Cases reported "Snake Bites"

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1/5. Multiple thrombotic occlusions of vessels after russell's viper envenoming.

    Systemic bleeding due to consumption coagulopathy and thrombocytopenia due to activation of procoagulants is the leading manifestation and cause of death in russell's viper systemic envenoming. Thrombotic occlusion of the blood vessels is rare in cases of snakebite. In this report, two adult patients with russell's viper systemic envenoming presented multiple cerebral infarctions, digital gangrenes and ischaemic organs in addition to typical clinical manifestations of bleeding diathesis and renal involvement. Our findings in these two special cases suggest that the venom-induced coagulopathy and endothelium damage, predisposed by toxin-induced vasoconstriction, might be the possible mechanism of multiple thrombotic vascular occlusions in systemic envenoming of Formosan russell's viper.
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2/5. Femoral vessel entrapment and compartment syndromes following snakebite.

    A 15-year-old patient who had been bitten on the ankle by a snake presented with swelling extending to the chest wall, with significant haemostatic abnormalities. Compartment and femoral vessel entrapment syndromes are presented. Compartment syndrome is easily mimicked by snakebite without a compartment syndrome. Current measurement of intracompartmental pressure, diastolic or mean arterial blood pressure and resulting equations used to determine the need for fasciotomy do not take into account regional venous or arterial pressures. Combined vessel entrapment and compartment syndromes due to snakebite warrant urgent surgery once hypovolaemia and coagulopathy have been controlled.
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3/5. Thrombotic stroke following snake bites by the "Fer-de-Lance"bothrops lanceolatus in martinique despite antivenom treatment: a report of three recent cases.

    BACKGROUNDS: The severity of envenoming from bothrops lanceolatus is determined by the development of cerebral, myocardial or pulmonary infarctions, and occasionnaly by serious local envenoming. Introduction of specific antivenom has resulted in a dramatic improvement in the prognosis of this envenoming. Against this background, we report 3 recent cases of patients bitten by B. lanceolatus who developed cerebral infarctions despite early administration of antivenom. methods: In 1991 a protocol was designed to apply the same evaluation and treatment to all envenomed patients. The clinical results have been continuously monitored. RESULTS: Between April 1993 and July 2003, 128 envenomed patients (age 6-83 (mean 45) years) were treated. No coagulopathy, thrombotic complication or death occurred in patients who were given early antivenom therapy--up to 6h following the bite--and 126 patients recovered. Between August 2003 and October 2004, 10 additional patients (18-66 (mean 46) years) were given antivenom at the time of admission at hospital. Of these, 3 developed cerebral infarctions within 24h. Effectiveness of antivenom was tested on mouse, and found to be lower than specified by the manufacturer. DISCUSSION: Our data shows that recently the antivenom may have lost some of its efficacy. Possible mechanisms include variability in venom composition or loss of activity of the antibodies produced more than 15 years ago. The question is whether we should attempt to produce improved antivenom. This could include activity against the venom of bothrops caribbaeus from the neighbouring island of St Lucia, which shares a monophyletic group with B. lanceolatus and whose venom produces a similar thrombotic syndrome. CONCLUSION: Prevention of systemic vessels thrombosis remains the main therapeutic challenge of B. lanceolatus envenoming in martinique.
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4/5. Fibrinogenolytic afibrinogenemia after envenomation by western diamondback rattlesnake (crotalus atrox).

    The absence of fibrinogen and the presence of plasmic fragments X, Y, D, and E were demonstrated in a patient bitten by a western diamondback rattlesnake, crotalus atrox. The factor viii level and the platelet count were within normal limits. There were distinct changes of protease inhibitors in the patient's plasma. Alpha-1-protease inhibitor was elevated. Antithrombin-III was only slightly decreased after the envenomation, but alpha 2-antiplasmin and alpha 2-macroglobulin were initially significantly lowered, returning to normal values in 38 and 3 days, respectively. Plasmin-alpha 2-antiplasmin complex was present until day 10 after the envenomation. However, purified plasminogen was not activated in vitro by the venom. Cultured endothelial and smooth muscle cells from human blood vessels released an increased amount of plasminogen activator upon incubation with the venom. The release did not result from cell lysis. Platelets in normal human platelet-rich plasma were aggregated by 10 micrograms/ml of the venom, without serotonin secretion. The aggregation kinetics and serotonin secretion induced by adenosine diphosphate (ADP) or arachidonate were not significantly affected by the venom at 1-10 micrograms/ml. It is concluded that the predominant mechanism of afibrinogenemia in the patient after crotalus atrox bite resulted from primary fibrinogenolysis and not from a consumptive coagulopathy. The lytic state seemed to be induced through an indirect activation of plasminogen by vascular plasminogen activator, which was probably released from endothelial cells and smooth muscle cells by the snake venom.
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5/5. A case of intestinal infarction following Vipera aspis bite.

    A case of Vipera aspis bite followed by severe envenomation, shock, neurotoxic symptoms, myoglobinuria and coagulation disorders with thrombosis of the iliac vessels and intestinal infarction is described. A right hemicolectomy had to be performed. Treatment is described in detail. European adder bites may cause, although uncommonly, severe envenoming with unusual symptoms. The attending doctor must be prepared to face unusual diagnostic and therapeutic problems.
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