Hypotony maculopathy - Glaucomanew-glaucoma-treatments.com/wp-content/imagesfiles/Hypotony maculopathy.pdfCystoid macular oedema caused by abnormal retinal capillary permeabil-ity

Definition, history andsynonyms

There are two definitions of hypo-tony. ‘Statistical’ hypotony can bedefined as an intraocular pressure(IOP) less than 6.5 mmHg, whichcorresponds to more than threestandard deviations below the mean;

‘clinically significant’ hypotony repre-sents the condition where the IOP islow enough to result in visual loss(Pederson 1996). There are severalcauses of visual loss secondary tolow IOPs, including hypotony macul-opathy, keratopathy, cataract forma-tion, choroidal effusion, optic nerveoedema, irregular astigmatism and

even phthisis bulbi (Fannin et al.2003). This review will explore thedefinition, mechanisms, clinical find-ings and treatment of hypotony mac-ulopathy.

Hypotony maculopathy was firstdescribed by Dellaporta (1954). Inthis publication, he assembled fourcases that had been reported between1946 and 1954 (Renard 1946; Della-porta 1948; Pau 1950). He recognizedthat the condition occurred usuallyafter antiglaucomatous surgery orafter perforating eye injuries, andstressed that ‘the striking commoncharacteristic of the four reportedeyes was ocular hypotony of about8–10 mmHg’. The syndrome wascharacterized by hypotony associatedwith fundus abnormalities, whichincluded papilloedema, vascular tortu-osity and chorioretinal folds. Sincethe papilloedema was usually of mod-erate degree and was not associatedwith retinal haemorrhages, the term‘papilloedema ex vacuo’ was proposedin order to clearly distinguish thiscondition from the true papilloedemabecause of increased intracranial pres-sure (Dellaporta 1954).

Several years later, Gass (1972)coined the term ‘hypotony maculopa-thy’, chosen only to emphasize thatalterations in the macular region wereprimarily responsible for the loss ofcentral vision. Although ‘hypotonychorioretinopathy’ might be a moreaccurate term to describe the fundo-scopic changes, which may involvevirtually the entire ocular fundus, wedecided to maintain the term ‘hypo-tony maculopathy’ throughout this

Review Article

Hypotony maculopathy

Vital Paulino Costa1,2 and Enyr Saran Arcieri1,3

1Glaucoma Service, Department of Ophthalmology, University of Campinas, SaoPaulo, Brazil2Department of Ophthalmology, University of Sao Paulo, Sao Paulo, Brazil3Department of Ophthalmology, School of Medicine, Federal University ofUberlandia, Minas Gerais, Brazil

ABSTRACT.

Hypotony maculopathy, first described in 1954 by Dellaporta, usually occurs

after antiglaucomatous surgery or after perforating eye injuries; it is charac-

terized by hypotony associated with fundus abnormalities, including papilloede-

ma, vascular tortuosity and chorioretinal folds. In hypotony maculopathy, the

scleral wall collapses inward, resulting in redundancy of the choroid and

retina, leading to chorioretinal wrinkling. As the antero-posterior diameter of

the vitreous cavity decreases, the very thick perivofeal retina surrounding the

very thin foveal retina is thrown into radial folds around the fovea. It has been

reported that hypotony maculopathy occurs in up to 20% of cases of glaucoma

filtering surgery and has become more common after the introduction of anti-

metabolites. Young age, myopia, primary filtering surgery, systemic illnesses

and elevated preoperative intraocular pressure (IOP) have been found to be

associated with hypotony maculopathy. Hypotony maculopathy is treated with

procedures designed to elevate IOP, which may reverse the inward scleral bow-

ing and improve visual acuity. The successful treatment of hypotony maculo-

pathy depends on the correct identification of its cause. Once the cause is

detected, treatment should be employed as soon as possible because delayed

normalization of the IOP may result in permanent macular chorioretinal chan-

ges and poor vision. This review will explore the definition, mechanisms, clin-

ical findings and treatment of hypotony maculopathy.

Key words: hypotony maculopathy – clinical findings – mechanisms – tonometry – ocular –

ciliary body – glaucoma – trabeculectomy

Acta Ophthalmol. Scand. 2007: 85: 586–597ª 2007 The Authors

Journal compilation ª 2007 Acta Ophthalmol Scand

doi: 10.1111/j.1600-0420.2007.00910.x

Acta Ophthalmologica Scandinavica 2007

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article because it is more commonlyused in the medical literature.

Clinical findings

Hypotony maculopathy correspondsto a condition where hypotony leadsto papilloedema associated withwrinkling or folding of the retina andchoroid throughout the posterior pole.In the macular area, there are several

fine retinal folds radiating outwardfrom the fovea (Fig. 1). The foldingresults in distortion of the neurosenso-rial elements of the retina and reduc-tion of the antero-posterior diameterof the eye, leading to a relative hyper-opia. The chorioretinal folds are par-ticularly evident in the macula. In thisarea, the very thick perifoveal retinasurrounding the very thin fovealretina is thrown into radial foldsaround the fovea (Gass 1972).

With the onset of hypotony, theposterior scleral wall probably beginsto shrink or collapse, throwing thechoroid and retina into folds. As thewrinkling or folding becomes moreprominent, the relative compression ofpigment epithelial cells in the troughof the fold and the relative thinningof the pigment epithelium over thecrest produce the alternate dark andlight coloured streaks that can beobserved ophthalmoscopically (Fig. 2).In prolonged hypotony, the intensifi-cation of the alternate light and darkstreaks in the fundus is probablycaused by alterations in the structureand pigment content of the retinalpigment epithelial cells (Figs 2 and 3).

Acutely acquired chorioretinal foldsusually produce visual dysfunctioncaused by distortion of the overlyingretinal receptors. In hypotony macul-opathy, the distortion of the photore-ceptors is probably associated withother hypotony-induced changes(such as irregular astigmatism) thatexacerbate the visual disturbancecaused by the chorioretinal folds.These folds may have a horizontal,oblique or vertical orientation,although an irregular or radiatingpattern may be present. The longerthe duration of the folds, the moreprominent they appear.

Cystoid macular oedema caused byabnormal retinal capillary permeabil-ity may ensue secondary to a reduc-tion in the interstitial pressure(Kokame et al. 2001; Stefansson2006). However, this is not a commonfinding, and – even if present – is ofsecondary importance as a cause ofvisual loss in these eyes. The retinalvessels appear tortuous, and the ret-inal veins engorged (Figs 1 and 3).Serous detachment of the peripheralchoroid is usually absent at indirectophthalmoscopy (Gass 1972), but maybe recognized with ultrasound bio-microscopy (Coleman 1995).

Papilloedema is probably the resultof anterior bowing of the laminacribrosa, constricting axonal bundlesin the lamina scleralis and redu-cing orthograde and retrogradeaxoplasmic transport (Minckler &Bunt 1977) (Figs 1 and 3). Discswelling is less frequent in patientswith advanced optic nerve dam-age, because there are fewer axonsleft to suffer changes in axoplasmicflow.

Fig. 1. Clinical photograph of an eye with hypotony maculopathy showing disc swelling and

several fine retinal folds radiating outward from the fovea at the macular area. The retinal ves-

sels appear tortuous and the retinal veins are engorged.

Fig. 2. Clinical photograph of hypotony maculopathy showing retinal folds and alternate light

and dark streaks in the fundus.


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Imaging

Fluorescein angiography is helpful indemonstrating the chorioretinal folds,which in relatively mild degrees maybe overlooked (Fig. 4). It is also usefulin differentiating folds of the choroidand retinal pigment epithelium (RPE)from folds in the retina, which do notalter background fluorescence. Earlyin the course of hypotony, fluoresceinangiography shows an irregular inc-rease in background choroidal fluores-cence corresponding to the crest of thechoroidal folds and also shows someevidence of leakage of dye from thecapillaries on the optic nerve head, butusually not from the retinal capillaries

(Gass 1972). Characteristic changes inthe background choroidal fluorescenceare caused by folding of the choroidand RPE. Intensification of the choroi-dal fluorescence occurs along the crestof the choroid and RPE and producesa series of relatively hyperfluorescentstreaks that are evident as early as thearterial phase. The hyperfluorescentstreaks are caused by the relative thin-ness of the RPE on the crest, thegreater thickness of the pool of choroi-dal dye beneath the crest and the shor-ter course of the incident blue andreflected yellow-green light throughthe RPE on the crest. The troughs ofthe folds appear relatively hypofluores-cent. This results in angiographic

finding of narrow dark lines runningwithin a background of normal orslightly intensified background choroi-dal fluorescence.

Indocyanine green angiographymay reveal multiple hypofluorescentspots in many parts of the fundus,sector hypofluorescent areas, dilata-tion and tortuosity of the choroidalvessels in the posterior pole of hypo-tonous eyes, even if fluorescein angi-ography is not able to detect them(Masaoka et al. 2000).

B-scan ultrasonography is especiallyuseful when the fundus is not easilyvisualized. It can help in excluding thepresence of ciliochoroidal detachment,suprachoroidal haemorrhage and ret-inal detachment, which are not com-monly seen in cases of hypotonymaculopathy. Ultrasonography usu-ally demonstrates some flattening andthickening of the posterior sclera andchoroid, but identifying the chorioreti-nal folds may be difficult (Cappaertet al. 1977) (Fig. 5).

Ultrasonic biomicroscopy can beemployed (Fig. 6) to further evaluatethe anterior chamber depth, the posi-tion of the ciliary body and the pres-ence of anterior ciliary detachment(Roters et al. 2002). Furthermore, itcan be used to identify a cyclodialysiscleft, one of the important causes ofhypotony maculopathy (Bhende et al.1999; Chan et al. 2000). Intraopera-tively, the ciliary body can be directlyvisualized to evaluate rotation andtraction using endoscopy (Hammer &Grizzard 2003; Gnanaraj et al. 2005).

Optical coherence tomography(OCT) of the posterior pole can helpto better demonstrate subtle macularfluid or folds. OCT can be helpful in

(A) (B)

Fig. 4. Picture and fluorescein angiography of a patient with hypotony maculopathy. Fluorescein angiography (B) is helpful in demonstrating the

chorioretinal folds, which in relatively mild degrees may be overlooked (A). (Reprinted from Handbook of Glaucoma, Azvara-Blanco A, Costa

VP, Wilson RP (eds.), 2002, London: Martin Dunitz.)

Fig. 3. Clinical photograph of an eye with hypotony maculopathy showing marked disc swell-

ing.


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diagnosing suspected hypotony macul-opathy in patients with reduced visualacuity (VA) and normal ocular exam-ination, except for low IOPs. Budenzet al. (2005) suggested that becauseretinal folds are typically oriented inthe 0–180� axis, careful review of allradial line scans may be necessary todiagnose this condition (Fig. 7).Martinez de la Casa et al. (2003)reported the case of a 40-year-oldman who underwent trabeculectomyand showed hypotony and VA loss.

Although no alterations were notedon opthalmoscopy or on fluoresceinangiography, OCT allowed the diag-nosis of hypotony maculopathy. Kok-ame et al. (2001) described a casewhere OCT allowed the detection ofnot only choroidal folds but also int-raretinal cysts and serous retinaldetachment associated with hypotonymaculopathy.

Westfall et al. (2004) reported themagnetic resonance appearance ofhypotony maculopathy in a 48-year-old

man with a long history of glaucoma,who underwent trabeculectomy in theright eye. Magnetic resonance imagingshowed an abnormal plaque-like thick-ening of the macula and flattening ofthe posterior globe.

Aetiology, histopathologyand mechanisms

Any condition leading to reduced IOPmay result in hypotony maculopathy.Causes of hypotony are listed inTable 1, although the discussion ofthese extends beyond the scope of thisarticle.

Hypotony occurs when aqueoushumour production does not keep pacewith outflow. Outflow may be greaterthan usual, as seen with a wound leak,an overfiltering bleb or a cyclodialysiscleft. Conditions that alter ciliary bodyfunction, such as iridocyclitis, ciliocho-roidal detachment or hypoperfusion,may cause inadequate aqueous humourproduction (Newhouse & Beyrer 1982;Toris & Pederson 1987; Pederson 1996;Kato et al. 1999; Fannin et al. 2003).Although hypotony maculopathy isusually seen after glaucoma filteringsurgery, especially with adjunctivemitomycin C (MMC), it can also beobserved following other ocular condi-tions (Hatton et al. 1998; Foster et al.1999; Deramo et al. 2001; Ichibe et al.2002).

Inflammation may play a key rolein the evolution of hypotony. It causesincreased permeability of the blood–aqueous barrier. Choroidal fluid isbelieved to accumulate as a result ofenhanced uveoscleral outflow anddecreased aqueous humour produc-tion, a cycle that is often perpetuatedonce choroidal effusion develops. Aring of anterior choroidal fluid canrotate the ciliary body forward,impairing its ability to produce aque-ous humour (Weekers & Delmarcelle1953; de Smet et al. 2005).

Dellaporta (1954) believed that, inhypotonic eyes, the protruding nervehead pulled the nerve-fibre layer caus-ing friction between the retina and thepigment epithelium of the retina alongthe nerve fibres. This friction wouldcause irritation and subsequent grad-ual increased pigmentation. He alsobelieved that the tendency for thechoroidal folds to have a linear branch-ing course radiating in a temporal

Fig. 6. Ultrasound biomicroscopy revealing fluid in the supraciliary space (arrow) with no

cyclodialysis cleft in a patient with hypotony maculopathy.

Fig. 5. B-scan ultrasonography of an eye with hypotony maculopathy showing thickening of

the choroid (between arrows).


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direction away from the optic disc,and to have a cobblestone, flagstone,hexagonal or quilt-like pattern nas-ally, was probably caused by severalfactors including structural differencesbetween the choroid and sclera andunequal forces exerted in the collapseof the ocular coats during eye move-ment by virtue of the oblique andnasal insertion of the optic nervehead.

Gass (1972) proposed the theorythat is now accepted to explain themechanism of hypotony maculopathy.He suggested that hypotony couldcause the scleral wall to collapseinward, resulting in redundancy of thechoroid and retina, which would leadto chorioretinal wrinkling. The unu-sual configuration of retinal folding isa result of the peculiar anatomy of

the retina in the macula. As the anter-o-posterior diameter of the vitreouscavity decreases in hypotony, the verythick perivofeal retina surrounding thevery thin foveal retina is thrown intoradial folds around the fovea (Gass1972) (Fig. 8).

Several authors have subsequentlyconfirmed that any condition causinga reduction in the area of the innersurface of the sclera (scleral thickeningor scleral shrinkage) may cause theinner portion of the choroids, theoverlying retinal pigment epitheliumand the outer retinal layers to bethrown into a series of folds or wrin-kles (Dellaporta 1950; Norton 1969;Hyvarinen & Walsh 1970; Kroll &Norton 1970; Francois & DeLaey1971; Von Winning 1972; Newell1973; Cangemi et al. 1978; Kalina &

Mills 1980; Morris & Sanders 1980;Lebuisson et al. 1981; Gass 1987).

The origin of papilloedema wasexplained in a series of experimentalstudies. According to Minckler &Bunt (1977), hypotony could lead toanterior bowing of the lamina cri-brosa, constricting axonal bundles inthe lamina scleralis and reducingorthograde and retrograde axoplasmictransport. In a subsequent study,Floyd & Minckler (1983) demon-strated that leakage from the chorio-capillaris could be an additionalsource of the fluid that accumulates inthe disc. They speculated that swollenaxons, caused by blockage of the axo-plasmic transport, could compromisethe blood flow to the optic nerve,resulting in hypoxia, endothelial celldamage and leakage.

Histopathologic findings in eyeswith hypotony have been described byCollins (1917), who demonstratedthickening and folding of the scleraand folding of Bruch’s membrane,associated with accumulation of ret-inal pigment epithelium in the depthsof the choroidal folds. Histopathologyof hypotonic eyes may also demon-strate generalized oedema of the uvea,retina and optic nerve, as well as aproteinaceous fluid in the suprachoroi-dal space (Volcker & Naumann 1979).

Incidence and riskfactors

The initial literature on hypotonymaculopathy included several reportsof cases; these did not allow the evalu-ation of its incidence. More recently,hypotony maculopathy has beenreported to occur in up to 20% ofcases of glaucoma filtering surgery(Whiteside-Michel et al. 1992; Costaet al. 1993c; Kitazawa et al. 1993;

Table 1. Causes of hypotony.

Postoperative hypotony Hypotony after trauma Bilateral hypotony Miscellaneous forms of hypotony

Wound leak Iridocyclitis Osmotic Vascular occlusive disease (ciliary body hypoperfusion)

Overfiltration Retinal detachment Dehydration Carotid occlusion

Iridocyclitis Cyclodialysis Diabetic coma Temporal arteritis

Ciliochoroidal detachment Scleral rupture Uremia Central retinal artery or vein occlusion

Retinal detachment Ciliochoroidal detachment Myotonic dystrophy PVR or cyclitic membrane pulling the ciliary body

Cyclodialysis Prephthisis bulbi

Scleral perforation

MMC-induced toxicity of the ciliary body

MMC, mitomycin C.

Fig. 7. Optical coherence tomography with macular scan using Stratus OCT (Zeiss Meditec,

Dublin, California, USA) showing folding of the retinal and choriocapillaris layers because of

hypotony maculopathy. (Reprinted from Archives of Ophthalmology 2005, 123: 113–114. Copy-

right ª 2005, American Medical Association. All rights reserved.)


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Shields et al. 1993; Megevand et al.1995; Bell et al. 1997; Cheung et al.1997; Zacharia & Schuman 1997;Perkins et al. 1998; Rasheed 1999;Lanzl et al. 2000; Martinez Garcia &Perez Garcia 2000; Mietz & Kriegl-stein 2001; Bindlish et al. 2002; Mietzet al. 2002; Tsai et al. 2003) (Table 2).

Although the description of hypo-tony maculopathy dates from 1955(Dellaporta 1954), reports of thiscomplication became frequent onlyafter the introduction of antimeta-bolites in glaucoma surgery. In areview of 40 eyes with hypotony(IOP < 10 mmHg) post-trabeculect-omy without antimetabolites followedfor 3.4 years, Cristiansson (1967)reported persistent degenerative macu-lar changes in four eyes, but there was

no mention of the presence of chori-oretinal folds or the effect of this find-ing on VA.

Costa et al. (1993b) reviewed thecharts of 440 patients (508 eyes) whounderwent trabeculectomy to detectcases of postoperative VA loss (two ormore Snellen lines or a categorychange). In this series, six eyes (1.2%)showed loss of VA because of hypo-tony maculopathy. Among thesix eyes, three (50%) had receivedpostoperative applications of 5-fluour-acil (5-FU) injections. Hypotonymaculopathy was associated with cor-onary artery disease (P ¼ 0.0397) andsystemic hypertension (P ¼ 0.0118).

Whiteside-Michel et al. (1992) eval-uated the effectiveness of initial trabe-culectomy with adjunctive 5-FU for

uncomplicated glaucoma in 20 eyes of20 patients younger than 40 years old.Subconjunctival injections of 5-FU(5 mg) were given 180� from theoperative site within 14 days of sur-gery. Hypotony maculopathy wasobserved in one patient (5%).

Mitomycin C appears to be evenmore likely to produce hypotony, withthe occurrence ranging from 3% to20% in various series (Costa et al.1993c; Kitazawa et al. 1993; Shieldset al. 1993; Megevand et al. 1995;Cheung et al. 1997; Zacharia &Schuman 1997; Perkins et al. 1998;Rasheed 1999; Lanzl et al. 2000; Mar-tinez Garcia & Perez Garcia 2000;Mietz & Krieglstein 2001; Bindlishet al. 2002; Mietz et al. 2002; Tsaiet al. 2003). In a prospective, random-ized study, Rasheed (1999) comparedthe overall efficacy of intraoperativeapplication of MMC in eyes with noprevious ocular surgery to standardtrabeculectomy without MMC.Twenty-five patients with primaryglaucoma were treated with trabecul-ectomy without antimetabolites in oneeye and trabeculectomy with MMC inthe contralateral eye. After a meanfollow-up of 18 months, hypotonymaculopathy developed in three eyes(12%) of the MMC group, and wasnot observed in the group that didnot receive antimetabolites.

Other studies have suggested thathigh concentrations of MMC orincreased exposure time to MMC maybe associated with the development ofhypotony maculopathy (Whiteside-Michel et al. 1992; Kitazawa et al.1993; Oppenheim & Ortiz 1993;Shields et al. 1993; Zacharia et al.1993; Neelakantan et al. 1994; Megev-and et al. 1995). Zacharia et al. (1993)reported an incidence of 32.7% ofhypotony (IOP < 5 mmHg) in 52eyes of 48 patients undergoing trabe-culectomy with MMC (0.4 mg ⁄mL for3.7–7 min). Twenty-two eyes requiringbilateral primary trabeculectomy wererandomized by Kitazawa et al. (1993)to intraoperative MMC (0.2 mg ⁄mLfor 5 min) in one eye and to low-doseintraoperative MMC (0.02 mg ⁄mL for5 min) in the contralateral eye. Twocases (18.2%) of transient hypotonymaculopathy were noted in the0.2 mg ⁄mL group exclusively.Megevand et al. (1995) compared theresults of 25 eyes that were consideredto be at high risk for surgical failure

Fig. 8. Normal eye (A, B). Mild hypotony with thickening of the choroid, initial scleral shrink-

ing and disc oedema (C, D). Severe hypotony maculopathy with choroidal and retinal folds,

macular striae, disc oedema, dilated retinal veins and scleral shrinking (E, F).


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and that received a single intraopera-tive application of MMC (0.2 mg ⁄mLfor 2 min) to a group of 48 patients –matched for age, race, type of refract-ory glaucoma and preoperativeIOP – who received a single intra-operative application of MMC(0.2 mg ⁄mL for 5 min). Hypotony-related maculopathy developed in oneeye (2.1%) in the 5 min group.

Costa et al. (1993a) reviewed thecharts of patients who underwentprimary trabeculectomies (group 1,n ¼ 39) or combined procedures(phacoemulsification+trabeculectomy )group 2, n ¼ 15) and received intraop-erative MMC (0.4 mg ⁄mL ) 1.5–3.5 min), and observed that hypotonymaculopathy developed in three casesof group 1 (7.7%).

Bindlish et al. (2002) investigatedthe 5 year incidence of hypotony mac-ulopathy after trabeculectomy withMMC at various concentrations.Hypotony (IOP < 6 mmHg) occurredin 42.2% of eyes after a mean follow-up of 26.1 months, whereas hypotonymaculopathy occurred in 8.9% of eyesat mean follow-up of 33.7 months.

The association between hypotonymaculopathy and the use of antime-tabolites is not exclusively because ofthe antifibrotic effect, leading toreduced scar formation and a ten-dency for overfiltration. It has beensuggested that MMC may have adirect toxic effect on the ciliary body,resulting in reduced aqueous humourproduction (Nuyts et al. 1994a). Addi-tionally, the application of antifibroticagents in filtering surgery, such asMMC or 5-FU, may induce changesin the conjunctiva. The tissue fre-quently becomes avascular, which pre-vents migration of cells via thevascular route to induce fibrosis(Shields et al. 1993; Hutchinson et al.1994; Sihota et al. 2000). Further-more, Sihota et al. (2000) suggestedthat a dysfunctional conjunctivalbarrier, as evidenced by the ‘sweating’of the bleb and histopathologic altera-tions in the epithelial barrier, could becoresponsible for the hypotonic mac-ulopathy in eyes undergoing trabecul-ectomy with MMC.

Certainly, the level of IOP alonedoes not determine who will develop

wrinkling of the choroid and retina.Factors such as scleral thickness,scleral rigidity, structural variations inthe choroid and its vessels, extraocularmuscle tone and duration of hypotonyare probably important in the patho-genesis of hypotony maculopathy(Gass 1972). It is also important tonotice the influence of central cornealthickness (CCT) on the diagnosis ofhypotony maculopathy. Eyes withthin corneas may not develophypotony maculopathy despite lowIOPs, artificially reduced by the CCTvalue. On the other hand, eyeswith thick corneas and IOPs of8–9 mmHg may exhibit hypotonymaculopathy despite apparently nor-mal IOPs.

Early on, Dellaporta (1954) noticedthat ocular hypotony preceded byocular hypertension and the relativelyyoung age of the patients involvedwere important prerequisites to thedevelopment of hypotony macul-opathy. The medical records of186 patients with ocular hypotonyfollowing glaucoma surgery werereviewed by Fannin et al. (2003) in a

Table 2. Incidence of hypotony maculopathy following trabeculectomy or combined (phacoemulsification + trabeculectomy) procedures in differ-

ent studies.

Author n Type of surgery Antimetabolites (dose) Follow-up (months) Incidence (%)

Whiteside-Michel et al. (1992) 20 TREC 5-FU (15–45 mg; mean 27.8 ± 8.8 mg) 31.1 ± 17.3 (11.5–70) 5%

Costa et al. (1993a) 39 TREC MMC (0.4 mg ⁄mL; 1.5–2.5 min) 6.7 ± 0.7 7.7%

15 PHACOTREC MMC (0.4 mg ⁄mL; 3.5 min) 6.8 ± 0.9 0

Shields et al. (1993) 59 TREC MMC (0.4 mg ⁄mL)

2 min (n ¼ 17) ⁄ 3 min (n ¼ 17) ⁄4 min (n ¼ 8) ⁄ 5 min (n ¼ 10)

2 to 12 (mean 5.0–6.3) 11.7% (2 min)

11.7% (3 min)

20% (5 min)

Kitazawa et al. (1993) 11 TREC MMC (0.02 mg ⁄mL; 5 min) 11.0 ± 3.4 0

11 TREC MMC (0.2 mg ⁄mL; 5 min) 10.7 ± 3.2 18.2%

Megevand et al. (1995) 25 TREC MMC (0.2 mg ⁄mL; 2 min) 12.0 (4–19) 0

48 TREC MMC (0.2 mg ⁄mL; 5 min) 20.2 (4–35) 2.1%

Cheung et al. (1997) 157 TREC MMC (0.2–0.5 mg ⁄mL; 0.5–5 min) 19.7 ± 9.0 3.2%

Zacharia & Schuman (1997) 20 PHACOTREC MMC (0.4 mg ⁄mL; 1.0–3.5 min) 14.4 ± 3.1 (9.2–19.3) 5%

Bell et al. (1997) 45 TREC 5-FU (25 mg ⁄mL; 5 min) 24.0 ± 6.9 (12–42) 4.4%

Perkins et al. (1998) 68 TREC MMC (0.5 mg ⁄mL; 0.5–5.0 min) 36.0 (93%) 5.9%

Rasheed (1999) 25 TREC No antimetabolite 17.8 ± 1.2 0

25 TREC MMC (0.3–0.4 mg ⁄mL; 4 min) 17.8 ± 1.1 12%

Lanzl et al. (2000) 10 TREC MMC (0.4 mg ⁄mL; 1.0–4.0 min) 14.9 (9–19) 10%

Martinez Garcia &

Perez Garcia (2000)

34 TREC MMC (dose not available) 28.1 8.8%

Mietz & Krieglstein (2001) 10 TREC Suramin (200 mg ⁄mL; 5 min) 18.0 0

10 TREC MMC (0.2 mg ⁄mL; 3 min) 18.0 10%

20 TREC No antimetabolite 18.0 0

Mietz et al. (2002) 24 TREC Postoperative MMC (0.05 mg ⁄mL)* 18.2 ± 6.5 0

24 TREC MMC (0.2 mg ⁄mL; 3 min) 19.0 ± 5.0 4.2%

Bindlish et al. (2002) 123 TREC MMC (0.25 ⁄ 0.33 ⁄ 0.5 mg ⁄mL;

0.5–5.0 min)

At least 60 8.9%

Tsai et al. (2003) 15 TREC MMC (0.2 mg ⁄mL; 2 min) 25.7 ± 21.4 20%

29 TREC No antimetabolite 27.7 ± 12.2 0

TREC, trabeculectomy; PHACOTREC, phacotrabeculectomy; MMC, mitomycin C; 5-FU, 5-fluouracil.*Mitomycin-C (0.05 mg ⁄mL) was applied topically to the filtering bleb on days 1, 2 and 3 after surgery (postoperative application).


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retrospective case series to determinerisk factors for hypotony maculopa-thy. The mean age for eyes with mac-ulopathy was 50.5 years versus70.7 years for those eyes without mac-ulopathy. Maculopathy was more fre-quent in myopic eyes and in eyesundergoing primary surgery. Further-more, eyes with hypotony maculopa-thy had a lower frequency ofchoroidal effusion than non-maculop-athy controls.

Several authors confirmed thatyounger age, myopia, male genderand primary filtering surgery are riskfactors for the development of hypo-tony maculopathy (Jampel et al. 1992;Stamper et al. 1992; Suner et al. 1997;Palmberg 1998). The first two factorssupport the theory of low scleral rigid-ity as an important element in thepathogenesis of hypotony maculopa-thy (Gass 1972; Stamper et al. 1992).It is possible that low scleral rigidityfacilitates the inward collapse of thescleral wall during hypotony, causingthe chorioretinal wrinkling. The scleraof young patients is thought to bemore elastic and flexible than that ofolder patients, and may shrink morein hypotonic conditions. Similarly, thesclera in patients with myopia tendsto be thinner, less rigid and, thus,more likely to contract in hypotony(Gass 1972).

Differential diagnosis

Chorioretinal folds may also developin the absence of hypotony. The fol-lowing situations may be associatedwith chorioretinal folds:

(1) Idiopathic chorioretinal folds.Incidental finding in patients who areseen because of presbyopia and thosewho have normal or near-to-normalVA. These patients typically havehyperopia (1–6 dioptres or more).When the folds occur in the macularregion, they are often roughly hori-zontal in their course or may radiateoutward from the optic disc (Gass1987).(2) Retrobulbar mass lesions. Orbitaltumours as well as orbital implants, insome cases, may cause scleral oedema,choroidal congestion and chorioretinalfolds (Kroll & Norton 1970; Wolter1974; Friberg & Grove 1983). Ifthe retrobulbar mass is removed orotherwise treated successfully, the

chorioretinal folds usually disappear(Kroll & Norton 1970).(3) Scleral inflammation. Thickeningand inflammation of the sclera in thy-roid eye disease, inflammatory pseu-dotumour of the orbit andrheumatoid scleritis may cause chori-oretinal folds (Coleman 1995).(4) Scleral buckle. Thickening of thesclera in the vicinity of a scleralbuckle for a rhegmatogenous retinaldetachment may occasionally producechorioretinal folds (Coleman 1995).(5) Choroidal tumours. Choroidaltumours, particularly malignant mel-anomas and metastatic carcinomas,may produce folds in the choroid andretina. These folds are produced bymechanical displacement of the sur-rounding choroid by the expandingtumour (Norton 1969).(6) Choroidal neovascularization.Contraction of a choroidal neovascu-lar membrane (CNVM) and theunderlying Bruch’s membrane occur-ring either spontaneously or afterphotocoagulation may cause aradiating pattern of chorioretinal foldsaround the membrane (Gass 1981).

Prevention andtreatment

The advent of antimetabolite therapyin glaucoma filtration surgery hasresulted in an increased incidence ofpostoperative hypotony secondary tooverfiltration. Modifications of thesurgical technique, such as tighterscleral flap suturing and postoperativegradual increase in outflow with lasersuture lysis or releasable sutures,should be used in order to avoid over-filtration and the occurrence of hypo-tony maculopathy (Savage et al. 1988;Melamed et al. 1990).

Hypotony maculopathy is usuallytreated with procedures designed toelevate the IOP. Normalization ofIOP may then reverse the inwardscleral bowing. However, despite suc-cessful IOP elevation, VA may notreturn to normal, and permanent ma-cular chorioretinal changes may ensue(Duker & Schuman 1994).

The successful treatment of hypot-ony maculopathy depends on the cor-rect identification of its cause. Oncethe cause is detected, treatment shouldbe employed as soon as possible:delayed normalization of the IOP

may result in permanent macularchorioretinal changes and poor vision(Costa et al. 1993c; Nuyts et al.1994b).

Leakage of aqueous humour from afiltration bleb after glaucoma surgerymay cause hypotony maculopathy.Conservative management, includingthe use of aqueous suppressants,pressure patching, collagen shieldapplication or contact lens ⁄ shell ⁄ ringtamponade, may help to seal the leak(Ruderman & Allen 1985; Melamedet al. 1986; Fourman & Wiley 1989;Blok et al. 1990; Hill et al. 1990). Onepossible approach consists of aqueoussuppressants, use of a contact lens andtopical gentamicin therapy. Aqueoussuppressants decrease production ofaqueous humour and reduce bulk flowthrough the leak, thereby allowing epi-thelial proliferation; bandage contactlens facilitates epithelial migration; andtopical aminoglycoside (e.g. gentami-cin) incites mild conjunctival inflamma-tion and stimulates wound healing(Tomlinson et al. 1987).

There have also been successfulreports of bleb leaks treated with low-power argon laser application (Baum& Weiss 1993) or fibrin glue topicalapplication (Kajiwara 1990). Morerecently, intrableb or subconjunctivalperibleb injection of autologous bloodhas been described as a simple in-office technique for treating chronicpostfiltration hypotony (Wise 1993;Smith et al. 1995) (Fig. 9).

Conjunctival compression sutureshave also been used to induce adher-ence of conjunctiva to underlying tis-sues (Palmberg & Zacchei 1996;Palmberg 1996). Palmberg (1996) sug-gested that 9–0 nylon sutures could beemployed to isolate the area of leak-age, reducing the access of aqueous tothe leakage site, or to limit the size ofan overhanging bleb in cases of over-filtration (Fig. 10). The suturesapplied to sectors of the conjunctivain which the fibroblasts are viablemay help induce sufficient healingresponse. However, this techniqueonly affects the area of conjunctivathat is compressed, and, in our hands,this has been insufficient in caseswhere hypotony is caused by overfil-tration and no leakage. When thesesutures are used in association withsubconjunctival injections of autolo-gous blood, they may provide moreeffective management of hypotony


593

maculopathy following filtration sur-gery with mitomycin C (Haynes &Alward 1999).

Finally, bleb excision with surgicalrevision, donor scleral graft patchingand reconstruction of the filtering blebwith a free conjunctival autograftrepresent more invasive treatmentmodalities (Melamed et al. 1991;O’Connor et al. 1992; Buxton et al.1994; Wilson & Kotas-Neumann1994). These techniques are highlysuccessful in increasing IOP by closingconjunctival leakage or decreasing fil-tration in overfunctioning blebs, withsuccess rates varying from 80% to

94% (Budenz et al. 1999; Catoiraet al. 2000; Burnstein et al. 2002;Bashford et al. 2004; Tannenbaumet al. 2004). However, a large propor-tion (up to 50%) of eyes undergoingsurgery require antiglaucoma medica-tions to control IOP, and some (up to8%) may need new filtering proce-dures to reduce IOP (Budenz et al.1999; Catoira et al. 2000; Burnsteinet al. 2002; Bashford et al. 2004;Tannenbaum et al. 2004).

Burnstein et al. (2002) comparedthe outcomes of conjunctival advance-ment and non-incisional managementof late-onset glaucoma filtering bleb

leak in a retrospective, non-random-ized trial. Fifty-one eyes of 48 patientswho underwent management oflate-onset glaucoma filtering blebleaks were included. Thirty-seven eyeswere included in the non-incisionaltreatment group and 34 eyes wereincluded in the surgical revision group(conjunctival advancement with pre-servation of the preexisting bleb). TheKaplan-Meier cumulative probabilityof success at 24 months were 42%and 80%, respectively, for the non-incisional and surgical revision groups(P ¼ 0.0001, log-rank test).

In eyes with hypotony maculopathysecondary to an overfiltering bleb,measures to incite inflammation at thebleb site are recommended to promotescarring and consequent reduction ofaqueous flow. Multiple methods havebeen used in attempting to induce suf-ficient healing or fibrosis of the bleb toreverse the hypotony. It is recognizedthat cataract extraction performed inpreviously filtered eyes can causeinflammatory compromise of the filter,leading to postoperative increases inIOP (Oyakawa & Maumenee 1982;Shields 1982; Dickens & Cashwell1996; Sibayan et al. 1997). Inflamma-tion and scarring at the filtering sitemay also be stimulated by yttrium alu-minium garnet (YAG) laser (Bettinet al. 1999), cryotherapy (Jampel et al.1992; Stamper et al. 1992; Costa et al.1993c; Nuyts et al. 1994b), diathermy(Stamper et al. 1992) and trichloroace-tic acid application (Stamper et al.1992; Nuyts et al. 1994b).

Injection of autologous blood intothe bleb has been described but is notwithout risk. It was first employed byWise (1993), who successfully treatedfour eyes with chronic hypotony fol-lowing MMC trabeculectomy. Nuytset al. (1994b) reported that 17(77.3%) of the 22 eyes that underwentintrableb autologous blood injectionshowed IOPs of 6 mmHg or greaterafter a mean follow-up of 20.7 weeks.Leen et al. (1995) investigated theefficacy of intrableb autologous bloodinjection in 12 eyes with overfilteringor leaking blebs, and observed a58.3% success rate after an averagefollow-up of 6.8 months. Smith et al.(1995) demonstrated a 66.6% successrate following peribleb autologousblood injection into surrounding sub-conjunctival tissue after a minimumfollow-up of 4 months. Ellong et al.

Fig. 9. Intrableb injection of autologous blood.

Fig. 10. Conjunctival compression sutures (under circle) employed to isolate the area of leakage

of aqueous humour from a filtration bleb.


594

(2001) evaluated the effectiveness ofintrableb autologous blood injectionsin 12 eyes with hypotony associatedwith overfiltration. After a mean fol-low-up of 12.3 months, the averageIOP increased from 2.7 ± 1.2 mmHgto 8.2 ± 4.2 mmHg (P < 0.05).

Yieh et al. (2001) described the useof autologous fibrinogen concentrate(AFC) to treat seven eyes with persist-ent post-trabeculectomy hypotony.Under a microscope, 0.2 mL AFCand bovine thrombin was injected intothe blebs. On the second day, themean IOP of seven eyes elevatedfrom 3.4 ± 2.1 mmHg to 12.6 ±4.2 mmHg; within 2 weeks, VA wasnoted to improve in six eyes (85.7%).

Sometimes, the above-mentionedmeasures used to treat hypotony sec-ondary to overfiltration do not reversethe problem because failure of scleralhealing is the underlying cause. Inthese cases, resuturing the scleral flapor placing a scleral patch over the ori-ginal flap is effective in reversinghypotony and restoring VA, while stillmaintaining some degree of filtration(Cohen et al. 1995; Schwartz et al.1996; Halkiadakis et al. 2005;Harizman et al. 2005).

Schwartz et al. (1996) reported foureyes that underwent trabeculectomyusing topical mitomycin C and devel-oped hypotony maculopathy unre-sponsive to non-surgical therapies.After a minimum follow-up of18 months, the surgical revision withscleral flap closure increased the IOP,reversing the hypotony, and resultedin improved VA to 20 ⁄25 or better inall cases.

Harizman et al. (2005) reported amodified technique of bleb revisionwith the use of a donor scleral patch in15 eyes in which scleral melting did notallow effective suturing and closureof the aqueous leak. After a meanfollow-up of 22.0 months, mean IOPincreased from 2.9 ± 2.3 mmHg to14.1 ± 3.3 mmHg, and mean VAimproved from 20 ⁄50 to 20 ⁄ 30.Halkiadakis et al. (2005) employed thesame technique in 14 patients. The pre-operative IOP was 3.3 ± 2.6 mmHg,and the final IOP was 11.6 ± 3.4mmHg after 10.1 ± 6.8 months. VAimproved in 10 of 14 eyes. A secondscleral patch graft revision was neces-sary in three eyes, but bleb leaks andhypotony resolved in all 14 eyes at lastfollow-up.

Resolution

As IOP is normalized, the choroidalfolds become flattened and may com-pletely disappear. Residual changes inthe retinal pigment epithelium mayremain as a result of hyperplasia andhyperpigmentation. Fluorescein angi-ography may depict abnormal areasof hypo- and hyperfluorescence. Thechoroid and the sclera recover theiroriginal thickness, and the tortuosityand engorgement of the retinal vesselsdisappear.

The prognosis for visual recoveryapparently depends primarily on theduration of the hypotony. If retinalfolds are induced by scleral shrinkagein response to low IOP, the restor-ation of the normal smooth architec-ture to the retina and Bruch’smembranes allows realignment ofphotoreceptors. If not treatedpromptly, prolonged hypotony maycause irreversible fibrosis within theretina, choroid or sclera, maintainingthe choroid in a folded position(Jampel et al. 1992).

Conclusion

Hypotony maculopathy is an uncom-mon complication of glaucoma filter-ing surgery, trauma and otheranterior segment surgeries. Young age(Dellaporta 1948, 1950, 1954; Jampelet al. 1992; Stamper et al. 1992; Suneret al. 1997; Palmberg 1998), myopia(Jampel et al. 1992; Stamper et al.1992; Suner et al. 1997; Palmberg1998), primary filtering surgery (Suneret al. 1997), systemic illnesses (Costaet al. 1993b) and elevated preoperativeIOP (Stamper et al. 1992; Palmberg1998) have been found to be associ-ated with hypotony maculopathy.

Early detection of the characteristicfundoscopic findings of hypotony andthe search for its cause are fundamen-tal because the visual deficit can becorrected through appropriate meas-ures to restore normal IOP. The prog-nosis for VA recovery depends onseveral factors, including the durationof the hypotony. Delayed normaliza-tion of IOP may result in perma-nent macular chorioretinal changesand poor vision. This justifies animmediate recognition of the condi-tion, identification of the cause andinitiation of treatment.

Financial ⁄proprietaryinterest

The authors do not have any financialor proprietary interest in the drugs andinstruments mentioned in this article.

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Received on September 26th, 2006.

Accepted on January 23rd, 2007.

Correspondence:

Vital P. Costa

Rua Bauru, 40

Sao Paulo, SP 01248–010

Brazil

Tel: +55 11 3865 9630

Fax: +55 11 3865 9630

Email: [email protected]


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