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Multiple Intravenous Bolus Dosing and Invasive Hemodynamic Assessment in a Hypoxia-Induced Mouse Pulmonary Artery Hypertension Model

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Hypotension in severe dimethoate self-poisoning.

James Davies¹, Darren Roberts, Peter Eyer

¹Department of Critical Care Medicine, Guy's and St Thomas' Hospital, London, UK.

Clinical Toxicology (Philadelphia, Pa.)

|November 13, 2008

Summary

Acute dimethoate pesticide poisoning causes severe hypotension and shock, leading to death within 48 hours. This organophosphorus (OP) poisoning syndrome is distinct and requires further study for effective treatment.

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Area of Science:

Toxicology
Clinical Medicine
Pharmacology

Background:

Acute self-poisoning with organophosphorus (OP) pesticides like dimethoate presents a higher fatality rate compared to chlorpyrifos.
Severe dimethoate poisoning exhibits a distinct clinical presentation, often involving hypotension progressing to shock within 12-48 hours post-ingestion.

Observation:

Three patients with severe dimethoate poisoning presented with inappropriate peripheral vasodilatation and profound hypotension.
Despite standard treatments including atropine, i.v. fluids, pralidoxime chloride, and inotropes, patients' hypotension progressed.
Cardiac monitoring and troponin T levels showed minimal evidence of primary cardiotoxicity until shortly before death.

Findings:

Severe dimethoate poisoning induces a syndrome of marked hypotension and distributive shock, resistant to conventional therapies.
The primary mechanism appears to be OP-induced low systemic vascular resistance (SVR), rather than direct cardiotoxicity.

Implications:

Further invasive studies on cardiac function and SVR are necessary to elucidate the pathophysiology of dimethoate poisoning.
Investigating the efficacy of vasopressors and high-dose atropine in treating this specific OP poisoning syndrome is warranted.