Uveitic Glaucoma

Updated: Sep 30, 2020
Author: Leon Herndon, Jr, MD; Chief Editor: Inci Irak Dersu, MD, MPH 



In 1813, Joseph Beer first reported the association of uveitis and glaucoma, describing it as arthritic iritis followed by glaucoma and blindness. In 1891, Priesley Smith proposed the first modern classification of uveitic glaucoma. Later, specific types of uveitic glaucoma were described by Fuchs in 1906 (Fuchs heterochromic uveitis) and Posner and Schlossman in 1948 (glaucomatocyclitic crisis).


The mechanisms by which uveitis leads to elevated intraocular pressure (IOP) are numerous and poorly understood. In general, iridocyclitis affects both aqueous production and resistance to aqueous outflow, with the subsequent change in IOP representing a balance between these two factors. Inflammation of the ciliary body usually leads to reduced aqueous production, and combined with increased uveoscleral outflow often seen in inflammatory states, hypotony often is a consequence.

Prostaglandins, which have been demonstrated to be present in the aqueous of eyes with uveitis, are known to cause elevated IOP without a reduction in outflow facility. Mechanisms of increased resistance to aqueous outflow with both acute and subacute forms of uveitis usually are of the open-angle type and include obstruction of the trabecular meshwork by inflammatory cells or fibrin, swelling or dysfunction of the trabecular lamellae or endothelium, and inflammatory precipitates on the meshwork. Uveitis also may be associated with secondary angle-closure glaucoma.

Alteration of the protein content of the aqueous humor may be a cause of elevated IOP in uveitis. Increased levels of protein in the aqueous are a result of increased permeability of the blood-aqueous barrier, which leads to an aqueous that more closely resembles undiluted serum. This elevated protein content may, in fact, lead to aqueous hypersecretion and IOP elevation.

The treatment of the uveitis can lead to elevated IOP. Although corticosteroids have proven to be effective in relieving inflammation, prolonged administration can result in elevated IOP. Corticosteroids increase IOP by decreasing aqueous outflow. Several theories have been proposed to explain this phenomenon, including accumulation of glycosaminoglycans in the trabecular meshwork, inhibition of phagocytosis by trabecular endothelial cells, and inhibition of synthesis of certain prostaglandins.



United States

The prevalence of uveitis has been estimated at approximately 115 people per 100,000 in the United States. Approximately 20% of uveitis patients develop glaucoma.


The prevalence of uveitis has been estimated at 38-730 people per 100,000 worldwide. Approximately 20% of uveitis patients develop glaucoma.


Acute iridocyclitis usually produces symptoms; however, subacute iridocyclitis produces few or no symptoms but can have serious consequences because its complications may go undetected until advanced damage has occurred. If the inflammation is not controlled promptly, posterior synechiae and peripheral anterior synechiae (PAS) can form, leading to progressive angle closure and irreversible optic nerve damage.


No known racial predilection exists.


No known sexual predilection exists.


No known age predilection exists.


Few published reports are available that address the results of surgery in patients with uveitic glaucoma.

Hoskins et al achieved successful lowering of IOP in 6 of 9 eyes undergoing trabeculectomy for uveitic glaucoma.[1]

Hill et al showed a success rate of 81% at 12 months. The success rate of trabeculectomy with antimetabolite supplementation has been reported to be higher (71-100%).[2]

Wright et al reported that 3 of 24 patients undergoing trabeculectomy with mitomycin-C required subsequent drainage implants and that 7 of 24 patients lost 2 or more lines of Snellen acuity.[3]

Hill et al reported a success rate of 79% of eyes undergoing Molteno tube implantation.[4]

Ceballos et al reported a success rate of 91.7% in eyes undergoing Baerveldt drainage device placement for uveitic glaucoma.[5]

Ozdal et al showed a 2-year success rate of 60% in eyes undergoing Ahmed drainage device placement for uveitic glaucoma.[6]

Rachmiel et al reported similar 30-month results between eyes that underwent Ahmed glaucoma valve implantation with uveitic glaucoma compared to open-angle glaucoma eyes.[7]

Patient Education

For patient education resources, see the Glaucoma Center and Eye and Vision Center, as well as Glaucoma Overview, Anatomy of the Eye, Glaucoma FAQs, Understanding Glaucoma Medications, and Iritis.




Symptoms with acute iridocyclitis may include blurred vision, ocular pain, brow ache, and other ocular disturbances.

Blurred vision

It often is difficult to know if the blurred vision is due to glaucoma, uveitis, or complications associated with the uveitis.

Ocular pain

Pain is a frequent finding in acute iridocyclitis but often is not seen with subacute or chronic iridocyclitis. Some patients with markedly elevated IOP often have severe eye pain associated with corneal edema.

Brow ache

Ocular pain associated with elevated IOP often is referred to the brow on the affected side.

Ocular disturbances

Other ocular disturbances (eg, photophobia, colored halos) may be associated with acute iridocyclitis and corneal edema, respectively.


The cornea may reveal band keratopathy, epithelial dendrites, or stromal scarring from herpetic infections. Corneal epithelial edema associated with acutely elevated IOP may give rise to a steamy appearance. Keratic precipitates may be present on the endothelium and have different characteristics that signify various diagnoses.

The hallmark of anterior uveitis is the presence of cells and flare in the anterior chamber. Cellular infiltration is due to release of chemotactic factors into the anterior chamber, and flare results from leakage of protein into the anterior chamber.

The iris should be examined for evidence of stromal atrophy, nodules, and posterior synechiae and PAS. Inflammation can result in engorgement of the blood vessels in both the iris stroma and the angle, which can be confused with rubeosis iridis.

The lens may have pigment on the anterior capsule, and posterior subcapsular opacification may be due to uveitis or to chronic corticosteroid therapy.

The vitreous cavity may show the presence of cells or snowball opacities.

The IOP may be low, normal, or high due to variations in aqueous secretion, amount of outflow obstruction, and dose of corticosteroids being used.

Gonioscopy should be performed to detect the presence of PAS and to assess the degree of angle closure.

The posterior segment should be examined, paying particular attention to the optic nerve to document morphologic changes consistent with glaucoma. Other possible posterior segment findings include cystoid macular edema, retinitis, perivascular sheathing, choroidal infiltrates, or retinal detachment.


Many specific uveitic entities may lead to the development of glaucoma. Some of the more common syndromes are listed below.

Juvenile rheumatoid arthritis

Juvenile rheumatoid arthritis (JRA) is defined as an arthritis, with a duration of at least 3 months, that begins prior to age 16 years and is diagnosed after exclusion of other causes of arthritis.

Glaucoma is a common complication of chronic uveitis in patients with JRA and most frequently is caused by progressive closure of the angle by PAS.

Since the uveitis frequently is treated with prolonged topical corticosteroids, steroid-induced glaucoma may occur. The reported incidence of glaucoma varies from 14-22%.

Fuchs heterochromic iridocyclitis

Fuchs heterochromic iridocyclitis (FHI) usually is unilateral and appears between the third and fourth decades with the insidious onset of mild, chronic anterior uveitis that usually is asymptomatic.

The glaucoma associated with FHI resembles primary open-angle glaucoma.

Gonioscopic evaluation may reveal multiple fine blood vessels, arranged either radially or concentrically in the trabecular meshwork.

Cataract is a constant feature of FHI, whereas glaucoma has been reported to occur in 6-47% of cases.

Low-grade inflammation does not need treatment with anti-inflammatory or immunosuppressive agents.

Posner-Schlossman syndrome

Posner-Schlossman syndrome is characterized by a number of unusual features, including unilateral involvement, recurrent attacks of often very mild cyclitis, marked elevation of IOP, open angle, and occasional heterochromia. The condition typically affects individuals aged 20-50 years and resolves spontaneously regardless of treatment.

Herpetic uveitis

Herpes simplex

Ocular manifestations of herpes simplex virus have been classified in accordance with the site of the corneal involvement and the presence or absence of associated uveitis, including herpetic superficial keratitis, disciform keratitis, disciform keratouveitis, and necrotic stromal keratitis. Disciform keratouveitis and necrotic stromal keratitis are associated more commonly with elevated IOP than epithelial keratitis.

The elevated IOP may be caused by trabeculitis, inflammatory obstruction of the trabecular meshwork, and angle closure in severe keratouveitis. The management of elevated IOP initially is directed toward controlling the viral replication and inflammation.

Varicella zoster

Ocular involvement of cutaneous varicella zoster occurs in two thirds of patients when the ophthalmic division of the trigeminal nerve is involved. Dendritic keratitis, stromal keratitis, and exposure keratitis are common.

IOP elevation and glaucoma are believed to be caused by decreased outflow facility due to trabecular obstruction from inflammatory debris, trabeculitis, and damage to the trabecular meshwork by recurrent inflammation. Treatment with systemic acyclovir when the cutaneous lesions are still active appears to reduce the risk of elevated IOP.[8]


Complications of uveitis include the following:

  • Band keratopathy

  • Corneal decompensation

  • Posterior subcapsular cataract

  • Vitreous opacities

  • Retinal or choroidal detachment

  • Macular edema

  • Disc edema





Laboratory Studies

Laboratory investigation should be tailored to appropriate studies based on both the history and the physical findings and may include serology and/or skin tests.

Imaging Studies

See the list below:

  • Chest radiography

  • Computerized tomography

  • Magnetic resonance imaging

  • Gallium scanning

Ocular imaging studies, including anterior-segment optical coherence tomography (OCT) and ultrasound biomicroscopy, are used to identify possible causes of inflammation and to understand the extent of structural changes caused by inflammation. Optic nerve imaging studies and visual field tests are useful to evaluate the stage of glaucoma and to plan appropriate treatment.


See the list below:

  • Conjunctival biopsy

  • Vitreous biopsy

  • Anterior chamber paracentesis



Medical Care

Treatment of glaucoma in uveitis depends on the underlying disease and on the individual patient. The treatment rationale consists of (1) treating any underlying systemic disease, (2) treating the ocular inflammation, and (3) treating the glaucoma. The ocular inflammation and glaucoma usually can be controlled with eye drops. Often, treatment of the inflammation will control the IOP.

Surgical Care

It is a general rule that surgery should be avoided, when possible, in the inflamed eye. However, if surgery is required, the eye should receive maximal preoperative anti-inflammatory therapy to decrease the inflammation as much as possible.

In eyes with active uveitis, preparation for intraocular surgery should include perioperative topical and, occasionally, systemic corticosteroid therapy to avoid exacerbation of uveitis and failure of filtering surgery. If an elective surgical case is to be performed, the uveitis should be as quiet as possible for 3 months prior to surgery. One week prior to surgery, topical prednisolone 1% solution should be given hourly, and oral prednisone 40 mg daily should be considered.

At the conclusion of surgery, a depot of corticosteroid should be injected subconjunctivally. Postoperatively, topical and oral corticosteroids may be tapered according to control of the inflammation. In emergency cases, severe postoperative exacerbation of existing inflammation should be anticipated; therefore, aggressive perioperative topical and systemic corticosteroid therapy is warranted.

More recently, the injection of intraocular corticosteroids such as triamcinolone has been found to be effective in reducing macular edema and improving vision in uveitic eyes that have proved refractory to systemic or periocular corticosteroids. The effect is usually transient but can be repeated, although the adverse effects of cataract and raised intraocular pressure (IOP) are increased in frequency with intraocular versus periocular corticosteroid injections. This has led to the development of new intraocular corticosteroid devices designed to deliver sustained-release drugs and obviate the need for systemic immunosuppressive treatment.

The first such implant was Retisert (0.59 mg fluocinolone acetonide intravitreal implant), which is surgically implanted and is designed to release fluocinolone over a period of about 30 months. Callanan et al reported a reduced recurrence rate of uveitis from 62% to 20% during the 3-year postimplantation period after Retisert implantation.[8] Despite successful control of the uveitis, IOP elevation was common, and 40% of implanted eyes required glaucoma surgery. The most common adverse events associated with a sustained delivery fluocinolone acetonide device include eye pain, procedural complications, cataract progression (managed by standard cataract surgery), and elevated IOP (managed with the use of IOP-lowering eye drops or surgery. In one retrospective study, almost 50% of eyes followed over the course of the 8-year study period required glaucoma surgical intervention following Retisert implantation.[9]

Ozurdex, a bioerodible dexamethasone implant (0.7 mg intravitreal dexamethasone) that can be inserted in an office setting, has gained approval for the treatment of macular edema and noninfectious posterior uveitis. This implant lasts approximately 6 months and has been found to be effective with a much better adverse effect profile than Retisert or intravitreal triamcinolone injection, at least for one injection.[10] Lowder et al studied the safety and efficacy of two doses of dexamethasone intravitreal implant for the treatment of noninfectious intermediate or posterior uveitis. The proportion of eyes with a vitreous haze score of 0 at week 8 was 47% with the 0.8-mg dexamethasone implant, 36% with the 0.35-mg dexamethasone implant, and 12% with the sham treatment. The percentage of eyes with IOP of 25 mm Hg or more peaked at 7.1% for the 0.7-mg dexamethasone implant, 8.7% for the 0.35-mg dexamethasone implant, and 4.2% for the sham treatment.[11]

Yutiq (0.18-mg intravitreal fluocinolone acetonide implant) has been studied extensively for the management of chronic noninfectious uveitis affecting the posterior segment of the eye. Jaffe et al randomized 129 patients to Yutiq injection or sham treatment. The 6-month and 12-month uveitis recurrence rates were significantly lower in the Yutiq group versus the sham group. IOP lowering treatment use was equal between both groups.[12]

Laser iridotomy

Extensive posterior synechiae formation can lead to pupillary block glaucoma, so it is important to reestablish communication between the posterior and anterior chambers before a full-blown attack of pupillary block occurs. Performing laser iridotomy prophylactically is preferable to performing this procedure during an attack of acute angle-closure glaucoma because visualization of the iris may be difficult due to corneal edema caused by high IOP.

An argon laser or an Nd:YAG laser may be used to perform the iridotomy. In patients with uveitis, the Nd:YAG laser may have the advantage of inducing less postoperative inflammation and requiring less energy compared with the argon laser. Combined Nd:YAG laser and argon laser is preferable in eyes with thick brown irides. Also, combined laser may allow for a larger iridotomy, which may be less prone to close.

Transient anterior chamber inflammation occurs in all eyes after this procedure, so topical corticosteroids should be used as warranted postoperatively. When laser iridotomies are unsuccessful or when the use of a laser is not possible, a surgical iridectomy should be performed in cases of inflammatory angle-closure glaucoma. Since this procedure can lead to increased postoperative inflammation, topical and, sometimes, systemic corticosteroids are required in the perioperative period.


Trabeculectomy surgery is indicated for eyes with closed-angle, open-angle, or combined mechanism glaucoma when IOP is believed to be too high, despite maximum tolerated medical and laser therapy. Due to an accelerated wound healing response in uveitis, the results of trabeculectomy generally are poor, particularly in young patients.

Antimetabolite therapy in association with trabeculectomy has been shown to improve the success rate of trabeculectomy in patients with a high risk of failure. Intraoperative application of mitomycin-C is used widely to supplement standard trabeculectomy. The mitomycin can be applied to the eye for a variable duration prior to or after dissection of the scleral flap. Irrigation of the subconjunctival tissues should be carried out to prevent intraocular exposure.

A 2017 retrospective study evaluated intermediate and long-term outcomes of mitomycin C–enhanced trabeculectomy as a first glaucoma procedure in uveitic glaucoma.[13] Seventy eyes were studied for a mean follow-up period of 77 months, with the probability of success at only 35.7% at 60 months. Hypotony was a common complication, seen in 30% of eyes.

Dhanireddy et al studied the outcomes of the Ex-Press filtration device in patients with uveitic glaucoma. Surgical success was seen in 90.9% of the eyes in the simple glaucoma group, compared to 75% of eyes in the uveitic glaucoma group.[14]

Drainage implantation

Drainage implants are designed to route aqueous from the anterior chamber to a posterior reservoir. They are particularly useful in cases with significant conjunctival scarring due to previous surgery. Drainage valves, such as the Ahmed valve, may be safer than trabeculectomy, as less risk of hypotony exists, which can be seen in postoperative uveitic eyes due to decreased aqueous production.

In eyes with chronic uveitis, long-term corticosteroid therapy may induce glaucoma or glaucoma may occur secondary to the ocular inflammation. In these eyes, it would be beneficial to simultaneously control inflammation and IOP. To this end, a retrospective case series described 7 eyes of 5 patients in which a fluocinolone acetonide implantation was inserted and a glaucoma tube shunt was placed in a single surgical session.[15] This procedure was well tolerated and was associated with reduced inflammation, decreased concurrent systemic immunosuppressive therapy, and good IOP control.

Zivneyet al conducted a study to determine whether patients who underwent combined Ahmed tube shunt and Retisert implantation had superior outcomes than did patients with Ahmed implants only in the setting of uveitic glaucoma.[16] At 6 months, no significant differences in terms of mean IOP, mean number of IOP-lowering medications, visual acuity, surgical success, or adverse events were noted between Ahmed implantation alone or combined Ahmed and Retisert implantation in patients with uveitic glaucoma. However, Hennein et al found that patients who received Retisert implantation had lower IOP and used fewer glaucoma eye drops compared with control eyes at 1-year following Ahmed valve surgery.[17]

Chow et al conducted a retrospective comparative study to compare clinical outcomes of trabeculectomy with mitomycin-C, Ahmed shunt, and Baerveldt shunt surgery specifically in uveitic glaucoma. The postoperative hypotony rate differed significantly across trabeculectomy (53%), Baerveldt (24%), and Ahmed (18%) groups (P = 0.027); other complication rates were similar. Baerveldt eyes had a lower failure rate compared to trabeculectomy (P = 0.0054) and Ahmed (P = 0.0008) eyes.[18]


As a last resort, cycloablative techniques can be employed. Diode or Nd:YAG laser cyclophotocoagulation can be used to destroy the secretory ciliary epithelium, leading to decreased aqueous production. Unfortunately, cycloablative procedures often exacerbate the inflammation. These methods are reserved for eyes with poor visual potential due to the relatively high risk of further vision loss and phthisis bulbi.


See the list below:

  • Uveitis specialist

  • Rheumatologist

  • Glaucoma specialist


No special diet is required.


Avoid strenuous exercise and heavy lifting in the early postoperative period.


Postoperative complications include the following:

  • Postoperative complications (eg, choroidal effusion, choroidal hemorrhage, shallow anterior chamber, hypotony) may be higher in eyes with uveitic glaucoma than with primary open-angle glaucoma after trabeculectomy with wound modulation.

  • Postoperative inflammation is fairly common in eyes with uveitic glaucoma, although this incidence can be lowered by treating the patients with preoperative and postoperative corticosteroids.

  • The combination of postoperative inflammation and shallow anterior chamber can lead to the formation of PAS, which may interfere with the function of the glaucoma filter. Cataract formation also is very common with this scenario; therefore, prolonged periods of postoperative shallowing of the anterior chamber should be avoided.

  • Phthisis bulbi may occur after any surgical procedure for uveitic glaucoma but is particularly common after cycloablative therapy. Eyes that may be at high risk of developing phthisis include those with a totally occluded angle and a relatively low preoperative IOP.

Long-Term Monitoring

Patients should receive follow-up care as needed.



Medication Summary

Common anti-inflammatory treatment entails use of nonsteroidal anti-inflammatory drugs (eg, topical, systemic); corticosteroids (eg, topical, subconjunctival, systemic); and, rarely, immunosuppressive agents. Mydriatic-cycloplegic agents may be used to prevent or break posterior synechiae and to relieve pain and discomfort of ciliary muscle spasm. Available agents include atropine 1%, homatropine 1-5%, scopolamine, phenylephrine 2.5-10%, and tropicamide 0.5-1%.

Topical corticosteroids are effective in the control of anterior uveitis but vary in strength, ocular penetration, and adverse effect profile. Systemic corticosteroids are widely used for the management of posterior segment inflammation, which requires treatment, particularly when it is associated with systemic disease or when bilateral ocular disease is present. However, when ocular inflammation is unilateral, or is active in one eye only, local therapy has considerable advantages, and periocular injections of corticosteroid is a useful alternative to systemic medication and is very effective in controlling mild or moderate intraocular inflammation.

Many agents are available for lowering of IOP, including topical beta-blockers, adrenergic agents, and topical and systemic carbonic anhydrase inhibitors.

Miotics are avoided in uveitic glaucoma because of the risk of formation of posterior synechiae or a pupillary membrane. They also may increase inflammation by enhancing breakdown of the blood-aqueous barrier.

The role of prostaglandin analogs (PGAs) in uveitic glaucoma is unknown; PGAs have been used to help lower IOP in these often difficult to manage eyes. However, controversy exists concerning their use in uveitic patients owing to the theoretically higher risk of anterior uveitis, development of cystoid macular edema, and reactivation of herpes simplex keratitis. Little evidence suggests that PGAs disrupt the blood-aqueous barrier and only anecdotal evidence suggests an increased risk of these rare findings. PGA may be used in uveitic glaucoma if other topical treatments have not lowered IOP to the patient's target range.[19]

Markomichelakis et al, reported that latanoprost was safe and equally effective compared with a fixed combination of dorzolamide and timolol in the treatment of uveitic glaucoma.[20]


Class Summary

Lower IOP by decreasing the production of aqueous humor.

Carteolol 1% (Ocupress, Cartrol)

Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic effects.

Levobunolol (AKBeta, Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production.

Carbonic anhydrase inhibitors

Class Summary

Lower IOP by decreasing aqueous production. Oral and topical forms are available.

Acetazolamide (Diamox)

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP.

Methazolamide (Neptazane, GlaucTabs)

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

Dorzolamide 2% (Trusopt); Brinzolamide 1% (Azopt)

Both act by inhibition of carbonic anhydrase in the ciliary processes that decreases aqueous humor formation.

Adrenergic agonists

Class Summary

Lower IOP by a combination of decreasing production of aqueous and increasing aqueous outflow.

Apraclonidine (Iopidine)

Reduces IOP whether or not accompanied by glaucoma. Selective alpha-adrenergic agonist (alpha2) without significant local anesthetic activity. Has minimal cardiovascular effect.

Brimonidine (Alphagan)

Selective alpha2-receptor that reduces aqueous humor formation and possibly increases uveoscleral outflow.

Prostaglandin analogs

Class Summary

Lower IOP by increasing aqueous outflow.

Latanoprost (Xalatan, Xelpros)

Decreases IOP by increasing outflow of aqueous humor.

Bimatoprost ophthalmic solution (Lumigan)

A prostamide analogue with ocular hypotensive activity. Mimics the IOP-lowering activity of prostamides via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

Travoprost ophthalmic solution (Travatan)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension. Now with BAK-free formulation called travoprost-Z.

Nonsteroidal anti-inflammatory agents

Class Summary

Have analgesic and anti-inflammatory activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms also may exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Ketorolac tromethamine 0.5% (Acular)

The mechanism of action is believed to be due, in part, to its ability to inhibit prostaglandin biosynthesis.

Diclofenac ophthalmic (Voltaren)

Believed to inhibit cyclooxygenase, which is essential in the biosynthesis of prostaglandins.

Topical corticosteroids

Class Summary

Treatment of ocular inflammation.

Prednisolone acetate 1% (Pred Forte)

Inhibits the edema, fibrin deposition, capillary dilation, and phagocytic migration of the acute inflammatory response and capillary proliferation. Causes the induction of phospholipase A-2 inhibitory proteins.

Fluorometholone 0.1% (FML)

Believed to act by the induction of phospholipase A-2 inhibitory proteins. Shows a lower propensity to increase IOP than dexamethasone in clinical studies.

Nonsteroidal Anti-Inflammatory Drug (NSAID), Ophthalmic

Nepafenac ophthalmic suspension (Nevanac)

Nonsteroidal anti-inflammatory prodrug for ophthalmic use. Following administration, converted by ocular tissue hydrolases to amfenac, an NSAID. Inhibits prostaglandin H synthase (cyclooxygenase), an enzyme required for prostaglandin production. Indicated for treatment of pain and inflammation associated with cataract surgery.

Bromfenac ophthalmic (BromSite, Prolensa)

Nonsteroidal anti-inflammatory drug for ophthalmic use. Blocks prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2. Indicated to treat postoperative inflammation and reduce ocular pain after cataract extraction.

Corticosteroid, Ophthalmic

Difluprednate ophthalmic emulsion (Durezol)

Ophthalmic corticosteroid indicated for inflammation and pain associated with ocular surgery. Available as a 0.05% ophthalmic emulsion.

Beta-blocker / Alpha Agonist Combination

Brimonidine tartrate, timolol maleate ophthalmic solution (Combigan)

Selective alpha-2 adrenergic receptor agonist with a nonselective beta-adrenergic receptor inhibitor. Each of them decreases elevated IOP, whether or not associated with glaucoma.

Carbonic Anhydrase Inhibitor

Dorzolamide hydrochloride-timolol maleate (Cosopt)

Carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.

Timolol is a nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility.

Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.


Questions & Answers


What is uveitic glaucoma?

What is the pathophysiology of uveitic glaucoma?

What is the US prevalence of uveitic glaucoma?

What is the global prevalence of uveitic glaucoma?

What is the morbidity and mortality associated with uveitic glaucoma?

What is the racial predilection of uveitic glaucoma?

What is the sexual predilections of uveitic glaucoma?

Which age groups have the highest prevalence of uveitic glaucoma?

What is the prognosis for uveitic glaucoma?


What are the signs and symptoms of uveitic glaucoma?

What causes blurred vision in uveitic glaucoma?

Which ocular pain findings are characteristic of uveitic glaucoma?

What causes brow ache in patients with uveitic glaucoma?

Which ocular disturbances are associated with acute iridocyclitis and corneal edema in patients with uveitic glaucoma?

Which ocular exam findings are characteristic of uveitic glaucoma?

What causes uveitic glaucoma?

What are the possible complications of uveitic glaucoma?


What are the differential diagnoses for Uveitic Glaucoma?


What is the role of lab testing in the workup of uveitic glaucoma?

Which imaging studies are performed in the workup of uveitic glaucoma?

Which procedures are performed in the workup of uveitic glaucoma?


How is uveitic glaucoma treated?

What is the role of surgery in the treatment of uveitic glaucoma?

What is the role of laser iridotomy in the treatment of uveitic glaucoma?

What is the role of trabeculectomy in the treatment of uveitic glaucoma?

What is the role of drainage implants in the treatment of uveitic glaucoma?

What is the role of cycloablation in the treatment of uveitic glaucoma?

Which specialist consultations may be beneficial to patients with uveitic glaucoma?

Which dietary modifications are used in the treatment of uveitic glaucoma?

Which activity modifications are used in the treatment of uveitic glaucoma?

What are the possible postoperative complications following surgical treatment of uveitic glaucoma?

What is included in the long-term monitoring of patients with uveitic glaucoma?


What is the role of medications in the treatment of uveitic glaucoma?

Which medications in the drug class Carbonic Anhydrase Inhibitor are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Beta-blocker / Alpha Agonist Combination are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Corticosteroid, Ophthalmic are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Nonsteroidal Anti-Inflammatory Drug (NSAID), Ophthalmic are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Topical corticosteroids are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Nonsteroidal anti-inflammatory agents are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Prostaglandin analogs are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Adrenergic agonists are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Uveitic Glaucoma?

Which medications in the drug class Beta-blockers are used in the treatment of Uveitic Glaucoma?