Aishwarya Gupta,  B.Optom

Fellow Optometrist, Dr. Shroff Charity Eye Hospital, Delhi, India


Glaucoma is more commonly attributed to anterior and posterior uveitis. The term uveitic glaucoma is defined as glaucoma resulting indirectly or directly from uveitis, as it causes a rise in Intra Ocular Pressure (IOP). A persistent rise in IOP can lead to glaucomatous optic neuropathy and visual field loss. (1) Intraocular pressure elevation in uveitis can lead to secondary to open angle or angle closure glaucoma. It can also be to due corticosteroid-induced glaucoma. (2)

Types and Pathophysiology

  • The pathogenesis may be acute in onset, with rapid onset inflammation, obstruction of intertrabecular spaces, and subsequent raise in IOP. This effect is more often transient and innocuous
  • The chronic pathogenesis, of uveitis, leads to fibroblastic infiltration and the formation of scar tissue that slowly obstructs the anterior chamber angle.

In uveitic glaucoma, obstruction of the outflow pathways, comprising the uveal and juxtacanalicular trabecular meshwork structures, follows disruption of the blood-aqueous barrier (BAB) due to inflammation rather than due to idiopathic causes as in Primary Open Angle Glaucoma (POAG). This allows inflammatory cells to enter the anterior chamber and disrupt the aqueous outflow equilibrium. (3)

These inflammatory cells are capable of physically obstructing the outflow in Trabecular Meshwork (TM), as well as producing cytotoxic agents that can lead to permanent scarring of the TM lamellae and endothelial cells which line Schlemm’s canal. (4,5) Inflammatory cells are known to act by PGE1- and PGE-2 mediated biochemical pathways which can lead to the breakdown of the BAB. (6) This may explain the similarities between uveitic glaucoma and corticosteroid-induced glaucoma. Complications may include neovascularization of the anterior chamber angle with haemorrhage and worsening obstruction.



  • Control IOP is likely to be achieved if the angle is completely open.
  • The requirement therapy in terms of IOP level to be attained depends on the healthy optic nerve head; eyes with advanced damage require a low target IOP.
  • In terms of steroid reactors, it is essential to control inflammation for fear of steroid-induced IOP elevation. Long-standing depot preparations should be used with great caution in patients with a history of a steroid response respectively.
  • The IOP-lowering effect of ocular hypotensive drugs is less predictable in uveitis and some cases may be unexpectedly sensitive to topical carbonic anhydrase inhibitors.
  • The use of prostaglandin analogues in uveitic glaucoma is tempered by the small risk of precipitating uveitic sequences.

Surgical treatment

In secondary angle-closure glaucoma due to pupillary block, laser peripheral iridotomy (LPI) is usually the treatment of choice, however, the LPI may close secondary to inflammatory membranes with recurrence of the pupillary block. If there is active inflammation, a better treatment is a surgical iridotomy with posterior synechiolysis. (7)


Patients with uveitis episodes should be worked on underlying systemic causes. Assessment for arthritis, infections, mucosa or skin lesions, and cough may lead one to order targeted tests. Uveitic glaucoma includes ankylosing spondylitis, syphilis, tuberculosis, sarcoidosis. Specific ocular inflammations attributed with a high rate of secondary glaucoma that should be considered in cases of uveitic glaucoma include Fuch’s heterochromic iridocyclitis, glaucomatocyclitic crisis, sarcoidosis, juvenile rheumatoid arthritis, and herpetic keratouveitis.



  1. Bodh, S. A., Kumar, V., Raina, U. K., Ghosh, B., & Thakar, M. (2011). Inflammatory glaucoma. Oman journal of ophthalmology, 4(1), 3.
  2. Armaly, M. F. (1963). Effect of corticosteroids on intraocular pressure and fluid dynamics: I. The effect of dexamethasone* in the normal eye. Archives of ophthalmology, 70(4), 482-491.
  3. Freddo, T. F., Patterson, M. M., Scott, D. R., & Epstein, D. L. (1984). Influence of mercurial sulfhydryl agents on aqueous outflow pathways in enucleated eyes. Investigative Ophthalmology & Visual Science, 25(3), 278-285.
  4. Roth, M., & Simmons, R. J. (1979). Glaucoma associated with precipitates on the trabecular meshwork. Ophthalmology, 86(9), 1613-1618.
  5. Richardson, T. M., Hutchinson, B. T., & Grant, W. M. (1977). The outflow tract in pigmentary glaucoma: a light and electron microscopic study. Archives of ophthalmology, 95(6), 1015-1025.
  6. Chiang, T. S., & Thomas, R. P. (1972). Ocular hypertension following intravenous infusion of prostaglandin E1. Archives of Ophthalmology, 88(4), 418-420.
  7. Kulkarni, A., Shaarawy, B. K., Sherwood, M. B., Crowston, J. G., & Hitchings, R. A. (2009). Uveitic glaucoma. Glaucoma. China: Saunders Ltd, 393-407.