Current medical and surgical therapeutic approaches to cystoid macular edema in uveitis

Abstract

Cystoid macular edema (CME), a frequent complication of uveitis, is defined as central retinal thickening caused by accumulation of intra-retinal fluid in the outer plexiform and inner nuclear layers of the retina. Chronic retinal edema can lead to vision loss secondary to photoreceptor impairment and retinal pigment epithelium dysfunction. Patients suffering from CME often complain of decrease in visual acuity, contrast sensitivity and difficulty performing near tasks such as reading. The pathophysiology of CME revolves around disruption of the blood-retinal barrier due to release of pro-inflammatory mediators and/or Muller-cell dysfunction. Imaging modalities have advanced in recent years allowing earlier detection and better management of uveitic CME. Though often managed medically, when CME is refractory to anti-inflammatory therapy such as corticosteroids and/or immunomodulators, underlying mechanical causes such as vitreo-macular traction and internal limiting membrane gliosis must be considered as causes of CME formation. In such cases, Pars-plana vitrectomy with internal limiting membrane peel may be undertaken. New intraoperative imaging modalities, such as intraoperative optical coherence tomography, carry the promise of better and more accurate surgical manipulations.

Keywords:

• corticosteroids
• cystoid macular edema
• immunosuppressive therapy
• internal limiting membrane stripping
• intraoperative OCT
• intra-vitreal triamcinolone acetonide
• pars plana vitrectomy
• vitreo-macular traction

Financial & competing interests disclosure

This study is supported in part by an unrestricted institutional grant from Research to Prevent Blindness. S Schaal serves on the Allergan advisory board. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Key issues

• Cystoid macular edema (CME) is defined as central retinal thickening caused by cystic accumulation of intra-retinal fluid in the outer plexiform layer and inner nuclear layers of the retina secondary to release of inflammatory mediators or mechanical factors.

• Medical management of CME primarily involves controlling intraocular inflammation through the use of corticosteroids and immunomodulatory therapy.

• The posterior hyaloid/internal limiting membrane plays an important role in uveitic cystoid macular edema that is unresponsive to medical management. The taut posterior hyaloid causing vitreo-macular traction and gliosis of the internal limiting membrane are mechanical forces possibly contributing to the persistence of CME.

• Patients who present with persistent CME and decreased ) visual acuity despite the resolution of inflammation and medical attempts to resolve the CME are candidates for Pars-plana vitrectomy with stripping of the residual posterior hyaloid and/or internal limiting membrane.

• Preoperative examination with Optical Coherence Tomography (OCT) (either TD-OCT or SD-OCT) cannot exclude the presence of tangential traction from an adherent residual posterior hyaloid.

• Intraoperative OCT can provide high-resolution visualization of any residual membranes and help identify whether the traction has been relieved.