Effects of laser in situ keratomileusis (LASIK) on the corneal endothelium

Effects of Laser In Situ Keratomileusis (LASIK) on the Cornea1 Endothelium

SARAH S. JONES, MD, RAMZY C. AZAR, BS, STEPHEN M. CRISTOL, MD, MPH, DAYLE H. CEROSKI, PHD,

GEORGE 0. WARING III, MD, R. DOYLE STULTING, MD, PHD, KEITH P. THOMPSON, MD, AND HENRY F. EDELHAUSER, PHD

l PURPOSE: To assess the effects of laser in situ keratomileusis (LASIK) on the cornea1 endothelium. l METHODS: Ln a prospective study, the cornea1 endothelium of 98 eyes of 65 consecutive patients (mean age, 41 years; range, 22 to 66 years) was photographed before, 2 weeks after, and 12 weeks after LASIK for the correction of 2.75 to 14.5 diopters of myopia. Theoretical ablation depths were 200 to 330 pm below the cornea1 surface. Cell density, coefficient of variation, and percent of hexagonal cells were determined using 150 to 200 cells from each image. Eighty-eight eyes (91%) of 59 patients had a history of contact lens wear. l RESULTS: The mean * SD preoperative endothelial cell density was 2,549 +: 365 cells per mm2, and the mean coefficient of variation was 0.35 f 0.06. There was no statistically significant change in the mean endothelial cell density or mean coefficient of variation of cell size at the 2eweek (2,561 +, 360 cells per mm’ and 0.35 +, 0.06) or 12-week (2,541 + 364 cells per mm2 and 0.35 + 0.05) postoperative examinations. The percent of hexagonal cells was not significantly changed 2 weeks postoperatively; however, 12 weeks postop-

Accepted for publicanon July 30, 1997. From the Emory Eye Center, Emory University School of Medicine,

Atlanta, Georgia. Supported in part by grants P30 EY06360 and EY00933 from the National Institutes of Health. Bethesda, Marvland. and bv Research to Prevent Blindness, Inc, New York, New York. Dr Edelhauser 1s a Research to Prevent Blindness Senior Scientific Investigator Awardee. Dr Waring is a consultant for Chiron Vision.

Reprint requests to Henry F. Edelhauser, PhD, Emory Eye Center, 1365B Clifton Rd NE, Ste B2600, Atlanta. GA 30322; fax: (404) 778-4143; e-mail: [email protected]

eratively (P = ,0413, twostailed t test), the percent of hexagonal cells was decreased by 1%. l CONCLUSIONS: Cornea1 endothelial cell density and morphology were unchanged 2 and 12 weeks after LASIK for the correction of up to 14.5 diopters of myopia. In this LASIK study, the correction of up to 14.5 diopters of myopia appears to cause no clinically significant effect on cornea1 endothelial cell density or morphology. (Am J Ophthalmol 1998;125:465-471. 0 1998 by El- sevier Science Inc. All rights reserved.)

L ASER IN SITU KERATOMILEUSIS USING THE 193-NM

excimer laser is a promising surgical technique because it avoids disruption of the Bowman layer

in the central cornea and can correct high degrees of myopia. However, this procedure might damage the cornea1 endothelium. The potential mechanisms for endothelial injury by excimer laser photoablation include thermal damage, mechanical damage from shock waves, and actinic damage from the ultraviolet light.1’2 In previous photorefractive keratectomy studies,3*9 there were no reported changes in endothelial cell density at 1 year as measured with contact specular microscopy. However, ablations within 130 to 200 km of the rabbit cornea1 endothelium in- creased endothelial permeability and caused morphometric alterations.‘” In another study, endothelial cell density decreased after photorefractive keratectomy to a depth of 150 pm in human corneas cultured in serum-free medium.” These studies suggest that deep excimer ablation of the cornea may damage endothelial cells under certain conditions.

Although superficial ablation of the human cornea

0002..9394/98/$19.00 0 1998 BY ELSEVIER SCIENCE JNC. ALL RIGHTS RESERVED. 465

by photorefractive keratectomy for the correction of mild to moderate myopia does not appear to damage the cornea1 endothelium, little information is avail- able about the effects of laser in situ keratomileusis on the human cornea1 endothelium. Because ablations with laser in situ keratomileusis are significantly closer to the cornea1 endothelium than those of photorefractive keratectomy are, we evaluated the effects of laser in situ keratomileusis on the cornea1 endotheli- urn using a noncontact specular microscope and morphometric analysis 2 and 12 weeks after excimer laser in situ keratomileusis.

PATIENTS AND METHODS

IN A PROSPECTIVE STUDY, 65 CONSECUTIVE PATIENTS (98

eyes) who met the inclusion criteria for a clinical investigation of excimer laser in situ keratomileusis for the treatment of myopia were enrolled between Sep- tember 1 and October 3 1, 1995. Patients were eligible for inclusion when they were aged 18 years or older, had a manifest spherical equivalent refractive error of -2.00 to -30.00 diopters with no more than 4.00 diopters of refractive astigmatism, had normal video- keratography with no signs of keratoconus, had a normal anterior segment by slit-lamp microscopy, did not have glaucoma or ocular hypertension, did not have systemic collagen vascular disease, were not pregnant, were not using systemic corticosteroids, had a realistic understanding of the risks and benefits of refractive surgery, were capable of returning for follow-up examinations, and were willing to discontinue contact lens wear for 3 days (soft) or 2 weeks (rigid) before baseline preoperative measurements. All eyes underwent laser in situ keratomileusis with a 193-nm argon fluoride excimer laser at the Emory Vision Correction Center. The mean age of the patients was 41 years (range, 22 to 66 years), and the mean attempted correction was 7.40 diopters (range, 2.75 to 14.5 diopters). Eighty-eight eyes of 59 patients (91%) had a history of contact lens wear. Eyes were evaluated 2 and 12 weeks after surgery; 10 eyes were lost to follow-up after the 2-week evaluation. The experimental protocol was approved by the Emory Univer- sity Human Investigations Committee; informed consent was obtained from all patients participating in the study.

The laser was calibrated according to the manufacturer’s instructions. The dioptric power entered into the laser’s computer was determined from the Emory Vision Correction Center nomogram. The number of pulses and diaphragm mask settings were determined by the manufacturer’s software algorithms.

Patients were prepared and draped for the procedure in the customary fashion. An eyelid speculum was inserted. An eight-blade radial keratotomy mark- er coated with methylene blue was used to mark the cornea. The suction ring of the automated cornea1 shaper was applied to the surface of the globe, and the intraocular pressure was verified to be greater than 65 mm Hg with a Barraquer applanation tonometer. A microkeratome with a 160+m plate was inserted into the suction ring, advanced to the stop, reversed, and removed. The lamellar flaps were typically 8.5 mm in diameter with a OS-mm-wide nasal hinge. The thickness of the flap was not measured. After the flap was folded back with forceps, the excimer laser was centered on the patient’s pupil, and the ablation was performed. Single-zone (6.0-mm) or multizone treatment was used for correction of 7.0 diopters or less. Multizone treatments were used for corrections greater than 7.0 diopters, with a central diameter of 5.5 mm, an intermediate zone of 6.0 mm diameter, and a peripheral zone of 6.5 mm diameter (Figure 1). The cornea1 flap was replaced using the methylene blue lines for alignment. The speculum was removed after approximately 5 minutes, and the security of the flap was verified after eyelid movement. Patients were examined by slit- lamp 10 minutes after removal of the speculum, on the first postoperative day, and at 2 and 12 weeks postoperatively.

Endothelial specular microscopy was done preoper- atively and at 2 and 12 weeks postoperatively. The Konan ROB0 Non-contact Specular Microscope (Konan Medical Corporation, Fairlawn, New Jersey) enabled postoperative morphometric evaluation with- out disturbing the flap. Sampling error was reduced by analyzing as many cells (150 to 200) as possible. Images were captured from the central cornea be- neath the area of ablation. The microscope’s image analysis software computed cell density, coefficient of variation of cell size, and percentage of hexagonal cells. Preoperative images were captured with the “autofocus” on the specular microscope (focal plane approximately 500 pm behind the epithelial surface).

466 AMERICAN JOURNAL OF OPHTHALMOLOGY APRIL 1998

(4D=40wm)

(8D=84pm)

(12D=125pm)

(>12D=172,um)

FIGURE 1. Diagram of laser in situ keratomileusis. The cornea1 flap is approximately 160 pm thick. Theoretic ablation depths of the cornea1 stroma are shown for selected corrections (with the nomogram used in this study, an assumed ablation rate of 0.25 pm per pulse) and an assumed preoperative cornea1 thickness of 540

Pm-

Postoperatively, manual setting of the focal plane was necessary for most eyes to obtain good specular images of the endothelium. A single instrument and two operators (two of us, S.S.J. and R.G.A.) were used throughout the study.

The microscope was calibrated according to the manufacturer’s specifications. To determine precision, 36 images of each eye of one author (R.G.A., aged 23 years) were recorded on 18 different days from Sep- tember 1995 to January 1996. The 36 images showed a mean cell density of RE, 2,545 + 45 cells and LE, 2,600 + 41 cells; mean coefficient of variation was RE, 0.28 t 0.02 and LE, 0.27 + 0.02; and mean percent of hexagonal cells was RE, 78% 5 3% and LE, 75% + 4%.

The changes in cell density, coefficient of variation, and percent of hexagonal cells from preoperative values were determined at 2 weeks and 12 weeks postoperatively (Student two-tailed e test). Changes in the cell density and percent of hexagonality were also modeled using multiple linear regression to adjust for covariates including patient age, history of contact lens wear, refractive error, and preoperative endothe-

lial cell density. Colinearity among the covariates precluded a general analysis of interaction (all possible interaction terms), but interaction among significant covariants in models was investigated. The coefficient of variation was modeled nonparametrical- ly with each of the covariates (Kruskal-Wallis test). Data from all eyes were assumed to be statistically independent. To validate this assumption, the overall results of the study were reanalyzed using data from only one eye per patient (the eye to be excluded was selected by a coin toss). The exclusion of the poten- tially nonindependent data did not alter the results. Tests used a significance level of alpha = 0.05. Power calculations were performed for selected analysis.

RESULTS

THE MEAN PREOPERATIVE CENTRAL ENDOTHELIAL CELL

density for all 98 eyes was 2,549 + 365 cells per mm* (range, 1,364 to 3,278 cells per mm”) (Table 1). After surgery, no significant change in cell density from the preoperative value was observed at 2 weeks (2,561 + 360 cells per mm’, P = .3586, two-tailed t test) or 12 weeks (2,541 + 364 cells per mm2, P = .9211, paired t test; Figure 2, left). There were also no changes in cell density at the 2-week and 12-week examinations using multivariate regression to adjust for age, refractive error, and contact lens wear. Similarly, the coefficient of variation remained unchanged from the preoperative values at 2 weeks (P = .3710, Wilcoxon signed rank test) and 12 weeks (P = 6938, Wilcoxon signed rank test; Figure 2, middle). The percent of hexagonal cells did not differ significantly from the preoperative value 2 weeks after surgery (P = .3236, two-tailed t test), but there was a 1% decrease at 12 weeks (P = .0413, two-tailed t test; Figure 2, right). The power of the study to detect a 2% change in the cell density at 2 and 12 weeks exceeded 95% and 99%, respectively.

Preoperative endothelial cell density was inversely related to age (Table 1). Statistical modeling suggests that patients with higher cell densities lost more cells than did those with lower cell densities; moreover, the number of cells lost was proportional to the preoperative cell density. There was no statistical relation between preoperative cell density and preoperative refractive error.

VOL. 12.5, No. 4 LASER IN SITU KERATOMILEUSIS 467

1 2 nks l2wks

(R 0.4

z 0 0 1

z m-o.4 m til

I -0.6

E 8 -1.2 &

0 .E -1.6

8 s -2

6 -2 4

2 wks I2 wks

FIGURE 2. Change from preoperative values at 2 and 12 weeks after laser in situ keratomileusis. Bars show mean and 95% confidence intervals. Only the percent of hexagonal cells at 12 weeks (right) shows a statistically significant difference.

The overall coefficient of variation remained unchanged. Adjusting for preoperative refractive error disclosed a small but statistically significant change in the coefficient of variation at both 2 weeks (I’ = .0044, Kruskal-Wallis test) and 12 weeks (I’ = .0134, Kruskal-Wallis test) postoperatively (Table 2). The percent of hexagonal cells remained unchanged from the preoperative value at 2 weeks and 12 weeks (Table 2) when compared with the preoperative refractive error.

The 10 eyes of six patients with no history of contact lens wear were compared with the 88 eyes of 59 patients who previously had worn either soft or rigid contact lenses. Prior contact lens wear did not affect the change in cell density, coefficient of variation, or percent of hexagonal cells at either follow-up visit. However, eyes with a longer history of contact lens wear (more than 25 years) had the lowest preoperative cell density, the lowest percent of hexagonal cells, and the highest coefficient of variation within the contact lens-wearing group (Table 3). An unexpected finding was that the 10 patients who did not wear contact lenses had the lowest preoperative cell density (Table 3).

DISCUSSION

LASER IN SITU KERATOMILEUSIS IS A NEW PROCEDURE

that allows correction of high degrees of myopia.TJ* However, this type of treatment may cause cornea1 endothelial damage.

Experimental studies on rabbits and nonhuman primates have shown that superficial excimer laser ablation of the cornea1 surface does not damage the cornea1 endothelium.“~‘” More recent studies demon- strated endothelial cell loss with deep excimer laser ablations.1”J7,23 In two studies, Marshall and associates”“’ reported that endothelial cells were lost after nonpenetrating excimer laser incisions to within 40 pm of the Descemet membrane. Rabbit studies by Koch and associates” and Deham and associates*’ reported that ablation of 90% of the stromal depth structurally altered the endothelium. In the present study, the depth of ablation was not measured direct- ly. However, it can be calculated to be from 208 to 340 km from the cornea1 endothelium, assuming 0.25 km per laser pulse, a flap thickness of 160 pm, and a preoperative central cornea1 thickness of 540 pm (Figure 1). Thus, the residual cornea1 thickness after excimer laser ablation in this study approached that at which morphometric endothelial changes have been seen experimentally.”

After radial keratotomy’ and photorefractive keratectomy, a number of studies have shown no clinically significant changes in cornea1 endothelial cell density, coefficient of variation, or percent of hexagonal cells with follow-up of up to 2 years after surgery.2-5 However, Pallikaris and Siganos,7 in a series of 10 eyes after photorefractive keratectomy for severe myopia (corrections of -8.80 to - 17.60 diopters), reported that the central endothelial cell density was reduced by 5.69% at 6 months and 10.56% at 1 year postoperatively. One recent study’ showed a transient loss of


Mean t SD

Patient

Age (YW

Cell Density (cells/mm2) Coefficient of Variation of Cell Size Hexagonal Cells (%)

preop- 2 Weeks Post- 12 Weeks Post- PreOp- 2 Weeks Post- 12 Weeks Post- preop- 2 Weeks Post- 12 Weeks Post-

erative operative operative eratlve operative operative era&e operative operative

(n = 13) (n = 13)

%I- 2,w@ 3 m 2, d 3’12 28)

(n = 40) (n = 40)

(n = 98) (n = 98)

, Mean r SD

Preoperative Spherical

Cell Density (cells/mm2) Coefficient of Variation Hexagonal Cells (%)

Equwalent preop- 2 Weeks Post- 12 Weeks Post- Preop- 2 Weeks Post- 12 Weeks Post- Preop- 2 Weeks Post- 12 Weeks Post-

(D) erative operative operative erative operative operative eratlve operatlve operative

-%nJlo-4.00 2,627Srcll RPillSam 0;&&*4&3 @‘m *&Ml l.a!smO,Q% Qi,iw~o‘m eDa@ Ik:b gshllas (n = 22) (n = 22) (n = 21)

-5.00 to -7.00 2,454 * 372 2,486 -t 366 2,416 r 376 0.37 + 0.06 0.36 t 0.08 0.35 or 0.04 5Q 6 + 58 7 i 57 ?z 6

(n = 26) (n = 26) (n = 23)

-7.00 to -9.50 2,561 zt 299 2,5Q7 rt 321 2,685 r 304 0.36 r 0.06 0.36 rt 0.07 0.35 A 0.06 58 6 t 68 iz 7 5627

(n = 24) (n = 24) (n = 21)

2,%44 x cm 2,%%1 1340 'O+aLv * 0.0% 0440 * o.tw O.&s f: B.06 erl f e, f# r4t 0‘ @%*a

(n = 26) (n = 26) (n = 23)

All 2,549 + 3f% 2,561 A 380 2,641 it 364 0.35 k 0.08 0.38 f 0.06 035 rt 0.06 59 tt 6 89*6 56c8

(n = 98) (n = 98) (n = 88)

peripheral cornea1 endothelial cells 1 year after post- photorefractive keratectomy, which reversed by 2 years.”

Toda and associates24 reported endothelial edema and inflammatory cells attached to the endothelium 4 days after photorefractive keratectomy. The endothelial cell area did not change significantly, and there was no change in the cell number 1 month after photorefractive keratectomy. Rosa and associates2’ compared the cell number and the shape of cornea1 endothelial cells in 25 eyes before and 6 months after photorefractive keratectomy with ablation depths of 25 to 170 pm for corrections ranging from -2.5 to - 17 diopters. They also found no change in endo-

thelial cell number or shape at 6 months. One study, however, described excimer laser-induced changes in the human cornea1 endothelium shortly after photorefractive keratectomy. Carones and associates26 found a small increase in cell density at 1 month and a significant change in the coefficient of variation and percent of hexagonal cells in patients after photorefractive keratectomy, for an average correction of 5.7 1 diopters with a maximum ablation depth of 160 km.

’ They found no correlation between endothelial change and the depth of ablation.

In this prospective study of 98 eyes that underwent laser in situ keratomileusis for the correction of 2.75 to 14.5 diopters of myopia, there was no significant

VOL. 125, No. 4 LASER IN SITU KERATOMILEUSIS 469

Duration of Mean + SD

contact Coefficient of Variation

LSW Cell Density (cells/mm2) Hexagonal Cells (“6)

Wear preop- 2 Weeks Post- 12 Weeks Post- preop- 2 Weeks Post- 12 Weeks Post- Preop- 2 Weeks Post- 12 Weeks Post-

(YW erative operative operative erative operative operatwe erative operative operative

NCltle 2,366 c 333 2,446 It 321 2,472 f 335 0.35 + 003 0.34 k 0.03 0.37 iz 0.04 6f + 7 82+? go+5

(rl = 10)

l-9 2,919 ?r 173

(l-l = 12)

10-18 2,644 zt 287

(n = 24)

19-25 2,495 k 469

(n = 22)

>25 2,419 2 262

(n = 30)

All 2,549 f 365

(n = 98)

(n = 10) (n = 9) 2,915 r 158 2,937 t 176 0.30 i: 0.02 0.32 i: 0.02 0.29 + 0.03 64 k 6 63rte 64 -+ 6

(n = 12) (n = 8)

2,662 rt 312 2,661 -c 279 0.33 r 0.04 0.33 + 0.04 0.32 + 0.03 83 zt 4 6225 80 " 6

(n = 24) (n = 22) 2,S13 + 470 2,477 + 4651 0.36 " 0.10 0.36 A 0.09 0.35 + 0.06 56 " 5 57 + 5 56i4

(n = 22) (n = 22) 2,397 + 241 2,410 -c 254 0.37 rt 0.05 0.39 + 0.08 0.37 It 0.06 56 k 5 5s f s 55 +- 6

(n = 30) (n = 27)

2,561 rrr 360 2,541 + 364 0.35 rt 0.06 0.35 + 0.06 0.35 -c 0.05 59 f. 8 59 f 8 58 + 6

(n = 98) (n = 88)

change in endothelial cell density or coefficient of variation, whereas the percent of hexagonal cells decreased 1% at 12 weeks postoperatively (Figure 2). We do not think that this small change in the percent of hexagonal cells is clinically meaningful. Pallikaris and Siganos7 reported that laser in situ keratomileusis did not induce significant endothelial cell loss in 10 eyes of 10 patients with an attempted myopic correction range from -8.00 to - 16.00 diopters. Our data confirm their findings.

In a recent laser in situ keratomileusis study, Perez-Santonja and associates27 reported the cornea1 endothelial findings on 45 eyes of 31 patients, 30 of whom were contact lens wearers. Their results showed that laser in situ keratomileusis caused no change in endothelial cell number, coefficient of variation, and hexagonality to the central endothelium in both groups of eyes at 3,6, and 12 months after laser in situ keratomileusis. The results of our study confirm their findings and show that 2 weeks after laser in situ keratomileusis, the central endothelium is similar to that of control eyes.

We were concerned that contact lens wearers who have polymegathism’” would be predisposed to further endothelial cell changes after laser in situ keratomileusis. In this study, 91% of the population were contact lens wearers, with 25% having more than 25 years of contact lens wear. Our results suggest

that contact lens wear did not predispose the cornea to further endothelial cell damage by laser in situ keratomileusis.

Long-term effects of laser in situ keratomileusis have been reported in only 3 1 patients (45 eyes) in a study by Perez-Santonja and associates.27 Based on our short-term observation and data, our study suggests that laser in situ keratomileusis is unlikely to cause endothelial damage. However, long-term follow-up studies are needed to confirm endothelial safety at 5 and 10 years.

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Authors Interactive@ We encourage questions and comments regarding this article via the Internet on Authors Interactive@ at http://www.ajo.com/ Questions, comments, and author responses are posted.

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Effects of laser in situ keratomileusis (LASIK) on the corneal endothelium

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