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Delayed Ectasia Following LASIK With No Risk Factors: Is a 300-µm Stromal Bed Enough? PDF Print E-mail
Sunday, 07 October 2007 06:03

Journal of Refractive Surgery Vol. 23 No. 6 June 2007

Sonal S. Tuli, MD; Sandhya Iyer, MD, FRCS

PURPOSE: To report a case of ectasia occurring >4 years following LASIK with no risk factors and a residual stromal bed >300 µm.

METHODS: A 33-year-old woman presented 4 years after LASIK with mild blurring in the left eye. Uncorrected visual acuity (UCVA) had been 20/20 in both eyes previously.

RESULTS: Uncorrected visual acuity was 20/20 and 20/40 in the right and left eyes, respectively. Best spectacle-corrected visual acuity (BSCVA) was 20/20 with –0.75 +2.25 X 70° refraction in the left eye, which matched topography. Preoperative corneal thickness was 595 µm, and topography showed no risk factors preoperatively or immediately postoperatively. Calculated residual stromal bed was 342 µm and measured 400 µm with ultrasound microscopy. One year postoperatively, UCVA decreased to 20/400, and BSCVA decreased to 20/60 with refraction of –4.50 +5.00 X 90°. The patient was intolerant of contact lens wear and is considering collagen cross-linking, Intacs, or corneal transplantation.

CONCLUSIONS: Ectasia can occur more than 4 years after LASIK. Its etiology is unknown and management is challenging. [J Refract Surg. 2007;23:620-622.]>

From the full text:

Quote: There was no documentation of intraoperative corneal thickness.

Quote: The posterior float on Orbscan increased to 55 μm (Fig 2). A Paradigm UBM microscope (Paradigm Medical Industries, Salt Lake City, Utah) was used to measure the residual stromal bed directly, which showed flap thickness of 150 μm and residual stromal bed of 400 μm.

Quote: This report shows that ectasia can occur >4 years following uncomplicated LASIK in a patient with no risk factors.

Quote: Confocal microscopy of corneas after LASIK have shown 20% loss of keratocytes above and below the flap interface by apoptosis immediately following surgery, which progressed to 40% at 5 years postoperatively.6 This loss of keratocytes has been seen in histology specimens of corneas removed during keratoplasty for ectasia.7 The decrease in keratocytes could progressively weaken the stromal bed and cause ectasia. It is conceivable that individual corneas differ in stromal keratocytes density, and the loss of keratocytes could cause ectasia in corneas with fewer keratocytes. Although most people develop ectasia much earlier, a weakened stromal bed may explain its development in our patient 4 years after LASIK.

Quote: Management of ectasia after LASIK is challenging due to its rapid progression. The use of contact lenses may correct vision but could be diffi cult to fi t, and patients may be intolerant due to dry eye, as was our patient.

Quote: One third of ectasia cases following LASIK require penetrating keratoplasty. 1 However, penetrating keratoplasty may result in unacceptable lifestyle changes in patients who often choose LASIK due to their active lifestyle. Also, a large graft may be necessary to include the entire LASIK flap and the donor cornea would be sutured to an intact recipient rim, which would increase risk of rejection. Other options are implantation of intrastromal rings (Intacs) and riboflavin with collagen cross-linking.8,9 However, these merely stabilize the cornea, and vision does not improve to the same levels noted before ectasia. In addition, cross-linking involves ultraviolet light, and its long-term effects are unknown.