Ischemic stroke after Russel’s Viper snake bite, an infrequent event: a case report

S. Yogeshwaran^1,*, P. Saravana Kumar², C.M. Santhosham³, P. Sasikumar⁴

¹ MEM-Post Graduate, Kauvery Hospital, Cantonment-Trichy, Tamilnadu, India

²HOD Critical Care, Kauvery Hospital, Cantonment-Trichy, Tamilnadu, India

³Critical Care Specialist, Kauvery Hospital, Cantonment-Trichy, Tamilnadu, India

⁴Anaesthesiologist, Kauvery Hospital, Cantonment-Trichy, Tamilnadu, India

Abstract

Snake bites are a well-known medical emergency in many parts of the world including India. This results in tens of thousands of deaths every year and many chronic disabilities in South Asian countries. Though much is now known about the species of venomous snake, the nature of their bites and clinical effects of envenomation, cerebral arterial thrombosis following snake bite has been sparsely described in the literature. We describe a case of acute multiple cerebral infarction following Russel viper bite and envenomation.

Background

Many snake bites patients are treated by traditional healers in South Asian regions and thus the epidemiology of snake bites has not been adequately studied. According to WHO Direct estimate, India measures highest number of cases of snake bite worldwide, with a mortality estimated 46,000 annual death [1]. A new study has found an estimated 1.2 million people died from snake bites India in the past two decades, averaging 58,000 deaths every year, with nearly half of the victims aged 30 to 69 years, and over a quarter being children under 15 years. Snake bite envenomation is a neglected but important public health problem in rural areas of South Asia, South east Asia and Sub Saharan Africa [2]. The big four medically significant species in India are naja naja, Bungarus carefues, Debois russelli and Echis carinatus. Viper being the most common cause of bite, local envenomation is the frequent manifestation, followed by haemostatic abnormalities and neurotoxicity [3]. Coagulopathy if present is diagnostic of viper bites in South Asia. Viper bites have been associated rarely with cerebrovascular complications, most commonly due to haemorrhages, and rarely due to infarct. Ischemic stroke following viper bite is quite rare [4].

Most common and serious central nervous system complication following snake bite is intracranial haemorhage [5]. Ischemic stroke, when present, commonly involves anterior circulation. Here we describe a polyvalent anti venom treated patient with multiple infarcts in the Right temporo-parietal and left fronto-parietal region and cerebellar cortex, with mass effect.

Case Presentation

A 42-years-old female with no co-morbidities was admitted to our ER with alleged history of snake bite on her left hand. The snake was killed and brought by the relatives in a cover to ER and it was identified as Russell’s viper (Fig. 1), within 10 minutes after bite, she noticed mild swelling over the bite area and was brought to ER within an hour in an unresponsive and gasping state. She was immediately intubated and put on mechanical ventilation, her whole blood clotting time was more than 20 min and ASV 10 vials was administered subsequently she received 20 more vial. Her initial labs showed leukocytosis, thrombocytopenia, elevated international normalised ratio, prothrombin time and activated prothrombin time. Kidney function was normal. CT brain was normal.

Fig. 1. Russell’s viper from the wild

Patient sensorium did not improve in the first 48 h, on the third day withdrawal to pain, on left side was appreciated, MRI Brain was done in view of Right-side paucity, which showed – acute infarct in Right Tempero – Parietal and Left Fronto Parietal region and Right Cerebellar Cortex, with mass effect.

She was managed on mechanical ventilator, antibiotics and supportive care, tracheostomy was done in view of long-term ventilation and was weaned off accordingly. On 35th day of admission, she was discharged with a GCS-E4VTM5 with right side paucity.

On Examination

HB	10.3
PCV	32.1
Platelets	1,24,000
Total Leucocyte Count	18,000
PT	>2 min
INR	10
APTT	>2 min
Sr Urea	30.6
Sr Creatinine	0.65
Sr Na	145
Sr K	2.99
Sr Chloride	111
Sr HCo3	19.0

MRI – Brain

MRI Brain – Acute infarct in Right Tempero- Parietal and Left Fronto Parietal region and Right Cerebellar Cortex, with mass effect

Discussion

Viper bite is the most frequent snake bite in the Indian subcontinent. Envenomation by viper bite leads to local manifestations, followed by abnormal coagulation [6]. The various toxins present in the viper venom can be categorized both as pro-coagulant and anticoagulant. The toxins with well-established pro-coagulant/platelet aggregating properties are cerastobin [6], factor IVA [7], cerastocytin [8], cerastotin [9], and afaacytin [10].

These various protein products have thrombin like enzymatic activity. Different toxins activate different parts of the coagulation cascade [6-10]. Their activity is inhibited by monoclonal antibodies against GP1b or GPIIb/IIIa or thrombin receptor. Disseminated intravascular coagulation and hypotension are also associated risk factors in viper bite patients. Disseminated intravascular coagulation can be a cause of neurological deficits, largely due to vessel occlusion [11]. The toxin itself can cause vasospasm which can lead to a cerebrovascular catastrophe. Reported case reports of infarct following snake bite are mostly due to viper bite. Most of the patients had features of local envenomation with disseminated intravascular coagulation. The infarct commonly involved the anterior circulation, with hemiparesis being the frequent presentation [12-15]. As a matter of fact, cerebral infarction after snake envenomation occurs due to a complex multifactorial mechanism. It includes direct cardiotoxic effects of venom leading to dysrrhythmias. This may cause cardiac thromboembolism. Hyperviscosity due to hypovolemia and hypoperfusion secondary to hypotension may also be a contributing factor to causation of ischemic strokes [16-18].

Conclusion

After viper bite, neurological manifestations can be attributed to various reasons, such as toxin induced vasculitis, procoagulant effect, endothelial damage, disseminated intravascular coagulation and hypotension. In a snake bite prone country like India, it is necessary to evaluate the incidence of ischemic stroke and other neurological disorders from possible viper bite. The early detection of the viper bite and administration of anti-snake venom can prevent this infrequent but devastating complication.

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