Organophosphorus compound poisoning continues to be a significant clinical concern in developing countries, presenting with diverse neurological and systemic complications. While cholinergic crisis and intermediate syndrome are well-recognised sequelae, serotonin syndrome remains a rare and underreported complication in such cases. We describe the case of a 48-year-old man who intentionally ingested a large amount of a chlorpyrifos-based pesticide (Killer 505) in an act of self-harm. Upon admission, he was drowsy but arousable, with a Glasgow Coma Scale (GCS) score of 14/15, and was initially managed with atropine and pralidoxime infusions. By the fourth day, he developed signs of intermediate syndrome and required mechanical ventilation. On day 7, he was started on ondansetron 8 mg intravenously every eight hours for persistent nausea. Within 24 hours, he developed fever, agitation, spontaneous clonus, and hyperreflexia. Clinical assessment, supported by Hunter’s Criteria, led to a diagnosis of serotonin syndrome. His brain Magnetic Resonance Imaging (MRI) showed old infarcts but no new findings to explain the sudden change in his neurological status. After stopping ondansetron, his condition improved rapidly, confirming the diagnosis. He was later decannulated and discharged with a full recovery. This case illustrates that ondansetron, a 5-HT3 antagonist, can trigger serotonin syndrome in high-risk individuals, especially those already affected by neurotoxicity from organophosphorus compound poisoning. Early detection and withdrawal of the triggering drug are critical. Clinicians must remain vigilant for unusual symptoms and drug-induced effects in complex toxicology cases.
Reddy et al. (Fri,) studied this question.