Mechanisms Of Coagulopathy After Envenomation By The Eastern Diamondback Rattlesnake

Abstract

All 34 patients seen at this hospital during the 19781980 period who were envenomated by poisonous snakes were studied in a prospective manner with respect to their hemostatic system. Blood was drawn on the patient’s arrival to the emergency room and every 6 h thereafter. Blood was analysed for platelet count; routine coagulation tests; levels of factors II, VIII, IX, XII; clottable fibrinogen; fibrinogen antigen; fibrin degradation products (FDP); plasminogen (PI); antithrombin III (AT III); α2 plasmin inhibitor (API); and plasminogen activator (PA). Twelve of the 34 patients underwent a coagulopathy as described below. These patients included all 10 patients envenomated by the Eastern diamondback rattlesnake (Crotalus adamanteus) and 2 of 17 patients bitten by the pygmy rattlesnake (Sistrurus miliarius). Values of all the above coagulation tests in 15 pygmy rattlesnake and 7 moccasin (Agkistrodon piscivorus) victims were indistinguishable from normal. Patients undergoing coagulopathy rapidly developed noncoagulable blood as defined by a thrombin time (TT) >120 s; blood remained incoagulable for an average of 18 h. The nadir clottable fibrinogen (0 mg/dl), fibrinogen antigen (99 mg/dl), Pl (20% of normal), API (17% of normal), and maximal levels of FDP (1:4096) and PA (20 times normal) were all significantly (p < 0.001) altered when compared with normal values. The platelet count and AT III levels were only midly decreased. Factors II, VIII, IX, and XII were normal. Because venom from the Eastern diamondback rattlesnake does not directly activate Pl, we conclude that the coagulopathy following envenomation by that reptile appears to be due to partial proteolysis of the fibrinogen with secondary activation of Pl by PA released from the endothelium. The resulting defibrination is distinguishable from disseminated intravascular coagulation.