Ectasia Without Risk Factors

Does this really occur, and can it be avoided?
By Shawn R. Klein, MD; Randy J. Epstein, MD; J. Bradley Randleman, MD; and R. Doyle Stulting MD, PhD

Corneal ectasia is a progressive bowing forward and thinning of the cornea that can diminish UCVA and BCVA. Its occurrence after LASIK can be a serious complication, and its cause is not always completely apparent.

WHO IS AT RISK?
Recognized Factors

Previous studies1-9 suggest that ectasia primarily occurs in patients who have demonstrable preoperative risk factors or rarely in association with complications from the surgery. Several risk factors may predispose patients to post-LASIK ectasia, including a preoperative pachymetry <500µm, calculated residual bed <250µm, steep corneas or high attempted corrections for myopia, signs suggestive of keratoconus, forme fruste keratoconus or pellucid marginal degeneration on topography or other imaging modalities, multiple retreatments, and surgical/flap complications.

Post-LASIK Cases

Anecdotally, cases of ectasia have occurred following LASIK for which the surgeons have, even retrospectively, been unable to identify any recognizable preoperative risk factors. We attempted to determine the incidence and characteristics of cases where ectasia occurred in the absence of any of the risk factors mentioned earlier. We polled ophthalmologists who participate on Kera-net, ASCRS-net, and the ISRS/AAO's ISRSnet Internet bulletin boards (between April and October 2003) in order to collect cases that might satisfy rather rigid criteria for the “absence of identifiable risk factors.”

Data collected regarding the eyes in our study10 have been submitted for publication elsewhere. However, we can relate that a significant number of patients developed post-LASIK ectasia without any of the aforementioned recognizable risk factors. We believe that most surgeons would have performed surgery on any of these patients because the surgeons would have no reason to anticipate postoperative ectasia.

Ectasia occurred with several different types of excimer lasers and microkeratomes. All preoperative central corneal pachymetries were greater than 500µm. Calculated residual stromal bed thickness was greater than 250µm in every case. Following LASIK, all cases demonstrated increasing myopia and astigmatism as well as a progressive loss of both UCVA and BCVA. Many eyes required rigid gas permeable contact lenses for visual rehabilitation, and one required penetrating keratoplasty.

A TYPICAL LASIK CANDIDATE?

A 41-year-old male was corrected to 20/20 with a preoperative manifest refraction of -7.25 +0.75 X 115 in his left eye. He had keratometries of 42.6 X 96 and 40.7 X 6. His preoperative ultrasonic pachymetry was 556µm. Preoperative topography of his left eye demonstrated mild with-the-rule astigmatism without inferior corneal steepening. His right eye was similar to his left.

The patient underwent uneventful LASIK in his left eye, using a CB microkeratome (Moria, Antony, France) fitted with a 130-µm head and a “-1” ring. Ablation was carried out with a Technolas 217C laser (Bausch & Lomb) with a calculated ablation depth of 119µm. His intraoperative pachymetry measured 416µm. His calculated residual stromal bed was 307µm.
At 1 month postoperatively, a manifest refraction of

-2.25 +0.75 X 004 yielded 20/20 visual acuity. The patient's BCVA with -5.00 +4.00 X 025 was 20/30 8 months postoperatively. A diagnosis of ectasia was made at that time. An Orbscan (Bausch & Lomb) analysis 17 months after surgery revealed inferior corneal steepening consistent with ectasia (Figure 1). The patient was fitted with a rigid gas permeable lens in his left eye, that left him with 20/30 vision.

POSSIBLE ETIOLOGIES FOR ECTASIA

In order to avoid ectasia in patients without apparent risk factors, it is important to ascertain possible reasons for its occurrence.

Although all eyes in our study had calculated residual stromal beds thicker than 250µm, only one eye had intraoperative pachymetry. We estimated residual stromal bed thickness by subtracting the labeled microkeratome head thickness and the theoretical laser ablation depth from the preoperative pachymetry. There are several sources of error in this calculation. Several studies11-14 have demonstrated a wide distribution for flap thicknesses cut by many types of microkeratomes. It is not always safe to assume that a microkeratome will cut its labeled head thickness. Additionally, factors such as dehydration of the bed, variation in tissue ablation at different stromal depths, and fluctuations in pachymetry measurements add to flap-thickness uncertainty.

The limitations of our diagnostic technologies may make forme fruste keratoconus difficult to diagnose. For example, asymmetry of the astigmatic bowtie on topography, classically seen with forme fruste keratoconus, may be mimicked by keratoconjunctivitis sicca or can be a normal variant.

Some cases may be the result of biomechanical instability within the cornea itself that makes it unable to withstand the insult of LASIK. As Piccoli15 discussed, corneas that have the same thickness may not have the same strength. LASIK surgeons currently do not have the capability to recognize corneas that may have a decreased tissue density or tissue that is less than structurally sound.

Age may also be an important factor. Keratoconus often presents clinically in subjects in their midteens. If the age of onset of keratoconus follows its normal distribution, a small number of subjects will not become keratoconic until their early twenties. Because LASIK is often performed on patients who are 21 years old, there will be a small subset of the LASIK population who will develop keratoconus later on as a function of their eyes' natural predisposition to do so. Instead, these patients will develop ectasia after LASIK, and the refractive surgery blamed.

In comparing our patients to Randleman's study2 of ectasia patients, we found that ours were significantly younger by a margin of more than 14 years. They may represent (in part) those who were predisposed to developing ectasia because they may have developed keratoconus even without LASIK.

LIMITATIONS OF THE STUDY

This is a retrospective case series in which different surgeons performed LASIK surgeries with various techniques and equipment. In order to identify more definitively the characteristics of a patient who may unexpectedly develop ectasia postoperatively, a prospective study using a standardized surgery and technique would be more useful. Additionally, only one of our enrolled patients had his intraoperative pachymetry recorded. This makes it difficult to rule out thick flaps as a source for ectasia. It is also possible that some patients may have corneas biomechanically predisposed to developing ectasia.

CONCLUSIONS AND RECOMMENDATIONS

In addition to eliminating patients with the risk factors mentioned earlier from undergoing LASIK surgery, there may be other pertinent considerations in order to prevent ectasia. First, when calculating the residual stromal bed thickness, it is important to take into account the possible wide range of flap thicknesses achieved with mechanical keratomes. In patients who have borderline pachymetry, surface ablation or the use of the Intralase FS laser (Intralase Corp., Irvine, CA) to make the flap may be advisable. Second, surgeons should utilize intraoperative pachymetry both before and after cutting the flap when performing LASIK. This technique can detect a thick flap, which might be an indication for modificating or cancelling an ablation that would further weaken the thinned stromal bed. Lastly, young patients must be carefully considered, because some may have ectatic predispositions that would become manifest if given more time.

Shawn R. Klein, MD, is in private practice with Klein & Scannapiego in Roseland, New Jersey, and is a clinical instructor at the Institute of Ophthalmology and Visual Sciences of New Jersey Medical School in Newark. He states that he holds no financial interest in any of the products or companies mentioned herein. Dr. Klein may be reached at (908) 289-1166; kleinshawn@hotmail.com.
Randy J. Epstein, MD, is Professor of Ophthalmology at Rush University Medical Center in Chicago and is the CEO of Chicago Cornea Consultants, Ltd. He is a paid consultant for Bausch & Lomb. Dr. Epstein may be reached at (847) 432-6010; repstein@chicagocornea.com.
J. Bradley Randleman, MD, is an Assistant Professor in the Department of Ophthalmology at Emory University in Atlanta. He states that he holds no financial interest in any of the products or companies mentioned herein. Dr. Randleman may be reached at (404) 778-2264; jrandle@emory.edu.
R. Doyle Stulting, MD, PhD, is Professor and Director of the Cornea and Refractive Surgery Service in the Department of Ophthalmology at Emory University in Atlanta. He states that he holds no financial interest in any of the products or companies mentioned herein. Dr. Stulting may be reached at (404) 778-6166; ophtrds@emory.edu.

1. Seiler T, Koufala K, Richter G. Iatrogenic keratectasia after laser in situ keratomileusis. J Refract Surg. 1998;14:312-317.
2. Randleman JB, Russell B, Ward MA, et al. Risk factors and prognosis for corneal ectasia after LASIK. Ophthalmology. 2003;110:267-275.
3. Joo CK, Kim TG. 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.
4. Argento C, Cosentino MJ, Tytiun A, et al. Corneal ectasia after laser in situ keratomileusis. J Cataract Refract Surg. 2001;27:1440-1448.
5. Jabbur NS, Stark WJ, Green WR. Corneal ectasia after laser-assisted in situ keratomileusis. Arch Ophthalmology. 2001;119:1714-1716.
6. Lafond G, Bazin R, Lajoie C. Bilateral severe keratoconus after laser in situ keratomileusis in a patient with form fruste keratoconus. J Cataract Refract Surg. 2001;27:1115-1118.
7. Barraquer JI. Keratomileusis for myopia and aphakia. Ophthalmology. 1981;88:701-708.
8. Ou RJ, Shaw EL, Glasgow BJ. Keratectasia after laser in situ keratomileusis (LASIK): evaluation of the calculated residual stromal bed thickness. Am J Ophthalmol. 2002;134:771-773.
9. Buzard KA, Tuengler A, Febbraro JL. Treatment of mild to moderate keratoconus with laser in situ keratomileusis. J Cataract Refract Surg. 1999;25:1600-1609.
10. Klein SR, Epstein RJ, Randleman JB, Stulting RD. Corneal ectasia following LASIK in patients without apparent preoperative risk factors. Paper presented at: The World Cornea Congress Meeting; April 14, 2005; Washington, DC.
11. Yildirim R, Aras C, Ozdamar A, et al. Reproducibility of corneal flap thickness in laser in situ keratomileusis using the Hansatome microkeratome. J Cataract Refract Surg. 2000; 26:222-228.
12. Jackson DW, Wang L, Koch DD. Accuracy and precision of the Amadeus microkeratome in producing LASIK flaps. Cornea. 2003;22:504-507.
13. Solomon KD, Donnenfeld E, Sandoval HP, et al. Flap thickness accuracy: comparison of 6 microkeratome models. J Cataract Refract Surg. 2004;30:964-977.
14. Binder PS. Flap dimensions created with the Intralase FS laser. J Cataract Refract Surg. 2004;30:26-32.
15. Piccoli PM, Gomes AAC, Piccoli FVR. Corneal ectasia detected 32 months after LASIK for correction of myopia and asymmetric astigmatism. J Cataract Refract Surg. 2003;29:1222-1225.
For a downloadable pdf of this article, including Tables and Figures, click here.