Neurotoxic snake envenomation — DTM&H MCQ

Correct answer: B — Neurotoxic (elapid) envenomation

The correct answer is B, neurotoxic (elapid) envenomation. In India, elapids (cobras and kraits) produce descending flaccid paralysis with ptosis, dysarthria, and respiratory muscle weakness developing over hours, without significant local swelling, pain, or necrosis at the bite site. This pattern reflects pre and post synaptic neuromuscular blockade rather than tissue-destructive venom components. The absence of local swelling or necrosis argues strongly against a viper bite, and the progressive bulbar and respiratory involvement is the hallmark of elapid neurotoxicity requiring urgent antivenom and ventilatory support. Why the other options are wrong: A. Cytotoxic (viperid) envenomation: Viper bites typically cause marked local swelling, pain, blistering, and necrosis at the bite site plus coagulopathy, none of which are present here. C. Haemotoxic envenomation: This causes systemic bleeding, incoagulable blood, and often local swelling from vascular damage, not isolated cranial nerve and respiratory signs. E. Myotoxic envenomation: Myotoxicity (seen with some sea snakes and Russell's viper) produces muscle pain, tenderness, and myoglobinuria (dark urine) rather than ptosis and dysarthria, which are neurological, not myopathic, signs. D. Non-venomous bite: A non-venomous bite would not produce progressive systemic neurological deterioration; the evolving ptosis, dysarthria, and respiratory weakness confirm true envenomation. Key point: Progressive ptosis, dysarthria, and respiratory weakness without local tissue damage after an Indian snakebite indicates elapid (cobra or krait) neurotoxic envenomation, demanding urgent antivenom and airway/ventilatory support.

Reference: WHO Regional Office for South-East Asia, Guidelines for the Management of Snakebites, 2nd Edition, 2016: sections on clinical features of elapid (neurotoxic) envenoming versus viperid (cytotoxic/haemotoxic) envenoming.