Cerebral infarction in a young female following snake bite.

Abstract

SUMMARYWe present a normal 13-year old female who developed left cerebral infarction following envenomation by the carpet viper (Echis car inat us). We have read of only one other case of cerebral infarction following viper envenomation (Viperi russelli). Possible mechanisms for cerebral infarction in these circumstances are discussed. It is believed that this complication may be more common than is reported in the literature. Stroke Vol 16, No 2, 1985ECHIS CARINATUS, the saw-scaled viper, occurs throughout the Middle East and there have been sightings in many areas of Saudi Arabia. 1 Envenomation by this snake causes local swelling and severe tissue necrosis. Systemic complications are primarily related to bleeding due to blood depleted of fibrinogen and factors V, VII, II and XIII. This is manifested as hemorrhage in different parts of the body including the gums, nasopharynx, gastrointestinal tract, urinary tract and central nervous system. 2 The neurological symptoms include drowsiness, confusion and convulsions. Subarachnoid hemorrhage was seen in three of 115 patients reported from Nigeria, two of whom died. 2Arterial thrombotic complications in vessels near the site of some viper bites have been well described, 3 but arterial thromboses at distant sites are quite rare. We are aware of only two such instances reported in the literature. -5 In this communication, a Saudi Arabian patient who had cerebral infarction after a bite from Echis carinatus is described, and possible mechanisms for this phenomenon are discussed. Case HistoryA 13-year old right-handed Saudi Arabian female was clearing the ground for her sheep when she was bitten on her hand by a snake. She described the snake as being 50 centimetres long. When we showed her colored pictures of different snakes, she consistently pointed out Echis carinatus. A few minutes after the bite the patient developed severe pain and swelling in the right arm. She was taken to a nearby infirmary where she was given three 10 ml intravenous injections of polyvalent anti-snake serum (Behringwerke). She showed no immediate reaction to the antivenom and was subsequently transferred to a local hospital. On examination, the vital signs were stable. Two deep fang marks were seen on the right middle finger and the right arm was markedly swollen. A neurological examination was normal. Four hours after admission (ten hours after envenomation), she developed right hemiplegia with aphasia which evolved over one to two hours. Complete blood count including platelets, bleeding studies and prothrombin time, were normal. She received two more 10 ml injections of polyvalent anti-snake serum with no change in condition. Seventeen days later she was transferred to the King Faisal Specialist Hospital for investigation. The fang marks on the right middle finger were visible and healing, and there was mild swelling of the right arm. She had non-fluent aphasia with difficulty in expression and understanding. She also had right spastic hemiparesis involving the face and the arm, and to a...

Acute Cerebral Infarct on Evolution in Middle Cerebral Artery Following Viper Snake Bite

“….Bashir and jinkin reported patient in whom envenomation with Russell viperbite resulted in hemiplegia and aphasia. 7 The possible cause of infarct in our patient may be due to toxic vasculitiesbyendothelial damage by viper snake bite. Betteroutcome have been reported by early ASVS treatment by Thomas et al 12 Viper venom contains complex toxin affecting haemostatic mechanism 9 .…”

“…4,[7][8] . Mosquario et al, reported only 2.6% cases that is 8 patients in 309 cases of viper bite studied.…”

“…In large doses it can cause massive intravascular coagulation leading to small and large vessel occlusion resulting in infarction 10 .Direct action of venom on endothelial cell as reported by bashir. 7 Haemorrhagin the complement mediated toxic component leading to vascular spasm ,endothelial damage and increased vascular permeability resulting in vascular occlusion. 7,8 Hypercoagulation due to procoagulation in venom such as arginine ,esterase and hydrolase.…”

“…7 Haemorrhagin the complement mediated toxic component leading to vascular spasm ,endothelial damage and increased vascular permeability resulting in vascular occlusion. 7,8 Hypercoagulation due to procoagulation in venom such as arginine ,esterase and hydrolase. 7 hyper viscosity is mainly caused by hypo volume and hypoperfusion secondary to hypo perfusion contributes to vascular occlusion .The infarction is not related to inherent deficiency of protein c ,s and antithrombin3.…”

Cerebral infarction: an unusual manifestation of viper snake bite

“…3) Hypercoagulability -it can be due to procoagulants in the venom such as arginine, esterase, hydrolase, hyper viscosity due to hypotension, 4) Vascular -hemorrhaging are complement mediated toxic components of viperidae that causes severe vascular spasms followed by vasodilatation, while at capillaries they causes increased vascular permeability, resulting in hemorrhagic infarct. 3,7 Reports of thrombotic phenomenon following viper bite are small in number.…”