Uveitic glaucoma consists of a complicated triad of intraocular inflammation, elevated intraocular pressure, and optic nerve damage. This is a clinical challenge that requires nuanced multidisciplinary management.
Glaucoma arises secondarily to intraocular inflammation, and this demands a great deal of attention.1 Uveitic glaucoma is present in up to 20% of patients diagnosed with chronic uveitis.2 The multifaceted etiology comprises trabecular meshwork damage and synechiae.3
Additionally, the most common treatment of uveitis, corticosteroids, may induce or further exacerbate glaucoma by elevating intraocular pressure (IOP).4 Meanwhile, even uncontrolled uveitis can lead to glaucoma due to the accumulation of inflammatory debris that contributes to the blockage of aqueous humour outflow.5
The pathophysiology is characterized by a dynamic and unpredictable clinical course of hills and valleys, marked by episodic fluctuations in inflammatory activity, IOP variability, and inconsistent therapeutic responses.
Although this condition may manifest across a broad age spectrum, it frequently presents earlier than primary open-angle glaucoma and necessitates a highly individualized management strategy.6
Signs and symptoms of uveitic glaucoma
Patients presenting with uveitic glaucoma may present with a wide range of signs and symptoms depending on both the elevation of IOP and the inflammatory extent of uveitis. One simplifying factor in the diagnosis is that usually, patients are known to have pre-existing glaucoma.
Patients with uveitic glaucoma often experience symptoms like:7
- Pain
- Photophobia
- Rapidly progressive diminution of visual acuity
- Acute visual blurring
A key concern is the potential for asymptomatic elevation of IOP, which may progress unnoticed and remain undetected in the absence of routine ophthalmic evaluation. This underscores the importance of regular monitoring, as individuals may not experience symptoms that would otherwise prompt medical attention.8
Clinical characteristics of uveitic glaucoma
Ocular hyperemia may be observed on physical examination and can be accompanied by conjunctival or ciliary injection; however, the absence of these findings does not exclude the diagnosis of uveitic glaucoma.
Furthermore, on slit lamp examination, several characteristic findings may be observed, including keratic precipitates, which are deposits of inflammatory cells on the corneal endothelium; anterior chamber “cell and flare,” reflecting the presence of inflammatory cells, and protein in the aqueous humor and indicating active intraocular inflammation.
For example:
- Iris synechiae, which are adhesions between the iris and either the lens or cornea, develop as a result of chronic inflammation.
- Posterior subcapsular cataracts, characterized by opacification of the posterior aspect of the lens, are often associated with prolonged inflammation or corticosteroid use.
Fundoscopic examination may reveal glaucomatous optic nerve changes, such as an increased cup-to-disc ratio or thinning of the neuroretinal rim, which are indicative of optic nerve damage secondary to elevated IOP.9
Figure 1: Cytomegalovirus (CMV) anterior uveitis with characteristic large keratic precipitates.7
Figure 1: Uveitic Glaucoma©Ioannis Halkiadakis et al. Image used under CC BY 4.0.
Diagnostic workup: Imaging is integral
The diagnostic evaluation for uveitic glaucoma incorporates several specialized tools and imaging modalities:10
- Tonometry: Crucial for frequent monitoring of IOP, as pressure levels can fluctuate significantly in these patients.11
- Gonioscopy: Performed to assess the anterior chamber angle and can help identify angle closure due to synechiae formation or accumulation of inflammatory debris.12
- Optical coherence tomography (OCT): OCT imaging of the retinal nerve fiber layer (RNFL) and macula is utilized to monitor the structural integrity of the optic nerve and to detect concurrent complications such as cystoid macular edema.13
Pro Tip: Although visual field testing can be challenging during episodes of active uveitis, it remains an important tool for the longitudinal assessment and follow-up of glaucomatous damage.14
Additionally, anterior segment imaging techniques, such as ultrasound biomicroscopy (UBM) or anterior segment OCT (AS-OCT), are particularly valuable in complex or post-surgical cases.
These imaging modalities provide detailed visualization of the angle structures and can assist in identifying features such as iris bombe, where the iris bows forward due to a blockage of fluid flow within the eye, leading to pupillary block and exacerbating angle closure glaucoma.15
Figure 2: Slit lamp image of angle-closure glaucoma with iris bombe.7
Figure 2: Angle-Closure Glaucoma with Iris Bombe©Ioannis Halkiadakis et al. Image used under CC BY 4.0.
Potential causes of uveitic glaucoma
Several underlying conditions are commonly associated with the development of uveitic glaucoma, including:
- Fuchs’ heterochromic iridocyclitis (FHI)
- Posner-Schlossman syndrome (PSS)
- Juvenile idiopathic arthritis (JIA)
One such condition is Fuchs’ heterochromic iridocyclitis, which is characterized by chronic, low-grade inflammation of the eye. Patients with FHI often exhibit heterochromia, a difference in coloration between the two irises, and fine stellate keratic precipitates (KPs), which are star-shaped deposits of inflammatory cells on the inner surface of the cornea. Despite the relatively mild inflammation, elevated IOP is frequently observed.16
Another cause is Posner-Schlossman syndrome, which typically presents as recurrent, unilateral episodes of markedly elevated IOP accompanied by mild inflammation. Between these episodes, patients are often asymptomatic, and the eye appears normal.17
Juvenile idiopathic arthritis is also a significant contributor, particularly in pediatric populations. JIA-associated uveitis tends to be silent and chronic, meaning children may not report symptoms despite ongoing inflammation.
This can lead to the early onset of severe glaucoma, especially when the disease is complicated by the formation of synechiae and the use of corticosteroids, which themselves can increase IOP.18
Best practices for management of uveitic glaucoma
The management of uveitic glaucoma is complex, as it requires both effective control of intraocular inflammation and reduction of IOP—objectives that can sometimes conflict with each other.
Corticosteroids—which include medications administered as eye drops (topical), injections around the eye (periocular), or oral/systemic drugs—are the primary treatment for acute inflammation.19
However, corticosteroids can cause an increase in IOP, a phenomenon known as steroid-induced glaucoma, which may worsen the underlying condition. Therefore, their use must be carefully balanced, and patients should be closely monitored.
Immunomodulatory therapy
For cases where inflammation is chronic or does not respond adequately to steroids, immunomodulatory therapy (IMT) may be employed.20
IMT involves the use of systemic medications such as methotrexate, mycophenolate mofetil, or adalimumab, which suppress the immune system to reduce inflammation. By lowering the need for steroids, IMT helps minimize the risk of steroid-induced IOP elevation and supports long-term IOP stability.21
IOP-lowering medications
To directly address elevated IOP, several classes of medications are available. Beta-blockers, alpha-agonists, and carbonic anhydrase inhibitors are generally considered safe and effective for lowering eye pressure in patients with uveitic glaucoma.22
Prostaglandin analogs, another class of IOP-lowering drugs, are typically avoided during periods of active inflammation because they can potentially worsen intraocular inflammation.23
Rho kinase inhibitors (such as netarsudil) represent a newer class of medications that may help lower IOP, although clinical experience and data regarding their use in uveitic glaucoma are still evolving.24
Surgical therapies
Surgical therapy becomes necessary for patients whose IOP remains uncontrolled despite the use of multiple medications, or in those who develop angle closure—a condition in which the drainage angle of the eye becomes blocked, preventing fluid outflow and causing a rise in eye pressure.25
This procedure involves creating a new drainage pathway for the aqueous humor (the fluid inside the eye) to lower IOP. However, its success in uveitic glaucoma is often limited because inflammation can lead to excessive scarring, which may block the new drainage channel.
To reduce the risk of scarring, surgeons commonly use antimetabolites such as mitomycin C (MMC), which are medications that inhibit cell growth and scar formation.26
Achieving and maintaining pre-operative inflammation control is crucial to improving surgical outcomes. These are small tubes or shunts (such as the Ahmed or Baerveldt devices) that are implanted to divert aqueous humor from inside the eye to an external reservoir, thereby lowering IOP.
Glaucoma drainage devices (GDDs) are often preferred in cases of uveitic glaucoma, particularly in children or in patients with JIA, because their effectiveness is less dependent on the healing of the conjunctiva, which can be compromised by inflammation.
Nevertheless, it is still essential that the eye is free of active inflammation at the time of surgery to reduce complications and improve success rates.27
Laser procedures
Laser procedures can play a role in the management of uveitic glaucoma. Nd:YAG laser iridotomy is sometimes required when angle closure occurs due to the formation of posterior synechiae or a pupillary block.28 This laser treatment creates a small opening in the iris to restore normal fluid flow within the eye.
Cyclophotocoagulation is a laser procedure reserved for advanced or treatment-refractory glaucoma. It works by targeting and reducing the activity of the ciliary body, the part of the eye that produces aqueous humor, thereby lowering IOP.29 However, this procedure must be performed with caution, as it carries a risk of worsening intraocular inflammation.
To watch a narrated surgical video of endoscopic cyclophotocoagulation, check out Revisiting the Benefits of Endoscopic Cyclophotocoagulation!
Co-managing patients with uveitic glaucoma
Achieving the best outcomes for patients with uveitic glaucoma requires close collaboration between glaucoma and uveitis specialists. Several key principles guide this process. It is essential that the eye remains free of active inflammation for at least 3 months before elective glaucoma surgery, as this reduces the risk of post-operative complications.30
Steroid medications should be reduced slowly rather than stopped abruptly, since sudden withdrawal can trigger a rebound of inflammation and cause a rapid increase in intraocular pressure.31 The use of systemic immunomodulatory medications can help control both ocular and systemic inflammation, improving overall disease management.
It is vital to educate patients about the unpredictable and fluctuating nature of their disease, and to set realistic expectations regarding the need for long-term follow-up, ongoing management, and most importantly, compliance with treatment.32,33
Conclusion
Uveitic glaucoma represents a complex and evolving challenge for eyecare providers, necessitating a tailored and collaborative approach.
The unpredictable nature of both intraocular inflammation and pressure fluctuations requires ongoing vigilance, adaptability in management strategies, and close cooperation with uveitis specialists.
Clinicians must consider uveitic glaucoma in any patient who presents with elevated IOP alongside evidence of intraocular inflammation. Additionally, clinicians must monitor and manage steroid-induced IOP elevation proactively, as corticosteroids can themselves raise eye pressure.
In chronic or difficult cases, early referral for immunomodulatory therapy is recommended. Surgical intervention is frequently required to control IOP, but the likelihood of success is greatly improved if the eye is in a state of pre-operative quiescence.
Long-term, multidisciplinary co-management, involving glaucoma specialists, uveitis specialists, and the patient, is essential for preserving both vision and quality of life.
