Coagulopathy after snake bite byBothrops neuwiedi: Case report and results of in vitro experiments

Abstract

Coagulation studies were performed in a patient who had been bitten by a snake of the species Bothrops neuwiedi. The patient presented with hemorrhagic necrosis at the envenomization site and considerable bleeding from venous puncture sites. He developed a severe defibrination syndrome with a clottable fibrinogen level of approximately 0.1 g/l. Fibrinogen was not measurable by clotting time assay. Fibrin degradation products were greatly elevated. Treatment with antivenom caused an anaphylactic reaction within ten minutes and serum sickness after three days. In vitro experiments revealed that B. neuwiedi venom directly activates Factors II and X, but does not activate Factor XIII. In vivo consumption of Factor XIII after B. neuwiedi envenomization is ascribed to the action of Factor IIa. At low venom concentrations clotting is initiated by activation of prothrombin by the venom either directly or via Factor X activation. Treatment with heparin might be beneficial in coagulopathy secondary to snake bite by reducing circulating active thrombin. The venom contains thrombin-like proteases which cause slow clotting of fibrinogen, and plasmin-like components causing further proteolysis of fibrinogen and fibrin. Antivenom has no effect on the proteolytic action of the snake venom. The in vivo effects of antivenom are presumably caused by acceleration of the elimination of venom components from the circulation. Intravenous administration of antivenom caused normalization of blood coagulation parameters within 48 h.

Bothrops jararaca Venom Metalloproteinases Are Essential for Coagulopathy and Increase Plasma Tissue Factor Levels during Envenomation

“…In fact, FVII has the shortest mean-life (4–7 h) of blood coagulation factors in the circulation, and the lack of diminished FVII levels may be ascribed to an increased hepatic synthesis that may occur in stressful situations [32]. A steady decrease in FVII levels has been reported for one patient bitten by Bothrops neuwiedi [74], although most snakebites in humans do not induce a marked FVII consumption [75]–[78]. As shown elsewhere [42], the coagulant activity of BjV does not depend on FVII in vitro .…”

Clinical characteristics of children with snakebite poisioning and management of complications in the pediatric intensive care unit

“…The venom of the snake results in capillary leak syndrome, platelet dysfunction, breakdown of vascular integrity and hemolysis, thrombotic squeals and shock by effecting stimulatory and inhibitory hemolytic mechanisms such as fibrinolysis 3,22 . Snake venom may cause clotting abnormalities by decreasing the levels of active thrombin and fibrinogen in the circulation with plasmin‐like proteases, thrombin‐like proteases and other enzymes they contain 23 . On laboratory evaluation, thrombocytopenia, elongation of PT and aPTT, DIC, and markers of hemolysis and rhabdomyolysis may be seen 5,18,24–26 .…”

“…3,22 Snake venom may cause clotting abnormalities by decreasing the levels of active thrombin and fibrinogen in the circulation with plasmin-like proteases, thrombin-like proteases and other enzymes they contain. 23 On laboratory evaluation, thrombocytopenia, elongation of PT and aPTT, DIC, and markers of hemolysis and rhabdomyolysis may be seen. 5,18,[24][25][26] Serum fibrinogen concentration may be decreased due to the thrombin-like activity of snake venom and fibrin degradation products may be increased due to the secondary activation of fibrinolytic system; however, AT III may be either normal or increased.…”

Estudo dos efeitos das serinoproteinases PA-BJ e Giroxinas isoladas de venenos de serpentes em cultura de células endoteliais

“…Os distúrbios da coagulação estão entre os efeitos mais graves do envenenamento causado pelas serpentes da família Viperidae (KAMIGUTI et al, 1986;DEMPFLE et al, 1990;SANO-MARTINS e SANTORO, 2003). Dentre os componentes desses venenos, as metaloproteinases e serinoproteinases são as principais enzimas envolvidas em eventos relacionados aos distúrbios na hemostasia, decorrentes do envenenamento (para revisões vide BJARNASON e FOX, 1988/89;SERRANO e MAROUN, 2005).…”