Chapter 54D
Inflammatory Glaucoma
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Intraocular inflammation affects both aqueous inflow and outflow. A decrease in aqueous production frequently leads to a reduction in intraocular pressure (IOP). Elevated IOP can occur if aqueous outflow is decreased to a greater extent than aqueous production.1 In many eyes with uveitis, the IOP is normal or low acutely, but may become elevated later when aqueous production returns to normal and outflow remains compromised.2 Inflamed eyes should be monitored closely to detect a late rise in IOP.

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.



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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.


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

Fig. 1. Histopathologic slide of the iridocorneal angle of a patient with congenital syphilis. Granulomatous inflammation is present on the surface of this eye, and the angle is closed by peripheral anterior synechieae. (Courtesy of Robert Folberg, MD. Copyright University of Iowa. Alward WLM: Color Atlas of Gonioscopy. London, Mosby-Year Book, 1994.)

Fig. 2. Gonioscopic view of the iridocorneal angle in a child with uveitis. The trabecular meshwork can be seen only at the left of this illustration. The remainder of the angle has been closed by peripheral anterior synechiae. Central posterior synechiae are present at the pupil, and keratic precipitates are visible on the corneal endothelium. (Illustration by Lee Allen. Copyright University of Iowa. Alward WLM: Color Atlas of Gonioscopy. London: Mosby-Year Book, 1994.)

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

Fig. 3. Central posterior synechiae leading to pupillary block and iris bombe. (Courtesy Paul F. Palmberg, MD, PhD, Bascom Palmer Eye Institute, University of Miami. Alward WLM: Color Atlas of Gonioscopy. London: Mosby-Year Book, 1994.)

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.

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Glaucoma is most commonly associated with anterior uveitis. Pain, photophobia, and blurred vision are characteristic symptoms of acute iridocyclitis. Chronic inflammation may be asymptomatic, and extensive glaucomatous damage can occur before diagnosis. On examination, conjunctival injection with perilimbal ciliary flush is present. Cell and flare are present in the anterior chamber. Keratic precipitates are present on the corneal endothelium, and if the IOP is elevated, microcystic epithelial edema may be seen. Gonioscopy may reveal increased pigmentation, inflammatory precipitates, or peripheral anterior synechiae. The iris may exhibit inflammatory nodules. Central posterior synechiae may develop, and if confluent may result in seclusion of the pupil, iris bombe, and angle closure. In the majority of patients with anterior uveitis, an underlying etiology is never determined.
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Arthritis is often associated with ocular inflammation. In a review of 1927 patients with uveitis, an underlying joint disease was found in 10%.43 Anterior uveitis and joint disease are also frequently associated with the genetic marker HLA-B27.44,45 HLA-B27-positive anterior uveitis is usually recurrent, unilateral, and nongranulomatous. Extensive anterior chamber cellular reaction and fibrin formation are characteristic.44,46 Of patients with acute nongranulomatous iridocyclitis, 52% to 56% are HLA-B27 positive compared with 4% to 8% of controls without uveitis.44,47 About half (45% to 58%) of patients with HLA-B27-positive anterior uveitis have a systemic disorder associated with joint disease, such as ankylosing spondylitis, Reiter's syndrome, psoriatic arthritis, or inflammatory bowel disease.44,46,48 In one review, half of the patients with a systemic disease were diagnosed after ophthalmic consultation.48

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

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Juvenile rheumatoid arthritis is defined as arthritis of at least 6 weeks' duration in a child younger than age 16.52,53 It is the most common cause of anterior uveitis in childhood4 and is complicated by secondary glaucoma in 15% to 26% of patients.4,8,54–57 The chronic, nongranulomatous uveitis is more common in pauciarticular disease and in girls who are both antinuclear antibody (ANA)-positive and rheumatoid factor negative.8,57

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

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Keratouveitis due to herpes virus infections often leads to secondary glaucoma. A large study of patients with uveitis revealed that herpes simplex virus (HSV) and herpes zoster-associated uveitis carried the greatest risk of development of secondary glaucoma, with 23% of cases developing this complication.3

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

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Secondary glaucoma may also be associated with congenital rubella. In one study of 125 patients with this disease,72 9% developed glaucoma. Another review of 328 patients73 found 15 with secondary glaucoma, and all but 1 had bilateral disease. All 15 required surgery, and 8 were blind in both eyes by 7 years of age. Glaucoma in rubella is usually infantile in onset and often associated with buphthalmos and persistent corneal haze.73 Late-onset forms have also been reported in older children and young adults who were aphakic and microphthalmic.74 Another form presenting later is characterized by iris stromal hypoplasia in patients without cataract or microphthalmia.75
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Interstitial keratitis is usually a late manifestation of congenital syphilis due to an immune hypersensitivity reaction to treponemal antigen in the corneal stroma.76 Acutely it produces an opacified, edematous cornea with deep vascularization. It is bilateral in 90% of cases.47 Glaucoma can occur in the acute inflammatory stage but more commonly develops later. In one study,77 the interval from diagnosis to development of secondary glaucoma ranged from 7 to 50 years, with a mean of 27 years. One quarter of patients with interstitial keratitis in one review developed glaucoma.78 In another report,3 24% of patients with syphilitic uveitis had ocular hypertension, and 60% of these went on to develop glaucoma.

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.

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Sarcoidosis is a disorder of noncaseating granulomatous inflammation affecting multiple organ systems, including the eyes. It is more common in young adults and persons of African ancestry. In a study of 183 patients with sarcoidosis, 19% had uveitis and 6% had secondary glaucoma.81 A larger report of 532 patients82 found 53% with chronic anterior uveitis and 11% with secondary glaucoma. A review of 119 patients with sarcoid uveitis revealed 24% with elevated IOP, half of whom developed glaucoma.3 Blacks have a higher incidence than whites of ophthalmic involvement,81 uveitic glaucoma, and blindness.82

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

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Vogt-Koyanagi-Harada syndrome (VKH) is a bilateral panuveitis with central nervous system and dermatologic manifestations occurring most commonly in darkly pigmented races.85 Secondary glaucoma, reported to develop in 18% to 38%,3,85,86 may be due to open or closed angle mechanisms. In one study of 42 patients with VKH,85 56% had open angle glaucoma and 44% had angle closure. Acute angle closure has been reported as a presenting sign of VKH87,88 and may be due to edema and anterior rotation of the ciliary body. Angle closure attacks should be broken with laser peripheral iridotomy, but ongoing inflammation may result in closure of these iridotomies and surgical iridectomy may be required.85 The success of standard or antimetabolite augmented trabeculectomy is often low because of chronic inflammation in these patients, many of whom are young.85 Aqueous drainage devices may be the preferred filtering procedure.85
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Behçet's disease is a multisystem occlusive vasculitis that may be associated with uveitis in 66%.90 Other hallmarks include retinal vasculitis, aphthous oral lesions, genital ulcers, and erythema nodosum.90 Acute uveitis may be accompanied by sterile hypopyon.91 Chronic or recurrent anterior uveitis has been reported to be complicated by glaucoma92 in 3%.3 The uveitis can be difficult to control and often requires the use of immunosuppressive agents.91
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Pars planitis, or intermediate uveitis, is a chronic inflammatory disorder of children and young adults. Clinical findings include inflammatory exudates over the inferior pars plana (“snowbank formation”), vitreous cells and debris, and retinal periphlebitis.25 Although the most common cause of visual loss is cystoid macular edema,25 glaucoma is reported to occur in 7% to 8%.25,93 Reported mechanisms include peripheral anterior synechiae, iris neovascularization, and iris bombe.94 Treatment consists of periocular and systemic corticosteroids,25 which may be a contributing factor in the development of ocular hypertension.93 Resistant cases may require pars plana cryotherapy, vitrectomy, or systemic immunosuppressive agents.25
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Sympathetic ophthalmia is a rare bilateral granulomatous panuveitis in response to traumatic or surgical injury to one eye. In one review with an average follow-up of 10 years, 7 of 17 patients developed glaucoma.95 Only 2 of 32 patients in another study had this complication.24
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Episcleritis is a benign, recurrent inflammation that uncommonly causes glaucoma. In two separate series of patients, 4% developed glaucoma, but this complication could not be attributed to the episcleritis alone. Some patients had preexisting primary open angle glaucoma, and in others the problem was thought to be steroid induced.27,37 Secondary glaucoma has also been reported where the IOP improved with steroid therapy. In these cases, inflammation of angle structures was believed to be the cause.96 Although topical corticosteroids are often prescribed for this condition, topical or oral NSAIDs can decrease symptoms without the risk of inducing ocular hypertension.37,97 Because the symptoms are usually self-limited and transient, in many cases no treatment is necessary.
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Scleritis is a painful inflammation of the sclera that is associated with systemic disease in approximately half of cases.27,37 Secondary glaucoma develops in 12% to 18%27,31,37 and most commonly complicates sclerokeratitis37 and necrotizing scleritis.27 It is especially likely to occur when scleritis involves the entire limbal circumference.31 Mechanisms for elevated IOP in scleritis include damage to trabecular meshwork by associated uveitis, edema and inflammation around outflow channels, angle neovascularization, and corticosteroid treatment.31,37 Although usually associated with anterior scleritis, glaucoma is also reported secondary to posterior disease in which annular choroidal detachment may result in forward rotation of the ciliary body and angle closure.27,31,41 In eyes enucleated due to uncontrolled scleritis, evidence of glaucoma was found in 49%.31

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.

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Chandler and Grant described this rare form of inflammatory glaucoma in 1965.98 It presents as open angle glaucoma unresponsive to medical treatment. The eye appears quiet, with minimal anterior chamber cellular reaction and few keratic precipitates. On gonioscopy, multiple broad, flat, clear to yellow precipitates are seen that may be solitary or confluent (Fig. 4). Eventually peripheral anterior synechiae develop in these areas.98 The number and extent of precipitates do not correlate with IOP.98 The disease is usually bilateral and found most commonly in patients older than 50.99 Many cases remain idiopathic, but some patients develop other signs of ocular or systemic inflammation,99 such as sarcoidosis.29 The condition responds well to intensive topical steroids29 and aqueous suppressants, but patients with extensive synechiae may need filtering surgery. Recurrences are common and can be asymptomatic. In one study nine of nine patients experienced recurrent disease, one patient 16 years after the original episode.99 Some patients require chronic suppression with topical steroids or long-term treatment with glaucoma medicines.99

Fig. 4. Gonioscopic view of the iridocorneal angle showing inflammatory precipitates of the trabecular meshwork. (Van Bus-kirk EM: Clinical Atlas of Glaucoma. Philadelphia: WB Saunders, 1986.)

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Glaucomatocyclitic crisis is a syndrome of episodic ocular hypertension associated with mild anterior segment inflammation. First described in 1948 by Posner and Schlossman,23 it is usually unilateral, although bilateral cases have been reported. The disease primarily occurs in the third to seventh decade of life and is rare over age 60.23,101,102 One case has been described in a child.103,104 Symptoms consist of recurrent attacks of blurred vision and haloes without photophobia or significant pain. Many patients are asymptomatic.23 The episodes usually last a few days, occasionally persist for months, and often recur months to years later. During attacks, the IOP may reach 40 to 60 mmHg but returns to normal between recurrences.105 Immediately after an attack the eye may be hypotonous.102 Elevated pressure may precede the anterior chamber inflammation105 but usually coincides with it. The degree of IOP elevation is not proportional to the level of inflammation.106

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

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In 1906, Fuchs described a syndrome of hetero-chromia and cataract associated with mild inflammation.117 Secondary glaucoma is the main cause of permanent vision loss with this condition, and it is reported to occur in 13% to 59% of cases.3,22,118,119 The incidence and severity of glaucoma may be greater in black patients120 and more prevalent in bilateral disease.121 The ocular hypertension may be a result of chronic trabecular meshwork inflammation producing sclerosis.122 Inflammatory membranes of plasma cells and lymphocytes have been found to cover the inner meshwork on histopathologic examination.123

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 absent22,128 or very mild.120 Some patients report floaters.120

Iris heterochromia (Fig. 5), due to stromal atrophy, develops slowly121,125 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

Fig. 5. Left and right eye of patient with Fuchs' heterochromic iridocyclitis. Affected left eye appears gray due to iris stromal atrophy. The iris surface is featureless. Left eye is also aphakic.

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

Fig. 6. Keratic precipitates in Fuchs' heterochromic iridocyclitis may be stellate and connected by fine filaments.

Fig. 7. Retroillumination of an eye with Fuchs' heterochromic iridocyclitis reveals diffuse distribution of keratic precipitates.

Fig. 8. Fine neovascularization of the anterior chamber angle may be seen in patients with Fuchs' heterochromic iridocyclitis, but this does not usually result in formation of peripheral anterior synechiae. (Alward WLM: Requisites in Ophthalmology: Glaucoma. St Louis: Mosby, 2000.)

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

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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 uveitis156–158 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 uveitis160,161 and cystoid macular edema161 and should be used with caution or avoided in patients with uveitis.161


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-FU166–168 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.

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In 1950, McClean reported that systemic adrenocorticotropic hormone (ACTH) given for uveitis led to ocular hypertension in some patients.178 Four years later, it was reported that topical cortisone could also elevate IOP.179 Steroid-induced ocular hypertension may result in glaucoma, which may be difficult to distinguish from glaucoma secondary to the inflammation for which the steroids were prescribed. In one study of patients with chronic uveitis and ocular hypertension, corticosteroid treatment was shown to be the cause of the elevated IOP in 75%.180

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 skin194,195 as well as chronic application of large doses to skin far from the eyes.196 Glaucoma can occur with systemic191,197–199 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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