Neuromuscular Effects of Common Krait ( Bungarus caeruleus) Envenoming in Sri Lanka

Abstract

Objective

We aimed to investigate neurophysiological and clinical effects of common krait envenoming, including the time course and treatment response.

Methodology

Patients with definite common krait ( Bungarus caeruleus) bites were recruited from a Sri Lankan hospital. All patients had serial neurological examinations and stimulated concentric needle single-fibre electromyography (sfEMG) of orbicularis oculi in hospital at 6wk and 6–9mth post-bite.

Principal Findings

There were 33 patients enrolled (median age 35y; 24 males). Eight did not develop neurotoxicity and had normal sfEMG. Eight had mild neurotoxicity with ptosis, normal sfEMG; six received antivenom and all recovered within 20–32h. Seventeen patients developed severe neurotoxicity with rapidly descending paralysis, from ptosis to complete ophthalmoplegia, facial, bulbar and neck weakness. All 17 received Indian polyvalent antivenom a median 3.5h post-bite (2.8–7.2h), which cleared unbound venom from blood. Despite this, the paralysis worsened requiring intubation and ventilation within 7h post-bite. sfEMG showed markedly increased jitter and neuromuscular blocks within 12h. sfEMG abnormalities gradually improved over 24h, corresponding with clinical recovery. Muscle recovery occurred in ascending order. Myotoxicity was not evident, clinically or biochemically, in any of the patients. Patients were extubated a median 96h post-bite (54–216h). On discharge, median 8 days (4–12days) post-bite, patients were clinically normal but had mild sfEMG abnormalities which persisted at 6wk post-bite. There were no clinical or neurophysiological abnormalities at 6–9mth.

Conclusions

Common krait envenoming causes rapid onset severe neuromuscular paralysis which takes days to recover clinically consistent with sfEMG. Subclinical neuromuscular dysfunction lasts weeks but was not permanent. Antivenom effectively cleared venom but did not prevent worsening or reverse neuromuscular paralysis.

Author Summary

Common krait bites cause muscular paralysis due to the venom disrupting communication between the nerves and muscles. This becomes life-threatening for the patient if there is paralysis of the muscles used for breathing. We studied the severity of paralysis, long term effects and the value of antivenom treatment in authenticated Indian krait bite patients from Sri Lanka. In addition to standard treatment with antivenom, the patients had single-fibre electromyography done, a sensitive neurophysiological test that detects the abnormalities of communication between the nerves and muscles. Half of the patients had severe paralysis and required mechanical ventilation, and the remainder had mild or no effects. Antivenom was given to all patients with severe paralysis and most with mild effects. However, despite antivenom binding all free venom after it was administered, it did not prevent or reverse already developed paralysis. Clinically evident paralysis resolved after a few days, but the neurophysiological abnormalities lasted for weeks. No permanent neurological damages were noted at 6 to 9 months after the snake bite.