角膜内皮炎

目的探讨角膜内皮炎的发病原因．证实角膜内皮细胞的改变．阐述角膜内皮炎的临床表现特征。方法①用多聚酶链反应检测患眼房水中的单纯疱疹病毒DNA；用间接免疫荧光法检测患眼房水细胞中和小梁组织中的单纯疱疹病毒抗体。②用角膜内皮镜检查患眼愈后角膜内皮细胞密度和形态改变。结果多聚酶链反应检测20只眼房水．单纯疱疹病毒阳性率为60．0％。间接免疫荧光法检测14只眼房水涂片．荧光抗体阳性率为28．6％；1只眼的小梁组织切片检测荧光抗体亦呈阳性。角膜内皮镜检查10只患眼．表明内皮细胞密度降低．细胞异形性比率增高。结论单纯疱疹病毒是角膜内皮炎的主要感染原。感染的主要部位在角膜内皮细胞，也可同时感染虹膜睫状体和小梁网。该病特有的临床表现有别其他眼病。     

角膜内皮炎的角膜内皮细胞形态改变

目的探讨角膜内皮炎对患者中央角膜内皮细胞形态的影响。方法用EM-1000型接触式角膜内皮镜对10例单眼角膜内皮炎愈后4-12周的患者的双眼分别摄取中央角膜内皮像并对其图像进行电脑分析。患眼作为实验组。健眼作为对照组。观察其角膜内皮细胞密度。六角形细胞的百分比及异形性的变化。用计量资料配对设计的2样本均数的t检验进行统计分析（双侧检验，P〈0．01为统计学有差异）。结果在10例临床诊断角膜内皮炎愈后的患者中，中央角膜内皮细胞密度实验组平均为（1981±181）／mm^2。对照组平均为（2284±315）／mm^2。六角形细胞比例实验组平均为34％，对照组平均为43％．变异系数实验组平均为53％，对照组平均为45％．以上各项观察指标实验组与对照组之间在统计学上都存在显著性差异（P〈0．01）。结论角膜内皮炎对角膜内皮细胞造成损伤，导致严重的形态改变，在临床工作中应给予充分重视。[眼科新进展2007；27（2）：138-139]     

准分子激光原位角膜磨镶术后角膜内皮细胞的变化

目的 研究LASIK手术对角膜内皮细胞的影响。方法 对197例(370只眼)行LASIK手术治疗的患者,分别于术前、术后1周、术后1、3个月行角膜内皮镜检查,观察角膜内皮细胞的形态和密度的变化。结果 LASIK术后随访3个月。角膜内皮细胞形态无明显改变,角膜内皮细胞密度亦无显著性改变。结论 LASIK手术对角膜内皮细胞无损伤,不会造成角膜中央部内皮细胞形态改变和密度降低。     

两种角膜内皮显微镜测量近视屈光手术前后角膜内皮细胞密度的比较

目的比较两种非接触角膜内皮显微镜测量近视屈光手术前后角膜内皮细胞密度。方法近视91例（182只眼）,用SP-1P及EM-3000两种角膜内皮显微镜检查,行SMILE术34例（67只眼）,术后1周完成检查,余未手术。比较两种仪器测量术前和术后中央角膜内皮细胞密度结果,用Bland-Altman法比较两种仪器测量结果的一致性。结果近视91例（182只眼）术前两种仪器测量中央角膜内皮细胞密度组内相关系数分别为0.976、0.961,变异系数分别为0.086、0.068,角膜内皮细胞密度95%可信区间为148.27～209.87个/mm2;34例（67只眼）SMILE术后1周,两种仪器测量结果组内相关系数分别为0.973、0.879,变异系数分别为0.076、0.090, 95%可信区间为225.86～316.84个/mm2。术前、术后两种仪器测量中央角膜内皮细胞密度差异均有统计学意义（P〈0.05）。结论SP-1P及EM-3000两种角膜内皮显微镜测量近视SMILE术前结果一致性好,术后早期测量结果间一致性不佳。     

应用共焦显微镜观察Fuch角膜内皮营养不良患者的病变形态学特征

目的探讨应用共焦显微镜观察我国Fuch角膜内皮营养不良患者角膜各层的活体形态学特征。方法对19例(38只眼)Fuch角膜内皮营养不良患者的中央部角膜进行活体共焦显微镜检查,分为有症状组(19只眼)和无症状组(19只眼),并选取30只眼作为正常对照组,应用NAVIS软件测量、分析角膜各层组织细胞形态和密度,以及滴状赘疣和角膜神经的直径。结果 (1)有症状组:19只眼的角膜内皮层均见到滴状赘疣,直径20-60 μm,内皮细胞密度与正常对照组比较差异有显著意义(t=18.74,P<0.01);9只眼后弹力膜增厚;14只眼角膜后基质层有长条形暗区结构;19只眼角膜基质反光普遍增强;17只眼Bowman膜有局灶性高反光区域;19只眼基底上皮细胞形态大致正常;10只眼显示正常的角膜神经结构;后、前基质细胞密度,与正常对照组比较差异无显著意义(t=0.854、1.173,P=0.38、0.24)。(2)无症状组:19只眼的角膜内皮层均见到滴状赘疣,数目较有症状组者少,直径15-40μm;内皮细胞密度,与正常对照组比较,差异无显著意义(t=1.998,P=0.053);角膜其余各层未见异常。有症状组与无症状组的内皮细胞密度计数比较,差异有非常显著意义(t=8.352,P<0.01)。结论活体共焦显微镜检查有助于Fuch角膜内皮营养不良患者的诊断,特别适用于角膜水肿、角膜内皮镜无法成像的患者。(     

LASIK手术对角膜内皮细胞影响的研究

目的　研究 L ASIK手术对角膜内皮细胞的影响。方法　 5 1例 96眼近视眼患者进行 L ASIK治疗 ,等效球镜度数 - 1.5 0 D～ - 15 .75 D(- 6 .92± 3.43D) ,并按照准分子激光切削后角膜基质床的厚度分别分成三组 : .2 0 0～ 2 5 0μm ; .2 5 0～ 30 0μm; .30 0μm以上。各组患眼于术前和术后 3个月进行角膜内皮镜检查 ,观察角膜内皮细胞形态和内皮细胞密度。结果　 L ASIK手术前后角膜内皮细胞形态结构无明显改变 ,术前、术后角膜内皮细胞密度分别为 316 5± 32 4/ mm2 和 315 1± 30 5 / mm2 ,配对 t检验 ,无显著性差异 (P >0 .0 5 )。按照激光切削后角膜基质床的厚度分成的三组术前、术后角膜内皮细胞密度也没有出现显著性改变 (P >0 .0 5 )。结论　 L ASIK术后早期不会损伤角膜内皮 ,不会造成中央部角膜内皮细胞密度降低和细胞形态结构的改变 ,其对角膜内皮细胞的远期影响有待进一步的观察。     

小切口下角膜后弹力层剥除联合深板层内皮移植术的实验研究

目的 探讨小切口下角膜后弹力层剥除联合深板层内皮移植术(DSEK)的手术方法、疗效、并发症、内皮细胞的评价及组织学检查.方法 为实验研究.将24只新西兰大白兔随机分为3组,每组8只兔(8只眼),供体为新西兰大白兔16只眼.A组于角膜缘处行5 mm长隧道切口,剥去角膜中央直径10 mm的后弹力层,将等大的带有少量基质的后弹力层内皮细胞膜片植入受体眼;B组行单纯角膜后弹力层环形撕除术;C组在角膜后弹力层剥除后行去内皮细胞的带少许角膜基质和后弹力层膜片植入.术后观察1个月,比较3组兔角膜的透明性、植片贴附情况、角膜内皮细胞密度及并发症情况.结果 A组8只眼术前角膜内皮细胞密度平均值为(2728±108)个/mm2,术后角膜均恢复透明,内皮细胞密度平均为(2195±77)个/mm2,差异有统计学意义(t=12.455,P＜0.001);组织切片证实角膜内皮细胞植片与受体植床愈合良好,层间无瘢痕形成.B组8只眼术后均有严重的角膜水肿,持续1个月未恢复,组织学检查术后28 d时仅在后弹力层剥除的交界处有极少数的内皮细胞长入.C组8只眼术后1周内角膜植片均水肿,5只眼植片脱位;术后至观察1个月,角膜中央水肿仍较明显,伴有角膜新生血管长入,组织学检查植片部位未见内皮细胞长入.结论 角膜后弹力层剥除联合深板层内皮移植术具有安全、损伤小、术后恢复快及无层间瘢痕的优点,是治疗大泡性角膜疾病的优选术式.     

低密度角膜内皮细胞白内障超声乳化术的临床观察

目的评价超声乳化吸除术在治疗低密度角膜内皮细胞白内障患者的可行性和手术效果。方法对10例（12只眼）角膜内皮细胞密度〈1500个/mm^2的白内障患者行白内障超声乳化吸除人工晶状体植入术。其中Fuchs角膜营养不良3只眼,抗青光眼术后4只眼,颗粒状角膜营养不良2只眼,穿透性角膜移植术后3只眼。使用角膜内皮显微镜检查所有患者术前术后角膜内皮细胞密度,并观察术后视力及角膜水肿变化。结果所有患者术后视力均有不同程度提高,术后3个月最佳矫正视力0.1-0.4者8只眼,≥0.5者4只眼。术后角膜水肿为轻中度,常于术后5-7 d恢复,无角膜内皮细胞失代偿。内皮细胞损失率8.83%。结论低密度角膜内皮细胞白内障患者在一定程度上可行白内障超声乳化联合人工晶状体植入术。严格掌握手术适应证、术中注意保护角膜内皮细胞和由经验丰富的术者完成手术是疗效满意的重要保证。     

传导性角膜成形术后眼压及角膜内皮细胞的变化

目的 探讨传导性角膜成形术（CK）对眼压和角膜内皮细胞的影响。方法 对20例（36眼）接受CK治疗的患者，于术前和术后第4周分别用非接触式眼压计（NCT）和Goldmann眼压计（GAT）测量眼压，行角膜内皮镜检查，观察中央区角膜内皮细胞形态和密度的变化。结果 和术前比较，术后眼压显著降低。眼压变化和年龄、性别、角膜曲率以及拟矫正屈光度无关。角膜内皮细胞形态和密度无显著性改变。结论 CK手术对角膜内皮细胞无损伤，不会造成角膜内皮细胞形态改变和密度降低。但术后压平式眼压计和非接触式眼压计测量眼压值偏低。为避免CK术后青光眼的误诊，不能按传统的正常眼压值衡量术后结果。     

角膜内皮面硅油的形态学及定量分析

目的观察贴附在角膜内皮面的硅油形态学变化及对角膜内皮细胞损害的形态学定量分析。方法选择已行经睫状体平部玻璃体手术联合硅油玻璃体腔内注射手术后1周～1a并出现硅油进入前房且已贴附在内皮面的患者11例(11眼,有晶状体眼),应用角膜内皮细胞分析系统(角膜内皮镜)观察进入前房并已贴附在内皮面的硅油,手术取出前后角膜内皮细胞形态学改变及形态定量指标的变化。结果硅油取出术前角膜内皮镜检查,镜下清晰可见贴附在内皮面的硅油液面与内皮细胞层紧密粘贴,并形成特殊的明亮反光,内皮细胞边界发亮(即“亮度颠倒”现象),在角膜后表面皱褶的边缘有亮暗相间的轮廓线;角膜内皮细胞四项形态定量指标中:细胞面积和细胞密度2项手术前后(术后4～7d)改变无统计学差异,六棱细胞比率和变异系数2项改变有统计学差异。结论角膜内皮面贴附硅油时,出现特有的角膜内皮镜下改变,且在短期内即可直接造成内皮细胞的损害,应尽早取出。     

Effects of intraocular irrigating solutions on the corneal endothelium after in vivo anterior chamber irrigation

We used wide-field specular microscopy and corneal pachymetry to evaluate the effect of anterior chamber irrigation with BSS and BSS Plus on the corneal endothelium of cats. Endothelial changes were quantitated by computerized morphometric analysis of individual cells. After short-term (15 and 30 minutes) and long-term (one and two hours) irrigation, endothelial cell density remained unchanged. Corneal thickness increased significantly in the BSS group after one hour of irrigation. BSS Plus caused minimal changes in endothelial morphologic characteristics regardless of the irrigation time. By comparison, BSS caused a significant increase in the coefficient of variation of cell area (polymegethism) and a decrease in the percentage of hexagonal cells (pleomorphism). These changes were more prominent after prolonged irrigation. The morphologic changes caused by BSS irrigation are indicative of a stressed endothelial monolayer that may be more susceptible to additional surgical trauma.     

Sporadic diffuse corneal endotheliitis

We studied two patients with acute diffuse corneal endotheliitis who had no family history of the disease. Endothelial specular photographs taken during and after an attack of endotheliitis demonstrate the deposition of inflammatory material on edematous endothelial cells, with areas of focal endothelial cell loss that resolved with treatment. These cases are distinctly different than the previously described "idiopathic" primary endotheliitis entities, which have included focal or sectoral areas of corneal edema, corneal edema in association with a migrating rejection line, or diffuse edema occurring as a dominantly inherited condition. No definitive causative agents have been established. It is likely that the disease results from an immune response to autoantigens or antigens from an unidentified viral infection. The pathogenesis may be similar to that of corneal homograft rejection.     

白内障术后角膜内皮炎5例临床分析

目的 探讨对白内障术后角膜内皮炎的诊断及治疗方法 .方法 对一组白内障术后角膜内皮炎采用抗病毒药物、糖皮质激素及降眼压等对症治疗.观察疗效并进行随访.结果 全部病例均获得良好疗效,随访4～9个月,未发现复发.结论 白内障术后发生角膜内皮炎,早期足量糖皮质激素治疗,可以迅速缓解内皮细胞及小梁网的炎症,对控制眼压,挽救角膜内皮细胞生理功能起主要作用.同时使用抗病毒药物,以及对症降眼压处理.可以获得良好的疗效.     

Long-term corneal endothelial changes after intraocular lens implantation

We studied the morphologic characteristics of the corneal endothelium in a series of patients who had undergone phacoemulsification with intraocular lens implantation performed by one surgeon. Specular microscopy and computer-assisted morphometry were performed preoperatively and three years after surgery. Nineteen eyes that received posterior chamber lenses with intracapsular fixation had a mean endothelial cell loss of 18.1%, without any significant change in cell size (polymegethism) or shape variability (pleomorphism). Implantation of anterior chamber lenses with the posterior capsule left intact (18 eyes) caused a similar degree of cell loss (23.5%) but caused marked polymegethism and pleomorphism of the cells. Endothelial cell loss (28.5%) and morphologic changes were greatest in five eyes that received anterior chamber lenses because of a rupture of the posterior capsule.     

Corneal endothelium in penetrating keratoplasty

Specular microscopy of endothelium after corneal transplantation has often shown a sharp reduction in its number density immediately after surgery and long-term cell loss during the next three to four years in addition to continuous morphologic changes. We examined flat preparations of the endothelium of three corneal buttons removed three weeks, eight weeks, and 11 months after penetrating keratoplasty and compared them to similar preparations from the corneal rims of the respective donors. We did not find significant morphologic changes, and direct endothelial cell counts disclosed an endothelial cell loss of 3.8% at three weeks, 2.6% at eight weeks, and 5.6% at 11 months after keratoplasty. We believe the lack of endothelial cell loss and absence of morphologic changes in these specimens are direct results of our surgical technique.     

Clinical specular microscopy

Clinical specular microscopy (CSM) has recently been introduced as a means of qualitative and quantitative examination of the human corneal endothelium at high magnification. With the aid of CSM, a decline in endothelial cell density with age has been documented and several endothelial abnormalities from disease or trauma can be detected. Donor material for corneal grafting can be examined by CSM and keratoplasty procedures can be designed to decrease endothelial damage. Cataract surgical procedures can cause endothelial cell loss. According to most studies, intracapsular extraction causes less cell loss than does phacoemulsification, and cataract extraction with intraocular lens (IOL) insertion causes the greatest loss. Cell loss from IOL can be minimized by decreasing lens-corneal contact. Elevated intraocular pressure may lead to endothelial cell loss, as may therapy with epinephrine. Endothelial toxicity of other drugs and solutions can be studied by CSM. While long term studies are necessary to correlate the morphologic changes detected by CSM with future endothelial function, shortterm studies can be helpful in developing medical and surgical techniques that minimize corneal endothelial trauma.     

共聚焦显微镜对角膜移植术后内皮型免疫排斥反应观察

目的 应用激光共聚焦显微镜(Confocal LaserScaning Microscope,CLSM)观察角膜移植术后内皮型免疫排斥反应的特征及抗排斥治疗后的转归.方法 应用CLSM对16例角膜移植术后内皮型免疫排斥反应的病例,分别在抗排斥治疗前、治疗3～7d和1月后,对其病灶的特定位点进行检查,分析角膜上皮细胞、基质细胞、内皮细胞及免疫细胞的数量及形态学变化.结果 (1)16例患者中,8例可见典型的内皮排斥线,CLSM下:内皮排斥线是由体积较小反光明亮的炎症细胞和体积较大边界不清的异常内皮细胞构成.排斥线经过的区域上皮细胞体积增大,上皮基底层大量树突状Langerhans细胞,基质层水肿增厚,呈网格状改变.内皮细胞体积增大,边界模糊,六边形结构消失,可见多核细胞.基质水肿较重的病例,内皮层面见大量强反光团,内皮细胞无法成像.排斥线以上角膜植片相对透明的部分则各层细胞排列基本规则,内皮面少量免疫细胞附着.另8例表现为植片弥漫水肿混浊,CLSM下表现与内皮排斥线经过区域类同.(2)药物治疗3～7d后,12例患者明显好转.CLSM下见上皮基底层下树突状Langerhans细胞明显减少;基质细胞核清晰可见;内皮细胞恢复六边形结构,密度增加,其表面免疫细胞数量减少.4例患者基质层水肿减轻,中深基质层细胞有变性纤维化现象,内皮细胞层强反光团明显减少,但内皮细胞仍不能清晰成像.此4例患者用药1月后基底膜下仍有局限性树突Langerhans细胞聚集,中深基质层变性纤维化,内皮细胞排列不规则,有变圆或拉长现象.结论 应用CLSM可在细胞学水平对角膜移植术后内皮型免疫排斥反应的过程与转归进行活体的动态观察,对指导抗排斥治疗,有效提高角膜移植排斥反应的诊治水平,具有重要的临床意义.

Abstract：

Objective To demonstrate the features and the outcomes after treatment of endothelial rejection in human corneal allograft rejection by in vivo confocal microscopy. Methods Sixteen patients with endothelium rejection ofallogratt after penetrating keratoplasty were examined by confocal microscopy, to analyze the quantity and morphological changes of corneal epithelial cells, stroma cells, endothelium cells and immune cells before treatment and 3-7days and 1 month after treatment. Results Among the 16 patients, typically endothelial rejection line were seen in 8 cases, another 8 cases' keratic precipitates was diffusely scattered.Confocal microscope images revealed that the endothelial rejection lines were formed by cellular aggregate of small inflammatory cells and damaged larger endothelial cells with pyknotic highly reflective nuclei. With the progression of endothelial endothelia line, epithelium cells were large in size and lose distinct boundaries, numerous Langerhans cells (LCs) were seen in the basement epithelial cell region, keratocytes were altered in appearance with increased visibility of the cytoplasm, damaged endothelial cells decreased in number, increased in size with loss of normal polygonal shape and sticked by highly reflective immune cells which scattered or gathered. In the severely edematous area, the endothelial cells were not visualized with confocal microscopy.After 3 or 7 days of treatment, 12 cases were cured. Confocal microscopy examination revealed that the density of LCs reduced gradually and normal keratocytes were detected, the endothelial cells restored to hexagon structure and the density of immune cells decreased. Endothelial cells of 4 cases still were not visualized with confocai microscopy because of the degeneration fibrosis of deep stromal layer. LCs in the basement epithelial cell region still could be found after I month of treatment, and their endothelial cells appeared elongated or rounded with loss of their normal cell junctions. Conclusions In vivo confocal microscopy can provide us with detailed histopathology proofs and appear dynamically the transformation after treatment of endothelial rejection at cell level. It plays an important role in improving the diagnostic level and directing anti-rejection medication in our clinical practicing works.     

Experimental corneal endotheliitis in rabbit

PURPOSE: Corneal endotheliitis may cause permanent visual loss due to endothelial decompensation. The pathogenesis underlying this distinct clinical entity is not known. In the current study, a rabbit herpetic corneal endotheliitis model was made of induced anterior chamber-associated immune deviation (ACAID). METHODs: One group of rabbits received left-eye intracameral inoculation of UV-inactivated herpes simplex virus (HSV)-1 (strain McKrae). The second group received cell medium in the same manner as the first group. The third group subcutaneously received the same inoculum as the first group. Seven days later, all right eyes were intracamerally infected with 2.5 x 10(4) plaque-forming units of infectious HSV-1. Eyes were evaluated by slit lamp examination. Two weeks after infection, rabbits were killed, and right eyes were examined by immunohistochemical staining and electron microscopy. Aqueous humor was detected for HSV-1 DNA and antibody. RESULTS: Nonspecific inflammation occurred in the anterior segments of the eyes from the second and third groups. In contrast, at 14 days after infection, the first group of rabbits showed a specific pattern of inflammation that greatly resembled clinical features of corneal endotheliitis. Viral antigen was detected only in the endothelial layer. Electron microscopy revealed enlarged intercellular gaps and infiltration of inflammatory cells that are characteristic of endothelial defects. HSV-1 DNA was detected at a significantly higher number in the aqueous humor aspirates from endotheliitis rabbits. In addition, ACAID was shown to be induced in the rabbits with corneal endotheliitis. CONCLusIONS: HSV-1 infection can induce corneal endotheliitis and ACAID may play the pivotal role in this entity.     

Changes in the normal corneal endothelial cellular pattern as a function of age

Human endothelial morphologic changes were quantitated by specular microscopy and computer-assisted morphometry to establish normal baselines of various morphologic parameters. Cellular polymegethism and cellular pleomorphism increases with age, and normal baseline parameters are detailed. Furthermore, no significant difference in any morphologic parameters between the right and left eye and between central and peripheral endothelium was detected in the normal corneas examined. These normal morphologic baselines can possibly be utilized to detect early corneal endothelial pathology and/or cell loss nondetectable by cell density measurement.     

我国正常人角膜内皮细胞的计算机分析

目的 探讨我国正常人角膜内皮细胞密度和形态特征，建立细胞密度和形态学的生理学参数。方法 应用接触式角膜内皮细胞显微镜（日本Ｔｏｍｅｙ公司ＥＭ－１０００）及与其联网同步显示的角膜内皮细胞分析仪（日本Ｔｏｍｅｙ公司－１０２０），对我国１５４例（２４４眼）正常人角膜内皮细胞进行了观察和分析。结果 建立了细胞密度和形态学参数。发现：年龄和平均面积、面积标准差、最大细胞面积、最小细胞面积以及五、七角形细胞出