomation.

Correct. VICC can develop in a delayed fashion — an initially normal 20WBCT does not rule out subsequent coagulopathy. Serial 20WBCT monitoring is mandatory. A non-clotting result at 6 hours, even after an initial normal result, confirms development of VICC and is an indication for ASV. This patient now has systemic envenomation and must receive antivenom.

Serial 20WBCT monitoring schedule: on admission, at 6 hours, and at 12 hours (some protocols also test at 24h). The 20WBCT can normalise then become positive again — venom from lymphatic depots can be absorbed over time. Never discharge a snakebite patient before completing the 24-hour serial monitoring.

The 20WBCT must be repeated at regular intervals (on admission, at 6h, and at 12h minimum) even if the initial test is normal, because VICC can be delayed. A non-clotting result at any serial measurement = ASV indication. The shift from normal to non-clotting is clinically significant and must be acted upon.

Correct. Jellyfish first aid: do NOT rub (rubbing fires undischarged nematocysts). Remove visible tentacles carefully without touching them directly (use a card or gloves). Rinse with seawater (NOT fresh water — hypotonic solution triggers nematocyst discharge). Vinegar (5% acetic acid) is recommended for Box jellyfish stings to inactivate nematocysts. Hot water immersion (45°C for 20 min) is the preferred analgesic measure for most jellyfish in Indian waters.

Jellyfish management: (1) Do NOT rub; (2) Remove tentacles carefully; (3) Rinse with seawater — NEVER fresh water (hypotonic water triggers nematocyst discharge); (4) Hot water immersion 45°C for 20 min for analgesia; (5) Vinegar for Box jellyfish to inactivate remaining nematocysts; (6) Analgesia (paracetamol/NSAIDs); (7) Watch for systemic features in large-area stings — rare but can include cardiac arrhythmias.

Jellyfish first aid: never rub (fires nematocysts). Remove tentacles without touching. Rinse with seawater (not fresh water). Vinegar for Box jellyfish. Hot water immersion (45°C, 20 min) is effective for pain relief for most Indian species. Ice packs are less effective for jellyfish venom pain.

Correct. Polyvalent ASV is administered as an IV infusion (not IM — IM route is not recommended for Indian polyvalent ASV). Dilute in 100-200 mL of normal saline (or 5% dextrose) and infuse over 1 hour. Always have adrenaline drawn up and ready BEFORE starting the infusion. IM route has unreliable absorption and may be used only when IV access is impossible.

ASV administration: Dilute in 100-200 mL NS or 5% dextrose; infuse IV over 60 minutes; monitor continuously during infusion; have adrenaline 0.5 mg (1:1000) IM drawn up and ready before starting. Indian polyvalent ASV is not recommended IM. Dose in children is the SAME as adults — the amount of venom injected is independent of body weight.

ASV administration route and rate: IV infusion (never IM unless IV access impossible), diluted in 100-200 mL normal saline, given over 1 hour. Undiluted IV bolus increases the risk of anaphylaxis. Have adrenaline 0.5 mg IM drawn up and at the bedside BEFORE starting. Monitor the patient throughout the infusion.

Correct. Once VICC has been neutralised (20WBCT normal), further ASV vials do not prevent or reverse established AKI. Venom-induced AKI in Russell's viper envenomation results from multiple mechanisms: VICC with microthrombi in glomerular capillaries, direct renal tubular toxicity, hypotension causing ischaemia, and haemoglobinuria. Management is supportive: IV fluids (if euvolaemic or hypovolaemic), strict input-output charting, and renal replacement therapy (dialysis) if oliguric AKI persists. Most cases are reversible with appropriate supportive care.

Post-ASV complications requiring supportive care: AKI (Russell's viper — most common cause of death in survivors; monitor creatinine, urine output; dialyse if needed), local necrosis (surgical review, secondary infection prophylaxis), residual coagulopathy (monitor until normalisation), neurological recovery (krait/cobra — may take weeks). ASV does not treat established organ damage.

After 20WBCT normalises, additional ASV is not indicated for AKI — ASV neutralises circulating venom; it does not repair established renal injury. AKI in Russell's viper envenomation is multifactorial (VICC, direct tubular toxicity, hypotension, haemoglobinuria) and requires supportive care. Dialysis may be needed but supportive measures and fluid management must be tried first.

Correct. Propranolol is ABSOLUTELY CONTRAINDICATED in scorpion envenomation. The pathophysiology is massive catecholamine release causing combined alpha-1 vasoconstriction and beta-2 vasodilation. Beta-blockade with propranolol eliminates the beta-2 vasodilatory component, leaving unopposed alpha-1 vasoconstriction — this precipitates catastrophic hypertension and cardiovascular collapse. Prazosin (alpha-1 blocker) is the correct specific treatment for Grade II/III.

WHY beta-blockers are fatal in scorpion envenomation: Mesobuthus tamulus toxin causes massive ACh/noradrenaline release → alpha-1 (vasoconstriction) + beta-2 (vasodilation) + beta-1 (tachycardia/inotropy) effects. Propranolol blocks beta-1 + beta-2 → only alpha-1 left unopposed → severe hypertension + no beta-2 vasodilatory escape → acute pulmonary oedema + cardiogenic shock. This is the highest-yield fact in scorpion management.

Propranolol is the most dangerous drug in scorpion envenomation. Blocking beta-2 receptors while alpha-1 vasoconstriction remains unopposed causes fatal hypertension. The correct specific treatment is prazosin (alpha-1 blocker). If cardiogenic shock develops, dobutamine (beta-1 agonist, inotropic) is used — but the primary error to avoid is propranolol.

Correct. Evidence-based community first aid: Immobilise the limb (improvised splint if available), keep below heart level, remove rings/bangles/tight clothing from the bitten limb to allow for swelling, keep the patient calm (panic increases heart rate and lymphatic flow), and transport to the nearest healthcare facility as rapidly as possible. Do NOT incise, suck, tourniquet, apply electric shock, apply ice, or apply traditional herbal remedies.

The WHO and Indian National Guidelines for snakebite first aid: DO: immobilise, keep below heart level, remove jewellery/tight items, calm and reassure, transport immediately. DO NOT: tourniquet, incise/suck, apply electricity, herbal remedies, give food/water/alcohol, delay transport. For suspected neurotoxic bites, pressure immobilisation bandage (firm crepe from fingers/toes to axilla/groin) is used in Australia — evidence is limited in India but some centres recommend it for cobra/krait.

Evidence-based snakebite first aid: immobilise limb + keep below heart level + remove constricting items + calm patient + RAPID transport. ALL of these are harmful and contraindicated: tourniquet (compartment syndrome, no benefit), incision/suction (no benefit, introduces infection, delays transport), electric shock (no benefit, causes burns), ice (causes frostbite, delays transport).

Correct. This is anaphylaxis (urticaria + angioedema + stridor + hypotension after bee sting). The only life-saving drug in anaphylaxis is adrenaline (epinephrine) 0.5 mg IM (1:1000 solution) into the anterolateral thigh. This must be given FIRST — before IV access, before antihistamines, before steroids. Corticosteroids and antihistamines take 30-60 minutes to act and do not reverse life-threatening anaphylaxis.

Anaphylaxis management sequence: 1) IM adrenaline 0.5 mg (adults) into anterolateral thigh — FIRST; 2) Call for help, lay patient flat, raise legs; 3) High-flow oxygen; 4) IV access + fluid bolus (500 mL NS); 5) Second dose of adrenaline if no improvement in 5-15 min; 6) IV chlorphenamine 10 mg + hydrocortisone 200 mg (adjuncts); 7) Salbutamol nebulisation if bronchospasm persists. Never use IV adrenaline outside cardiac arrest settings.

Anaphylaxis with stridor and hypotension is immediately life-threatening. Adrenaline IM is the ONLY first-line treatment — it works within minutes, reverses bronchospasm (beta-2), raises BP (alpha-1), and reduces mucosal oedema. Steroids take 30-60 minutes to act — they are adjuncts given AFTER adrenaline. IV fluids are also important but second to adrenaline.