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Results of Phototherapeutic Keratectomy in the Management of Flap Striae after LASIK Roger F. Steinert, MD,1,2 Amin Ashrafzadeh, MD,1,3 Peter S. Hersh, MD4 Objective: To evaluate the efficacy of phototherapeutic keratectomy (PTK) in reducing or resolving visually significant surface irregularities resulting from flap striae after LASIK. Design: Retrospective, noncomparative case series. Participants: Twenty-three eyes of 22 patients with flap striae after LASIK and reduced best-corrected visual acuity or visual symptoms that resolved with diagnostic contact lens fitting treated between January 2001 and April 2002 with at least 1 month of follow-up. The mean follow-up interval was 134 days (range, 30 –354 days). Intervention: Transepithelial PTK. Main Outcome Measures: Uncorrected visual acuity (UCVA), resolution or reduction of preoperative symptoms, corneal haze, and best spectacle-corrected visual acuity (BSCVA). Results: Mean BSCVA and UCVA improved significantly from 20/32 and 20/48 to 20/22 and 20/33 (P⬍0.0001 and P ⫽ 0.027), respectively, after PTK. There was a significant mean hyperopic shift of 0.88 diopters (D; P ⫽ 0.002, range, ⫺1.38 to ⫹3.88 D). Fourteen eyes (61%) were clinically clear, 6 eyes (23%) had trace haze, and 3 eyes (16%) had 1⫹ haze at the last follow-up visit. Mean spherical equivalent refractive error before LASIK was ⫺7.23 D (range, ⫺2.88 to ⫺13.55 D). Twenty-two of 23 eyes had significant qualitative resolution or reduction of preoperative visual symptoms. Conclusions: In cases of visually significant LASIK flap striae, PTK is effective in improving best-corrected visual acuity and reducing visual symptoms. High myopia may be a risk factor for development of visually significant microstriae. Development of anterior stromal haze did not exceed 1⫹ density and was not correlated to either the number of laser pulses or the length of the follow-up period. Ophthalmology 2004;111:740 –746 © 2004 by the American Academy of Ophthalmology. A safe and effective LASIK procedure requires creating, lifting, repositioning, and healing of a corneal flap that does not degrade the corneal optics. Wrinkles in the flap may cause loss of best-corrected visual acuity and symptoms such as multiplopia resulting from optical aberrations. Strategies to reduce or eliminate flap wrinkles include lifting the flap, hydration, stroking, smoothing, suturing, heating, use of a bandage contact lens, and discarding the flap with or without replacement lamellar keratoplasty.1– 8 A useful clinical classification of flap wrinkles distinguishes between macrostriae and microstriae. Macrostriae are large, full-thickness folds in the LASIK flap, usually Originally received: October 21, 2002. Accepted: June 25, 2003. Manuscript no. 220854. 1 Center for Eye Research and Education, Boston, Massachusetts. 2 Harvard Medical School, Boston, Massachusetts. 3 Tufts University School of Medicine, Boston, Massachusetts. 4 Department of Ophthalmology, University of Medicine and Dentistry of New Jersey, Newark, New Jersey. Presented at: American Society of Cataract and Refractive Surgery meeting, June, 2002; Philadelphia. Authors have no proprietary interest in any product or technique discussed in this article. Correspondence to Roger F. Steinert, MD, Ophthalmic Consultants of Boston, 50 Staniford Street, Suite 600, Boston, MA 02114. E-mail: [email protected]. 740 © 2004 by the American Academy of Ophthalmology Published by Elsevier Inc. occurring spontaneously in the first postoperative day after direct corneal trauma or later. Characteristically, macrostriae are readily visible at the slit-lamp biomicroscope, with a “washboard” appearance of parallel or semiparallel lines. If detected and treated acutely by repositioning the flap, macrostriae usually resolve; if left untreated, however, these folds may become fixed and unresponsive to conservative measures. Microstriae, in contrast, are finer, randomly directed wrinkles in the anterior cornea. Most microstriae are not optically significant because of the masking effect of the overlying epithelium. Microstriae are best seen with retroillumination (Fig 1). Optically significant microstriae generally are not detectable on corneal topography color maps but may disrupt the placido mire reflection pattern. After a small amount of fluorescein is placed in the tear film, a characteristic “negative” staining pattern of reduced fluorescence over the microstriae9 resulting from disruption of the tear film is helpful in identifying optically significant microstriae (Fig 2). Excimer laser phototherapeutic keratectomy (PTK) is successfully used in the treatment of numerous corneal surface irregularities, including anterior basement membrane dystrophy,10 Bowman membrane dystrophies, anterior stromal dystrophies,11 superficial corneal scars,12 and Salzmann’s nodular degeneration.13,14 We investigated the ISSN 0161-6420/04/$–see front matter doi:10.1016/j.ophtha.2003.06.015 Steinert et al 䡠 Phototherapeutic Keratectomy for Flap Striae Figure 1. Slit-lamp retroillumination photomicrograph of microstriae. Figure 2. “Negative staining” pattern of fluorescein in the tear film resulting from disruption by microstriae. Figure 3. Sequential operative photographs of the epithelial fluorescence pattern seen during phototherapeutic keratectomy (PTK) for microstriae. A, With successive pulses, epithelial fluorescence over the most highly elevated striae disappears as the thinnest epithelium becomes fully ablated. Reprinted with permission from Roger F. Steinert, MD. PTK treatment of chronic flap striae. Refractive Surgery Quarterly 2003;2(4):2⫺3. ©2003 Slack Inc. B, With further pulses, the epithelium between the striae recedes, along with a further reduction in fluorescence. C, At the end of the transepithelial phase of the PTK, most of the epithelium is removed, with only minimal residual fluorescence in the areas of thickest epithelium between the striae. Figure 4. Schematic diagram of the mechanism of reduction in optical disturbance of striae by transepithelial phototherapeutic keratectomy (PTK). Rx epi ⫽ transepithelial treatment. Reprinted with permission from Roger F. Steinert, MD. PTK treatment of chronic flap striae. Refractive Surgery Quarterly 2003;2(4):2⫺3. ©2003 Slack Inc. efficacy of PTK to improve corneal optics in the presence of chronic macrostriae and microstriae. A MEDLINE literature search did not reveal any previous reports of this technique for treatment of microstriae Patients and Methods Patients were either referred after LASIK treatment elsewhere or had been treated primarily by the authors. All treated eyes exhib- 741 Ophthalmology Volume 111, Number 4, April 2004 Table 1. Patient Characteristics Patients Eyes Analysis Age (yrs) 22 patients 14 female 8 male 23 eyes 13 right eyes 10 left eyes Mean Median Standard deviation Minimum Maximum 44 46 7 30 56 Pre-LASIK Refraction Pre-LASIK K Sphere Cylinder SE Vertical K Horzizontal K Average K ⫺6.81 ⫺6.50 2.90 ⫺13.30 ⫺2.00 ⫺0.84 ⫺0.50 0.96 ⫺3.25 0.00 ⫺7.23 ⫺7.13 2.80 ⫺13.55 ⫺2.88 45.00 44.50 1.82 41.12 48.75 43.84 44.00 1.39 41.50 47.00 44.42 44.25 1.48 41.31 46.83 K ⫽ keratometric power; SE ⫽ spherical equivalent. ited flap striae and either loss of best spectacle-corrected visual acuity (BSCVA) or symptoms such as hazy view, ghost images, monocular multiplopia, or nighttime glare. Patients often described a fleeting clear view immediately after a blink or placement of artificial tears in the eye. All patients underwent a complete preoperative eye examination. Specific attention was given to uncorrected visual acuity (UCVA), BSCVA, manifest and cycloplegic refractions, corneal topography, and examination of the tear film staining pattern. Specific details of the patient symptoms were delineated. If the patient’s symptoms could not be resolved with refraction, the next step was to place a soft contact lens to neutralize the optical significance of the microstriae. If a soft contact lens failed to improve the symptoms, a hard contact lens refraction was performed. Patients were selected for PTK only if their symptoms significantly improved or fully resolved with the clinic trial of the contact lenses. Before surgery, patients received 2 to 10 mg diazepam and drops of topical antibiotics, either ofloxacin (Ocuflox; Allergan, Irvine, CA) or levofloxacin (Quixin; Santen, Napa, CA). A broadbeam excimer laser programmed for PTK with an optical zone of 6.5 mm (Summit Apex Plus [Alcon Summit Autonomous, Orlando, FL] or Star S3 [VISX, Sunnyvale, CA]) was used in all cases. The nominal depth per pulse specified by the manufacturer is 0.24 m per pulse with the Summit laser and 0.25 m per pulse with the VISX laser. Transepithelial PTK was used, monitoring the pattern of epithelial fluorescence through the operating microscope. Because epithelium is thinnest over the elevated ridges of the striae, the initial epithelial breakthrough, heralded by the loss of fluorescence, typically had the pattern of the underlying striae (Figs 3, 4). Phototherapeutic keratectomy was continued until epithelial fluorescence began to recede between striae. A thin layer of medium viscosity artificial tears (Refresh Plus; Allergan) then was applied with a lightly moistened surgical spear, and PTK was resumed to decrease further the height of the striae. The goal was to achieve reduction but not elimination of all striae. In a typical treatment, the transepithelial phase was completed with 180 to 220 pulses, and a total of 80 to 100 further pulses were applied with the masking artificial tears. In the second phase of the PTK in which artificial tears were used, 8 to 10 laser pulses were delivered, and then the artificial tears were reapplied with a lightly moistened surgical spear sponge to reestablish a thin layer of masking fluid. Because much of the laser energy is absorbed by the masking fluid, it is impossible to calculate the depth of stromal ablation, but it probably is less than 10 m. On completion of the procedure, 1 drop of prednisolone acetate 1% (Pred Forte; Allergan) and 1 drop of one of the above antibiotics were placed. A soft bandage contact lens was placed (Model 66, medium base curve; Bausch & Lomb, Rochester, NY). The patient was instructed to use the steroid and antibiotic drops 5 minutes apart, 4 times daily for the next 5 days. Patients were 742 examined early in the postoperative period, at a minimum of day 1 and days 3 to 5. The soft contact lens was removed when epithelial coverage was achieved, and the patient was instructed to use a nonpreserved or rapid deactivating preservative ocular surface lubricant for a minimum of every 2 hours while awake for at least the first postoperative month. At the 1-month and subsequent postoperative examinations, a full eye examination along with manifest refraction and notation of patient symptoms was performed. Statistical analysis was by paired t test (Microsoft Excel 2000; Microsoft Corporation, Redmond, WA). Results Thirteen right eyes (57%) and 10 left eyes (43%) of 14 female patients (64%) and 8 male patients (36%) underwent PTK. One patient underwent PTK in both eyes. The mean patient age was 44 years (range, 30 –56 years). Patient characteristics are summarized in Table 1. The mean spherical equivalent refractive error before LASIK was ⫺7.23 diopters (D; range, ⫺2.88 to ⫺13.55 D). The corneal keratometric power before LASIK was available for 17 of the 23 eyes. The mean vertical keratometric power was 45.00 D, the mean horizontal keratometric power was 43.84 D, and the mean overall keratometric power was 44.42 D (range, 41.31– 46.83 D). The difference in the vertical versus horizontal keratometric corneal powers was statistically significant (P ⫽ 0.002). Fifteen of 17 eyes (88%) had steeper vertical meridians, and 2 eyes (12%) had steeper horizontal meridians. Treatment history is detailed in Table 2. The average interval between the primary LASIK and PTK was 307 days (range, 19 –992 days). The mean follow-up interval after the PTK (to the last examination or any other subsequent intervention) was 134 days (range, 30 –354 days). Before PTK, eyes 3, 7, and 18 had 1 flap refloat, and eyes 8 and 20 had 2 flap refloats. Eye 6 had a flap refloat and a subsequent Donnenfeld heating treatment. Eye 15 had a flap refloat followed by a second refloat combined with epithelial debridement. Ten eyes had undergone LASIK retreatments before Table 2. Treatment Intervals Analysis LASIK to Phototherapeutic Keratectomy (days) After Phototherapeutic Keratectomy (days) Mean Median Standard deviation Minimum Maximum 307.00 285.00 250.00 19.00 992.00 134 106 81 30 354 Steinert et al 䡠 Phototherapeutic Keratectomy for Flap Striae Table 3. Changes in Best Spectacle-corrected Visual Acuity Best Spectacle-corrected Visual Acuity before Phototherapeutic Keratectomy Best Spectacle-corrected Visual Acuity after Phototherapeutic Keratectomy Analysis Snellen Decimal Snellen Decimal Safety Index Improvement in Lines of Snellen Acuity Mean Median Standard deviation Minimum Maximum 20/32 20/30 0.63 0.66 0.20 0.29 1.00 20/22 20/20 0.90 1.00 0.21 0.50 1.33 1.55 1.52 0.58 0.76 2.80 1.70 2 1.66 ⫺1 5 20/70 20/20 20/40 20/15 PTK, 8 with lifting of the original flap and 2 with microkeratome cutting of a new flap. Two eyes (eyes 3 and 19) had been noted to have minor nonvision impairing microstriae before LASIK retreatment, and visually impairing microstriae developed afterward. After the PTK treatment, 4 eyes had subsequent LASIK retreatments by lifting the flap that had been treated by PTK. Three eyes (eyes 1, 5, and 16) were treated successfully with no redevelopment of microstriae afterward. In 1 eye (eye 19) with a known very thin primary flap, a frank buttonhole developed with relifting; retreatment was aborted. Mean BSCVA improved significantly from 20/32 (0.63) before PTK to 20/22 (0.90) after PTK (P⬍0.0001; Table 3). Uncorrected visual acuity improved significantly from a mean of 20/48 (0.42) before PTK to 20/33 (0.60) after PTK (P ⫽ 0.027; Table 4). Phototherapeutic keratectomy improved BSCVA in 21 of 23 eyes (Figs 5, 6). Uncorrected visual acuity also improved in most patients, although this was not a primary goal of the PTK treatment (Fig 7). The mean safety index was 1.70, calculated as decimal BSCVA value after PTK divided by decimal BSCVA value before PTK.15 Two eyes (eyes 15 and 19) in this study each had a 1-line loss of BSCVA. In eye 15, some macular pigment epithelial changes developed that were consistent with myopic degeneration. This patient noted improvement in vision symptoms after PTK, even though a hard contact lens refraction did not improve her BSCVA. Eye 19 had a very thin flap (77 m) initially. This eye had minor microstriae that became visually significant after a flap-lift enhancement procedure. The eye then underwent PTK, and mild irregular astigmatism and 1⫹ haze developed. The mean spherical equivalent manifest refraction showed a hyperopic shift of ⫹0.88 D (range, ⫺1.38 to ⫹3.88 D; P ⫽ 0.002; Table 5). A small mean reduction of 0.14 D of absolute cylinder (range, ⫺2.00 to ⫹1.50 D) occurred that was not statistically significant. Table 6 tabulates the operative parameters. Total pulses averaged 286 (range, 163–348 pulses). The transepithelial phase was recorded in 20 of 23 eyes, with a mean of 196 pulses (range, 60 –289 pulses). Flap thickness measurements determined by ul- trasonic pachymetry were available for 9 of 23 eyes from the primary surgery. Eye 1 had LASIK retreatment after PTK with flap thickness measurement at that time. Including eye 1, the mean flap thickness was 150 m (range, 77–196 m). Table 7 lists the clinical haze ratings at the last follow-up examination and the total number of PTK laser pulses. Fourteen eyes (61%) were completely clear, 6 eyes (23%) had trace haze, and 3 eyes (16%) had 1⫹ haze. The mean total number of laser pulses for patients with haze and without haze was 294 (range, 235–348 pulses) and 281 (range, 163–321 pulses), respectively; the difference approached but did not reach statistical significance (P ⫽ 0.08). Stromal pulses calculated mathematically as the difference between total number of pulses and the epithelial phase pulses also are reported. The mean number of stromal pulses in eyes with haze (100 pulses) and without haze (91 pulses) was not significantly different (P ⫽ 0.69). The mean follow-up period for patients with haze and without haze was 100 days (range, 48 –189 days) and 130 days (range, 30 –354 days), respectively; the difference was not statistically significant (P ⫽ 0.13). Discussion Phototherapeutic keratectomy directly reduces the anterior elevations of the striae, thereby reducing or eliminating the optical disruption of the tear film. The smoothing effect of the laser pulses is aided by the masking effect of the epithelium in the transepithelial phase and the use of artificial tears as a masking agent after the laser pulses penetrate through the basal epithelium. Twenty-one of 23 eyes in this series experienced improvement in BSCVA and reduc- Table 4. Change in Uncorrected Visual Acuity Uncorrected Visual Acuity before Phototherapeutic Keratectomy Uncorrected Visual Acuity after Phototherapeutic Keratectomy Analysis Snellen Decimal Snellen Decimal Mean Median Standard deviation Minimum Maximum 20/48 20/50 0.42 0.40 0.20 0.10 0.80 20/33 20/30 0.60 0.66 0.34 0.05 1.25 20/200 20/25 20/400 20/16 Figure 5. Change in best spectacle-corrected visual acuity (BSCVA). 743 Ophthalmology Volume 111, Number 4, April 2004 Figure 6. Distribution of best spectacle-corrected visual acuity (BSCVA) before and after phototherapeutic keratectomy (PTK). tion of undesirable vision disruption. Seven of 23 patients had undergone prior interventions that failed to resolve their vision impairments. Macrostriae are full-thickness folds of the flap that occur as a result of flap slippage that may occur secondary to direct trauma, drying, and adhesion of the flap to the tarsal conjunctiva, and the altered central convexity and stromal support referred to as the “tenting effect.”16 Macrostriae are best treated immediately. To remedy acute macrostriae, we lift the involved area of the flap, most commonly the entire flap. The flap is refloated with balanced salt solution and is stroked gently and smoothed back into proper position, taking care to remove any peripheral epithelium that would become trapped in the interface. If macrostriae are not recognized and treated immediately, however, the flap wrinkles become fixed and resistant to smoothing. More aggressive maneuvers, such as stretching with forceps, suturing, hydration with hypotonic solutions, heating, and sandwich compression, have been proposed.5– 8,16 –18 These maneuvers are not without risk. Figure 7. Distribution of uncorrected visual acuity (UCVA) before and after phototherapeutic keratectomy (PTK). 744 Potential complications of these flap manipulations include interface epithelial ingrowth, interface inflammation and infection, tearing the flap edge, induction of new striae, and creation of irregular astigmatism. The flap may seem to improve initially, with later return of striae. Phototherapeutic keratectomy also has been suggested for chronic macrostriae with a 6-m ablation depth to “make the (Bowman) membrane thinner and minimize its ‘mechanical memory.’”5 This technique differs from the methodology used in our series. In contrast to macrostriae, microstriae occur, despite good flap repositioning. Microstriae are virtually universal in LASIK flaps, although often they are invisible or optically insignificant. Vesaluoma et al19 detected microstriae in 60 of 62 eyes (96.8%) that had undergone LASIK using confocal microscopy but in only 25 eyes (40.3%) that had undergone LASIK by biomicroscopy. Our data suggest that visually significant microstriae may be more prevalent in patients with higher levels of myopic correction. After a myopic laser photoablation, the bed is flatter. When the flap is repositioned, it must conform to the altered contour. This causes a relative compression of the anterior surface while stretching the posterior surface of the flap, resulting in microstriae at the level of Bowman’s and the anterior stroma. In our series, the mean prerefractive surgery spherical equivalent was ⫺7.23 D (range, ⫺2.88 to ⫺13.55 D), which probably exceeds the average level of myopic LASIK, although we do not have data on the mean level of myopia in all patients treated contemporaneously with the patients who received PTK for striae. In our experience, microstriae often do not respond to smoothing maneuvers or to the other interventions discussed. Seven eyes had undergone specific procedures to remove the microstriae; all of these procedures failed to relieve the symptoms. The limited number of patients with data on flap thickness precludes drawing a conclusion about whether a thin flap is predisposed to developing striae. In 10 patients, corneal flap thickness was available, with a mean flap thickness of 150 m and a wide range from 77 to 196 m. Four of 10 patients (40%) had a flap thickness of less than 135 m. This suggests that a thinner flap may be at increased risk of developing striae, but a thicker flap is not immune from striae. In 15 of 17 eyes (88%) for which data were available, the vertical keratometric power was steeper than horizontal (P ⫽ 0.002). This finding may represent simply a preponderance of with-the-rule astigmatism before surgery. We cannot exclude the possibility that the corneal curvature plays a role in the cause of visually significant striae, although our data on keratometry (Table 1) do not suggest that the mean keratometry values deviated from a typical patient population. Ten eyes (43%) had retreatment before development of visually significant microstriae, suggesting that lifting (8 eyes) or recutting (2 eyes) a flap may have an increased risk of developing striae compared with primary flap creation. In contrast, 3 eyes with adequate flap thickness underwent LASIK retreatment after PTK and did not develop new striae. Formation of corneal haze after PTK on the flap was one of our foremost concerns. Carones et al20 noted grade 3 and 4 haze formation in 82.3% of patients who underwent photorefractive keratectomy (PRK) on top of a previous Steinert et al 䡠 Phototherapeutic Keratectomy for Flap Striae Table 5. Change in Refraction after Phototherapeutic Keratectomy MR before Phototherapeutic Keratectomy MR after Phototherapeutic Keratectomy Analysis Sphere Cylinder SE Sphere Cylinder SE Change in SE Change in Cyl Mean Median Standard deviation Minimum Maximum 0.00 0.00 0.94 ⫺1.75 ⫹2.00 ⫺0.89 ⫺0.75 0.52 ⫺2.25 0.00 ⫺0.45 ⫺0.50 0.98 ⫺2.50 ⫹2.00 ⫹0.80 ⫹0.50 1.51 ⫺1.75 ⫹5.00 ⫺0.75 ⫺0.50 0.68 ⫺2.50 0.00 ⫹0.43 ⫹0.25 1.40 ⫺2.00 ⫹3.75 ⫹0.88 ⫹0.75 1.21 ⫺1.38 ⫹3.88 ⫹0.14* ⫹0.25* 0.83 ⫺2.00 ⫹1.50* MR ⫽ manifest refraction; SE ⫽ spherical equivalent. *Indicates a reducation in overall astigmatism. Rojas and Manche22 used PTK on LASIK flaps for treatment of anterior basement membrane dystrophy-related epitheliopathy occurring after LASIK. Epithelial removal was performed with placement of 20% alcohol for 30 seconds, followed by mechanical debridement and PTK. A total of 6 pulses of laser were performed centrally (6.0-mm optical zone) and another 6 pulses of laser peripherally (3.0-mm optical zone). In their study of 10 patients, Rojas and Manche noted 2 eyes with diffuse lamellar keratitis stages 1 and 2 and another eye with trace corneal haze.22 All of the above complications resolved over time. In our study, diffuse lamellar keratitis did not develop in any eyes. Phototherapeutic keratectomy for vision-impairing chronic striae may seem undesirably aggressive because it represents a permanent alteration of the flap. However, PTK has the advantage of being the only intervention that directly reduces the optically disruptive elevations caused by striae. By limiting the amount of tissue removed to the ridges, we hypothesize that the stimulus for haze is minimized, whereas the PTK directly smoothes the optical surface to a level at which regrowth of epithelium is adequate to mask the remaining optical irregularities. For optically disruptive microstriae and for chronic macrostriae that do not respond adequately to the above intervention, the surgeon must determine that the epithelium has been supported adequately and has been allowed to heal. Epithelial hyperplasia between striae and hypoplasia over the striae ridges often mask the optical disruption of the striae. The first step in alleviating optically symptomatic striae, therefore, is to encourage optimal surface integrity with lubrication, punctal occlusion, consideration of an extended wear bandage contact lens in some cases, and time. One study showed that the corneal epithelial thickness peaks at the third month after LASIK in high myopes and LASIK flap. Unlike PRK, which removes anterior flap tissue to the depth necessary for the optical correction, PTK for striae by our technique is intended to remove only the elevated ridges of the striae, without violating most of the anterior Bowman layer. Because of the frequent reapplication of masking fluid during PTK, much of the laser energy was absorbed, and the depth of ablation cannot be calculated from the number of pulses delivered. However, the small hyperopic shift of 0.9 D, if performed as a PRK with a 6.5-mm optical zone, calculates to an ablation depth of less than 11 m. In the study by Carones et al, the deepest ablation was 60 m. Most patients in that series had excellent results at 1 month after PRK but a decline in vision and marked haze formation at 3 to 10 months after PRK. Some of the patients in our study were referred from long distances and were not available for long-term follow-up. However, 15 eyes were followed up for more than 3 months, including 7 eyes that were followed up for more than 6 months; late-onset haze did not develop in any of these eyes. In 9 of 23 eyes, trace to 1⫹ haze developed within the first postoperative month. Six of the 9 eyes with haze were followed up for more than 90 days without any evidence of haze progression. The 1 eye with loss of 1 line of BSCVA had only trace haze; the loss of BSCVA was believed to be the result of slight progression of myopic macular degeneration. Development of haze did not correlate with either the total number of laser pulses or the number of pulses applied to the stroma (Table 7). Kapadia and Wilson21 reported transepithelial PRK for optical correction after complicated flaps and caps in LASIK. In their series, 1 patient had a 30-m cap and the other had a 50-m flap. Transepithelial PTK was performed followed by PRK. By this method, the cap and the flap were completely ablated centrally. The authors reported no haze. Table 6. Operative Parameters Phototherapeutic Keratectomy Exposure Flap and Stromal Bed Thickness Analysis Total Pulses Transepithelial Phase Stromal Phase Pachymetry At Primary LASIK Bed Thickness Flap Thickness Mean Median Standard deviation Minimum Maximum 286 288 42 163 348 196 211 54 60 289 95 91 50 31 223 563 548 37 517 632 416 430 35 337 444 150 155 40 77 196 745 Ophthalmology Volume 111, Number 4, April 2004 Table 7. Laser Parameters, Follow-up Interval, and Corneal Haze Rating Eye No. Total Pulses 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 240 235 245 321 300 321 256 306 286 288 342 283 268 289 341 286 263 318 303 266 163 308 348 286 288 42 163 348 Stromal Phase Pulses 57 48 90 32 121 117 91 67 123 223 44 62 142 31 112 93 91 62 97 189 95 91 50 31 223 Interval After Phototherapeutic Keratectomy (days) Haze after Phototherapeutic Keratectomy 262 235 222 58 125 204 75 354 193 211 131 30 112 66 48 84 117 106 78 60 105 105 105 129 106 80 30 354 Trace Trace 1⫹ 0 1⫹ 0 0 0 0 0 Trace 0 0 Trace Trace 0 0 0 1⫹ 0 0 0 Trace Mean Median Standard deviation Minimum Maximum remains stable thereafter.23 Therefore, it may be advisable to wait at least 3 months after LASIK to determine if the symptoms attributable to striae are relieved. In some cases, however, loss of vision may be so impairing that the functional needs of the patient justify earlier intervention. If conservative measures fail, we believe that the results of PTK as demonstrated in this series merits consideration of PTK as the definitive intervention to ameliorate visual disruption attributable to striae. The key elements in successful PTK on a LASIK flap are (1) determination of which striae are optically significant by examination of the fluorescein tear pattern, the placido mires, and the effect of a diagnostic contact lens refraction; (2) transepithelial treatment while monitoring fluorescence to determine when the masking effect of the epithelium is diminishing; (3) limited further PTK pulses using an artificial tear as a masking agent, recognizing that the flap may be thin and that the goal is reduction but not elimination of the striae; (4) postoperative support of the regenerating epithelium with administration of intensive lubrication. References 1. Gimble HV, Penno EE, van Westenbrugge JA, et al. Incidence and management of intraoperative and early postoperative complications in 1000 consecutive laser in situ keratomileusis cases. Ophthalmology 1998;105:1839 – 47; discussion 1847– 8. 746 2. Tham VM, Maloney RK. Microkeratome complications of laser in situ keratomileusis. Ophthalmology 2000;107:920 – 4. 3. Stulting RD, Carr JD, Thompson KP, et al. Complication of laser in situ keratomileusis for correction of myopia. Ophthalmology 1999;106:13–20. 4. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999;127:129 –36. 5. Hernandez-Matamoros J, Iradier MT, Moreno E. Treating folds and striae after laser in situ keratomileusis. J Cataract Refract Surg 2001;27:350 –2. 6. Muñoz G, Alio JL, Perez-Santonja JJ, Attia WH. Successful treatment of severe wrinkled corneal flap after laser in situ keratomileusis with deionized water. Am J Ophthalmol 2000; 129:91–2. 7. Ambrosio R Jr, Wilson SE. Complications of laser in situ keratomileusis: etiology, prevention, and treatment. J Refract Surg 2001;17:350 –79. 8. Melki SA, Azar DT. LASIK complications: etiology, management, and prevention. Surv Ophthalmol 2001;46:95–116. 9. Rabinowitz YS, Rasheed K. Fluorescein test for the detection of striae in the corneal flap after laser in situ keratomileusis. Am J Ophthalmol 1999;127:717– 8. 10. Cavanaugh TB, Lind DM, Cutarelli PE, et al. Phototherapeutic keratectomy for recurrent erosion syndrome in anterior basement membrane dystrophy. Ophthalmology 1999;106:971– 6. 11. Dinh R, Rapuano CJ, Cohen EJ, Laibson PR. Recurrence of corneal dystrophy after excimer laser phototherapeutic keratectomy. Ophthalmology 1999;106:1490 –7. 12. Migden M, Elkins BS, Clinch TE. Phototherapeutic keratectomy for corneal scars. Ophthalmic Surg Lasers 1996; 27(suppl 5):S503–7. 13. Zuckerman SJ, Aquavella JV, Park SB. Analysis of the efficacy and safety of excimer laser PTK in the treatment of corneal disease. 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Evaluation of photorefractive keratectomy retreatments after regressed myopic laser in situ keratomileusis. Ophthalmology 2001;108: 1732–7. 21. Kapadia MS, Wilson SE. Transepithelial photorefractive keratectomy for treatment of thin flaps or caps after complicated laser in situ keratomileusis. Am J Ophthalmol 1998;126:827–9. 22. Rojas MC, Manche EE. Phototherapeutic keratectomy for anterior basement membrane dystrophy after laser in situ keratomileusis. Arch Ophthalmol 2002;120:722–7. 23. Spadea L, Fasciani R, Necozione S, Balestrazzi E. Role of the corneal epithelium in refractive changes following laser in situ keratomileusis for high myopia. J Refract Surgery 2000;16: 133–9.