EPIDEMIOLOGY W-Methyl carbamates are cholinesterase inhibitors that are structurally related to the organophosphates. Commonly used carbamates are Sevin, Baygon, Lannate, and Aldicarb.

PATHOPHYSIOLOGY Carbamates transiently and reversibly inhibit the cholinesterase enzyme through carbamoylation. Regeneration of enzyme activity by dissociation of the carbamyl-cholinesterase complex occurs within minutes to a few hours. This involves rapid, spontaneous hydrolysis of the carbamate from the cholinesterase enzymatic site. Unlike organophosphate poisoning, it is not necessary for new enzyme to be synthesized for normal function to be restored.

CLINICAL FEATURES Symptoms of acute intoxication are similar to the cholinergic crisis observed with organophosphates but are of shorter duration. Because carbamates do not effectively penetrate the CNS, less central toxicity is seen, and seizures do not occur. Presentation of carbamate poisoning in childhood with a predominance of CNS depression and nicotinic effects differs clinically from that of adults.13

DIAGNOSIS Cholinesterase levels and thus enzymatic activity may return to normal spontaneously 4 to 8 h after exposure. Measurement of RBC cholinesterase activity is therefore not useful unless done shortly after poisoning.

TREATMENT Initial treatment is the same as for organophosphates. Atropine is the antidote of choice and is administered for muscarinic symptoms. This is usually all that is necessary while waiting for the carbamoylated acetylcholinesterase complex to dissociate and recover function. Therapy is usually not needed for more than 6 to 12 h. The use of 2-PAM in carbamate poisoning is controversial. The carbamate-binding half-life to cholinesterase is approximately 30 min, and irreversible binding does not occur; therefore, there is little need for 2-PAM. The older literature suggests that 2-PAM may potentiate toxicity of the carbamate carbaryl, but a recent study found benefit.14 Thus, it should not be avoided in severe carbamate poisonings. 2-PAM is indicated in mixed poisonings with an organophosphate and a carbamate or if the type of insecticide is unknown.

DISPOSITION Morbidity and mortality are limited because of the transient cholinesterase inhibition and rapid enzyme reactivation. These are less toxic and the clinical course more benign. Most patients recover completely within 24 h. In mild poisonings, observation suffices, and the patient may be discharged with follow-up. Moderate poisonings necessitate 24-h observation that includes ruling out concomitant exposure to or toxicity from inactive ingredients or vehicles such as hydrocarbons.

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