Introduction. In the contemporary world, the problem of poisoning caused by organophosphorus compounds (OPs) is of great concern, with the risk of exposure to OP nerve agents remaining a reality in military settings. Healthcare professionals can utilize clinical cases of OP intoxication to prepare for the treatment of affected individuals. This study aims to investigate the characteristics of poisoning in a patient who suffered from acute oral exposure to OPs. Description of the clinical case. The patient was discovered in a state of unconsciousness on the staircase, with a bottle of AgranTM insecticide nearby. It was estimated that the patient had ingested approximately 600 milligrams of the substance per kilogram of their body weight. The acetylcholinesterase (AChE) activity in their serum was significantly diminished, measuring at 12 units per liter. Furthermore, the patient was also exposed to another organophosphorus (OP) substance, cypermethrin, at an estimated dose of 50 milligrams per kilogram. Upon admission, the severity of the patient’s condition was attributed to a cholinomimetic syndrome, accompanied by acute respiratory failure of mixed origin, decompensated mixed acidosis, and toxic encephalopathy. No abnormalities in neuromuscular conduction or transmission were observed. Timely etiological therapy with atropine and detoxification measures such as gastric lavage and hemosorption contributed to the normalization of the patient’s condition. Nonetheless, fourteen days following the exposure, there was a persistent and substantial reduction in the activity of serum cholinesterases and erythrocyte acetylcholinesterase. Conclusion. Consequently, it is reasonable to infer that acetylcholinesterase activity may not consistently correlate with the severity of OP intoxication in the prolonged post-toxic period. In the absence of comprehensive treatment for OP, extracorporeal detoxification emerges as a recommended approach. Limitations. In the performed study, the activity of erythrocyte AChE and serum butyrylcholinesterase was not evaluated, electromyography was not performed at the time of admission and during the start of treatment, the patient did not receive antidote therapy with cholinesterase reactivators.
Толкач et al. (Mon,) studied this question.