19 Cystoid Macular Edema and Management

Cystoid macular edema (CME) following cataract surgery was initially reported by Irvine in 1953 and is known as the Irvine–Gass syndrome.1,2 CME is one of the most common causes of unexpected decreased visual acuity after ophthalmic surgery. Despite recent advances in cataract surgery technique and instrumentation, pseudophakic cystoid macular edema (PCME) occurs most frequently after cataract surgery even after uncomplicated surgery ( Fig. 19.1).³ The incidence of PCME in different cataract extraction techniques in uncomplicated cataract operations are as follows: after intracapsular cataract extraction 8%, after extracapsular cataract extraction 0.8 to 20%, after phacoemulsification 0.1 to 2.35%, and after femtosecond-assisted cataract surgery 1.18%.³ CME exhibits dilation of normal retinal capillaries around the fovea, with consequent fluid leakage and microcystoid formation.

19.2 Histology

CME consists of a localized expansion of the retinal intracellular and/or extracellular space in the macular area. This predilection to the macular region is probably associated with the loose binding of inner connecting fibers in Henle’s layer, allowing accumulation of fluid leaking from perifoveal capillaries ( Fig. 19.2).⁴ Recently, Antcliff et al⁵ concluded that the inner and outer plexiform layers constitute high-resistance barriers to fluid flow through the retina, which accounts for the characteristic distribution of CME. In CME associated with cataract extraction, the cysts were most prominent in the inner nuclear layer and less prominent in the outer plexiform layer.

Fig. 19.1 (a) Photography of the anterior segment after uneventful cataract surgery showing a multifocal intraocular lens in the posterior chamber. (b) Fluorescein angiography shows pseudophakic cystoid macular edema.

Fig. 19.2 Histology of pseudophakic cystoid macular edema showing cystic spaces in the outer plexiform layer (black arrows). Retinal detachment is an artifact. (These images are provided courtesy of Dr. Deepak Edward.)

Several theories exist regarding the pathogenesis of CME.6,7 The theories involve changes in the perifoveal retina where the vascular permeability of the retinal capillaries is altered, leading to leakage of plasma into the central retina, which causes it to thicken because of excess interstitial fluid. The excess interstitial fluid is likely to disrupt ion fluxes, and the thickening of the macula results in stretching and distortion of neurons. There is reversible reduction in visual acuity, but over time the perturbed neurons die, which results in permanent visual loss ( Fig. 19.3).^{8,9,10,11,12,13}

Cataract surgery in diabetic patients may result in a dramatic acceleration of preexisting diabetic macular edema leading to poor functional visual outcome ( Fig. 19.4). This can be prevented provided the severity of the retinopathy is recognized preoperatively and treated appropriately with prompt laser photocoagulation either before surgery, if there is adequate fundal view, or shortly afterward.

Fig. 19.3 Inflammatory hypothesis on the pathogenesis of pseudophakic cystoid macular edema. (Adapted from Miyake K, Ibaraki N. Prostaglandins and cystoid macular edema. Surv Ophthalmol 2002;47 (suppl 1):S203–S218)

Fig. 19.4 (a) Photograph of the anterior segment after uneventful phacoemulsification cataract surgery showing anterior chamber fibrin in a patient with diabetes. (b) Photograph of the anterior segment post-treatment with tissue plasminogen activator in the anterior chamber showing disappearance of the fibrin. (c) Fluorescein angiography after cataract surgery showing macular edema and proliferative diabetic retinopathy.

Approximately 20% of the patients who undergo uncomplicated phacoemulsification or extracapsular extraction develop angiographically proven CME. However, a clinically significant decrease in visual acuity is seen only in about 1% of these eyes. Spontaneous resolution of the CME with subsequent visual improvement may occur within 3 to 12 months in 80% of the patients. Chronic CME is defined as a persistent decline in visual acuity for more than 6 months. Interestingly, complicated cataract extraction is associated with an increased risk for clinically significant CME, such as disruption of the anterior vitreous hyaloid ( Fig. 19.5), vitreous loss, retention of lens cortex, vitreous strands to the wound ( Fig. 19.6), dislocated intraocular lens (IOL), inadequate wound closure, and chronic inflammation¹⁴ and in patients with significant postoperative inflammation.

19.4 Clinical Presentation

PCME should be suspected when a patient without underlying risk factors complains of decreased vision or metamorphopsia following cataract extraction. Clinically, intraretinal edema contained in cystlike spaces in a honeycomb pattern around the fovea can be seen. Diagnosis is based on the clinical findings and characteristic appearance on fundus fluorescein angiography and optical coherence tomography (OCT).

The fluorescein angiography pattern is characteristic. Early phases of fluorescein angiography demonstrate dye leakage from the parafoveal retinal capillaries, and later phases of the angiogram demonstrate the petaloid pattern of leakage into the parafoveal intraretinal spaces along with optic disc hyperfluorescence ( Fig. 19.7).

OCT is a sensitive noninvasive tool that can clearly demonstrate these cystoid spaces as well as calculate central macular thickness and total macular volume. Spectral-domain OCT (SD-OCT) can show an increased thickness of the fovea and presence of large cystoid spaces in the outer plexiform layer with stretching of the Müller cell processes. OCT can also show increased thickness of the outer nuclear layer. Photoreceptor layer (as represented by inner segment–outer segment line [IS-OS line]) can be intact and the continuity of the external limiting membrane (ELM) can be maintained ( Fig. 19.8). Choroidal thickness is increased and decreases following edema resolution. These findings may strengthen the hypothesis of an inflammatory pathogenesis in PCME. Optical coherence tomography angiography (OCT-A) shows capillary changes in PCME; the deep capillary plexus is mainly altered and disorganized with a significant decrease of capillary density in the acute phase of PCME. After macular edema resolution, the pattern of deep capillary plexus recovers and the capillary density returns to normal.

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