It is difficult to judge which patients bitten by coral snakes are envenomated. The venom has rapid venous absorption, but symptoms may have delayed onset for 12 or more hours after the bite and are difficult to reverse or may even progress after administration of antivenin. If a patient has been bitten by a snake positively identified as a coral snake, with a history of the snake having chewed the affected area and fang marks present, administration of antivenin is warranted, even without any other signs or symptoms (33,35).
Eastern coral snake envenomation requires antivenin (Micrurus fulvius). It is derived from horses, and can cause allergic reactions immediately in someone with previous sensitization, or later cause serum sickness. The Arizona coral snake (Micruroides) is not associated with human fatality and has no specific antivenin (76).
Envenomation by the Eastern coral snake can result in major neurologic dysfunction, including cranial nerve paralysis. Elective endotracheal intubation is recommended if any signs of bulbar paralysis develop (including slurred speech and diplopia) to minimize the potential of aspiration before respiratory paralysis develops (35).
Elapidae venom can produce respiratory compromise followed by death within 10 minutes. The neurotoxic-acting polypeptides are known to act as a curare-like nondepolarizing paralytic agent. A therapy to consider in patients envenomated by cobras are the acetylcholinesterase inhibitors; a test dose of edrophonium followed by an infusion of neostigmine has occasionally been successful (77).
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