Snake Envenomation

Snake envenomation pathophysiology varies by species. In the US, 99% of venomous snakebites are from pit vipers (Crotalidae: rattlesnakes, copperheads, cottonmouths/water moccasins). Pit viper venom is a complex mixture of enzymatic proteins: metalloproteinases (cause tissue destruction, hemorrhage, and edema by degrading extracellular matrix and capillary basement membranes), phospholipase A2 (destroys cell membranes, causes myonecrosis), serine proteases (consume fibrinogen causing consumptive coagulopathy — venom-induced consumptive coagulopathy, VICC), and hyaluronidase (facilitates venom spread through tissues). The result is local tissue destruction with progressive swelling, ecchymosis, and pain spreading proximally, combined with systemic effects including coagulopathy (hypofibrinogenemia, thrombocytopenia, elevated PT/INR), hypotension, and rarely rhabdomyolysis. Coral snake (Elapidae) venom is primarily neurotoxic: postsynaptic neurotoxins block nicotinic acetylcholine receptors at the neuromuscular junction, causing progressive descending paralysis similar to myasthenia gravis — ptosis, dysarthria, dysphagia, respiratory failure. Approximately 25-50% of pit viper bites are 'dry bites' with no envenomation. The severity of envenomation depends on species, fang penetration depth, amount of venom injected, and bite location.