|Year : 2017 | Volume
| Issue : 3 | Page : 192-193
Ischemic stroke consequent to snake bite
Pothukuchi Venkata Krishna1, Shaik Ahmed2, Katreddy Venkata Narasimha Reddy3
1 Professor of Medicine, Guntur Medical College, Guntur, Andhra Pradesh, India
2 Assistant Professor of Medicine, Guntur Medical College, Guntur, Andhra Pradesh, India
3 PG in Medicine, Guntur Medical College, Guntur, Andhra Pradesh, India
|Date of Web Publication||25-Sep-2017|
Pothukuchi Venkata Krishna
Professor, Siddhartha Medical College (Formerly Guntur Medical College), Vijayawada, Andhra Pradesh - 520 008
Source of Support: None, Conflict of Interest: None
Neurological deficits following snake bite are usually due to intracerebral hemorrhage as a result of depletion of clotting factors. Ischemic stroke following snake bite is rare. We are presenting a case report of a female who developed seizures within 4 hours of snake bite; her computed tomography scan of the brain revealed an infarct.
Keywords: Ischemic, snake bite, stroke
|How to cite this article:|
Krishna PV, Ahmed S, Reddy KV. Ischemic stroke consequent to snake bite. J NTR Univ Health Sci 2017;6:192-3
| Introduction|| |
Neurological deficit following snake bite is not uncommon and is usually caused by intracerebral or subarachnoid bleed. Cerebral infarction following snake bite is rare and only few cases have been reported since 1966.,,,
| Case History|| |
A 30-year-old female presented to our emergency department with a 4-hour history of snake bite on the tip of her great toe. She could not recognize the type of snake as it was small and rapidly disappeared. On examination, there were fang marks but there was no fresh bleeding from the site. There was no history of ptosis, ophthalmoplegia, neck drop, weakness, blurring of vision, hematuria, or petechiae. After 5 min, patient had generalized seizures of clonic and tonic type lasting for 1 min. There was no past history of seizures or any past history suggestive of connective tissue disorders or coagulation disorders either in her or in her family. Twenty minute whole blood clot test (20WBCT) was done, which was positive at that time. Patient was treated with anticonvulsants and anti-snake venom immediately and was sent for a computerized tomogram (CT) scan. Six hours after administering anti-snake venom, 20-min clot test was repeated, which was negative. On follow up, her blood sugar, serum creatinine, blood urea, serum bilirubin, and liver function tests were with in normal limits. Bleeding time was 2 min and 5 s; clotting time was 3 min and 24 s. Her CT brain [Figure 1] showed an acute left capsuloganglionic infarct. Patient was kept on aspirin and clopidogrel and was discharged after recovery.
| Discussion|| |
Snake venoms can cause cellular injury through enzymes, polypeptide toxins, cytokines, and mediators. Important venom enzymes consist of proteases, hydrolases, hyaluroxidase, oxidases, phospholipases, and esterases. Among these enzymes, phospholipases A2 and proteases (especially metalloproteases) contribute significantly to tissue injury. Cytokines and vasoactive mediators are responsible for inflammatory changes and hemodynamic alterations that can ultimately lead to cellular injury.
The occurrence of vascular thrombosis in vessels adjacent to the site of envenomation is common. It is extremely rare for thrombosis to occur in distant vessels. Cerebral infarction following snake bite is rare and only few cases have been reported. There are several mechanisms by which cerebral infarction occur in snake envenomation.
- Hypotension due to hypovolemia from sweating, vomiting, decreased fluid intake, and bleeding tendencies. This leads to low flow state and watershed infarct.,
- Hypercoagulability can be due to procoagulants in the venom such as hydrolase, consumption coagulopathy phase of DIC.,
- Endothelial injury due to toxic vasculitis by the components of venom can lead to thrombosis.,
The infarct in our patient was not in classical watershed territory and hence hypotension may not be the cause. Clotting time and bleeding time were normal, which ruled out DIC; there are no other clinical manifestations of DIC (only 20WBCT was positive). The possible cause of infarct in this case was toxic vasculitis which causes injury to the endothelial cells by snake venom toxin.
Other causes of stroke in young, including connective tissue disorders, are also important and should be considered in differential diagnosis of our case. However, our patient was a case of snake envenomation only because the initial 20-min clot test, which was positive initially was corrected after giving anti-snake venom (ASV) to the patient. There was history of snake bite and fang marks were noted and then only she was given ASV in the casualty. There was no history suggestive of connective tissue disorders in our patient. Of course, the mechanism of action of envenomation of snake bite includes vasculitis, thinking snake bite possibility appears to be more reasonable rather than the connective tissue disorder presenting at the same time of snake bite, as fang marks were present. Hence, it may not be a case of stroke in young due to connective tissue disorders, and other differential diagnoses of stroke in young can be ruled out. In the context of correction of 20-min WBCT with ASV, it may not be logical to think about other causes of stroke in young.
The 20-min blood clot test was adopted as the standard test of coagulopathy. It is simple to carry out and give reliable indication of consumption coagulopathy. Evidence of coagulopathy determines that the biting species is viperine. Neither of the Elapids, i.e., cobra or krait are known to give anti-hemostatic symptoms. In our case, the 20-min blood clot test was positive initially and become negative after giving ASV. Hence, it must be a viper snake bite. Primary coagulopathies should also be an important differential diagnosis. However, if it is a case of primary coagulopathies, patient could not recover with ASV (as the 20-min clot test after ASV is normal) and also there was no past history of bleeding. Therefore, other primary coagulopathies can be ruled out.
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| References|| |
Mugundhan K, Thruvarutchelvan K, Sivakumar S. Posterior circulation stroke in young male following snake bite. J Assoc Physicians India 2008;56:713-4.
Rifant B, John J. Cerebral Infarction in a young female following snake bite. Stroke 1985;16:328-30.
Upadhyaya AC, Murthy GL, Sahay RK, Srinivasan VR, Shantaram V. Snake bite presenting as acute myocardial infarction, ischaemic cerebrovascular accident, acute renal failure and disseminated intravascular coagulopathy. J Assoc Physicians India 2000;48:1109-10.
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.
] [Full text]
Sitprija V. Snakebite nephropathy (Review Article). Nephrology 2006;11:442-8.
Christ A, Loannidis PJ, Ktenasjohn. Acute M1 and CVA in a young girl after a viper bite. Br Heart J 1982;47:500-3.
Panicker JN, Madhusudhanan S. Cerebral infarction in a Young Male following Viper envenomation. J Assoc Physicians India 2000;48:744-5.
Ghosh S. Management of Snake Bite-An Update. Med Update 2008;18:691-6.