injuries poisoning
Snakebites
Pathophysiology of Snakebites
Snake venoms are complex substances, chiefly proteins, with enzymatic activity. Although enzymes play an important role, the lethal properties of venom are caused by certain smaller polypeptides. Most venom components appear to bind to multiple physiologic receptors, and attempts to classify venom as toxic to a specific system (eg, neurotoxin, hemotoxin, cardiotoxin, myotoxin) are misleading and can lead to errors in clinical judgment. The complex venom of most North American pit vipers has local effects as well as systemic effects such as coagulopathy. Effects may include Local tissue damage, causing edema and ecchymosis Vascular endothelial damage Hemolysis A disseminated intravascular coagulation (DIC)–like (defibrination) syndrome Pulmonary, cardiac, renal, and neurologic defects Venom alters capillary membrane permeability, causing extravasation of electrolytes,albumin, and red blood cells through vessel walls into the envenomated site. This process may occur in the lungs, myocardium, kidneys, peritoneum, and, rarely, the central nervous system. Common clinical syndromes secondary to severe pit viper envenomation include the following: Edema:Initially, edema, hypoalbuminemia, and hemoconcentration occur. Hypovolemia:Later, blood and fluids pool in the microcirculation, causing hypotension, lactic acidemia, shock, and, in severe cases, multisystem organ failure. Effective circulating blood volume falls and may contribute to cardiac and renal failure. Bleeding:Clinically significant thrombocytopenia (platelet count<20,000/mcL) is common in severe rattlesnake bites and may occur alone or with other coagulopathies. Venom-induced intravascular clotting may trigger DIC-like syndrome, resulting in bleeding. Renal failure:Renal failure may result from severe hypotension, hemolysis, rhabdomyolysis, nephrotoxic venom effects, or a DIC-like syndrome. Proteinuria, hemoglobinuria, and myoglobinuria may occur in reaction to severe rattlesnake bites. The venom of most North American pit vipers causes very minor changes in neuromuscular conduction, except for Mojave and eastern diamondback rattlesnake venom, which may cause serious neurologic deficits. Venom of these snakes contains primarily neurotoxic components, which cause a presynaptic neuromuscular blockade, potentially causing respiratory paralysis. The lack of significant proteolytic enzyme activity accounts for the paucity of symptoms and signs at the bite site. 