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ity to 28% of baseline within 2 hours of ingestion, with resolution of symptoms by 4 hours.6 In vitro the half life of cholinesterase inhibition activity is 30 to 40 minutes.24 In rats, drinking water concentrations of 19.2 parts per million of a 1:1 mixture of aldicarb sulfoxide and aldicarb sulfone resulted in a decrease in plasma pseudocholinesterase levels to 23% to 32% of normal with a decrease in RBC cholinesterase to 37% to 43% of normal.25

The treatment of carbamate poisonings is supportive in the majority of cases. Patients with dermal exposures should have their contaminated clothing removed and the involved skin cleansed with alkaline soap and water, with appropriate care to prevent exposure of the medical staff. For ingestions, gastric lavage and the administration of activated charcoal are recommended. In severe poisonings atropine may be useful in controlling secretions, and large quantities may be required. Since carbamates do not readily cross the blood-brain barrier, glycopyrrolate may be substituted for atropine to avoid significant central neurologic effects. Administration of cholinergic drugs, such as the succinylcholine given in our patient, should be avoided in carbamate poisonings.

The use of pralidoxime for carbamate pesticide poisoning is controversial. Most carbamate poisonings resolve within several hours without treatment other than atropine. Since the binding to cholinesterase enzymes is reversible, there is usually no need for oxime therapy. Clinical worsening after administration of pralidoxime, toxogonin, and obidoxime to animals has been described in animal experiments with the carbamate pesticide carbaryl.1,2 Obidoxime also interfered with the protective effect of atropine in carbaryl poisonings.2 However, for aldicarb poisoning, pralidoxime and obidoxime have been shown to improve mortality in rats,2 and toxogonin reduced toxicity in rats.1 In our patient we noted hypertension with the bolus administration of pralidoxime, but not with continuous intravenous infusion. While it is impossible to determine if the patient’s seizure was related to the second dose of pralidoxime, his clinical status was clearly deteriorating prior to the pralidoxime with documented acidemia and progressive difficulty maintaining his airway. Subsequent doses of pralidoxime appeared to improve our patient’s weakness without significant adverse effects.

In summary, we presented an unusual case of severe poisoning with aldicarb, a carbamate pesticide. To our knowledge, this is the first article on prolonged cholinesterase inhibition with aldicarb poisoning, and documents the highest combined blood concentration of aldicarb and its metabolites of any human poisoning in the medical literature. The patient appeared to benefit from oxime therapy, demonstrating neuromuscular improvement temporally associated with pralidoxime administration. Severe aldicarb poisonings may be life threatening and can be successfully managed in the same manner as organophosphate poisonings.

Accepted for publication June 8, 1993.

Presented at the American Academy of Clinical Toxicology in Tampa, Fla, September 19–22, 1992. Reprints not available.

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