Severe organophosphate intoxication without classic cholinergic signs: A case report and updated literature review

Organophosphate compounds such as dichlorvos, a widely used pesticide, account for a substantial proportion of acute poisonings globally. These agents irreversibly inhibit acetylcholinesterase, leading to cholinergic overstimulation. A subgroup of these compounds, alkyl phosphates-originally developed as nerve agents such as tabun, sarin and soman-has been increasingly implicated in intentional ingestions. Diagnosis can be challenging, particularly in the absence of classic cholinergic features such as bradycardia, bronchorrhea and miosis. We present a case of a male patient in his early 20s who was admitted to the intensive care unit with impaired consciousness, respiratory failure, tachycardia and severe metabolic acidosis following ingestion of unidentified substances. Imaging revealed chemical gastritis and aspiration pneumonia. A profoundly reduced serum cholinesterase level prompted empiric initiation of obidoxime therapy. Admission toxicology was positive for amphetamines, plausibly explaining the patient's atypical tachycardia and attenuation of classical cholinergic signs. The patient recovered following intensive supportive care and later confirmed ingestion of dichlorvos in a suicide attempt. This review discusses the clinical presentation, diagnostic challenges and current evidence-based management of alkyl phosphate intoxication. Particular emphasis is placed on the utility of serum cholinesterase measurement, the role of oximes such as obidoxime, and adjunctive interventions including seizure control, and ventilatory support. Clinicians should be aware that severe organophosphate poisoning may occur even in the absence of classical cholinergic signs, requiring a high index of suspicion and timely antidotal therapy.