Indian common krait envenomation presenting as coma and hypertension: A case report and literature review.

Neuroparalytic snake bite is a common emergency situation encountered in India. Common krait (Bungarus caeruleus) and cobra (Naja naja) are important snakes causing neuroparalysis in North India. Despite severe neuroparalysis, patients who receive antivenin and ventilator support in time recover completely. Autonomic disturbances resulting in resting tachycardia, labile hypertension and sweating have been described in common krait envenomation. We present a case of common krait (B. caeruleus) envenomation presenting in the locked-in state and severe hypertension that remained in such a state for over 96 h before a gradual and sustained recovery.

INTRODUCTION

Neuroparalytic snake bite is a common emergency situation encountered in tropical countries. Severe envenomation may mimic brain death or a locked-in state with absent reflexes and total ophthalmoplegia.[1] Despite appearances, patients who receive antivenin and ventilator support in time may recover completely. In addition, some forms of envenomation may be associated with severe and labile hypertension. We present a case of common krait (Bungarus caeruleus) bite that remained in such a state for over 96 h before a gradual and sustained recovery.

CASE REPORT

A 35-year-old agricultural worker was brought to the emergency department of a tertiary care center in Northern India with a history of being bitten by a snake on his left ear. The snake had been spotted and killed and examination of the carcass revealed it to be a common krait (B. caeruleus) approximately three feet in length. Patient had a Glasgow Coma Scale of three on arrival and was deeply cyanosed. He was promptly intubated and put on mechanical ventilation with an ambu bag. On detailed examination, the patient had total ophthalmoplegia with absent pupillary, vestibulo-ocular and corneal reflexes. Blood pressure measurement on arrival was 190/100 mm of Hg. The site of bite showed two fang marks with no local signs of inflammation. As per the national snake bite protocol, 20 vials of polyvalent antivenin (Biological E. Limited, Hyderabad) were administered with no immediate complications. Blood pressure was unresponsive to injectible labetalol and therefore nitroglycerin infusion was initiated. Optimal supportive care and ryles tube feeding was initiated. As the patient had been completely paralyzed on arrival and had thus been apneic for an indeterminate period of time, hypoxic encephalopathy leading to brain death was suspected. A cold caloric stimulation test was performed and was negative. Magnetic resonance imaging of the brain showed no gross abnormality. Electroencephalography was suggestive of diffuse encephalopathy. Patient remained in a comatose state for the next 4 days and showed no change in neurological status. Blood pressure remained elevated but was effectively managed with intravenous nitroglycerine and later by a combination of amlodipine, metoprolol and prazosin administered through Ryle's tube. On day 5 of admission, the patient developed a cough reflex to endotracheal suctioning, which had earlier been absent. Further examination revealed slight pupillary constriction to bright light. Over the next 48 h, the patient had a gradual improvement in ophthalmoplegia with vertical movements recovering before horizontal movements. Simultaneous recovery of muscle power of the extremities was also noted with the patient being able to move the fingers of his right hand voluntarily. Higher mental functions appeared to be intact as the patient responded to commands by blinking or moving his fingers. Mechanical ventilation was continued for another 5 days due to persistent respiratory weakness complicated by ventilator associated pneumonia, which was managed with antibiotics. After a period of 12 days, the patient was successfully weaned off mechanical ventilation. With intensive physiotherapy and supportive care, the patient was able to walk unaided. Blood pressure control improved and anti-hypertensives were tapered gradually. Patient was discharged after 19 days of admission.

DISCUSSION

In India, the mortality from snake bite is 40,900 to 50,900/year.[2] Most deaths occur in rural areas with poor access to basic health-care. Persistence of many myths and superstitions regarding snake bite management prevail in these areas further complicating emergency management. The venomous snakes most often encountered are the Indian spectacled cobra (Naja naja), common krait (B. caeruleus), Russell's viper (Daboia russelli) and the Saw scaled viper (Echis carinatus). Cobra and krait envenomation is typically neuroparalytic, whereas envenomation by Viperidae species shows characteristic vasculotoxic and hemotoxic features. Neuroparalytic snake bite is associated with higher mortality rates due to the rapid onset of respiratory paralysis and as most envenomations occur in rural areas, these patients may not reach a center capable of providing mechanical ventilation in time.[3] Overall mortality in patients admitted for the management of snake bite was found to be approximately 3.5% in a study performed at our center.[4]

Neuromuscular paralysis in elapid bites occurs as a result of blockade of neuromuscular transmission. The bungarotoxins present in krait venom act preferentially on the pre-synaptic membrane of the neuromuscular junction. These neurotoxins have phospholipase A2 activity and hydrolyze phosphoglycerides thereby producing neuromuscular blockade by inhibiting the release of acetylcholine from the presynaptic membrane.[56] Bites of the common krait (B. caeruleus) have been associated with profound neurotoxicity, but relatively few local signs or symptoms. Cases have been reported with patients having severe neuroparalytic features without any history of snake bite due to lack of local symptoms.[78] Only on careful examination for fang marks and a dramatic response to antivenin was the diagnosis established in these cases. In most cases, abdominal pain is a frequent early symptom of envenomation. Neuroparalysis progresses and patients develop ptosis, ophthalmoplegia (manifesting as ocular cranial neuropathies), bulbar symptom (lower cranial nerves involvement) and progressive muscular weakness culminating in respiratory paralysis. Unlike in cobra envenomation, local signs are absent and neostigmine is ineffective in improving neuroparalytic features caused by krait envenomation.[9]

Autonomic disturbance in relation to krait bite characterized by hypertension, tachycardia and mydriasis has been well described in the literature. Elevated blood pressure was seen in over half the patients of krait bite enrolled in a study conducted in Sri Lanka.[10] Decreased cholinergic activity and marked sympathetic activity causing hypertension, tachycardia and mydriasis was seen in all cases of Malaysian krait (Bungarus candidus) envenomation in one series.[11] In another series from Vietnam, bites from Malayan and Chinese kraits (Bungarus multicinctus) were associated with autonomic disturbances in one-third of patients.[12] Typical of krait bites, local symptoms were minimal or absent in all cases. The autonomic abnormalities are thought to result both from the action of the pre-synaptic neurotoxin which causes reduced parasympathetic activity, as well as by producing blockade of receptor sites such as presynaptic-2 adrenoceptors, thereby inhibiting the inhibition of neurally mediated release of norepinephrine with resultant sympathetic hyper-reactivity.[11]

Management protocols should include provisions for the management of such manifestations in cases of krait bite. Whereas adequate ventilation and general supportive care is paramount, control of blood pressure and other autonomic manifestations should be useful in improving the overall course and outcome. Due to the unique pathogenesis of hypertension, beta blockers alone should not be used for fear of causing increased alpha adrenergic activity.[13] A combination of alpha and beta blockers is considered appropriate as shown in this case. Initial control of hypertension may be more effective through a nitroglycerin infusion thereby enabling titration of the drug to achieve the desired effect. No accounts of prolonged hypertension after krait bite have been reported and antihypertensive agents can be tapered and stopped once target blood pressure is attained.

CONCLUSION

Coma and hypertension are unusual neurological complications of common krait envenomation. Bulbar involvement and ophthalmoplegia in common krait bite can mimic brain death in a patient. Autonomic dysfunction should be considered in these patients whenever labile hypertension is encountered.