Acute Corneal Decompensation After Magnetic Resonance Imaging Due To A Retained Metallic Intraocular Foreign Body

To report acute corneal endothelial failure caused by magnetic field–induced displacement of a long-standing retained metallic intraocular foreign body (IOFB) and to emphasise the pathophysiological mechanism of rapid corneal decompensation following endothelial trauma.

Ophthalmology Clinic, Clinical Hospital Centre Zagreb, Croatia

A 37-year-old male presented to the ophthalmic emergency department with sudden visual deterioration in the right eye approximately 30 minutes after MRI of the spine. Best-corrected visual acuity was 20/100. His medical history revealed ocular trauma 20 years earlier, when a metallic fragment struck the right eye while hammering metal, resulting in traumatic hyphema. At that time, no intraocular foreign body had been identified despite the reported mechanism of injury, and the patient remained asymptomatic thereafter. On presentation, slit-lamp examination demonstrated diffuse stromal oedema with Descemet membrane folds, consistent with acute endothelial decompensation. The iris showed focal traumatic changes. A small metallic IOFB was identified within the iridocorneal angle at the 9 o’clock position. Magnetic field–induced displacement of the retained metallic IOFB was presumed to have caused direct mechanical endothelial trauma and acute disruption of endothelial barrier and pump function. Ultrasound biomicroscopy confirmed localisation of the foreign body within the anterior chamber angle without posterior segment involvement. Surgical removal of the foreign body was performed. Postoperatively, intensive topical therapy was initiated, including dexamethasone eye drops and dexpanthenol gel, combined with hypertonic saline eye drops. Progressive resolution of corneal oedema and visual improvement were observed within seven days.

A long-standing retained metallic intraocular foreign body may remain clinically silent for decades; however, exposure to MRI can induce migration of a ferromagnetic fragment, leading to displacement into the iridocorneal angle and direct endothelial trauma. This may result in acute endothelial cell loss, disruption of barrier and pump function, persistent corneal oedema, anterior chamber inflammation and hyphema. Severe endothelial damage can progress to bullous keratopathy, irreversible stromal scarring and, in advanced cases, the need for endothelial keratoplasty. Thorough trauma history and careful pre-imaging assessment are essential to prevent avoidable vision-threatening corneal complications.