CARBAMATE POISONING AND OXIME TREATMENT IN CHILDREN - A CLINICAL AND LABORATORY STUDY

Citation
M. Lifshitz et al., CARBAMATE POISONING AND OXIME TREATMENT IN CHILDREN - A CLINICAL AND LABORATORY STUDY, Pediatrics, 93(4), 1994, pp. 652-655
Citations number
24
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00314005
Volume
93
Issue
4
Year of publication
1994
Pages
652 - 655
Database
ISI
SICI code
0031-4005(1994)93:4<652:CPAOTI>2.0.ZU;2-H
Abstract
Objective. (1) Retrospective evaluation of the clinical course of carb amate poisoning and the effect of oxime therapy in children. (2) In vi tro study of the effect of oximes on the reactivation of carbamylated cholinesterase. Design. (1) Clinical survey: The records of 26 childre n intoxicated with carbamates were examined retrospectively. The poiso ning agents in all cases were positively identified as methomyl or ald icarb by gas chromatography-mass spectrometry. (2) Laboratory study: T he direct effect of obidoxime and of pralidoxime on acetylcholinestera se activity in vitro was investigated in normal human packed red blood cells pretreated with an organophosphate (paraoxon) or a carbamate (a ldicarb or methomyl). Clinical setting. Pediatric intensive care unit of a teaching hospital. Patients. Twenty-six infants and young childre n (aged 1 to 8 years) admitted to the pediatric intensive care unit wi th severe carbamate intoxication. Interventions. All cases had been tr eated with repeated doses of atropine sulfate (0.05 mg/kg) administere d every 5 to 10 minutes until muscarinic symptoms disappeared. Obidoxi me chloride (Toxogonin, 6 mg/kg) was administered on admission, and ag ain after 4 to 5 hours. Results. Predominant symptoms were related to central nervous system and nicotinic effects. All the patients showed marked improvement within several hours and recovered completely withi n 24 hours. None of the children deteriorated and none showed exacerba tion of cholinergic symptoms after obidoxime treatment. In vitro, oxim es reactivated acetylcholinesterase inhibited with paraoxon, whereas n o significant effect of oximes on carbamylated enzyme activity was obs erved. Conclusions. Based on the recovery of all cases, as compared wi th other reports of carbamate poisoning treated with atropine alone, i t is concluded that, in the case of aldicarb or methomyl poisoning, ox ime therapy apparently does not contribute to the recovery of poisoned patients. In cases of poisoning by an unknown pesticide or of mixed p oisoning, oxime therapy can prove beneficial because no negative effec ts of the therapy can be discerned.