Fig 1.
An adult common krait (Bungarus caeruleus) specimen, 92.5 cm in total length, that caused severe neuromuscular paralysis.
Table 1.
Demographic features of 33 definite Indian Krait bite patients.
Table 2.
Comparison of the clinical effects and treatment of the patients who developed no neurotoxicity, mild neurotoxicity and severe neurotoxicity following common krait envenoming.
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.