Neurotoxic Envenomation
Definition
Venom-induced paralysis from blockade of the neuromuscular junction. The Indian cobra produces post-synaptic blockade through alpha-neurotoxins binding the acetylcholine receptor. The common krait produces pre-synaptic blockade through beta-bungarotoxin, which is harder to reverse with antivenom once paralysis is established.
- Mechanism
- Neuromuscular junction blockade
- Indian cobra
- Post-synaptic block via alpha-neurotoxins
- Common krait
- Pre-synaptic block via beta-bungarotoxin
- Clinical note
- Krait paralysis harder to reverse once established
Common questions
Why is krait envenomation harder to treat once paralysis sets in?+
Pre-synaptic beta-bungarotoxin damages the nerve terminal itself, so antivenom cannot reverse an already-established block, unlike the more reversible post-synaptic cobra mechanism.
Why does distinguishing cobra from krait bite matter forensically?+
The differing mechanisms affect antivenom timing and prognosis, and combining clinical presentation with bite-site or circumstantial evidence helps establish which species was responsible.
Related terms
- 20WBCT
- Twenty minute whole blood clotting test. A few millilitres of fresh venous blood are placed in a clean dry glass tube, left...
- Autonomic Storm
- The biphasic cardiovascular crisis of Indian red scorpion envenomation. An initial cholinergic phase of vomiting, salivation and bradycardia is followed by an...
- The Big Four
- The four Indian snake species responsible for the bulk of medically significant envenomation: Naja naja (Indian cobra), Bungarus caeruleus (common krait), Daboia...
- Venom ELISA
- An enzyme-linked immunosorbent assay in which species-specific anti-venom antibodies are used to detect residual venom antigen in serum, urine, bite-site exudate or...
- VICC
- Venom-induced consumption coagulopathy, the haemotoxic syndrome of Russell's viper and saw-scaled viper bites in which the venom activates coagulation factors, consumes fibrinogen...