Poisonous snake bites

Of the 3,000 species of snakes in existence, only about 15% worldwide and 20% in the United States are dangerous to humans because they have venom or venomous secretions. Every U.S. state except Alaska, Maine, and Hawaii has at least one naturally occurring species of venomous snake. Almost all of these are pit vipers (also called pit vipers because of the pit-like depressions on either side of their heads that act as heat-sensing organs) and include rattlesnakes, copperheads, and water moccasins. About 7,000 to 8,000 snake bites occur each year. Rattlesnakes bite more often than other snakes, and almost all of their bites are fatal. Copperheads and, to a lesser extent, water moccasins cause the majority of other venomous bites. Bites from coral snakes (aspid) and imported species (zoos, schools, snake farms, hobby and professional collections) account for less than 1% of all bites. Most victims are males aged 17-27, 50% of whom grabbed or teased the snakes while drunk. Snakes most often bite the upper limbs. Five to six fatalities are recorded each year. Fatalities are influenced by age (old or very young), handling of captive snakes (more important than in the case of wild snakes), delay in treatment and insufficient treatment.

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Prevalence of venomous snakes

Snake habitat	Snakes
Africa	Pig-faced snake
	Gaboon viper
	Ground viper
	Natal Black Snake
	Boomslang
	Tarantula snake
	Ground viper
	Mamba
Asia	Asian Rattlesnake
	Russell's viper
	Red-spotted Asian water snake
	Malaysian Rattlesnake
	Krait
	King Cobra
Australia	Taipan
	Tiger snake
	Royal Brown
	Deadly Snake
	Red-bellied black
Central and South America	Rattlesnake
	Yam ko head viper
	Bush Master
	Coral snake
	Tree pit viper
	Mexican Copperhead (Pit Viper)
Europe	Common viper
	Asp viper
	Long-nosed viper
	Turkish viper
	Blunt-nosed viper
Indian and Pacific Oceans	Sea snakes
	Sea kraits
Middle East	Sand viper
	Horned viper
	Ground viper
	Natal Black Snake
	Ground viper
	Egyptian Cobra
	Sinai viper
	Palestine viper
North America	Rattlesnakes (e.g., American or Texas diamondback rattlesnake, horned rattlesnake, banded rattlesnake, green rattlesnake, Mojave rattlesnakes)
	Copperhead snake
	Water pit viper
	Coral snake

Pathophysiology of venomous snake bites

Snake venoms are complex substances consisting mainly of proteins with enzymatic activity. Although enzymes play an important role, smaller polypeptides may contribute to the lethal properties of the venom. Most venom components bind to a variety of physiological receptors, so attempts to classify venoms by their effect on a specific system (e.g., neurotoxin, hemotoxin, cardiotoxin, myotoxin) are misleading and may lead to incorrect clinical judgment.

The venom of most North American rattlesnakes is local, causing coagulopathy and other systemic effects. Local vascular damage, hemolysis, disseminated intravascular coagulation (DIC)-like syndrome, pulmonary, cardiac, renal, and neurological impairment are possible. The venom alters the permeability of the capillary membrane, causing leakage of electrolytes, albumin, and red blood cells in the affected area. This process can occur in the lungs, myocardium, kidneys, abdomen, and, less commonly, the central nervous system. Edema, hypoalbuminemia, and hemoconcentration initially develop. Later, congestion of blood and fluid in the microcirculatory bed develops, causing arterial hypotension, lactic acidosis, shock, and, in severe cases, multiple organ failure. The effective circulating blood volume decreases, which can cause cardiac or renal failure. Clinically significant thrombocytopenia (platelet count <20,000 cells/μL) may occur after a rattlesnake bite, alone or in combination with other coagulopathies. Venom-induced intravascular coagulation may cause disseminated intravascular coagulation (DIC) with epistaxis, gingival bleeding, hematemesis, hematuria, internal hemorrhage, and spontaneous bleeding at the bite and venipuncture sites. Renal failure may result from severe hypotension, hemolysis, rhabdomyolysis, nephrotoxicity from the venom, or DIC. Proteinuria, hemoglobinuria, and myoglobinuria may occur after a rattlesnake bite. The venom of most North American rattlesnakes produces very little alteration in neuromuscular conduction, with the exception of the Mojave Desert rattlesnake and the diamondback rattlesnake, which can cause severe neurological damage.

Coral snake venom contains mainly neurotoxic components that cause presynaptic neuromuscular blockade and may cause respiratory paralysis. The lack of sufficient proteolytic enzymatic activity explains the minor severity of symptoms at the site of the snake bite.