Keratectasia is a known, albeit rare, complication of LASIK that results when the mechanical strength of the cornea is compromised by flap creation and tissue ablation. High myopes have an increased risk for developing post-LASIK ectasia because of their thin residual stromal beds1 and deep primary keratotomies.2 It is critical to screen these patients for other risk factors, including a family history of keratoconus and corneal topography that indicates inferior steepening or possible forme fruste keratoconus. Interestingly, post-LASIK ectasia has also been observed in patients with low-to-moderate myopia.3,4
STUDY AND RESULTS
In order to identify cases of forme fruste keratoconus unrecognized during the screening process and to determine an incidence of post-LASIK iatrogenic ectasia, we conducted a retrospective chart analysis at the John A. Moran Eye Center at the University of Utah in Salt Lake City. This analysis involved slightly fewer than 2,000 eyes with myopia of between -1.00 and -6.00D that underwent LASIK with a Chiron Automated Corneal Shaper (Bausch & Lomb, Rochester, NY) (with a 160-µm plate) over a period of approximately 2 years and with at least 3 years of follow-up.
We defined ectasia as inferior topographic steepening of 5.00D or more relative to immediate postoperative topographies and a decrease in UCVA of two or more Snellen lines. We also defined iatrogenic ectasia as that which developed in patients without any risk factors.
Upon re-examination of the preoperative data, we found a total of 69 eyes (3.5%) that had forme fruste keratoconus (Figures 1 and 2). These included four eyes of three patients who developed post-LASIK ectasia (Figures 3 and 4). The total incidence of eyes with unrecognized preoperative forme fruste keratoconus that also developed post-LASIK ectasia was 5.8 cases per 100 eyes. We also found one eye with post-LASIK ectasia without any identifiable preoperative risk factors; the incidence for this purely iatrogenic ectasia was one case per 1,931 eyes. The patient had undergone bilateral LASIK for moderate myopia. Although the other three cases had suspicious corneal topographies upon evaluation at the time of the screening visit, the corneal topography for this case was entirely normal. All of the patients who were diagnosed with ectasia underwent uncomplicated bilateral LASIK with satisfactory initial postoperative results.
All of our patients met the most conservative recommendations for the degree of myopia, residual stromal bed thickness, and flap thickness. The more conservative recommendations have suggested that LASIK should be contraindicated in patients with myopia of greater than -8.00D and a corneal thickness of less than 500µm.5 All four of our post-LASIK ectasia cases had preoperative pachymetry readings of more than 500µm. Because there have been reports of ectasia in much lower levels of myopia as well, we feel that perhaps the combined effect of the level of myopia and the corneal thickness on the residual stromal bed thickness may serve as a more accurate measurement of a patient's risk for post-LASIK ectasia.
Although there is no general agreement regarding the optimal residual thickness of the stromal bed, the most commonly accepted value is 250µm. However, even after preserving more than 300µm of the stromal bed, it is still possible for the cornea to bulge anteriorly after LASIK.6 Similarly, not only are there no definite guidelines regarding the minimal residual corneal thickness required to prevent post-LASIK ectasia, but the accuracy of these measurements is strongly debated. Although ultrasonic and Orbscan (Bausch & Lomb) pachymetry remain the most popular methods for acquiring these measurements, they often give different values. Ultrasonic pachymetry remains the current standard, but the Orbscan was less operator-dependent and more reproducible in one study.7 Furthermore, it is worth noting that the measurement of the central corneal thickness using partial coherence interferometry shows less variability than either ultrasonic or Orbscan pachymetry.8
Thicker flaps lead to thinner residual stromal beds, another variable that may potentially cause post-LASIK corneal ectasia. Flap thickness itself depends on the brand and plate size of the microkeratome, thus leading to even greater unpredictability. Variable flap thickness has been observed with certain microkeratomes. In one study that compared the cutting depths of various microkeratomes, flaps made with the ACS (Bausch & Lomb) were thinner than the others.9 In another study involving different types of microkeratomes, not only were thicker corneas associated with thicker flaps, but the first cuts in bilateral LASIK were thicker than the second cuts.10 We performed LASIK on the subject's right eye first in our bilateral cases, and two of our post-LASIK ectasia cases occurred in right eyes. Perhaps these complications were a result of thicker flaps in the those eyes.
Even with the 160-µm ACS microkeratome, we did not observe consistent flap thickness. Inaccurate microkeratome cuts may produce thicker flaps, which may potentially lead to corneal ectasia (such cases are seen in the literature11). Our case of iatrogenic ectasia involved using the same microkeratome blade on the patient's left eye. This complication occurred despite the eye's having greater pachymetry (520µm) and residual stromal bed values (290µm) than even conservative suggested values.
In our study, we could not include patients who were ruled poor candidates or who had unrecognized forme fruste keratoconus preoperatively but did not develop ectasia postoperatively. Nonetheless, it is possible that the incidence of purely iatrogenic post-LASIK ectasia is higher than what we found.
We suggest the following in relation to the prevention of post-LASIK ectasia. First, surgeons should have a very low threshold for signs detected on corneal topography. Second, we suggest using the criterion of a minimal thickness of more than 500µm regardless of the level of myopia. Third, we recommend the mandatory implementation of routine intraoperative measurements of the flap and the residual stromal bed.
We would like to emphasize the importance of postoperative vigilance in LASIK patients. Although most cases of ectasia are evident within the first year, we found the detection time of ectasia to range from 5 months to nearly 4 years. As we argue herein, there are aspects of LASIK that require further study to establish more exact criteria and standardization. Universally accepted standards for LASIK are lacking. Refractive surgeons must take great care when testing for forme fruste keratoconus prior to LASIK, and they should be aware of ectasia as a potential complication of LASIK, even when applying the most rigorous screening criteria.
Majid Moshirfar, MD, FACS, is Associate Professor of Ophthalmology and Director of the Cornea and Refractive Division at the John A. Moran Eye Center, University of Utah, Salt Lake City. He states that he holds no financial interest in any product or company mentioned herein.
Dr. Moshirfar may be reached at (801) 585-3937; email@example.com.
Garen Mirzaian, MD, is a graduate of the Trinity College Dublin School of Medicine in Ireland. He conducts research in the Cornea section of the John A. Moran Eye Center, University of Utah, Salt Lake City. He states that he holds no financial interest in any product or company mentioned herein. Dr. Mirzaian may be reached at firstname.lastname@example.org.
Doug P. Marx, MD, is a graduate of Georgetown University School of Medicine in Washington, DC. He states that he holds no financial interest in any product or company mentioned herein. Dr. Marx may be reached at email@example.com.
1. Randleman JB, Russell B, Ward MA, et al. Risk factors and prognosis for corneal ectasia after LASIK. Ophthalmology. 2003;110:267-275.
2. Haw WW, Manche EE. Iatrogenic keratectasia after a deep primary keratotomy during laser in situ keratomileusis. Am J Ophthalmol. 2001;132:920-921.
3. Amoils SP, Deist MB, Gous R, et al. Iatrogenic keratectasia after laser in situ keratomileusis for less than -4.0 to -7.0 diopters of myopia. J Cataract Refract Surg. 2000;26:967-997.
4. Geggel HS, Talley AR. Delayed onset keratectasia following laser in situ keratomileusis. J Cataract Refract Surg. 1999;25:582-586.
5. Seiler T, Koufala K, Richter G. Iatrogenic keratectasia after laser in situ keratomileusis. J Refract Surg. 1998;14:312-317.
6. Miyata K, Tokunaga T, Nakahara M, et al. Residual bed thickness and corneal forward shift after laser in situ keratomileusis. J Cataract Refract Surg. 2004;30:1067-1072.
7. Fakhry MA, Artola A, Beld JI, et al. Comparison of corneal pachymetry using ultrasound and Orbscan II. J Cataract Refract Surg. 2002;28:248-252.
8. Rainer G, Findl O, Petternel V, et al. Central corneal thickness measurements with partial coherence interferometry, ultrasound, and the Orbscan system. Ophthalmology. 2004;111:875-879.
9. Javaloy EJ, Vidal MT, Quinto A, et al. Quality assessment model of 3 different microkeratomes through confocal microscopy. J Cataract Refract Surg. 2004;30:1300-1309.
10. Solomon KD, Donnenfeld E, Sandoval HP, et al. Flap thickness accuracy. J Cataract Refract Surg. 2004;30:964-977.
11. Sezitz B, Rozsival P, Feurermannova A, et al. Penetrating keratoplasty for iatrogenic keratoconus after repeat myopic laser in situ keratomileusis: histologic findings and literature review. J Cataract Refract Surg. 2003;29:2217-2224.