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Figure 12-14 Lipid keratopathy secondary to corneal vascularization. (Courtesy of Cornea Service, Paulista School of Medicine, Federal University of São Paulo.)

Endothelial Degenerations

Iridocorneal endothelial syndrome

Iridocorneal endothelial (ICE) syndrome is a spectrum of disorders characterized by varying degrees of iris changes, abnormal corneal endothelium, and peripheral anterior synechiae.

The pathogenesis of ICE syndrome is unknown but appears to involve an abnormal clone of endothelial cells that takes on the ultrastructural characteristics of epithelial cells. The abnormal clone could originate at birth or before. Herpesvirus DNA has been identified in some corneal specimens following keratoplasty and in the aqueous humor of some patients.

Varying degrees of progressive endothelialization take place in the anterior chamber angle and on the iris surface. Frequently, the border between the abnormal and normal endothelium can be seen at the slit lamp using specular reflection. When the abnormal endothelium migrates over the anterior chamber angle, the resultant peripheral anterior synechiae and outflow obstruction produce glaucoma. Three clinical variations of the syndrome have been described in the literature. When the disease is confined to the inner corneal surface, corneal edema may result from subnormal endothelial pump function, producing the Chandler variant of ICE syndrome. When the abnormal endothelium spreads onto the surface of the iris, the resulting contractile membrane may produce iris atrophy, corectopia, and polycoria, hallmarks of the essential iris atrophy variant of ICE syndrome (Fig 12-15). The Cogan-Reese variant shows multiple pigmented iris nodules, also produced by the contracting endothelial membrane. Iris nevus syndrome, considered by some a possible fourth variant of ICE syndrome, can be distinguished from the Cogan-Reese variant by the presence of diffuse nevi or heterochromia of iris.