Premonitory signs and symptoms of envenoming by common krait (Bungarus caeruleus )

Introduction

Bungarus caeruleus is an Indian krait common in tropical countries. Krait, a venomous snake, is active during the night hours. It enters homes to hunt prey: rats, lizards and small krait. The krait enters and finds a warm environment in bedding and if a person rolls on to a krait, the krait misinterprets this as prey and will bite a person asleep on the floor. As the fangs of the krait are small and short, the victim will experience only tingling or numbness and mild or no pain ¹ . Though the venom is of small molecular size, the delayed manifestation is attributed to poor muscular movement, dermal circulation and slow reflexes during sleep. The high fatality due to krait bite is attributed to the unavailability of anti-snake venom (ASV), delayed and inappropriate administration of ASV, and inexperienced doctors ² . Abdominal colic and vomiting are usually attributed to indigestion. Doctors who examined such cases have initially misdiagnosed acute appendicitis, stroke, head injury, ischemic heart disease, food poisoning, trismus, hysteria and Guillain-Barré syndrome. Victims are sent for unnecessary investigations including MRI scans of the brain and lumbar puncture.

Methods, patients and treatment

We analyzed krait bite cases admitted between January 2005 and August 2011. The approximate time of bite was suggested by the onset of abdominal pain, vomiting, excessive salivation, difficulty in deglutition, heaviness of the eyelids, parenthesis, suffocation, dysphonic, nasal twang of voice, weakness in limbs and inability to lift the neck from the pillow (broken neck sign), the inability to protrude the tongue beyond teeth margin, eyelid paresis, pooling of saliva, intensity of expiratory nasal breathing, 1-minute breath interval, power and hypo-reflexia in limbs, all of which were specifically looked for. The blood pressure, pulse and oxygen saturation were measured and the body searched with a magnifying lens for the site of the bite (Figure 1). The snake was identified by examining the killed specimen or by showing the patient photographs of kraits (Figures 2 and 3). A total of 100 mL of polyvalent anti-venom was administered intravenously. Endotracheal intubation and artificial ventilation were administered to a victim with poor nasal expiration, SPO2 <90%, pooling of saliva and the broken neck sign OPEN IN VIEWER

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Figure 2.

Faint copper color krait (Kokan krait).

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Figure 3.

Dark black krait (Bunareus caeruleus).

Intubation and artificial ventilatory support by Ambu bag or ventilator are mandatory in victims with the broken neck sign, pooling of saliva and respiratory paralysis.

Results

In total, 140 out of 141 victims reported having slept on the floor. 75% reported to hospital between midnight and 5 am. Twenty-six percent of victims had neuroparalysis on arrival. Although many denied any history of snake bite, all had signs and symptoms suggestive of krait bite. Fifty-six percent of patients were male. 85% of patients were woken due to abdominal pain while 23 victims reported to hospital 8h after the bite; 16 victims had respiratory paralysis and needed ventilator support but seven of these victims died.

Forty-five killed specimens of krait brought in by relatives of the victims were analyzed. The colour of 29 specimens was steel black (Figure 3); of the victims bitten by these 29 kraits, seven died and the remaining patients required ventilatory support for recovery. Sixteen specimens were a faint copper colour (Figure 2). Of these, 15 victims recovered with ASV and neostigmine 25 ug/kg over 4-h intervals for the next 24 h (Figures 4 and 5. One victim died of massive pulmonary edema with severe hypertension. Nineteen victims saw the kraits after they were bitten and the species was confirmed by showing the victims photographs of kraits and preserved specimens in the hospital. In the present study, 38 cases were unaware of the bite. Twelve patients misinterpreted it as a rat bite, six cases as ant bites. Seventeen victims were brought in already dead. An autopsy confirmed by verbal testimony that they were victims of krait bite. OPEN IN VIEWER

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Figure 5.

Improvement with neostigmine and atropine.

Discussion

In the present study, 140 of 141 victims were bitten while they slept on the floor without a mosquito net. Of these, 138 were Hindu and three were Muslim. The lower incidence of bites in the Muslim community is attributed to their religious obligation of not sleeping on the floor.^1,2,3 The small molecular size of krait venom components facilitates the rapid absorption into the blood stream from the bite site. A 31% fatality rate is attributed to the delay in hospitalisation of more than 8 h. In this time, the venom reaches nerve receptors site and cannot be neutralized by ASV. Krait venom blocks both pre- and postsynaptic receptors. Beta bungarotoxin is a phospholipses A2, attached to the presynaptic acetyl choline receptors – it causes initial release of acetyl choline and then the blocking and destruction or irreversible damage of receptors. ASV and acetyl-choline esterase inhibitors, reverses the postsyanptic block.^2,3 The severity of clinical manifestations depends upon the dose of venom injected, the darkness of snake colour and time lapsed between the bite and administration of ASV. Krait is a cold-blooded animal. The venom remains in a thin liquid form in a dark-coloured snake. Dark skin is a poor temperature conductor responsible for raised body temperature (Figure 3). With the faint coppery coloured snake (Kokan krait) (Figure 2), because of its low body temperature, the venom is thick and viscid and is injected slower and in a lesser amount as compared to a dark-coloured snake. In the present study, 15 of 16 cases bitten by a light-coloured krait (Figure 2) recovered with ASV, neostigamine and atropine. Both dark and light-skinned kraits are actually of the same species.

By the time victims are hospitalised many develop full-fledged bulbar palsy or respiratory arrest, or others are brought in dead or in respiratory failure with coma,⁴ hence the common belief that the krait ‘licks the skin but bites the respiratory system’. In a rural setting, an important amount of time is wasted by attending to tantrik or through the failure of making the diagnosis at a primary health centre (PHC). At the PHC, medical officers who have never examined these cases before delay the diagnosis. Failure of early detection of respiratory failure and endo-tracheal intubations add to fatality. Hypertension due to krait poisoning is attributed to blockade of presyanptic alpha-2 receptors by beta bungarotoxin.^5,6 In endemic areas of krait bite such as in India, Pakistan and Bangladesh, villagers should be trained when to suspect krait bite. Routine use of cots with mosquito nets is preventative. ⁷

The chemical sequence homology of glycoprotein of the rabies virus is similar to the elapid venom neurotoxin alpha-bungarotoxin. It is possible that a drug derived from krait venom may act as a competitive antagonist with rabies virus glycoprotein at central nervous system and at peripheral nicotinic receptors and so might help to arrest the progress of rabies disease. ⁸