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We report a 12–year old boy, who was
admitted in our hospital with history of snake bite over left side of
pinna, while he was sleeping on the floor in the house during night. Child
was immediately brought to hospital. He had one episode of vomiting on way
to the hospital. On examination, he was drowsy and having insufficient
respiratory efforts. The pulse rate was 56/min, BP was 90/60 mm of Hg and
SPO
2 was 70% with 3L/min O2.
He had ptosis and sluggish deep tendon reflexes with absent plantar. Child
was immediately intubated and kept on ventilator. Polyvalent antisnake
venum and neostigmine were started as per the standard protocol on snake
bite.
Over a period of about 6
hours, child became areflexic. Pupils were dilated and not reacting to
light. Corneal and occulocephalic reflexes were absent. There were no
spontaneous respiratory efforts and apnea test was negative. Ventilatory
support continued despite finding suggestive of brain stem dysfunction.
The child was showing some movements of hands and feet on the next
morning. In the evening, spontaneous respiration was present. Child was
weaned off from ventilator after 72 hours and discharged after 5 days.
The snakes most commonly
associated with mortality in India are cobra (Naja naja), krait (Bungarus
caeruleus), Russel’s viper (Vipera russelli) and saw scalled
wiper (Echis Carinatus)(1). Although snake bite is a frequently
encountered problem in rural and tribal areas, it is infrequently seen in
urban Surat. Common neurotoxic snake include cobra and krait. Krait bites
are commonly reported during night, and those sleeping on the floor are at
greater risk (2).
Venom from neurotoxic
snake has a curare like effect by blocking neurotransmission at neuro-muscular
junction. Cobra venom acts post synaptically while krait venom acts pre
synaptically(3).
ASV
is most effective when administered within a few hours of krait bite.
Ventilator support forms a cornerstone of krait envenomation therapy.
Anticholinesterase (neostigmine) had been tested and no benefit was found
in reversing paralysis in common krait bite(4).
This case highlights
that potential reversible causes of brain death must be excluded before
diagnosis of brain death. Electrocerebral silence on EEG for at least 30
minutes and absence of blood flow in 4 vessels cerebral angiography are
confirmatory test for brain death(5).
References
1. Whittaker R. Common Indian snakes: a Field Guide.
New Delhi: McMillan India Limited; 2001.
2. Kularatne SA. Common krait (Bungarus caeruleus)
bite in Anuradhapura, Sri Lanka: a prospective clinical study, 1996-98.
Postgrad Med J 2002; 78: 276-280.
3. Warrell DA. International panel of experts:
Guideline for the clinical management of snake bite in South-East Asia
Region. Southeast Asian J Trop Med Public Health 1999; 30 (supplement 1):
1-85.
4. Singh G, Pannu HS, Chawla PS, Malhotra S.
Neuromuscular transmission failure due to common krait (Bungarus
Caeruleus) envenomation. Muscle Nerve 1999; 22: 1637-1643.
5. Eleco FM, Wijdicks N. The diagnosis of brain death. N Eng J Med
2001; 344: 1215-1221.
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