CLINICAL CHALLENGES
A Fortuitous Finding
Cystoid macular edema may appear when you're looking for something else.
Eric Schmidt, O.D.

In everyday practice, we can usually find some thing if we set out to discover it; a foreign body or the TV remote for instance. But occasionally things find us even when we aren't looking for them.

Higher expectations

Last month I introduced you to Mr. Harvey, a 74-year-old white man whom I diagnosed with pigmentary glaucoma. Mr. Harvey had undergone uneventful small-incision cataract surgeries OU 4 and 5 months earlier, with the incisions made superiorly using the scleral tunnel technique. No complica tions occurred during surgery, and his postoperative course was also normal.

I treated Mr. Harvey postoperatively with ciprofloxacin (Ciloxan) q.i.d. for 1 week and with prednisolone (Econo-pred) q.i.d. for 1 week; t.i.d. for 1 week; b.i.d. for 1 week, and q.d. for 1 week after each procedure. Mr. Harvey was pleased with his visual outcome of 20/30-2 OD and 20/30 OS -- after all, he'd been 20/60 before the surgery. But I expected better. As smoothly as his surgeries went, I felt that his vision should be crisper and closer to 20/20.

Looking for a problem

Six months after Mr. Harvey's surgery, I worked him up for glaucoma, as discussed last month. I took a detailed look at his macula and posterior pole with a 78D lens and saw no overt macular cysts, edema or retinal thickening. As part of the glaucoma work up, I scanned his optic disk and macular region using the Talia Retinal Thickness Analyzer (RTA).

The RTA revealed abnormal macular thickening and elevation OD > OS (see photo below). When I superimposed the scans on a photograph of his fundus, the thickest areas were juxta-foveolar. The probability plots showed that the thickest areas were significant, with values of less than 1%, meaning that these areas were present in less than 1% of "normals."

This elevation at the foveal region is consistent with cystoid macular edema (CME) and were enough to cause Mr. Harvey's somewhat diminished visual acuity (VA).

When I looked closely at individual slit scans, which are "real time" optical sections of small areas of the retina, I saw individual cysts lying within the retina. Clearly, Mr. Harvey had post-operative CME.

Understanding CME

In the past, CME was common after cataract surgery, especially when doctors used larger incisions. Postoperative CME, or Irvine-Gass syndrome, arises from surgical trauma and the inflammation it induces.

Large incisions that require more tissue dissection cause increased intraocular inflammation. Longer surgical times, specifically longer phacoemulsification times, also increase CME. The longer the surgical trauma is inflicted on the eye, the more inflammation is induced and the more likely CME is to develop.

Individual cells in the retina will decompensate and leak fluid. This now extracellular fluid organizes as intraretinal cysts. If enough cysts form, retinal thickening and edema will develop. These conditions can cause a moderate decrease of VA to the 20/80 level.

Fortunately, CME has become much rarer since the advent of small-incision and clear-cornea cataract extractions. Now you'll see postoperative CME mainly in diabetics or in patients who have other inflammatory conditions and note it incidentally on fluorescein angiography or with retinal scanners, as in this case. Most cases are considered sub-clinical and of little visual consequence.

Clinically, CME presents as mild to moderately decreased VA, usually ranging from 20/30 to 20/60. Using a 78D lens, you'll see retinal thickening. Small intraretinal cysts may be apparent but often an irregularity of the foveal region is the only overtly visible sign. It's a diagnosis predicated on clinical suspicion and traditionally confirmed by intravenous fluorescein angiography.

Clinically significant?

The question for this case was whether the CME required treatment. Mr. Harvey's cataract procedures had both been eventful and his VA was decent. Glare while driving bothered him and he noticed that his vision OD wasn't as good as OS. But was this reason enough for treatment?

In a case like this where multiple treatment options exist and the results of each can't be well predicted, I feel that it's important to let the patient decide what to do. I laid out the options for Mr. Harvey. Treatment for postoperative CME varies from case to case. It typically depends on the level of VA, the duration of the condition and, in a large part, the doctor's preference. Topical non-steroidal anti-inflammatory agents (NSAIDs) have been shown to be successful in reducing mild to moderate CME cases.

Some doctors prescribe oral NSAIDs, such as indomethacin (Indocin) 25 mg t.i.d. Others advocate a 2-week burst of systemic prednisone up to 50 mg. Many retinal specialists feel that the best treatment is a subtenons injection of triamcinolone (Kenalog), especially for more severe cases, whether acute or chronic. I also informed Mr. Harvey that often CME will resolve itself up to 6 months post-operatively.

Treating Mr. Harvey

After discussion, we opted to initiate a regimen of the topical NSAID diclofenac (Voltaren) q.i.d. OU. Diclofenac penetrates well to the posterior pole and has been shown effective in combating posterior segment inflammation.

After 6 weeks of treatment, Mr. Harvey's VA had improved to a crisp 20/25 in each eye. The retinal elevation that was present on the original RTA was greatly diminished on the repeat scan. And, most importantly, Mr. Harvey reported an improvement in his vision.

Without the benefit of new technology, I wouldn't have detected this CME and Mr. Harvey would have had sub-optimal VA. As you can see, it's important that all of us have access to instruments such as the RTA to benefit our patients. They deserve and appreciate it!

Contributing Editor Eric Schmidt, O.D., is director of the Bladen Eye Center in Elizabethtown, N.C. E-mail him at KENZIEKATE@aol.com.