What makes uveitic glaucoma particularly difficult to manage?

Corticosteroids for the uveitis can themselves raise pressure Pressure can rise by several coexisting mechanisms, and the steroids used to control the inflammation may raise it further, so treating one problem risks worsening the other.

Inflammation makes intraocular pressure impossible to measure

The optic nerve resists all pressure-lowering treatment

Topical drops cannot penetrate an inflamed cornea

What is trabeculitis as a mechanism of raised pressure in uveitis?

Direct inflammation of the meshwork reducing aqueous outflow Trabeculitis is inflammation of the trabecular meshwork itself, which reduces outflow, distinct from mechanical blockage by inflammatory cells and debris.

Scarring of the trabecular meshwork after laser treatment

Pigment deposition in the meshwork from iris chafing

Collapse of the meshwork from sustained ocular hypotony

How does iris bombe raise intraocular pressure in uveitis?

Extensive posterior synechiae cause pupillary block Posterior synechiae produce pupillary block, and when extensive enough to cause iris bombe they can precipitate acute angle closure.

Ciliary body swelling pushes the lens forward

Inflammatory cells obstruct the episcleral veins

New vessels grow across the trabecular meshwork

Why is gonioscopy essential in assessing uveitic glaucoma?

It shows synechial closure and the open angle remaining Gonioscopy assesses synechial angle closure, angle neovascularization, and how much open, functioning angle is left to drain aqueous.

It measures the individual steroid response directly

It quantifies anterior chamber cell and flare

It confirms the depth of optic disc cupping

Which agents are generally first-line for lowering pressure in uveitic glaucoma?

Beta-blockers and carbonic anhydrase inhibitors Aqueous suppressants, namely topical beta-blockers and carbonic anhydrase inhibitors, are preferred as first-line pressure-lowering therapy in uveitic glaucoma.

Topical miotics such as pilocarpine

Prostaglandin analogues given at bedtime

Why are miotics generally avoided in uveitic glaucoma?

They worsen posterior synechiae and pupillary block risk In an inflamed eye miotics promote posterior synechiae formation and increase the risk of pupillary block, so they are generally avoided.

They suppress aqueous production too profoundly

They accelerate steroid-induced cataract formation

They cause corneal endothelial decompensation

Why are prostaglandin analogues used cautiously in uveitic glaucoma?

Of a theoretical concern about promoting inflammation There is a theoretical concern that prostaglandin analogues promote further intraocular inflammation, although they are still used in many cases once inflammation is well controlled.

They fail to work once the angle is partly synechial

They raise pressure transiently in the first week

They cannot be combined with aqueous suppressants

How is pupillary block from posterior synechiae treated in uveitic glaucoma?

Peripheral iridoplasty with argon laser

In which patients with uveitis is steroid-sparing immunosuppression considered earlier?

Those showing a pronounced steroid pressure response Patients with a marked steroid pressure response are moved toward systemic steroid-sparing immunosuppression earlier, to reduce reliance on corticosteroids long term.

Those with neovascular glaucoma from chronic ischaemia

Those whose uveitis is confined to one eye

Those with established synechial angle closure

Which glaucoma operation is frequently favoured in eyes with uveitic glaucoma?

Trabeculectomy without any antimetabolite

Laser trabeculoplasty of the inflamed angle

Uveitic Glaucoma: Mechanisms & Management

Uveitic glaucoma is elevated intraocular pressure occurring in the setting of intraocular inflammation, and it is genuinely complex to manage because it can arise from several different, sometimes coexisting, mechanisms, and because one of the standard treatments for the underlying uveitis, corticosteroids, can itself raise pressure further, creating a situation where controlling one problem risks worsening the other.

Mechanisms of Elevated Pressure in Uveitis

Trabeculitis: direct inflammation of the trabecular meshwork itself, reducing aqueous outflow
Inflammatory cells and debris mechanically obstructing the trabecular meshwork
Posterior synechiae, causing pupillary block and, if extensive (iris bombe), acute angle closure
Peripheral anterior synechiae, forming over time from chronic inflammation and progressively closing the angle
Neovascular glaucoma, from chronic ischemia in severe or prolonged uveitis
Steroid-induced ocular hypertension, from the anti-inflammatory treatment itself, in susceptible patients (see steroid-induced glaucoma)
Rarely, hypotony alternating with pressure spikes in eyes with fluctuating ciliary body function

More than one mechanism is often present simultaneously, which is part of why management requires a broader assessment than simply lowering pressure with the usual glaucoma medications.

Clinical Evaluation

Gonioscopy is essential, to assess for synechial angle closure, neovascularization, and the degree of open, functioning angle remaining
Assessment of anterior chamber activity, to determine whether active inflammation is contributing to current pressure elevation
A careful medication history, including the type, potency, route, and duration of any corticosteroid use, since steroid response varies by individual and by formulation
Optic nerve and visual field assessment, interpreted with the understanding that uveitic eyes may have baseline optic nerve or macular changes from the underlying inflammatory disease that complicate standard glaucoma assessment

Test your knowledge 10 questions from this article

Management

Treating the Underlying Inflammation

When active inflammation is a significant contributor to elevated pressure, controlling the uveitis itself is a core part of pressure management, not a separate issue, since resolving trabeculitis and clearing inflammatory debris can substantially lower pressure without escalating glaucoma-specific treatment.

Choosing a Steroid Strategy That Limits Pressure Risk

Where possible, using the lowest effective corticosteroid potency and route for adequate inflammatory control, recognizing that some patients need potent or prolonged steroid treatment regardless
Considering steroid-sparing systemic immunosuppression earlier in patients who show a pronounced steroid pressure response, to reduce reliance on corticosteroids for long-term control
Close IOP monitoring after starting or escalating any corticosteroid, particularly in known steroid responders

Uveitic Glaucoma: When Two Problems Are Feeding Each Other

Medical IOP-Lowering Therapy

Aqueous suppressants, including topical beta-blockers and carbonic anhydrase inhibitors, are generally preferred as first-line pressure-lowering agents in uveitic glaucoma
Prostaglandin analogues are used more cautiously, given a theoretical concern about promoting further intraocular inflammation in some patients, though they are still used in many cases, particularly when inflammation is well controlled
Miotics are generally avoided, since they can worsen posterior synechiae formation and pupillary block risk in an inflamed eye

Managing Synechiae and Angle Closure

Laser peripheral iridotomy addresses pupillary block from posterior synechiae or iris bombe, and prompt recognition and treatment of this mechanism is important given its potential for rapid, severe pressure elevation (see Nd:YAG laser peripheral iridotomy).

Surgical Management

When medical therapy and treatment of the underlying inflammation are insufficient, surgical options include trabeculectomy, often with antimetabolite use, and glaucoma drainage device implantation, which is frequently favored in uveitic glaucoma given generally better outcomes than trabeculectomy in eyes with a history of significant intraocular inflammation, along with cyclophotocoagulation for refractory cases.

Surgery in an actively inflamed eye carries a higher risk of complications, so achieving reasonable inflammatory control before elective surgical intervention, when the clinical situation allows, improves the likelihood of a good outcome.

Prognosis

Outcomes depend heavily on how well the underlying uveitis can be controlled and on the specific mechanism or mechanisms driving pressure elevation in a given patient.

Uveitic glaucoma tends to require more intensive, individualized, and closely monitored management than primary open-angle glaucoma, reflecting the interplay between two active disease processes rather than a single, more predictable pathway to optic nerve damage.

References

Sng CC, Ang M, Barton K. Uveitic glaucoma: a review. Clin Exp Ophthalmol. 2015;43:1-14.
Kesav N, Palestine AG, Kahook MY, Pantcheva MB. Current management of uveitis-associated ocular hypertension and glaucoma. Surv Ophthalmol. 2020;65:397-407.
Sallam A, Sheth HG, Habot-Wilner Z, Lightman S. Outcome of trabeculectomy with mitomycin C in uveitic glaucoma. Ophthalmology. 2010;117:1655-1660.
Ceballos EM, Beck AD, Lynn MJ. Trabeculectomy with antiproliferative agents in uveitic glaucoma. J Glaucoma. 2002;11:189-196.

Test yourself

A few questions straight from this article.

1 / 10 0 correct

What makes uveitic glaucoma particularly difficult to manage?
Pressure can rise by several coexisting mechanisms, and the steroids used to control the inflammation may raise it further, so treating one problem risks worsening the other.
What is trabeculitis as a mechanism of raised pressure in uveitis?
Trabeculitis is inflammation of the trabecular meshwork itself, which reduces outflow, distinct from mechanical blockage by inflammatory cells and debris.
How does iris bombe raise intraocular pressure in uveitis?
Posterior synechiae produce pupillary block, and when extensive enough to cause iris bombe they can precipitate acute angle closure.
Why is gonioscopy essential in assessing uveitic glaucoma?
Gonioscopy assesses synechial angle closure, angle neovascularization, and how much open, functioning angle is left to drain aqueous.
Which agents are generally first-line for lowering pressure in uveitic glaucoma?
Aqueous suppressants, namely topical beta-blockers and carbonic anhydrase inhibitors, are preferred as first-line pressure-lowering therapy in uveitic glaucoma.
Why are miotics generally avoided in uveitic glaucoma?
In an inflamed eye miotics promote posterior synechiae formation and increase the risk of pupillary block, so they are generally avoided.
Why are prostaglandin analogues used cautiously in uveitic glaucoma?
There is a theoretical concern that prostaglandin analogues promote further intraocular inflammation, although they are still used in many cases once inflammation is well controlled.
How is pupillary block from posterior synechiae treated in uveitic glaucoma?
Laser peripheral iridotomy relieves pupillary block from posterior synechiae or iris bombe, and prompt recognition matters because pressure can rise rapidly and severely.
In which patients with uveitis is steroid-sparing immunosuppression considered earlier?
Patients with a marked steroid pressure response are moved toward systemic steroid-sparing immunosuppression earlier, to reduce reliance on corticosteroids long term.
Which glaucoma operation is frequently favoured in eyes with uveitic glaucoma?
Drainage devices generally give better outcomes than trabeculectomy in eyes with a history of significant intraocular inflammation, with cyclophotocoagulation kept for refractory cases.

Ahmed Ophthalmologist

Writes and reviews the clinical articles on Educate. Every post is checked against peer-reviewed sources before it goes live.

Uveitic Glaucoma: When Two Problems Are Feeding Each Other