Methidathion Poisoning.
10.4266/kjccm.2016.00073
- Author:
Ki Hoon KIM
;
Se Hun KIM
;
Charles HER
- Publication Type:Case Report
- Keywords:
acetylcholine;
aspergillosis;
ganglia;
sympathetic;
organophosphate poisoning
- MeSH:
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
- From:Korean Journal of Critical Care Medicine
2017;32(4):363-369
- CountryRepublic of Korea
- Language:English
-
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.
