Severe envenomation by Cerastes cerastes viper: an unusual mechanism of acute ischemic stroke.

J Stroke Cerebrovasc Dis

Department of Anesthesia and Intensive Care Medicine, Mohammed VI's University-Hospital of Marrakech, Cadi Ayyad University, Marrakech, Morocco.

Published: January 2014

AI Article Synopsis

  • Cerebral complications, especially ischemic events, from snake bites are rare, with only a few cases linked to viper bites reported in medical literature.
  • Three cases involving severe envenomation by Cerastes cerastes vipers demonstrated extensive local swelling and severe systemic effects, leading to unusual neurological symptoms like impaired consciousness and hemiparesis.
  • The ischemic strokes observed in these patients were associated with thrombotic complications occurring about 36 hours after the bites, likely due to the venom causing coagulopathy, vasculitis, or damage to blood vessel linings.

Article Abstract

Cerebral complications after snake bites--particularly ischemic complications--are rare. Very few cases of cerebral infarction resulting from a viper bite have been reported, and we call attention to this uncommon etiology. We discuss 3 authenticated reports of acute ischemic cerebrovascular accidents after 3 typical severe envenomations by Cerastes cerastes vipers. The 3 patients developed extensive local swelling and life-threatening systemic envenomation characterized by disseminated intravascular coagulopathy, increased fibrinolysis, thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure. This clinical picture involved atypical neurologic manifestations. These patients had either low Glasgow Coma Scale (GCS) or hemiparesis within hours to 4 days after being bitten, and they were found to have computed tomographic evidence of single or multiple ischemic (nonhemorrhagic) strokes of small- to large-vessel territories of the brain. One patient had good clinical recovery without neurologic deficits. Thrombotic complications occurred an average of 36 hours after being bitten, and their importance depends on the degree of envenomation. The possible mechanisms for cerebral infarction in these cases include generalized prothrombotic action of the venom (consumptive coagulopathy), toxin-induced vasculitis, and endothelial damage.

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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2012.07.008DOI Listing

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