Snake Envenomation

Meet the patient

A 30-year-old farmer in monsoon Kerala is brought at dawn with profuse bleeding from his gums and bite site, a swollen right ankle, and dark urine. He was bitten six hours earlier by a snake with a loud hiss. The blood drawn for tests has not clotted at twenty minutes.[1][3]

Across the district, a child is found at sunrise unable to open his eyes or swallow his saliva; he slept on the floor and no bite is visible. Two patients, two families, and one demand on you: recognise the syndrome, run the 20WBCT, and give antivenom for significant envenomation while adrenaline sits drawn up at the bedside. Everything below exists to do exactly that.[1][2]

Two families, one bedside fork

A bite mark alone does not mean envenomation — a dry bite injects no venom in 20 to 50 per cent of cases. Envenomation is declared by systemic or severe local signs, and the family of the snake decides which syndrome you are chasing. Snakebite is a WHO category-A neglected tropical disease and one of the most lethal accidental rural emergencies in South and Southeast Asia, sub-Saharan Africa and Latin America.[1][2]

The clinical skill is threefold: recognise the syndrome — neurotoxic, haemato or cytotoxic, or myotoxic — give specific antivenom promptly for significant envenomation while preparing for anaphylaxis, and support the complications of respiratory failure, acute kidney injury, coagulopathy and compartment syndrome. The single most important process lever is rapid transport to a hospital that holds antivenom.[1][4]

Elapid versus viper — the fork that drives everything

The family sets the syndrome, and the syndrome sets the first aid and the antidote. Elapids are predominantly neurotoxic with little local swelling; vipers are haemato and cytotoxic with immediate local destruction. The discriminator is the local limb and the clotting test.[1]

[1]

The Big Four — and who covers them

The Indian polyvalent antivenom covers the Big Four, and knowing them by syndrome is viva gold. Name the snake and you have named the dying organ and the dose.[1][3]

[1]

Australia carries its own Fab Five — brown snake, tiger snake, taipan, death adder and mulga — covered by the CSL polyvalent antivenom or monovalent antivenoms guided by the venom detection kit. Severity then grades the response: a dry bite or fang marks alone needs no antivenom and 24 hours of observation; moderate envenomation has local swelling beyond the bite site or early systemic features; severe envenomation brings neurotoxicity, a positive 20WBCT, spontaneous bleeding, shock, acute kidney injury, rhabdomyolysis, or rapidly extending local swelling — and antivenom is indicated.[1][2]

How common, and where the deaths fall

Globally the WHO estimates 81,000 to 138,000 deaths and about three times as many amputations or disabilities a year, overwhelmingly in rural agricultural communities. India carries the largest single burden — the nationally representative Million Death Study recorded about 45,000 snakebite deaths a year from 2000 to 2019, highest in Uttar Pradesh, Bihar, Andhra Pradesh, Madhya Pradesh and Odisha, with a marked monsoon peak.[1][3]

[1]

The host and environmental risks cluster usefully: rural agricultural occupation with knee or hand bites during fieldwork; sleeping on the floor or a mat, the classic krait exposure as the snake enters dwellings at night; walking barefoot at night without a light; the monsoon season from June to September when flooding drives snakes indoors; alcohol intoxication, which delays presentation and impairs first aid; and children and low body weight, which raise the venom dose per kilogram and accelerate progression. Vigorous limb movement accelerates systemic absorption through the lymphatics — the mechanistic basis of immobilisation.[1][3]

Four toxins — and why VICC is not DIC

Venom spreads systemically through the lymphatics, which is why the pressure-immobilisation bandage works — it compresses superficial lymphatics and arrests lymph flow for many hours. Venom is not one toxin but a complex mixture, and four dominant classes map to the clinical syndromes.[1][2]

Neurotoxins (predominantly elapid) come in two forms. Postsynaptic alpha-neurotoxins — alpha-bungarotoxin of krait, alpha-cobratoxin — are three-finger proteins that bind the nicotinic acetylcholine receptor at the neuromuscular junction to cause flaccid paralysis; because the receptor is intact, this is at least partially reversible by antivenom and may respond transiently to neostigmine. Presynaptic phospholipase A2 neurotoxins — beta-bungarotoxin of krait, taipoxin — destroy the presynaptic nerve terminal, causing irreversible paralysis that does not respond to antivenom or neostigmine because the terminal must regrow over days to weeks. Krait and Russell's viper venoms carry presynaptic toxins.[1]

Haemotoxins (predominantly viper and Australian elapid) are procoagulant enzymes — prothrombin activators and factor X activators, metalloproteinases and serine proteases — that directly activate the coagulation cascade, generating massive thrombin and consuming fibrinogen and factors V and VIII in a venom-induced consumption coagulopathy. The blood becomes incoagulable, with an unrecordable INR and fibrinogen and a massively elevated D-dimer. Cytotoxins (vipers, spitting cobras) — phospholipase A2, matrix-degrading metalloproteases and the spreading factor hyaluronidase — destroy local skin, subcutaneous tissue and muscle to cause pain, oedema, blistering and necrosis, and massive local oedema within a tight fascial compartment produces compartment syndrome. Myotoxins (sea snakes, Australian elapids, some vipers) — phospholipase A2 — lyse the skeletal-muscle sarcolemma to cause rhabdomyolysis with myoglobinuria, hyperkalaemia and pigment-cast acute kidney injury.[1][2]

Why VICC differs from DIC is a high-yield distinction. Both share an elevated INR and aPTT, a low fibrinogen and a high D-dimer. The difference is that VICC platelets are normal — venom directly activates the clotting cascade without the diffuse platelet consumption and microvascular thrombosis of true DIC. VICC is also self-limited once antivenom halts venom activity, and recovery is by hepatic factor resynthesis; heparin is ineffective and is not given.[1]

The clinical face — read the family

The presentation is dictated by the family, the species, the venom load and the time since bite. Recognise the syndrome and you have chosen the first aid and the antidote.[1]

The elapid neurotoxic syndrome begins 30 minutes to several hours after the bite — krait paralysis may develop overnight after a painless bite. Ptosis is often the first sign, followed by ophthalmoplegia, diplopia and blurred vision, then bulbar palsy with dysarthria, dysphagia and pooling of secretions that heralds airway compromise, then proximal more than distal limb weakness descending to respiratory failure — the killer. Assess the respiratory reserve with single breath count, peak flow and forced vital capacity, and intubate before arrest. Local signs are minimal or absent in kraits and many Australian elapids; cobra bites may show local necrosis and blistering. Sensorium and pupils are typically spared until the terminal event — the patient remains awake while paralysed.[1][2]

The viper haemato or cytotoxic syndrome brings immediate local pain, swelling and tenderness at the bite site, with swelling extending proximally over hours — measure the circumference and mark the leading edge every 15 to 30 minutes — followed by blistering, ecchymosis and necrosis in severe cases. Bleeding from the gums, bite site, haematuria, haemoptysis, haematemesis or melaena, and catastrophic intracranial or intra-abdominal haemorrhage, mark the consumption coagulopathy. Shock follows from hypovolaemia, capillary leak, bleeding and direct cardiotoxicity, and acute kidney injury is classical in Russell's viper. Regional tender lymphadenopathy indicates systemic absorption.[1]

The krait bite is the atypical missed presentation, and it is the one examiners set as a trap. Bites occur at night while the victim sleeps on the floor; the bite is painless with negligible local signs, so the victim often wakes already envenomed. Abdominal pain is a frequent early feature and may be misdiagnosed as an acute abdomen — exploratory laparotomy is harmful and must be avoided. Descending paralysis develops over hours and the airway is the threat; the clues are the ptosis and evolving neurological signs, the nocturnal setting, and the absence of true peritonism.[1][3]

The sea snake and Australian elapid myotoxic syndrome brings generalised muscle pain, tenderness and stiffness within 30 minutes to a few hours, with dark tea or cola-coloured urine from myoglobinuria, hyperkalaemia from muscle lysis that can cause arrhythmia, and rising creatine kinase and creatinine with acute kidney injury. Australian elapids may show a combined neurotoxic, consumption-coagulopathy and rhabdomyolysis picture. The spitting cobra aims a jet of venom at the eyes to cause intense pain, blepharospasm, lacrimation, chemosis and corneal erosions — treat with copious irrigation.[1][2]

The mimics — and the discriminator that ends each

A swollen painful limb is not always snakebite, a flaccid paralysis is not always neurotoxic, and incoagulable blood is not always VICC. The discriminator is the companion signs and the bedside tests.[1]

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The krait abdominal pain versus an acute abdomen is the single most dangerous mimic. The clues are the ptosis and other evolving neurological signs, the nocturnal setting, and the absence of true peritonism; imaging is normal, and laparotomy is harmful.[3]

The bedside assessment — and the 20WBCT

A standardised bedside assessment drives both the severity grade and the antivenom decision. Run ABCDE and the bite site together, then the focused neurological examination, then the clotting test.[1][4]

Assess the airway and breathing with the respiratory rate, oxygen saturation, single breath count, peak flow and forced vital capacity — intubate once the FVC falls below about 12 to 15 mL/kg or secretions pool. Assess the circulation for shock. Examine the bite site for the number and pattern of fang marks, the local pain and swelling, and measure the limb circumference at fixed reference points every 15 to 30 minutes, marking the leading edge of swelling with a time stamp — the rate of proximal extension is a severity marker. Palpate the regional lymph nodes; tender nodes draining the limb indicate systemic absorption.[1]

For evolving paralysis, look for ptosis by asking the patient to sustain upgaze, test the extraocular movements and diplopia, assess the bulbar function through voice quality, swallow, gag and tongue protrusion and the pooling of secretions, grade the limb power with the MRC scale (proximal more than distal), and measure the respiratory reserve. Sensorium and pupils are characteristically preserved in elapid neurotoxicity until the terminal event.[1][2]

[1]

Investigations — confirm and grade

The first-line panel confirms the syndrome and grades its complications. Draw a full blood count — haemoconcentration from capillary leak or a fall with bleeding, platelets normal in VICC, stress leucocytosis — coagulation with PT, INR, aPTT, fibrinogen and D-dimer plus the bedside 20WBCT, urea, creatinine and electrolytes for acute kidney injury and the hyperkalaemia of rhabdomyolysis, creatine kinase which may exceed 10,000 U/L, LFTs, urine dipstick where blood-positive with few or no red cells means myoglobinuria, a blood group and cross-match before antivenom, and an ECG for hyperkalaemia or arrhythmia.[1][2]

The VICC laboratory signature is a markedly prolonged or unrecordable INR, a prolonged aPTT, an unrecordable fibrinogen under 0.5 g/L, a massively elevated D-dimer, and platelets that are usually normal. Once antivenom halts venom activity, the liver resynthesises factors: factor VII, with a half-life of about 6 hours, recovers first so the INR begins to improve within 24 hours, while prothrombin, with a half-life of about 72 hours, recovers last and full normalisation may take 1 to 2 weeks. The INR may therefore remain abnormal for days despite adequate antivenom — this is not treatment failure, and antivenom should not be endlessly repeated for an isolated abnormal INR in a clinically stable patient. The rhabdomyolysis signature is a creatine kinase over 1000 U/L, often over 10,000, with myoglobinuria, hyperkalaemia, hyperphosphataemia, hypocalcaemia and a rising creatinine.[1]

Image selectively: a CT brain for intracranial haemorrhage or altered sensorium with coagulopathy, an abdominal ultrasound for a suspected intra-abdominal bleed, and compartment pressure measurement when compartment syndrome is suspected — a delta pressure, diastolic BP minus compartment pressure, under 30 mmHg. In Australia the venom detection kit on a bite-site swab or urine guides monovalent antivenom; it is not available in India or Africa, where management is clinical and rests on the 20WBCT.[1][2]

First aid — RIGHT, and the actions that harm

[1]

The first-aid mnemonic is RIGHT, and half of it is a list of things you must never do. Reassure the patient, because panic accelerates venom spread. Immobilise the bitten limb with a splint at heart level, because immobility slows lymphatic flow. Get to hospital — rapid transport is the single most important community action. Hold the pressure-immobilisation bandage for elapid and neurotoxic bites, wrapping the entire limb firmly — a finger should slip under — from the bite site proximally with a splint, and do not remove it until hospital, IV access and antivenom are ready. And avoid the toxins people reach for: cutting, sucking, a tourniquet, ice, electric shock, herbal pastes, alcohol, and food or drink in case intubation is needed.[1][4]

[1]

The pressure-immobilisation bandage compresses the lymphatics and delays systemic absorption of both neurotoxin and myotoxin for many hours. If a tourniquet is already in place on arrival, be prepared for sudden envenomation on its removal — have IV access and antivenom ready. Cutting and suction do not remove meaningful venom and introduce infection; ice increases tissue necrosis; and traditional remedies and alcohol delay definitive care.[1][4]

Resuscitation — airway first, then the antivenom

Begin with ABCDE and secure the airway early, because in elapid neurotoxicity the airway is what kills. Establish the airway, give oxygen, secure two large-bore cannulae, take bloods including the 20WBCT and cross-match, and start IV access before removing any pressure-immobilisation bandage — removal can trigger sudden systemic venom release.[1][2]

Watch the single breath count, peak flow and forced vital capacity, and intubate early and electively when bulbar secretions pool or the FVC falls below about 12 to 15 mL/kg. Ventilate — paralysis may last days to weeks with presynaptic toxins, and this is the single most life-saving supportive measure after antivenom. Neostigmine with atropine may transiently improve postsynaptic cobra neurotoxicity while antivenom works, but it does not help presynaptic krait paralysis. For shock give IV crystalloid boluses of 10 to 15 mL/kg, reassessing, add noradrenaline if fluid-refractory, and transfuse blood for anaemia from haemorrhage once antivenom is running.[1]

Antivenom — the definitive therapy

Specific antivenom is indicated only for significant envenomation, not for a dry bite or trivial local signs — giving it for a dry bite exposes the patient to anaphylaxis for no benefit. The indications are any one of haematotoxicity — a positive 20WBCT, spontaneous bleeding, or unequivocal VICC on laboratory coagulation — neurotoxicity with ptosis, ophthalmoplegia, bulbar palsy or any weakness progressing to respiratory compromise, cardiovascular toxicity with shock or arrhythmia, renal toxicity with acute kidney injury or haematuria or myoglobinuria, myotoxicity with a raised creatine kinase or dark urine, and severe local envenomation with swelling extending beyond the bite site, blistering or necrosis.[1][2]

The Indian polyvalent antivenom is raised in horses and active against the Big Four. Reconstitute each 10 mL vial of lyophilised powder in 10 mL of sterile water for injection by gentle rolling to avoid foaming, then dilute the total dose in normal saline. Give an initial 8 to 10 vials IV over an hour as soon as an indication is met — the dose is the same in adults and children, because antivenom neutralises a fixed venom load, not body weight, and under-dosing children is a classic error. Reassess the 20WBCT and coagulation at 6 hours; if VICC persists, repeat 5 to 10 vials, and continue to reassess every 6 hours while watching for recurrent VICC over the next 24 to 48 hours. If paralysis is progressing despite two doses, particularly from presynaptic krait toxins, antivenom may have limited efficacy and the priority shifts to ventilation.[1][3]

Prepare for anaphylaxis before you start the infusion, every time. Early anaphylactic or anaphylactoid reactions — urticaria, pruritus, hypotension, bronchospasm, angioedema, vomiting — occur in 10 to 40 per cent of Indian whole-IgG recipients within minutes to hours; pyrogenic endotoxin reactions bring fever and rigors; and late serum sickness at 5 to 14 days brings fever, arthralgia and urticaria. Before starting, have adrenaline drawn up, oxygen and IV fluids running, a doctor at the bedside, and resuscitation equipment ready.[1][5]

When anaphylaxis strikes, stop or slow the infusion and give IM adrenaline 0.5 mg — 0.5 mL of 1 in 1000 — into the anterolateral mid-thigh, repeated every 5 minutes as needed, with high-flow oxygen, an IV crystalloid bolus of 10 to 15 mL/kg, IV hydrocortisone 200 mg and chlorphenamine 10 mg. Once the patient is stable, resume the antivenom cautiously at a slower rate — the indication has not disappeared, and untreated envenomation is more dangerous than a controlled reaction. The Habib 2011 meta-analysis found that premedication with adrenaline, antihistamine or hydrocortisone modestly reduced early reactions, particularly with lower-quality antivenoms; many Indian centres do not routinely premedicate but always have adrenaline ready, and the move to purified Fab and F(ab')2 fragment antivenoms is lowering reaction rates.[1][2][5]

Supportive care — the measures that save after the antivenom

Ventilation, dialysis, blood products and the timing of surgery are where snakebite is won or lost after the antivenom. Ventilation for respiratory failure is often needed for days to weeks and is the life-saving measure after antivenom. Haemodialysis is reserved for established acute kidney injury with refractory hyperkalaemia, acidosis, fluid overload or uraemia.[1]

Give blood products only after antivenom — cryoprecipitate for fibrinogen and fresh-frozen plasma for factors, with packed red cells for anaemia — because giving them before antivenom is futile: ongoing venom consumes the new factors as fast as you infuse them. Give tetanus prophylaxis if not immune, antibiotics only for secondary wound infection (most bites are not initially infected; consider Staphylococcus, Streptococcus and Gram-negatives, including in sea-snake bites), and surgical debridement of frankly necrotic tissue once coagulopathy is corrected.[1][4]

Fasciotomy for compartment syndrome comes only after coagulopathy has been corrected with antivenom and blood products. Operating on an incoagulable patient is catastrophic; the indication is a confirmed compartment syndrome — a clinically tight compartment with neurovascular compromise, or a delta pressure under 30 mmHg — that persists after haematological stabilisation. Add wound care and physiotherapy to prevent contracture. Neostigmine 0.5 to 2.5 mg IV with atropine 0.6 mg IV, always given with atropine to prevent bradycardia and excess secretions, can transiently improve postsynaptic cobra weakness by raising synaptic acetylcholine; it does not work for presynaptic krait or Russell's toxins, where the priority is ventilation.[1]

Subtypes that change the plan

The krait, Russell's, saw-scaled, cobra, sea-snake and spitting-cobra subtypes each pivot the algorithm. Name the snake and the dominant syndrome.[3]

The common krait bites at night while the victim sleeps on the floor, painlessly, so the victim often wakes already envenomed with descending paralysis and prominent abdominal pain. The pressure-immobilisation bandage is essential and rapid transport matters; antivenom efficacy is limited by presynaptic beta-bungarotoxin, so ventilation is the life-saver and recovery may take weeks. Russell's viper is the most lethal Indian viper — consumption coagulopathy with a positive 20WBCT and bleeding, acute kidney injury from direct nephrotoxicity with capillary leak and hypovolaemia, shock, anterior pituitary haemorrhage causing a Sheehan-like hypopituitarism, and rarely presynaptic neurotoxicity, with monsoon clustering and a characteristic loud hiss. Saw-scaled viper is small with a large venom yield per body weight, causing consumption coagulopathy, local swelling and bleeding with significant case fatality from haemorrhage.[1][2]

The Indian cobra causes local necrosis at the bite site plus postsynaptic neurotoxicity — ptosis, ophthalmoplegia, bulbar and respiratory paralysis — and neostigmine-atropine may transiently help while antivenom works, with a pressure-immobilisation bandage useful. Spitting-cobra venom ophthalmia is treated with copious irrigation with water or saline for 10 to 15 minutes, topical local anaesthetic and antibiotic, and ophthalmology referral — do not instil antivenom into the eye. The sea snake and Australian elapid bite mandates a pressure-immobilisation bandage and brings a combined neurotoxic, consumption-coagulopathy and rhabdomyolysis picture with dark urine, hyperkalaemia and acute kidney injury; give monovalent or polyvalent CSL antivenom guided by the venom detection kit where available, with supportive ventilation and dialysis.[1]

The preventable deaths — pitfalls that recur

The recurring failures trace to a short list, and most are preventable. Giving antivenom for a dry bite exposes the patient to anaphylaxis for no benefit, while not giving it when indicated — waiting too long for absolute proof while the patient deteriorates — is the other face of the same error. Fasciotomy before correcting coagulopathy causes catastrophic bleeding, and tourniquet harm causes ischaemia, reperfusion and worsened necrosis.[1][4]

Relying on a single 20WBCT misses coagulopathy that develops later — repeat at 6 hours — and missing delayed or recurrent VICC at 24 to 48 hours sends a stabilised patient backwards. Missing a krait bite because of absent local signs is the classic cognitive error: a paralysis with a clean limb, a nocturnal history and abdominal pain is krait envenomation until proven otherwise. Oral suction or incision of the bite site and exploratory laparotomy for krait abdominal pain close the list of harmful interventions.[1]

Prognosis and disposition

Time to antivenom is the strongest predictor of death — earlier is better — alongside time to hospital and to ventilation for neurotoxicity. Russell's viper and krait carry high mortality, children receive more venom per kilogram, and the elderly, malnourished, pregnant and those with renal or cardiac disease do worse.[1][3]

Disposition follows severity: ICU for neurotoxicity needing ventilation, shock, severe acute kidney injury needing dialysis, severe VICC with bleeding, and severe local envenomation or compartment syndrome; the ward for moderate envenomation under observation and post-antivenom stabilisation. Discharge only when the patient is asymptomatic, the 20WBCT and coagulation are stable and improving over at least 24 hours, renal function is stable, and the wound is healing — and counsel the patient to return for serum sickness at 5 to 14 days with fever, rash and joint pain. Reinforce community advice on footwear, lighting at night, sleeping off the floor, and rapid transport.[1]

Special populations

Children receive a higher venom dose per kilogram, so they progress faster and more severely — and the antivenom dose is the same adult vial count, because it neutralises a fixed venom load. Under-dosing children is a classic error. Give weight-based fluid boluses of 10 to 20 mL/kg for shock with reassessment, monitor the work of breathing continuously, and prepare for early intubation; for a neostigmine trial in postsynaptic elapid toxicity use neostigmine 0.025 to 0.1 mg/kg with atropine 0.02 mg/kg. Avoid IM injections when the patient is coagulopathic.[1][3]

In pregnancy the risks are miscarriage, preterm labour, placental abruption from coagulopathy, and fetal distress from maternal hypoxia or shock — do not withhold antivenom when indicated, because maternal stabilisation is fetal stabilisation and the benefit exceeds the theoretical fetal risk. Monitor with cardiotocography when gestation allows, involve obstetrics early, and give Anti-D if indicated. The elderly and comorbid have reduced respiratory and renal reserve and higher mortality from VICC, AKI and aspiration during paralysis; use cautious fluids if heart failure risk and plan dialysis early after Russell's viper envenoming. In remote rural tropical settings most deaths occur before hospital arrival, so prevention — footwear, a torch at night, sleeping on a raised bed, reducing rodent attractants — and a health system with rapid transport, uninterrupted antivenom supply, staff trained in the 20WBCT and airway, and partnership with traditional healers for early referral are the priorities.[1][3]

Evidence, guidelines, and regional practice

The WHO classifies snakebite as a category-A neglected tropical disease and the 2019 guidelines endorse the 20WBCT, polyvalent antivenom, the pressure-immobilisation bandage for elapids, and the avoidance of harmful first aid. The Indian national protocol — the ASI and National Snakebite Initiative — uses polyvalent antivenom 8 to 10 vials IV as the initial dose in VICC repeated per 20WBCT, the 20WBCT as the bedside test, avoidance of tourniquet incision and suction, and hospital-based stocking; snakebite is a notifiable condition in several Indian states.[1][3]

The Australian approach uses monovalent or polyvalent CSL antivenom guided by the venom detection kit on a bite-site swab or urine, a pressure-immobilisation bandage for all suspected Australian snakebites because all Australian elapids are neurotoxic, and lower reaction rates with highly purified antivenoms. The live controversies are premedication before antivenom — the Habib meta-analysis shows a modest reduction in early reactions, increasingly considered where low-purity antivenom is used — low-dose versus high-dose antivenom, with randomised trials from Sri Lanka and India suggesting lower initial doses may be as effective with fewer reactions, the move to Fab and F(ab')2 fragment antivenoms that are purer and faster-distributing, and prehospital antivenom, which is generally not recommended except in carefully resourced remote settings.[1][5]

[1] [2]

Ward-round test — four stems

Stem 1 — the farmer with bleeding gums and incoagulable blood (answer)

A 30-year-old farmer in monsoon Kerala has bleeding gums, a swollen ankle, dark urine, and blood that has not clotted at 20 minutes after a Russell's viper bite. What is the bedside test, the antivenom dose, and the timing of blood products? Model: The 20WBCT is positive — incoagulable blood at 20 minutes in a glass tube means venom-induced consumption coagulopathy, and the normal platelet count distinguishes it from DIC. Give Indian polyvalent antivenom 8 to 10 vials IV over an hour, the same dose whatever the body weight, with adrenaline drawn up at the bedside because anaphylaxis occurs in 10 to 40 per cent. Reassess the 20WBCT and coagulation at 6 hours and repeat 5 to 10 vials if VICC persists. Give cryoprecipitate and fresh-frozen plasma only AFTER antivenom — giving them before is futile because ongoing venom consumes the new factors. Watch the renal function — Russell's viper classically causes acute kidney injury — and arrange dialysis for refractory hyperkalaemia, acidosis or uraemia.[1][3]

Stem 2 — the child who wakes paralysed (answer)

A child is found at sunrise unable to open his eyes or swallow his saliva; he slept on the floor and no bite is visible. What is the diagnosis, the threat, and the priority? Model: This is a common krait bite — painless and nocturnal while sleeping on the floor, so the child wakes already envenomed with descending flaccid paralysis (ptosis, ophthalmoplegia, bulbar palsy). The threat is respiratory failure from progressive paralysis, and the priority is early intubation and ventilation — assess with single breath count, peak flow and FVC and intubate before arrest. Give polyvalent antivenom 8 to 10 vials IV over an hour, but know that krait presynaptic beta-bungarotoxin makes antivenom efficacy limited, so ventilation is the life-saver and recovery may take weeks. The abdominal pain, if present, is not peritonism — do not send this child to theatre.[1][3]

Stem 3 — anaphylaxis during the antivenom infusion (answer)

Ten minutes into the antivenom infusion a patient develops urticaria, wheeze and hypotension. What do you do, and do you abandon the antivenom? Model: This is an early anaphylactoid reaction to the horse whole-IgG antivenom. Stop or slow the infusion immediately, give IM adrenaline 0.5 mg (0.5 mL of 1 in 1000) into the anterolateral mid-thigh repeated every 5 minutes as needed, high-flow oxygen, an IV crystalloid bolus of 10 to 15 mL/kg, IV hydrocortisone 200 mg and chlorphenamine 10 mg. Do NOT abandon the antivenom — the indication has not disappeared and untreated envenomation is more dangerous than a controlled reaction. Once the patient is stable, resume the antivenom cautiously at a slower rate, and counsel the patient about serum sickness at 5 to 14 days.[1][5]

Stem 4 — a tense, swollen calf and incoagulable blood (answer)

Twelve hours after a viper bite a patient has a tense, swollen calf with pain on passive stretch, paraesthesia, and a positive 20WBCT. What is the complication, and what is the trap in its management? Model: This is compartment syndrome from massive local cytotoxic oedema within a tight fascial compartment. The trap is operating before the coagulopathy is corrected — fasciotomy on an incoagulable patient causes catastrophic bleeding. First give antivenom 8 to 10 vials IV and correct the coagulopathy with cryoprecipitate and fresh-frozen plasma, then confirm the compartment syndrome with a delta pressure (diastolic BP minus compartment pressure) under 30 mmHg, and only then perform the fasciotomy. Continue antivenom per 20WBCT, give antibiotics for secondary infection, and arrange surgical debridement of any frankly necrotic tissue once the blood clots.[1][4]

References

1. [1]Gutiérrez JM, Calvete JJ, Habib AG, et al. Snakebite envenoming Nat Rev Dis Primers, 2017.PMID 28980622
2. [2]Seifert SA, Armitage JO, Sanchez EE Snake Envenomation N Engl J Med, 2022.PMID 34986287
3. [3]Suraweera W, Warrell D, Whitaker R, Menon G, Rodrigues R, Fu SH, et al. Trends in snakebite deaths in India from 2000 to 2019 in a nationally representative mortality study Elife, 2020.PMID 32633232
4. [4]Russell JJ, Schoenbrunner A, Janis JE Snake Bite Management: A Scoping Review of the Literature Plast Reconstr Surg Glob Open, 2021.PMID 33936914
5. [5]Habib AG Effect of pre-medication on early adverse reactions following antivenom use in snakebite: a systematic review and meta-analysis Drug Saf, 2011.PMID 21879781