ICU · toxicology

Acute Snake Envenomation — Comprehensive (ANZ Context)

Also known as Snakebite envenomation · Snake envenoming · Elapid envenomation · Brown snake bite · Tiger snake bite · Taipan bite · Death adder bite · Venom-induced consumption coagulopathy · VICC · Australian snakebite · Pressure immobilisation bandage · Snake antivenom

Acute snake envenomation in Australia and New Zealand — the world's most venomous snakes belong to the family Elapidae (front-fanged: brown snake [Pseudonaja — 1 cause of snakebite death — procoagulant + presynaptic neurotoxin + rarely thrombotic microangiopathy], tiger snake [Notechis — procoagulant + neurotoxic + myotoxic], taipan [Oxyuranus — most toxic land snake — procoagulant + neurotoxic + myotoxic], death adder [Acanthophis — postsynaptic neurotoxin — curare-like; mechanistically reversible but ASP cohort showed no reversal by antivenom (median resolution 21 h)], black snake [Pseudechis — myotoxic + anticoagulant], rough-scaled snake [Tropidechis — procoagulant + myotoxic], sea snakes [Hydrophiidae — myotoxic + neurotoxic]). Clinical syndromes: (1) PROCOAGULANT → venom-induced consumption coagulopathy [VICC] — prothrombin activators → massive consumption of fibrinogen and factors V, VIII, X → INR 5 + fibrinogen <0.5 + D-dimer massively elevated + PLATELETS NORMAL — but BLEEDING IS RARE despite extreme coagulopathy because the venom clots AND lyses simultaneously (unlike warfarin or DIC — no true anticoagulated state) — give antivenom NOT FFP unless actively bleeding — recovery takes 24-36 h as the liver resynthesises factors (ASP-10). (2) NEUROTOXIC → descending flaccid paralysis: ptosis → ophthalmoplegia → bulbar palsy → limb weakness → respiratory failure — resembles myasthenia gravis (postsynaptic: death adder) or botulism (presynaptic: tiger, brown, taipan) — the pupil reflex and deep tendon reflexes distinguish. (3) MYOTOXIC → muscle pain, tenderness, rising CK (10,000-100,000+), myoglobinuria, AKI — tiger, black, taipan, sea snakes. (4) NEPHROTOXIC → AKI from rhabdomyolysis + direct nephrotoxicity + thrombotic microangiopathy — brown snake. (5) CARDIOVASCULAR COLLAPSE → sudden early collapse (within 1h of bite) — brown snake — thought to be transient hypotension from venom cardiotoxicity or anaphylactoid reaction — high-risk feature. Management: (1) FIRST AID: pressure immobilisation bandage [PIB] — broad bandage over bite site + splint + immobilise the limb — slows LYMPHATIC venom spread (NOT venous — venom moves via lymphatics) — DO NOT remove until antivenom ready in hospital (removal causes venom surge). (2) SNAKE VENOM DETECTION KIT [SVDK] — bite site swab or urine — identifies snake GROUP (brown, tiger, black, death adder, taipan) — guides monovalent antivenom choice — BUT 5% false negative in envenomed patients + 36% false positive in non-envenomed patients — clinical syndromic diagnosis is more reliable. (3) ANTIVENOM: monovalent if snake identified by SVDK or clinical/geographic assessment OR polyvalent if snake unknown — ONE VIAL is sufficient to bind all circulating venom (recent evidence: median dose declined from 4 to 1 vial without harm) — pre-medicate with adrenaline (subcutaneous 0.25 mg) to reduce hypersensitivity reactions (24% reaction rate, 6% severe) — large volumes if polyvalent (dilute in crystalloid, infuse over 30 min). (4) VICC MANAGEMENT: give antivenom — DO NOT give blood products (FFP, cryoprecipitate, platelets) UNLESS actively bleeding — the coagulopathy resolves within 24-36 h as the liver resynthesises factors (ASP-10) — giving FFP 'feeds' the venom prothrombin activator more substrate to consume (paradoxical worsening) and risks transfusion reactions. (5) SUPPORTIVE: mechanical ventilation for neurotoxicity, renal replacement therapy for AKI, treat rhabdomyolysis with fluids. Mortality ~1-2% with antivenom (23 deaths over 10 years in ASP-20; 17 from brown snake).

Checked against its sources on 2 Sept 2026