Primary acute angle-closure glaucoma damage to cornea and lens.

The following corneal conditions will be considered: (1) pressure oedema; (2) oedema following endothelial damage; (3) persistent folds in Descemet's membrane; (4) vascularization; (5) lipoid infiltration; (6) band-shape degeneration. Oedema of the cornea caused by a sudden elevation of intra-ocular pressure is a diagnostic feature of acute angle-closure glaucoma. If the intra-ocular pressure rises to 40 mm. Hg within some hours, corneal oedema is likely to occur, but corneal oedema may not accompany intra-ocular pressures of 80 mm. Hg if the increase has occurred slowly over some months or years. The acute pressure oedema tends to involve all the cornea, but not infrequently only the central area may be affected leaving the periphery clear. The pressure oedema affects especially the epithelium and superficial stroma so that it can be temporarily cleared with topical glycerine to permit gonioscopic and other examinations (Cogan, 1943). With reduction in intra-ocular pressure it disappears quickly. When a severe attack of angle-closure glaucoma has persisted for twenty-four hours or more, the intra-ocular pressure may still be reduced rapidly by appropriate treatment, but the cornea remains oedematous. This type of oedema then shows as a thickening of the cornea with folds in Descemet's membrane. It is slow to clear, taking several days or even some weeks. It is less readily cleared with glycerine, and its persistence in the presence of low intra-ocular pressures is a striking feature. It is not cleared by hypertonic infusions such as 20 per cent. mannitol. It is probably caused by aqueous seeping through damaged endothelium and its clearing is dependent upon the recovery of these cells. Its regression is frequently assisted by topical corticosteroid eyedrops. Folds in Descemet's membrane may persist long enough for them to develop hyaline appearances and they may then become permanent.