The term inflammatory glaucoma implies an elevation in intraocular pressure (IOP), secondary to a variety of ocular inflammatory processes, that may result in glaucomatous damage to the optic nerve head and visual fields.
(a) Secondary open angle glaucoma can occur if aqueous outflow is embarrassed by inflammatory cells and debris blocking the trabecular meshwork or from trabecular inflammation. Chronic inflammatory processes can lead to scarring of the trabecular meshwork.
(b) Secondary angle closure can also occur either with or without pupil block. Pupil-block with secluded pupil from extensive posterior synechiae can result in iris bombe and peripheral anterior synechiae (PAS). Alternatively, in non-pupil block, there is progressive PAS causing a gradual rise in IOP.
(c) Associated non-uveitic glaucoma: The patient could already have primary open angle glaucoma, anterior chamber dynamics that predispose to primary closed angle glaucoma, or the rise in IOP could result from the use of steroid medications to treat the inflammation (See Steroid-induced glaucoma).
Severe symptoms of acute uveitis could be present such as pain, photophobia, lacrimation and vision loss, or alternatively, symptoms could be very mild or even be non-existent.
The eye may show signs of anterior uveitis such as conjunctival and ciliary hyperaemia, aqueous and vitreous cells, posterior synechiae and keratic precipitates. With gonioscopy, the angle may appear open or reveal evidence of PAS. Trabecular exudation, pigmentation and neovascularisation can occur. The pupil of the involved eye may be smaller than its fellow.
In cases of secondary angle closure with pupil block, the slit lamp should reveal a shallow anterior chamber, a secluded pupil and iris bombe. The presence of iris atrophy, PAS and cataract is indicative of a chronic recurrent inflammation. In time, typical glaucomatous optic disc and visual field changes may develop. A careful examination of and comparisons with the fellow eye is essential.
Inflammatory glaucoma is more common in chronic recurrent ocular inflammations.
Inflammatory glaucoma should be differentiated from other conditions where elevated IOP may be associated with ocular inflammation such as in Fuchs’ heterochromic iridocyclitis and glaucomatocyclytic crisis. Steroid induced glaucoma and acute closed angle glaucoma, as well as pigmentary dispersion syndrome, pseudoexfoliation syndrome and neovascular glaucoma must be considered.
Consideration must be given to the cause of the elevation in IOP as outlined above. Systemic medical investigations may be required to try and establish a cause for the uveitis, especially in chronic recurrent cases.
Appropriate control of the ocular inflammation with steroid and cycloplegic medications may cause IOP return to normal without any further intervention and also prevent complications.
Topical aqueous suppressants such as beta blockers and additionally an alpha agonist or topical carbonic anhydrase inhibitor should be used if a reduction in IOP is needed. Prostaglandin and miotic agents are contraindicated.
If medical management fails to adequately control IOP, filtering surgery with antimetabolites may be considered.
Recurrent uveitis and secondary glaucoma resulting in blindness. The temporal iris is atrophic. Pigmented deposits on the anterior capsule of the lens are evidence of previous posterior synechiae.