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 6 wk and 6-9 mth post-bite.

Principal findings: There were 33 patients enrolled (median age 35 y; 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 20-32 h. 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 3.5 h post-bite (2.8-7.2 h), which cleared unbound venom from blood. Despite this, the paralysis worsened requiring intubation and ventilation within 7 h post-bite. sfEMG showed markedly increased jitter and neuromuscular blocks within 12 h. sfEMG abnormalities gradually improved over 24 h, 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 96 h post-bite (54-216 h). On discharge, median 8 days (4-12 days) post-bite, patients were clinically normal but had mild sfEMG abnormalities which persisted at 6 wk post-bite. There were no clinical or neurophysiological abnormalities at 6-9 mth.

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.

Fig 1. Common krait.

An adult common krait (Bungarus caeruleus) specimen, 92.5 cm in total length, that caused severe neuromuscular paralysis.

Fig 2. Time related change of neuromuscular paralysis.

A, Noodle plot showing the evolution of paralysis in 14 patients with severe neurotoxicity. Note the pre-antivenom events are in red; B, Scatter plots of the time taken for the complete resolution of five major clinical effects of neurotoxicity (muscle groups), including ptosis, diplopia, external ophthalmoplegia, facial weakness, upper limb weakness and lower limb weakness in the 17 patients with severe neuromuscular paralysis.

Fig 3. Superimposed and non-superimposed sfEMG recordings of the orbicularis oculi muscle of patients following krait bites.

A, recordings of a patient on admission with no neurotoxicity indicating the normal jitter (14.5μs) and no blocks; B, high jitter (61.6μs) with intermittent blocks seen in a patient on admission with severe neuromuscular paralysis. (The distance between two dots represents 200μV vertically and 3ms horizontally.)

Fig 4. sfEMG jitter comparison across no, mild and severe neurotoxicity groups.

Scatter plots of the median MCD in jitter of the three groups of patients with common krait bites on admission (A) and 6–12 hours after the bite (B) compared to the median MCD in jitter values of normal subjects. Median and interquartile range is shown for each group in the graph. On both occasions, the severe neurotoxicity group has significantly high median jitter compared to the normal subjects (P<0.0001; one-way ANOVA followed by multiple comparison test).

Fig 5. Time related change of sfEMG jitter and blocks in patients developed severe neurotoxicity.

A, Scatter plots showing the time related change of the median MCD in jitter of the 17 patients with severe neurotoxicity, compared to normal subjects. Note the high median of the MCD in jitter values seen even at 6 weeks after the snakebite, compared to the normal subjects; B, scatter plots showing time related changes in the percentage of recorded fibres with neuromuscular blocks in these patients at the same times. Neuromuscular blocks are still present 6 weeks after the snakebite.

Fig 6. Serum venom concentrations of 9 patients with pre-antivenom blood samples, in relation to the time of initiation of the antivenom therapy.

Pre-antivenom venom concentrations are indicated by filled black circles and post-antivenom concentrations by filled red circles.