PERSPECTIVEPeripheral Retinal Degenerations and the Risk of

Retinal Detachment

HILEL LEWIS, MD

● PURPOSE: To review the degenerative diseases of theperipheral retina in relationship with the risk to developa rhegmatogenous retinal detachment and to presentrecommendations for use in eyes at increased risk ofdeveloping a retinal detachment.● DESIGN: Focused literature review and author’s clinicalexperience.● RESULTS: Retinal degenerations are common lesionsinvolving the peripheral retina, and most of them areclinically insignificant. Lattice degeneration, degenera-tive retinoschisis, cystic retinal tufts, and, rarely, zonulartraction tufts, can result in a rhegmatogenous retinaldetachment. Therefore, these lesions have been consid-ered for prophylactic therapy; however, adequate studieshave not been performed to date.● CONCLUSIONS: Well-designed, prospective, random-ized clinical studies are necessary to determine thebenefit-risk ratio of prophylactic treatment. In the mean-time, the evidence available suggests that most of theperipheral retinal degenerations should not be treatedexcept in rare, high-risk situations. (Am J Ophthalmol2003;136:155–160. © 2003 by Elsevier Inc. All rightsreserved.)

N ON-TRAUMATIC RHEGMATOGENOUS RETINAL DE-

tachment occurs in approximately 1 in 10,000persons per year.1–3 The prevalence in pseudopha-

kic patients is higher, approximately 1% to 3%.4,5 Despitethis relatively low incidence, a retinal detachment is animportant cause of visual disability and severe visual lossand is the most common potential cause of blindness aftercataract surgery.

The pathogenesis of a rhegmatogenous retinal detach-ment includes vitreous syneresis followed by posteriorvitreous detachment, resulting in vitreoretinal traction

with formation of retinal break(s). Intraocular fluid cur-rents separate the neurosensory retina from the retinalpigment epithelium resulting in a retinal detachment.6–7

Degenerative conditions of the peripheral retina canlead to the formation of atrophic retinal holes or tractionalretinal tears, and thus predispose patients to the develop-ment of a rhegmatogenous retinal detachment. Atrophicretinal holes within areas of peripheral retinal degenera-tions rarely cause a retinal detachment when the liquidvitreous passes through the atrophic hole and separates theneurosensory retina from the retinal pigment epithelium.This process can occur even in the absence of a posteriorvitreous detachment. Tractional retinal tears are morelikely to occur in areas of abnormal vitreoretinal adhesionswithin peripheral retinal degenerations. As the posteriorvitreous detaches from the retina, the vitreous exertstraction on the abnormal vitreoretinal attachment, whichcan lead to a retinal tear and subsequent retinal detach-ment. In patients with a rhegmatogenous retinal detach-ment in one eye and a predisposing peripheral retinaldegeneration in the fellow eye, the risk of a retinaldetachment increases greatly and is at least 10%.8–12

In this article, I review the peripheral retinal degenera-tions that pose a higher risk for development of a rheg-matogenous retinal detachment and the evidence availableregarding prophylactic treatment.

LATTICE DEGENERATION OFTHE RETINA

LATTICE DEGENERATION OF THE RETINA WAS PROBABLY

first described by Gonin13 and since then, it has beenbetter defined by Straatsma and Allen14 and others.15–19 Itis typically characterized by sharply demarcated, circum-ferentially oriented, oval or round areas of retinal thinningwith overlying vitreous liquefaction and exaggerated vit-reoretinal attachments along its edges. Other features thatcan be, but are not always, present include fine white lines(latticelike) in the crossing retinal vessels, alterations ofretinal pigment, small white-yellow particles at the marginof the surface of the lesion, punched out areas of extreme

Accepted for publication Jan 20, 2003.InternetAdvance publication at ajo.com Jan 24, 2003.From the Cole Eye Institute, Division of Ophthalmology, The Cleve-

land Clinic Foundation, Cleveland, Ohio.Supported by the Retina Research Foundation, Houston, Texas.Inquiries to Hilel Lewis, MD, Cole Eye Institute, The Cleveland Clinic

Foundation, 9500 Euclid Avenue, i-30, Cleveland, OH 44195; fax: (216)445-7654; e-mail: lewish@ccf.org

© 2003 BY ELSEVIER INC. ALL RIGHTS RESERVED.0002-9394/03/$30.00 155doi:10.1016/S0002-9394(03)00144-2

retinal thinning, or excavations and atrophic retinal holes.Retinal tears can occur at the posterior or lateral margin ofthe lesion from vitreous traction following posterior vitre-ous detachment.

Lattice degeneration can occur early in life and peaks inthe second decade.16,20 The number of lattice lesions in aneye can vary from 1 to more than 20, with an average ofbetween 2 and 24.12,20 The lattice lesions can be arrangedin multiple rows and are most commonly located near thevertical meridian between 11 and 1 o’clock and between 5and 7 o’clock. The lesions are usually located slightlyanterior to the equator, but they can be present posteriorto the equator where they are frequently radially orient-ed.12,16,20

The pathogenesis of lattice degeneration is unknown.Several theories have been proposed, including develop-mental anomalies of the internal limiting membrane,vitreous traction, embriologic vascular anastomosis, andchoroidal abnormalities.12,21,22 Inner retinal ischemia asthe cause of lattice degeneration was postulated byStraatsma and colleagues.16 None of the hypotheses havebeen proven to date, however.

Lattice degeneration is present in 6% to 10.7% and isbilateral in 34% to 48% of nonselected patients.12,16,20 Itsincidence is higher in myopic patients, occurring in 15% ofeyes with axial length of 30 mm or more.12,16,23 Theprevalence of lattice degeneration of the retina in thefellow eye of patients with rhegmatogenous retinal detach-ment ranges from 9.2% to 35%.24,25

Lattice degeneration is the most important peripheralretinal degeneration that predisposes to a rhegmatogenousretinal detachment. Most rhegmatogenous retinal detach-ments seen in patients with lattice degeneration are due totractional retinal tears following posterior vitreous detach-ment. Atrophic retinal holes within lattice lesions cancause a localized retinal detachment, and rarely, a progres-sive retinal detachment.

Retinal tears, due to vitreous traction to the stronglyadherent posterior and lateral vitreoretinal margins oflattice lesions follow a posterior vitreous detachment. Inclinical series, they were found to be present in 1.5% ofeyes with lattice degeneration followed for 3 to 10 years.26

In autopsy series, they were found in 2.5% of eyes withlattice degeneration, but in only 1.4% of the eyes, theretinal tears were associated with lattice lesions.16 Retinaltears occur within areas of lattice in 21% of autopsy eyes,12

and in 64% to 83% of eyes in clinical series.12,25,27 Theprevalence of posterior vitreous detachment and retinaltears is higher in eyes with lattice degeneration. In a largeclinical series, 30% of eyes with acute retinal detachmentand retinal breaks had lattice degeneration.27 In 83% ofthese cases, the retinal tear was associated with a latticelesion. The 3- to 10-year incidences of retinal detachmentin phakic eyes with lattice degeneration and a history ofretinal detachment in the fellow eye is 6% to 15%.25,28

The cause for the higher incidence of retinal detachment

may be the older age of these patients, which predisposesthem to posterior vitreous detachment in the fellow eye.

Retinal holes can be single or multiple. They have beenfound in 16% to 24% of eyes with lattice degeneration inclinical series12 and in 25% of eyes with lattice degenera-tion in an autopsy series.16 They cause a retinal detach-ment when fluid passes through the hole within the latticeto the subretinal space. Vitreous traction at the edge of thelattice lesion may also play a role in the process. Approx-imately 2.8% of rhegmatogenous retinal detachments aredue to retinal holes within lattice degeneration.28,29 Ac-cording to Byer,12 the risk of a retinal detachment in eyeswith atrophic retinal holes is 0.274%, and the risk appearsto be higher in young, myopic patients. There is noevidence that eyes with lattice degeneration and retinalholes are more likely to develop a retinal detachment afterposterior vitreous detachment.

Although lattice degeneration is a risk factor for devel-opment of a rhegmatogenous retinal detachment, the greatmajority of patients with lattice degeneration do notdevelop a retinal detachment, and up to 80% of rhegmat-ogenous retinal detachments are not associated with latticedegeneration of the retina.12

Because lattice degeneration is present in 30% of phakicrhegmatogenous retinal detachments, these lesions havebeen frequently considered for prophylactic therapy.30,31 Ineyes without other predisposing factors, however, latticedegeneration rarely causes a retinal detachment.12,26 Therisk for a rhegmatogenous retinal detachment in eyes withlattice degeneration that were followed between 1 and 10years is 0 to 1.4%.26,32 In a study by Byer33 of 423 eyes in276 patients followed for an average of almost 11 years,atrophic retinal holes were present in 35% of eyes, and ofthese 150 eyes, 9 (6%) had stable, nonprogressive limitedsubretinal fluid; only one eye (0.7%) had asymptomaticposterior extension of the subretinal fluid. In this sameseries, asymptomatic retinal tears occurred in three eyes(0.7%) and were observed; symptomatic retinal tearswithout retinal detachment developed in five eyes(1.18%), and they were treated. Only three eyes (0.7%)developed a clinical retinal detachment.33

To determine if prophylactic treatment to eyes withlattice degeneration with or without retinal holes is ben-eficial, it is necessary to design a study with appropriatestatistical methods and power to produce either statisticalsignificant results or show no difference. Unfortunately,this study has not yet been performed. To date, thereported studies on prophylactic therapy for lattice degen-eration have not been prospectively randomized and havenot separated the cases based on family history, thepresence or absence of symptoms, the refractive error, thestatus of the lens, the presence or absence of a posteriorvitreous detachment, or the history of retinal detachmentin the fellow eye.

Currently, there is no scientific evidence to suggest thatprophylactic treatment of lattice degeneration with or

AMERICAN JOURNAL OF OPHTHALMOLOGY156 JULY 2003

without retinal holes in phakic, nonfellow eyes, is benefi-cial. Prophylactic treatment has failed to prevent a retinaldetachment in between 2.2% and 2.9% of treated eyesreported in two series.32,34 The natural history of latticedegeneration and the results of prophylactic treatmentmight not be different in these patients; therefore, inasymptomatic patients without other risk factors, we donot recommend prophylactic treatment.

Prophylactic treatment might be considered in somepatients with lattice degeneration in the fellow eye of apatient with a history of rhegmatogenous retinal detach-ment in the first eye, especially if the visual function ispoor in this eye, if the patient does not have or hasminimal access to ophthalmic care, or if the patient ismentally retarded and might not recognize the symptomsof a posterior vitreous separation. In a retrospective study,Folk and colleagues studied 388 consecutive patients withlattice degeneration in one eye and a history of rhegmat-ogenous retinal detachment associated with lattice degen-eration in the fellow eye. In 151 eyes, no prophylactictreatment was performed; in 164 eyes, all lattice lesionsand retinal breaks were treated; and in 73 eyes, partialtreatment of lattice degeneration was given. During anaverage follow-up of more than 7 years, new retinal tearswithout a detachment occurred in 6.6% of untreated eyes,in 9.6% of partially treated eyes, and in 3% of fully treatedeyes. The prevalence of retinal detachments was 5.9% inuntreated eyes, 6.8% in partially treated eyes, and 1.8% ineyes receiving prophylactic treatment of all lattice lesions.This beneficial effect was statistically significant (P �.0001) except for eyes with myopia of 6 diopters or moreand more than 6 clock hours of lattice degeneration.11

Based on this study, retinal detachments would be pre-vented in only three eyes for every 100 patients withlattice degeneration that we treat in a phakic fellow eyeand a history of retinal detachment in the other eye.

DEGENERATIVE RETINOSCHISIS

DEGENERATIVE RETINOSCHISIS WAS PROBABLY FIRST RE-

ported by Bartels in 1933.35 Straatsma and Foos36 describedtwo forms based on histopathology, typical or flat retino-schisis, and reticular or bullous retinoschisis. In degenera-tive retinoschisis, there is a coalescence of cystic lesions asa result of degeneration of neuroretinal and glial support-ing elements within areas of peripheral cystoid degenera-tion. This area enlarges slowly as a substance containingacid mucopolysacharide accumulates.37 This results inseparation or splitting of the retina into an inner and anouter layer with severing of neurons and leads to irrevers-ible and complete loss of visual function in the affectedarea. In typical retinoschisis, the retinal separation occursdeeper in the retina compared with reticular retinoschisis,which is the more severe form. By histopathology, typicalretinoschisis shows that the inner layer contains the inner

limiting membrane, retinal vessels, and inner plexiformlayer, whereas the outer layer has portions of the outerplexiform, outer nuclear, and photoreceptor layers. Incontrast, reticular retinoschisis demonstrates an extremelythin inner wall consisting of inner limiting membrane,remnants of the nerve fiber layer, attenuated blood vessels,and there is complete loss of the supporting radial pillars.

Degenerative retinoschisis is an idiopathic, degenerativeprocess, and there is no evidence to suggest the genetic,vascular, nutritional, or tractional etiology. In autopsystudies, typical retinoschisis is present in 1%, is bilateral in33% of cases, and has a prevalence of 0.7%. Reticularretinoschisis is present in 1.6%, is bilateral in 16% of cases,and has a prevalence of 0.95%.36,38 In an unselectedclinical series, the incidence of retinoschisis was found tobe 3.7% in patients 10 years or older and 7% for patients40 years of age or older, with 82% of cases being bilateral.39

Normally, the inferotemporal quadrant is the most fre-quent location where retinoschisis is encountered.

A rhegmatogenous retinal detachment can rarely occurin eyes with retinoschisis and retinal breaks. Retinoschisiswithout retinal breaks in either layer does not cause retinaldetachment. In retinoschisis, inner retinal holes are rareand probably occur in less than 4% of cases.40 Theincidence of tractional retinal tears in retinoschisis, al-though not known, is extremely low. Retinal tears, sec-ondary to posterior vitreous detachment, may, however, beimportant in causing progressive rhegmatogenous retinaldetachment. Outer retinal holes are more common thaninner retinal breaks, and they are present in 23% ofautopsy cases and in up to 17% of clinical series.37,40,41

They can be single or multiple, can be large in size, anddemonstrate a prominent rolled posterior border.

There are two types of retinal detachments associatedwith retinoschisis, a localized and relatively stable formwith outer retinal holes only and a symptomatic, rapidlyprogressive detachment with retinal breaks in both layers.Retinoschisis is present in up to 6% of rhegmatogenousretinal detachments, but retinoschisis is responsible forless than 2.5% of all rhegmatogenous retinal detach-ments.37,40–42

Localized and relatively nonprogressive retinal detach-ments occur more frequently than a progressive retinaldetachment by a ratio of 178:1,40 but they are rarelyclinically relevant. A localized retinal detachment wasfound in 6.4% of eyes with retinoschisis followed clinically,and in 60% of autopsy eyes with retinoschisis and outerretinal holes.40,43 A progressive symptomatic retinal de-tachment is rare in patients with retinoschisis who areinitially asymptomatic. In a study by Byer40 of 218 sucheyes followed for an average of 9 years, none developed asymptomatic rhegmatogenous retinal detachment. In aseries by Hagler and Woldoff, however, which included 90patients seen with rhegmatogenous retinal detachmentand retinoschisis, 79% of the detachments were of theprogressive form.44

PERSPECTIVEVOL. 136, NO. 1 157

Based on the information presented, treatment forretinoschisis should be limited to patients who developedsymptomatic, progressive retinal detachments.40 Prophy-lactic treatment is not recommended for asymptomaticpatients with retinoschisis with or without outer retinalholes or with localized, nonprogressive, retinal detach-ments. In reports in which such prophylactic treatmentswere performed, a retinal detachment occurred in 1.2% to13% of cases, and adverse effects developed in severalpatients, including epimacular proliferation, new retinalbreaks, and vitreous hemorrhage.40 Routine treatment ofasymptomatic patients with localized retinal detachmentand posterior progression also is not recommended becausethis posterior extension frequently stops spontaneously,macular involvement is extremely rare, and demarcationtreatment has been associated with severe complications.40

Patients with retinoschisis with or without outer retinalholes and with or without limited retinal detachmentshould instead be followed periodically and instructed toreturn immediately in the unlikely event that they becomesymptomatic.

CYSTIC RETINAL TUFT

THE RETINAL LESION THAT FOOS AND ALLEN45 NAMED

cystic retinal tuft in 1967 was first illustrated in 1936 byVogt.46 It is clinically characterized by a round or oval,elevated vitreoretinal lesion which is small, discreet, andsharply circumscribed and has a chalky-white color. Vit-reous condensations are attached to its surface, and its basemay have pigmentary changes. The lesion occurs mostfrequently (78%) in the extra basal or equatorial zone ofthe eye, is single in most cases, and is unilateral in 80% ofpatients.38

Cystic retinal tuft is a congenital abnormality in thedevelopment of the peripheral retina. Histologically, accu-mulations of glial tissue form in nodules on the retinalsurface that enclose crypts of formed vitreous within thelesion. Large tufts demonstrate an absence of photorecep-tors.47 Cystic retinal tufts are present at birth and affectapproximately 5% of the population.38

The dense vitreoretinal adherence present in cysticretinal tufts explains why they are commonly associatedwith retinal tears that can have either a flap or anoperculum and can occur with or without a posteriorvitreous detachment.47–49 It is estimated that up to 10% ofrhegmatogenous retinal detachments are caused by retinaltears in areas of cystic retinal tufts.50 Rarely, atrophicretinal holes in an area of chronic vitreoretinal tractioncan be the cause of the rhegmatogenous retinal detach-ment.50 Because the natural history and the results oftreatment of cystic retinal tufts have not been studied, andknowing that the risk of developing a rhegmatogenousretinal detachment from a cystic retinal tuft is 0.28%,prophylactic treatment is not indicated.48

ZONULAR TRACTION TUFT

IN ZONULAR TRACTION TUFTS, THICKENED ZONULES ARE

displaced posteriorly toward the anterior retina resulting inan anterior projection or tuft of the retina. By histopathol-ogy, these lesions show attachments of zonular fibers at theapex of the tuft, neuroglial cells within the tuft, and retinalthickening and degeneration at the base.51

Zonular traction tufts are present at birth and are foundin 15% of cases seen at autopsy, being bilateral in 15%.They are mostly single and, in the majority of patients,they are located in the nasal quadrant within the vitreousbase close to the ora serrata.51 Retinal detachment canrarely occur, caused by the development of retinal breaksin association with the zonular traction tuft. The tractionat the apex can result in a retinal tear (flap or operculated),and the trophic changes at the base can cause a retinalhole. Foos found that in autopsy cases, 6% of all full-thickness retinal tears were due to a zonular traction tuft.49

Because these lesions are mostly intrabasal, retinal breaksare mostly clinically insignificant. When a retinal detach-ment occurs, it is frequently localized and nonprogressive.Therefore, prophylactic treatment of these lesions is notindicated.

CLINICAL RECOMMENDATIONS

PREVENTION OF RHEGMATOGENOUS RETINAL DETACH-

ment is important because, in many cases, surgical andanatomic success is not followed by visual success. Prophy-lactic treatment of retinal detachment could be achievedby preventing a posterior vitreous detachment, reducingvitreoretinal traction, or creating a chorioretinal adhesionaround precursors of retinal detachment, such as someperipheral retinal degenerations. Unfortunately, we do notknow how to prevent vitreous syneresis or posterior vitre-ous detachment. Reducing vitreoretinal traction can beaccomplished with a scleral buckle or vitrectomy, but therisks of surgery far outweigh their possible benefits. Thus,we are left with consideration of treating peripheral retinaldegenerations with either laser or cryotherapy.

Although there are several studies on prophylaxis ofretinal detachment for patients with peripheral retinaldegenerations, these studies are retrospective and thepatients have not been randomized nor stratified accordingto important factors, such as the presence or severity ofmyopia, the status of the lens, the presence or absence ofa posterior vitreous separation, the history of retinaldetachment in the fellow eye, and so on. As evidencepresently suggests, prophylactic treatment is of question-able value, and there is risk to the treatment.

Based on current evidence, it is recommended thatpatients with peripheral retinal degenerations that are at ahigher risk for developing a retinal detachment be told ofthe signs and symptoms of posterior vitreous detachment

AMERICAN JOURNAL OF OPHTHALMOLOGY158 JULY 2003

and instructed to return immediately if these symptomsoccur. Fellow eyes of patients with retinal detachment dorelatively well, and the surgical outcomes are better be-cause they are seen relatively early. So, we can preventmany retinal detachments by educating high-risk patients.Treatment of fellow eyes with lattice degeneration of theretina is still controversial but might have some merit ifthe eye has less than 6 diopters of myopia and the latticeis present in less than 6 clock hours, particularly if aposterior vitreous separation has not yet occurred.11

The important studies by Straatsma and others charac-terizing peripheral retinal degenerations and presentingthe natural history of these conditions need now to befollowed by well-designed, prospective, randomized, clini-cal trials to determine if prophylactic treatment of patientswith eyes that are highly predisposed to retinal detachmentis of value.52 In the meantime, we should observe andeducate.

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