In large reviews of uveitis patients, the reported prevalence of secondary glaucoma ranges from 9.6% to 23%.^3–5 Although all types of ocular inflammation can lead to glaucoma, it is seen most frequently with iridocyclitis. In a study of 1254 consecutive patients at a uveitis clinic,³ glaucoma was seen most frequently with anterior, chronic, and granulomatous disease. Of those with glaucoma, 67% had anterior segment inflammation, 4% had intermediate uveitis, and 13% had posterior uveitis. The remaining patients had panuveitis. In this study, the types of uveitis that were most likely to result in glaucoma were secondary to herpes simplex and herpes zoster (22% developed glaucoma), Fuchs' heterochromic iridocyclitis, Vogt-Koyanagi-Harada syndrome, juvenile rheumatoid arthritis (JRA), syphilis, and sarcoidosis. Table 1 outlines the many types of uveitis reported to be associated with secondary glaucoma.

OPEN ANGLE MECHANISMS

Aqueous outflow is decreased when the trabecular meshwork becomes clogged with macrophages and inflammatory debris.^30,31 The iridocorneal angle may also be infiltrated with lymphocytes, polymorphonuclear leukocytes, and fibrin, and the trabecular beams may become swollen.³² Aqueous protein alone has been shown to reduce outflow significantly.³³ In acute inflammation, angle obstruction is usually temporary. In chronic or recurrent disease, however, inflammation can permanently damage the trabecular meshwork. A basement membranelike material may develop over the angle.³⁴ Trabecular endothelial cells that phagocytize debris may migrate away from the collagen beams or undergo autolysis, resulting in permanent impairment of function.^2,35,36

Increased outflow resistance distal to Schlemm's canal is proposed as a mechanism for ocular hypertension in scleritis. Histopathologic study has demonstrated lymphocytic cuffing of the scleral outflow channels in scleritis patients with glaucoma.³⁷

Although most ocular hypertension due to inflammation is a result of decreased outflow, increased aqueous production due to prostaglandins may also play a role.³⁸ Prostaglandins have been demonstrated in the anterior chamber of uveitis patients³⁹ and have been implicated in the pathogenesis of glaucomatocyclitic crisis.⁴⁰

Finally, chronic treatment of inflammation with corticosteroids may elevate IOP. This is discussed in detail later in the chapter.

CLOSED ANGLE MECHANISMS

Disruption of the blood-aqueous barrier allows inflammatory cells, fibrin, and debris to collect in the anterior chamber angle. The peripheral iris can then become adherent to the trabecular meshwork, resulting in the formation of peripheral anterior syn-echiae (Figs. 1 and 2).² The areas of open angle between synechiae are often heavily pigmented and function poorly.² Chronic inflammation may be associated with angle neovascularization, which can also cause synechiae to develop.²

Anterior segment inflammation may also cause adhesions to form between the iris and anterior lens capsule. In aphakic and pseudophakic patients, the iris may adhere to the vitreous face or intraocular lens, respectively. Seclusion of the pupil occurs when these central posterior synechiae block the flow of aqueous from the posterior to the anterior chamber through the pupil. Increased pressure in the posterior chamber pushes the peripheral iris forward (iris bombe, Fig. 3) against the trabecular meshwork, leading to appositional angle closure. In an inflamed eye, this can quickly lead to synechial angle closure.²

Ciliary body edema may cause anterolateral rotation of the ciliary body about its attachment to the scleral spur. This relaxes the lens zonules, resulting in forward movement of a rounder lens. The anterior face of the ciliary body and peripheral iris are then brought into contact with the trabecular meshwork, causing angle closure.^41,42 This mechanism of angle closure is treated with cycloplegics and steroids.^41,42 Cholinergic agonists should be avoided.

Associated ocular hypertension is reported in 8% to 23% of patients with HLA-B27-positive anterior uveitis,^48,49 and 4% to 8% develop secondary glaucoma.^46,48 In one report of patients with ankylosing spondylitis, 28% developed uveitis, and in some the ocular disease presented before joint symptoms.⁵⁰ Another study of 47 patients with ankylosing spondylitis and uveitis found that 4% developed ocular hypertension and 2% had secondary glaucoma.³ In a review of 113 patients with Reiter's syndrome, 12% had iritis and 1% had glaucoma.⁵¹ Of 26 patients with Reiter's syndrome and uveitis in another study, 12% developed glaucoma.³

Ocular inflammation is often asymptomatic and usually bilateral.⁵⁴ It can precede joint symptoms or persist long after the arthritis is quiet.^54,58 The activity of the joint inflammation is independent of the ocular disease.⁵⁸ When uveitis is the initial manifestation, the visual prognosis is poorer than if the arthritis is the presenting sign.⁸ In one study, presentation with advanced inflammation (posterior synechiae) was associated with glaucoma in 45% compared with 17% of patients with mild or no inflammation at onset.⁸

Glaucoma secondary to JRA can be challenging to treat. In one report, filtering surgery was required in 19% of cases.⁵⁷ Other studies indicate that filtering surgery provided adequate control in only 18% to 38% of cases.^4,54 Cyclocryotherapy may be effective in lowering pressure, but one report suggests this result may last only a few months.⁵⁹ Control of the uveitis is essential, and a stepwise approach to treatment has been advocated, with no tolerance for any active inflammation.⁶⁰ Anterior chamber cellular response should always be treated, but flare alone becomes chronic and is not an indicator of active disease.^60,61 Therapy begins with topical corticosteroids and progresses to periocular steroid injection, systemic nonsteroidal anti-inflammatory agents (NSAIDs), systemic steroids, and immunosuppressants.⁶⁰ Glaucoma and cataracts can be exacerbated by steroid therapy.⁸ Oral NSAIDs have been reported to improve chronic iridocyclitis and allow reduction of the steroid dose.⁶² Methotrexate isalso steroid sparing⁶³ and is effective in resistantcases of the disease.^57,64,65 The reported visual prog-nosis for patients who develop glaucoma is poor,with half of the eyes in one study with vision of20/200 or worse⁵⁵ and 35% with no light perception in another.⁴

A review of patients with herpes simplex uveitis revealed that 28% developed ocular hypertension, with 10% of these progressing to visual field loss.⁹ HSV keratitis associated with elevated IOP is usually disciform or stromal.⁹ Management of secondary glaucoma is initially directed at controlling the viral infection and treating the inflammation.⁴⁷ Topical trifluorothymidine penetrates the cornea better than other antiviral agents and may be best for treatment of HSV keratitis.⁶⁶ Systemic acyclovir may also be helpful.⁶⁷ Topical corticosteroids must always be used in conjunction with antiviral coverage to prevent reactivation of epithelial disease.⁴⁷ Cycloplegics relieve ciliary spasm, and aqueous suppressants are best for treatment of elevated pressure.

In a study of 86 patients with herpes zoster ophthalmicus,¹⁰ 43% had uveitis, and 27% of these had ocular hypertension. Only one patient developed visual field loss. In another report of 14 patients,⁶⁸ 5 had elevated IOP. The use of oral acyclovir⁶⁹ or related antivirals (valacyclovir, famciclovir)⁷⁰ within 72 hours of onset of skin lesions reduces the incidence and severity of secondary uveitis that can lead to glaucoma. Topical acyclovir has also been shown to be more effective than topical corticosteroids in shortening the course of zoster uveitis.⁷¹

Both open and closed angle mechanisms have been described. Open angle glaucoma may occur with increased pigmentation and a hyalinized appearance to the trabecular meshwork resulting from acute inflammation early in life.^34,79 These cases usually respond poorly to medical treatment.⁷⁹ Angle closure may occur acutely or subacutely due to posterior synechiae and pupillary block, or chronically with peripheral anterior synechiae.⁴⁷ Patients with congenital syphilis and interstitial keratitis in infancy may have small anterior segments, microcornea, and narrow angles, predisposing them to pupillary block angle closure later in life.⁸⁰ Acute cases of angle closure may respond well to laser peripheral iridotomy, but if extensive synechiae are present, medical or surgical treatment may be needed.⁷⁹ Intraepithelial cysts of the iris and ciliary body²⁸ and lens subluxation or dislocation⁷⁶ have also been reported as causes of angle closure glaucoma in syphilis.

Although most commonly associated with anterior uveitis, sarcoidosis has been shown to be the leading cause of posterior, intermediate, and panuveitis associated with secondary glaucoma.³ One study found that nodular infiltration of the trabecular meshwork was the most common cause of ocular hypertension.⁸³ In patients with sarcoid uveitis, secondary glaucoma is often the major prognostic factor in a poor visual outcome.^81,84 Eight of 11 patients with secondary glaucoma in one review experienced severe visual loss.⁸¹

Treatment of scleritis includes systemic NSAIDs, topical and systemic steroids, and immunosuppressive agents.^31,37 Ocular hypertension is usually improved with control of inflammation unless synechiae have developed.³⁷ In posterior disease with ciliary body rotation and angle closure, cycloplegics should be used and cholinergic drugs avoided.⁴¹ Aqueous suppressants are used as needed to lower IOP.

On examination, the conjunctiva is minimally injected or quiet. A subtle anterior chamber reaction is present. The corneal epithelium may be edematous, and a few small round keratic precipitates may be present inferiorly.¹⁰⁵ The pupil may be slightly dilated,^23,107 and the iris may become hypochromic.²³ Iris fluorescein angiography demonstrates focal ischemia with a late diffuse leak from the pupillary border.¹⁰² On gonioscopy, the anterior chamber angle is open and not excessively pigmented. Peripheral anterior synechiae do not develop.^23,106

Tonographic studies demonstrate a decrease in aqueous outflow during attacks,¹⁰⁸ but increased aqueous production has also been reported to contribute to the pressure elevation.^109,110 Prostaglandins can increase aqueous production in animal models and are believed to be the cause of the pressure rise.¹¹¹ They are also known to cause breakdown of the blood-aqueous barrier, allowing protein and inflammatory cells to leak into the anterior chamber.¹¹¹ Elevated levels of prostaglandins have been measured in the anterior chamber during attacks but fall to normal levels between attacks.⁴⁰ IOPs during attacks have been correlated with anterior chamber prostaglandin levels.⁴⁰ Therapy with the prostaglandin inhibitor indomethacin was shown in one study to lower pressure more rapidly than acetazolamide, epinephrine, and dexamethasone.⁴⁰ Inflammatory changes in the trabecular meshwork may also be a factor in the elevated pressures: one trabeculectomy specimen obtained during an attack revealed a trabecular mononuclear cell infiltrate and a lack of vacuoles in Schlemm's canal.¹¹²

Many theories have been proposed as to the underlying cause of this disease, including an autonomic defect,²³ a vascular process,¹⁰² an allergic disorder,¹⁰⁷ a variant of developmental glaucoma,¹⁰⁶ and a viral infection.^113,114 In one study, cytomegalovirus antibodies were found in the aqueous of 7 of 11 eyes with glaucomatocyclitic crisis compared with 3 of 379 eyes with other uveitides.¹¹³ HSV DNA has also been demonstrated in aqueous aspirates during acute attacks.¹¹⁴ The disease has been associated with peptic ulcer disease and allergic disorders.¹¹⁵ Evidence also suggests a relationship to primary open angle glaucoma, because glaucomatous optic nerve damage has occurred in both the affected and unaffected eyes of some patients,^101,102 and these patients also exhibit a response to corticosteroid therapy similar to those with primary open angle glaucoma.¹⁰¹ Many patients eventually develop primary open angle glaucoma that may be masked by the relative hypotony in the affected eye after the attack.¹⁰²

Treatment for attacks includes control of inflammation with topical steroids¹⁰⁷ and lowering of IOP with ocular antihypertensive medications. Oral indomethacin may also be helpful.⁴⁰ Cycloplegia is not necessary because there is little discomfort and synechiae do not develop. The pressure returns to normal on resolution, but glaucomatous damage can develop that may require chronic therapy. There is no evidence supporting the use of prophylactic antiinflammatory treatment between episodes. If needed, IOP control can be achieved with filtration surgery, although recurrence of attacks is not prevented.¹¹⁶

Fuchs' heterochromic iridocyclitis was found in 2% to 3% of uveitis patients studied by a large clinic,¹²⁴ and it is believed to be the most frequently misdiagnosed cause of ocular inflammation.¹²² Although it commonly presents between age 30 and 60, cases have been reported in patients in their teens to over age 70.²² Its occurrence is equal in men and women.¹²¹ It is most commonly unilateral; the reported prevalence of bilateral disease is 7.8% to 13%.^121,125 Most cases are sporadic, but familial cases have been reported.²² Both concordance¹²⁶ and discordance¹²⁷ have been reported in monozygotic twins. The onset is typically insidious, and the condition is often asymptomatic until significant cataract develops. Pain and photophobia are usually absent^22,128 or very mild.¹²⁰ Some patients report floaters.¹²⁰

Iris heterochromia (Fig. 5), due to stromal atrophy, develops slowly^121,125 and is subtle or absent in some patients. The affected eye is usually lighter,¹²⁸but in light blue eyes, the darker eye may be affected as the pigment epithelium is visible though the atrophic iris stroma.¹²¹ In one report, 67% of the affected eyes were hypochromic, 11% were hyper-chromic, and 22% had no heterochromia.²² Very dark irides may not exhibit heterochromia.^120,128 In one study, 92% of whites and 76% of blacks exhibited this sign.¹²⁰ The most consistent finding is a featureless iris with blunted crypts and a dull, flat surface.¹²³ Transillumination defects may be seen near the pupillary margin.¹²¹ Inflammatory nodules were present in 20% of white patients and 30% of blacks in one study.¹²⁰ The finding of unilateral iris nodules may aid in making the diagnosis in a patient of African descent.¹²⁹ Iris neovascularization is present in many patients.¹²³ Histologically, the iris in patients with Fuchs' exhibits decreased stromal melanocytes with atrophy and stromal fibrosis. There is infiltration of histiocytes, plasma cells, and lymphocytes.^130,131

Chronic, mild anterior chamber cell and flare is common.¹²⁴ Keratic precipitates are characteristically small, round, or stellate, with fine filaments between them (Fig. 6).¹²¹ Unlike other inflammatory conditions, they are distributed over the entire endothelium (Fig. 7).¹²¹ The anterior chamber angle is open. Inflammatory synechiae rarely develop spontaneously¹²¹ but may arise after cataract surgery.¹³² Neovascularization of the angle may occur (Fig. 8),^22,123 but neovascular glaucoma is rare.¹³³ Angle vessels are extremely fragile and have been reported to bleed with minor trauma such as gonioscopy,¹³⁴ applanation tonometry,¹²⁵ or Honan balloon application.¹³⁵ Significant intraoperative hemorrhage is unusual,¹³⁶ but minor bleeding may occur after a paracentesis, resulting in a discrete column of blood in the opposite angle (Amsler's sign).¹³⁷ Ingeneral, angle abnormalities do not correlate well with the presence or severity of glaucoma.¹¹⁹

Chorioretinal lesions similar in appearance to toxoplasmosis scars have been reported in 10.2% to 100% of cases.^138–141 In one study, only 60% of those with scars had positive toxoplasmosis titers,¹⁴⁰ and in another, no toxoplasma antigen was detected in patients with these lesions.¹⁴¹ Moreover, no antibodies to toxoplasmosis were found in the aqueous of these patients.¹⁴¹

Cataracts develop late in the course of the disease and do not help with early diagnosis.¹²⁴ For most patients, cataract extraction has a good prognosis, with only a minimal increase in the incidence of complications.^{121,124,132,136,142–144} Reported complications include hyphema,¹⁴⁵ development of synechiae,^132,143 and postoperative fibrinous reaction.^142,143 Cataract surgery may also lead to the onset or exac-erbate the course of glaucoma.¹¹⁸ In one study, placement of an intraocular lens in patients with preexisting glaucoma was more likely to result in severe postoperative uveitis; the uveitis did not seem to affect visual outcome, however.¹⁴⁵ Increased postoperative inflammation has been associated with preoperative severe iris atrophy and marked iris vascular abnormalities as well as preoperative glaucoma.¹⁴⁶ Preoperative steroid treatment has been advocated for these high-risk patients.^145,146 Nevertheless, patients with heterochromic iridocyclitis generally have a better course with cataract surgery than other uveitides.¹⁴⁶

The etiology of this disease is unclear. Fuchs postulated that it was due to an intrauterine insult.¹¹⁷ Others have proposed vascular disease,¹⁴⁷ toxoplasmosis,¹³⁸ a degenerative process,¹⁴⁸ or a sympathetic disorder¹⁴⁹ as the cause. There is some evidence supporting an immunologic mechanism. Cellular immunity to corneal antigens¹⁵⁰ and circulating antibodies against corneal epithelium¹⁵¹ have been found in many of these patients.

No treatment is required for this condition unless glaucoma develops. Treatment of the inflammation with steroids is unnecessary; it will not help control elevated pressure and may instead hasten the development of cataracts or induce glaucoma in steroid-responsive patients. Control of the glaucoma with medical management alone is often difficult: reported success rates vary from 27% to 63%.^22,118,119 Many patients require filtering surgery, and reported success rates are 45%,¹¹⁸ 57%,²² and 72%, the latter of which involved use of 5-fluorouracil (5-FU)-augmented trabeculectomy.¹¹⁹

MEDICAL THERAPY

Treatment of glaucoma associated with uveitis begins with control of the inflammation. This alone may lower the IOP. Topical corticosteroids are used initially,⁸⁹ with hourly or every-2-hour frequencies in severe cases. Concomitant use of topical antiviral agents should be considered if HSV is the suspected etiology.⁴⁷ Topical corticosteroids may be supplemented with sub-Tenon's injection or systemic administration. Topical or oral NSAIDs may be helpful in selected cases.^40,152,153 Resistant disease may require immunosuppressive agents.^154,155

Topical cycloplegic-mydriatic agents help to relieve the discomfort of ciliary spasm and may prevent formation of central posterior synechiae. By deepening the anterior chamber, they may also helplimit the development of peripheral anterior synechiae. One may attempt to break formed posterior synechiae with strong mydriatic agents such as 10% phenylephrine and 1% atropine.

Aqueous suppressants are the main therapy for the control of ocular hypertension associated with inflammation. Topical beta-adrenergic blocking drugs, topical alpha-2 agonists, and topical or oral carbonic anhydrase inhibitors can be used. Metipranolol, a nonspecific beta antagonist, has been reported to cause granulomatous uveitis^156–158 and should probably be avoided in the treatment of uveitic glaucoma. Systemic hyperosmotic agents may be helpful to lower IOP rapidly, but they may fail because of blood-ocular barrier breakdown due to inflammation.¹⁵⁹ Cholinergic agonists are contraindicated for several reasons. Induced miosis promotes posterior synechiae and pupillary membrane formation. Shallowing of the anterior chamber may lead to peripheral anterior synechiae. These agents may also further weaken the blood-ocular barrier, worsening inflammation. Prostaglandin analogs, such as latanoprost, have been associated with anterior uveitis^160,161 and cystoid macular edema¹⁶¹ and should be used with caution or avoided in patients with uveitis.¹⁶¹

SURGICAL MANAGEMENT

Laser peripheral iridotomy should be performed in eyes with pupillary block that cannot be broken with dilation. In an inflamed eye a large iridotomy should be made because a smaller opening is more likely to close. If this occurs, the iridotomy may be enlarged with repeat laser treatment, multiple iridotomies can be created, or a larger surgical opening can be fashioned. Iridotomies made with an argon laser are more likely to close than those created with the Nd-YAG laser.¹⁶² The Nd-YAG laser, however, should be used with caution in inflamed eyes with engorged iris vasculature because significant bleeding can occur. Pretreatment with the argon laser may limit bleeding at the iridotomy site.¹⁶² Because laser iridotomy may exacerbate or reactivate anterior segment inflammation, topical corticosteroids should be administered after surgery.⁴⁷ The Nd-YAG laser may induce less postoperative inflammation than the argon laser.¹⁶²

There is no place for argon laser trabeculoplasty in the treatment of uveitic glaucoma. Trabeculoplasty is ineffective, may exacerbate inflammation, and may induce the formation of peripheral anterior synechiae in an eye with uveitis.¹⁶³

Goniosynechiolysis is a procedure for opening an angle with extensive, recently formed peripheralanterior synechiae. Campbell and Vela described four cases of synechial angle closure glaucoma that were cured with their technique, and a fifth that was significantly improved.¹⁶⁴ The technique is thought to be less successful when synechiae are more than 1 year old. In these cases, chronic pathologic changes in the meshwork that occur behind the synechiae can significantly increase resistance to outflow.¹⁶⁴

Eyes in which medical treatment fails to control IOP require filtering surgery. Results of trabeculectomy in the setting of chronic inflammation are poor⁴ but improve with adjunctive use of antifibrotic agents. Reported results of complete success (IOP less than 21 without medication) with 5-FU range from 47% to 83%^165–168 and from 62% to 88% with mitomycin C.^165,169,170 Qualified success rates (IOP less than 21 with or without medication) are higher: 80% to 100% for 5-FU^166–168 and 65% to 92% for mitomycin C.^169–171 When 5-FU and mitomycin C were directly compared in glaucoma patients with poor surgical prognoses (including inflammatory glaucoma), patients receiving mitomycin-C were more likely to have complete success (88% vs. 47% with 5-FU)¹⁶⁵ and had a lower IOP with fewer medications.¹⁷² Eyes with active uveitis at the time of surgery should have intense topical and possibly systemic corticosteroids before surgery and in the postoperative period to avoid exacerbation of uveitis and failure of the filtering surgery.⁴⁷

When postoperative inflammation is expected to be significant or prolonged, aqueous drainage devices may offer better control of IOP.¹⁷³ Success rates of 57% to 94% are reported with the Ahmed valve,^174,175 79% with the Molteno implant,¹⁷³ and 90% with the Baerveldt device in patients with uveitic glaucoma.¹⁷⁶

Modified goniotomy (trabeculodialysis) was reported to be successful in 60% in one study of JRA patients.¹⁷⁷

As with other forms of glaucoma, cyclodestructive procedures are used as a therapy of last resort because of their risk of exacerbating inflammation and the potential for the development of phthisis.

Elevation of IOP will occur in normal subjects when given 6 weeks of topical corticosteroids. In one study,¹⁸¹ about two thirds responded with a rise in IOP of 5 mmHg or less. Less than one third (29%) responded with increases between 6 and 15 mmHg, and 5% developed pressures of greater than 16 over baseline. In another study, 30% of normals developed pressures greater than 20 and 4% rose to above 31 mmHg.¹⁸² Ninety-two to 94% of primary open angle glaucoma patients reportedly respond with significant elevations.^182,183 Steroid response is also more common in patients with a family history of glaucoma,¹⁸² high myopia,¹⁸⁴ diabetes,¹⁸⁵ and connective tissue diseases.¹⁸⁶ A response to corticosteroids has also been reported to occur in children.^187,188

Elevated IOP usually occurs after 3 to 8 weeks of chronic treatment but can occur earlier.¹⁸⁹ Acute rises have been reported after intensive topical or systemic administration of corticosteroids.^190,191 Patients should be monitored for this complication throughout the course of therapy. Previous corticosteroid therapy should also be in the differential diagnosis of normal tension glaucoma.

The mechanism of elevated IOP is thought to be an increase in resistance to aqueous outflow.^182,193 Glucocorticoid receptors are present in the trabecular meshwork, and steroids have been shown to have a high affinity for binding to them.¹⁹² It is unclear how this results in compromised outflow, but it has been proposed that the normal phagocytic activity of trabecular endothelial cells is inhibited, resulting in a buildup of debris in the meshwork.³⁰ Another theory is that steroids prevent the release of enzymes that depolymerize glycosaminoglycans, leading to their accumulation in the outflow system.^190,193

The steroid response effect is most frequently seen with ocular topical corticosteroids¹⁹⁰ but has also been reported with every other route of administration. A response has been observed with topical steroids applied to lid skin^194,195 as well as chronic application of large doses to skin far from the eyes.¹⁹⁶ Glaucoma can occur with systemic^{191,197–199} administration as well as with excess endogenous steroids, as in Cushing's syndrome.²⁰⁰

Periocular injection (subconjunctival, sub-Tenon's, and retrobulbar) carries a significant risk of secondary glaucoma.²⁰¹ This is more likely to occur with anterior than posterior injection. In one study, 30% of eyes receiving a posterior sub-Tenon'sinjection experienced an increase in pressure to greater than 25 mmHg.²⁰² The duration and severity of pressure elevation are inversely related to the solubility of the injected steroid.²⁰¹ Triamcinolone acetate, the least soluble and longest-acting repository steroid, is the highest-risk agent.²⁰¹ A patient's response to chronic topical steroids is not always predictive of a response to periocular injection,²⁰¹ although in one study of 202 patients who did not respond to topical or systemic steroids, deep posterior sub-Tenon's injection also did not cause an elevated pressure.²⁰³ Multiple periocular injections may increase the risk of developing glaucoma.²⁰² When maximal medical therapy is unsuccessful in controlling elevated pressure, surgical removal of the tissue containing the depot steroid can be effective.^201,204

Induced ocular hypertension due to inhaled steroids has been reported,^105,206 especially with chronic high-dose therapy.²⁰⁶ In one study, the relationship was found only in persons with a family history of glaucoma.²⁰⁷ Reports of response with intranasal administration are conflicting in the literature, with case reports suggestive of this complication²⁰⁸ but one large study demonstrating no significant risk.²⁰⁶

Elevated IOP is related to steroid potency,²⁰⁹ frequency of administration, and duration of treatment.¹⁸³ Several topical steroids have been developed that have a lower risk of secondary glaucoma. Fluoromethalone is a steroid structurally related to progesterone that has less hypertensive effect than other steroids of similar potency.²¹⁰ Its anti-inflammatory effect is less than that of 1% prednisolone acetate or dexamethasone,²¹¹ but it may be more potent when used in the acetate form without additional risk.²¹² Medrysone, also related to progesterone, has minimal ocular hypertensive effects primarily because it has poor ocular penetration.^213,214 It may be useful for external inflammation.²¹³ Rimexolone was shown to be as effective as prednisolone acetate in one report but less likely to cause elevated IOP.²¹⁵ In a study of known steroid responders, rimexolone was less likely to cause a10-mmHg rise in pressure than prednisolone acetate or dexamethasone sodium phosphate, and patients taking the latter medicines had a pressure response in a significantly shorter interval than the former.²¹⁶ Loteprednol is a site-active steroid that undergoes transformation to inactive metabolites.²¹⁷ Although found to be somewhat less effective for the treatment of anterior uveitis than prednisolone acetate,²¹⁸ loteprednol caused significantly less ocular hypertension.²¹⁷ Pressure elevations greater than10 mmHg occurred in 1.7% of patients using chronic 0.5% loteprednol compared with 6.7% of those using 1% prednisolone acetate.²¹⁷

Management of induced glaucoma should begin with tapering or discontinuing the corticosteroid if possible. In most cases IOP returns to normal within 1 to 4 weeks,¹⁹⁰ but it has been reported to cause permanent ocular hypertension in some patients.^190,219 If the severity of the uveitis precludes discontinuing therapy, substitution with a steroid less likely to induce ocular hypertension may be beneficial. Topical NSAIDs also show some efficacy in the treatment of uveitis²¹⁵ and do not affect IOP.²²⁰ Excision of depot corticosteroids may be necessary in some patients to normalize IOP.^201,204 Finally, concurrent treatment of inflammation and ocular hypertension may be necessary with standard antiglaucoma medicines or filtering surgery.

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