|Year : 2015 | Volume
| Issue : 1 | Page : 51-53
Multiple infarctions involving cerebral and cerebellar hemispheres following viper bite
Rajesh M Kumar1, Ramesh P Babu1, Amit Agrawal2
1 Department of Medicine, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
2 Department of Neurosurgery, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
|Date of Web Publication||17-Jun-2015|
Dr. Rajesh M Kumar
Department of Medicine, Narayana Medical College Hospital, Nellore - 524 003, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
The Russell's viper is one of the most dangerous and commonly encountered vasculotoxic poisonous snakes in India that is responsible for most snakebite mortalities. Usually hemorrhagic stroke is the sequel of viper bite; however, ischemic stroke is increasingly recognized and reported in the literature. In rural areas, there is a need to keep the possibility of cerebral infarction as one of the differential diagnoses of neurological deterioration following Russell's viper's bite, as early identification of neurological complications can lead to a more effective treatment. In the present article, we discuss a case of a young male who was presented with both supra- and infratentorial infarcts.
Keywords: Cerebral infarction, Cerebellar infarction, Russell′s viper, Snakebite
|How to cite this article:|
Kumar RM, Babu RP, Agrawal A. Multiple infarctions involving cerebral and cerebellar hemispheres following viper bite. J Med Soc 2015;29:51-3
|How to cite this URL:|
Kumar RM, Babu RP, Agrawal A. Multiple infarctions involving cerebral and cerebellar hemispheres following viper bite. J Med Soc [serial online] 2015 [cited 2019 Oct 17];29:51-3. Available from: http://www.jmedsoc.org/text.asp?2015/29/1/51/158938
| Introduction|| |
The Russell's viper is one of the most dangerous and commonly encountered vasculotoxic poisonous snakes in India, and it is responsible for most snakebite mortalities. ,,,, Usually, hemorrhagic stroke is the sequel of viper bite; however, ischemic stroke is increasingly recognized and reported in the literature. ,,,,,,,,, In the present article, we discuss a case of a young male who was presented with both supra- and infratentorial infarcts.
| Case Report|| |
A 32-year-old man was admitted to our Emergency Department for snakebite (around half an hour after the bite) on his left foot, which he sustained in the fields. The onlookers identified the snake as Russell's viper. He received primary treatment at an outside hospital. At the time of bite, he complained of severe pain and when he was received in the emergency, he was in altered sensorium, irritable and restless. Local examination showed two deep fang marks with associated erythema and edema. There was bleeding from the mouth. His pulse rate was 146 beats per minute. Respiratory rate was 28 per minute. Blood pressure was 100/60 mmHg; SpO 2 was 98% at 4 L/min oxygen. Neurologically, he was in altered sensorium (Glasgow coma scale - E1V2M5). Pupils were bilaterally equal and reacting to light. In view of the poor Glasgow coma scale, the patient was immediately intubated. After stabilizing the vitals, he was shifted for CT scan, following which he was kept on elective ventilation in intensive care unit. Blood investigations at the time of admission revealed hemoglobin, 13.9 g/dL, normal urea and creatinine levels (CPK) 10,045 IU/L (<200 IU/mL) and urine myoglobin >700 ng/ml (<40 ng/ml). Prothrombin time was 15.7 s (range, 11-16 s; control, 13.4 s), INR was 1.19 and APTT was 13.4 (control,13.2); bleeding and clotting time were in normal range. Carotid and vertebral Doppler were normal. Echocardiography was normal. After the test dose, the patient received 10 vials of anti-snake venom (ASV) followed by seven vials three times a day for a period of five days. In view of oral bleeding, he received fresh frozen plasma (FFP). CT scan on the day of admission was apparently normal [Figure 1]. Supportive measures, including injection tetanus toxoid and prophylactic antibiotics were also given. However, he did not make any significant improvement and on day 4 after admission, he underwent MRI brain that showed multiple infarcts involving right temporal, occipital and left cerebellar hemispheres [Figure 2]. He was continued on elective ventilation and on 10 th day tracheotomy was performed. He could be weaned off from ventilator; however, he did not improve significantly in his neurological status. At the time of discharge, the patient was opening eyes spontaneously and obeying commands, but weakness of all the four limbs was persistent.
|Figure 1: Day 1: CT scan brain plain study- an axial section through the posterior fossa showing normal appearance of the structures|
Click here to view
|Figure 2: MRI brain FLAIR and diffusion-weighted images showing extensive infarctions involving right temporal, parietal, occipital lobes and small infarct in the left cerebellar hemisphere|
Click here to view
| Discussion|| |
The viper venom comprises a mixture of numerous enzymes with opposing effects, some of the enzymes causes hypofibrinogenemia, hypoprothrombinemia, thrombocytopenia and fibrinolysis; few are potent proteases (e.g., arginine esterase hydrolase) acting as activators of clotting factors X and V, thereby promoting coagulation.  In addition to these, few enzymes (i.e., hyaluronidase) cause damage to the connective tissues, leading to enhanced toxin dissemination.  Following snakebite, complex interactions of these enzymes usually lead to consumption coagulopathy, coagulation failure and intracranial hemorrhage. ,,,, Apart from the local manifestations such as pain, edema, bleeding and necrosis, there may be systemic features, including hypotension, shock, acute renal failure, weakness, dizziness and nausea. ,,, Most common neurological complications include drowsiness, confusion, fainting, dizziness, blurred vision, loss of muscle coordination and convulsions. ,,, Recently, ischemic infarction following viper bite is increasingly reported and various mechanisms for ischemic infarction have been proposed. ,,,,,,,, The possible explanations for cerebral infarction can be vessel wall-damaging toxin in the venom leading to thrombosis, microthrombi formation as a sequel to low-grade dissemination of intravascular coagulopathy, and hypotension leading to ischemia and infarction. ,,,,, The basic principles of management are adequate hydration, control of blood pressure and central venous pressure, and management of local infection with appropriate antibiotics and dressings.  In spite of the normal coagulation profile, the patient had clinical evidence of bleeding (oral bleeding). There are reports from Indian subcontinent that FFP or cryoprecipitate can be recommended when there is clinical bleeding despite giving antivenin therapy;  however, there are no well-designed studies to support this assumption and a need for trials to demonstrate effectiveness of transfusion therapy in the setting of clinical bleeding despite giving antivenin therapy has been recommended.  It has been reported that with immediate ASV treatment, the outcome is better; ,,, however, there are reports of development of cerebral infarct despite early treatment with ASV (even within 1 hour of envenomation).  In spite of the aggressive management, outcome of patients of snakebite presenting with features of infarction remain poor, more so when the posterior circulation is involved. 
| Conclusion|| |
In summary, snakebites are common particularly in rural areas and there is a need to keep the possibility of cerebral infarction as one of the differential diagnosis of neurological deterioration following Russell's viper's bite, as early identification of neurological complications can lead to a more effective treatment.
| References|| |
Simpson ID, Norris RL. Snakes of medical importance in India: Is the concept of the "Big 4" still relevant and useful? Wilderness Environ Med 2007;18:2-9.
Bhargava RK, Hakim A, Shah PK, Mathur SB, Ujjwal JS. Disseminated intravascular coagulation in cases of snake bite (Echis carinatus). J Assoc Physicians India 1976;24:671-5.
Hoskote SS, Iyer VR, Kothari VM, Sanghvi DA. Bilateral anterior cerebral artery infarction following viper bite. J Assoc Physicians India 2009;57:67-9.
Krishna K, Diwan AG, Mendiratta N, Jadhav S, Reddy S. Acute ischaemic stroke following viper bite in the elderly. J Indian Acad Geriatr 2011;7:30-2.
Narang SK, Paleti S, Azeez Asad MA, Samina T. Acute ischemic infarct in the middle cerebral artery territory following a Russell′s viper bite. Neurol India 2009;57:479-80.
Deepu D, Hrishikesh S, Suma M, Zoya V. Posterior fossa infarct following Viper bite: A paradox. J Venomous Anim Toxins Trop Dis 2011;17:358-60.
Gouda S, Pandit V, Seshadri S, Valsalan R, Vikas M. Posterior circulation ischemic stroke following Russell′s viper envenomation. Ann Indian Acad Neurol 2011;14:301-3.
Rebahi H, Nejmi H, Abouelhassan T, Hasni K, Samkaoui MA. Severe envenomation by cerastes cerastes viper: An unusual mechanism of acute ischemic stroke. J Stroke Cerebrovasc Dis 2012;23:169-72.
Hsaini Y, Satte A, Balkhi H, Karouache A, Bourezza A. Stroke following a viper bite. Ann Fr Anesth Reanim 2010;29:315-6.
Gawarammana I, Mendis S, Jeganathan K. Acute ischemic strokes due to bites by Daboia russelii in Sri Lanka - first authenticated case series. Toxicon 2009;54:421-8.
Malbranque S, Piercecchi-Marti MD, Thomas L, Barbey C, Courcier D, Bucher B, et al
. Fatal diffuse thrombotic microangiopathy after a bite by the "Fer-de-Lance" pit viper (Bothrops lanceolatus) of Martinique. Am J Trop Med Hyg 2008;78:856-61.
Singh S, Chattopadhya A, Sud A, Wanchu A, Bambery P. Acute paraplegia following viper bite. J Assoc Physicians India 2002;50:1427-9.
Mugundhan K, Thruvarutchelvan K, Sivakumar S. Posterior circulation stroke in a young male following snake bite. J Assoc Physicians India 2008;56:713-4.
Siigur J, Aaspollu A, Tonismagi K, Trummal K, Samel M, Vija H, et al
. Proteases from Vipera lebetina venom affecting coagulation and fibrinolysis. Haemostasis 2001;31:123-32.
Murthy JM, Kishore LT, Naidu KS. Cerebral infarction after envenomation by viper. J Comput Assist Tomogr 1997;21:35-7.
Than-Than, Hutton RA, Myint-Lwin, Khin-Ei-Han, Soe-Soe, Tin-Nu-Swe, et al
. Haemostatic disturbances in patients bitten by Russell′s viper (Vipera russelli siamensis) in Burma. Br J Haematol 1988;69:513-20.
Sarangi A, Jena I, Sahoo H, Das JP. A profile of snake bite poisoning with special reference to haematological, renal, neurological and electrocardiographic abnormalities. J Assoc Physicians India 1977;25:555-60.
White J. Clinical toxicology of snakebite in Australia and New Guinea. Handbook of Clinical Toxicology of Animal Venoms and Poisons 1995:5954il.
Boviatsis EJ, Kouyialis AT, Papatheodorou G, Gavra M, Korfias S, Sakas DE. Multiple hemorrhagic brain infarcts after viper envenomation. Am J Trop Med Hyg 2003;68:253-7.
Lee BC, Hwang SH, Bae JC, Kwon SB. Brainstem infarction following Korean viper bite. Neurology 2001;56:1244-5.
Panicker JN, Madhusudanan S. Cerebral infarction in a young male following viper envenomation. J Assoc Physicians India 2000;48:744-5.
Minagar A, David NJ. Bilateral infarction in the territory of the anterior cerebral arteries. Neurology 1999;52:886-8.
Gupta S, Tewari A, Nair V. Cerebellar infarct with neurogenic pulmonary edema following viper bite. J Neurosci Rural Pract 2012;3:74-6.
Thomas L, Tyburn B, Ketterle J, Biao T, Mehdaoui H, Moravie V, et al
. Prognostic significance of clinical grading of patients envenomed by Bothrops lanceolatus in Martinique. Members of the Research Group on Snake Bite in Martinique. Trans R Soc Trop Med Hyg 1998;92:542-5.
Godpower MC. Cerebellar infarct with neurogenic pulmonary edema following viper bite. J Neurosci Rural Pract 2012;3:4-5.
[Figure 1], [Figure 2]