Mechanism of defibrination in humans after envenomation by the eastern diamondback rattlesnake

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Abstract
We prospectively studied the hemostatic system of ten persons bitten by the Eastern diamondback rattlesnake (Crotalus adamanteus) during 1978–1980. Blood was drawn when the patients arrived in the emergency room and every 6 hr thereafter. All envenomated victims developed incoagulable blood (defined by a thrombin time ≥ 120 sec, normal < 20 sec). Platelet counts and plasma levels of antithrombin III and factors II and VIII were not drastically altered, which distinguished this disorder from classic disseminated intravascular coagulation. Fibrinogen levels were markedly decreased (mean coagulable level of 0 mg/dl and antigenic levels of 99 mg/dl). Plasminogen levels were 20% of normal, alpha‐2‐plasminogen inhibitor was 17% of normal, and plasminogen activator was 20 times normal. Levels of fibrin degradation products peaked at a mean of 7,680 μg/ml. The magnitude and duration of the coagulopathy were proportional to the clinical severity of envenomation. Treatment with antivenin blunted the coagulopathy. Because venom from the Eastern diamond‐back rattlesnake does not directly activate plasminogen, we conclude that coagulopathy following envenomation by that reptile appears to be due to partial proteolysis of fibrinogen with secondary activation of plasminogen by released plasminogen activator, probably of endothelial orgin.