Australian Envenomation — Written Clinical Reasoning

SAQ 1 — Brown snake bite with VICC and thrombotic microangiopathy (15 marks, 30 minutes)

Prompt: Outline your assessment, the clinical syndrome, the integrated management plan addressing each problem, and the communication framework. Justify each decision with reference to evidence. [1]

Model Answer

Step 1 — The clinical syndrome synthesis (3 marks): [1]

This man has systemic brown snake envenomation with three overlapping syndromes: venom-induced consumption coagulopathy (VICC), early thrombotic microangiopathy (TMA), and cardiovascular compromise. The unrecordable INR with undetectable fibrinogen and extreme D-dimer is VICC — the hallmark of brown snake envenomation, occurring in 100 per cent of envenomed patients in the ASP-14 cohort [2]. The thrombocytopenia (platelets 85), schistocytes on the blood film and the rising creatinine are the early triad of TMA, which complicates approximately 10 per cent of brown snake envenomations [3]. The hypotension and tachycardia reflect cardiovascular compromise, seen in one-third of brown snake envenomations. The normal CK excludes significant myotoxicity — brown snake venom is not a dominant myotoxin.

Step 2 — The VICC versus DIC distinction (2 marks): [1]

It is critical to recognise that this is VICC, NOT DIC. The mechanism is direct prothrombin activation by pseutarin C (the brown snake prothrombin activator), which generates a massive thrombin burst that consumes fibrinogen and clotting factors through defibrination and secondary fibrinolysis. There are no microthrommi causing end-organ damage, and there is no systemic inflammatory trigger — the distinction Isbister has argued should replace the misleading label "snakebite DIC" [4]. The management implications are profound: VICC is treated with antivenom, not with activated protein C, heparin, or the DIC paradigm.

Step 3 — The problem list (2 marks): [1]

1. VICC (INR unrecordable, fibrinogen undetectable) — the central problem; risk of spontaneous haemorrhage, though major bleeding is uncommon (under 5 per cent).
2. Thrombotic microangiopathy (platelets falling, schistocytes, AKI) — may progress to dialysis-dependent renal failure.
3. Cardiovascular compromise (hypotension) — from anaphylactoid reaction or direct cardiotoxicity.
4. Acute kidney injury (creatinine 145) — from TMA and possible pigment nephropathy.
5. Risk of major haemorrhage — avoid all non-essential invasive procedures during the coagulopathic window.
6. Risk of serum sickness at 5 to 14 days. [1]

Step 4 — The integrated management plan (5 marks): [1]

Pillar 1 — Resuscitation and first aid: The pressure immobilisation bandage must stay in situ until antivenom is ready at the bedside. I would establish two large-bore IV cannulae (on the opposite limb), give a fluid bolus (500 mL crystalloid) for the hypotension, and set up full monitoring including continuous ECG and oxygen saturation. I would draw blood for group and hold, cross-match, and a venous gas. I would NOT remove the bandage to inspect the bite site — this releases the trapped venom as a systemic bolus [7].

Pillar 2 — Antivenom: The SVDK is positive for brown snake venom, confirming the monovalent antivenom choice. 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 antivenom dose fell from four vials to one over the study decade with no change in outcomes [1][2]. I would NOT give routine premedication (adrenaline, antihistamines, corticosteroids) — current Australian guidelines do not recommend it because Australian antivenom is a purer product with a lower reaction rate than the Indian polyvalent used in the Premawardhena trial [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 must resynthesise the factors (6 to 12 hours for fibrinogen, 12 to 24 hours for a normal INR) [5]. 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 cases of severe VICC — the ASP-18 trial showed that FFP after antivenom accelerates correction [6], but routine FFP exposes the patient to transfusion risk. I would give vitamin K only if there was a suggestion of concurrent warfarin use (confirmed by history), because vitamin K is useless in VICC — the mechanism is consumption, not impaired synthesis.

Pillar 4 — TMA and AKI management: TMA is managed supportively — there is no specific treatment. I would monitor urine output, creatinine and the blood film daily. If AKI progresses to oliguria or uraemia, I would involve nephrology for renal replacement therapy (continuous or intermittent, depending on haemodynamic stability). Transfusion of platelets or red cells is guided by the clinical picture — platelet transfusion is rarely needed unless there is life-threatening bleeding, and red cell transfusion is given for symptomatic anaemia from haemolysis. [1]

Pillar 5 — Avoidance of harm during the coagulopathic window: I would avoid all non-essential invasive procedures (central lines, arterial gases, lumbar punctures, intramuscular injections) until the INR is below 2. If a central line is essential (for example, for dialysis access), I would give FFP first to partially correct the coagulopathy. Nasogastric tubes and urinary catheters can be placed with caution. [1]

Step 5 — Communication (3 marks): [1]

I would explain to the patient and his wife that the brown snake bite has caused a severe but treatable envenomation. The bandage his wife applied was excellent first aid and has contained the venom. The blood tests show a coagulopathy that looks alarming but is expected and will recover over 24 hours with antivenom. I would explain that the kidney function needs close monitoring because of a complication called thrombotic microangiopathy that affects some patients. I would warn him about serum sickness at 1 to 2 weeks (fever, joint pains, rash) and advise him to return if it occurs. I would involve the toxicologist and the renal team, and arrange retrieval to a tertiary centre if dialysis becomes likely. [1]

SAQ 2 — Tiger snake bite with neurotoxicity: the antivenom-versus-ventilation decision (10 marks, 20 minutes)

Prompt: A 35-year-old bushwalker in Tasmania is bitten on the calf by a snake later identified as a tiger snake. She had pressure immobilisation applied by her walking companion. Six hours after the bite, despite one vial of tiger snake monovalent antivenom, she develops progressive ptosis, ophthalmoplegia and bulbar weakness. Her vital capacity is falling. Coagulation has normalised. Discuss the mechanism of the neurotoxicity, why antivenom has not reversed it, and the management priorities. [1]

Model Answer

Step 1 — The mechanism (3 marks): [1]

Tiger snake venom contains notexin, a presynaptic phospholipase A2 neurotoxin that destroys the presynaptic nerve terminal membrane. The mechanism is physical destruction of the terminal — the vesicles are released in a massive burst (causing initial fasciculations), then the terminal is incapable of further acetylcholine release, producing a flaccid paralysis. Because the damage is structural (membrane destruction), antivenom can neutralise circulating toxin and prevent further damage, but it CANNOT reverse the destruction that has already occurred — the nerve terminal must regenerate, which takes days to weeks. [1]

This is fundamentally different from death adder neurotoxicity, where the venom is a postsynaptic alpha-neurotoxin that competitively blocks the receptor. Postsynaptic blockade IS reversible by antivenom and by neostigmine. The presynaptic/postsynaptic distinction is the key to understanding why this patient's paralysis is progressing despite antivenom. [1]

Step 2 — Why antivenom has not reversed the paralysis (2 marks): [1]

The antivenom was given correctly and has neutralised the circulating venom — the coagulation has normalised, confirming the VICC component is resolving. However, the presynaptic nerve terminal destruction occurred BEFORE the antivenom was given (within the first few hours), and antivenom cannot regenerate destroyed tissue. The paralysis will persist until the nerve terminals regrow. This is the expected course for presynaptic neurotoxicity — it is NOT a treatment failure. [1]

Step 3 — The management priorities (4 marks): [1]

1. Airway protection and mechanical ventilation. The falling vital capacity and bulbar weakness (pooled secretions, poor gag) indicate impending respiratory failure. I would intubate early using a rapid sequence induction, before the vital capacity falls below 15 mL/kg or the patient aspirates. Once intubated, the patient is managed in ICU with lung-protective ventilation. [1]

2. Continue antivenom as indicated. A second dose of antivenom may be considered if there is evidence of ongoing venom activity (worsening coagulopathy, rising CK), but it will not reverse the established paralysis. The role of further antivenom is to prevent ongoing presynaptic destruction at terminals not yet affected. [1]

3. Supportive ICU care. Sedation and analgesia (propofol and fentanyl, titrated to allow neurological assessment), pressure area care, DVT prophylaxis (mechanical, given the recent coagulopathy), nasogastric feeding, and physiotherapy. The patient may need ventilation for days. [1]

4. Monitor for recovery. A train-of-four monitor can assess neuromuscular recovery. The patient is extubated when the vital capacity exceeds 15 mL/kg, the bulbar function returns (able to manage secretions), and the train-of-four shows full recovery. [1]

Step 4 — Communication (1 mark): [1]

I would explain to the patient (once recovered enough to communicate) and her family that the paralysis is from a venom component that destroys nerve endings. The antivenom prevented further destruction but could not reverse the damage already done. The nerve endings will regrow over days, and the ventilator is supporting her breathing until they do. The prognosis is excellent — full recovery is expected. [1]