In their letter1 about my 2007 article,2 Mohammadpour and Jabbavand asked whether the assumed risk factors for developing ectasia, in and of themselves, increased the risk in a population of eyes that had been screened for topographic abnormalities. Before the 1998 article by Seiler et al.,3 keratoconus was considered a contraindication to laser vision correction. As corneal and refractive surgeons, we were aware of the topographic appearance of keratoconus eyes well before that date.4 I screened potential laser refractive patients for the then accepted signs of keratoconus and, subsequently, forme fruste keratoconus.5 Of the 3 eyes (2 patients) in my series that developed ectasia, 1 patient had keratoconus in 1 eye, but I did not see that topography before surgery because of a computer printer error; only the fellow-eye topography was available and that was normal. I now have 8 years of follow-up for that particular patient and the uninvolved fellow eye did not develop ectasia. One issue in reviewing retrospective cases is that our diagnostic and surgical skills, as well as our screening criteria, are constantly evolving. What I might have approved for surgery in 1996, would certainly not meet the same approval criteria in 2008. For example, I previously used 250 μm of residual stromal bed thickness (RSBT) as a cut-off and if I felt I could not safely leave an eye with more than that thickness, I would perform photorefractive keratectomy (PRK). I have subsequently increased my minimal RSBT to more than 300 μm. In the second patient with bilateral ectasia, who was operated on in 2000, there was a 10-degree skewing of the radial axis; based on today's criteria, this would have accounted for a 3-point score in the Randleman system and the patient would definitely have been eliminated as a laser in situ keratomileusis (LASIK) candidate. However, at the time, this feature was not fully appreciated as a risk. Interestingly, the RSBTs were 340 and 345 μm in this case. I agree with Mohammadpour and Jabbarvand that one should not perform LASIK in “high risk” patients. Today, in 2008, we agree that any topographic abnormality carries the highest risk for developing ectasia, but having a preoperative topographic abnormality does not guarantee that one will develop ectasia. Patients may not develop ectasia in an eye with abnormal preoperative topography or in a fellow eye with keratoconus or forme fruste keratoconus when the topography is normal in the other eye. Ectasia can occur in 1 eye of a patient who has had LASIK in both eyes. It has been reported to occur after LASIK in 1 eye and not after PRK in the fellow eye. It may occur after PRK, conductive keratoplasty, keratomileusis, hexagonal keratotomy, or hyperopic automated lamellar keratoplasty. However, the absence of risk factors does not protect against the risk for developing ectasia6 because we simply do not know which eyes are biomechanically stable. Unfortunately, the only good biomechanical test of the cornea that we have today is LASIK surgery. For these reasons, I disagree that the best way to analyze risk factors is to survey post-refractive surgery keratectasia patients. Over time, we have learned that thin preoperative corneas, steep keratometry readings, or high refractive errors, previously assumed to be risk factors based on literature reviews, do not, in and of themselves, guarantee the onset of ectasia. Operating on thin corneas increases the risk for a thin RSBT. A mechanical microkeratome may create an unexpected thick flap, which will also produce an unexpected thin RSBT; both factors (thin corneas and unexpected thick flaps) may increase the risk for ectasia. Since patients with forme fruste keratoconus tend to develop significant refractive errors early in life and tend to be younger, operating on such patients would tend to skew the review of ectasia cases toward younger patients with thinner corneas. I have to conclude that in 2008 we should be conservative and if there are any questions as to the candidacy for surgery, we should perform PRK or offer another form of vision correction such as a phakic intraocular lens. I agree that we need to better understand/determine risk factors that lead to post-LASIK ectasia. For the time being, we can look at all the assumed risk factors and when they are present, offer surgical or optical alternatives.
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Perry S. Binder (2008) studied this question.
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