Preoperative Considerations

Figure 10.1 The advanced keratoconus with a hydrop in the central cornea. This patient does not pose a risk of being misdiagnosed. It is the more subtle changes on topography and examination that may be missed, if attention to this problem is not provided in the preoperative evaluation of LASIK surgery.

B. DIAGNOSIS

The diagnosis is based on clinical history, clinical examination, placido-based topography using modified Rabinowitz criteria, and scanning slit topography.

Videokeratographic signs (7,8) include increased K (anterior central corneal power) and I-S value (inferior versus superior difference in anterior central corneal power) (9).

The diagnosis of keratoconus is important for proper management with hard contact lenses (10,11) or penetrating keratoplasty (12) and to avoid unexpected adverse outcomes with refractive surgery (13–15). Rabinowitz and McDonnell classified keratoconus based on K, I-S value, and asymmetry of K between a patient’s two eyes (16). Maeda, Klyce, and Smolek calculated the I-S value as corneal power difference between five inferior and five superior spots at 30° intervals 3 mm from the corneal vertex (17,18).

Maeda et al. developed a TMS-1 videokeratoscope guided by an automated system with eight indices (Simulated K1, Simulated K2, Surface Asymmetry Index, Differential Sector Index, Opposite Sector Index, Center/Surround Index, Irregular Astigmatism Index, Analyzed Area) which were used to diagnose keratoconus as differentiated from other causes of corneal irregularities (18). Patients were selected from the Louisiana State University Eye Center and had one of eight diagnoses: normal, keratoconus, keratoplasty, epikeratophakia, excimer laser photorefractive keratectomy, radial keratotomy, contact- lens-induced warpage (19,20), or other. Sensitivity and specificity were 98% and 99%, respectively (17).

The TMS-2 videokeratoscope used the modified Rabinowitz criteria to determine K and I-S value only. K of 47.2–48.7 D (diopters) was considered suspect for keratoconus, and K 48.7 D was suggestive of keratoconus. Likewise, inferior–superior central anterior corneal power asymmetry between 1.4 and 1.9 D was considered suspect for keratoconus, and I-S value 1.9 D was suggestive of keratoconus (21). Sensitivity and specificity of the modified Rabinowitz method were 96–100% and 85–89%, respectively (17,21).

Considerations Preoperative

Figure 10.2. The Azar-Lu MEEI keratoconus scoring system.

155

Considerations Preoperative

Figure 10.3 (Top lane) The central axial keratometry maps: normal controls (A), keratoconus suspects (B), early keratoconus (C), and advanced keratoconus (D). (Middle lane) The Pachymetry maps: normal controls (E), keratoconus suspects (F), early keratoconus (G), and advanced keratoconus (H). Note that corneal thinning is greatest in advanced keratoconus. (Bottom lane) The posterior best fit (B.F.) sphere maps: normal controls (I), keratoconus suspects (J), early keratoconus (K), and advanced keratoconus (L). Note increased posterior corneal curvature in advanced keratoconus. [Color in original.]

157

‡: Tukey Multiple Comparison, CI confidence interval, KC keratoconus, * statistically significant. Suspects KC suspects.

Ultrasonic pachymetry may provide corroborative evidence for the diagnosis of keratoconus, but Rabinowitz et al. have shown that this technique is less valuable than videok- eratography-derived indices in distinguishing keratoconus from the normal condition (24). Other studies suggest that pachymetry data are important because corneal stromal thinning may be associated with disease progression (22,23). Bohm et al., using ultrasound pachymetry, showed that normal subjects had a central corneal thickness of 548 30 m, compared to 505 42 m in the corneal center and 424 41 m on the conus peak in keratoconus subjects (23). Stromal thinning occurs commonly in the inferotemporal quadrant; in one study, comparisons of pachymetry of keratoconus and normal eyes showed similarities in all except this quadrant (26).

These variations in corneal pachymetry findings in the normal population may contribute to its inability to differentiate keratoconus eyes from normal controls. Our study revealed significant differences in pachymetry in normal controls vs. early keratoconus and advanced keratoconus, keratoconus suspects vs. advanced keratoconus, and early keratoconus vs. advanced keratoconus, but not in normal controls vs. keratoconus suspects. This finding implies that pachymetry is a predictor of progression of keratoconus, especially in the much advanced stage.

Measurements of posterior best sphere (25,27) may be important, possibly because it may represent advanced disease progression. As the cornea thins and protrudes forward, the posterior corneal curvature may show more dramatic steepening than does the anterior corneal curvature. Posterior corneal curvature is a minor determinant of dioptric corneal power. Our study revealed significant difference in posterior best sphere in advanced keratoconus vs. controls, keratoconus suspects, and early keratoconus, suggesting that posterior corneal curvature changes to an extreme extent at the end stage of keratoconus progression.

Most previous keratoconus classifications used either topographical (28–32) quantitative indices or clinical findings only. The MEEI classification, using a scoring system, combines history, examination, topographical maps, and modified Rabinowitz criteria to establish stricter criteria for distinguishing normal controls, keratoconus suspects, and early and advanced keratoconus. Smolek and Klyce (21) modified the Rabinowitz criteria and identified the anterior central corneal power (K) between 47.2 and 48.7 D as suspect and K48.7 D as suggestive of keratoconus. The modified Rabinowitz criteria also identified the inferior–superior central anterior corneal power asymmetry (I-S value) between 1.4 and 1.9 D as suspect and I-S 1.9 D as suggestive of keratoconus. Given these limits, we es-

tablished three groups of central cornea power (K) ( 47.2 D, 47.2–48.7 D, 48.7D) and inferior–superior corneal power asymmetry (I-S value) ( 1.4 D, 1.4–1.9 D, 1.9 D) and assigned 0, 1, and 2 points, respectively. In other words, the higher the K and I-S value measurement, the more severe the disease and the higher the score assigned. Asymmetry of the central corneal power between one eye and the fellow eye greater than 1.9 D is assigned one point only because this asymmetry can be a normal variant. If asymmetry 1.9 D is present, the eye with the higher corneal power is assigned 1 point and the other is assigned 0 points. The presence of two or more findings by examination (Fleischer ring, Vogt’s striae, Munson’s sign, prominent nerves, scarring) and history (atopy, Down’s, family history) is assigned two points, but the presence of one finding is assigned zero points. Corneal hydrops of examination or from history is assigned two points because it is easily diagnosed and is of definitive value since it is a sign of severe late stage keratoconus. Future studies incorporating optical pachymetry and posterior corneal curvature into current videokeratography-derived indices may improve the accuracy in distinguishing among keratoconus suspects and early and advanced keratoconus.

E. KERATOCONUS AND LASIK/PRK

LASIK/PRK are effective and precise refractive surgery. Recently, however, there are many articles reporting disappointing results after performing LASIK or PRK on keratoconus suspects or early keratoconus patients (33–37). Seiler and Quurke reported a case of forme fruste keratoconus revealing a central steeping with rapid progression one month postoperatively (33). Speicher and Gottinger reported 4 eyes from 2 patients that got progressive corneal ectasia of up to 7 diopters within a few months after LASIK treatment (34). Buzard et al. used LASIK to treat mild to moderate keratoconus in 16 eyes of 9 patients and conclude that longer term results, even the initial visual results, appear promising, and they revealed regression of the refractive outcome in some cases. Moreover, despite improvement in the postoperative spherical equivalent and uncorrected visual acuity in most cases, the risk of loss of BCVA and the necessity of performing PKP in three cases lead us to consider LASIK as not a primary solution for keratoconus (35). Holland et al. also noted that 4 eyes in 2 patients with possible forme fruste keratoconus showed worsening irregular astigmatism after LASIK or PRK treatments (36). Schmitt-Bernard et al. reported a keratoconus suspect receiving two LASIK procedures and one PRK performed on his left eye, and three LASIK procedures on his right eye. After these surgeries, a dramatic corneal ectasia and grade III haze occurred in both eyes, with a clinical diagnosis of keratoconus. The best spectacle-corrected visual acuity was as low as 20/1200 bilaterally. Both eyes displayed dramatic corneal protrusion with corneal scarring (37).

F. THE PATIENTS WITH ECTASIA AFTER LASIK/PRK

The cases revealing ectasia after LASIK or PRK treatments may be the undiagnosed keratoconus, forme fruste keratoconus (33,34,36,37), or may be due to corneal weakening and unstable after surgery. We cannot overemphasize the need for thorough preoperative evaluations of corneal conditions, such as slit lamp examination, corneal thickness measurement, and detailed analysis of videokeratographs. Thinning corneal disorders such as keratoconus, keratoconus suspects, or pellucid marginal degeneration should be considered as contraindications for excimer laser ablative refractive procedures (35–37).

G. INTRAOPERATIVE PACHYMETRY TO AVOID COMPLICATIONS

For cases without keratoconus, if the pachymetry is less than 500 m or the refractive error more than -6 diopters, in order to preserve posterior corneal residual thickness, more than 250 m (note the variable flap thickness); intraoperative pachymetry can be used to avoid serious complications after LASIK or PRK treatments. If the residual corneal thickness cannot meet that criterion undercorrection is recommended.

REFERENCES

1.YS Rabinowitz, AB Nesburn, PJ McDonnell. Videokeratography of the fellow eye in unilateral keratoconus. Ophthalmology 1993;100:181–186.

2.SE Wilson, DTC Lin, SD Klyce, JJ Reidy, MS Insler. Topographic changes in contact lens-in- duced corneal warpage. Ophthalmology 1990;97:734–744.

3.YS Rabinowitz, J Garbus, PJ McDonnell. Computer-assisted corneal topography in family members of patients with keratoconus. Arch Ophthalmol 1990;108:365–371.

4.J Parker, WW Ko, G Pavlopoulos, PJ Wolfe, YS Rabinowitz, ST Feldman. Videokeratography of keratoconus in monozygotic twins. J Refract Surg 1996;12:180–183.

5.V Gonzalez, PJ McDonnell. Computer-assisted corneal topography in parents of patients with keratoconus. Arch Ophthalmol 1992;110:1412–1414.

6.RH Kennedy, WM Bourne, JA Dyer. A 48-year clinical and epidemiologic study of keratoconus. Am J Ophthalmol 1986;101:267–273.

7.YS Rabinowitz. Videokeratographic indices to aid in screening for keratoconus. J Refract Surg 1995;11:371–379.

8.SE Wilson, DTC Lin, SD Klyce. Corneal topography of keratoconus. Cornea 1991;10:2–8.

9.YS Rabinowitz. Keratoconus. Surv Ophthalmol 1998;42:297–319.

10.YS Rabinowitz, JJ Garbus, C Garbus, PJ McDonnell. Contact lens selection for keratoconus using a computer-assisted video-photokeratoscope. CLAO J 1991;17:88–93.

11.MJ Mannis, K Zadnik. Contact lens fitting in keratoconus. CLAO J 1989;15:282–289.

12.MJ Crews, WT Driebe Jr, GA Stern. The clinical management of keratoconus: 6 year retrospective study. CLAO J 1994;20:194–197.

13.JH Lass, RG Lembach, SB Park, DL Hom, ME Fritz, GM Svilar, IF Nuamah, WJ Reinhart, EG Stocker, RH Keates. Clinical management of keratoconus: a multicenter analysis. Ophthalmology 1990;97:433–445.

14.AB Nesburn, S Bahri, J Salz, YS Rabinowitz, E Maguen, J Hofbauer, M Berlin, JI Macy. Keratoconus detected by videokeratography in candidates for photorefractive keratectomy. J Refract Surg 1995;11:194–201.

15.YS Rabinowitz, SD Klyce, J Krachmer, L Nordan, J Rowsey, J Sugar, S Wilson, P Binder, R Damiano, M McDonald, A Neumann, T Seiler, K Thompson, P Wyzinski, L O’Dell. Keratoconus, videokeratography, and refractive surgery. Refract Corneal Surg 1992;8:403–407.

16.YS Rabinowitz, PJ McDonnell. Computer-assisted corneal topography in keratoconus. Refract Corneal Surg 1989;5:400–408.

17.N Maeda, SD Klyce, MK Smolek. Comparison of methods for detecting keratoconus using videokeratography. Arch Ophthalmol 1995;113:870–874.

18.N Maeda, SD Klyce, MK Smolek, HW Thompson. Automated keratoconus screening with corneal topography analysis. Invest Ophthalmol Vis Sci 1994;35:2749–2757.

19.J Ruiz-Montenegro, CH Mafra, SE Wilson, JE Jumper, SD Klyce, EN Mendelson. Corneal topographic alterations in normal contact lens wearers. Ophthalmology 1993;100:128–134.

20.N Maeda, SD Klyce, H Hamano. Alteration of corneal asphericity in rigid gas permeable contact lens induced warpage. CLAO J 1994;20:27–31.

21.MK Smolek, SD Klyce. Current keratoconus detection methods compared with a neural network approach. Invest Ophthalmol Vis Sci 1997;38:2290–2299.

22.V Yaylali, SC Kaufman, HW Thompson. Corneal thickness measurements with the Orbscan Topography System and ultrasonic pachymetry. J Cataract Refract Surg 1997;23:1345–1350.

23.A Bohm, M Kohlhaas, RC Lerche, B Bischoff, G Richard. Messung des intraokularen druckes bei keratokonus: einfluss der veränderten biomechanik. (Measuring intraocular pressure in keratoconus: effect of the changed biomechanics.) Ophthalmologe 1997;94:771–774.

24.YS Rabinowitz, K Rasheed, H Yang, J Elashoff. Accuracy of ultrasonic pachymetry and videokeratography in detecting keratoconus. J Cataract Refract Surg 1998;24:196–201.

25.PC Lu, S Samapunphong, DT Azar. Posterior corneal curvature and keratoconus: quantitative and qualitative analysis. Asia-Pacific Journal of Ophthalmology 1999;11:28–31.

26.J Colin, Y Sale, F Malet, B Cochener. Inferior steepening is associated with thinning of the inferotemporal cornea. J Refract Surg 1996;12:697–699.

27.C Edmund. Posterior corneal curvature and its influence on corneal dioptric power. Acta Ophthalmol (Copenh) 1994;72:715–720.

28.TT McMahon, JB Robin, KM Scarpulla, JL Putz. The spectrum of topography found in keratoconus. CLAO J 1991;17:198–204.

29.JS Chan, RB Mandell, DS Burger, RE Fusaro. Accuracy of videokeratography for instantaneous radius in keratoconus. Optom Vis Sci 1995;72:793–799.

30.DA deCunha, EG Woodward. Measurement of corneal topography in keratoconus. Ophthalmic Physiol Opt 1993;13:377–382.

31.SE Wilson, SD Klyce. Advances in the analysis of corneal topography. Surv Ophthalmol 1991;35:269–277.

32.LJ Maguire, WM Bourne. Corneal topography of early keratoconus. Am J Ophthalmol 1989;108:107–112.

33.T Seiler, AW Quurke. Iatrogenic keratectasia after LASIK in a case of forme fruste keratoconus. J Cataract Refract Surg 1998;24:1007–1009.

34.L Speicher, W Gottinger. Progressive corneal ectasia after laser in situ keratomileusis. Klin Monatsbl Augenheilkd 1998;213:247–251.

35.KA Buzard, A Tuengler, JL Febbraro. Treatment of mild to moderate keratoconus with laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1600–1609.

36.SP Holland, S Srivannaboon, DZ Reinstein. Avoiding serious corneal complications of laser assisted in situ keratomileusis and photorefractive keratectomy. Ophthalmology 2000;107:640– 652.

37.CF Schmitt-Bernard, C Lesage, B Arnaud. Keratectasia induced by laser in situ keratomileusis in keratoconus. J Refract Surg 2000;16:368–70.

that, assuming the biomechanical parameters are constant throughout the cornea, a normal corneal thickness can be reduced twofold before its elasticity is reduced to that of a keratoconic cornea. That is, assuming a normal corneal thickness of about 540 m, a total residual corneal thickness of more than 270 m should be sufficient to provide the elasticity of a normal cornea. Unfortunately, this assumption is proven wrong by the long-term results of corneal refractive surgeries. Iatrogenic keratectasia, that is, progressive corneal thinning and weakening, remains an uncommon yet vision-threatening complication following refractive surgery.

B. LESSONS FROM INCISIONAL REFRACTIVE SURGERY

Refractive keratotomy was first described by European ophthalmologists in the late 1800s, developed in Japan after the Second World War, and evolved into its modern form in Russia in the 1970s (5–7). The first radial keratotomy in the United States was performed in 1978 (8). Before the LASIK era, radial keratotomy was the most widely used refractive surgical procedure to correct myopia. Approximately 250,000 radial keratotomy operations were performed annually in the United States (9).

Numerous articles described the initial short-term favorable outcomes of this procedure. In 1986, Deitz et al. (10) first reported a trend toward progressive hyperopic shift in postoperative refraction in a series of 150 patients who had undergone 225 metal-blade radial keratotomy procedures. Between 12 months to 4 years after surgery, 31% of the patients had hyperopic shifts of at least 1.00 D (mean shift, 0.51 D). Then in the Prospective Evaluation of Radial Keratotomy (PERK) series (11), in which patients received diamondblade radial keratotomy, 43% of 693 eyes underwent a hyperopic change in refractive power of 1.00 D or more, 10 years after surgery. The mean rate of change was approximately 0.10 D per year. The investigators estimated that each year, an additional 5% of eyes would reach the level of 1.00 D hyperopic shift. The hyperopic shift showed no signs of slowing, confirming the long-term results of the metal-blade study that hyperopic shift could last as long as 12 years after the radial keratotomy procedure (12).

Most corneal surgeons initially thought the hyperopic shift was due to a continuation of the basic biomechanical change in the cornea that produces the initial central corneal flattening after surgery—perhaps an increase in the length of the incision. It took more than five years to recognize that the progressive hyperopic shift was in fact due to weakening of the paracentral cornea leading to iatrogenic keratectasia.

C. LESSONS FROM LAMELLAR CORNEAL SURGERY

Automated lamellar keratoplasty provided the most extensive experience with lamellar refractive surgery before the LASIK era. In this procedure, a 4.2 mm diameter lamellar disc is removed from the center of the visual axis, creating a uniform thinning of the entire corneal bed in that area. In LASIK, however, excimer ablation using the single-zone or multizone technique results in a gradient of thinning in the ablation zone. Maximum removal of tissue occurs only at the central 0.25 mm, depending on the first opening of the diaphragm, while the remaining posterior stromal tissue maintains substantially more thickness.

The type of lamellar surgery that penetrates most deeply into the cornea is hyperopic automated lamellar keratoplasty. This procedure uses a 5.6 to 6.6 mm diameter lamellar dissection extending to 53 to 74% of the corneal thickness to induce central ectasia. The

Ruiz nomogram for hyperopic automated lamellar keratoplasty suggested that a 300 m cut in corneas ranging in thickness from 490 to 575 m would produce a 1.0 D myopic shift due to the subsequent controlled corneal ectasia (13). Ruiz observed that microkeratome cuts of more than 60% of the central corneal thickness could produce uncontrolled ectasia (14). Similarly, Gris et al. (15) found that a microkeratome cut of more than 350 m could produce corneal ectasia. Given the average central corneal thickness of approximately 540.5 38.5 m, automated lamellar keratoplasty can produce corneal ectasia with 180 to 275 m of posterior stromal tissue. Lyle and Jin (16) reported a 26% incidence of iatrogenic keratoconus following hyperopic automated lamellar keratoplasty with a lamellar cut depth of 52 to 70% of corneal thickness. However, this series included corneas that had undergone prior radial keratotomy and were presumably weaker than naive corneas. Although a residual corneal stromal bed of less than 250 m thickness is usual in hyperopic automated lamellar keratoplasty, when performed in primary cases this procedure rarely leads to keratectasia (17). Ghiselli et al. (18) looked for evidence of corneal ectasia in 38 eyes that had undergone hyperopic automated lamellar keratoplasty; mean residual corneal bed thickness was 195 m (range, 126 to 230 m). Multiple regression analysis showed no statistical evidence of corneal ectasia in the short term.

Barraquer (19), based on his extensive experience with myopic keratomileusis, in which corneal tissue is removed from the entire 7 to 8 mm diameter of the resected bed, suggested the need for a minimum of 300 m total thickness of treated cornea, including a 100 m sutured lamella. Slade has pointed out that a 15 year follow-up of his earlier myopic keratomileusis studies has not shown any loss of structural integrity or ectasia in eyes with a residual bed thickness of 200 m (personal communication, October 1998).

D. CORNEAL BIOMECHANICS AFTER LASIK

Since Barraquer more than 50 years ago first introduced the myopic keratomileusis procedure with cryolathing of a freehand dissected corneal disc (20), substantial improvements have been made in lamellar corneal refractive surgery. LASIK combines the lifting of a corneal flap with a microkeratome and refractive photoablation of the stromal bed by means of a 193 nm argon fluoride excimer laser (21). Because of the accurate and consistent flap cut and the extreme precision of tissue removal, along with patients’ more comfortable recuperation and rapid visual recovery, LASIK has become the most popular corneal refractive surgery.

This procedure, however, substantially weakens the mechanical strength of the cornea, the extent of weakening depending on the degree of refractive error. Depth of keratectomy is related to the diameter of the ablation zone and the attempted correction (22) (Fig. 11.1) by the equation

(Diameter of ablation)2 Attempted correction in diopters Ablation depth (2)

3

The state-of-the-art diameter for photorefractive keratectomy (PRK) is 6 mm, and from the early PRK reports we know that ablation zones less than 5 mm in diameter result in severe glare and halos (23,24). Therefore, according to Eq. (2), the excimer laser ablates about 12 m per 1.00 D of myopic correction for a 6 mm ablation zone (Fig. 11.2). Similarly, for a 6.5 mm ablation zone the excimer laser ablates about 14 m for the correction of 1.00 D myopia. One advantage of LASIK over older forms of lamellar corneal surgeries is that, as noted earlier, maximum removal of tissue occurs only at the central 0.25 mm, de-

Figure 11.1 The schematic diagram of keratotomy depths for particular diopters of myopia according to Munnerlyn formula.

pending on the first opening of the diaphragm, and the remaining posterior stromal tissue maintains more of its normal thickness. A 200 m LASIK-created bed therefore has more stress-bearing tissue than a 200 m automated lamellar keratoplasty-created bed.

E. POSTERIOR CORNEAL CHANGES AFTER LASIK

Corneal shape is determined by the interplay among intraocular pressure, the elastic properties of the corneal tissue, and the amount and central/peripheral distribution of the corneal tissue mass (3). Thus the photosubtraction of corneal tissue with the lamellar cut during LASIK may affect corneal shape and lead to ectasia. Indeed, in a study of postoperative

Figure 11.2 The difference of ablation depths in microns with different ablation diameters for attempted correction of particular diopters of myopia.

changes in the posterior corneal surface after LASIK, Wang et al. (25) reported that the thinner the residual corneal bed after ablation, the greater the postoperative ectasia. A residual corneal bed thickness of 250 m was found to be a reasonable limit to prevent iatrogenic keratoconus. The authors also suggested that the post-LASIK regression might be due in part to induced central corneal ectasia. However, mainly because of the limitations of currently available corneal topography units (26), more investigations need to be performed before a final conclusion can be drawn.

F. IATROGENIC KERATECTASIA AFTER LASIK

One vision-threatening complication of LASIK is iatrogenic keratectasia (Fig. 11.3). Seiler et al. (27) first reported the occurrence of post-LASIK keratectasia in three eyes 1 to 8 months after surgery for 10.00 to 13.00 D of myopia. In all three cases the estimated residual corneal bed thickness was less than 250 m. In a recent report, Joo and Kim (28) described two cases of postoperative corneal ectasia occurring 1.5 to 9 months after surgery (28). These surgeons used a manual microkeratome and an estimated flap thickness of 150 m. The residual stromal bed thickness after the procedure was 232 to 257 m. The authors recommended that half the original stromal bed thickness and more than 250 m of residual stroma should be preserved after LASIK. They also reported corneal perforation during LASIK in two other patients (29). In both cases the residual bed thickness was less than 250 m and there was a lag between the creation of the corneal flap and the laser application. The authors concluded that excessive dehydration of the cornea must be avoided and that the corneal shape should be carefully watched to prevent corneal perforation during LASIK.

Figure 11.3 An Orbscan corneal tangential topography showing keratectasia after LASIK. (Courtesy of Donald Sanders, M.D., Ph.D.)

168

Figure 11.4 (A) Pre-LASIK topography in the right eye. (B) Pre-LASIK topography in the left eye. (C) Right eye: Frank inferior keratectasia 20 months postoperatively. (D) Left eye: topography showing marked inferonasal keratectasia 15 months postoperatively. (From Ref. 34.)

169

Geggel and Talley (30) described a patient who developed iatrogenic keratectasia after bilateral LASIK with enhancements. The authors documented a thinning of the total central corneal thickness; initial pachymetry was 449 m and gradually decreased to 260m over a period of 9 months.

Several different authors have also reported progressive keratectasia induced by LASIK in keratoconic corneas (31,32). One interesting finding is the occurrence of keratectasia even in corneas with a residual stromal bed thickness of more than 250 m in patients with keratoconus.

Preoperative corneal thickness measurement is of utmost importance in ruling out any corneal thinning disorders as well as in estimating the possible maximum amount of tissue ablation. Schmitt-Bernard et al. (33) reported on a patient with post-LASIK keratectasia resulting from a failure to perform preoperative pachymetry even though the topographic findings suggested keratoconus. They emphasized that corneal disorders with thinning such as keratoconus, suspected keratoconus, forme fruste keratoconus, or pellucid marginal degeneration are absolute contraindications for any corneal stromal ablative refractive procedures.

In a case series of 13 eyes, Amoils et al. (34) reported iatrogenic keratectasia following LASIK for myopia of 4.0 to 7.0 D. In one of the cases the calculated corneal bed thickness was 297 m (right eye) and 300 m (left eye). Preoperative topographic evaluation did not suggest keratoconus. However, the patient developed keratoconus with marked inferior steepening and thinning of the corneas 18 months postoperatively (Fig. 11.4A–D). The occurrence of LASIK-induced keratectasia even with a residual corneal bed thickness of more than 250 m can perhaps be attributed to the considerable variation in biomechanical properties of individual corneas (35).

G. IS THERE A SAFE CORNEAL BED THICKNESS AFTER LASIK?

As is apparent from the ocular rigidity equation, Eq. (1), corneal thickness is clearly one parameter of concern in LASIK. T in this equation represents total central corneal thickness. Given that the strength of a normal cornea is only twice that of the keratoconic cornea (4), as noted earlier, one might conclude that a normal 540 m cornea could be reduced to 270m before its elasticity is reduced to that of a keratoconic cornea. This assumption is too optimistic, however, because the anterior corneal flap after LASIK does not contribute to the tensile strength of the cornea; the stress is supported only by the residual bed (27). Also, current ablation depth nomograms are based on results of PRK, in which Bowman’s membrane and the anterior part of the stroma are ablated (36). In midstroma and deeper layers, however, per-pulse ablation rates are higher. Hence, owing to differences in water content, the actual ablation depth might be greater than calculated in LASIK (37). We also know that the deep posterior stroma has less biomechanical strength than the anterior layer (35). Thus ablating the same amount of tissue under a 160 m flap might leave a weaker residual bed than ablating under a 130 m flap, even though the final bed thickness is the same.

In order to extend the range of refractive correction by LASIK, thinner flaps would be an option. Ideally, a microkeratome should produce consistent corneal flap thickness within a 10% range of error, controlled by the thickness of the microkeratome plate. However, clinical studies have shown that actual flap thickness is usually thinner than intended and the range of error is wider (38,39). Thin, incomplete, or irregular flaps are difficult to deal with and may result in glare, decreased spectacle-corrected acuity, or loss of best-cor- rected visual acuity. Seiler et al. (27) estimated that an intended flap thickness of less than 110 m would automatically create cutting errors in more than 5% of cases.

Corneal radius of curvature (R) is another parameter that affects corneal tensile strength. As the steepness of the cornea increases, tensile strength decreases by the fourth power of the increase in radius of curvature; Eq. (1). Therefore patients with high myopia are expected to have a significantly decreased corneal tensile strength. Maldonado et al. (40) have recently demonstrated that when performing LASIK in eyes with 12.0 D or more of myopia, a thicker than intended flap may occur due to unusual steepness of the cornea, leaving an unexpectedly thinner residual bed. Another, striking finding of the same study was a statistically significant mean difference (14.6 m) between the predicted and the actual central ablation depth. This difference was weakly associated with the degree of preoperative ametropia and accordingly with the dose and duration of the laser treatment. The authors recommended adding a safety margin of 15 m thickness to preoperative calculations for LASIK corrections.

Another factor to be considered is that the tensile strength (Yi) of normal cornea varies by as much as 25% (35). Unfortunately, because currently available technology cannot measure patients’ corneal elasticity preoperatively, the safe minimal residual bed thickness will have to be established by trial and error. At present it seems that a thickness of at least 250 m is reasonable to minimize the risk of ectasia. However, a long-term follow-up of 5 years or more is required to establish reliable guidelines.

REFERENCES

1.YCB Fung. Stress-strain-history relations of soft tissue in simple elongation. In: YCB Fung, N Perrone, M Anliker, eds. Biomechanics, Its Foundation and Objectives. Englewood Cliffs, NJ: Prentice Hall, 1972, pp 181–208.

2.GW Nyquist. Rheology of the cornea: experimental techniques and results. Exp Eye Res 1968;7:183–188.

3.C Edmund. Corneal elasticity and ocular rigidity in normal and keratoconic eyes. Acta Ophthalmol 1988;66:134–140.

4.TT Andreassen, AH Simonsen, H Oxlund. Biomechanical properties of keratoconus and normal corneas. Exp Eye Res 1980;31:435–441.

5.BH Schimmelpfenning, GO Waring. Development of refractive keratotomy in the nineteenth century. In: GO Waring, ed. Refractive Keratotomy for Myopia and Astigmatism. St Louis, MO: Mosby—Year Book, 1992, pp 171–178.

6.K Akiyama, H Shibata, A Kanai. Development of radial keratotomy in Japan, 1939–1960. In: GO Waring, ed. Refractive Keratotomy for Myopia and Astigmatism. St Louis, MO: Mosby–Year Book, 1992, pp 179–220.

7.GO Waring. Development of refractive keratotomy in the Soviet Union, 1960–1990. In: GO Waring, ed. Refractive Keratotomy for Myopia and Astigmatism. St Louis, MO: Mosby–Year Book, 1992, pp 221–236.

8.GO Waring. Development of refractive keratotomy in the United States, 1978–1990. In: GO Waring, ed. Refractive Keratotomy for Myopia and Astigmatism. St Louis, MO: Mosby–Year Book, 1992, pp 237–258.

9.DV Leaming. Practice styles and preferences of ASCRS members: 1993 survey. J Cataract Refract Surg 1994;20:459–467.

10.MR Deitz, DR Sanders, MG Raanan. Progressive hyperopia in radial keratotomy: long term follow-up of diamond knife and metal blade series. Ophthalmology 1986;93:1284–1289.

11.GO Waring, M Lynn, PJ McDonnell, and the PERK Study Group. Results of the Prospective Evaluation of Radial Keratotomy study 10 years after the surgery. Arch Ophthalmol 1994;112: 1298–1308.

12.MR Deitz, DR Sanders, MG Raanan, M DeLuca. Long-term (5- to 12-year) follow-up of metalblade radial keratotomy procedures. Arch Ophthalmol 1994;112:614–620.

13.GM Kezirian, CM Gremillion. Automated lamellar keratoplasty for the correction of hyperopia. J Cataract Refract Surg 1995;21:386–392.

14.American Academy of Ophthalmology. Automated lamellar keratoplasty. Ophthalmology 1996;103:852–861.

15.O Gris, JL Guell, A Muller. Keratomileusis update. J Cataract Refract Surg 1996;22:620–623.

16.WA Lyle, GJ Jin. Hyperopic automated lamellar keratoplasty: complications and visual results. Arch Ophthalmol 1998;116:425–428.

17.Y Burnstein, AL Robin. Pressure or progression? (letter). Arch Ophthalmol 1999, 117:417– 419.

18.G Ghiselli, EE Manche, R Maloney. Factors influencing the outcome of hyperopic lamellar keratoplasty. J Cataract Refract Surg 1998;24:35–41.

19.JI Barraquer. Querato Mileusis y Queratofaquia. Bogota, Colombia: Instituto Barraquer de America, 1980, p 342.

20.JI Barraquer. Queratomileusis para la correccion de la miopia. Arch Soc Am Oftamol Optom 1964;5:27–48.

21.IG Pallikaris, DS Siganos. Excimer laser in situ keratomileusis and photorefractive keratectomy for correction of high myopia. J Refract Corneal Surg 1994;10:498–510.

22.CR Munnerlyn, SJ Koons, J Marshall. Photorefractive keratectomy: a technique for laser refractive surgery. J Cataract Refract Surg 1988;14:46–52.

23.DS O’Brart, DS Gartry, CP Lohmann, M Kerr Muir, J Marshall. Excimer laser photorefractive keratectomy for myopia: comparison of 4.0 and 5.0 millimeter ablation zones. J Refract Corneal Surg 1994;10:87–94.

24.T Seiler, J Wollensak. Results of a prospective evaluation of photorefractive keratectomy at 1 year after surgery. Ger J Ophthalmol 1993;2:135–142.

25.Z Wang, J Chen, B Yang. Posterior corneal surface topographic changes after laser in situ keratomileusis are related to residual corneal bed thickness. Ophthalmology 1999;106:406– 410.

26.RK Maloney. Discussion of “Posterior corneal surface topographic changes after laser in situ keratomileusis are related to residual corneal bed thickness.” Ophthalmology 1999;106:409– 410.

27.T Seiler, K Koufala, G Richter. Iatrogenic keratectasia after laser in situ keratomileusis. J Refract Surg 1998;14:312–317.

28.C-K Joo, T-G Kim. Corneal ectasia detected after laser in situ keratomileusis for correction of less than 12 diopters of myopia. J Cataract Refract Surg 2000;26:292–295.

29.C-K Joo, T-G Kim. Corneal perforation during laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1165–1167.

30.HS Geggel, AR Talley. Delayed onset keratectasia following laser in situ keratomileusis. J Cataract Refract Surg 1999;25:582–586.

31.FM Clair, B Schmitt, C Lesage, B Arnaud. Keratectasia induced by laser in situ keratomileusis in keratoconus. J Refract Surg 2000;16:368–370.

32.T Seiler, AW Quurke. Iatrogenic keratectasia after LASIK in a case of forme fruste keratoconus. J Cataract Refract Surg 1998;24:1007–1009.

33.CFM Schmitt-Bernard, C Lesage, B Arnaud. Keratectasia induced by laser in situ keratomileusis in keratoconus. J Refract Surg 2000;16:368–370.

34.SP Amoils, MB Deist, P Gous, PM Amoils. Iatrogenic keratectasia after laser in situ keratomileusis for less than 4.0 to 7.0 diopters of myopia. J Cataract Refract Surg 2000;26: 967–977.

35.DA Hoetzel, P Altman, K Buzard, K Choe. Strip extensiometry for comparison of the mechanical response of bovine, rabbit and human corneas. J Biomech Eng 1992;114:202–215.

36.DD Koch. The riddle of iatrogenic keratectasia. J Cataract Refract Surg 1999;25:453–454.

37.R Turss, J Friend, M Reim, CH Dohlman. Glucose concentration and hydration of the corneal stroma. Ophthalmic Res 1971;2:253–260.

38.W-M Yi, C-K Joo. Corneal flap thickness in laser in situ keratomileusis using an SCMD manual microkeratome. J Cataract Refract Surg 1999;25:1087–1092.

39.A Behrens, B Seitz, A Langenbucher, MM Kus, C Rummelt, M Kuchle. Evaluation of corneal flap dimensions and cut quality using the automated corneal shaper microkeratome. J Refract Surg 2000;16:83–89.

40.MJ Maldonado, L Ruiz-Oblitas, JM Munuera, D Aliseda, A Garcia-Layana, J Moreno-Mon- tanes. Optical coherence tomography evaluation of the corneal cap and stromal bed features after laser in situ keratomileusis for high myopia and astigmatism. Ophthalmology 2000;107:81– 87; discussion 88.