Citation

Michael AP, Mostafa A, Cooper JM, Grice J, Roberts MS, Isbister GK. Clin. Toxicol. (Phila) 2015; 53(7): 633-635.

Affiliation

Emergency Department, Bundaberg Hospital , Bundaberg, Queensland , Australia.

Copyright

(Copyright © 2015, Informa - Taylor and Francis Group)

DOI

10.3109/15563650.2015.1054504

PMID

26065362

Abstract

OBJECTIVE: To describe the clinical effects, pharmacokinetics, and pharmacodynamics of plasma and acetylcholinesterase in an aldicarb (a carbamate insecticide) overdose. CASE REPORT: A 57-year-old female was found unconscious and incontinent of urine after ingesting aldicarb. She was bradycardic, hypotensive, hypersalivating, clammy, had small pupils, and generalized weakness. She was intubated, ventilated, and treated with large atropine doses (50 mg and 20 mg/h infusion) and adrenaline. She improved hemodynamically over 24 h, but remained comatose for another 24 h, before recovering without sequela. Aldicarb concentration at admission was 2.18 μg/ml and concentration-time data best fitted a two compartmental model with first order absorption and a time of ingestion 4.5 h preadmission. The half-life of distribution was 0.4 h and half-life of elimination, 13 h. Plasma cholinesterase concentration at admission was 0.3 kU/L (Reference range[RR]:4.3-10.6 kU/L) and red cell cholinesterase was 10 U/gHb (RR:38-66 U/gHb). The IC50 was 0.15 μg/ml and 0.26 μg/ml for plasma and red cell cholinesterase, respectively.

DISCUSSION: Aldicarb poisoning causes rapid onset severe toxicity with muscarinic and nicotinic excess, seizures, and decreased consciousness. Cholinesterases rapidly recover once aldicarb concentrations decrease and precede clinical recovery.

Language: en