Clinical CME peaks at approximately 4 to 6 weeks postoperatively and has been defined as the presence of postoperative macular edema reducing visual acuity to 20/40 or worse or to two lines below the expected visual outcome.16 However, as stated previously, with increased patient expectations, smaller reductions of visual acuity should be considered clinically significant, as long as the patient is symptomatic and edema can be demonstrated. Angiographic edema, by definition, requires fluorescein angiography for diagnosis, but with the ubiquitous use of noninvasive OCT analysis, the definition is expanded to include presence of demonstrable macular edema in an asymptomatic patient not discernible by biomicroscopy. This could be referred to as nonclinically significant macular edema, although tests, such as contrast sensitivity or reading vision, may detect subtle abnormalities in these patients.

Cystoid macular edema represents the leakage of intravascular fluid from perifoveal vessels, causing an expansion of the outer retina at the level of the outer plexiform and inner nuclear layers of the retina. These retinal changes, if subtle, are easily identified by loss of the foveal light reflex on slit lamp exam with a noncontact, high magnification handheld lens. When the edema is more pronounced, thickening of the central macula can be observed, especially when a handheld fundus contact lens is used during biomicroscopy. Chronic CME can result in hyperpigmentation of the Retinal pigment epithelium (RPE) layer and can mimic RPE changes caused by nonexudative Age-related macular degeneration (AMD). It may be distinguished by the lack of associated drusen. However, when underlying nonexudative AMD is present, the diagnosis is more difficult to differentiate. The vitreoretinal interface should also be inspected carefully for the presence of an epiretinal membrane, presenting as a grayish, sometimes glistening membrane that can distort or partially obscure the retinal vasculature.

Fluorescein angiography has been the longstanding gold standard in the diagnosis of CME. In the early phase of the angiogram, dilation of the perifoveal capillaries can be seen, which manifest as small, punctate hyperfluorescent lesions, followed by pooling of fluorescein dye into the perifoveal cystoid spaces in a distinct petaloid pattern (Fig. 5A.2). Late phases of the angiogram typically show leakage from the optic disc, which can be helpful in distinguishing pseudophakic CME from other causes of CME such as subfoveal occult choroidal neovascular membranes in patients with exudative AMD, or leakage secondary to diabetic retinopathy or epiretinal membranes.

OCT has become widely adopted and allows convenient monitoring of disease activity. It is characterized by loss of the foveal depression, retinal thickening, and cystic hyporeflective lesions, and may show a small amount of subretinal fluid (Fig. 5A.3). It has the advantage of yielding a quantitative measurement of central foveal thickness and macular volume that can be followed over time to determine whether the edema is resolving. If subretinal fluid is the major component with little or no intraretinal cysts, other diagnoses, such as central serous chorioretinopathy or exudative AMD, should be considered. OCT is also extremely helpful in demonstrating subtle epiretinal membranes or vitreomacular traction. However, despite OCT’s superior sensitivity and convenience, fluorescein angiography remains the gold standard because it can rule out other causes of CME.

While the incidence of CME in healthy patients after uncomplicated cataract surgery is low, systemic disease, preoperative eye drops, and surgical complications can increase the risk for developing visually significant edema in the postoperative period. Therefore, the presence of systemic diseases needs to be taken into consideration when the risks of cataract surgery are discussed with the patient. Diabetes, even in the absence of visible diabetic retinopathy, is a well-established risk factor for the development of CME,17, 18, 19 and 20 increasing the incidence from 1.73% to 3.05% in a large cost-analysis study of nearly 140,000 patients.12 The compromised retinal vasculature in diabetic patients with loss of pericytes as well as higher levels of inflammatory cytokines appears to be more sensitive to the trauma induced by cataract surgery. It may be difficult to distinguish pseudophakic CME from progression of diabetic macular edema (DME). A history of uveitis21, 22 as well as retinal vein occlusion (RVO)16 increases the risk of formation of postsurgical macular edema. A retrospective series of 108 eyes with various causes of uveitis demonstrated a 21% incidence of clinical CME, with 74% achieving final visual acuity of 20/40 or better.23 Systemic hypertension has been established as a risk factor for retinal vein occlusions and can therefore indirectly contribute to the risk for CME, but it may also directly increase the risk of postsurgical edema in the absence of venous-occlusive events.24 It is uncertain whether presence of drusen or prior CNV associated with AMD increases the risk for CME, but patients with AMD and postoperative CME present a diagnostic challenge. A careful exam with use of fluorescein angiography and OCT analysis is necessary to prevent misdiagnosis of progression to neovascular AMD as postsurgical CME and vice versa.

The preoperative presence of an epiretinal membrane increases the risk of postcataract CME,16, 25 but care has to be taken to separate cause and effect, as epiretinal membranes can cause macular edema in the absence of cataract surgery, and CME can lead to the formation or progression of epiretinal membranes. The only condition identified to date that appears to decrease the risk of CME is the presence of a complete Posterior vitreous detachment(PVD).26 It is possible that the absence of vitreomacular traction transmitted through the posterior hyaloid is protective of the perifoveal zone during and after cataract surgery.

Use of preoperative eye drops can increase the risk of postoperative edema, and patients need to be counseled about possible substitution of drops in the perioperative period. Prostaglandin analogs used as ocular antihypertensive drops are known to increase risk of CME27, 28, 29, 30 likely due to the proinflammatory properties, but even ocular antihypertensive beta blockers and preservatives in ocular medications such as benzalkonium chloride have been implicated as risk factors for CME.31 One randomized clinical trial of 80 patients demonstrated that glaucoma patients treated with prostaglandin analogs were more likely to develop angiographic CME compared with patients randomized to placebo (P = .03).32 If the patient cannot be safely switched to a different class of antihypertensives during the perioperative period, addition of preoperative topical NSAIDs should be considered.

The transition from extracapsular cataract extraction to phocoemulsification has greatly reduced the incidence of CME.33 However, surgical complications during phacoemulsification remain a major risk factor for development of macular edema. While ECCE procedures with rupture of the posterior capsule and vitreous loss result in CME in 31% of patients,34 similar complications in phacoemulsification lead to macular edema in 11% to 20% of cases.35, 36 Vitreous strands to the wound, abnormal pupil shape, retained lens fragments, and placement of anterior chamber intraocular lenses are all associated with increased rates of CME.36, 37, 38 and 39 While the current generation of open haptic anterior chamber intraocular lenses are less irritating and inflammatory compared to the older design of closed haptic lenses, placement of intraocular lenses anterior to the iris increases the risk of CME in comparison with a lens positioned in the capsule. Posterior secondary IOLs stabilized by scleral fixation40 or iris fixation appear to confer a smaller or no increased risk of CME in patients without sufficient capsular support. Surprisingly, prolonged surgical time in the context of cataract extractions performed by ophthalmology residents under the guidance of attending surgeons does not increase the risk of development of postoperative CME.16

Patients who develop visually significant posterior capsular opacification after successful cataract surgery and require Nd:YAG capsulotomy have a 1% to 2.5% risk of developing CME in the months following the procedure.41, 42 This risk appears not to be correlated with the amount of laser energy used, but may reflect the altered intraocular fluidics created by the discontinuity of the posterior capsule.41

As the definitions of clinical and angiographic edema indicate, not all patients with measurable postoperative macular edema are visually impacted.43 It is well established that the correlation between fluorescein leakage or OCT thickness and visual acuity is surprisingly poor. Cystoid edema in retinal layers not affecting the photoreceptors may be asymptomatic. Therefore, the visual acuity and subjective complaints of the patient need to be taken into consideration when diagnosing and treating cystoid macular edema. However, onset of CME typically occurs several weeks to several months after cataract surgery, allowing sufficient time for postsurgical recovery of the anterior segment of the eye. The typical patient with postcataract macular edema will complain of decreased acuity after an initial period of clear vision. Some patients may notice central or paracentral metamorphopsia, whereas others report photosensitivity or a pink tint. Similar to patients with diabetic macular edema, reduction in contrast sensitivity may be the earliest symptom the patient experiences,44 which may not be picked up with the high contrast visual acuity measurements of projected Snellen charts.

The natural course of postsurgical CME is often prolonged, but generally favorable. In a study of 20 eyes, resolution of symptoms and apparent resolution of the macular edema were observed in 78% of cases within 1 year and in 94% within 2 years. In eyes with resolved macular edema, visual acuity returned to 20/40 or better.45 However, untreated, prolonged CME may not simply be annoying to the patient but can lead to irreparable damage of photoreceptors and RPE and permanent decrease of vision. In addition, in today’s age of increased expectations, there is a general unwillingness among both patients and surgeons to wait a prolonged period for visual recovery.