Sbarbaro James A, Eagle Ralph C, Thumma Prathima, Raber Irving M
Department of Ophthalmology, Drexel University, Philadelphia, PA 19107, USA.
Cornea. 2008 Sep;27(8):900-4. doi: 10.1097/ICO.0b013e318170aeb7.
To describe the histopathologic findings and relevant clinical details of 3 patients undergoing penetrating keratoplasty (PK) after failure of posterior lamellar endothelial keratoplasty (EK).
Retrospective clinicopathologic case series. Patients 1 and 2 underwent EK for pseudophakic bullous keratopathy. Patient 3 underwent EK for persistent corneal edema secondary to a Descemet membrane (DM) detachment after cataract extraction. Patient 1 had persistent diffuse corneal edema and broad, long-standing iridocorneal adhesions that precluded repeat EK. Patient 2 had high intraocular pressure and severe anterior chamber inflammation 1 day postoperatively with subsequent noncorneal clearing and elected PK over repeat EK. Progressive corneal edema with resultant poor visual acuity after EK was the reason for PK in patient 3.
Histopathologic examination disclosed thickened, edematous corneas with attenuated endothelium consistent with graft failure caused by endothelial decompensation in all 3 cases. Although various degrees of posterior lamellar graft detachment were observed in each instance, significant parts of each graft remained adherent to the host stroma or to segments of residual host DM. The wounds in the adherent areas, although discernible, were relatively inconspicuous, resembling those seen at the flap-stromal interface after laser in situ keratomileusis. The donor graft endothelium was atrophic in all cases, and a delicate retrocorneal fibrous membrane was present in 2 cases. Most of the graft in cases 1 and 2 remained adherent, with small areas of peripheral detachment. In contrast, the graft in case 3 adhered peripherally but had separated from the stroma centrally, forming a thin cleft.
Histopathology suggests endothelial decompensation, incomplete graft adherence, and the formation of retrocorneal fibrous membranes as possible etiologies for EK failure. The adherence of endothelial grafts to residual host DM suggests that it may not be necessary to remove optically clear DM before endothelial graft placement. The inconspicuous nature of the EK interface suggests that it may not play a large role in image degradation, although more study is needed.
描述3例后板层内皮角膜移植术(EK)失败后接受穿透性角膜移植术(PK)患者的组织病理学发现及相关临床细节。
回顾性临床病理病例系列研究。患者1和患者2因人工晶状体性大泡性角膜病变接受EK。患者3因白内障摘除术后Descemet膜(DM)脱离继发持续性角膜水肿接受EK。患者1存在持续性弥漫性角膜水肿以及广泛、长期的虹膜角膜粘连,无法再次进行EK。患者2术后1天出现高眼压和严重前房炎症,随后角膜未恢复透明,选择PK而非再次EK。患者3因EK后角膜水肿进展导致视力不佳而接受PK。
组织病理学检查显示,所有3例患者的角膜均增厚、水肿,内皮细胞变薄,符合内皮失代偿导致的移植失败。尽管在每个病例中均观察到不同程度的后板层移植片脱离,但每个移植片的大部分仍与宿主基质或残留宿主DM段粘连。粘连区域的伤口虽然可见,但相对不明显,类似于准分子原位角膜磨镶术后瓣-基质界面处的伤口。所有病例中供体移植片内皮均萎缩,2例出现薄的角膜后纤维膜。病例1和病例2的大部分移植片仍粘连,周边有小面积脱离。相比之下,病例3的移植片周边粘连,但中央与基质分离,形成一个薄间隙。
组织病理学提示内皮失代偿、移植片不完全粘连以及角膜后纤维膜形成可能是EK失败的病因。内皮移植片与残留宿主DM的粘连表明,在内皮移植片植入前可能无需去除透明的DM。EK界面不明显的性质表明,尽管需要更多研究,但它可能在图像退化中不起主要作用。