Katarak Pada Diabetes

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Cataracts and Diabetes Mellitus;Javadi et al

JOURNALOFOPHTHALMIC ANDVISIONRESEARCH2008; Vol. 3, No. 152

Cataracts in Diabetic Patients: A Review ArticleMohammad-Ali Javadi, MD; Siamak Zarei-Ghanavati, MD

Shaheed Beheshti Medical University, Tehran, Iran

The number of people with diabetes mellitus is increasing and cataracts are one of themost common causes of visual impairment in these subjects. Advances in cataract sur-gical techniques and instrumentation have generally improved the outcomes; however,surgery may not be safe and effective in certain individuals with pre-existing retinalpathology or limited visual potential. This review article aims to address different as-

pects surrounding cataracts in diabetic patients. In a computerized MEDLINE search,relevant studies were selected by two authors using the keywords diabetes mellitus,cataract, diabetic retinopathy and diabetic maculopathy.

J Ophthalmic Vis Res2008; 3 (1): 52-65.

Correspondence to: Mohammad-Ali Javadi, MD. Professor of Ophthalmology; Ophthalmic Research Center,No. 5, Boostan 9 St., Amir Ebrahimi Ave., Pasdaran, Tehran 16666, Iran; Tel: +98 21 22585952, Fax: +98 21 22590607;

e-mail: [email protected]

INTRODUCTIONPopulation growth, ageing, urbanization, sed-entary lifestyles and an increasing prevalenceof obesity are increasing the number of peoplewith diabetes mellitus. The global prevalenceof diabetes was estimated to be 2.8% in 2000and is expected to reach 4.4% by 2030. The totalnumber of people with diabetes mellitus world-wide is projected to rise from 171 million in2000 to 366 million in 2030.1 Globally, cataractsremain the leading cause of blindness, affectingapproximately 18 million people.2 Cataractsoccur at an earlier age and 25 times more freq-uently in patients with diabetes, thus the visualloss has a significant impact on the workingpopulation.3,4

Overall, up to 20% of all cataract proced-ures are estimated to be performed for diabeticpatients.5 Epidemiologic studies have demon-strated that cataracts are the most commoncause of visual impairment in older-onset dia-betic patients6,7 and the rate of cataract surgeryis correspondingly high. The Wisconsin study

identified that the ten-year cumulative inci-

dence of cataract surgery was 27% in patientswith early onset diabetes and 44% in cases witholder onset disease.3

Advances in cataract surgery have gene-rally improved the outcomes, however diabeticindividuals do not always share the same favo-rable outcomes. Some studies have reportedthat cataract surgery may have adverse effects,including progression of retinopathy, vitreoushemorrhage, iris neovascularization and dec-rease or loss of vision.8-10 This study will reviewrelated articles to highlight current agreementsand controversies regarding cataract develop-ment, extraction and complications with great-er attention to clinical aspects.

RISK FACTORS FOR OCULARCOMPLICATIONS IN DIABETIC PATIENTSDiabetes mellitus is a systemic condition affect-ting numerous organs other than the eye. Onthe other hand, concomitant systemic disorderscan significantly influence the development


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JOURNALOFOPHTHALMIC ANDVISIONRESEARCH2008; Vol. 3, No. 1 53

and progression of ocular complications in dia-betic patients. Intensive control of blood glu-cose and systemic hypertension reduce the riskof new onset diabetic retinopathy and slow theprogression of existing diabetic retinopathy.11,12Severe renal disease affects the progression ofdiabetic retinopathy, elevated serum lipids areassociated with macular exudation and moder-ate visual loss, excessive exercise in patientswith advanced retinopathy may predispose tovitreous hemorrhage, transient progression ofdiabetic retinopathy can occur during preg-nancy, anemia can result in progression ofdiabetic retinopathy and smoking in general

should be discouraged.13Studies related to cataract formation in dia-

betic patients have shown that hyperglycemiais associated with loss of lens transparency ina cumulative manner.14 Rapid decline of serumglucose levels in patients with marked hyper-glycemia may induce temporary lens opacifi-cation and swelling as well as transient hyper-opia. It has also been suggested that rapid gly-cemic control can irreversibly increase lens opa-cities.15

RISK FACTORS FOR CATARACTS INDIABETESCataracts are among the earliest complicationsof diabetes mellitus. Klein et al3 demonstratedthat patients with diabetes mellitus are 25times more likely to develop cataracts thantheir nondiabetic counterparts; this risk mayreach 15-25 times in diabetics less than 40 yearsof age.16 Even impaired fasting glucose (IFG),a pre-diabetic condition, has been considered

as a risk factor for the development of corticalcataracts.17 In a study from Iran, Janghorbaniand Amini18 evaluated 3,888 type 2 diabeticpatients who were free of cataracts at initialvisit and reported a rate of cataract formationof 33.1 per 1000 person-years of observationafter a mean follow-up of 3.6 years.

PREVENTION OF CATARACTSThree molecular mechanisms seem to be in-

volved in the development of diabetic cataracts:non-enzymatic glycation of lens proteins, oxi-dative stress and activated polyol pathway.Despite the fact that a wide variety of agents,including inhibitors of glycation (Aspirin, Ibu-profen, Aminoguanidine and Pyruvate), anti-oxidants (Vitamin C, Vitamin E, Carotenoids,Trolox and Hydroxytoluene) and aldose reduc-tase inhibitors (Zenarestat, Eplarestat, Imirestat,Ponalrestat, Zopolrestat, M-79175 and BAL-AR18) have demonstrated potential for preven-tion of cataracts in animal models, it would bepremature to recommend them in humans.19

ANTERIOR SEGMENT CHANGES INDIABETESDiabetes mellitus significantly impacts the mor-phological,metabolic,physiologicalandclinicalproperties of the cornea. The corneal abnor-malities, generally termed diabetic keratopathy,are present in more than 70% of diabetic pa-tients20andincludeclinicallydetectablechangessuch as increased epithelial fragility and recur-rent erosions,21 reduced corneal sensitivity,22-25

increased autofluorescence,26

impaired woundhealing,27 altered epithelial and endothelial bar-rier functions,28 and predisposition to cornealedema29 and infectious ulcers.21-24

Confocal microscopy has revealed lowerbasal cell density in diabetic patients whichmay due to decreased innervation at the sub-basal nerve plexus level, basement membranealterations and higher turnover rate in the basalepithelial cells. Both stromal and sub-basal cor-neal nerve plexuses in diabetic subjects appearabnormalonconfocalmicroscopy;patientswith

proliferative diabetic retinopathy show morepronounced alterations than patients with nodiabetic retinopathy. The sub-basal nerve ple-xus has been reported to appear significantlythicker and more tortuous.30 Cell density alsoseems to be reduced at the mid corneal stromalevel in diabetic patients.31 Inoue et al32 demon-strated that corneal endothelial cell density wasdecreased and the coefficient of variation in cellarea was increased in diabetic patients as com-pared to healthy controls. However, no signi-


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ficant difference in central corneal thickness(CCT) was observed.

The most important change in the crys-talline lens is cataract formation. The basementmembrane of the lens (or lens capsule) isknown to be thicker in diabetics, which is simi-lar to the thickened vascular basement mem-brane in these subjects. This thickened capsuleis more friable and inadvertent rupture duringintracapsular lens extraction seems to be morecommon in diabetics.33 Lens capsule changesmay also affect performing capsulorrhexis du-ring phacoemulsification.

Several studies have compared different

types of cataracts in diabetics vs non-diabetics.Schafer et al34 reported a higher percentage ofcortical opacities in diabetics as documented byScheimpflug photography and densitometricanalysis. They also demonstrated correlationbetween type 2 diabetes mellitus and corticallens opacities. Saxena et al17 found a 2-foldhigher incidence of cortical cataracts in subjectswith diabetes mellitus over 5 years. In theirstudy, posterior subcapsular cataracts weremore frequent in diabetic patients, but the

association was statistically significant only forsubjects with newly diagnosed diabetes. Theseinvestigators found no significant associationbetween nuclear cataracts and diabetes mellitusor IFG. An uncommon type of lens opacity,true diabetic cataract or snowflake cataract,consists of widespread bilateral subcapsularlens opacities of abrupt onset and acute prog-ression, typically in young people with uncon-trolled diabetes mellitus. This is rare and maybe the initial presentation of diabetes.35

Iris changes such as leathery consistency

and a miotic pupil were found to occur morefrequently in diabetic patients. The iris pigmentepithelium is often vacuolized due to the accu-mulation of glycogen and pigment dispersionmay occur with iris trauma or surgery.36 Insome cases, abnormal iris transillumination hasbeen noted. This tends to be associated withmore severe degrees of retinopathy. Hypoxiahas been implicated as the cause of changes inthe iris pigment epithelium.37

Studies have reported a higher prevalence

of both elevated mean IOP and POAG amongsubjects with diabetes. On the other hand, glau-coma patients have been reported to have ahigher prevalence of abnormal glucose meta-bolism.38 It is possible that diabetes mellitusincreases the susceptibility of the optic nervefibers to glaucomatous damage because of itseffect on small vessels of the eye. Whetherdiabetes is an independent risk factor for thedevelopment of POAG remains controversial;some studies have found a positive association(BlueMountainsEyeStudy39)whileothershavenot. Diabetes was not associated with an incr-eased risk of conversion of ocular hypertension

to frank glaucoma in the Ocular HypertensionTreatment Study (OHTS).40

One of the most important anterior seg-ment complications of diabetes is neovas-cularization of the iris (NVI) which is usuallydue to tissue hypoxia or ischemia and charac-terized by fine arborizing blood vessels on theiris stroma and trabecular meshwork, accom-panied by a fibrous membrane. Contraction ofthe fibrovascular membrane results in peri-pheral anterior synechiae formation, leading to

a severe type of secondary angle-closure glau-coma, neovascular glaucoma, which is causedby a variety of disorders characterized by re-tinal or ocular ischemia, the most common ofwhich is diabetes mellitus.41,42

TIMING OF CATARACT SURGERYThe approach to timing for cataract surgeryin diabetic patients seems to be changing. Adecade ago, a more conservative attitude wasprevalent. Pollack et al43 reported VA better

than 20/40 in 31% of patients and notedmacular edema as the main cause of poorvisual outcome. These investigators proposedthat cataract extraction should not be reco-mmended for eyes with diabetic retinopathyuntil visual acuity has deteriorated to 20/10020/200. This view was later endorsed bySchatz et al44 reporting a study in which only9% of eyes achieved postoperative VA betterthan 20/40. These authors stated that Apatient with diabetes and cataract might wish


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to postpone surgery or elect not to have it at all,given the chance of a markedly poor result,especially if any retinopathy is present pre-operatively.

There is growing evidence in support ofa more interventional approach. A shift inattitude towards earlier cataract extraction indiabetes mellitus has contributed to an impro-ved visual outcome. This approach facilitatespanretinal photocoagulation therefore preven-ting progression of retinopathy and also en-ables timely treatment of underlying macularedema.45 Visual outcomes are likely to be worsein studies in which surgery is deferred until it

was not possible to identify or adequately treatclinically significant macular edema (CSME)prior to surgery. Additionally, if surgery isundertaken before lens opacity prevents therecognition of retinal thickening, the risk ofCSME is decreased and the visual outcomemay be improved considerably.46

PREOPERATIVE CONSIDERATIONSPrior to surgery, patients should have good

glycemic control and no evidence of ocular orperiocular infection. Due to the range of an-terior segment changes in diabetic patients, it isadvisable that cataract extraction be undertakenby an experienced surgeon. A thorough andcomprehensive ophthalmologic examination in-cluding assessment of visual acuity (VA), bestcorrected visual acuity (BCVA), relative affe-rent pupillary defect (RAPD), slitlamp biomic-roscopy, gonioscopy (with particular attentionto new vessels), tonometry and dilated fundus-copy is mandatory. Ancillary diagnostic evalu-

ations such as fluorescein angiography, opticalcoherence tomography (OCT) and B-scan ultra-sonography may be helpful in selected cases.Some authors recommend consultation withvitreoretinal subspecialist, especially in compli-cated cases.47

Patients with pre-existing proliferative dia-betic retinopathy are more likely to progressrapidly after cataract surgery, therefore pan-retinal photocoagulation (PRP) is recommen-ded preoperatively. When lens opacity pre-

cludes PRP, it can be performed after surgery48or the surgeon may consider preoperative pan-retinal cryopexy or combined cataract surgerywith vitrectomy and endolaser photocoagu-lation, especially for cases with posterior poletractional retinal detachment (TRD). Macularedema should be adequately treated prior tosurgery because pre-existing maculopathy mayaggravate postoperatively and is strongly asso-ciated with a poor visual outcome.49

Patients with NVI also need prompt PRP.When neovascular glaucoma (NVG) has de-veloped, medical therapy alone is usually noteffective. Topical beta-adrenergic antagonists,

alpha2-adrenergic agonists, carbonic anhydraseinhibitors, cycloplegics and corticosteroids maybe useful in reducing IOP and decreasinginflammation. The risk of intra- and post-operative complications are high with activeNVI. Antivascular endothelial growth factor(VEGF) agents such as bevacizumab appear tohave a promising role in the treatment of neo-vascular glaucoma. Patients have demonstrateddramatic short-term response in terms of intra-ocular pressure reduction and regression of

neovascularization.50,51

The authors have limi-ted experience with the combination of intra-vitreal bevacizumab injection to induce NVIregression prior to cataract surgery followed byPRP briefly after surgery (unpublished data).

Hyperglycemia is the major cause of tran-sient refractive changes in diabetic patients.The refractive changes observed during periodsof unstable blood sugar are thought to be re-lated to both morphologic and functional cha-nges in the crystalline lens.52 With intensivemedical therapy, a considerable number of pa-

tients tend to become more hyperopic as com-pared to the hyperglycemic state. Changes incorneal topographic parameters during periodsof glycemic changes are a potential source oferror in keratorefractive and cataract surgery.53

CATARACT SURGERYCataract surgery is more complicated in dia-betic patients overall. Phacoemulsification isassociated with better visual results, less in-


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flammation and less need for capsulotomy ascompared to extracapsular cataract surgery.54

Corneal hypoesthesia is common in dia-betic patients. Special care should be taken toprotect the corneal epithelium during surgery.Corneal abrasions during or after surgery maybe slow to heal and lead to recurrent cornealerosions. Small-incision surgery can minimizefurther decrease in corneal sensation.21,22 Due tocorneal hypoesthesia and the increased risk ofinfection, patients with diabetes are poorcandidates for long-term aphakic contact lenswear. Thus a posterior chamber intraocular lens(IOL) should be inserted when possible.

If the pupil is small preoperatively, it maybe enlarged during cataract surgery using in-tracameral atropine and adrenaline, multiplesphincterotomies, pupil-stretching techniquesor mechanical iris retractors. A generous anteri-or capsulotomy and complete cortical cleanupwill enhance the view of the peripheral retinapostoperatively. Anterior capsular phimosis ismore common in diabetic patients, thereforethe capsulorrhexis size should be larger thannormal but smaller than IOL optic diameter

to prevent posterior capsular opacification. Alarge diameter optic (i.e. 6.0 mm or larger) willfacilitate diagnosis and treatment of peripheralretinal pathology postoperatively.55

The surgeon's skill affects surgical time,decreases the chance of intraoperative compli-cations and is associated with less postopera-tive inflammation. Longer and complicatedcataract surgery is associated with a greater riskof progression of retinopathy and subsequentvisual compromise.56 It is prudent to makeevery effort to minimize surgical trauma in

diabetic eyes.Altug et al57 showed that photic retino-

pathy during cataract surgery was more pre-valent in diabetic patients than non-diabetics.They suggested that diabetic patients may bemore vulnerable to photic injury and surgeonsshould take necessary precautions.

INTRAOCULAR LENS CHOICELarge diameter IOLs are required to facilitate

visualization and treatment of the peripheralretina. A 6.5-mm IOL, for example, provides39.7% larger optical area than a 5.5-mm IOL,this difference may be crucial for optimalmanagement of diabetic retinopathy.

Posterior capsular opacification (PCO) is amajor concern following cataract extraction.Diabetic patients seem to develop more severePCO than non-diabetic patients.58 PCO may berelated to the shape of the optic edge; a square-edge design seems to inhibit lens epithelial cellproliferation and may therefore prevent PCOformation.59

Three common materials used for manu-

facture of foldable IOLs are silicone, hydro-phobic acrylic and hydrophilic acrylic. Severalstudies have evaluated the biocompatibility ofthese materials in diabetic patients. One studycompared the rate of PCO with hydrophobicacrylic and plate-haptic silicone IOLs in dia-betic patients; although hydrophobic acrylicIOLs were associated with more anteriorchamber flare in the early postoperative period,PCO developed less frequently. Hydrophobicacrylic lenses have the lowest propensity to

silicone oil adhesion and may be the IOL ofchoice in diabetic patients anticipating vitreo-retinal surgery. Silicone IOLs can develop con-densations during pars plana vitrectomy andthus may be relatively contraindicated in suchindividuals.60

The level of phosphorus in the serum andaqueous humor of diabetic patients, parti-cularly those with proliferative diabetic retino-pathy, is significantly higher than normal indi-viduals, which may lead opacification of hydro-philic acrylic IOLs. There are increasing reports

of progressive calcific opacification of hydro-philic acrylic IOLs in diabetic patients.61,62

Rodriguez-Galietero et al63 evaluated chan-ges in contrast sensitivity and color discri-mination in diabetic patients who had cataractsurgery and implantation of a blue-light fil-tering IOL compared with an ultraviolet-onlyfiltering IOL. Their results suggested blue-lightfiltering IOLs did not cause chromatic discri-mination defects and even improved colorvision in the blue-yellow chromatic axis. The


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use of multifocal and accommodative IOLs indiabetics remains controversial.

INTRAOCULAR LENS IMPLANTATION SITEConcerns have arisen regarding the use of an-terior chamber angle-fixated lenses and sulcus-fixated posterior chamber IOLs in diabeticpatients. Anterior chamber IOLs including iris-claw lenses should generally not be used inpatients with diabetes who are at an increasedrisk for iris neovascularization. Most studiessuggest that the safest procedure for diabetics iscontrolled extracapsular surgery with careful

cleaning of cortical material and in-the-bagimplantation of a posterior chamber IOL. Theposterior chamber lens will act as a barrier tothe anterior movement of vitreous in the eventof posterior capsulotomy.47,54

VISUAL PROGNOSIS FOLLOWINGCATARACT SURGERYRecent studies on cataract surgery in diabeticstend to report a lower incidence of compli-

cations and better visual outcomes.64,65

Thistrend of improvement may be due to betterpreoperative management of retinopathy,66evolutions in operative techniques and app-reciation of the importance of systemic factorssuch as glycemic and hypertensive control.

In general, the visual prognosis followingcataract surgery in diabetic patients is favor-able. Diabetic patients with little or no retino-pathy enjoy the same good prognosis as indi-viduals without diabetes.67 However, in thepresence of significant diabetic retinopathy,

postoperative VA may be suboptimal and theresults of surgery may be disappointing. Pre-sence of CSME and poor preoperative visualacuity (reflecting diabetic maculopathy, ische-mia and traction) have been recognized as riskfactors for poor postoperative visual acuityfollowing cataract surgery.68

Previous reports have focused primarily onVA and less attention has been given to theeffect of surgery on quality of life in termsof vision-dependent activities or satisfaction

with outcomes of surgery. Mozaffarieh et al69in a prospective study evaluated patientswith different stages of diabetic retinopathy.Patients were assessed using the VF-14 (VisualFunction-14) questionnaire. Their study sugges-ted that patients with more advanced diabeticretinopathy may show no functional improve-ment despite apparent improvement in VA.This emphasizes the importance of patient edu-cation prior to surgery.

INDICATORS OF POOR VISUAL OUTCOMESFOLLOWING CATARACT SURGERYSeveral variables have been associated withpoor visual outcomes following cataract sur-gery in diabetic patients. According to the EarlyTreatment of Diabetic Retinopathy Study(ETDRS), the presence of CSME at the time ofcataract surgery is significantly associated withpoor postoperative visual acuity and a pre-dictor of final VA worse than 20/200. Theseverity of diabetic retinopathy at the time ofcataract surgery is also a significant deter-minant of postoperative visual acuity: more

severe retinopathy seems to be associated withan increased prevalence of macular ischemia, oras natural history studies suggest, reducedtendency for spontaneous resolution of post-operative macular edema. Analysis of deter-minants of postoperative visual acuity in theETDRS also identified poor preoperative visualacuity as a risk factor for poor postoperativeoutcome. Macular ischemia, edema and trac-tion seem to be probable causes for the latterfinding.

COMBINED CATARACT SURGERY ANDVITRECTOMYAdvances in vitreoretinal and cataract surgicaltechniques have led to several studies oncombining cataract and vitrectomy surgery indiabetic patients. Diabetic patients undergoingvitrectomy often have coexisting cataracts, onthe other hand lens opacities often progressfollowing vitrectomy. Combined surgery hasbeen shown to be safe, effective and com-


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parable to sequential surgery in terms of finalvisual outcomes. Careful patient selection andcombining the two procedures can offer morerapid visual rehabilitation, avoid a secondoperation and simplify surgical interventions inpatients who are likely to require multiple pro-cedures.70-72 Several studies have suggestedthat the vitreoretinal interface is a contributingfactor in the development of persistent CSMEfollowing laser photocoagulation and havedemonstrated significant anatomic and visualimprovement with combined surgery whenindicated.73-75

Patient selection is crucial for a successful

outcome following combined procedures. Pa-tients over 60 years of age are more likely tohave progressive lens opacification followingvitrectomy. Combined surgery may be reco-mmended for patients with cataracts preclu-ding membrane dissection or those with pre-existing cataracts who are likely to suffer fromvisual loss due to cataract progression in thenext two years. Patients with severe tractionand ischemia and those with active rubeosis areless suitable candidates and younger patients

with little preoperative lens opacity may bebetter managed without lens extraction.71

CATARACT SURGERY AND INTRAVITREALINJECTIONSCataract surgery provides the ideal setting foradministration of intravitreal medications in asterile surgical field allowing for control of IOP.Experience with intravitreal steroids has de-monstrated their efficacy in reducing macularedema as measured by optical coherence tomo-

graphy (OCT). Intravitreal steroids may be con-sidered during cataract surgery in eyes withCSME but no epiretinal membrane or tractionalcomponent particularly if the patient has notbeen treated or if a favorable response has beenobtained previously.76,77 Intravitreal injectionsof bevacizumab (Avastin) have been employedfor the treatment of neovascular and exudativeocular diseases since 2005. Since then, severalstudies have evaluated its effect on neovascularcomplications of diabetes,50,51,78,79 however its

use during cataract surgery has been notevaluated and could be the subject of futurestudies.

POSTOPERATIVE CONSIDERATIONSAll patients diagnosed with nonproliferativediabetic retinopathy should undergo a detailedretinal examination within three months ofcataract extraction. Patients with proliferativeretinopathy or those with inadequate view ofthe retina prior to cataract extraction should beevaluated closely after surgery for monitoring

retinal status.10NVI is the most dreaded anterior segment

complication in diabetic subjects following ca-taract surgery. The incidence has been reducedwith modern cataract surgery which is lesstraumatic and leaves the posterior capsule in-tact. In addition to PRP, intravitreal injectionsof bevacizumab have been reported to controlNVI but the effect has been short-lived.50,51,78,79

Other anterior segment complicationswhich occur more frequently in diabetic sub-

jects are posterior synechiae, pupillary block,pigmented precipitates on the IOL and severeiritis.80 The incidence of fibrin reaction is highand reported in up to 13.7% of diabeticpatients.81 Although not definitely confirmed,diabetes may be a risk factor for postoperativeendophthalmitis and is associated with a poorvisual prognosis following the development ofendophthalmitis.82

Corneal complications may occur spon-taneously but more often follow excessivesurgical manipulations. Diabetic patients are

prone to corneal epithelial defects and per-sistent erosions due to impaired corneal sen-sation, these occur more frequently with in-creasing patient age and duration of diabetes.83Wavelike epitheliopathy following phaco-emulsification reflecting neurotrophic cornealdamage has also been reported.84

Numerous measures for promoting cornealepithelial healing have been explored. Discon-tinuing topical medications may be adequateto heal the epithelial defect because many pre-


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parations contain toxic preservatives. Patientsshould be treated with frequent lubricatingdrops and ointments, goggles and closure ofthe eyelid by patching, or by temporary or per-manent tarsorrhaphy. Another effective treat-ment for persistent epithelial defects is thera-peutic soft contact lens fitting but the majordrawback is the increased risk of infectious cor-neal ulceration.85 Newer therapeutic options in-clude: fibronectin,86 growth factors (includingepidermal growth factor, substance P and in-sulin-like growth factor-1),87,88 plasminogenactivator/plasmin89 and amniotic membranetransplantation.90 In a randomized study, topi-

cal application of insulin (4 times daily for 7days) normalized the delayed corneal woundhealing in rats with diabetes mellitus.91

Eyes of patients with diabetes mellitusshow more severe corneal endothelial celldamage following cataract surgery and delayedrecovery of corneal edema.92 Lee et al93 com-pared corneal endothelial cell damage follow-ing phacoemulsification and intraocular lensimplantation in diabetic patients categorized bythe severity of diabetic retinopathy and normal

patients. Their findings revealed significantlygreater reduction in corneal endothelial celldensity and increased coefficient of variation incell size in patients with high risk PDR.

EFFECT OF CATARACT SURGERY ONRETINOPATHYNumerous studies have addressed whethercataract surgery influences diabetic retino-pathy. The progression of diabetic retinopathyafter intracapsular (ICCE) and extracapsular

(ECCE) cataract extraction is well documen-ted,94-97 however controversy surrounds theeffect of phacoemulsification. Some studieshave demonstrated a similar trend of prog-ression in diabetic retinopathy after phaco-emulsification surgery, while others reportedno significant change.49,98,99 These discrepanciesmay be attributed to the different criteria usedto define progression of diabetic retinopathy.Many authors believe cataract surgery actuallyinfluences diabetic retinopathy progression in

an independent fashion while others feel thatthe natural history of the condition per se ismore important than the effect of surgery.

In a retrospective study, Hauser et al100evaluated the occurrence and progression ofdiabetic retinopathy; their data suggested thatdiabetic retinopathy was associated with malesex, disease duration and poor glycemic con-trol. Progression of pre-existing diabetic retino-pathy was associated with poor blood sugarcontrol. This study is limited by its retros-pective nature, the relatively small number ofcases and not being able to differentiate thenatural course of the disease from the effect of

surgery.To differentiate the effect of cataract sur-

gery from the natural course of the disease,Dowler et al46 designed a prospective studyin which monocular surgery was performedand the fellow eyes served as controls. Theseauthors showed that uncomplicated phaco-emulsification cataract surgery does not acce-lerate progression of diabetic retinopathy.

In another prospective study by Squirrell etal,49 monocular phacoemulsification was per-

formed and the grade of diabetic retinopathyand diabetic maculopathy was assessed for 12months postoperatively in the operated andnon-operated fellow eye. This study also re-vealed that uncomplicated phacoemulsificationdoes not accelerate the course of diabeticretinopathy and any observed progressionprobably represents the natural course of thedisorder.

ETDRS report number 25 is one of the mostimportant studies on cataract surgery in dia-betes. It has a low rate of loss to follow-up,

well-documented BCVA measurements, accu-rate annual fundus photographs and well do-cumented interventions. This report suggests atrend towards accelerated retinopathy prog-ression in operated eyes compared to un-operated fellow eyes. However, this trend didnot reach statistical significance.45

The progression of diabetic retinopathy,particularly in studies evaluating ECCE andICCE, may be caused by breakdown of theblood ocular barrier or enhanced inflammation


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in diabetic patients after cataract extraction.The smaller incision size and shorter surgicaltime in phacoemulsification decrease inflam-mation and may induce less breakdown of theblood ocular barrier. The lack of clinicallysignificant effects in certain studies does notrule out any adverse effect from surgery. Oneday after uneventful phacoemulsification andIOL implantation VEGF, hepatocyte growthfactor, interleukin-1 and pigment epithelium-derived factor concentrations increase but takeone month to decline to preoperative levels.These results confirm altered concentrations ofangiogenic and growth factors after cataract

surgery, which may induce subclinical or evenclinical worsening of diabetic retinopathy andmaculopathy.101

EFFECT OF CATARACT SURGERY ONMACULAR EDEMAAltered concentrations of angiogenic factorsafter cataract surgery may aggravate maculo-pathy.101 Following uneventful cataract sur-gery, OCT imaging has revealed increased re-

tinal thickness in diabetic eyes without retino-pathy which was comparable to nondiabetics,however there was a trend toward more in-crease in retinal thickness in diabetics whichwas evident up to 3 months after surgery.102

In eyes without CSME at the time of sur-gery, either because the condition had not de-veloped or was successfully treated, ETDRSreport number 25 showed no statistically signi-ficant difference in the prevalence of macularedema before and one year after surgery.45Another study reported a 56% incidence of new

clinically detectable macular edema one yearafter surgery but spontaneous resolution occu-rred without treatment in 50% by six months,and in 75% by one year after surgery.46 Otherdata showed that, although macular edema iscommon after cataract surgery it may followa benign course and in many patients thedevelopment of clinically significant macularedema postoperatively probably representsprogression in the natural course of the diseaserather than a direct effect of surgery.49

Eyes with established CSME at the time ofsurgery behaved quite differently, none resol-ved spontaneously within a year and the ma-jority showed clinical and angiographic evi-dence of deterioration. Overall, CSME presentin diabetic eyes at the time of cataract surgery isunlikely to resolve spontaneously. It seems po-ssible that case reports of severe macularedema after cataract surgery describe post-operative deterioration of pre-existing macularedema which was untreated because of the lensopacity.45

Studies on diabetic macular edema aftercataract surgery are difficult to perform be-

cause they must be able to differentiate diabeticmacular edema from pseudophakic cystoidmacular edema (Irvine-Gass syndrome). Fluor-escein angiography may help make the distinc-tion; if angiography shows a petaloid patternassociated with optic disc hyperfluorescencewithout retinopathy or microaneurysms, onemay consider the edema to be the result ofIrvine-Gass syndrome. However, some authorsdo not agree that optic disc hyperfluorescencenecessarily indicates the presence of pseudo-

phakic macular edema.45,103

Postoperative laser photocoagulation fordiabetic macular edema is controversial.Pollack et al104 performed the first prospectivecontrolled trial to evaluate the natural course ofdiabetic macular edema after cataract surgery.They found that only a minority of patientswho developed macular edema required focallaser photocoagulation. Similarly, Dowler etal46 reported that macular edema resolvesspontaneously if it arises after surgery but notwhen it is present prior to surgery, suggesting

that early laser treatment of all cases ofpostoperative diabetic macular edema isunnecessary. In general, specialists do notperform argon laser treatment until 6 monthsafter cataract surgery.

POSTERIOR CAPSULE OPACIFICATIONPosterior capsule opacification (PCO) remains acommon complication of modern cataract sur-gery with a reported rate of 20 to 50% five years


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after surgery. Modifications in surgical tech-nique and improvements in IOL technologyhave reduced the rate of PCO.55,105 Lens epi-thelial cells (LECs) are the source and cause ofPCO; the proliferation of these cells is affectedby several factors including optic edge design,optic-haptic junction and IOL material.

Another important determinant is post-operative inflammation. The degree of post-operative inflammation may be related to thedevelopment of PCO. It has been suggestedthat surgical trauma and contact with the IOLstimulate residual LECs to produce cytokines.These cytokines may affect LECs in an auto-

crine or paracrine fashion and induce collagenproduction and fibrous metaplasia.106 Eyes ofdiabetic patients already have incompetentblood-aqueous barrier function and are predis-posed to postoperative inflammation. Althoughmany surgeons believe that PCO is morecommon and severe in diabetic patients, thematter still remains controversial. Using retro-illumination images, Zaczek and Zetterstrom107demonstrated less PCO in diabetic patientsthan in nondiabetic controls.

New diagnostic systems have facilitatedthe evaluation of PCO. Hayashi et al108 quan-titatively measured PCO density using anScheimpflug slit-image analysis system andfound no significant difference between dia-betic and non-diabetic patients up to 12 monthsafter cataract surgery. However, at 18 monthsand later, PCO increased significantly in thediabetic group. Their results also demonstratedthat diabetic patients were significantly morelikely to require laser capsulotomy than con-trols. Ebihara at al58 using the POCO system (a

software for semiobjective assessment of PCO)also found that diabetic patients had signifi-cantly more severe PCO after cataract surgerythan non-diabetic patients. Another study re-ported anterior capsular contraction to be morecommon in diabetic patients, especially thosewith diabetic retinopathy.109

CONCLUSIONThe number of people with diabetes mellitus is

increasing exponentially. Diabetics have notalways shared the same favorable outcomesafter cataract surgery as their nondiabetic coun-terparts. New surgical and pharmacologic the-rapies may now allow for safer and more effect-tive surgery in diabetic individuals. Specialattention to systemic and ocular conditions isneeded.

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