Cystoid Macular Edema

Cystoid macular edema (CME), also known as Irvine-Gass syndrome, is a common cause of decreased vision after cataract surgery. Although the exact pathogenesis of CME is unknown, the final common pathway appears to be increased perifoveal capillary permeability with accumulation of fluid in the inner nuclear and outer plexiform layers. CME is often associated with intraocular inflammation and may be mediated through the release of prostaglandins and leukotrienes.

Figure 11-19 Cystoid macular edema (CME). A, Fluorescein angiogram demonstrates late pooling of dye in a petaloid pattern in the macula and staining of the optic nerve head. B, Spectral-domain optical coherence tomography scan shows diffuse retinal thickening with cystic areas of low reflectivity predominantly in the inner nuclear and outer plexiform layers.

(Courtesy of Thomas L. Beardsley, MD.)

CME may be recognized by an otherwise unexplained reduction in vision, by the characteristic petaloid appearance of cystic spaces in the macula on ophthalmoscopy or fluorescein angiography (Fig 11-19A), or by cystic areas of low reflectivity and retinal thickening on OCT (Fig 11-19B). Most affected patients are asymptomatic, although there may be some loss of contrast sensitivity even in the absence of reduced Snellen visual acuity. In addition, patients with angiographic CME after phacoemulsification score substantially lower in logMAR (logarithm of the minimum angle of resolution) visual acuity than do patients with no CME, even though their Snellen visual acuities remain better than 20/40. Table 11-4 summarizes the incidence of CME according to the type of cataract surgery and the basis of diagnosis of CME.

The incidence of both angiographic and clinical CME peaks 6–10 weeks after surgery. Spontaneous resolution occurs in approximately 95% of uncomplicated cases, usually within 3–12 months. In rare cases, CME may develop many years after surgery, especially in association with delayed postoperative rupture of the anterior vitreous face. CME has also been associated with the use of topical epinephrine and dipivefrin for the treatment of aphakic glaucoma. Prostaglandin analogues have been associated with reversible CME in eyes that have undergone recent intraocular surgery, although a causal relationship has not been established. The risk is believed to be greater in the absence of an intact posterior capsule. Table 11-5 lists risk factors for CME.

The risk of early postoperative CME is reduced with prophylactic postoperative use of topical corticosteroids and NSAID drops. An American Academy of Ophthalmology report found that topical NSAIDs after cataract surgery were effective in reducing the incidence of CME and hastened postoperative visual recovery in the short term. However, level 1 evidence that NSAID therapy prevents vision loss from CME at 3 months or longer after cataract surgery is lacking.

Table 11-4 Incidence of CME According to Basis of CME Diagnosis and Type of Surgery

Table 11-5 Risk Factors for Cystoid Macular Edema

Medical treatment of chronic postoperative CME typically begins with a course of anti-inflammatory drugs such as topical corticosteroids and/or NSAIDs. A prospective randomized clinical trial of chronic CME found that combination therapy with ketorolac 0.5% and prednisolone acetate 1.0% 4 times a day was more effective than either drug alone in improving visual acuity. Topical anti-inflammatory therapy may take 3–6 months to resolve chronic CME, and the condition may recur after cessation of therapy. Sub-Tenon steroid injection or intravitreal injections of corticosteroids alone or via a sustained drug-delivery system may be effective. In refractory cases, systemic carbonic anhydrase inhibitors may be beneficial. Intravitreal vascular endothelial growth factor inhibitors have been successful in chronic CME cases that do not respond to conventional treatment.

When the inciting source of chronic CME can be defined and the edema fails to respond to medical therapy, surgical therapy may be indicated. Any retained lens fragments should be removed. Nd:YAG laser vitreolysis or vitrectomy can be used to remove vitreous adhering to the cataract incision and relieve iris deformity or vitreomacular traction. If the IOL is malpositioned and contributing to chronic uveitis, repositioning or exchange may be helpful. For further discussion of CME, see BCSC Section 12, Retina and Vitreous.

• Kim SJ, Schoenberger SD, Thorne JE, Ehlers JP, Yeh S, Bakri SJ. Topical nonsteroidal anti-inflammatory drugs and cataract surgery: a report by the American Academy of Ophthalmology. Ophthalmology. 2015;122(11):2159–2168.

• Wielders LHP, Schouten JSAG, Winkens B, et al; ESCRS PREMED Study Group. Randomized controlled European multicenter trial on the prevention of cystoid macular edema after cataract surgery in diabetics: ESCRS PREMED Study Report 2. J Cataract Refract Surg. 2018;44(7):836–847.

Excerpted from BCSC 2020-2021 series: Section 11 - Lens and Cataract. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.