OD News Articles

1st July 2013

Managing Post-op CME

by Oliver Kuhn-Wilken, OD Tacoma, WA

Confident management of cystoid macular edema (CME), one of the more frequent complications of cataract surgery, can build tremendous trust with patients. Though the discovery of CME is concerning, treatment is fortunately straightforward and falls well within the scope of primary care optometry.


Cystoid macular edema (CME) is an inflammatory swelling, similar to a blister. It is not an actual disease, but a clinical finding (like drusen or infiltrates) and a common endpoint of many inflammatory pathologies.1,2

Edema is a frequent sequel to injury. In most tissues it is transient and does not generally become a serious or permanent problem. However, edema of the retina does not clear as quickly as elsewhere and can dramatically affect a patient’s vision. Chronic macular edema can even result in mild long-term color desaturation and degradation of contrast sensitivity despite normal recorded Snellen vision.

There are many causes of CME. The most common are:

  • retinal venous disease
  • epiretinal membrane
  • uncontrolled diabetes or hypertension
  • cataract surgery

CME following cataract surgery is often referred to as Irvine-Gass syndrome, in honor of the doctors who first identified it. Although post-op CME can occur following any cataract surgery, it is much more common after surgical complications, such as a tear in the posterior capsule, vitreous prolapse into the anterior chamber or vitreous incarceration into the wound. A patient who develops post-op CME in one eye has a 50% chance of developing it in the other eye. With modern cataract surgical approaches, post-op CME has become less frequent. The current incidence nationwide is between 1 and 2%.

How it Works

When pro-inflammatory chemical messengers suffuse the posterior segment, immune cells begin the process of inflammation by breaching the blood-retinal barrier. Weakened blood vessels are still able to contain the relatively large red blood cells, but small gaps in the vessel endothelial walls allow serum to leak out into retinal tissues. Müller cells are initially able to pump the retina dry. So, early in the process, there are no cystoid spaces—only swelling within the cytoplasm of the Müllers. As fluid leaks continue, the Müllers rupture or liquefy, creating the characteristic cystoid spaces.

Why does CME affect the macula preferentially? One theory is that the horizontal structural adhesions are not as robust in the macula as elsewhere. However, scanning electron imaging has shown that CME does cause subclinical edema in blood vessels and pericytes throughout the retina and optic nerve.3


A typical post-op CME patient will have good vision after surgery, but then lose acuity to 20/40 or worse. Patients may complain of constant monocular blur. Common descriptions include, “My vision is like looking through water” or “through a shower door.” This vision loss is occasionally accompanied by conjunctival injection, photophobia and an anterior chamber reaction. Symptoms typically peak 6 to 10 weeks after cataract surgery, though may present much later.


Clinically, a CME blister will appear as a diffuse red area around the macula. Often the macula will have apparent thickening with a honeycomb-like pattern that decreases in size away from the fovea. The cystoid spaces will be most apparent with a stereoscopic view and a thin slit-beam retro-illuminating the macula. Frequently the retina may show evidence of an old BRVO, CRVO, ERM or diabetic retinopathy.

Critically, the optometrist must rule out other causes of post-op blur, including corneal edema, uveitis, posterior capsular opacification, retinal disease including detachment,n and endophthalmitis. If CME with uveitis presents, look for vitreous to the wound or retained lens material, both of which require a return visit to the surgeon.4

On OCT, the cystic voids are unmistakable. Though OCT is now more frequently used, fluorescein angiography can provide additional evidence to diagnose CME. Fluorescein will leak slowly into the cystoid spaces, which are extracellular and not fed by vessels. Therefore, the characteristic petalloid pattern will not appear for up to 10 minutes after injection.


The majority of patients with mild to moderate CME will recover whether you do anything or not. We probably miss many such cases simply because patients are so much happier with their vision after cataract surgery.

Consider treating CME when patients notice blur and clinical signs are present. Fundamental management begins with a topical NSAID. Those that have been studied and shown to be effective are:

  • diclofenac sodium 0.1% (Voltaren)
  • ketorolac tromethamine 0.5% (Acular)5
  • bromfenac (Bromday)
  • nepafenac (Nevanac)

Many (but not all) studies point to a more complete recovery with the addition of prednisolone acetate 1% qid. Although there is debate about the usefulness of carbonic anhydrase inhibitors, some doctors add oral acetazolamide to the regimen.

Depending on severity, follow-up exams are every 1-3 weeks until resolved. Discontinue medications once all clinical signs have resolved.

Prostaglandin analogues can have a pro-inflammatory effect. For glaucoma patients taking one of these popular medicines, consider the possibility that it may be contributing to post-op CME, particularly if the case is not resolving.

Proceed cautiously and with frequent follow-ups when patients exhibit characteristics that are likely to lead to chronic and debilitating CME:

  • florid CME (obvious and large cystoid spaces seen clinically)
  • poor acuity
  • vitreous wicks
  • retinal risk factors (in particular, epiretinal membranes, diabetic retinopathy and prior retinal vascular occlusions)

Some cases will not quiet even with aggressive proper management. If the situation is worsening or unresolved within 2 months, consider referral to a retinal specialist for possible further treatments, such as a sub-Tenon’s steroid injection, intravitreal steroid injection or vitrectomy.


When referring patients for cataract surgery, alert the surgery center to any known retinal vessel disease or ERMs. Consider placing patients with a history of retinal vein occlusions on an NSAID for 7 days prior to surgery. This will often help smooth their transition through what should be an uneventful and life-enhancing procedure.

Clinical Pearls
  • The easiest way to see macular cysts is with a stereoscopic view and a thin slit-beam retro-illuminating the macula.
  • Rule out other causes of post-op blur, especially retinal disease or detachment and endophthalmitis.
  • Most mild cases of post-op CME will resolve nicely no matter what you do.
  • Prescribe an NSAID and pred acetate for mild-to-moderate cases.
  • If available, use OCT to monitor resolution of macular thickness.
  • Identify CME most likely to become chronic, then schedule frequent follow-up exams and refer promptly if they do not improve. 

  1. Irvine SR. A newly defined vitreous syndrome following cataract surgery: Interpreted according to recent concepts of the structure of the vitreous. Am J Ophthalmol. 1953;36:599-619.
  2. Gass JDM, Norton EWD. Cystoid macular edema and papilledema following cataract extraction: a fluorescein funduscopic and angiographic study. Arch Ophthalmol. 1966;76:646.
  3. Benitah NR, Arroyo JG. Pseudophakic Cystoid Macular Edema. Intl Ophthalmol Clinics. 2010;50,1:139-153.
  4. Murrill C, Stanfield D, VanBrocklin M. Primary Care of the Cataract Patient. East Norwalk, CT: Appleton & Lange; 1994.
  5. Heier JS, Topping TM, Baumann W, et al. Ketorolac versus prednisolone versus combination therapy in the treatment of acute pseudophakic cystoid macular edema. Ophthalmology. 2000;107:2034-2038.