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Oman J Ophthalmol. 2011 Jan-Apr; 4(1): 3–9.
PMCID: PMC3110445

Inflammatory glaucoma


Glaucoma is seen in about 20% of the patients with uveitis. Anterior uveitis may be acute, subacute, or chronic. The mechanisms by which iridocyclitis leads to obstruction of aqueous outflow include acute, usually reversible forms (e.g., accumulation of inflammatory elements in the intertrabecular spaces, edema of the trabecular lamellae, or angle closure due to ciliary body swelling) and chronic forms (e.g., scar formation or membrane overgrowth in the anterior chamber angle). Careful history and follow-up helps distinguish steroid-induced glaucoma from uveitic glaucoma. Treatment of combined iridocyclitis and glaucoma involves steroidal and nonsteroidal antiinflammatory agents and antiglaucoma drugs. However, glaucoma drugs can often have an unpredictable effect on intraocular pressure (IOP) in the setting of uveitis. Surgical intervention is required in case of medical failure.

Method of Literature Search:

Literature on the Medline database was searched using the PubMed interface.

Keywords: Intraocular pressure, glaucoma, inflammation, uveitis


Inflammatory glaucoma, also known as uveitic glaucoma, is a condition in which ocular inflammation causes apersistent or recurrent IOP elevation resulting in anatomical and physiological changes characteristic of primary open angle glaucoma. The anatomical changes include progressive optic nerve cupping with corresponding retinal nerve fiber layer loss. When anatomical changes progress beyond the physiological reserve of the optic nerve, the visual field defects become detectable. Joseph Beer first reported the association of uveitis and glaucoma in 1813, describing it as arthritic iritis.[1] In 1891, Priestley Smith proposed the first modern classification of uveitic glaucoma.[2] Elliot proposed several hypotheses for its mechanism: An alteration of aqueous composition, obstruction of filtering angle by inflammatory cells, and debris. Unilateral glaucoma should raise the suspicion of an inflammatory glaucoma. The overall prevalence of glaucoma in eyes with uveitis varies from 10 to 20%, but it is much more common in chronic uveitis and can be as high as 46%.[3]

Method of Literature Search — literature was searched for on the Medline database using the Pubmed interface.

Pathophysiology: The relationship between IOP and inflammation is complex. At any one time IOP depends on the comparative rates of aqueous production and drainage. Both these processes and intraocular circulation of the aqueous can be altered by inflammation, its effects on the ocular tissue involved, and its treatment.

Mechanisms of Intraocular Pressure Elevation

  1. Secondary open angle glaucoma
    1. Trabecular meshwork (TM) obstruction is the most common mechanism and can be caused by: Disruption of the blood aqueous barrier [BAB], which allows entry of inflammatory cells into the aqueous humor and entrapment of normal serum components in the aqueous outflow system.[4] Swelling of trabecular lamellae and endothelial cells with both a physical narrowing of trabecular pores and dysfunction also leads to aqueous outflow obstruction,[5] ultimately leading to permanent damage and scarring of the trabecular meshwork.[6]
    2. Hypersecretion caused by PGE1 - and PGE2 -mediated increase in the rate of aqueous secretion or by a breakdown in BAB, with an associated increase in aqueous protein concentration and thus aqueous viscosity.[7]
    3. Corticosteroid-induced elevation of IOP
  2. Pre-existing primary open angle glaucoma
  3. Secondary angle closure glaucoma: The inflammatory cell and protein in the aqueous humor can form an adhesion between the iris and lens resulting in the formation of posterior synechiae leading to pupillary block, iris bombe, and peripheral anterior synechiae. Subsequently neovascularization of the anterior chamber angle and its fibrovascular closure may ensue.
  4. Pre-existing predisposition to primary angle closure glaucoma: In eyes with shallow anterior chamber.
  5. Combined mechanism glaucoma: Scarring and obstruction of outflow channels.

General Symptoms and Signs

Symptoms with acute iridocyclitis may include blurred vision, ocular pain, brow ache, and other ocular disturbances like photophobia and colored haloes. The cornea may reveal band keratopathy, epithelial dendrites, or stromal scarring from herpetic infections. The iris should be examined for evidence of stromal atrophy, nodules, posterior synechiae, peripheral anterior synechiae (PAS), and neovascularization of iris (NVI). The lens may have a pigment on the anterior capsule, and the posterior subcapsular opacification may be due to uveitis or to chronic corticosteroid therapy. These patients require regular IOP monitoring. Note has to be made on the timing and the extent of the pressure rise. If the pressure is elevated at the time of diagnosis, it is more likely that the inflammation is contributing to pressure elevation. In this case, the priority has to be in the escalating anti-inflammatory treatment, until the inflammation has been controlled. Gonioscopy must be performed to detect the presence of PAS and to assess the degree of angle closure. The posterior segment must be examined, paying particular attention to the optic nerve, to document the morphological changes consistent with glaucoma. Other possible posterior segment findings include cystoid macular edema, retinitis, perivascular sheathing, choroidal infiltrates, or retinal detachment.

Major Ocular Inflammations Associated with Secondary Glaucoma

Fuch's Heterochromic Iridocyclitis (FHIC): First described by Fuch's in 1906, FHIC is an idiopathic, painless, chronic, low-grade iridocyclitis with heterochromia, due to iris stromal atrophy. The typical age of onset is 20 – 40 years of age, with men and women affected equally.[8] It is typically unilateral, but in 13% of the cases it has presented bilaterally.[9] Slit lamp examination shows fine, diffuse, scattered, stellate-shaped keratic precipitates (KP) with fine filaments between them, with iris atrophy and patchy transillumination, secondary to loss of pigment epithelium, with characteristic moth-eaten appearance.[8] Histology reveals anterior stromal depigmentation, hyalinization of blood vessels, cellular infiltrations and Russell bodies. Infiltration of TM by mononuclear inflammatory cells, typically lymphocytes and plasma cells, causes rubeosis, trabeculitis, and collapse of the Schelmm's canal, leading to TM obstruction and rise in IOP.[10] Gonioscopic examination typically reveals an open angle and possible neovascularization, which may bleed with minor trauma.[11] Iris angiography can show leakage of the iris vessels and possibly ischemic changes of the iris. Complications are posterior subcapsular cataract (PSC) and secondary glaucoma. Reported incidence of glaucoma varies from 13 – 59%, with higher figures seen on long-term follow-up. Typically, glaucoma more commonly develops in persons of African descent and bilateral cases.[9] The glaucoma typically persists after uveitis has subsided and does not respond to steroids. Fuch's rarely causes synechiae formation. Unless glaucoma develops, Fuch's cyclitis is a benign disorder and does not require therapy. Use of steroids may only accelerate PSC formation and increase IOP.

Glaucomatocyclitic crisis: First described by Posner and Schlossman in 1948, presents in the 20 – 60 years age group, typically with unilateral recurrent episodes of mild cyclitis and heterochromia. Its pathogenesis still remains unknown, with suggested possible associations including an immunogenetic factor involving HLA-Bw54,[12] viral infections (HSV and CMV),[13,14] gastrointestinal disease, and various allergic factors.[15] The IOP is in the range of 40 – 70 mmHg during an acute attack and usually resolves spontaneously. The levels of prostaglandins in the aqueous humor have been found to be correlated with the level of IOP.[16] Slit lamp examination shows fine, small, flat, non-pigmented KP's in inferior corneal endothelium.[17] Gonioscopy reveals an open angle, with occasional trabecular precipitates.The treatment includes corticosteroids to control inflammation, and antiglaucoma medications notably beta-blockers and carbonic anhydrase inhibitors to control IOP. Apraclonidine has been shown to be effective during acute attacks.[18] Oral indomethacin may be effective because prostaglandins have been implicated in the disease.[16] If severe residual glaucoma persists after being maximally treated by medications, filtration surgery is indicated.

Grant's syndrome: First described by Chandler and Grant, it is an acute onset bilateral condition, affecting patients above 50 years of age.[18,19] Patients are usually asymptomatic. Gonioscopy reveals gray-to-yellowish inflammatory precipitates on the TM. The magnitude of IOP does not correspond to the amount of precipitates. It shows a good response to topical steroids and is typically unresponsive to antiglaucoma medication, but shows an excellent response to topical corticosteroid therapy. In most cases, the IOP returns to a normal level within one to two weeks after administration of topical corticosteroid, which clears the inflammatory precipitates. If severe angle closure is present secondary to the formation of extensive PAS, filtration surgery may be indicated.

Sarcoidosis: Sarcoidosis is a multisystem inflammatory disorder seen in the 20 – 40 year age group. It is more common in females than males and in blacks more than whites.[20] The ocular findings seen are panuveitis, mutton fat KP's, Bussaca and Koeppe's nodules, snow balls, candle wax dripping, and phlebitis. Glaucoma is seen in 11% of the cases. Gonioscopy shows obstruction of TM by inflammatory debris or nodules. Corticosteroids are the mainstay of the treatment.[21]

Juvenile Rheumatoid Arthritis (JRA): JRA is an autoimmune disease typically affecting children under the age of 16 years and lasts more than six months.[22] The uveitis is typically bilateral, nongranulomatous, asymptomatic anterior uveitis, usually preceded by arthritis.[23] Children with iridocyclitis rarely have a positive serology for a rheumatoid factor, but they frequently have antinuclear antibody[23,24] and HLA-B27 antigen, and some eventually are found to have typical ankylosing spondylitis.[24] Secondary glaucoma is seen in 19-25% of the patients with longstanding uveitis, due to secondary pupillary block acute angle closure. Topical steroids and mydriatics are the mainstay of treatment. The antiglaucoma drugs are required for control of IOP. In many cases, visual acuity is threatened enough to warrant further glaucoma surgery. Trabeculectomy or tube shunt surgeries are the first-line procedures. Goniotomy has been reported to be a safe and effective procedure and could be a first-line surgical treatment for JRA patients, although many patients may continue to require medication even after surgery.[25] Other potential surgical options that have been shown to have some positive outcomes include, nonpenetrating deep sclerectomy with the collagen glaucoma drainage device[26] and Molteno implant.[27] The complications that may cause significant visual loss in children with iridocyclitis and JRA include cataracts, band keratopathy, and glaucoma.

Herpetic Keratouveitis: This viral infection may cause recurrent conjunctivitis, keratitis, and uveitis. In one study of patients with herpes simplex keratouveitis, 28% had IOP elevation and 10% had glaucomatous damage.[28] The period of elevated IOP from herpetic keratouveitis has a mean duration of two months. Increase in IOP is due to an increase in the aqueous viscosity, trabecular blockade due to inflammatory debris, and trabeculitis with edema of the meshwork. Management of this condition requires that attention be given to the infection, inflammation, and glaucoma, and one suggested regimen includes topical trifluorothymidine, corticosteroids, and cycloplegics, along with antiglaucoma agents that reduce aqueous production.[29]

Syphilis: Fifteen percent of the patients of syphilis develop interstitial keratitis, of which 96% are bilateral. Twenty percent of the patients with interstitial keratitis (IK) develop secondary glaucoma. Both open and closed types of glaucoma have been reported.[30] In the open-angle, deep chamber type, there is usually no active inflammation. The glaucoma appears later in life, with an elevated IOP. The anterior chamber may have irregular pigmentation with varying amount of synechiae. Gonioscopy reveals open angles with a ‘dirty appearance,’ having varying amounts of old PAS that do not correlate with the amount of outflow obstruction.[30] The pathological mechanism of the condition appears to be endothelialization of the open portions of the angle, with formation of a hyaline membrane.The glaucoma tends to respond poorly to antiglaucoma medications and eventually requires filtering surgery. The closed-angle, narrow chamber type is characterized by small anterior segments, which could be due to IK in early infancy.[31] Peripheral iridectomy can be curative in eyes without permanent synechial angle closure.[30] In other eyes with permanent PAS, medical therapy, surgical goniosynechialysis, or filtering surgery may be necessary.

Scleritis: Scleritis is a painful ocular inflammation, which may primarily involve the anterior or posterior segment of the eye.[32] It affects patients in the 40 – 60 year age group; 12 – 46% of the patients of posterior scleritis show elevated IOP.[33] Unilateral acute angle closure glaucoma could be the presenting feature of scleritis due to choroidal effusion and subsequent detachment. Other mechanisms of glaucoma are uveitis, trabeculitis, primary angle closure glaucoma, pupillary block glaucoma, and neovascular glaucoma.[34] Treatment includes systemic anti-inflammatory agents, antiglaucoma medication, and laser iridotomy for pupillary block glaucoma.

Episleritis: Four percent of the patients develop open angle secondary glaucoma due to inflammation of the angle structure or due to steroids.[35]


In any patient with recurrent or bilateral uveitis, an underlying ocular or systemic cause should be sought. The ocular syndrome will dictate the workup and directed history. An appropriate systemic workup, focusing on arthritis, infections, mucosa or skin lesions, and cough should be conducted. A complete blood count and syphilis serology may be appropriate for all patients, while specific tests such as angiotensin converting enzyme and chest x-ray may be advisable for patients of African descent. Many syndromes may have unique characteristic features, either in the clinical presentation or examination findings. Findings such as disciform keratitis or a characteristic distribution of skin lesions may implicate herpetic infection. A rapid episodic rise in IOP with minimal cellular reaction may suggest Posner-Schlossman syndrome.


Treatment of uveitic glaucoma is aimed at controlling the intraocular inflammation and elevated IOP, as well as treating any underlying systemic disease.

Treatment of the inflammation: The major goals of treatment of inflammation are to provide symptomatic relief, prevent posterior synechiae formation, and reduce the severity and frequency of attacks or exacerbation of uveitis.


Corticosteroids remain the first line treatment in noninfectious ocular inflammation and can be administered topically, periocularly, intravitreally, and systemically. They exert anti-inflammatory effects by inhibiting the release of arachidonic acid and a subsequent production of prostaglandins. Topical steroids are favored for anterior segment disease.[36] If a long-term anti-inflammatory is needed, corticosteroid-sparing medications, or less potent corticosteroids, should be slowly replaced because of the potential side effects of long-term use, such as cataract, glaucoma, and local immunosuppression.[37] Periocular administration is used when more posterior effects are needed or when a patient's compliance is unsure. Several techniques have been advocated for the periocular application of corticosteroid, including subconjuctival, sub-Tenon's capsule, transeptal, orbital floor, and retrobulbar injections. Intravitreal injections of triamcinolone (IVTA) can also be used to deliver a high concentration of corticosteroids, to treat inflammation involving both anterior and posterior segments. IVTA is associated with over a 50% chance of an IOP elevation, although only 1 – 2% of these elevations necessitate surgical intervention.[38] Systemic steroids can be used to treat ocular inflammation recalcitrant to topical and periocular injections or when the uveitis is associated with systemic disease. Implantation of intraocular slow-release drug delivery devices using fluocinolone acetonide has been studied,[39,40] and could be a potential surgical treatment of uveitis. A concerning ocular side effect of corticosteroids is ocular hypertension especially with long-term use (more than three months).[41,42]


Cycloplegics are frequently prescribed together with corticosteroids to decrease the photophobia and pain caused by ciliary muscle or iris sphincter spasm. Cycloplegia can also break or prevent the formation of posterior synechiae.

Immunosuppressive agents

Immunosuppressive agents like antimetabolites, T-cell suppressors, and cytotoxic agents are generally reserved for cases refractory to corticosteroids or when chronic side effects of systemic corticosteroids, such as, bone demineralization, diabetes, or psychosis, are being avoided. Most immunosuppressive agents take several weeks to achieve efficacy and should be used in conjunction with oral corticosteroids, initially. Patients should be monitored very closely.


Methotrexate: Methotrexate (MTX) is an effective first-line corticosteroid-sparing medication. In a retrospective case series review of 160 patients, control of inflammation was achieved in more than 70% of the uveitic patients, with 90% having improved or stable visual acuity.[43] However, MTX is associated with a 30% discontinuation rate in the first year, due to toxicity, which includes liver dysfunction, nausea and vomiting, and alopecia. Folate supplementation should be used concurrently, to minimize the toxicity.

Mycophenolate Mofetil: Mycophenolate mofetil (MMF) is another corticosteroid-sparing medication that has favorable outcomes in treating ocular inflammation, with a low risk of side effects. MMF could be a potentially valuable alternative to other immunosuppressive therapy.[44]

T-cell Suppressors

Cyclosporine: Cyclosporine is an effective second-line agent in treating uveitis, but its therapeutic use is greatly limited by its toxicity, namely, renal dysfunction and systemic hypertension, even with low-dose regimens.[45]

Cytotoxic Agents

Cyclophosphamide: Cyclophosphamide has been used as a second-line immunosuppressive agent and has been seen to have stronger immunosuppressive power than MTX and MMF. Scleritis has an excellent response rate to cyclophosphamide.[46]

Chlorambucil: Chlorambucil is an alkylating agent of the nitrogen mustard type. It is recommended for use in patients with (1) severe ocular inflammation unresponsive to corticosteroids and / or a corticosteroid-sparing agent, (2) serious progressive reduction in vision despite other treatments, or (3) when blindness is an unavoidable consequence without further attempted therapy.[47]

Treatment of Glaucoma

Usually, abating the ocular inflammation normalizes the IOP, but in refractory cases, antiglaucoma medications, surgical management, or cyclodestructive laser treatment of glaucoma may be required.

Antiglaucoma Agents

Beta-blockers: Beta-blockers are first-line drugs to lower IOP in inflammatory glaucoma by reducing aqueous humor production. They are usually administered once or twice daily.[48]

Carbonic anhydrase inhibitors: Carbonic anhydrase inhibitors (CAIs) reduce aqueous production through an alteration of ion transport mechanism in the ciliary epithelium. CAIs can be administered topically, orally, or intravenously. Topical administration has the least potential for side effects, but also the least potent IOP-lowering effect

Selective alpha-2 adrenergic agonists: Alpha-2 adrenergic agonists lower IOP primarily by decreasing aqueous production. Brimonidine may have a delayed onset of enhanced uveoscleral outflow as well.[49,50] Nonselective adrenergic agents, such as epinephrine and dipivefrin, are not typically used. However, the mydriatic effect of epinephrine can be used to prevent posterior synechiae.

Prostaglandin analogs: Use of prostaglandin analogs (PGAs) in the setting of uveitic glaucoma has been limited due to potential concerns of worsening inflammation and increasing the risk of cystoid macular edema.[51,52] Although prostaglandins are to be avoided as the first-line therapy, they may prove to be very useful in a quiet eye with continuous pressure elevation.

Hyperosmotic agents: Hyperosmotic agents reduce IOP by dehydrating the vitreous, and thus, reducing the vitreous volume. They are used to lower IOP rapidly in an acute setting. However, hyperosmotic agents carry a significant risk of intravascular fluid overload in a patient with suppressed cardiovascular function.

Miotics: Miotics should not be used in uveitic glaucoma due to their potential to induce formation of posterior synechiae, aggravate the symptoms of inflammation caused by ciliary spasm, and worsen inflammation by disrupting the BAB.

Surgical Treatment

Surgery for uveitic glaucoma is reserved for uncontrolled elevated IOP, despite maximally tolerated medical therapy, as well as in cases of pupillary-block angle-closure glaucoma. Intraocular surgery should be avoided whenever possible in eyes with active inflammation. However, when medical therapy is inadequate, surgery may be required. In these cases, it is best to do the least amount of surgery possible. A laser iridotomy is safer than an incisional iridectomy when an angle closure mechanism is present, although the fibrin may tend to close a small iridotomy in an inflamed eye. Antimetabolite therapy in association with trabeculectomy has been shown to improve the success rate of trabeculectomy in patients with a high risk of failure.[36] A study by Kaburaki et al.,[53] has concluded that initial trabeculectomy with mitomycin C in uveitic glaucoma eyes with inactive uveitis that had not undergone any previous ocular surgery had results comparable to those of primary open angle glaucoma, suggesting that pre-existing uveitis itself is not a risk factor for failure of trabeculectomy, with mitomycin C, when uveitis is under control. Drainage implants 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.[5458] Standard goniotomy represents an alternative, safe, and effective surgical option for the treatment of young patients with medically refractory glaucoma, complicating chronic childhood uveitis. Candidates for goniotomy include children and young adults, both phakic and after cataract surgery. Angle surgery should be considered in these young patients, as it may be appropriate to utilize before more invasive surgical techniques such as trabeculectomy and glaucoma implant surgery. Future consideration of goniotomy for the surgical treatment of glaucoma, secondary to adult-onset uveitis, might also be warranted.

Freedman et al.[59] reported an overall success rate of 75% with standard goniotomy surgery for the treatment of young patients with medically refractory glaucoma associated with chronic childhood uveitis, with few complications, and without worsening of the existing uveitis.Trabeculodialysis is a modified goniotomy used in children and young adults with uncontrolled uveitic glaucoma.[60] 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.

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

  • Wright et al. reported that three of the 24 patients undergoing trabeculectomy with mitomycin-C required subsequent drainage implants and that seven of the 24 patients lost two or more lines of Snellen acuity.[61]
  • Hill et al. reported a success rate of 79% in eyes undergoing Molteno tube implantation.[62]
  • Ceballos et al. reported a two-year success rate of 91.7% in eyes undergoing Baerveldt drainage device placement for uveitic glaucoma. There were no intraoperative complications in this series. Ten eyes had postoperative complications. The most common were choroidal effusions (four eyes, 16.7%), hypotony maculopathy (three eyes, 12.5%), cystoid macular edema (three eyes, 12.5%), and failure of corneal grafts (two eyes, 8.3%). One patient in whom a corneal graft failed had undergone penetrating keratoplasty, three months before placement of the Baerveldt implant. The corneal graft remained clear for two years and then slowly failed. The second patient in whom a corneal graft failed had undergone penetrating keratoplasty at the same time as placement of the Baerveldt implant. Her corneal graft failed 12 months after surgery, at which time she underwent a second penetrating keratoplasty. Most complications were transient and of no visual consequence.[63]
  • Ozdal et al. showed a two-year success rate of 68.4% in eyes undergoing the Ahmed drainage device placement for uveitic glaucoma.[64] Postoperative complications were observed in 57.9% eyes. The majority of these complications were resolved either spontaneously or with an additional surgical procedure. Occlusion of the valve was the most common complication and occurred in 26.3% in which one additionally had extrusion of the valve. In one of these eyes, the AV implant was replaced and the second implant worked successfully. Another one was treated with irrigation of the implant. The remaining three eyes in which two had neovascular glaucoma (NVG) were considered as a failure. A success rate in eyes with NVG has been reported to be significantly lower. Another complication that required additional surgery was corneal decompensation due to the corneal-tube touch and was observed in one eye. Penetrating keratoplasty was performed in this eye. Choroidal effusion was observed in one and treated with systemic corticosteroid. Other complications such as hyphema (5.3%) and postoperative hypotony (15.8%) were resolved spontaneously within few days.
  • Rachmiel et al. reported a 30-month success rate of 60% in both primary open angle glaucoma and uveitic glaucoma in patients undergoing Ahmed glaucoma valve implantation. The most common side effect in the two groups was uveitis, 24.5% and 33.3% in the primary open angle glaucoma and uveitic groups, respectively, which was controlled with topical steroids. Other complications, such as wound dehiscence, choroidal effusion, and transient diplopia were comparable in the two groups and resolved spontaneously with no intervention. The single significant complication in the uveitic group was tube removal in three eyes (13.3%; P = 0.02) due to tube exposure in two cases and plate exposure in one case.[65]


Glaucoma is a common and potentially blinding complication of uveitis and is seen in about 20% of these patients. The pathogenic processes responsible for the underlying elevation in intraocular pressure are multiple involving both open angle and closed angle mechanisms.[66,67] The mechanisms by which iridocyclitis leads to obstruction of aqueous outflow include acute, usually reversible forms (e.g., accumulation of inflammatory elements in the intertrabecular spaces, edema of the trabecular lamellae, or angle closure due to ciliary body swelling) and chronic forms (e.g., scar formation or membrane overgrowth in the anterior chamber angle). Careful history and follow-up helps distinguish steroid-induced glaucoma from uveitic glaucoma. Successful management of uvetic glaucoma depends on recognition of the uveitis syndrome and clarification of the mechanisms contributing to it. Both the inflammation and raised intraocular pressure require treatment. The anti-inflammatory regimen includes corticosteroids, cytotoxic agents, and other immunosuppressive agents. When the angle is open IOP reduction may be achieved medically. When medical treatment fails surgical intervention may be required.


Source of Support: Nil

Conflict of Interest: None declared.


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