Organophosphate Poisoning: Peripheral Vascular Resistance – A Measure of Adequate Atropinization

Abstract

We report severe organophosphate poisoning complicated by hypotension and ischemic sequelae in two patients with pre-existing vascular disease. Both patients had a low total peripheral resistance and high cardiac output that were significantly reversed by doses of atropine in excess of those required to control other muscarinic symptoms. Cerebral infarcts and gangrene requiring a below knee amputation were complications of the poisonings. It is proposed that the ischemic complications are due to paradoxical vasoconstriction by acetylcholine at sites of endothelial injury. One patient, who had taken fenthion, also had a significantly delayed peak and prolonged, 2—3 week, systemic toxicity. We propose that stability of the plasma cholinesterase at 6 to 8 h after temporarily suspending oxime provides a rapid guide to the duration of therapy, especially in patients whose complications make clinical assessment difficult.

KEY WORDS:

• organophosphorus compound
• dimethoate
• fenthion
• cholinesterases
• poisoning
• human
• vascular resistance
• cardiac output
• vasoconstriction
• atropine
• pralidoxime
• intermediate syndrome