Post-laser refractive surgery complication identified in study

Noninflammatory central corneal opacification clears over several months, often leaving patients hyperopic.

Issue: October 1, 2007

ByAndy Moskowitz

Robert K. Maloney

Central toxic keratopathy, a syndrome characterized by noninflammatory central corneal opacification, can occur in some patients within 9 days after undergoing LASIK or PRK, according to a study.

Robert K. Maloney, MD, and Baris Sonmez, MD, reported results for 23 eyes of 14 patients who developed central toxic keratopathy in the immediate postoperative period after undergoing LASIK or PRK. All eyes had a central corneal opacification in the laser treatment area, and in 19 post-LASIK eyes, the opacification extended posteriorly into the stromal bed, the authors said.

The opacification lasted for a minimum of 2 months to a maximum of 18 months before clearing on its own. As the syndrome cleared, nine eyes experienced a hyperopic shift of more than 2 D. One eye lost two lines of best corrected visual acuity and two eyes lost one line. Laser re-treatments were successfully performed in six patients with no central toxic keratopathy recurrence, the author said in the American Journal of Ophthalmology.

“It’s a scary complication because the patients are hyperopic and they have poor quality of vision for a long period of time,” Dr. Maloney told Ocular Surgery News. “The good new is that in our experience the opacity always goes away. We can reassure patients that the long-term prognosis is good, even though they’re going to have a difficult road ahead.”

Easily misdiagnosed

According to Dr. Maloney, central toxic keratopathy is often mistaken for infectious keratitis, which also presents with a white opacity in the central cornea.

“But central toxic keratopathy is easily distinguished from infectious keratitis,” he said. “If you look carefully, infectious keratitis always contains a lot of inflammatory cells and the eye is red. There are no inflammatory cells in central toxic keratopathy and the eye is white and quiet.”

Dr. Maloney noted that 18 of 19 post-LASIK eyes had diffuse lamellar keratitis (DLK) preceding the onset of central toxic keratopathy. Not surprisingly, he said, central toxic keratopathy has also been called a stage 4 DLK.

“Central toxic keratopathy is related to DLK, and in fact many patients who get central toxic keratopathy have preceding DLK. But we think it’s distinct from DLK because DLK is confined to the interface and central toxic keratopathy extends into the anterior and posterior stroma,” he said. “DLK is always inflammatory by its nature, and central toxic keratopathy is not inflammatory. And DLK is diffuse, and central toxic keratopathy tends to be focal in the central cornea.”

“And while central toxic keratopathy often follows DLK, it does not always,” he said. “We have cases where this occurred in the absence of DLK. Also, DLK doesn’t occur after PRK, but we’ve reported four eyes where this [central toxic keratopathy] occurred after PRK. So we think it’s distinct, although it’s not well understood.”

Mild case of central toxic keratopathy with faint central opacification and the characteristic dark striae against a lighter background. No inflammation is present.

Severe central toxic keratopathy with dense central opacification and striae. Best corrected visual acuity dropped to 20/40 with a 3 D hyperopic shift.

Images: Maloney RK

Treatment

The best way to treat central toxic keratopathy is to let it clear on its own, Dr. Maloney said.

“We recommend tincture of time. This disorder is not responsive to topical steroids, and topical steroids have a whole set of extra risks,” he said, adding that surgeons should use steroids to treat any coexisting DLK but should stop using them once the DLK clears.

“We also don’t recommend lifting the flap and trying to scrape or irrigate the opacity,” he said. “The tissue is necrotic when you lift the flap, and our concern is that scraping it may increase the hyperopic shift that commonly accompanies central toxic keratopathy.”

Once the opacity clears, surgeons can safely perform enhancements to correct the hyperopic shift and remove any residual stria, Dr. Maloney said.

Possible cause

Although the exact etiology of central toxic keratopathy is unknown, Dr. Maloney hypothesizes that a toxin is entering the flap and causing corneal apoptosis.

“I’m suspicious that the photoactivation of Betadine (10% povidone iodine, Purdue Pharm) may be a contributor in some cases,” he said. Betadine is used to sterilize the skin before surgery and could easily get under the flap, he said.

“And [the opacification] almost always occurs dead center in the area of the laser treatment. If it were just a toxic substance alone, it should occur anywhere under the flap, wherever the toxic substance was. So it appears that photoactivation by the laser is part of the pathophysiology,” he said.

Dr. Maloney has ruled out genetics as a possible cause, as he has never seen central toxic keratopathy recur after laser re-treatments, he said.

“We thought maybe these patients had something in their genetics that makes the cornea wither up when it’s lasered. But it doesn’t seem to happen with re-treatments, and so we don’t think it’s something intrinsic to the response of these patients,” he said.

For more information:

Robert K. Maloney, MD, can be reached at Maloney Vision Institute, 10921 Wilshire Blvd., Suite 900, Los Angeles, CA 90024; 310-208-3937; fax: 310-208-8058; e-mail: russell@maloneyvision.com.

Reference:

Sonmez B, Maloney RK. Central toxic keratopathy: Description of a syndrome in laser refractive surgery. Am J Ophthalmol. 2007;143;420-427.

Andy Moskowitz is an OSN Correspondent based in Media, Pa.