The Common Krait (Bungarus caeruleus) is active at night and its bite may not be noticed. There is little local reaction but paralysis occurs quickly. Mortality of untreated cases may be as high as 70%.
Thirty-three patients with confirmed envenoming by the Common Krait were subject to detailed and repeated neurological examination and stimulated EMG jitter determination by concentric needle electrode in Orbicularis oculi.
Descending paralysis progresses from ptosis, ophthalmoplegia, facial, bulbar and neck weakness and respiratory failure. The full syndrome developed in 17/33. Eight patients showed no neurotoxic signs and another 8 showed mild signs only. All those with severe toxicity received anti-venom serum within a median of 3.5 hours after the bite which cleared unbound venom from the serum but did not prevent development of paralysis. Blood samples from 8 patients before anti-venom serum was given revealed 0.3 - 52.2 ng/ml of venom.
Jitter values were increased at 6-12 hrs with blocking but improvement began after 24-36 hrs. Two patients had complete neuromuscular block lasting 9 and 10.5 hrs. Jitter values were still raised at discharge in 11 patients but paralleled the clinical paralysis.
Recovery began on day 2 and patients were discharged 4 - 12 days post bite. Follow-up at 6 weeks showed residual numbness in the area of the bite and persisting mild jitter abnormalities. They were totally recovered at 6 months.
Anti-venom serum caused severe adverse reactions in 19 of 23 patients and 6 had life threatening anaphylaxis, systolic BP <90 mmHg and SpO2 <92%.
Neuromuscular abnormalities lasting for 6 weeks suggests that the major toxin is β bungarotoxin acting at the presynaptic site of the neuromuscular junction. It causes excess release of ACh and destruction of the presynaptic structures. The venom also contains α bungarotoxin which binds to the ACh receptors.
Universities of Rajarata and Peradeniya, Sri Lanka, Sydney, NSW and Anuradhapura Hospital, Sri Lanka.
