Visual impairment following aluminum phosphide poisoning: A rare case

• Published in: Clinical case reports Vol. 11; no. 6; pp. e7422 - n/a
• Main Authors: Kargar, Alireza, Noroozian, Maryam, Ramezani, Mahtab, Shadnia, Shahin, Mostafazadeh, Babak, Erfan Talab Evini, Peyman, Rahimi, Mitra
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01-06-2023; John Wiley and Sons Inc; Wiley
• Subjects: Acidosis; Aluminum; aluminum phosphide; Blood pressure; cardiogenic shock; Case Report; Case reports; cerebral atrophy; Consciousness; Cytochrome; Entrance examinations; Extubation; Glasgow Coma Scale; Heart rate; Hospitalization; hypoperfusion; Hypoxia; Insulin; Laboratories; Magnetic resonance imaging; Metabolism; Neurology; Pharmacology and Pharmacy; Poisoning; Psychiatrists; Psychiatry; Psychotherapy; Suicides & suicide attempts; Toxicology; Visual acuity; Visual impairment; visual loss; Iran; cerebral atrophy; cardiogenic shock; hypoperfusion; poisoning; visual loss; aluminum phosphide
• ISSN: 2050-0904; 2050-0904
• DOI: 10.1002/ccr3.7422

Key Clinical Message
Aluminum phosphide poisoning may cause rare visual impairment. In a case, a 31‐year‐old female, visual loss was linked to shock‐induced hypoperfusion, causing oxygen lack and cerebral atrophy, emphasizing the need for identifying atypical symptoms.
This case report describes the multidisciplinary evaluation of a 31‐year‐old female patient who suffered from visual impairment as a result of aluminum phosphide (AlP) poisoning. Phosphine, which is formed in the body when AlP reacts with water, cannot cross the blood–brain barrier; therefore, visual impairment seems unlikely to be the direct result of phosphine. To our knowledge, it is the first documented report of such impairment due to AlP.
This case report illustrates a rare consequence of aluminum phosphide (AlP) poisoning ‐ visual impairment ‐ in a 31‐year‐old female. In the pursuit of understanding the underlying pathophysiology, MRI scans were performed. The axial FLAIR sequence (A) revealed bilateral cortical hyperintensity, while the sagittal T1‐weighted sequence (B) showed no signal abnormality. While the toxic compound phosphine released by AlP cannot cross the blood‐brain barrier, the impairment was attributed to cerebral atrophy due to shock‐induced hypoperfusion.