In primary angle closure glaucoma, the aqueous outflow is obstructed by apposition of the iris to the inner surface of the cornea and the trabecular meshwork. The acute form of the disease occurs unilaterally in middle-aged and elderly patients and presents with a rapid and painful rise in intraocular pressure. Both in acute and chronic angle closure glaucoma, three ageing processes seem to cause the closure of the angle: shrinkage of the eye, reduction in depth of the anterior chamber and increased size of the lens.
Fig. 10.18. Trauma caused by a wooden stick: this eye was enucleated 1 week after the trauma and showed scleral perforation, retinal detachment and haemorrhagic vitreous most cases not be detected in the tissue without the complete clinical history. Depending upon the rapidity of the rise in pressure, glaucoma causes tissue damage. In a pressure rise to 80 mmHg within 1 or 2 days (acute glaucoma) severe corneal oedema, infarction of the iris, necrosis of the lens and retinal oedema occur. When the pressure rises over a longer period of time more chronic changes can be found. The cornea shows fibrovascular tissue ingrowth at the periphery. The angle is closed by a corneal endothelial downgrowth and the trabecular tissue is fused and hyalinised. The iris stroma and ciliary body become atrophic and fibrotic. The nucleus of the lens becomes sclerotic. The vitreous may be unaffected, but in cases of retinal vascular disease, the vitreous contains blood and macrophages with fibrous strands. Atrophy of the optic disc is visible by cupping and shrinkage down to the lamina cribro-sa, which becomes bowed posteriorly. The choroid and retinal pigment epithelium are able to withstand high pressure and will only show atrophy and fibrosis in end-stage disease. Pathologic examination of enucleated glaucomatous eyes is often complicated by previous surgical procedures. Glaucoma can be divided into four subgroups.
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