Modern strategies in therapy of organophosphate poisoning

Toxicol Lett. 1999 Jun 30;107(1-3):233-9. doi: 10.1016/s0378-4274(99)00052-1.

Abstract

Considering the various microscopic reactions as well as toxicokinetic and pharmacokinetic principles in therapy of organophosphate poisoning, the administration of obidoxime by an initial bolus dose followed by continuous infusion appears rational. Using this protocol, six patients each with parathion or oxydemeton methyl poisoning were treated. In parathion poisoning, reactivation was possible up to 7 days. At paraoxon concentrations > 0.1 microM obidoxime only partially reactivated acetylcholinesterase (AChE) of erythrocytes in vivo although reactivation could be assessed in vitro, which roughly fitted theoretical calculations. AChE-inhibitory material was detected up to 5 days. Cholinergic signs soon subsided when AChE was above 20% of normal, and atropine plasma levels could be kept below 7 ng/ml. In one patient brain damage persisted. Oxydemeton methyl poisoning responded to obidoxime therapy only when the oxime was instituted shortly after poisoning. Out of six patients one died. No intermediate syndrome and no signs of permanent hepatic dysfunction were found in the 12 patients.

MeSH terms

  • Acetylcholinesterase / blood
  • Cholinesterase Reactivators / therapeutic use*
  • Erythrocytes / enzymology
  • Humans
  • Insecticides / poisoning*
  • Obidoxime Chloride / therapeutic use*
  • Organothiophosphorus Compounds / poisoning*
  • Parathion / poisoning*

Substances

  • Cholinesterase Reactivators
  • Insecticides
  • Organothiophosphorus Compounds
  • Obidoxime Chloride
  • Parathion
  • methyl demeton
  • Acetylcholinesterase