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EM TopicsToxicology and environmental emergencies

EM · Toxicology and environmental emergencies

Snake envenomation

Also known as Australian snakebite · Elapid envenomation · Venom-induced consumption coagulopathy · VICC · Brown snake bite · Tiger snake bite

ANZ snake envenomation — elapid bites from the brown snake, tiger snake, taipan, death adder, mulga/black snake and rough-scaled snake. The four venom syndromes are venom-induced consumption coagulopathy (VICC — INR above 3, D-dimer markedly raised, fibrinogen low, from procoagulant prothrombin-activator venoms), neurotoxicity (descending paralysis — ptosis, ophthalmoplegia, bulbar palsy, respiratory failure — from presynaptic phospholipase A2 and postsynaptic three-finger toxins), rhabdomyolysis, and renal failure. First aid is the pressure immobilisation bandage. Diagnosis is clinical plus the snake venom detection kit (SVDK). Treatment is monovalent antivenom (brown snake 1 to 2 vials, tiger snake 2 to 4 vials) or polyvalent antivenom when the snake is unidentified, with adrenaline premedication and blood products only after antivenom. ACEM-primary, globally tagged.

high6 referencesUpdated 26 July 202621 min readSource-verified · Sept 2026

Checked against its sources on 2 Sept 2026

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Target exams

ACEMFRCEMABEMFRCPCCCFPEMEBEEM

Red flags

  • VICC is NOT DIC — the INR is unrecordable, the fibrinogen is undetectable, the D-dimer is off-scale, but the platelet count is preserved. Giving clotting factors before antivenom simply feeds the venom and is re-consumed within hours.
  • Brown snake bite causes sudden prehospital cardiac collapse — the patient found dead in the paddock with an unrecordable INR has been envenomed until proven otherwise.
  • The bite mark is often invisible and the snake is unidentified in over half of cases — diagnose and treat on the venom syndrome, the geography, and the coagulation profile, not on a bite mark.
  • Presynaptic neurotoxicity (tiger, taipan, rough-scaled) is irreversible once nerve terminals are damaged — antivenom prevents further injury but does not reverse established paralysis; anticipate and intubate before respiratory failure.
  • Do not remove the pressure immobilisation bandage to inspect the bite unless antivenom and resuscitation are ready — removal releases a lymphatic bolus of venom and precipitates envenomation.
  • Antivenom reactions are common — premedicate with low-dose adrenaline 0.25 mg subcutaneously (the randomised-trial regimen: 0.25 mL of 1 in 1000) and give antivenom in a monitored area with adrenaline drawn up.
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Related topics

  • Salicylate poisoning
  • Paracetamol poisoning
  • Tricyclic antidepressant poisoning (emergency department diagnosis and management)
  • Upper airway obstruction in the emergency department
  • Acute ischaemic stroke
  • Spider and marine envenomation
Study tools

Your progress

Saved on this device.

Target exams

ACEMFRCEMABEMFRCPCCCFPEMEBEEM

Red flags

  • VICC is NOT DIC — the INR is unrecordable, the fibrinogen is undetectable, the D-dimer is off-scale, but the platelet count is preserved. Giving clotting factors before antivenom simply feeds the venom and is re-consumed within hours.
  • Brown snake bite causes sudden prehospital cardiac collapse — the patient found dead in the paddock with an unrecordable INR has been envenomed until proven otherwise.
  • The bite mark is often invisible and the snake is unidentified in over half of cases — diagnose and treat on the venom syndrome, the geography, and the coagulation profile, not on a bite mark.
  • Presynaptic neurotoxicity (tiger, taipan, rough-scaled) is irreversible once nerve terminals are damaged — antivenom prevents further injury but does not reverse established paralysis; anticipate and intubate before respiratory failure.
  • Do not remove the pressure immobilisation bandage to inspect the bite unless antivenom and resuscitation are ready — removal releases a lymphatic bolus of venom and precipitates envenomation.
  • Antivenom reactions are common — premedicate with low-dose adrenaline 0.25 mg subcutaneously (the randomised-trial regimen: 0.25 mL of 1 in 1000) and give antivenom in a monitored area with adrenaline drawn up.
The one-line answer

ANZ snake envenomation is an elapid bite read off the venom syndrome, not the bite mark. It produces one of four patterns — venom-induced consumption coagulopathy (VICC), descending neurotoxicity, rhabdomyolysis, or early cardiovascular collapse — and the coagulation profile plus the neurology give you both within an hour. First aid is the pressure-immobilisation bandage, left on until antivenom is ready; definitive treatment is monovalent antivenom when the snake group is known (brown snake 1 to 2 vials, tiger snake 2 to 4 vials) or polyvalent when it is not, with low-dose adrenaline 0.25 mg subcutaneous premedication (reduces severe reactions by about 43 percent; antihistamine or steroid alone does not) and clotting factors only after antivenom, and only in the actively bleeding patient.[1][6]

Meet the patient

A 45-year-old farmer is flown in from regional New South Wales three hours after a witnessed snake bite while fencing. The bite mark is barely visible and the snake was not seen clearly, but the geography favours the brown snake. He is alert, with oozing from his gum and his cannula site. The INR is unrecordable, the APTT is unrecordable, the fibrinogen is 0.3 g/L, the D-dimer is 45 mg/L, and the platelet count is 230.[1]

The two questions that decide his next hour are the two that decide every snakebite: which venom syndrome is this? (the coagulation profile and the neurology answer within the hour) and which antivenom, and how much? (the snake group, from the SVDK or the geography, answers that). Hold those two and the rest of the topic slots into place.[1]

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References6ShowHide
  1. [1]Johnston CI, Ryan NM, Page CB, et al. The Australian Snakebite Project, 2005-2015 (ASP-20). Med J Aust, 2017.PMID 28764620
  2. [2]Isbister GK, Noutsos T, Jenkins S, et al. D-dimer testing for early detection of venom-induced consumption coagulopathy after snakebite in Australia (ASP-29). Med J Aust, 2022.PMID 35670073
  3. [3]Isbister GK, Isoardi KZ, Chiew AL, et al. Early cardiovascular collapse after envenoming by snakes in Australia, 2005-2020: an observational study (ASP-31). Med J Aust, 2025.PMID 40058771
  4. [4]Johnston CI, Ryan NM, O'Leary MA, et al. Australian taipan (Oxyuranus spp.) envenoming: clinical effects and potential benefits of early antivenom therapy - Australian Snakebite Project (ASP-25). Clin Toxicol (Phila), 2017.PMID 27903075
  5. [5]Brown SG, Caruso N, Borland ML, et al. Clotting factor replacement and recovery from snake venom-induced consumptive coagulopathy. Intensive Care Med, 2009.PMID 19547954
  6. [6]de Silva HA, Pathmeswaran A, Ranasinha CD, et al. Low-dose adrenaline, promethazine, and hydrocortisone in the prevention of acute adverse reactions to antivenom following snakebite: a randomised, double-blind, placebo-controlled trial. PLoS Med, 2011.PMID 21572992
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Related topics

  • Salicylate poisoning
  • Paracetamol poisoning
  • Tricyclic antidepressant poisoning (emergency department diagnosis and management)
  • Upper airway obstruction in the emergency department
  • Acute ischaemic stroke
  • Spider and marine envenomation