Neuromuscular transmission failure due to common krait (Bungarus caeruleus) envenomation

Neurophysiological studies were performed in 12 patients with neuromuscular paralysis due to envenomation by the common krait (Bungarus caeruleus). All patients presented with an acute, reversible, oculofaciobulbar paresis. In addition, 7 patients had weakness of the limb muscles and 4 required assisted mechanical ventilation. Neurophysiological abnormalities included: (1) a reduction in the amplitude of the median-elicited compound muscle action potential (CMAP) in 4 patients; and (2) a decremental response (>10%) to 3-Hz repetitive nerve stimulation (RNS) in 4 patients. With 1 exception, these abnormalities were noted only in clinically weak muscles. The administration of edrophonium to 6 patients produced an insignificant increase in CMAP amplitudes as well as partial (not significant) improvement in the decremental response to 3-Hz RNS. Neurophysiological studies were performed in 2 patients before and after the administration of 20 mL of polyvalent antivenom. A decrease in amplitude of the median-elicited CMAP amplitude occurred after the administration of antivenom. In 1 patient, administered 100 mL of antivenom, the median-elicited CMAP amplitude increased and the decrement to 3-Hz RNS decreased. Neurophysiological studies can provide useful information regarding the nature, severity, and therapy of the neuroparalytic syndrome of krait envenomation.