Snake Scorpion and Spider Venoms

Pathogenesis and Pathophysiology. Most animal neurotoxins affect the cholinergic system through either enhancement or blockade. Snake venoms are extremely toxic to cardiac muscle, coagulant pathways, and the nervous system. y Snake venom acts either presynaptically as a toxin that inhibits the release of acetylcholine from presynaptic cells in the neuromuscular junction or postsynaptically as an agent that produces a nondepolarizing neuromuscular block. The resulting effect is a depression of cholinergic function at the neuromuscular junction. There is little evidence that snake bites act directly on the nervous system. Spider venom causes a release of acetylcholine, producing tetanic spasms followed by paralysis.

Epidemiology and Risk Factors. Poisonous snakes include vipers, rattlesnakes, cobras, kraits, mambas, and the American coral snake. Spiders such as the black widow probably account for most of the neurotoxic syndromes that occur after spider bites. Fatalities associated with spider bites occur in approximately 2.5 to 6 percent of cases.y Tarantula bites are probably similar to those of the black widow spider.

Clinical Features and Associated Findings. The clinical presentation of persons with a snake bite include localized pain and swelling, headache, vomiting, loss of consciousness, paresthesias, ptosis, loss of vision secondary to coagulation disturbances, and hemorrhage into the retina. Symptoms after snake bite may develop in from 1 to 10 hours. Beginning signs of paralysis include difficulty with swallowing and opening the mouth. Depending on the species, scorpion stings may include both local and systemic complications. Early symptoms include pain, swelling, excessive salivation, sweating, and abdominal pain. Death may result from hypertension, peripheral circulatory collapse, and cardiac failure. Neurological sequelae are more common in children than in adults and include overexcitement, muscle rigidity, convulsions, and alteration of mental status, which is probably secondary to hypoxia. In those with spider bites, neurological sequelae include paresthesias, fasciculations, tremor, and hyperreflexia during the excitatory phase.

Differential Diagnosis and Evaluation. In patients with snake bites it is especially important to attempt to identify the specific snake involved, since a number of antivenins have been developed against specific poisons.

Management. Treatment of snake bites involves administration of anticholinesterases and specific antivenin as early as possible after the bite. If these are administered prior to the development of major weakness, both pre-and postsynaptic toxic effects can be aborted. Mechanical respiration may also be warranted. During the acute stages after a spider bite, atropine can be administered to control the cardiac muscle effort; gradual recovery will occur over approximately 2 days. Treatment for scorpion bites focuses primarily on supportive respiratory and cardiac measures and attention to coagulation. y

Prognosis and Future Perspectives. Survival depends heavily on the control of cardiac and coagulation defects. The development of effective antitoxins and more rapid access to supportive care centers may improve the prognosis.

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