Description

A 25-year-old Afro-Caribbean woman was bitten by a snake in her right inner thigh while in a forest reserve in Trinidad and Tobago. As an ardent nature lover and animal rights activist, she had entered the rainforest with companions to release a wounded owl that had been rehabilitated. The snake was photographed by digital phones and later identified by a toxicologist as Micrurus lemniscatus, a coral snake species (figure 1A). The patient experienced local minor bleeding, followed 5 min later by regional swelling, pain and paraesthesia radiating to her upper thigh. She arrived at our tertiary care hospital 4 hours later. She had a history of allergic reactions to insect bites manifesting as local swelling, but no history of consumption of medications, recreational drugs, alcohol or tobacco. On admission, vital signs were normal. Neurological examination demonstrated bilateral palpebral ptosis (figure 1B), slurred speech, dysarthria, dysphagia, sialorrhoea and flaccid quadriparesis (grade 4/5). The deep tendon reflexes were preserved with no sensory abnormalities. The right inner thigh puncture is shown in figure 1C. The rest of the physical examination was normal. Her course in the hospital is shown in table 1.

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Figure 1

Images of (A) Micrurus lemniscatus and the patient showing (B) bilateral palpebral ptosis and (C) a small puncture mark in the right inner thigh (black arrow) caused by the snake bite. The patient experienced full recovery of the ptosis 10 days after treatment with neostigmine (D).

Laboratory studies revealed normal full blood count, erythrocyte sedimentation rate, C reactive protein, coagulation, and renal and liver function tests. Serum calcium, phosphorous, magnesium, creatine kinase and amylase were also normal. Arterial blood gas remained normal during hospitalisation. Chest X-ray, ECG and echocardiogram were normal. An ultrasound examination of the right leg was normal. Electromyography and edrophonium test were not performed.

Diagnosed with progressive descending myasthenic syndrome of coral snake envenomation, we administered 80 mL of monovalent equine lyophilised coral antivenom intravenously with no adverse reactions or significant improvement. Atropine 0.6 mg followed by neostigmine 1.5 mg were given intravenously stat. Half an hour later, atropine 0.6 mg followed by neostigmine 0.5 mg were given intravenously stat again. Improvement in single breath count from 12 to 35, muscle strength and sialorrhoea by more than 75%, and ptosis in more than 25% in 1 hour were documented. No further administration of atropine-neostigmine was necessary in our patient due to appropriate and significant response thereafter. When the symptoms are not completely resolved, five additional doses of atropine-neostigmine (0.6 mg/0.5 mg) should be given every half-hourly intravenously and then 2–12 hourly according to recovery. For severe cases, intravenous infusion of neostigmine at 12 µg/kg/hour can be administered.1–3 Respiratory distress was resolved, and oxygen therapy and nebulisations were discontinued. The patient recovered and was discharged from hospital 5 days from admission.

Neostigmine is a reversible acetylcholinesterase inhibitor that restores neuromuscular transmission by increasing concentrations of acetylcholine at the neuromuscular junction, counteracting postsynaptic blockade at the nicotinic receptors. Neostigmine increases bronchial, gastric, sweat gland and salivary secretions at the muscarinic receptors. Atropine is an anticholinergic agent that inhibits smooth muscle and glands which are innervated by postganglionic cholinergic nerves, and is administered together with neostigmine most commonly to reduce the unwanted muscarinic effects of neostigmine by preventing excessive secretions.3

Coral snake venom contains α-neurotoxins of the three-finger (3FTx) protein superfamily that cause muscle weakness by competitive inhibition of the nicotinic acetylcholine receptors at the neuromuscular junction. Phospholipase A2 may cause myotoxicity and rhabdomyolysis.1–3

Hypersalivation from envenomation by coral snakes is uncommon. In 2006 Bucaretchi et al3 reported 1 case of moderate hypersalivation out of 11 (9.09%) cases of envenomation with Micrurus species in Brazil. The concomitant manifestation of excessive salivation and neuromuscular features in that patient was not described. The first line of therapy for the neuromuscular blockade manifestations of neurotoxic snake envenomation is the specific snake antivenom. The administration of the combination of atropine-neostigmine is indicated when the antivenom is unavailable, if there is a delay in obtaining a sufficient amount, or in patients given the highest recommended doses of antivenom without improvement in paralysis or with delayed recovery. The glycopyrrolate-neostigmine combination can also be used with success.1–3

M. lemniscatus is a highly venomous coral snake indigenous to the forests of Brazil, Bolivia, Colombia, Venezuela, Ecuador, Guyana, French Guiana, Suriname, Argentina, Paraguay, Peru and Trinidad and Tobago.1–3 M. lemniscatus characteristically has bright, bold-coloured rings, triad of black bands, small head, and a blunt and rounded snout (figure 1A).

This is the first published case from the Caribbean of acute myasthenic syndrome following coral snake envenomation causing respiratory paralysis. Timely intervention prevented death and disability.3 Snake bite is a neglected public health issue in the world, and education, improvement in healthcare and ongoing research are all essential.1–3