Late posterior migration of glass intraocular foreign bodies.

ocular complications and resultant poor visual acuity, whereas the cases reported herein responded well to topical corticosteroid therapy and had better visual outcomes. One patient did develop a choroidalneovascularmembrane formation 11 years after the initial diagnosis of VKH syndrome that has previously been reported to occur in 11% ofaffectedeyes. Ithasbeensuggested that chronic AU may lead to inflammatory events in the retina and choroid that damage the retinal pigment epithelium and Bruch’s membrane, causingchorioretinaldegenerationand choroidalneovascularmembraneformation,basedon thehistopathologic condition. However, this was localized and unassociated with any other posterior segment changes. The trigger for this recurrent AU remains unknown, but it cannot be purely a reflection of syndrome reactivation as the choroid and retina remained uninvolved in each case. Therefore, it seems probable that it may represent a secondary immune event. A similar phenomenon has been reported in patients with healed acute retinal necrosis, who may also demonstrate recurrent AU in the absence of posterior segment inflammation or recurrence of acute retinal necrosis. It has been suggested that the destruction of retinal tissue may release antigen that initiates an immune response to ocular tissue; similar to the sensitiztion to retinal S-antigen that follows panretinal photocoagulation. As this phenomenon does not occur in all patients with VKH syndrome, there may be the additional involvement of a genetic predisposition.