Hematologic Changes with Crotalid Envenomation

Blood in the local tissues is anticoagulated. Ecchymosis and discoloration of the skin often appear in the area of the bite within several hours. Vesicula-tions may be found within three hours. Hemorrhagic vesiculations and petechiae are common, and thrombosis may occur in superficial vessels. Necrosis develops in many untreated victims. Subcutaneous hemorrhage has been reproduced in mice with injection of venom damaging capillaries by a direct lysis of endothelial cells, which resulted in hemorrhage by rhexis (rupture of vessel) (26,41).

The proteolytic activity of some enzymes can activate the coagulation or fibrinolytic system. The Eastern diamondback rattlesnake can cause nearly total defibrination (with relative sparing of platelets), yet the patient rarely bleeds. Envenomation by the Southern Pacific rattlesnake (C. viridis helleri) is associated with rapid, severe thrombocytopenia with little evidence for fibrinogenolysis (23).

Laboratory evaluation after envenomation reveals hemoconcentration, coagulation abnormalities, with thrombocytopenia followed by decreased fibrinogen, increased fibrin split products from fibrinolysis, prolonged pro-thrombin time and partial thromboplastin time (4,42).

The mechanism of venom-induced thrombocytopenia is unclear, but is thought mainly to be secondary to the action of phospholipases contained in the venom that damage platelet membranes and trigger platelet destruction. Prompt antivenin administration is usually followed by a sustained rise in platelet counts. Thrombocytopenia can be recurrent in a crotaline enveno-mation and can be resistant to antivenom therapy (43-46).

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