Australian Envenomation — Clinical Case

DCE Long Case

Patient profile

Mr K is a 42-year-old farmer who was bitten on the right ankle by a brown-coloured snake while walking through a paddock on his property in rural Victoria at 1400 hours. His wife, a former ambulance volunteer, applied a crepe bandage from the toes to the groin and splinted the leg with a fence paling. The Royal Flying Doctor Service retrieved him, arriving at the regional hospital emergency department at 1530 hours. [1]

Presenting concern: Mr K was walking through long grass in a paddock when he felt a sharp sting on his right ankle. He saw a brown-coloured snake, approximately 1.5 metres long, moving away quickly. Within 15 minutes he felt nauseated, diaphoretic and lightheaded. His wife applied the pressure immobilisation bandage immediately, kept him still, and called the RFDS. On arrival at the emergency department he is anxious, pale and diaphoretic, with nausea but no vomiting. He has no bleeding from the gums, no haematuria and no headache. [1]

Past medical history: Hypertension (on ramipril 5 mg daily) and mild asthma (salbutamol prn). No prior snake bite. No known allergies. No bleeding disorders. Not on anticoagulants or antiplatelet agents. Non-smoker, drinks 10 to 20 grams of alcohol per day. [1]

Social: Married with two school-age children. Works the family farm (sheep and crops). Lives 45 minutes from the nearest hospital. He is the primary income earner and is anxious about the financial impact of being off work. [1]

Examination:

• Alert, anxious, pale, diaphoretic. GCS 15.
• Blood pressure 95/60, heart rate 110, respiratory rate 20, oxygen saturation 97 per cent on room air, temperature 36.8.
• Pressure immobilisation bandage in situ on the right lower limb (well applied, firm, from toes to groin, with a splint).
• Two fang marks on the lateral right ankle, 1 cm apart. Minimal local swelling. No bleeding from the bite site.
• Right inguinal lymph nodes are tender and mildly enlarged.
• Cardiovascular: regular tachycardia, no murmurs. Lungs clear.
• Abdomen: soft, non-tender. No organomegaly.
• Neurological: no ptosis, full extraocular movements, normal facial power, normal bulbar function, normal limb power and reflexes, normal sensation. (This confirms the brown snake VICC-dominant pattern — no neurotoxicity.) [1]

Investigations at 1530 (90 minutes post-bite):

• INR unrecordable (above 10). aPTT unrecordable. Fibrinogen undetectable (below 0.1 g/L). D-dimer markedly elevated.
• Platelets 85 x 10^9/L. Haemoglobin 142 g/L. White cell count 14.5 x 10^9/L (neutrophilia).
• Blood film: schistocytes present (fragmented red cells).
• Creatinine 145 micromol/L (baseline unknown). Urea 9.2 mmol/L. CK 350 U/L (normal — no myotoxicity).
• Venous gas: pH 7.35, lactate 3.1 mmol/L.
• Urine: dipstick positive for blood (possible myoglobin or haemoglobin), no red cells on microscopy.
• SVDK from bite-site swab: positive for brown snake venom. [1]

Candidate's opening statement (SASPOP)

"This is Mr K, a 42-year-old farmer presenting with systemic brown snake envenomation acquired while walking through a paddock on his property in rural Victoria. His wife applied an excellent pressure immobilisation bandage immediately — 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, and the normal neurological examination confirms the brown snake VICC-dominant pattern — no neurotoxicity. 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]

Structured problem list (numbered, prioritised)

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; occurs in 10 per cent of brown snake bites.
3. Cardiovascular compromise (hypotension, tachycardia) — from anaphylactoid reaction or direct cardiotoxicity; risk of cardiac arrest in 5 per cent.
4. Acute kidney injury (creatinine 145) — from TMA; may progress to oliguria requiring renal replacement therapy.
5. Risk of major haemorrhage — avoid all non-essential invasive procedures until INR is below 2.
6. Risk of serum sickness at 5 to 14 days after antivenom (20 to 40 per cent incidence).
7. Psychosocial impact — primary income earner, anxious about work and finances, lives in a remote location. [1]

Integrated management plan

Step 1 — Resuscitation and first aid management: [1]

The pressure immobilisation bandage stays in situ until antivenom is drawn up and ready at the bedside. Removing the bandage before antivenom is available releases the trapped venom as a systemic bolus, which can precipitate collapse, worsen the VICC, or trigger neurotoxicity [6]. I would establish two large-bore IV cannulae on the left arm (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, a venous gas, and a repeat coagulation profile.

Step 2 — Antivenom: [1]

The SVDK confirms brown snake venom. 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 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 [7]. The Premawardhena 1999 trial of prophylactic subcutaneous adrenaline was conducted with Indian polyvalent antivenom, which has a much higher reaction rate than Australian antivenom; the risk-benefit does not transfer. I would have adrenaline drawn up and ready at the bedside.

Step 3 — Coagulopathy management: [1]

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) [4]. I would monitor coagulation at 1, 3, 6, 12 and 24 hours. The INR should begin to fall within hours of antivenom and be below 2 within 24 hours.

I would reserve fresh frozen plasma for: (a) active bleeding (gum bleeding, haematuria, gastrointestinal bleeding, suspected intracranial haemorrhage); (b) before an essential invasive procedure that cannot be delayed (central line for dialysis, surgery for a concurrent problem); or (c) selected cases of severe VICC not recovering as expected. The ASP-18 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, TACO, infection) for a coagulopathy that is self-limiting in most patients.

I would NOT give vitamin K — the mechanism is consumption, not impaired hepatic synthesis. The liver's function is intact; the problem is that the venom has consumed the factors. [1]

Step 4 — TMA and AKI management: [1]

TMA is managed supportively — there is no specific treatment. I would monitor urine output (indwelling catheter), creatinine, and the blood film daily. I would involve nephrology early. If the AKI progresses to oliguria, uraemia, or fluid overload, I would arrange renal replacement therapy (continuous venovenous haemofiltration if haemodynamically unstable, intermittent haemodialysis if stable). Platelet transfusion is reserved for life-threatening bleeding; red cell transfusion for symptomatic anaemia from haemolysis. Antivenom does not reverse established TMA — it prevents further venom-driven injury but cannot undo the endothelial damage. [1]

Step 5 — Avoidance of harm during the coagulopathic window: [1]

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 access), I would give FFP first to partially correct the coagulopathy. Nasogastric tubes and urinary catheters can be placed with caution. Venepuncture sites require firm pressure. [1]

Step 6 — Cardiovascular monitoring: [1]

I would monitor the ECG continuously for the first 12 hours, as brown snake venom can cause direct cardiotoxicity and arrhythmia. The initial hypotension is managed with IV fluids; if it persists or worsens, I would involve ICU for vasopressor support. [1]

Step 7 — Communication and psychosocial support: [1]

I would explain to Mr K and his wife that his wife's 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 is expected and will recover over 24 hours with antivenom. I would explain that his kidney function needs close monitoring because of TMA, and that he may need temporary dialysis. I would warn him about serum sickness at 1 to 2 weeks and advise returning if he develops fever, joint pains or a rash. I would involve the toxicologist, nephrology, and the retrieval service for transfer to a tertiary centre with ICU and dialysis capability. I would address his anxiety about work and finances and involve the social worker. [1]

Probing questions the examiner would ask

Q: You said this is VICC, not DIC. Explain the distinction and why it matters for management. [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. DIC is a systemic inflammatory process triggered by sepsis, malignancy or an obstetric catastrophe, characterised by microthrombi deposition causing end-organ damage and a consumptive coagulopathy driven by the full cascade. VICC is a toxin-driven defibrination — brown snake venom contains pseutarin C, a prothrombin activator that directly converts prothrombin to thrombin, producing massive consumption of fibrinogen and factors through defibrination and secondary fibrinolysis. There are no microthrombi and no end-organ damage from thrombosis. The management is different: VICC is treated with antivenom and supportive care, not with the DIC paradigm of activated protein C or heparin. 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 what is the evidence base? [1]

A: "One vial of brown snake monovalent antivenom intravenously over 15 to 30 minutes. 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 [1]. The brown snake-specific ASP-14 study confirmed this for brown snake envenomation specifically — one vial is sufficient to neutralise the venom load [2]. The reason is that the actual venom yield 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. Current Australian guidelines do not recommend routine premedication. The Premawardhena 1999 trial 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 [7]. Australian snake antivenom is a purer equine IgG preparation, and prophylactic adrenaline carries its own risks — hypertension, cardiac ischaemia, arrhythmia. The clinical rule is: have adrenaline drawn up and ready at the bedside, but do not give it prophylactically. If a reaction occurs, stop or slow the infusion and give intramuscular adrenaline 0.5 mg as for any anaphylaxis."

Q: When would you give fresh frozen plasma in this patient? [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. The ASP-18 trial showed that FFP after antivenom accelerates correction of the INR at 6 hours [5], but routine FFP exposes the patient to transfusion risk for a coagulopathy that is self-limiting and corrects spontaneously in most patients. The unrecordable INR itself is not dangerous — it is the procedures performed during the coagulopathic window that cause the bleeding."

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 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. 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. The AKI may require dialysis for days to weeks but usually recovers fully."

Q: If this patient had been bitten by a tiger snake instead, how would the management differ? [1]

A: "Tiger snake venom produces VICC (biochemically identical) PLUS neurotoxicity from notexin, a presynaptic PLA2 neurotoxin. The key management difference is the need for close neurological monitoring — I would check for ptosis, external ophthalmoplegia and bulbar weakness every 30 minutes, and measure the vital capacity. If neurotoxicity develops, the patient may need intubation and ventilation for days, because presynaptic neurotoxicity is NOT reversible by antivenom once the nerve terminal is destroyed. Antivenom prevents further destruction but cannot reverse established damage. I would still give one vial of the appropriate monovalent antivenom (tiger snake antivenom, guided by the SVDK), and the coagulopathy management is identical. The additional challenge is the airway and the potential prolonged ICU stay." [1]

Q: This patient lives 45 minutes from the nearest hospital. What advice would you give him for prevention? [1]

A: "I would advise him to: wear thick boots and gaiters when walking through long grass or paddocks, particularly in the warmer months when snakes are active; carry a pressure immobilisation kit (a broad crepe bandage and a splint) in his vehicle and his farm kit, and ensure his wife and farm workers know the technique; keep the grass around the house and sheds short; remove rubbish piles and sheet metal where snakes may shelter; teach his children snake awareness and the first-aid technique; and ensure the local emergency number and the RFDS contact are saved in his phone. I would also advise him that the pressure immobilisation bandage his wife applied was textbook-perfect and almost certainly saved his life by containing the venom until hospital treatment was available." [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 is expected and will recover over 24 hours with 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 temporary dialysis support. 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 address his anxiety about being off work and involve the social worker. 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]

Outcome and follow-up

Mr K receives one vial of brown snake monovalent antivenom at 1600 hours over 20 minutes, with adrenaline drawn up but not needed. No immediate reaction occurs. The pressure immobilisation bandage is removed after the antivenom is infused. [1]

Coagulation monitoring shows the fibrinogen begins to rise at 6 hours (0.3 g/L), the INR becomes recordable at 8 hours (above 5.0), and the INR falls below 2 at 18 hours. The D-dimer remains elevated but is trending down. Platelets fall to a nadir of 45 x 10^9/L on day 2, then begin to recover. [1]

The creatinine rises to 220 micromol/L on day 2, with oliguria (less than 0.5 mL/kg/hour). Nephrology is involved. Mr K is transferred to the tertiary hospital in Melbourne for renal support. He receives three sessions of intermittent haemodialysis on days 3, 5 and 7. The TMA resolves — schistocytes clear from the blood film by day 5, platelets recover to above 150 by day 8, and the creatinine normalises by day 14. [1]

Mr K is discharged on day 16 with normal coagulation, normal renal function and a normal full blood count. He is warned about serum sickness and given a return plan. At the 2-week follow-up he reports mild arthralgia of the knees and wrists with a faint maculopapular rash — consistent with serum sickness. He is given a 5-day course of oral prednisone (30 mg daily, tapering), and the symptoms resolve within 4 days. [1]

At the 6-week follow-up Mr K is well, has returned to farm work, and has purchased pressure immobilisation kits for his vehicle, his motorbike and his wife's car. His GP has been provided with the discharge summary and the serum sickness advice. [1]