LASIK surgery is generally considered to be safe and effective for the treatment of myopia when patients are carefully screened for risk factors. The incidence of complications is fortunately quite low, and most problems are relatively easy to handle. In contrast, the management of progressive corneal thinning and ectasia following keratorefractive surgery has become a major postoperative challenge and remains of great concern. Clinically, eyes with iatrogenic ectasia develop progressive steepening centrally or inferiorly, leading to significant and progressive increase in myopia, irregular astigmatism, increase in high order aberrations (coma), loss of uncorrected visual acuity (UCVA), and corneal thinning. Central ectasia can usually be adequately corrected with glasses or contact lenses, but inferior ectasia is often associated with loss of bestcorrected visual acuity (BCVA). Ectasia can occur from a few weeks to 45 months after the primary surgery.¹ The median time of diagnosis of postoperative LASIK ectasia was reported to be 13 months.²

Corneal ectasia after LASIK was first described in 1998³; more than 200 cases have now been reported in the literature. The incidence of post-LASIK ectasia has been estimated to be between 0.04% (1:2,500)^4,5 and 0.66% (1:150).⁶ Fortunately, however, the predicted epidemic of iatrogenic ectasia 20 years after LASIK has not occurred.⁷

In LASIK both the lamellar cut and the tissue ablation contribute to a reduction in the biomechanical strength of the cornea.⁶ This is because the LASIK flap no longer contributes to the load-bearing function of the cornea and the posterior stroma is significantly less stable biomechanically.⁸ Both LASIK and radial keratotomy (RK) patients seem to be predisposed to the development of iatrogenic ectasia^9,10,11 while it is less likely following photorefractive keratectomy (PRK).¹² Using the Ocular Response Analyzer (ORA), a decrease in mean corneal hysteresis (CH) from 11.52 to 9.48 mmHg and in mean corneal resistance factor (CRF) from 11.68 to 8.47 mmHg has been found following LASIK surgery.^13,14 Also, the effect of creating flap without stromal ablation reduces CH by 1 mmHg and CRF by 1.8 mmHg.¹⁵ Clinically, the LASIK flap can still be lifted after many years. Histopathologically, only epithelial thickening at the flap edge and a hypocellular primitive scar without myofibroblasts¹⁶ composed primarily of large proteoglycans and a disorganized network of interspersed smaller than normal diameter collagen fibrils have been found.^17,18 Measurements of the tensile wound strength of the flap margin at its peak of healing had a tensile strength of 28% of normal controls, while the central and paracentral flap scar
showed an average of only around 2% to 3% of normal controls.¹⁹ In porcine eyes with 300-µm thick flaps, a significant decrease in CH from 8 to 5.1 mmHg and CRF from 8.2 to 4.1 mmHg was measured, whereas there were no significant changes in 100-µm thin flaps, demonstrating that thick LASIK flaps have a more profound biomechanical insult.²⁰ Similar to keratoconus, the decreased biomechanical strength eventually can lead to a so-called “interfiber fracture” with interlamellar and interfibrillar slippage,²¹ while simple stretching of the fibrils could not be confirmed. Breaks of Bowman layer are rare in post-LASIK ectasia.²²

While the risk factors for ectasia have been presented elsewhere in this handbook (Chapters 1 and 11), these issues are of such significance that they are again presented here to provide context and completeness for the discussion of collagen cross-linking (CXL). It is hoped that it will be particularly helpful for readers who use the book as a “go to” reference and not an inconvenience for those reading cover to cover.

Risk factors for the development of post-LASIK ectasia include young age, high myopia (>8 diopters [D]), reduced corneal thickness, low residual stromal bed (RSB) thickness, preexisting keratoconus, pellucid marginal degeneration or forme fruste keratoconus, greater residual myopia, and greater stromal ablation.^{1,2,4,5,6,23,24} A practical scoring system with a cumulative risk score has been proposed by Randleman, taking into account the following five factors: topography pattern, RSB thickness, age, preoperative corneal thickness, and preoperative spherical equivalent manifest refraction (see Chapter 1 [Tables 1.6 and 1.7] and Chapter 11).²⁰ Anterior bulging of the posterior corneal surface has been described as an early indication of imminent corneal ectasia.²¹ This can be seen on a posterior elevation map, the so-called “posterior float.” When the posterior float is created on an Orbscan (Bausch & Lomb, Rochester, NY), the maximum elevation above a best fit sphere should not exceed 50 µm centrally because this might indicate forme fruste keratoconus.^5,25 Caution is advised when this Orbscan value is >40 µm. Using the Pentacam (Oculus, Lynnwood, WA), it has been recommended that the maximum central elevation for a pre-LASIK cornea should not exceed 11 µm anteriorly or 20 µm posteriorly. A LASIK screening algorithm based on corneal topography indices and Orbscan II analysis measuring the posterior float has been proposed to exclude keratoconus suspects from LASIK.²⁵ A more detailed discussion of corneal topography can be found in Chapter 2.

Although it is still somewhat controversial, it has been suggested that one leave a residual stromal bed thickness of ≥250 µm or ≥50% of the total preoperative corneal thickness.⁵ The total corneal thickness should generally not be <500 µm.

Rare cases of post-LASIK ectasia in the absence of the typical preoperative risk factors and only low to moderate myopia have been described and are alarming.^5,26 Therefore, potential risk factors like young age or an innate biomechanical weakness of the cornea of the individual have been suggested.⁵ The concept of a chronic disease process due to an increased activity of degradative proteolytic enzymes, subclinical interface inflammation, and loss of keratocytes in the anterior flap instead of a purely mechanical process has been hypothesized as well.²⁷

In addition, the accuracy of the flap thickness, especially with mechanical microkeratomes, can vary significantly with diameter deviations of up to 300 µm and thickness standard deviations of up to 30 µm.^{1,5,28,29,30,31} Thick flaps can lead to a greater decrease of the biomechanical strength. Therefore, thin flaps using a femtosecond laser may be advantageous.²⁰ Dehydration of the stromal bed caused by prolonged exposure during surgery can increase the ablated tissue mass, leading to more ablation than calculated.⁵

Management of these patients is directly related to the degree of ectasia and the level of
visual disability. Careful documentation of the refractive status, including cycloplegic refraction, slit-lamp examination, and corneal contour mapping, including power, elevation, and pachymetry maps, is essential. Optical coherence tomography (OCT) imaging, if available, can be helpful as well (see Chapter 3). This careful evaluation and documentation enables the clinician to adequately follow the patient and determine the rate of progression. These patients are often confused and frightened, and a clear, calm explanation of both the condition and an appropriate management strategy will be much appreciated. Improving visual function will, however, be the most helpful way of reducing anxiety.

The refractive consequences of post-LASIK ectasia usually can be corrected effectively with rigid gas-permeable contact lenses, but bestcorrected visual acuity is often significantly worse than it was preoperatively, and about 20% of the cases may require deep anterior lamellar keratoplasty (DALK) or penetrating keratoplasty due to contact lens intolerance.^32,33 Secondary glaucoma, graft rejection, or other untoward effects do occur and must be explained. The keratoplasty rate has been reported to be 10% to 35% in post-LASIK ectasia patients,^2,32 just as in progressive keratoconus. Alternatively, intrastromal corneal ring segments (ICRS), inserted into a corneal tunnel, may improve visual acuity in iatrogenic ectasia. The ring segments induce central corneal flattening by occupying peripheral space in the stroma. The magnitude of flattening is directly proportional to the thickness of the implant and inversely proportional to its diameter. They are placed on the steep keratometric axis or around the cone. Possible problems are patient discomfort, infection, ring segment extrusion, anterior stromal necrosis, intrastromal deposits, and regression of the refractive effect.^34,35,36