LA number of clinical entities described as DLK were not included in the original spectrum of post-LASIK complications familiar to refractive subspecialists. DLK, however, has become a well-known entity to today's refractive surgeons, and I predict that newer, previously unreported LASIK complications will become more prevalent. A surgeon's continued vigilance in updating his knowledge of the latest complications is crucial to providing the best patient care.
CASE PRESENTATION
A 42-year-old white male sought refractive surgery for a preoperative refractive error of -5.00 D sphere OU. In all respects (including personality traits, corneal thickness, corneal topography, pupil size, and overall ocular health), this gentleman was an excellent candidate for LASIK. After a detailed informed consent discussion, I performed LASIK on the patient using the STAR S3 excimer laser system (VISX, Inc., Santa Clara, CA) and an Amadeus microkeratome (Advanced Medical Optics, Inc., Santa Ana, CA). Intraoperatively, a small epithelial abrasion occurred superiorly near the edge of the flap in each eye. After completing laser ablation, I carefully repositioned the flaps and placed a therapeutic soft contact lens on each eye. I placed the patient on Econopred (Alcon Laboratories, Inc., Fort Worth, TX) and Ciloxan (Alcon Laboratories, Inc.) q.i.d.
On the first postoperative day, the patient's UCVA was 20/40 OU. There was no evidence of interface inflammation in either eye, and I carefully removed the bandage contact lenses. I continued the patient on Econopred and Ciloxan q.i.d. and instructed him to return in 1 week. On the third postoperative day, the patient presented with a complaint of ?foggy? vision. His UCVA was 20/30 OD and 20/40 OS. I observed stage I DLK with inflammatory cells localized to the area of the epithelial defect in both of the patient's eyes.
As is my standard protocol, I treated the DLK aggressively with hourly applications of Pred Forte 1% (Allergan, Inc., Irvine, CA) and prescribed oral methylprednisolone (Medrol dose pack; Pharmacia Corporation, Peapack, NJ). I saw the patient 24 hours later. The inflammation had increased to stage II DLK OU with more central corneal involvement, and his UCVA had decreased to 20/40 OD and 20/50 OS.
On the fifth postoperative day, the patient returned with stage II to stage III DLK in both eyes. The progression of inflammation prompted me to lift the flap and irrigate the interface of both eyes with BSS (Alcon Laboratories, Inc.).
I again placed a therapeutic soft contact lens on each eye, and I continued the patient on hourly Pred Forte. On the following day, the patient was much more comfortable, and the cellular infiltrate had disappeared. His visual acuity improved slowly over the next few days, and I tapered his topical steroids to once every 2 hours.
The patient was to return in 1 week, but he instead presented on the tenth postoperative day complaining of decreased vision. His UCVA was 20/60 OU, but the slit-lamp examination revealed no interface cells in either eye. I tapered the administration of Pred Forte to every 4 hours and instructed the patient to return in 3 days. By the thirteenth postoperative day, he had noticed a gradual worsening of vision. His UCVA was 20/80 OU, and his BCVA was 20/40 with a minimal myopic and astigmatic refraction. The slit-lamp examination revealed fine interface haze throughout the entire flap in both eyes.
DIAGNOSIS AND TREATMENT
At first glance, the condition could easily have been mistaken for recurrent DLK. I recognized, however, that the appearance of the interface fluid in this case differed subtly from what is seen with DLK in that no interface cells were present. I recalled that a significant percentage of patients treated with high-dose topical steroids will develop a steroid-induced increase in IOP. In affected patients who have not undergone LASIK, an acute increase in IOP will force fluid through the endothelium, stroma, and ultimately the epithelium in the form of microcystic edema (Figure 1). In those who have undergone lamellar surgery, the fluid is forced into the interface, where it will disperse in the same plane without affecting the epithelium (Figure 2). The fluid in these cases resembles frosted glass or a fine, diffuse haze.
With a tonopen, I measured the patient's IOP at 26 mm Hg centrally. Although this measurement was borderline-high, I recalled that the IOP following myopic LASIK is falsely lower due to the central corneal thinning. Additionally, the presence of interface fluid will further lower the IOP reading. To obtain the patient's true IOP, I measured his pressure peripherally, outside the LASIK flap, and found it to be 37 mm Hg. I immediately had the patient discontinue Pred Forte and placed him on Alphagan P (Allergan, Inc.) b.i.d., TIMOPTIC 0.5% Sterile Ophthalmic Solution (Merck & Co., Inc., West Point, PA), and TRAVATAN (Alcon Laboratories, Inc.).
OUTCOME
Within 48 hours, the patient's interface was clear, his UCVA had improved to 20/40, and his IOP had decreased to 10 mm Hg. Over the next 3 weeks, after the patient discontinued using the glaucoma medications, his IOP remained low, his cornea continued to be clear, and his UCVA improved to 20/20 OD and 20/40 OS (monovision).
My patient was lucky. The incorrect diagnosis of chronic or recurrent DLK would likely have resulted in a knee-jerk response of increasing the amount of topical steroids administered. Clearly, that choice would have perpetuated the high IOP and could have led to irreversible complications in this case. A similar reported incident led to severe glaucomatous optic neuropathy and resulted in light-perception vision due to unrecognized high IOP.1-3 This case illustrates how important it is for surgeons to keep their knowledge of complications current.
Parag A. Majmudar, MD, is Assistant Professor of Ophthalmology at Rush Medical College in Chicago and is in private practice as a partner with Chicago Corneal Consultants. He does not hold a financial interest in any product mentioned herein. Dr. Majmudar may be reached at (847) 882-5900; pamajmudar@chicagocornea.com.
1. Lyle WA, Jin GJC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg. 1999;25:1009-1012.
2. Najmann-Vainer J, Smith RJ, Maloney RK. Interface fluid after LASIK: Misleading tonometry can lead to end-stage glaucoma. J Cataract Refract Surg. 2000;26:471-472.
3. Hamilton DR, Manche EE, Rich LF, et al. Steroid-induced glaucoma after laser in situ keratomileusis associated with interface fluid. Ophthalmology. 2002;109:659-665.
