OD News Articles

1st April 2004

Cataract Post-op CME

by Douglas Hansen, OD Silverdale, WA

Inflammation after cataract surgery is the most common post-op finding. And sterile inflammation of the anterior segment with cystoid macular edema (CME) is the main reason for post-op acuity loss in pseudophakia—with or without intraoperative complications. As optometric physicians, we must be familiar with the prevention and treatment options.

Although post-op inflammation is usually benign, and the incidence of CME after cataract surgery is low and often resolves on its own, care must be taken to rule out endophthalmitis when signs of inflammation are out of the norm.

Even though the occurrence rate of CME is low, it is an important cause of persistent vision loss in cataract surgery patients because of the large number of surgeries performed each year.


The direct cause of CME is unknown but preexisting conditions such as epiretinal membranes and diabetic macular edema increase the risk. Intraoperative trauma from cataract surgery complications can also increase the incidence of CME by as much as 30%. These complications include:

  • loss of vitreous
  • pupillary capture
  • retained lens material
  • uveitis
  • posterior-capsule rupture
  • vitreous to the wound

Although the exact mechanism of CME is still in debate, breakdown in the blood-retinal barrier secondary to the inflammatory process is an important factor in fluid accumulation. Surgical trauma causes a release of inflammatory mediators—such as prostaglandins and leukotrienes—that are thought to increase perifoveal capillary permeability and serous leakage.


Conventional strategy for preventing CME is:

  1. use of topical steroids in the post-op period
  2. and periocular subconjunctival injection of steroid after surgery

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been used before surgery or in conjunction with steroids after surgery to reduce the incidence of uncomplicated CME. No large clinical study has shown dramatic results of improved visual acuity using NSAIDs alone or in combination with steroids. However, there have been many studies suggesting that NSAIDs are of some benefit in reducing the percentage of angiographic CME in post-op patients.

Evaluation and Diagnosis

When evaluating a case of presumed CME, a dilated exam should be performed to rule out capsular clouding and retinal disease or detachment. We should not presume that decreased vision after cataract surgery is caused by CME. A revealing study found that a significant number of patients being followed for CME actually had retinal detachment instead.1 Not surprisingly, the study showed that the best way to avoid misdiagnosis is by evaluating the retina with maximum mydriasis. Confrontation visual-field testing should also be performed.

Macular evaluation reveals thickening and sometimes a yellowish appearance with small parafoveal hemorrhages. The classic appearance is a cystic, honey-comb-like formation that is best seen stereoscopically with a thin slit-beam retroilluminating the central macula. Since CME is sometimes difficult to visualize, fluorescein angiography (FA) is helpful in obtaining a definitive diagnosis. In our clinics, we usually do not perform FA on non-diabetic post-op patients who have clinically visible CME. However, if there are macular degenerative changes present, along with persistence of the clinical picture, an FA is performed to rule out the presence of a subretinal neovascular membrane.

Treatment Options

The incidence of CME increases when surgery is complicated by posterior-capsule rupture—especially with vitreous loss and vitreous to the wound. In such cases, patients are generally considered for anterior vitrectomy or YAG laser vitreolysis. Well-defined vitreous strands associated with a peaked pupil are best treated with the laser. Patients are then treated with a 4 to 6 week regimen of topical steroids and topical NSAIDs. If CME develops or persists, steroidal injection, oral steroids, oral NSAIDs, or oral carbonic-anhydrase inhibitors are considered.

Topical steroids alone have been reported to be of benefit in acute cases of CME that are secondary to uncomplicated cataract surgery. In our clinics, we commonly use:

  • prednisolone acetate 1% q.i.d.
  • along with a topical NSAID q.i.d. for 2 to 4 weeks such as

~ suprofen—Profenal 1% (Alcon)
~ diclofenac sodium 0.1%—Voltaren Ophthalmic (Novartis)
~ flurbiprofen sodium 0.03%—Ocufen (Allergan)

Patients are reevaluated in 2 to 4 weeks. In nonresponsive cases, an intra-ocular steroidal injection, oral steroids, or oral NSAIDs are considered.

Clinical Pearls
  • CME is still the primary reason for post-op acuity loss.
  • Epiretinal membranes and diabetes are preexisting conditions that increase the risk of CME.
  • Patients with decreased vision after surgery should have a dilated exam to rule out capsular clouding, retinal detachment and CME.
  • CME is best seen stereoscopically at the slit-lamp with a noncontact or contact fundus lens.
  • Usually, cases of mild CME with no other surgical complications clear in time and with use of topical steroids and NSAIDs.

1 Lakhanpal V, Schocket SS: Pseudophakic and aphakic detachment mimicking cystoid macular edema. Ophthalmology. 1987; 94:785-791.

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