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30

LASEK After Penetrating Keratoplasty

Steven B.Yee, MD, Ning Lin, MD, OD, Corey B.Westerfeld, MD, and

Richard W.Yee, MD

Hermann Eye Center, University of Texas Health Science Center at

Houston

Houston, TX

LASEK IN THE PATIENT AFTER PENETRATING

KERATOPLASTY

As microsurgical techniques have improved, penetrating keratoplasty (PKP) has become more commonly performed with a higher probability of success. In the United States alone, more than 40,000 PKPs are performed annually (1). Anisometropia remains a challenging problem in the patient after PKP and the rehabilitation of this has changed little. The majority of patients are unable to tolerate more than 3 diopters (D) (sphere) of anisometropia because of the resulting aniseikonia (2,3). An astigmatism of 1.5 to 3 D is likewise poorly tolerated (2,3). Anisometropia may result in ocular burning, tearing, blurry vision, photophobia, diplopia, and headache. Many of the patients who cannot achieve adequate rehabilitation with spectacles can do so with contact lenses. Ten percent to 30% of patients wear contact lenses after PKP (4). Both soft and rigid gas-permeable contact lenses can be effective for visual rehabilitation after PKP (5). However, there remains a significant percentage of PKP patients (10%–20%) who cannot achieve adequate rehabilitation with spectacles or contact lenses (5).

Anisometropia aside, there are numerous concerns related to contact lens wear that can be problematic for patient status after PKP. They include topographical abnormalities resulting from the PKP wound, dry eyes, blepharitis, lid abnormalities, corneal neovascularization, occupational/environmental factors (wind, dust, smoke, chemical fumes, etc.), patient limitations (e.g., poor manual dexterity), and poor patient compliance.

In the past, various forms of refractive surgery have been attempted on cornea transplantation patients. Radial keratotomy (RK) in post-PKP patients has been fraught with problems, namely refractive instability, glare, haloes, increased risk of traumatic ruptured globe, and progressive hyperopia (6). Photorefractive keratectomy (PRK) in post-PKP patients has been associated with increased incidence of irregular astigmatism and corneal scarring (5). Laser in situ keratomileusis (LASIK) has been performed in post-PKP patients, also, and has shown better results than with RK and PRK. These advantages include rapid visual rehabilitation, less irregular astigmatism, less regression, and the ability to correct a greater range of refractive errors (7,8). However, even the proponents of LASIK have conceded that LASIK itself can induce irregular astigmatism.

LASEK, PRK, and excimer laser stromal surface ablation 372

Furthermore, there remain the risks associated with the creation of the lamellar flap. Buttonholes, partial flaps, thin/irregular flaps, and free flaps may occur (7–11).

Laser epithelial keratectomy (LASEK) offers the exciting possibility of visual rehabilitation in the post-PKP patient who has not had satisfactory rehabilitation with spectacles or contact lenses. Unlike LASIK, LASEK avoids flap creation and, thus, the problems associated with a flap. Compared to PRK, retaining the epithelium, as is performed in LASEK, would theoretically promote better healing and less postoperative haze (loss of corneal opacity).

OUR EXPERIENCE

We followed-up two patients with a previous PKP who underwent LASEK for myopia and astigmatism.

Patient 1 was a 59-year-old woman with a history of Fuchs endothelial dystrophy (with corneal decompensation). She has undergone the following operations: PKP right eye (OD) 1993, PKP left eye (OS) 1996, actinic keratosis (AK) OD 1994, AK OS 1998, and phacoemulsification with posterior chamber intraocular lens (PCIOL) OD 1994. Before LASEK, her manifest refraction was +1.25+3.00×043 (OD), and −10.25+4.25×175 (OS). She found her anisometropia to be extremely troubling; she reported constant blurry vision. She was unable to tolerate a contact lens in her left eye; her steep K reading (OS) was 52.59 at axis 164. She underwent LASEK OS using the Alcon Autonomous LADARVision 4000 Excimer Laser. Preoperative medications were ketorolac tromethamine ophthalmic solution (Acular) 0.5% one drop (gtt) OS four times daily and ofloxacin 0.3% one gtt OS four times daily both for 3 days before LASEK. Postoperative medications were ofloxacin 0.3% one gtt OS four times daily for 7 days, fluorometholone 0.1% 1 gtt OS four times daily for 7 days, autologous serum solution 1 gtt OS every 30 minutes for 4 days, then every 1 hour for 7 days, then four times daily. Ketorolac tromethamine (Acular) 0.5% 1 gtt OS four times daily was resumed 3 weeks after LASEK as treatment of overcorrection. Post-LASEK use of ketorolac tromethamine is reserved for overcorrection.

Patient 2 was a 16-year-old boy with a history of keratoconus of his right eye. He underwent PKP OD. After PKP OD and before LASEK, his manifest refraction was −5.00, +4.00, ×145 (OD), and Plano +0.25 and ×080 (OS). The patient was unable to tolerate a contact lens in his right eye. He underwent LASEK OD 6 months after PKP. LASEK was performed using the Alcon Autonomous LADARVision 4000 Excimer Laser. Preoperative medications were ketorolac tromethamine ophthalmic solution (Acular) 0.5% 1 gtt OS four times daily for 3 days before LASEK. Postoperative medications were ofloxacin 0.3% 1 gtt OD four times daily for 7 days, fluorometholone 0.1% 1 gtt OD four times daily for 7 days, then twice daily for 7 days, autologous serum solution 1 gtt OD every 30 minutes for 4 days, then every 1 hour for 7 days, then every 2 hours for 3 days, then four times daily. Prednisolone (Pred Forte) 1% 1 gtt OD four times daily was begun 1 month after LASEK as therapy for “undercorrection” (residual myopia).

After a standard preparation and drape, the cornea was marked at the 6 o’clock position. Using a LASEK trephine (60-to 80-—m trephine), epithelial micro-trephination

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was performed, leaving a hinge of approximately 60 degrees to 80 degrees at the 12 o’clock position (Fig. 1). A LASEK alcohol well was then placed on the eye and filled with a 20% ethanol solution for 40 seconds (Fig. 2). The ethanol solution was then blotted with a dry Weck sponge and rinsed with balanced salt solution (BSS). The epithelium was then detached using an epithelial hoe (Fig. 3). The epithelium was peeled back resulting in

Figure 1 Epithelial trephination.

Figure 2 Instillation of 20% alcohol

LASEK, PRK, and excimer laser stromal surface ablation 374

Figure 3 Epithelial detachment.

Figure 4 Recession of the epithelial flap.

a hinge at the 12 o’clock position (Fig. 4). After laser ablation by small spot-tracking laser (Fig. 5), mitomycin-C (0.05%) was applied to the stroma and left in place for 90 seconds before being rinsed with BSS (Fig. 6). The epithelium was then replaced with a spatula (Fig. 7). A soft bandage contact lens was applied. The soft bandage contact lens was removed in the clinic using jeweler’s forceps on post-LASEK day 4.

Patient 1 had preoperative manifest refractions of +1.25, +3.00, ×043 (OD), and −10.25, +4.25, ×175 (OS). Preoperative BCVA was 20/20 in both eyes. LASEK was

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375

performed on her left eye, and the sphere was reduced to −2.50 D at 12 months after LASEK. Her spherical equivalent was reduced from –8.13 D preoperatively to +3.25 D at 3 weeks after LASEK, +1.12 D at 4 weeks after LASEK, −0.75 D at 3 months after LASEK, and −2.00 D at 12 months after LASEK. The cylinder before the surgery was +4.25 D, and at 5 months after LASEK it was +1.00 D. Topography revealed a preLASEK color unit (CU) index of 50% (Fig. 8) and a post-LASEK CU index of 20% (Fig. 9). At 3 months after LASEK, the CU index was 50%, and at 5 months after LASEK,

Figure 5 Small spot excimer treatment.

Figure 6 Mitomycin-C (0.05%) administration

the CU index was 50%. The slit-lamp examination on post-LASEK day 5 revealed a central epithelial defect (OS). A soft bandage contact lens was placed, and 3 days later, the defect had healed completely. The slit-lamp examinations postoperatively revealed a clear cornea, completely free of haze. Her spherical equivalent anisometropia was

LASEK, PRK, and excimer laser stromal surface ablation 376

reduced from 11.88 D to 4.75 D. Her BCVA in the postoperative eye was 20/20 at 12 months postoperatively (uncorrected visual acuity was 20/80). (Figs. 8 and 9)

Patient 2 had preoperative manifest refractions of −5.00, +4.00, and ×145 (OD), and Plano +0.25 and ×080 (OS). Preoperative BCVA was 20/20 OD and 20/30 OS. LASEK was performed on his right eye, and the sphere was reduced to −0.75 D at 9 months after LASEK. His spherical equivalent was reduced from −3.00 D preoperatively to −0.38 D at 4 weeks after LASEK and −0.25 D at 9 months after LASEK. The cylinder before the surgery was +4.00 and at 1 month after LASEK was +0.75. At 9 months after LASEK, the cylinder was +1.00. Topography revealed a pre-LASEK CU index of 40% (Fig. 10) and a post-LASEK CU index of 60% (Fig. 11). The CU index at 3 months after LASEK was 90%. The slit-lamp examination on post-LASEK day 4 revealed no epithelial defects (OD). However, the right eye was somewhat red, and the patient reported light sensitivity. His medications were continued, and on post-LASEK day 6, the patient’s symptoms had abated. The slit-lamp examination at 1 week found the cornea to be clear and free of haze. The slit-lamp examinations at 1 month and 3 months revealed trace corneal haze. His BCVA in the postoperative eye was 20/20 at 9 months postoperatively (uncorrected visual acuity [UCVA] was 20/25). (Figs. 10 and 11)

Figure 7 Repositioning epithelial flap

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Figure 8 Patient 1. Preoperative topography showing astigmatism: +2.57 D, axis 167.

Figure 9 Patient 1. Postoperative (2 months) topography showing astigmatism: +0.92 D, axis 85.

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Figure 10 Patient 2. Preoperative topography showing astigmatism: +3.42 D, axis 138.

Figure 11 Patient 2. Postoperative (1 month) topography showing astigmatism: +1.29 D, axis 93.

BCVA remained within two lines of preoperative visual acuity in both patients. At the last follow-up visit, the mean sphere was reduced by 6.0 D (78%), and the mean cylinder

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379

was reduced by 3.12 D (76%) from the preoperative values. The mean spherical equivalent was reduced by 4.44 D (80%) from preoperative values.

The complications related to LASEK surgery included a central epithelial defect in patient 1 and trace cornea haze in patient 2. However, both complications resolved satisfactorily. No graft rejection was associated with LASEK. No other intra-operative or postoperative complications were observed.

CONCLUSION

We demonstrated that LASEK can be safely performed in post-PKP patients to reduce significant anisometropia and myopia. One of our patients demonstrated more irregular astigmatism at the center of the cornea at 2 months after LASEK than preoperatively. However, at 3 and 4 months after LASEK, additional time and healing resulted in an improvement in the patient’s irregular astigmatism. LASEK did decrease the amount of anisometropia in both post-PKP patients. Both patients were extremely pleased with the reduction in the amount of anisometropia that LASEK afforded them. Our hope is that in the future, more patients who are post-PKP, anisometropic, and unable to tolerate contact lenses will be able to benefit from LASEK on several counts: (1) reduction of anisometropia; (2) reduction of astigmatism; and (3) avoid the potential complications involving flap creation by a microkeratome (as in the case of LASIK). LASEK coupled with wavefront-guided or custom cornea ablation may provide even better outcomes.

REFERENCES

1.Statistical Report, Eye Bank Association of America. Washington. DC, 1993.

2.Brooks SE, Johnson D, Fischer N. Anisometropia and binocularity. Ophthalmology; 1996; 103:1139–1143.

3.Rubin ML. Anisometropia Faunfelder FT, Hampton RF, Grove J, Eds. Current Ocular Therapy 4. Philadelphia: Saunders, 1995:757–758.

4.Donnenfeld ED, Kornstein HS. LASIK for correction of myopia and astigmatism after penetrating keratoplasty. Ophthalmology; 1999; 106(10):1966–1975.

5.Lopatynsky MO, Cohen EJ. Post-keratoplasty fitting for visual rehabilitation Kastl PR, Ed. Contact Lenses: The CLAO Guide to Basic Science and Clinical Practice. Dubuque. Iowa: Kendal/Hunt Publishing Co., 1995:79–90.

6.Waring GO III, Lynn MJ, Gelender H. Results of the Prospective Evaluation of Radial Keratotomy (PERK) Study one year after surgery. Ophthalmology; 1985; 92:177–198, 307.

7.Pallikaris IG, Papatzanski ME, Stathi EZ. Laser in situ keratomileusis. Lasers Surg Med; 1990; 10:463–468.

8.Azar DT, Farah SG. Laser in situ keratomileusis versus photorefractive keratectomy. An update on indications and safety. Ophthalmology; 1998; 105:1357–1358.

9.Malecha MA, Holland EJ. Correction of Myopia and Astigmatism after Penetrating Keratoplasty with Laser in Situ Keratomileusis. Cornea; 2002; 21(6):564–569.

10.da Lima GS, Moreira H, Wahab S A. Laser in situ keratomileusis to correct myopia, hypermetropia and astigmatism after penetrating keratoplasty for keratoconus: a series of 27 cases. Can J Ophthalmol; 2001; 36(7):391–397.

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11. Kwitko S, Marinho DR, Rymer S, Ramos Filho S. Laser in situ keratomileusis after penetrating keratoplasty. J Cataract Refract Surg; 2001; 27(3):374–379.