Obidoxime in acute organophosphate poisoning: 1 - clinical effectiveness

• Published in: Clinical toxicology (Philadelphia, Pa.) Pa.), 2009-09, Vol.47 (8), p.798-806
• Main Authors: Eyer, Florian, Worek, Franz, Eyer, Peter, Felgenhauer, Norbert, Haberkorn, Mike, Zilker, Thomas, Thiermann, Horst
• Format: Article
• Language: English
• Subjects: Acetylcholinesterase - blood; Acute Disease; Antidotes - administration & dosage; Antidotes - therapeutic use; Atropine - therapeutic use; Cholinesterase Inhibitors - poisoning; Cholinesterase Reactivators - administration & dosage; Cholinesterase Reactivators - therapeutic use; Cholinesterases - blood; Critical Care; Dimethoate - poisoning; Drug Administration Schedule; Drug Overdose - drug therapy; Drug Overdose - mortality; Erythrocytes - enzymology; Germany - epidemiology; Humans; Intensified monitoring; Neuromuscular Junction - drug effects; Neuromuscular Junction - metabolism; Obidoxime; Obidoxime Chloride - administration & dosage; Obidoxime Chloride - therapeutic use; Observational clinical study; Organophosphate pesticides; Organothiophosphorus Compounds - poisoning; Parathion - poisoning; Suicide; Time Factors; Treatment Outcome
• ISSN: 1556-3650; 1556-9519
• DOI: 10.1080/15563650903206828

Objective. The effects of obidoxime in the treatment of organophosphate poisoning were assessed by comparing the clinical course with its effects on laboratory parameters relevant to poisoning. In this article we report clinical findings and activity of cholinesterase in plasma and acetylcholinesterase (AChE) in red blood cells. In a linked paper we describe changes in neuromuscular transmission and atropine concentrations in the same patient cohort. Methods. We studied 34 atropinized patients with severe parathion, oxydemeton methyl, and dimethoate self-poisoning who were treated with obidoxime in a standard protocol. We measured the AChE activity in blood and related it to clinical features of organophosphate poisoning. Results. Patients poisoned with parathion responded promptly to obidoxime (250 mg bolus followed by continuous infusion at 750 mg day up to 1 week) with improvement of neuromuscular transmission and increased AChE activity. The effects were only transient in cases with the other poisons. Death (7 34) occurred late and was mostly due to complications rather than due to ongoing cholinergic crisis. Conclusions. Obidoxime appeared safe and reactivated AChE in parathion poisoning.