|LETTER TO EDITOR
|Year : 2015 | Volume
| Issue : 2 | Page : 181-182
Viper-bite causing isolated lower motor neuron type facial nerve palsy: A rare scenario
Department of General Medicine, Institute of Post-Graduate Medical Education and Research (IPGMER), Kolkata, West Bengal, India
|Date of Web Publication||13-Jul-2015|
Dr. Subrata Chakrabarti
Doctor Hostel, Institute of Post-Graduate Medical Education and Research (IPGMER), AJC Bose Road, Kolkata - 700 020, West Bengal
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chakrabarti S. Viper-bite causing isolated lower motor neuron type facial nerve palsy: A rare scenario. Muller J Med Sci Res 2015;6:181-2
|How to cite this URL:|
Chakrabarti S. Viper-bite causing isolated lower motor neuron type facial nerve palsy: A rare scenario. Muller J Med Sci Res [serial online] 2015 [cited 2020 Dec 4];6:181-2. Available from: https://www.mjmsr.net/text.asp?2015/6/2/181/160712
Vasculotoxicity following viperbites can develop severe local reactions as well as systemic complications including coagulopathy, Disseminated Intravascular coagulation, acute renal failure. Neurological complications by systemic envenomation without evidence of intracranial vascular events from coagulopathy are distinctly uncommon. The author reports an unusual case of left sided isolated lower motor neuron type facial nerve paralysis following Russel's viper bite in the foot. To the best of the author's knowledge, this scenario of isolated lower motor neuron type facial nerve paralysis following systemic envenomation after Russel's viper-bite at a distant site has been previously reported only once in literature.
A 58 year-old male, a farmer by occupation, hailing from rural parts of West Bengal in India, presented to the emergency with severe swelling and pain in the left foot and gross haematuria and diminished urine output after being bitten by a snake 5 hours back. The snake (which was later killed by his relatives and brought to the emergency) was identified as a Russel's viper and confirmed by forensic experts. Examination revealed fang marks with severe swelling and oozing with inflammation in the dorsum of left foot (at site of bite). Vitals were stable and there was no suggestion of neurological deficits. The bedside 20 min Whole blood clotting time was prolonged (25 minutes). The patient was immediately administered polyvalent Anti-snake venom (after proper skin tests) along with local wound care (including tetanus prophylaxis). 16 hours after admission he noticed inability to close the left eye and deviation of angle of mouth to the right. Neurological examination revealed complete Lower Motor neuron type left sided facial nerve palsy with no other neurological deficits [Figure 1]. Initial laboratory parameters revealed haemoglobin level of 10.4 g/dl, WBC count 8100/mm 3 ; Platelet 52,000/mm 3 ; serum Urea 97 mg/dl and Creatinine 6.5 mg/dl. Coagulation parameters were deranged-prothrombin time (PT)- 20 s (control 13 s; INR-1.8); activated partial thromboplastin time (APTT)-31 s (control 25 s). Liver function test, chest radiograph and electrocardiographs were all normal. Urgent non contrast computed tomography of the brain did not reveal any vascular event. The patient underwent urgent haemodialysis in view of his acute renal failure. After 18 hours of AVS administration and haemodialysis, the facial palsy started to recover. Repeat testing at this time also showed improvement in coagulation parameters (PT -15 s; Control 13 s, APTT -29 s; control 25 s). Facial palsy completely disappeared over 3 days. Renal parameters normalised after 4 sessions of haemodialysis over 6 days. He was discharged in a stable condition after 7 days of admission with no residual neuro-deficit.
|Figure 1: Complete lower motor neuron type left sided facial nerve palsy|
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Facial nerve palsy as a neurological complication of vasculotoxic snakebite (including Russel's viper bite) is a rare occurrence and follow either local or systemic envenomation. Local envenomation has been reported to cause to develop persistent facial muscle palsy. Weinelt et al. reported a case of the left frontalis muscle palsy following viper bite on the left fronto-temporal area leading to possible exposure of the muscle fibres to the venom, spreading directly from the injection site and destroying the nerve terminals in the muscle tissue. Their proposition was supported by the electromyographic test results. 
In the index case, site of the bite being the dorsum of the right foot (i.e. away from the face), facial palsy occurring within a few hours after the snake bite(i.e. venom injection) and rapid recovery following antivenin administration suggest the facial palsy as a consequence of systemic envenomation. The neurological manifestation is not related to mass effect from intracranial haemorrhage or infarct due to coagulopathy (imaging excluded such possibilities, although coagulation parameters were deranged). Direct systemic effects of the neurotoxin blocking transmission at the neuromuscular junction can be a rational explanation.
Vipers can produce selective flaccid type of neuromuscular paralysis (like kraits). Both pre-synaptic as well as postsynaptic neurotoxins are involved. Muscles innervated by cranial nerves usually are involved. Ptosis and ophthalmoplegia are among the first symptoms found almost in all cases.  Neurological deficits may also include manifestations of other cranial nerve palsy like dysphonia, dysphagia, drooling, diplopia, etc. However, isolated facial palsy as in this case can be the sole neurological finding following systemic envenomation. Similar finding was reported earlier by Baig et al. from South India. 
Complete recovery of the neurological deficits usually occurs in snakebites if it follows systemic envenomation. Recovery can be rapid, occurring within hours, or it may be delayed for days or weeks. The anti-venin therapy is important in the management of neurological complications following snakebite, especially when there is clinical or laboratory evidence of systemic envenomation. 
It can be concluded that in a case of isolated cranial nerve palsy developing in vasculotoxic snakebite (like viperbite), the first and foremost job of the attending physician is to rule out the development of any intracranial haemorrhage or infarct by appropriate imaging study which becomes specially important if coagulation parameters are deranged. However if imaging is normal, a direct neurotoxic effect of the toxin at the neuromuscular junction is to be considered. In the latter scenario, administration of Antivenin is the key to recovery.
| References|| |
Weinelt W, Sattler RW, Mebs D. Persistent paresis of the facialis muscle after European adder (Vipera berus) bite on the forehead. Toxicon 2002;40:1627-9.
Mitra S. Snake bite in India and its management. J Indian Med Assoc 1987;85:129-31.
Baig WW, Prabhu AR, Kumar C. Viper bite causing an isolated lower motor neuron-type of facial palsy. Singapore Med J 2009;50:e368-70.
Williams DJ, Jensen SD, Nimorakiotakis B, Müller R, Winkel KD. Antivenom use, premedication and early adverse reactions in the management of snake bites in rural Papua New Guinea. Toxicon 2007;49:780-92.