EyeWorld India March 2012 Issue

36 EW REFRACTIVE March 2012 PISK appears similar to DLK. This patient experienced haze grade +1/+2 in a pat- tern suggestive of DLK. Source: Michael Berlin, MD PISK discoverer and recent researcher elucidate these kissing cousins W hat looks like diffuse lamellar keratitis (DLK) appears shortly after LASIK, but is there a significantly different pathology? It’s called pressure-induced interlamellar stromal keratitis (PISK), and case reports have been sporadic since its discovery in 2002. “PISK is a poorly documented phenomenon,” wrote Theofilos Tourtas, MD , resident, Department of Ophthalmology, University of Erlangen-Nuremberg, Germany, in the most recent of the few studies on PISK, published in the August issue of Cornea . “Whereas DLK has been well described in the literature, there have been only a few reports of PISK.” In interviews with EyeWorl d, both Dr. Tourtas and the first ophthalmologist to report PISK in 2002, Michael Belin, MD , professor, Ophthalmology and Vision Science, University of Arizona College of Medicine, Tucson, Ariz., USA, suggested that it’s critical to distinguish PISK from DLK for treatment purposes. Stumbling upon PISK Dr. Belin explained that in his initial report on PISK, a series of patients presented with classic-appearing DLK, but were not responsive to steroids or anti-inflammatory agents. In one patient, Dr. Belin noticed pressure was fairly high, and treated him both with continuous steroids and pressure medications, after which the patient improved. “Literally a week after that case, I was a visiting professor in Taiwan and one of the leading refractive surgeons presented an unknown case of DLK,” Dr. Belin said. “The first thing out of my mouth was, ‘What was his pressure?’ He looked at me like, ‘Why are you asking that?’” The patient’s pressure was indeed high and documented another case of PISK. Since then, there have been others—but relatively few reported in medical literature. Dr. Tourtas’ case involved a 42-year-old man who experienced blurred vision in both eyes, seeking treatment for the problem 3 months after LASIK. DLK was diagnosed and topical steroids were increased. There was no improvement, but IOP markedly increased to 48 mmHg. The patient was then diagnosed instead with PISK, and pressure- reducing drops were added. One week later, the patient’s visual acuity improved while interface haze decreased. Dr. Tourtas distinguishes DLK from PISK in his report as follows: DLK is an idiopathic interface inflammation that typically occurs within the first postoperative week, with clinical features ranging from asymptomatic infiltrate confined to the interface to stromal necrosis. PISK is a condition with DLK-like interface haze caused by steroid- induced ocular hypertension after LASIK. The clinical findings are not associated with an accumulation of inflammatory cells but caused by edema. Inflammatory mononuclear cells and granulocytes, typically seen in patients with DLK, are absent in patients with PISK. “You don’t hear or see much about [PISK],” Dr. Belin added. Part of the reason is that ophthalmologists are more cognizant of checking IOP after LASIK now. “You are going to treat IOP elevation if it’s clinically significant regardless of what the situation is,” Dr. Belin said. “We’re not seeing the cases because we’re catching and treating pressure elevation before it gets the chance to cause a problem.” Identifying and treating PISK It’s still very important to be able to distinguish PISK from DLK since treatments are different, and time is of the essence. Be mindful of the following in confronting a potential PISK problem, Dr. Belin said: • Anytime you see what looks like DLK, check the patient’s IOP; • Note that sometimes you can get a falsely low pressure reading with fluid accumulation; • If there is any suspicion of PISK, treat the patient with anti- glaucoma medications, and to be safe, use prudent anti-inflammatory medications that will cause few if any steroid responses; • DLK tends to be more focal. It’s diffuse but has focal areas. PISK tends to be more evenly distributed. “The last thing you want to do in classic DLK is to stop anti- inflammatory drugs,” Dr. Belin said. “If I was presented with a nuance that appeared to be DLK and the pressure also was elevated, I would not initially suggest discontinuing anti-inflammatories until I had a A fine line of difference between PISK and DLK by Matt Young EyeWorld Contributing Editor clear picture of what was going on.” Further, if a patient’s pressure is 50, Dr. Belin would be more comfortable diagnosing PISK. Alternatively, if pressure is in the 20s, he would not stop anti- inflammatories. “If the pressure is moderately elevated, it behooves the surgeon to treat the pressure in addition to the anti-inflammatory treatment for presumed DLK,” Dr. Belin said. There also are greater consequences to getting DLK wrong, Dr. Belin said. “DLK can progress to stromal necrosis and flap melt,” Dr. Belin said. “The consequence of [PISK] would only be long-term if pressure was high enough to induce nerve damage, which can happen. But acutely, untreated DLK risk is much more substantial.” Dr. Tourtas added a few more points about PISK, which differ from Dr. Belin’s somewhat. “DLK is diffuse lamellar keratitis that appears in the first few days after LASIK,” Dr. Tourtas said. “PISK appears after the first post-operative week.” But Dr. Belin said, “I wouldn’t want to keyhole this [difference] into a time period.” Dr. Tourtas also emphasized the consequence of PISK leading to glaucoma. “If it is not diagnosed, then the patient develops glaucoma with an optic nerve atrophy,” Dr. Tourtas said. He added that PISK can be a symptom of glaucoma. In his patient, he reported, “Funduscopic examination revealed an incipient glaucomatous optic atrophy with diffuse visual field sensitivity loss.” Finally, Dr. Tourtas found SL- OCT to be useful in diagnosing PISK. “The first step is to measure IOP,” he said. “If it’s normal, then we can do an SL-OCT to rule out fluid accumulation that would lead to a falsely normal IOP.” EW Editor’s note: Drs. Belin and Tourtas have no financial interests related to this article. Contact information Belin: 520-321-3677, mwbelin@aol.com Tourtas: theofilos.tourtas@uk-erlangen.de