Corneal ectasia after excimer laser keratorefractive surgery: histopathology, ultrastructure, and pathophysiology

To evaluate the histopathology and ultrastructure of corneas developing ectasia after LASIK or photorefractive keratectomy (PRK).

Retrospective case series.

Thirteen specimens from 12 patients undergoing corneal transplantation for progressive ectasia after LASIK (12 specimens) or PRK (1 specimen) were obtained for histopathologic and ultrastructural evaluation.

All 13 ectatic corneas were submitted in formalin for light microscopy. Nine specimens were bisected, and the second half was placed in 2.5% glutaraldehyde for transmission electron microscopy (TEM).

Corneal histopathology, ultrastructure, and pathophysiology.

Light microscopy of the post-LASIK specimens showed corneal epithelial hypoplasia and occasional foci of epithelial hyperplasia, Bowman's layer breaks, a normal stromal thickness of the LASIK flap, a normal thickness of the hypocellular primitive stromal scar, a thinned residual stromal bed (RSB), and larger than normal artifacteous interlamellar clefts in the RSB of the ectatic region. The post-PRK specimen showed similar findings with the addition of a thinned hypercellular fibrotic stromal scar. TEM showed thinning of the collagen lamellae and loss of lamellar number in the RSB of post-LASIK ectasia corneas or throughout the entire corneal stromal bed in the post-PRK ectasia cornea, with the posterior aspect of the corneal stroma being most affected.

Histopathologic and ultrastructural studies suggest that interlamellar and interfibrillar biomechanical slippage occurs when the cornea becomes ectatic after LASIK or PRK in the postoperative stress-bearing regions of the corneal stroma. This 2-phase chronic biomechanical failure process is similar to that seen in keratoconus. Composite sciences classify this chronic biomechanical failure process as interfiber fracture.

The authors have no proprietary or commercial interest in any materials discussed in this article.