## Viper Venom Coagulopathy **Key Point:** Serine proteases in viper venom are the primary agents responsible for coagulopathy and hemorrhagic manifestations. These enzymes directly activate coagulation factors, leading to consumption coagulopathy and fibrinolysis. ### Mechanism of Coagulopathy Serine proteases in viper venom: 1. Directly activate Factor X and prothrombin 2. Consume fibrinogen through thrombin-like activity 3. Trigger secondary fibrinolysis 4. Result in DIC (disseminated intravascular coagulation) ### Venom Component Functions | Component | Primary Effect | Clinical Manifestation | | --- | --- | --- | | Serine protease | Coagulation cascade activation | Hemorrhage, DIC | | Phospholipase A2 | Anticoagulant, hemolysis, myotoxicity | Hemolysis, rhabdomyolysis | | Neurotoxin | Neuromuscular blockade | Paralysis, respiratory failure | | Hyaluronidase | Tissue spreading factor | Edema, tissue damage | **High-Yield:** Viper bites (especially Russell's viper) cause predominantly **hemorrhagic and coagulation** manifestations, while elapid bites (cobra, krait) cause **neurotoxic** manifestations. This distinction is forensically important for determining snake species and time of death. **Clinical Pearl:** The 20-minute whole blood clotting test (WBCT) is used forensically to detect coagulopathy in suspected viper bite cases — a positive WBCT (blood remains unclotted after 20 minutes) confirms systemic envenomation. [cite:Parikh Textbook of Medical Jurisprudence Ch 15]
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