British Journal ofOphthalmology, 1990,74,223-227

Glaucoma in patients with uveitis

William C Panek, Gary N Holland, David A Lee, Robert E Christensen

AbstractThe records of 100 patients (161 eyes) withuveitis were reviewed retrospectively todetermine the prevalence of increased intra-ocular pressure, the forms of uveitis mostcommonly associated with glaucoma, and theforms that require specific glaucoma therapy.Secondary glaucoma was present in 23 patients(31 eyes): three of24 patients with acute uveitis(three eyes, 12% of acute uveitis patients) and20 of 76 patients with chronic uveitis (28 eyes,26% of chronic uveitis patients). Eighteenpatients (26 eyes, 78% of glaucoma patients)with chronic uveitis required long-termmedical therapy to control intraocularpressure. Three patients (three eyes, 12% ofglaucoma patients) with acute uveitis requiredshort-term therapy to control intraocularpressure. The remaining two patients hadtransient increases in intraocular pressure thatdid not require treatment or that responded totreatment of intraocular inflammation alone.One patient with chronic uveitis (two eyes, 4%of glaucoma patients) required filteringsurgery. At least five patients (eight eyes, 22%ofglaucoma patients) had glaucomatous visualfield defects. The results of this survey areconsistent with the concept that secondaryglaucoma is a management problem in patientswith anterior segment inflammation andchronic rather than acute uveitis. An algorithmfor the management of increased intraocularpressure in patients with uveitis is proposed.

uveitis referred to and examined by one author(GNH) at the Jules Stein Eye Institute, UCLASchool of Medicine, were reveiwed retrospec-tively. Uveitis was identified by the presence ofinflammation involving any intraocular structureat the time of examination or by a welldocumented history ofintraocular inflammation.Excluded were patients with self-limited anteriorchamber inflammatory reactions during a one-month period following intraocular surgery,patients with neoplastic disease mimickinguveitis ('masquerade syndromes'), and patientswith cytomegalovirus (CMV) retinopathy.*

Each case was examined for location ofinflammation, disease chronicity, and thepresence or history of increased intraocularpressure. For the purpose of this study, thepatients were considered to be glaucomasuspects or to have uveitic glaucoma ifintraocularpressure was above 21 mm Hg on more than oneexamination at UCLA, or if the patient wasreceiving antiglaucoma therapy at the time ofinitial examination at UCLA and previously hada well documented increase in intraocularpressure concurrent with intraocularinflammation. No patients had a history of pre-existing primary open angle glaucoma.The cases were divided into acute and chronic

uveitis as defined by the International UveitisStudy Group.' Cases of acute uveitis were lessthan three months in duration and cases ofchronic uveitis were of three months or more.

University of CaliforniaLos Angeles, UveitisCenter, Jules SteinInstitute, andDepartment ofOphthalmology, UCLASchool of Medicine, LosAngeles, California, USAW C PanekG N HollandD A LeeR E ChristensenCorrespondence to:William C Panek, MD, JulesStein Eye Institute, UCLAMedical Center, 10833 LeConte Avenue, Los Angeles,CA 90024-1771, USA.Accepted for publication23 October 1989

Particularly complex management decisionsarise when intraocular inflammation is coupledwith increased intraocular pressure. The delicatetissues of the anterior segment may becomeswollen, scarred, and distorted, or renderedmalfunctional by the inflammatory response,'leading to increase of intraocular pressure,glaucomatous damage to the optic nerve, andsubsequent loss of visual field. Steroids, themainstay of treatment for uveitis, may also causeincreased intraocular pressure.2 The physicianmust evaluate carefully the effects ofboth diseaseand therapy in order to provide proper

management for patients with uveitis andglaucoma.This study was undertaken to obtain data on

the prevalence of increased intraocular pressurein patients with uveitis and to identify the formsof uveitis most commonly associated withglaucoma and that require specific glaucomatherapy. With such information rationalapproaches to the management of uveitis-relatedglaucoma can be planned.

Subjects and methodsThe records of 100 consecutive patients with

ResultsThere were 161 eyes with uveitis among the 100patients investigated in this study (Table 1).Twenty-four patients (34 eyes) had acute uveitisand 76 (127 eyes) had chronic uveitis. All thepatients had cells and flare in the anteriorchamber, indicating anterior segmentinflammation, regardless of the primary site ofdisease. Of the patients with acute uveitis all hadprimary inflammation of the anterior segmentexcept three, who had toxoplasmic retino-choroiditis with secondary iridocyclitis. Elevenpatients with chronic uveitis had intermediateuveitis (pars planitis). Of the remaining 65patients with chronic uveitis, one with Vogt-Koyanagi-Harada syndrome, one of three withsarcoidosis, and one of 33 with uveitis ofunknown cause had inflammation of theposterior segment; all others had inflammationof the anterior segment alone.

Twenty-three patients (31 eyes) had secondaryuveitic glaucoma by our criteria. Three patients(three eyes) had acute uveitis and 20 patients (28eyes) had chronic uveitis. Glaucoma occurred in*The author examines a large number of patients with CMVretinopathy enrolled in clinical research protocols. They wouldhave made up a disproportionately large percentage of theconsecutive uveitis cases had they been included. No patient withCMV retinopathy had an increased intraocular pressure.

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Panek, Holland, Lee, Christensen

TABLE I Patients with uveitis and increased intraocular pressure (fOP)

Diagnosis Number of Total eyes Patients with Total eyespatients with increased IOP with

inflammation increased IOP

Acute uveitisHLA B27+ 1 1 15 0 0HLA B27- 9 13 0 0Toxoplasmosis 3 5 2 2Posner-Schlossman syndrome 1 1 1 1Total 24 34 3 3

Chronic uveitisUnknown cause 33 61 8 13Intermediate (pars planitis) 11 20 1 1Juvenile rheumatoid arthritis 7 14 3 5Intraocular lens-associated 6 6 2 2Fuchs' heterochromic iridocycitis 5 6 2 2Herpes simplex virus associated 5 5 2 2Sarcoidosis 3 6 1 2Syphilis 3 5 0 0Herpes zoster virus associated 2 2 1 1Vogt-Koyanagi-Harada syndrome 1 2 0 0Total 76 127 20 28

12% of patients with acute uveitis and in 26% ofpatients with chronic uveitis. There was no

statistically significant difference in the incidenceof glaucoma between these two groups. All 23glaucoma patients had at some time undergonesteroid therapy - oral, topical, or periocular.Treatment regimens at the time of this reviewvaried from prednisone 60 mg orally every daycombined with prednisolone acetate 1% solutionevery hour to fluorometholone 1% solution everyother day. Only one patient with glaucoma was

off steroid therapy. No cases of glaucoma were

shown to be secondary to steroid response.Toxoplasmic retinochoroiditis was the only

form of posterior uveitis in which secondaryanterior segment inflammation resulted inincreased intraocular pressure. Posner-Schlossman syndrome was the only acuteprimary anterior segment disorder that was

found to be associated with increased intraocularpressure. All the other patients had chronicuveitis, either primary anterior segmentinflammation alone or panuveitis. All thepatients with bilateral uveitis who developedglaucoma did so in both inflamed eyes. At leastfive patients (eight eyes, 22% of glaucomapatients) had glaucomatous visual field defects.

Twenty-one patients (29 eyes, 91% ofglaucoma patients) received antiglaucomamedications for control of intraocular pressure.

Eighteen patients (26 eyes, 78% of glaucomapatients) required continuous, ongoing therapy;all had chronic uveitis. The other three patients(three eyes, 13% of glaucoma patients), all ofwhom had acute uveitis, required brief medicaltherapy only during the initial period ofinflammation. The remaining two patients withglaucoma (two eyes, 9% of glaucoma patients),both of whom had chronic anterior uveitis, didnot require medical therapy; they had historiesof transient, self-limited increases in intraocularpressure that responded to treatment ofinflammation alone. One patient (two eyes, 4%of glaucoma patients) with chronic uveitisrequired filtering surgery to lower the intra-ocular pressure.

DiscussionThe spectrum of uveitic disorders in this series is

consistent with that seen in other referralpractices.4 Uveitis may be complicated by avariety of secondary problems including cataractformation, synechiae, macular oedema, andglaucoma. In the present series glaucoma wasone of the most common complications thatrequired therapeutic intervention.The factors most commonly associated with

problems in the management of glaucoma weredisease chronicity and primary anterior segmentinflammation. Toxoplasmic retinochoroiditiswas the only disorder in which secondaryanterior segment inflammation resulted in risesof intraocular pressure requiring medicaltherapy. Increased intraocular pressureassociated with acute uveitis was not a significantmanagement problem, generally respondingwell to brief periods of medical therapy.Glaucoma associated with chronic uveitis usuallyrequired prolonged medical therapy for controlof pressure. Even with chronic uveitis, however,treatment of inflammation alone brought intra-ocular pressure under control in some cases.Visual field loss was a problem only in patientswith chronic uveitis.

In this group of referral patients it is possiblethat the incidence of raised intraocular pressureamong patients with acute uveitis was under-estimated. A transient rise in pressure associatedwith the onset of intense inflammation thatresolved with the initiation of anti-inflammatorytherapy by referring physicians may have beenmissed. It is unlikely, however, that suchtransient increases in pressure pose a seriousproblem to the eye.

PATHOPHYSIOLOGY OF UVEITICGLAUCOMAThe status of the anterior chamber angle gives animportant anatomical division into either closedor open angle types of glaucoma, and hasimportant therapeutic and prognosticimplications. In patients with uveitis the anglecan be closed as a result of posterior synechiaeproducing pupillary seclusion and iris bombed5Angle closure also can occur without pupillaryblock. It can result from peripheral anteriorsynechiae (an iridotrabecular adherence-associated inflammation of iris and angle

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225Glaucoma in patients with uveitis

structures) and sometimes inflammatorynodules in the angle.'6 In addition rubeosis iridisleading to fibrovascular scarring and closure ofthe angle can occur in patients with uveitis.' Inthis series no cases of angle closure were seen,indicating that this mechanism may occurinfrequently in patients receiving anti-inflammatory therapy.

Increased intraocular pressure associated witha clinically open angle involves microscopicalchanges with the trabecular meshwork.Postulated mechanisms include (1) mechanicalblockage ofthe trabeculum by serum componentsthat are liberated because of vascularincompetence;8 (2) hypersecretion associatedwith prostaglandin mediated vascular hyper-permeability;910 (3) overtaxing of outflowmechanisms by protein that interferes withactive transport;" (4) inflammation of thetrabeculum itself with swelling that causesimpaired outflow;6 (5) damage to trabecularendothelial cells by the inflammatory process;'2(6) mechanical obstruction of outflow byprecipitates on the meshwork;'3 (7) sclerosis oftrabecular meshwork as a result of chronicinflammation;5 or (8) obstruction of thetrabeculum by a hyaline membrane.5

Steroid therapy is also a potential cause ofraised pressure,2 1415 though in the present seriesno cases of steroid induced glaucoma wererecorded. Steroid induced glaucoma is verysimilar to primary open angle glaucoma,'6occurring slowly over weeks to months.Occasionally, however, an acute increase inpressure is noted. In all cases the trabeculum isclinically normal in appearance. Cessation ofsteroids usually leads to a return to normal of thepressure. 16

In many patients with anterior segmentinflammation who are receiving chronic steroidtherapy it is not clear whether increased intra-ocular pressure is due to the effect of theinflammation or steroids. There is not always arelationship between the amount ofinflammation, as measured by cells and flare,and inflammation induced rise of intraocularpressure. One therefore cannot predict in whichpatients intraocular pressure will drop whensteroid therapy is increased. The authors haveseen patients with only 1 + cells in the anteriorchamber who had a dramatic drop in pressurewith an increased dosage of steroids.

GLAUCOMA ASSOCIATED WITH SPECIFICUVEITIC DISORDERSMany different types of uveitis have beenassociated with glaucoma, but certain disordersmay have a relatively higher risk. For example,glaucoma is believed to be the major long termthreat to vision in patients with Fuchs' hetero-chromic iridocyclitis. "' Though frequentlyintermittent and well controlled initially,glaucoma may become chronic and difficult totreat.Glaucoma is also a major component of the

Posner-Schlossman syndrome (glaucomato-cyclitic crisis).20 Though inflammatory signsmay be minimal, rises in intraocular pressuremay be severe, leading to blurred vision, haloes,and ocular discomfort. Pressures of40-50 mmHg are not uncommon. Raitta andVannas believe that there may be a relationshipbetween this syndrome and the eventualdevelopment of primary open angle glaucoma. 21

Segmental iris ischaemia, demonstrated on

Management of Intraocular Pressure in Patients with Uveitis

Monitor status onanti-inflammatory regimen

Figure 1: Algorithm for the management of raised intraocular pressure in patients with uveitis.

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Panek, Holland, Lee, Christensen

fluorescein angiography, implies a vascular causeor the Posner-Schlossman syndrome.2'Vasculature incompetence could be associatedwith a release of prostaglandins, inflammationand a subsequent rise in intraocular pressure.22Oral indomethacin and subconjunctivalpolyphloretin, both prostaglandin inhibitors,have been shown to lower intraocular pressuresduring attacks.22The prognosis for control of intraocular

pressure in patients with glaucomatocycliticcrisis is good.23 Current treatmentrecommendations include both topical steroidtherapy to reduce inflammation and anti-glaucoma medications to control pressure duringacute attacks. Future modes may include anti-prostaglandin therapy as well as treatment tomodify vascular instability.2'The chronic uveitis associated with systemic

disease is frequently complicated by severeglaucoma.24 The glaucoma associated withjuvenile rheumatoid arthritis commonly occurswith open angles but may be of the pupillaryblock, secondary angle closure type, as a result ofthe formation of posterior synechiae.2526 Whenglaucoma occurs in patients with sarcoid uveitis,medical and surgical therapy may have onlylimited success.27 28Glaucoma may be a prominent feature of the

uveitis that results from ocular infections. Theprevalence of secondary glaucoma associatedwith toxoplasmic retinochoroiditis was reportedto be 12% in one series.29 Although the glaucomain that group was described as transient, a morerecalcitrant form may occur with severeinfections.

Herpetic uveitis may be particularly prone tothe development of glaucoma.30 In severe caseslong term antiglaucoma therapy may beindicated even after active inflammation hassubsided.30 Herpes simplex virus keratouveitis isoften associated with a raised intraocularpressure; Falcon and Williams reportedglaucoma in 28% of 183 patients.30 Postulatedmechanisms include both blockage of the trabec-ulum with inflammatory debris and inflamma-tion of the trabeculum.3' Townsend and Kaufmanfound that glaucoma was also a problem in experi-mental herpes simplex virus keratouveitis in therabbit.32 Secondary glaucoma was attributed to amononuclear cellular infiltrate in the angle; inaddition occasional peripheral anterior synechiaewere seen in severe cases.

Secondary glaucoma also can be a seriousproblem in patients with herpes zoster viruskeratouveitis; Womack and Liesegang reporteduveitic glaucoma in 10 of 37 patients.33 Thepathophysiology is probably similar to thatassociated with herpes simplex viruskeratouveitis.30

Uveitis may complicate the use of irissupported or anterior chamber intraocularlenses,34 more likely as a result of mechanicalfactors such as chafing of the lens against oculartissues. The smouldering low-grade uveitis maylead to secondary glaucoma; Ellingson describeda distinct syndrome of uveitis, glaucoma, andhyphaema in such patients.35 The prognosis forthe control of pressure is good if inflammationcan be controlled.

EVALUATION AND TREATMENT OF UVEITICGLAUCOMAThe treatment of intraocular inflammation itselfis an important component of glaucomamanagement, because it prevents damage toangle structures and blockage of outflowchannels by inflammatory material and therebymaintains normal aqueous outflow.36 In one caseof the present series the control of inflammationby chlorambucil in a patient having a 20-yearhistory of uveitis associated with juvenilerheumatoid arthritis also resulted in lowering ofintraocular pressure that could not be controlledby antiglaucoma medications alone.There may be special considerations in the

medical management of glaucoma in patientswith uveitis. Miotics such as pilocarpine shouldbe used with caution in inflamed eyes, becausethey may exacerbate the underlying inflam-matory process.36 The ocular hypotensive effectof epinephrine is inhibited by cyclo-oxygenaseinhibitors such as indomethacin. Patients usingepinephrine should be monitored for thispressure-raising effect in those rare cases inwhich non-steroidal anti-inflammatory agentsare used in the management of uveitis.37The laser and surgical treatment of glaucoma

in patients with uveitis also involves specialconsiderations. Laser iridotomy may be difficultto perform in inflamed eyes36 and may causescarring. Should surgical peripheral iridectomybe required in cases ofuveitis for the treatment ofpupillary block glaucoma, surgical section orlarge peripheral iridectomies should beconsidered.36 The efficacy of laser trabeculo-plasty varies in these patients38 and may lead to aworsening of both inflammation and glaucoma.

For patients with chronic inflammatoryglaucoma some authors36 39 recommendtrabeculodialysis as the procedure of choice.Success rates as high as 63% with this techniquehave been reported, in contrast to rates of 18%with standard filtration surgery.39

Adjunctive methods of treatment are underinvestigation to decrease postoperativeinflammation and fibrosis after glaucomafiltering surgery. They include the use of locallyadministered agents such as 5-fluorouracil40 andtriamcinolone4' in the preoperative and post-operative periods. In future these regimens maybe shown to improve filter survival in patientswith uveitic glaucoma.On the basis of these concepts the authors

propose a stepwise approach to the evaluationand treatment of increased intraocular pressurein patients with uveitis (Fig 1). Because steroidassociated glaucoma is apparently uncommon,and because the effect of prolonged or increasedinflammation is potentially worse than atransient steroid induced rise in intraocularpressure, one should first increase steroid dosageand observe both intraocular pressure andinflammation. In cases where severeglaucomatous nerve damage previously exists,antiglaucoma therapy may be included whilesteroids are increased and then withdrawn ifpressure decreases.

If intraocular pressure remains unchanged orrises with increased steroids, and inflammationis stable or improved, steroid therapy should be

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Glaucoma in patients with uveitis

reduced to the least amount that will maintainthe lowest achievable level of inflammation. Ifintraocular pressure remains raised as steroidtherapy is reduced, glaucoma therapy is initiated.While the modes of therapy may be dictated bythe presence of inflammation, the intensity oftreatment - as with all forms of glaucoma - isbased on the level of intraocular pressure, visualfield changes, and status of the optic nerve.

Dr Panek was an Abe Meyer Fellow in Glaucoma, UCLADepartment of Ophthalmology. Dr Holland is recipient of theResearch to Prevent Blindness - James S Adams Scholar Award.The work was supported in part by a Research Manpower Awardfrom Research to Prevent Blindness, Inc., New York, NY (DrHolland), and Karl Kirchgessner Foundation, an unrestrictedgrant from Research to Prevent Blindness, Inc., NationalInstitutes of Health Grant EY07701, and the Lucille Ellis SimonGlaucoma Research Fund (Dr Lee), and the Elsie B BallantyneFund (Dr Christensen).

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doi: 10.1136/bjo.74.4.223 1990 74: 223-227Br J Ophthalmol

 W C Panek, G N Holland, D A Lee, et al. Glaucoma in patients with uveitis.

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