Australian Envenomation — Viva Defence

Long Case Viva Defence

The scenario

A 42-year-old farmer in rural Victoria is bitten on the right ankle by a brown-coloured snake while walking through a paddock. His wife applies a crepe bandage from the toes to the groin and splints the leg. On arrival at the emergency department 90 minutes later he is pale, diaphoretic and anxious. Blood pressure is 95/60, heart rate 110. Blood tests show INR unrecordable (above 10), fibrinogen undetectable, D-dimer markedly elevated, platelets 85 x 10^9/L, creatinine 145 micromol/L, CK 350 U/L. The blood film shows schistocytes. The SVDK is positive for brown snake venom. [1]

Opening statement (SASPOP)

"This is Mr K, a 42-year-old farmer presenting with systemic brown snake envenomation acquired while walking through a paddock in rural Victoria. His wife applied an excellent pressure immobilisation bandage — this has contained the venom in the limb and is the foundation of his pre-hospital care. The clinical picture is dominated by three overlapping syndromes: venom-induced consumption coagulopathy, or VICC, which is universal in brown snake envenomation and shown here by the unrecordable INR and undetectable fibrinogen; early thrombotic microangiopathy, shown by the thrombocytopenia, schistocytes and rising creatinine, which complicates about 10 per cent of brown snake bites; and cardiovascular compromise with hypotension and tachycardia, seen in about one-third. The normal CK excludes significant myotoxicity. His main problems are the VICC with its haemorrhage risk, the TMA with potential for dialysis-dependent renal failure, the cardiovascular compromise, the acute kidney injury, and the risk of serum sickness at one to two weeks. My priorities are to keep the pressure bandage in situ until antivenom is ready, give one vial of brown snake monovalent antivenom intravenously, manage the coagulopathy with observation and reserve FFP for bleeding or procedures, support the cardiovascular system with fluids, monitor the renal function closely with nephrology involvement, and avoid all non-essential invasive procedures during the coagulopathic window." [1]

Problem list (numbered, prioritised)

1. VICC (INR unrecordable, fibrinogen undetectable) — the central problem; risk of haemorrhage.
2. Thrombotic microangiopathy (platelets falling, schistocytes, AKI) — may progress to dialysis-dependent renal failure.
3. Cardiovascular compromise (hypotension, tachycardia) — from anaphylactoid reaction or direct cardiotoxicity.
4. Acute kidney injury (creatinine 145) — from TMA.
5. Risk of major haemorrhage — avoid invasive procedures during coagulopathy.
6. Risk of serum sickness at 5 to 14 days after antivenom. [1]

Integrated management plan

Pillar 1 — Resuscitation and first aid: "The pressure immobilisation bandage stays in situ until antivenom is drawn up and ready at the bedside — removing it releases the trapped venom as a systemic bolus [6]. I would establish two large-bore IV cannulae on the opposite limb, give a 500 mL crystalloid bolus for the hypotension, and set up continuous ECG and oxygen saturation monitoring. I would draw blood for group and hold, cross-match, venous gas, and repeat coagulation."

Pillar 2 — Antivenom: "The SVDK confirms brown snake venom, so I would give one vial of brown snake monovalent antivenom intravenously over 15 to 30 minutes. The ASP-20 study established that one vial is the standard dose — the median fell from four vials to one over the decade with no change in outcomes [1][2]. I would NOT give routine premedication — current Australian guidelines do not recommend prophylactic adrenaline, antihistamines or corticosteroids [8]. I would have adrenaline drawn up and ready at the bedside."

Pillar 3 — Coagulopathy management: "Antivenom neutralises circulating venom and prevents ongoing prothrombin activator activity, but it does not reverse the established consumption — the liver resynthesises fibrinogen over 6 to 12 hours and the INR normalises over 12 to 24 hours. I would monitor coagulation at 1, 3, 6, 12 and 24 hours. I would reserve fresh frozen plasma for active bleeding, before invasive procedures, or in selected severe cases — the ASP-18 trial showed FFP accelerates correction after antivenom [5], but routine FFP exposes the patient to unnecessary transfusion risk. I would NOT give vitamin K — the mechanism is consumption, not impaired synthesis."

Pillar 4 — TMA and AKI management: "TMA is managed supportively. I would monitor urine output, creatinine and the blood film daily, involve nephrology early, and prepare for renal replacement therapy if the AKI progresses to oliguria or uraemia. Platelet or red cell transfusion is guided by the clinical picture." [1]

Pillar 5 — Avoidance of harm: "I would avoid all non-essential invasive procedures — central lines, arterial gases, intramuscular injections, lumbar punctures — until the INR is below 2. If a central line is essential for dialysis, I would give FFP first to partially correct the coagulopathy." [1]

Probing questions the examiner would ask

Q: You said this is VICC, not DIC. Explain the difference and why it matters. [1]

A: "VICC and DIC look similar on the bloods — both produce a prolonged INR, low fibrinogen and elevated D-dimer — but they are fundamentally different conditions. DIC is a systemic inflammatory process triggered by sepsis, malignancy or an obstetric catastrophe, characterised by microthrombi deposition causing end-organ damage (renal, hepatic, cerebral, digital ischaemia) and a consumptive coagulopathy driven by the full coagulation cascade. VICC is a toxin-driven defibrination — the brown snake venom contains pseutarin C, a prothrombin activator that directly converts prothrombin to thrombin, bypassing the cascade and producing a massive consumption of fibrinogen and factors. There are no microthrombi and no end-organ damage from thrombosis. The management is different: VICC is treated with antivenom and supportive care; DIC is treated by addressing the underlying trigger. Isbister has argued that calling snakebite VICC 'DIC' is misleading and the terminology should change [4]."

Q: What dose of antivenom would you give, and why has this changed over time? [1]

A: "One vial of brown snake monovalent antivenom intravenously. This is a major change from the historical practice of giving multiple vials. The ASP-20 prospective registry of over 1500 suspected snakebites showed that the median antivenom dose fell from four vials to one over the decade 2005 to 2015, with no change in outcomes — no increase in complications, no delay in recovery, no excess mortality [1]. The brown snake-specific ASP-14 study confirmed this for brown snake envenomation specifically [2]. The reason is that the actual venom load in a human bite is lower than previously believed, and one vial contains sufficient antibody to neutralise it."

Q: Would you premedicate with adrenaline before the antivenom? [1]

A: "No, I would not give routine premedication. The Premawardhena 1999 trial from Sri Lanka showed that low-dose subcutaneous adrenaline reduced acute reactions to Indian polyvalent antivenom, but that antivenom is a cruder product with a much higher reaction rate than Australian antivenom [8]. Australian snake antivenom is a purer equine IgG preparation with a lower reaction rate, and prophylactic adrenaline carries its own risks — hypertension, cardiac ischaemia, arrhythmia. Current Australian guidelines recommend having adrenaline drawn up and ready at the bedside but NOT giving it prophylactically. If a reaction occurs, I stop or slow the infusion and give intramuscular adrenaline 0.5 mg as for any anaphylaxis."

Q: What is thrombotic microangiopathy from brown snake bite, and how do you manage it? [1]

A: "TMA from brown snake envenomation is a complication occurring in about 10 per cent of envenomed patients, characterised by the triad of thrombocytopenia, microangiopathic haemolytic anaemia with schistocytes on the blood film, and acute kidney injury [3]. It resembles atypical HUS pathologically — there is endothelial injury in the renal microvasculature leading to platelet consumption and red cell fragmentation. The management is supportive — there is no specific treatment. I would monitor renal function closely, transfuse platelets or red cells only for life-threatening bleeding or symptomatic anaemia, and involve nephrology for renal replacement therapy if the AKI progresses. Antivenom does not reverse established TMA — it prevents further venom-driven injury but cannot undo the endothelial damage. The AKI may require dialysis for days to weeks but usually recovers fully."

Q: The patient's INR is unrecordable. At what point would you give fresh frozen plasma? [1]

A: "I would give FFP in three situations: first, if there is active bleeding — gum bleeding, haematuria, gastrointestinal bleeding, or any suspected intracranial haemorrhage; second, before an essential invasive procedure that cannot be delayed — for example, a central line for dialysis, or surgery for a concurrent problem; third, in selected cases of severe VICC where the coagulopathy is not recovering as expected, after discussion with haematology and toxicology. I would NOT give FFP routinely to every VICC patient. The ASP-18 randomised trial showed that FFP after antivenom results in faster correction of the INR at 6 hours [5], but routine FFP exposes the patient to transfusion risk (TRALI, transfusion-associated circulatory overload, infection) for a coagulopathy that is self-limiting and corrects spontaneously in most patients within 24 hours. The unrecordable INR itself is not dangerous — it is the procedures performed during the coagulopathic window that cause the bleeding."

Q: What is the role of the Snake Venom Detection Kit in this case? [1]

A: "The SVDK confirmed that the snake is a brown snake, which tells me to give brown snake monovalent antivenom rather than polyvalent. But the SVDK did not determine whether to treat — the decision to give antivenom was made on the clinical and laboratory features of envenomation (VICC, cardiovascular compromise). The SVDK is a refinement tool, not a decision-to-treat tool. A positive SVDK in a patient with normal bloods and no clinical features would NOT warrant antivenom — it means venom is present at the bite site but the patient has not been systemically envenomed." [1]

Communication and shared decision-making

"I would tell Mr K and his wife that his wife's quick action with the pressure bandage was excellent and has contained the venom. The blood tests show a severe but treatable envenomation — the INR looks alarming but it is expected and will recover over 24 hours with the antivenom. I would explain that his kidney function needs close monitoring because of a complication called thrombotic microangiopathy that affects some patients, and that he may need dialysis support temporarily if the kidneys struggle. I would warn him about serum sickness — a flu-like illness with joint pains and a rash that can occur one to two weeks after the antivenom, and which is easily treated with a short course of steroids. I would involve the toxicologist and the renal team, arrange retrieval to a tertiary centre if the AKI progresses, and ensure his GP is informed for follow-up." [1]

Short Case Discussion — Neurological Examination in Snake Bite

Instruction: "Examine this patient's neurological system. They were bitten by a snake 8 hours ago." [1]

Systematic examination routine

1. End of bed — observe for ptosis (the earliest sign of neurotoxicity), facial weakness, drooling (bulbar weakness), respiratory pattern (accessory muscle use suggests impending respiratory failure), and the level of alertness.
2. Cranial nerves — test eye movements in all directions (external ophthalmoplegia is an early sign), eyelid position (ptosis), facial power (facial diplegia in severe neurotoxicity), bulbar function (gag, palatal movement, tongue protrusion), and pupil reflexes (preserved in neuromuscular junction blockade — distinguishes from brainstem lesions).
3. Motor system — test limb power systematically (MRC grading), assess for fatigability (sustained upgaze for 60 seconds reveals ptosis), and check reflexes (depressed or absent in presynaptic neurotoxicity).
4. Respiratory assessment — measure the vital capacity at the bedside (a falling vital capacity is the trigger for intubation; below 15 mL/kg or below 1 L in an adult is the threshold). [1]

Key physical signs the patient demonstrates (for a tiger snake neurotoxicity case)

• Bilateral ptosis (worsening with sustained upgaze)
• External ophthalmoplegia (inability to move the eyes laterally or vertically)
• Facial diplegia (inability to smile or close the eyes forcefully)
• Bulbar palsy (nasal voice, pooled secretions, poor gag)
• Generalised limb weakness with depressed reflexes
• Preserved consciousness and preserved pupil reflexes [1]

Presentation template

"I examined this patient who was bitten by a snake 8 hours ago. At the end of the bed she is alert but has obvious bilateral ptosis and a nasal quality to her speech. On cranial nerve examination, there is bilateral ptosis that worsens on sustained upgaze for 60 seconds, complete external ophthalmoplegia with preserved pupil reflexes, a bilateral facial nerve palsy, and bulbar weakness with a poor gag reflex and pooled oral secretions. On motor examination, there is generalised limb weakness, MRC grade 4, with depressed reflexes throughout. Sensation is intact. These findings — a descending flaccid paralysis with preserved pupil reflexes and preserved sensation — are consistent with presynaptic neuromuscular junction blockade from tiger snake (notexin) or taipan (taipoxin) envenomation. The vital capacity is my key concern — a falling vital capacity is the trigger for intubation. I would like to check the coagulation profile, the CK, and the SVDK, and I would involve the toxicologist and ICU immediately." [1]

Discussion questions

Q: How do you distinguish presynaptic from postsynaptic neurotoxicity at the bedside? [1]

A: "At the bedside, you cannot definitively distinguish them by examination alone — both produce a descending flaccid paralysis with depressed reflexes. The distinction is made by the snake species (identified by the SVDK or geography) and by the response to a neostigmine trial. Death adder venom is postsynaptic (alpha-neurotoxin blocking the nicotinic receptor), and a trial of neostigmine with glycopyrrolate will partially reverse the paralysis. Tiger snake (notexin) and taipan (taipoxin) venoms are presynaptic PLA2 toxins that destroy the nerve terminal, and neostigmine will NOT work — the terminal is destroyed, not blocked. The clinical importance is that postsynaptic neurotoxicity is rapidly reversible by antivenom, while presynaptic neurotoxicity is NOT reversible once the terminal is destroyed — the patient may need ventilation for days despite adequate antivenom." [1]

Q: What is the significance of preserved pupil reflexes in this patient? [1]

A: "Preserved pupil reflexes confirm that the paralysis is at the neuromuscular junction, not in the brainstem or the cranial nerves. The pupil constrictor muscles (sphincter pupillae) are controlled by parasympathetic fibres from the Edinger-Westphal nucleus via the oculomotor nerve, and they are relatively resistant to the neuromuscular blockade. If the pupils were dilated and fixed, I would be concerned about a brainstem lesion or a different toxin (such as botulism, which dilates the pupils, or anticholinergic poisoning). Preserved pupils in the setting of complete external ophthalmoplegia is a sign that the extraocular muscles are affected but the iris sphincter is spared — a pattern characteristic of elapid neurotoxicity." [1]

Q: What is the blue-ringed octopus, and how does its neurotoxicity differ from snake neurotoxicity? [1]

A: "The blue-ringed octopus (Hapalochlaena) delivers tetrodotoxin, a potent voltage-gated sodium channel blocker. The clinical picture is rapid onset flaccid paralysis with preserved consciousness and preserved pupil reflexes — similar to snake neurotoxicity in the descending pattern, but the mechanism is different. Snake neurotoxins act at the neuromuscular junction (presynaptic or postsynaptic). Tetrodotoxin blocks the action potential in the motor nerve and the muscle, preventing any signal from reaching the junction. There is no antivenom for tetrodotoxin — management is purely supportive with mechanical ventilation until the toxin wears off (hours to a day). The patient is fully conscious throughout, so sedation is not routinely needed." [1]

Q: What are the first-aid rules for the major Australian envenomations? [1]

A: "The first-aid rules by creature are: Australian elapid snake bite — pressure immobilisation bandage; funnel-web spider bite — pressure immobilisation bandage; red-back spider bite — cold compress, NOT a pressure bandage; box jellyfish sting — pour copious vinegar over the tentacles, then carefully remove them; blue-ringed octopus bite — pressure immobilisation bandage (the venom spreads via lymphatics); stonefish sting — hot water immersion at 40 to 42 degrees Celsius. These are frequently tested and are the most common first-aid errors in exams. The key discriminations are: PBI for snake and funnel-web, NOT for red-back; vinegar for box jellyfish, NOT fresh water; hot water for stonefish, NOT ice." [1]