Abstract
To the Editor:
Snakebite is common in India and other subtropical countries with heavy rainfall and humid climates. 1 Approximately 10,000 to 50,000 snake bite-related deaths occur each year in India. The majority are due to envenomation by neurotoxic kraits and cobras.2,3 Common venomous snakes found in India are kraits (genus Bungarus), cobras (genus Naja), and carpet vipers (Echis carinatus). 1 The common krait (Bungarus caereulus) is regarded as the most dangerous species of venomous snake in the Indian subcontinent, and a 35% to 50% fatality rate attributed to krait bites has been reported. 1 We report the case of a male army paratrooper who was on a military exercise in the Thar Desert of Rajasthan, India.
A 25-year-old soldier was brought at 2200 hours on July 26, 2013, from an exercise area with history of headache, mostly frontal, associated with retroorbital pain since the morning hours. He also divulged a history of body pain, mainly in the thighs. The patient had gone on an exercise patrol in the forested area the previous night, after which he slept on the ground in his sleeping bag at the exercise location. Examination in the hospital by the casualty medical officer revealed altered sensorium, tachypnea, and generalized muscle pain and tenderness. Other general and systemic examinations were documented as unremarkable, and urgent noncontrast computed tomography scan of the brain was read as normal. The patient was admitted and treated in the intensive care unit as a case of heat exhaustion. Examination of the patient in the morning revealed dizziness, slurred speech, difficulty in swallowing, ptosis, inability to open his mouth fully, limited tongue protrusion, and paresthesias all over his body. Pooling of secretions in the oral cavity was noted. There were no bite marks on the body whatsoever, no evidence of bleeding from any site, and no fasciculations were noted. Pupils were mid range in size with sluggish reaction. His pulse rate was 104 beats/min, blood pressure 160/90mm Hg, and respiratory rate 32 breaths/min. The rest of the systemic examination was within normal limits.
A provisional diagnosis of neurotoxic snake envenomation was made, and the patient was immediately given 10 vials (100 mL) lyophilized polyvalent (Naja naja, Bungarus caeruleus, Vipera russelli, Echis carinatus) anti-snake venom, manufactured by Serum Institute of India, in 200 mL normal saline over 1 hour. In addition, an injection of hydrocortisone 100 mg and pheniramine maleate 22.75 mg IV was given as premedication. Intravenous neostigmine 2.5 mg and 0.5 mg every 6 hours along with atropine 1.2 mg IV and 0.6 mg hourly were instituted, in addition to other supportive therapy. The patient was orally intubated with an 8.5-cm cuffed polyvinyl chloride endotracheal tube, connected with T-piece oxygenation. The patient was given 50 mL antivenom at 1130 hours and 50 mL more at 1700 hours the same day. He had improved subjectively by the next day with resolution of paresthesias and slight improvement of his ptosis. He remained conscious and oriented. He was kept on endotracheal tube ventilation for a total of 48 hours; by this time, his bulbar weakness had resolved and ptosis recovered fully in the right eye and to 50% in the left eye; ptosis recovered fully in both eyes by 72 hours. Investigations revealed normal hematological and biochemical parameters. Urine for myoglobin was negative. Coagulation parameters revealed prothrombin 75% (70%–100%), international normalized ratio 1.14 (1.00–1.20), activated partial thromboplastin time 28 s (27–35 s), and thrombin time 17.4 s (<22.0 s). The patient made an uneventful recovery and was discharged after 10 days of careful observation. Krait envenomation was considered as the most plausible diagnosis (Table).
Why Krait envenomation was considered the most plausible diagnosis
The Krait is a nocturnally active, terrestrial snake that lives close to human dwellings, but is not vicious by nature. It creeps into houses over the ground or through the roof and exhibits arboreal tendencies. It has also been observed by others that bites occur at night while the victims are asleep. 4 The common krait normally prefers to feed on small snakes. 4 While asleep, humans may be bitten either due to accidental handling or rolling over on the snake, or exposed parts of the human body might be misidentified as prey. These may be possible provocative factors for a krait bite even though the common krait is naturally indolent.
The seasonal pattern of common krait bites has been explained by mating behavior, 4 but Kularatne 5 has shown the influence of changing environment such as rain and severe drought as contributing factors. Our patient had generalized muscle pain and tenderness; Kularatne 6 observed myalgia in a significant number of patients. A study of 5 common krait bites by Theakston et al 7 demonstrated myoglobinemia in 1 patient who had myalgia. One of the patients envenomed by the Malayan krait (Bungarus candidus) had generalized muscle pain and tenderness. 8 These suggest that presynaptic phospholipase A2 could cause rhabdomyolysis. However, none of these patients had renal consequences of rhabdomyolysis. Our patient had tachycardia, increased secretions, dilated pupils, and elevated blood pressure. Excitation of both parasympathetic and sympathetic autonomic systems explains most of the clinical manifestations, including increased secretions, dilated pupils, tachycardia, and hypertension. A patient who had a Malayan krait bite was reported to have fixed dilated pupil, sweating, tachycardia, and hypertension due to parasympathetic abnormalities. 8
Altered mental status as noted in our patient, with progression to a deeply comatose state, is not simply explained by cerebral hypoxemia. The locked-in position is due to severe neuromuscular paralysis. Kularatne 6 noted that his patients were well oxygenated and the brainstem function tests were negative. Furthermore, associated anterograde memory loss is strongly suggestive of widespread depression of cerebral functions. There is little documentation of these observations in the literature. One patient with a Ceylon krait bite remained deeply unconscious until death. 9
This report illustrates how heat exhaustion as a diagnosis can be confused with neurotoxic snakebites. Although altered mental status, pain in the muscles, and tachycardia could have been explained by heat exhaustion or heat stroke, in our patient, background history along with ptosis, weakness of facial muscles, dysphagia, and paresthesias gave valuable clinical clues in favor of krait envenomation.