Dawson Daniel G, Randleman J Bradley, Grossniklaus Hans E, O'Brien Terrence P, Dubovy Sander R, Schmack Ingo, Stulting R Doyle, Edelhauser Henry F
Emory Eye Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Ophthalmology. 2008 Dec;115(12):2181-2191.e1. doi: 10.1016/j.ophtha.2008.06.008. Epub 2008 Aug 9.
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.
FINANCIAL DISCLOSURE(S): The authors have no proprietary or commercial interest in any materials discussed in this article.
评估准分子激光原位角膜磨镶术(LASIK)或准分子激光角膜切削术(PRK)后发生角膜扩张的角膜组织病理学及超微结构。
回顾性病例系列研究。
获取12例接受LASIK术后(12份标本)或PRK术后(1份标本)因进行性角膜扩张而接受角膜移植的患者的13份标本,进行组织病理学和超微结构评估。
所有13份扩张角膜标本均用福尔马林固定用于光学显微镜检查。9份标本一分为二,另一半置于2.5%戊二醛中用于透射电子显微镜(TEM)检查。
角膜组织病理学、超微结构及病理生理学。
LASIK术后标本的光学显微镜检查显示角膜上皮发育不全,偶尔可见上皮增生灶,Bowman层断裂,LASIK瓣的基质厚度正常,低细胞性原始基质瘢痕厚度正常,残余基质床(RSB)变薄,扩张区域的RSB中出现比正常更大的人为层间裂隙。PRK术后标本显示类似结果,此外还有变薄的高细胞性纤维化基质瘢痕。TEM显示,LASIK术后角膜扩张角膜的RSB中胶原板层变薄且板层数量减少,或PRK术后角膜扩张角膜的整个角膜基质床均如此,角膜基质后层受影响最严重。
组织病理学和超微结构研究表明,LASIK或PRK术后,在角膜基质的术后应力承受区域,当角膜发生扩张时,层间和纤维间会发生生物力学滑动。这种两阶段的慢性生物力学失败过程与圆锥角膜所见相似。综合科学将这种慢性生物力学失败过程归类为纤维间断裂。
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