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Forensic Medicine & Toxicology · 4 min read

Snake Bite in India: The Big Four, the 20WBCT and Antivenom

Snake Bite in India: The Big Four, the 20WBCT and Antivenom
All notes

Snake bite is a notifiable cause of death in much of India and a guaranteed examination topic. The whole subject becomes manageable once you organise it around two syndromes rather than four species.

At a glance — the Big Four

Snake Family Syndrome
Indian cobra (Naja naja) Elapid Neurotoxic, with local necrosis
Common krait (Bungarus caeruleus) Elapid Neurotoxic, minimal local signs
Russell’s viper (Daboia russelii) Viper Vasculotoxic, coagulopathy, kidney injury
Saw-scaled viper (Echis carinatus) Viper Vasculotoxic, severe bleeding

Neurotoxic envenomation

Elapid venom blocks neuromuscular transmission. The clinical sequence is remarkably consistent: ptosis first, then ophthalmoplegia and a broken-neck sign, then bulbar weakness with pooling of secretions and an inability to swallow, then respiratory muscle paralysis. Consciousness is preserved throughout — a paralysed patient is often fully aware.

The krait is the classic trap. Its bite is often painless, happens at night to someone sleeping on the floor, and leaves almost no local mark. The patient wakes in the early hours with severe abdominal pain, then develops ptosis and weakness. Any young patient with unexplained early-morning paralysis in an endemic area is a krait bite until proven otherwise.

Vasculotoxic envenomation

Viper venom causes local swelling, blistering, bruising and necrosis, plus a consumption coagulopathy with spontaneous bleeding from gums, old venepuncture sites and into the urine. Russell’s viper additionally causes acute kidney injury, capillary leak with hypotension, and — a favourite examination detail — anterior pituitary infarction producing a Sheehan-like syndrome months later.

The 20-minute whole blood clotting test (20WBCT)

Place a few millilitres of fresh venous blood in a clean, dry glass test tube, leave it undisturbed at room temperature for 20 minutes, then tip it once. If the blood is still liquid, coagulopathy is present and antivenom is indicated. It must be a glass tube; plastic does not activate the contact pathway. Repeat six-hourly to guide further doses.

First aid — what to do and what never to do

  • Do: reassure the patient, immobilise the bitten limb in a splint at heart level, remove rings and tight clothing, and transport to hospital urgently.
  • Do not: apply an arterial tourniquet, incise or suck the wound, apply ice or chemicals, or attempt to catch the snake. Photograph it from a safe distance if it is already dead.

Antivenom

Indian polyvalent antivenom covers all four species. Give it when there are signs of systemic envenomation — neurological features, a positive 20WBCT, spontaneous bleeding, rapidly progressive local swelling, or renal impairment. Bites without any of these do not need antivenom, and roughly a third of bites are “dry”.

Have adrenaline drawn up before starting the infusion; anaphylactic and pyrogenic reactions are common and are treated with adrenaline, not by abandoning the antivenom. Repeat doses are guided by re-testing coagulation and by clinical progress.

Neostigmine with atropine helps in cobra envenomation because cobra neurotoxin acts postsynaptically and is competitively displaceable. It does not help in krait envenomation, where the toxin acts presynaptically and destroys the release apparatus — those patients simply need ventilation until new nerve terminals form.

Last-minute checklist

  • Ptosis is the earliest neurotoxic sign.
  • Painless nocturnal bite with morning abdominal pain equals krait.
  • 20WBCT needs a glass tube and 20 undisturbed minutes.
  • Antivenom for systemic envenomation only; adrenaline ready first.
  • Neostigmine works for cobra (postsynaptic), not krait (presynaptic).

Frequently asked questions

Why must the 20WBCT use a glass tube?

Glass activates factor XII and the contact pathway, which is what makes normal blood clot within 20 minutes. Plastic does not, so a plastic tube gives a false positive in a patient with normal clotting.

Why does neostigmine help in cobra but not krait bite?

Cobra neurotoxin competes with acetylcholine at the postsynaptic receptor, so raising acetylcholine levels can outcompete it. Krait toxin acts presynaptically and prevents release altogether, so there is no acetylcholine to raise.

Should a tourniquet be applied after a snake bite?

No. Arterial tourniquets cause limb ischaemia, and their sudden release can deliver a bolus of venom into the circulation. Splinting and immobilisation without constriction is the recommended approach.

References

  • National Snakebite Management Protocol (India), current edition.
  • World Health Organization guidelines for the management of snakebites, South-East Asia Region.
  • Reddy KSN. The Essentials of Forensic Medicine and Toxicology.

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