Treatment of Massive Poisoning by the Organophosphate Pesticide Methidathion

Teitelman, U; Adler, Michaël; Levy, Itay; Dikstein, S.

doi:10.3109/15563657508988076

Cited by 7 publications

(1 citation statement)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The acute oral LI?5o in rats' ranges from 20 to 81 mg kg and up to 36% of the dose applied is recovered as carbon dioxide.2 Methidathion in itself is a poor cholinesterase inhibitor and it requires oxidation of the P-S bond to become active. 3 3 In chronic intoxication it does not produce alterations in cholinesterases in man.4 As far as we know, the only described case of massive poisoning with methidathion required admission to an Intensive Care Unit (ICU) and treatment with high doses of atropine and prolonged mechanical ventilation.5 5 We think that a case of acute methidathion poisoning in which we have used haemoperfusion, a treatment proposed to remove the phosphorus esters in severe poisoning,&dquo; could be of interest.…”

Section: Introductionmentioning

confidence: 98%

Acute Poisoning with Methidathion: A Case

et al. 1990

View full text Add to dashboard Cite

An acute poisoning in a 50-year-old man who ingested approximately 6.2 g of the phosphorus ester methidathion is described. The patient was treated with three haemoperfusions 23, 44 and 115 h after ingestion, with continuous gastric lavage, atropine and pralidoxime administration and with prolonged mechanical ventilation. Haemoperfusion was an ineffective epuration technique since it removed only 0.22% of the ingested methidathion. The clinical course wavered because of a probable redistribution of phosphorus ester from fat to blood. A plasma level higher than 100 μg l-1 was associated with the most serious phases. Methidathion was present in the plasma until the sixth day, in the urine until the seventh and in the gastric juice until the eighth. Its absence in the fat biopsy made on the tenth day was an aid to therapy. The phosphorus ester did not inhibit lymphocyte neuropathy target esterase (NTE), neither did it induce development of delayed polyneuropathy.

show abstract

Section: Introductionmentioning

confidence: 98%

Acute Poisoning with Methidathion: A Case

et al. 1990

View full text Add to dashboard Cite

show abstract

CNS involvement in acute organophosphate poisoning: Specific pattern of toxicity, clinical correlates and antidotal treatment

1988

View full text Add to dashboard Cite

The present review was designed to integrate both experimental and clinical data and to focus on the problems of management of severe cases of acute organophosphate poisoning, which always show CNS involvement. AChE activity, in discrete regions of the human brain, was studied by quantitative histochemistry of 40 mu thick sections. The regional effects of AChE inhibition by organophosphates was examined in a comparative study of the brains of two victims and two control brains, matched for age and sex. The pattern of AChE inhibition was regionally selective. The most significant decreases were observed in the neocerebellum, thalamic nuclei and the cortex. This specific distribution of AChE inhibition may be correlated with some of the clinical characteristics of acute organophosphate poisoning. The diagnostic value of blood AChE levels was examined in a personal series of 53 patients, who needed artificial ventilation, intensive care monitoring and antidotal treatment. The effects and side-effects of the antidotal treatment were reassessed. Recommended regimen of therapy was outlined, based upon experience in this series and in recent animal studies. The logical therapy would be and almost always in the co-administration of an anticholinergic drug (usually atropine) and an AChE reactivator (oximes) in order to rapidly obtain the most beneficial effect in the critically ill patient. Seizures that do not respond to the specific antidotal therapy, should be treated with I.V. benzodiazepines. Artificial respiration and supportive measures are essential for patient' survival. They enable the patient to gain the necessary time for sufficient recovery of AChE activity.

show abstract