With improved microsurgical techniques, penetrating keratoplasty (PKP) has become a more common and successful procedure, with approximately 35,000 surgeries performed annually. Visual rehabilitation following a penetrating keratoplasty is often challenging because of anisometropia and astigmatism. Most patients will not tolerate more than 3 diopters of anisometropia because of image size disparity or astigmatism of greater than 1.5 to 3 diopters.
Rigid gas-permeable (RGP) contact lenses have been the mainstay of refractive rehabilitation following PKP. However, surgical options may be the only alternative to treat post-PKP refractive error. Kirkness et al reported a series of 201 corneal transplants for keratoconus and found that 18% of patients required refractive surgery for the correction of post-PKP astigmatism.
With the demonstrated success of photorefractive keratectomy (PRK) in treating myopia and astigmatism, PRK has been studied and used to treat post-penetrating keratoplasty refractive errors. However, significant haze following PRK is especially problematic in patients who have undergone prior keratoplasty. The corneal haze may reduce best spectacle-corrected visual acuity (BSCVA), induce regression and irregular astigmatism, and cause visual symptoms including haloes, blurred vision, and glare. Maloney and colleagues described a 29% incidence of corneal haze in patients undergoing PRK for visual rehabilitation following PKP.
Laser in situ keratomileusis (LASIK) has been demonstrated to offer patients the opportunity to be visually rehabilitated following a corneal transplantation. The first series of LASIK following penetrating keratoplasty reported a mean reduction of myopia from 7.58 diopters to 1.14 diopters and cylinder from 3.64 diopters to 1.48 diopters. BSCVA improved or remained the same in 21 of 23 patients, and all patients had less than 3 diopters of anisometropia. Additional studies have confirmed the safety and efficacy of LASIK following PKP for the management of residual refractive errors. Although LASIK has revolutionized the visual rehabilitation of the corneal transplant patient, no surgical procedure is risk-free. The purpose of this study is to report 3 patients who experienced flap dislocation following penetrating keratoplasty for bullous keratopathy.
DISCUSSION
All 3 patients had bullous keratopathy as the indication for penetrating keratoplasty, and all had peripheral corneal edema at the time of the LASIK procedure, with flap slippage occurring at a mean of 7 days postoperatively (range 3 to 14 days). The incidence of flap dislocation in this population of eyes following PKP was 1.85% compared with an incidence of 1.22% of complete and partial flap dislocation after LASIK in normal corneas. The incidence of flap dislocation in a recent study of LASIK following PKP of 57 eyes was as high as 9%. The peripheral corneal edema was the common factor in these 3 post-LASIK patients who had had a prior PKP for bullous keratopathy. To our knowledge, this is the first report of a series of patients experiencing corneal flap dislocation following LASIK after PKP for bullous keratopathy.
The final results of treatment of flap slippage were varied. One patient had a 2-line loss of BSCVA after flap slippage and underwent flap suturing, with an UCVA of 20/40 and a return to preoperative BSCVA of 20/25. One patient had a flap suturing with no change in BSCVA of 20/40. The final patient initially had a 5-line loss of BSCVA following flap repositioning, and underwent a repeat PKP for decreased visual acuity due to irregular astigmatism. His final BSCVA demonstrated a 2-line decrease in BSCVA.
This small case series highlights the importance of the endothelial pump function in maintaining the adherence of the LASIK flap. The corneal flap following LASIK is initially held in place by suction created by the pumping function of the endothelium against an intact epithelium. Any evidence of epithelial or stromal corneal edema is a sign that the endothelial pump function has been reduced below the natural swelling pressure of the cornea, and the adherence of the flap may not be adequate to prevent flap slippage.
Risk for development of corneal edema is increased in corneal grafts because of their decreased number of endothelial cells. The mean human endothelial cell density starts at about 4000 cells/mm2 in the first decade of life. As the eye ages, the average cell density gradually levels off to approximately 2600 cells/mm2 by age 40 but decreases to less than 300 cells/mm2 in patients with bullous keratopathy. The average cell density of donor corneas is around 2665 cells/mm, but grafts undergo a more rapid and continual decline in endothelial cell count than do normal corneas, with cell loss of 7.8% per year for the first 5 postoperative years, followed by a 4.7% annual decline for years 5-10. This is contrasted to a 0.5% per year decline in normal controls.
If the corneal endothelial barrier is injured, the corneal thickness can increase more than two-fold. A wounded endothelial barrier will cause a much greater increase in corneal thickness than a damaged epithelial barrier. The corneal stroma swells once the barrier or metabolic pump function is damaged because of the hypertonicity of the stromal milieu, which contains collagen, proteoglycans, and salts that are hypertonic to both tears and aqueous humor. These factors contribute to the corneal stromal swelling pressure, which has been determined to be approximately 60 mm Hg. The corneal stroma will also become edematous if the endothelial barrier is disrupted because the normal intraocular pressure of 15 mm Hg will be unopposed, and aqueous will diffuse into the stroma.
Even if a corneal graft is clear and nonedematous before LASIK, the surgeon needs to consider the possibility of endothelial compromise from the LASIK procedure itself. Although some studies have found no long-term endothelial effects of LASIK, 1 study does demonstrate post-LASIK changes in corneal morphology. Jones and colleagues found no effect on the endothelium in 98 eyes followed up to 12 weeks after LASIK. Pérez-Santonja and associates who followed patients over 6 months found that endothelial parameters in contact lens wearers actually improved after LASIK because of the discontinuation of contact lens wear. One study of 4 patients who underwent LASIK after penetrating keratoplasty and were followed for 12 months found no change in the endothelium. However, changes in endothelial cell morphology, probably related to transient corneal edema, were noted at 15 minutes postoperatively by Kim et al. Although these changes resolved by the first postoperative day, they could compromise endothelial pump function in postkeratoplasty eyes.
As part of the LASIK evaluation in postkeratoplasty eyes, we recommend a careful examination of the corneal graft for evidence of corneal edema. Because corneal endothelial function is best measured by corneal pachymetry, the pachymetry should be reviewed not only for adequate post-LASIK bed thickness but also for evidence of edema. Specular microscopy may be performed if there is clinical suspicion of low endothelial cell density. Once epithelial edema or bullae have occurred, the pump function of the endothelium has been overwhelmed, resulting in decreased flap suction, which increases the risk of flap dislocation.
For LASIK performed on a postkeratoplasty eye with Fuchs dystrophy or pseudophakic bullous keratopathy, or any postkeratoplasty eye in which the endothelial pump function may be marginal, we recommend an 8.5-mm-diameter superior hinge flap, particularly when the peripheral host bed has frank edema. None of the cases in this series had a superior hinge combined with an 8.5-mm-diameter corneal flap. If the peripheral cornea is edematous and the pump function of the endothelium is decreased, it is more likely the peripheral flap will elevate and dislocate following a blink. A larger flap will have a greater surface area over the peripheral edematous bed, and the edge of the flap may elevate, whereas the smaller diameter flap has less tissue overlying the edematous peripheral bed and is less likely to elevate. We recommend a superior flap for patients who undergo LASIK following PKP for bullous keratopathy because the natural gravitational effect will tend to hold the flap in place better than a nasal hinge flap.
We also recommend that patients with endothelial compromise who undergo LASIK wear protective shields for a longer than normal period and be followed closely to reduce the risk of flap slippage. Endothelial cell density may be helpful in all patients after corneal transplant in whom refractive surgery is being considered. Eyes with corneal transplants may lose endothelial cells at a more rapid rate than normal eyes and not always display typical guttata; therefore, specular microscopy may also be helpful in recognizing those eyes at risk for poor failure.
Furthermore, for eyes undergoing LASIK after PKP, consideration could be given to suturing edematous flaps to prevent a flap dislocation. Another consideration is increasing the use of topical steroids every 2 hours in corneal transplant patients because of the slight increase in cornea rejection caused by the trauma of the surgery and the fact that the endothelial cells may experience some disruption in function, which can be ameliorated by additional steroids. We suggest that endothelial compromise should be added to the list of risk factors for flap dislocation.
Conclusion:
Flap displacement may occur following LASIK in patients who have undergone PKP for bullous keratopathy. The endothelial pump function, which is vital to maintaining flap adherence, may be compromised in these patients. We suggest that patients with a history of PKP and endothelial compromise who undergo LASIK wear protective shields for a longer than normal period and be followed closely to reduce the risk of flap slippage.
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