Autopsy findings and pathological correlates in delayed death due to aluminum phosphide (celphos) ingestion: A case report

Aluminum phosphide (AlP), commercially known as celphos, is a widely used agricultural fumigant and a highly lethal poison with high mortality rates. While death typically occurs within hours due to acute cardiogenic shock accompanied marked multiorgan congestion, extended survival (approximately 40 h) presents an atypical pathological picture. We present a case of a 62-year-old male who was admitted to the hospital following alleged consumption of celphos. Clinical evaluation revealed profound refractory metabolic and lactic acidosis alongside cardiovascular collapse. Despite resuscitation and aggressive supportive management, the patient succumbed. Postmortem examination by a forensic medicine expert revealed bilateral conjunctival icteric discoloration, gastric mucosal hyperemia with 45 mL pale white fluid, approximately 250 mL of straw colored serous peritoneal effusion, a markedly pale liver with yellowish discoloration suggestive of fatty change, and a pronounced pallor across brain, lungs, spleen, and kidneys with loss of corticomedullary differentiation. Chemical examination confirmed phosphine/AlP in preserved viscera. Extended survival of approximately 40 h can produce marked visceral pallor that is notably more pronounced than in classic congestive picture seen in rapid fatalities, alongside serous peritoneal effusion and gross hepatic changes suggestive of fatty change. Recognizing these delayed features within a balanced forensic interpretation is essential to differentiate delayed toxicological and ischemic sequelae from classical acute findings.