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Snakebite-Induced Coagulopathy and Bleeding Disorders

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Abstract

Snake venoms target mainly neuromuscular and/or hemostatic systems. Each of them is a combination of several toxins. Therefore, coagulopathy is only a part of multi-systemic involvement from envenomation including muscular weakness, rhabdomyolysis, renal failure and hypotension. Kinetics studies reveal that viper venoms comprise long half-life components resulting in a delay onset and prolonged duration of bleeding in a subset of patients. On the other hand, elapid venoms are more rapidly cleared from the circulation showing faster recovery. Remarkably, snake venoms affect almost every component of hemostasis including vascular wall, platelets, coagulation factors, natural anticoagulants and fibrinolysis. They can be stimulatory or inhibitory through enzymatic or binding mechanisms. These effects can contribute to hemorrhagic, as well as thrombotic, manifestations of snakebites. The most prominent clinical syndrome is consumptive coagulopathy from the thrombin-like enzymes and/or coagulation factor activators in the venoms. In addition, anticoagulation syndrome, thromboembolism and thrombotic microangiopathy have been reported in victims of particular snake species. The key treatment of snakebites is antivenom that can promptly reverse coagulopathy in most situations.

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Correspondence to Ponlapat Rojnuckarin .

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Rojnuckarin, P. (2010). Snakebite-Induced Coagulopathy and Bleeding Disorders. In: Kini, R., Clemetson, K., Markland, F., McLane, M., Morita, T. (eds) Toxins and Hemostasis. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-9295-3_39

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