Epithelial Ingrowth

The surface layer of the cornea is the epithelium. It makes up about 10% of the thickness of the cornea. If injured, the epithelial cells regenerate. Below the epithelium is the corneal stroma. The stroma does not regenerate. The blade that cuts the LASIK flap penetrates to approximately one-third of the thickness of the corneal stroma. Where the flap meets the corneal bed is called the interface. Epithelial cells may be implanted in the interface either during flap creation or migrate under the flap after surgery.

A medical study of postmortem corneas after "successful" LASIK demonstrated that epithelial ingrowth of varying degrees occurred in 47% of corneas (see abstract below). The risk of epithelial ingrowth is greater for reoperations involving lifting the flap.

Surgical intervention is required in some cases. A high recurrence of epithelial ingrowth is reported after surgical treatment. Epithelial ingrowth may lead to flap melt and vision loss.

"Epithelial ingrowth is a relatively common complication of LASIK. The risk factors for its development include epithelial defects at the time of or soon after surgery, epithelial basement membrane dystrophy, hyperopic LASIK corrections, repeated LASIK surgery, flap instability, presence of diffuse lamellar keratitis (DLK), and a history of epithelial ingrowth in the fellow eye. While the reported incidence is up to 20%, less than 1% of cases required treatment in 2 large reported series. Most patients with epithelial ingrowth are asymptomatic but have subtle findings on examination. Fluorescein staining can often be seen at the flap edge in the area of the ingrowth, as there usually is incomplete adhesion of the flap to the underlying stroma. Epithelial ingrowth probably occurs postoperatively with an invasion of epithelial cells under the flap. Another possibility is that implantation of epithelial cells in the interface intraoperatively leads to epithelial ingrowth. In most cases, there is continuity between the epithelium in the interface and the surface epithelium with incomplete adhesion of the flap edge, suggesting that a postoperative invasion is the likely etiology." Source: J Cataract Refract Surg. 2004 Apr;30(4):929-31. Advanced epithelial ingrowth 6 months after laser in situ keratomileusis. Latkany RA, Haq FE, Speaker MG.


Pathologic findings in postmortem corneas after successful laser in situ keratomileusis.
Kramer TR, Chuckpaiwong V, Dawson DG, L'Hernault N, Grossniklaus HE, Edelhauser HF.
Cornea. 2005 Jan;24(1):92-102.
Emory Eye Center, Emory University, Atlanta, GA 30322, USA. Theresa_Kramer@emoryhealthcare.org

PURPOSE: To examine the histologic and ultrastructural features of human corneas after successful laser in situ keratomileusis (LASIK).

METHODS: Corneas from 48 eyes of 25 postmortem patients were processed for histology and transmission electron microscopy (TEM). The 25 patients had LASIK between 3 months and 7 years prior to death. Evaluation of all 5 layers of the cornea and the LASIK flap interface region was done using routine histology, periodic acid-Schiff (PAS)-stained specimens, toluidine blue-stained thick sections, and TEM.

RESULTS: In patients for whom visual acuity was known, the first postoperative day uncorrected visual acuity was 20/15 to 20/30. In patients for whom clinical records were available, the postoperative corneal topography was normal and clinical examination showed a semicircular ring of haze at the wound margin of the LASIK flap. Histologically, the LASIK flap measured, on average, 142.7 microm (range, 100-200). A spectrum of abnormal histopathologic and ultrastructural findings was present in all corneas. Findings at the flap surface included elongated basal epithelial cells, epithelial hyperplasia, thickening and undulations of the epithelial basement membrane (EBM), and undulations of Bowman's layer. Findings in or adjacent to the wound included collagen lamellar disarray; activated keratocytes; quiescent keratocytes with small vacuoles; epithelial ingrowth; eosinophilic deposits; PAS-positive, electron-dense granular material interspersed with randomly ordered collagen fibrils; increased spacing between collagen fibrils; and widely spaced banded collagen. There was no observable correlation between postoperative intervals and the severity or type of pathologic change except for the accumulation the electron-dense granular material.

CONCLUSIONS: Permanent pathologic changes were present in all post-LASIK corneas. These changes were most prevalent in the lamellar interface wound. These changes along with other pathologic alterations in post-LASIK corneas may change the functionality of the cornea after LASIK.