A patient undergoes phacoemulsification with posterior capsule rupture (PCR) and vitreous loss. The anterior chamber IOL (ACIOL) is implanted. Two years later, the patient develops bullous keratopathy. The pathophysiological mechanism is:

• A Elevated IOP from pupillary block by the IOL
• B Endothelial contact with ACIOL haptic causing chronic corneal endothelial cell loss ✓
• C Chronic inflammation from residual lens epithelial cells
• D Persistent cystoid macular edema causing anterior segment changes

Explanation

Anterior chamber IOLs (ACIOLs), especially older angle-supported designs, cause progressive corneal endothelial cell loss through chronic microtrauma from haptic-angle contact and anterior movement. This leads to pseudophakic bullous keratopathy (PBK) — once the most common indication for penetrating keratoplasty. Modern flexible open-loop ACIOLs have reduced but not eliminated this risk. Iris-claw (Artisan) or scleral-fixated posterior chamber IOLs are preferred when posterior capsule support is absent. Iridocyclitis-glaucoma-hyphema (UGH) syndrome is another ACIOL-specific complication.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

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Written and medically reviewed by the StethoPrep medical team.