Serpent Strikes, Sapien Sways: A Rare Case of Bilateral Cerebellar Infarct following Viper Bite

Abstract

Ischemic stroke following snake bite is rare. We report a posterior circulation infarct involving bilateral cerebellum and occipital lobe following Russell’s viper bite in a previously healthy individual. A 50 years old healthy individual, soon after being bitten by the Russel viper on the left foot he developed pain and swelling followed by drooping of eyelids, slurring of speech and giddiness with multiple episodes of vomiting. The patient was administered ASV as well as neostigmine and atropine injections. Following this, the neurological manifestations resolved except dysarthria. CT brain study done was normal. On day 2 of hospitalization, he developed left cerebellar signs (positive finger nose finger test, rebound phenomenon, dysdiadochokinesia, a positive heel shin test). Subsequently, an MRI with MR angiogram was done which showed acute infarcts in bilateral cerebellar hemispheres, with the left superior cerebellar peduncle showing restricted diffusion and low ADC values. Ischemic infarction following viper envenomation has been described by only few authors. In majority of the cases reported, ischemic infarction involved the anterior circulation. The possible mechanisms of infarction in this scenario are discussed. Patient was treated with anti-snake venom and showed a good recovery. Early imaging and early treatment with anti-snake venom is important for a favourable outcome.

INTRODUCTION

Snakebite is an acute, life-threatening, and time-limited medical emergency. Viperidae species consisting of Russell’s viper and saw-scaled viper are the leading cause of fatal snakebite in India.[1] Snake venoms consist of highly complex mixtures of enzymes, polypeptides, glycoproteins, and other constituents. The common clinical characteristics of viper bite include local cellulitis, renal failure, and systemic hemorrhagic manifestation. Neurological deficit following viper bite is common and is usually due to intracerebral or subarachnoid bleed. Ischemic infarction following viper envenomation has been described by only a few authors.[2] In majority of the cases reported, ischemic infarction involved the anterior circulation.[3] We report a posterior circulation infarct involving bilateral cerebellum and occipital lobe following Russell’s viper bite.

HISTORY

A 50-year-old male, known hypertensive, presented to the emergency department with an alleged history of Russell’s viper bite on his right foot [Figure 1]. The incident occurred an hour back while he was cleaning his water tank [Figure 2]. He had pain and swelling at the bite site initially. Later over 4 h, he developed drooping eyelids, slurring of speech, and giddiness with multiple episodes of vomiting. There was no LOC, seizure, and COVID infection.

Figure 1.

Viper bite mark at medial surface of foot

Figure 2.

Viper snake found in water

Assessment

Upon arrival at the emergency department of the hospital, his pulse rate was 84 bpm and blood pressure was 200/100 mmHg. A local examination revealed two deep fang marks with surrounding redness and edema, as well as minimal bleeding over the right medial malleolus. The patient was drowsy, with a Glasgow Coma Scale of 13/15. His pupils were 3 mm bilaterally with a normal light reflex. He had drooping eyelids, dysarthria, and a flexor plantar response with normal fundus.

In view of neurological manifestations, the patient was administered ten vials of antisnake venom (ASV) as well as neostigmine and atropine injections. Following this, the neurological manifestations resolved except dysarthria. Computed tomography brain was normal. A complete hemogram revealed mild thrombocytopenia (1.4 lakh platelets) and neutrophilic leukocytosis (15,030/mm³, 94% neutrophils). His coagulation profile was found to be abnormal with an international normalized ratio of 2.26 and a prothrombin time of 26.9 s. The whole-blood clotting time was 20 min. Urine examination showed microscopic hematuria and hemoglobinuria. Liver function tests and renal functions were within normal limits. He received 10 more vials of ASV as well as 4 units of fresh frozen plasma for correction of deranged coagulation parameters.

Course

On day 2 of hospitalization, a detailed neurological examination revealed persistence of dysarthria with new onset of dysphonia and left upper- and lower-limb incoordination (positive finger–nose–finger test, rebound phenomenon, dysdiadochokinesia, and a positive heel shin test) along with swaying to the left while walking.

Subsequently, a magnetic resonance imaging (MRI) with magnetic resonance angiogram was done which showed acute infarcts in bilateral cerebellar hemispheres, with the left superior cerebellar peduncle showing restricted diffusion and low apparent diffusion coefficient values [Figure 3]. Electrocardiogram, lipid profile, carotid Doppler, echocardiogram, and magnetic resonance angiogram were normal, which negated the possibility of an ischemic or embolic stroke. Thrombophilic profile was sent for analysis.

Figure 3.

Magnetic resonance imaging brain study shows bilateral cerebellar infarct with the left superior cerebellar peduncle showing restricted diffusion and low apparent diffusion coefficient values

Management

After normalization of the thrombocytopenia, microscopic hematuria, and coagulation profile, the patient was started on dual antiplatelet therapy, neuroprotective medications, high-dose statins with speech, and limb physiotherapy. The patient’s further hospital stay remained uneventful. Postdischarge, tests for lupus anticoagulant and anticardiolipin antibodies were found negative. Protein C, protein S, and antithrombin III levels were normal. Over a period of 3 weeks, the patient showed an improvement in upper-limb incoordination but mild gait ataxia which improved after 6 weeks.

DISCUSSION

Russell’s viper venom contains C-type lectin-like proteins, snake venom serine proteases, esterases, hydrolases, and hemorrhagic agents.[4] These proteins create a procoagulant state by activating thrombocytes and the complement system, which leads to widespread endothelial damage, vasospasm, and ultimately thrombosis of the cerebral blood vessels.

In a literature search study carried out from 1995 to 2018 by Mohammed Al-Sadawi et al., there were only 18 case studies all over the world that reported a posterior circulation stroke following a viper bite.[5] Murthy et al. have reported a case of cerebral infarction and diffuse encephalopathy following a viper bite.[5] In a study of 309 patients with snakebite, Mosquera et al. reported cerebrovascular complications in 8 patients (2.6%), 7 hemorrhagic strokes and 1 ischemic stroke.[6] Bashir and Jinkins reported a patient in whom envenomation with Russell’s viper resulted in hemiplegia and aphasia, consistent with a middle cerebral artery infarction.[7]

Better outcomes have been reported with immediate ASV treatment. In the study by Thomas et al., of the 33 patients with envenomation who had not received ASV or received ASV after 8 h of envenomation, 14% developed thrombotic complications and 4 of the 14 patients who had not received ASV died. Of the 70 patients who received ASV within 6 h of envenomation, none had thrombotic complications.[8] Our patient, despite treatment with ASV within 1 h of envenomation, developed delayed cerebral infarction on the 2^nd day.

Ischemic stroke after viper bite has been reported less commonly in the literature; furthermore, the onset of ischemic stroke and reversibility is rare. We present a case of snakebite with ischemic stroke which has a clinically reversible outcome.

CONCLUSION

Cerebral infarction can be one of the differential diagnoses of neurological deterioration following Russell’s viper bite. Learning point from these cases is that snakebite should be one of the differential diagnoses for any young patient with stroke. We call the attention of physicians working in rural areas, to look for such less recognized etiologies of stroke in tropical countries and importance of timely radio imaging, especially MRI brain in recognizing the condition and to initiate appropriate therapy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.