Russell's viper bite with incoagulable blood and no on-site blood bank
A 42-year-old farmer is brought to a rural hospital 2 hours after being bitten on the right ankle while working in paddy fields in the dry zone. He has vomited once and complains of abdominal pain. BP is 92/60 mmHg, pulse 120/min, and blood is continuing to ooze from the fang marks and from his gums. A 20-minute whole blood clotting test performed on arrival shows blood that has still not clotted at 20 minutes. Platelets are 90,000/µL, haemoglobin 11.8 g/dL and creatinine 1.4 mg/dL. His urine is dark, and he has passed only 20 mL in the last 2 hours. The hospital stocks 10 vials of polyvalent antivenom, has no blood bank on site, and the regional blood bank is 90 minutes away.
1. Interpret the 20-minute whole blood clotting test and state your immediate management.
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A 20-minute whole blood clotting test in which the blood remains liquid at 20 minutes is a bedside surrogate for venom-induced consumptive coagulopathy. Together with continued bleeding from the bite site and gums, hypotension, tachycardia, abdominal pain and dark oliguric urine, this is systemic envenoming with coagulopathy and early hypotension - in this geographical setting, most consistent with Russell's viper envenoming. Do not wait for a coagulation profile or fibrinogen result; the bedside test is sufficient to act.
Give polyvalent antivenom immediately, using the current national protocol dose - in adult practice this is typically an initial 10 vials diluted in 0.9% sodium chloride and infused over about one hour; confirm the exact dose and dilution against the current Sri Lankan national snakebite guideline. Antivenom neutralises circulating venom but does not reverse coagulopathy already established, so the endpoint is a clotting 20-minute whole blood clotting test at 6 hours, not an immediate change. If the test remains incoagulable at 6 hours, repeat the antivenom dose.
Simultaneously secure two large-bore intravenous lines, take blood for cross-match and send it with the request to the regional blood bank, and treat hypotension with cautious crystalloid - venom-induced capillary leak and myocardial depression mean careless large-volume filling can cause pulmonary oedema.
2. Antivenom is the only specific treatment available on site. How do you anticipate and manage an early reaction, and which common interventions must you avoid?
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Early anaphylactoid reactions to antivenom are common and are not true IgE-mediated allergy. Anticipate them in every patient: keep adrenaline 1:1000, hydrocortisone, chlorphenamine, oxygen and suction at the bedside before the infusion begins, and infuse with the patient fully monitored.
If urticaria, cough, wheeze, flushing, hypotension or angioedema develop, stop or slow the infusion, give intramuscular adrenaline 0.5 mg into the anterolateral thigh for systemic features, give oxygen and a fluid bolus, and add hydrocortisone and chlorphenamine. Once the reaction is controlled, restart the antivenom slowly, because the venom is still circulating and abandoning antivenom altogether leaves the coagulopathy untreated; observe closely.
Avoid intramuscular injections other than adrenaline for a reaction - they cause haematoma in a coagulopathic patient and are poorly absorbed. Avoid aspirin, NSAIDs and other antiplatelet drugs for pain; use paracetamol. Do not give prophylactic fresh frozen plasma or platelets simply because the clotting test is abnormal - blood products are for active bleeding with haemodynamic compromise or a falling haemoglobin, or before surgery, and prophylactic use can worsen the coagulopathy. Avoid immediate surgical debridement or fasciotomy at the bite site; the coagulopathy must be corrected first, and swelling alone is not compartment syndrome. Also avoid using the clotting test result to withhold antivenom in a patient who is clearly envenomed.
3. Outline your monitoring and supportive plan for the next 24 hours, including how you will handle the renal risk.
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This patient has three overlapping problems: coagulopathy, hypotension and early acute kidney injury with dark urine. Monitor hourly pulse, blood pressure, respiratory rate, oxygen saturation and urine output, with a strict fluid balance chart. Aim for a urine output of at least 0.5–1 mL/kg/h. Use crystalloid cautiously to correct hypovolaemia, reassessing after each bolus for basal crepitations and falling saturation, because both venom and fluid overload can cause pulmonary oedema.
Dark urine with oliguria suggests haemoglobinuria or myoglobinuria from venom-induced haemolysis or muscle damage, and the creatinine of 1.4 mg/dL indicates the kidney is already affected. Maintain perfusion and urine output rather than forcing high-volume fluids; if oliguria persists despite adequate filling, transfer to a centre with dialysis capability. Recheck haemoglobin, creatinine, potassium and the 20-minute whole blood clotting test at 6 hours and then at least twice daily. Transfuse if there is active bleeding with a falling haemoglobin, using the cross-matched units from the regional blood bank and keeping the transfer option open.
Reassess the bitten limb for progressive swelling, pain and neurovascular compromise, but remember that swelling is expected and does not by itself mandate fasciotomy. Document tetanus prophylaxis (give toxoid, not into a bleeding muscle if avoidable) and arrange follow-up for delayed coagulopathy or serum sickness, which can appear 5–10 days after antivenom.