Korean J Crit Care Med.  2017 Nov;32(4):363-369. 10.4266/kjccm.2016.00073.

Methidathion Poisoning

Affiliations
  • 1Department of Surgery, Inje University Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea.
  • 2Department of Anesthesiology, Inje University Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea. charles6133@msn.com

Abstract

Although methidathion is an organophosphate insecticide, it is different from the other organophosphates in terms of toxicity. Because of its relatively high fat solubility, the apparent volume of methidathion distribution throughout the body is very high, indicating that hemoperfusion is not effective in removing this organophosphate from the body. Redistribution of methidathion from fat to blood can also occur when plasma levels diminish. Additionally, acetylcholinesterase aging, which is the loss of an alkyl side chain that prevents reactivation by oximes, is very rapid so that the effective reactivation by oximes is thwarted. Thus, methidathion's effect on acetylcholinesterase inhibition is long lasting, particularly with a high dose. In addition to its parasympatholytic effect and ability to induce muscle paralysis, methidathion poisoning is associated with a profound and long-lasting circulatory collapse due to sympathetic ganglion blockade. This report presents the case of a 55-year-old man who accidentally ingested a high dose of methidathion. He later developed enteroinvasive aspergillosis infection-induced multiple bowel perforations on two separate occasions while on mechanical ventilator support, resulting in a fatal outcome. The renin-angiotensin axis activated by sympathetic ganglion blockade may have reduced the patient's splanchnic blood flow, contributing to translocation of endotoxin. Also, the effect of excessive acetylcholine on non-neuronal acetylcholine receptors may have contributed to the development of fatal enteroinvasive aspergillosis in this patient.

Keyword

acetylcholine; aspergillosis; ganglia; sympathetic; organophosphate poisoning

MeSH Terms

Acetylcholine
Acetylcholinesterase
Aging
Aspergillosis
Fatal Outcome
Ganglia
Ganglia, Sympathetic
Hemoperfusion
Humans
Middle Aged
Organophosphate Poisoning
Organophosphates
Oximes
Paralysis
Parasympatholytics
Plasma
Poisoning*
Receptors, Cholinergic
Shock
Solubility
Ventilators, Mechanical
Acetylcholine
Acetylcholinesterase
Organophosphates
Oximes
Parasympatholytics
Receptors, Cholinergic

Figure

  • Figure 1. Responses to angiotensin II (AII) infusion. The splanchnic vascular bed responds selectively by disproportionate vasoconstriction to a central intravenous infusion of angiotensin II, mimicking its response to cardiogenic shock. TSR: total splanchnic vascular resistance; TPR: total peripheral vascular resistance; NSR: non-splanchnic vascular resistance. Adapted from Reilly and Bulkley. Crit Care Med 1993;21(2 Suppl):S55-68 with permission of Lippincott Williams & Wilkins [2].


Reference

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