Topical nepafenac for prevention of post-cataract surgery macular edema in diabetic patients: patient selection and perspectives

Abstract

Since its first description, the prevention of pseudophakic cystoid macular edema (PCME) continues to pose challenges for ophthalmologists. Recent evidence suggests that prophylaxis is unnecessary in patients without risk factors. Diabetes mellitus is generally considered as a risk factor for the development of PCME after cataract surgery since it causes breakdown of the blood–retinal barrier. Diabetic retinopathy (DR) increases the risk even further. Therefore, prophylactic nonsteroidal anti-inflammatory drugs (NSAIDs) should be considered in diabetic patients, especially if they have DR. NSAIDs block the cyclooxygenase enzymes responsible for prostaglandin production and reduce the incidence of PCME after cataract surgery. Nepafenac seems superior to other NSAIDs in terms of ocular penetration allowing higher and sustained therapeutic levels in retina and choroid. Topical steroids are less effective and may cause intraocular pressure increase limiting their long-term use. Nepafenac is cost effective, when the burden of PCME prevention is compared with the burden of treatment. Prevention is much cheaper and less harmful than invasive treatments like periocular or intravitreal injections. Overall, both nepafenac 0.1% and nepafenac 0.3% are well tolerated. They should be used carefully in patients with compromised corneas such as those with severe dry eye or penetrating grafts. If otherwise healthy cataract patients have ≥2 risk factors, like PCME in the other eye or posterior capsule rupture during surgery, treatment should be considered. Once-daily nepafenac 0.3% dosing may improve postoperative outcomes through increased patient compliance and may reduce treatment burden further. Every patient should be assessed in terms of risks/benefits of the treatment, in individual basis, before cataract surgery.

Progression of macular oedema following cataract surgery in a diabetic patient

“…Osim prostaglandina za koje se smatra da imaju vodeću ulogu, važni su i ostali medijatori, kao vaskuarni endotelni faktor rasta (VEGF, engl. vascular endothelial growth factor) i različiti proupalni citokini 8,9 . Pacijenti s dijabetičkom retinopatijom imaju prisutnu subkliničku okularnu upalnu reakciju u prednjoj sobici i vitreusu, što se može dodatno pogoršati nakon operacije katarakte u vidu razvoja novog ili pogoršanja postojećeg makularnog edema 9 .…”

“…cystoid macular edema) nakon operacije katarakte je dobro poznat uzrok slabije vidne oštrine postoperativno s incidencijom 1.17 % u operacija bez komplikacija kod zdrave populacije. Simptomi se obično povuku nakon 3 do 12 mjeseci, iako ponekad može zaostati permanentno oštećenje vida 9 . CME postoperativno nastaje radi nakupljanja tekućine između vanjskog plexiformnog i unutarnjeg nuklearnog sloja retine.…”

“…Kod DME-a imamo visok omjer debljine vanjskog nuklearnog i unutarnjeg nuklearnog sloja parafoveolarno, prisutnost mikroaneurizmi, tvrdih eksudata, cisti retinalnog živčanog sloja vlakana, nedostatak subretinalne tekućine i disrupciju fotoreceptora. Također, većina očiju s DME-om ima sačuvanu fovealnu depresiju 9 .…”

“…Kod svih pacijenata sa šećernom bolesti kao profilaksu za razvoj CME-a prije operacije katarakte trebali bi se dati topički nesteroidni antireumatici (NSAID, engl. Non-steroidal anti-inflammatory drugs) 9 . Učinkovitost NSAID-a kao profilakse postoperativnog makularnog edema kod dijabetičke retinopatije pokazale su dvije randomizirane, dvostruko maskirane studije kod kojih su samo 4.1 % očiju s DR-om koje su tretirane preoperativno NSAID-om razvile CME unutar 90 dana nakon operacije uspoređujući sa 16.1 % kontrolnih očiju koje nisu bile tretirane s NSAID-om.…”

“…advanced glycation end products) te povećana koncentracija proupalnih citokina IL-6, IL-8 i IL-12 (IL, engl. Interleukin) 9 . Multicentrična studija koja je uključivala 19 centara demonstrirala je da je rizik za razvoj DME-a povezan s preoperativnom težinom retinopatije i to 1.0 % kod dijabetičara bez DR-a, 5.4 % kod blagog neproliferativnog DR-a, 10.00 % kod srednjeg neproliferativnog DR-a, 13.1 % kod teškog neproliferativnog DR-a i 14.9 % kod proliferativnog DR-a 2 .…”