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Correspondence and reprintrequests to:Aniki Rothova, MD, PhDFC Donders Institute ofOphthalmologyUniversity Medical Center UtrechtE.03-136Heidelberglaan 1003584 CX UtrechtThe NetherlandsFax: +31-30-2505417
Abstract Although cystoid macular edema (CME) represents amajor cause of visual loss in uveitis, the consensus on its treatment hasnot yet been reached. We performed a literature review on the efficacyof diverse medical treatment modalities for uveitic CME and suggestnovel treatment recommendations. A literature search retrieved 173citations (MEDLINE, conducted in March 2002, terms: macularedema, uveitis, treatment) and relevant publications were studied. Theliterature contained information based mainly on case series; the spe-cific treatment targets were not clear. Causal treatment of the under-lying ocular condition was considered essential and various approachesof symptomatic treatment were attempted (immunosuppressive andimmunomodulatory agents, acetazolamide, octreotide), all with differ-ent inclusion criteria and evaluation protocols. The decision to initiatethe symptomatic treatment of CME was usually made in cases withalready compromised visual acuity. Despite aggressive treatment, theprogression of CME with accompanying visual loss was common. Onthe basis of published results, we recommend starting treatment ofCME at an early stage, even in eyes with full visual acuity. Random-ized clinical trials are needed to determine the efficacy of diverse treat-ment modalities and to evaluate the effects of early intervention oninflammatory CME.
Key words Cystoid macular edema; uveitis; treatment
Introduction Cystoid macular edema (CME), an accumulation offluid in the extra- and/or intracellular part of the macula, is a compli-cation common to various ocular disorders affecting the inner and/orouter blood-retina barrier.1–7 Once developed, CME represents acommon final pathway for diverse diseases.Treatment, therefore, mightbe divided into causal and symptomatic forms.
CME is a major cause of visual loss in uveitis.1 A large survey onuveitis indicated that 31% of patients with uveitis (33% of affectedeyes) developed CME.1,6 Of all the patients with uveitis, 9% developedbilateral visual acuity of less than 0.3, of which 50% was caused by
Medical treatment of CME 239
Ocular Immunology and Inflammation0927-3948/02/US$ 16.00
Ocular Immunology and Inflammation –2002, Vol. 10, No. 4, pp. 239–246© Swets & Zeitlinger 2002
Accepted 3 January 2003
Medical treatment of cystoid macular edema
Aniki Rothova
Uveitis Center, FC Donders Institute of Ophthalmology,University Medical Center Utrecht, The Netherlands
Invited review
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CME. Of those with unilateral visual loss (26% of all with uveitis), 40%was caused by CME.1,6 The prognosticators of poor visual outcome inuveitic eyes with CME included prolonged duration of inflammationand of CME, advanced age of patients, incomplete vitreous detach-ment, increased macular thickness and severe CME, and a large fovealavascular zone on angiography.8–11
There is no consensus on the symptomatic treatment of CME inuveitis.12 Usually, the treatment is recommended when visual acuitydrops below 0.5. We performed a literature review on the efficacy ofdiverse medical treatment modalities for uveitic CME and suggestnovel treatment recommendations based on the results of this review.
Methods A literature search retrieved 173 citations and relevantarticles were studied.The literature contained mainly information fromcase series, which lack a control group and randomization. Various therapeutic approaches were reported (immunosuppressive andimmunomodulatory agents, acetazolamide, octreotide), all with differ-ent inclusion criteria, follow-up, and evaluation protocols. Usually, bothcausative and symptomatic forms of treatments were used. As a result,the evaluation and interpretation of the above data were extremely dif-ficult and should be regarded with caution.
Results Despite aggressive treatment, the progression of CME withaccompanying visual loss was common.1,6,12–18 The treatment of CMEwas usually initiated late in the disease process with already compro-mised visual acuity; visual gains varied widely and complications werefrequent. Conventional treatment options included anti-inflammatorydrugs12–18 and carbonic anhydrase inhibitors.19–24 Additional possibilitiesconsisted of hyperbaric oxygen, octreotide, laser grid coagulation, andsurgical treatment.25–33 The effect of anti-inflammatory drugs on uveitisand on CME is impossible to distinguish; the majority of studies wereperformed on eyes with multiple medications. Studies performed onquiet eyes with persistent CME are infrequent and do not reflect thenatural development of inflammatory CME. Numerous studies pointedout that an aggressive treatment of the underlying inflammation isessential.
The effect of topical non-steroidal anti-inflammatory drugs(NSAIDs) on inflammatory CME has never been evaluated on a largescale.13,33 The beneficial effect of systemic NSAIDs, for a long time con-sidered controversial, was recognized in one study.13 It concluded thatoral NSAIDs have an effect similar to that of steroid periocular injec-tions, but only with prolonged use, at least for several months.
Diverse routes of corticosteroid (CS) administrations were used forinflammatory CME, including topical, periocular, intraocular, oral, andintravenous routes. The effect of CS was quick, but the value of a pro-longed treatment of CME was not established.12,13,16,24 Subtenon injec-tions of CS are widely used to treat CME, preferably in patients withasymmetric or unilateral disease.14 Advantages of periocular injectionsinclude high concentrations of CS in the posterior eye segment and lesssystemic adverse effects compared to systemic administration. Systemiceffects of periocular CS occurred especially in children and elevated
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serum levels of CS were noted following periocular dexamethasoneinjections.34,35 Ultrasonographic studies demonstrated the retromacularposition of depots in the superior subtenon injections (in contrast to subtenon inferior location); therefore, this route is preferred forpatients with macular edema.36 No differences in intraocular levels ofCS were reported between subtenbon and retrobulbar administra-tion.37 Intraocular administration of triamcinolone was effective in six patients in treating resistant macular edema.38,39 An intraocular sustained drug-delivery device containing fluocinolone acetonide wasinvestigated in five patients with severe intractable uveitis; however,the eventual effect on CME was not reported.40
With regard to oral administration, it is recommended that treatmentbe initiated with a high dose (1–1.5mg/kg) to achieve a quick effect,and that the dosage should be slowly tapered off according to clinicalresults.12,13,24 A large study on the relative toxicities of immunosup-pressive medications in inflammatory ocular disease revealed thatpatients on systemic CS treatment more frequently developed perma-nent disabilities than patients on immunosuppressive medications.41,42
Although more patients had to stop the treatment with nonsteroidalimmunosuppressive drugs other than CS because of (reversible) sideeffects, the authors recommend refraining from long-term CS use.41
The risk of malignancy in patients treated with systemic immuno-suppressive agents was similar to that in patients treated with systemicCS.42 The value of methylprednisolone pulse therapy on CME has not yet been systematically evaluated.43–45 Cyclosporine was reportedto decrease CME in patients with active, corticosteroid-resistant panuveitis15,17
The beneficial effect of acetazolamide was observed in about onethird of the patients with inflammatory CME.21,23 However, limited clin-ical benefit was noted in patients with long-standing CME associatedwith chronic uveitis.22 Octreotide was found effective in one case ofhereditary CME and a clinical study on inflammatory CME is underway.26 Hyperbaric oxygen, working especially at the level of the innerblood-retina barrier, thus in vascular diseases, had only a partial effectin uveitis.46–49 Grid laser was investigated in a prospective randomizedstudy and noted to diminish edema on angiography, but remainedwithout substantial visual gain in cases with long-standing edema.27 Thebest results were achieved in young patients with a shorter duration ofCME.
Pars plana vitrectomy was repeatedly reported to have a beneficialeffect on the course of uveitis and associated CME.50 As expected, themajority of patients with vitreous opacities improved their initial visualacuity, but CME was also noted to resolve in 32–59% of cases.51–55
Therefore, pars plana vitrectomy may achieve a tapering of immuno-suppression. However, randomized prospective trials are still neededto define the role and indications of vitrectomy in altering the courseof inflammatory CME.56
In intermediate uveitis, transconjunctival cryopexy of the peripheralretina was useful both in patients with snowbanking and neovascular-ization of the vitreous base and in patients with snowbanking who werenot responsive or did not tolerate corticosteroids. This procedure min-
Medical treatment of CME 241
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imized the CME leakage in occasional patients with pars planitis.57
Peripheral laser photocoagulation was reported to decrease clinicallyapparent cystoid macular edema in intermediate uveitis and therebydecrease the need for corticosteroids while stabilizing visual acuity.58 Itwas recommended that laser coagulation be performed in quiet eyesin patients with significant capillary closure in the peripheral retina.59
Clinical studies suggested that the efficacy of CME treatment isrelated to the age of the patients, the duration of CME, and pretreat-ment visual acuity.3,6,9,10 The most favorable prognosis was noted foryoung patients in the early stages of CME.27,60,61
Discussion Although all of the studies agreed that a causal treat-ment of the underlying ocular condition is essential, the recommenda-tions of specific treatment targets were not clear. Poor visual outcomesof eyes with inflammatory CME were probably in part due to thedelayed initiation of treatment, when photoreceptors had already suf-fered irreparable damage. So far, there is no consensus on the treat-ment of CME.12,13 Usually, the start of treatment is recommended ineyes with a visual acuity of less than 20/40, but this arbitrary decisionwas not based on clinical evidence. The poor visual outcome of CMEeyes described in the literature reveals that initiating CME treatmentat an early stage might improve visual prognosis. Dysfunction of pho-toreceptors is probably already present before detectable edema andvisible leakage manifest on fluorescein angiography. This is suggestedby the loss of visual pigment density, photoreceptor alignment, and adecrease in contrast sensitivity before the development of CME.62 Wewould recommend treating CME eyes with chronic uveitis even withfull visual acuity before the structural photoreceptor changes anddefinitive loss of vision sets in. At present, we use two schemes for thetreatment of inflammatory CME (Figs. 1, 2).
In the past, CS formed the classical treatment of inflammatory CME,but these drugs have the potential for serious side effects in all obtain-able topical and systemic routes of administration.12,13,14,33 The advan-tage of CS in uveitis includes a quick anti-inflammatory effect. Thebeneficial effect of CS on CME was also described for CME of nonin-flammatory origin, where CS were reported to diminish retinal thick-ness and are occasionally used before the laser coagulation.63 Thecomplications of short-term therapy are usually negligible; long-termtreatment is associated with widely known and frequent adverse effectswith systemic and ocular manifestations. Therefore, the expected ther-apeutic effects have to be critically weighed against possible adverseeffects, especially in children, immunosuppressed patients, and thosewith infectious disease.The specific clinical situation dictates the choiceof CS administration. For those in need of long-term medication, it isrecommended to start CS in the acute stage of the disease and taperoff subsequently with the use of CS-sparing medications.41
The value of cyclosporin, methotrexate, and other nonsteroidalimmunomodulatory drugs on CME has never been systematicallyassessed; it is to be expected, however, that due to a decrease in inflam-mation these drugs will have a beneficial effect.12,13 The literature on the efficacy of acetazolamide for inflammatory CME is controver-
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Medical treatment of CME 243
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Fig. 1. Treatment scheme forbilateral inflammatory CME.Fig. 2. Treatment scheme forunilateral inflammatory CME.
sial.22,23 Possibly, the differences between various studies are due to dif-ferent inclusion criteria, with variable percentages of patients with end-stage CME. The effect of acetazolamide on CME might be expected in approximately 20–30% of patients, possibly even more in the earlystages.19–24 Therapeutical trial is useful (125mg twice a day; if no effectappears in 2 weeks, increase dose to 250mg twice a day; if no effect in4 weeks, then stop trial). Administration of the somatostatine analogueoctreotide awaits further results; so far, the indications and effects havenot been identified.26
The effect of grid laser coagulation on long-term visual acuity andthe eventual development of age-related maculopathy is not yetknown. The enlargement of laser scars should be taken into account.We employ the treatment in unilateral edema or after other treatmentshave failed (Figs. 1, 2).
The use of surgical methods to treat CME is attractive since medicaltreatment options are associated with a high frequency of adverseeffects and prolonged treatment is usually needed. However, random-ized studies have not yet been performed and the results of pars planavitrectomy for inflammatory CME have so far not been compared tomedical treatment regimens. Therefore, the exact indications for theseprocedures have not yet been identified.
On the basis of the literature, we would recommend starting treat-ment of CME at an early stage, even in those with as yet uncompro-mised visual acuity (Figs. 1, 2). Randomized trials are urgently neededto evaluate the effect of early CME treatment.
CORTICOSTEROID& NSAID’S DROPS
PERIOCULAR CORTICOSTEROID INJECTIONSACETAZOLAMIDE
SYSTEMIC NSAID’S
SYSTEMIC STEROIDS and/ or CYCLOSPORIN
CYTOTOXIC AGENTS
LASER GRID / VITRECTOMY
INFLAMMATORY CMEBILATERAL
LASER OR CRYO IN
PARS PLANITIS
CORTICOSTEROID& NSAID’S DROPS
PERIOCULAR CORTICOSTEROID INJECTIONSACETAZOLAMIDE
SYSTEMIC NSAID’S
SYSTEMIC STEROIDS?(short cycle)
VITRECTOMY
INFLAMMATORY CMEUNILATERAL
LASER GRID
LASER OR CRYO IN
PARS PLANITIS
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