Organophosphate & carbamates, acute poisoning


Acute Poisoning



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The organophosphate and N-methyl carbamate insecticides cause accumulation of acetylcholine at nerve endings by poisoning the acetylcholinesterase enzyme. In carbamate poisoning, the inhibition of the enzyme is rapidly reversible, and the workers are often improved by the time of arrival at the clinic or emergency room. Organophosphates (OPs) can irreversibly bind to the enzyme so that normal enzyme activity can only be restored after the cells synthesize new acetylcholinesterase. This process takes up to 60 days. The primary route of occupational exposure is through the skin. FINDINGS: D--diarrhea; U--urination; M--miosis; B--bradycardia, bronchorrhea, bronchospasm; E--emesis; L--lacrimation; S--salivation, secretions, sweating; TREATMENT: Decontamination in the field should include undressing and washing with water and mild liquid detergent. Irreversible binding of OPs to the enzyme can be prevented by initiating treatment immediately with pralidoxime. Large doses of atropine are often necessary, especially after suicidal ingestions that are common in the third world. SURVEILLANCE: Routine biological monitoring of field workers and pesticide applicators exposed to OPs can be accomplished by periodic measurement of plasma and red blood cell acetylcholinesterase levels. Removal from exposure is recommended if enzyme activity drops below 70-75% of baseline. [LaDou, p. 583-92; AHLS, p. 237-52]


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Decreased activity of serum or red cell acetylcholinesterase

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