Avellino角膜营养不良在共焦显微镜下的形态学特征

目的 探讨Avellino角膜营养不良（ACD）患者的共焦显微镜图像特点。方法对经基因型检测明确为ACD患者（R124H突变）的10例20眼角膜进行共焦显微镜检查，其中1例2眼为穿透角膜移植（PK）术后眼，一眼病变复发，另一眼无复发表现。并取颗粒状角膜营养不良I型（GCD I，R555W突变）患者9例18眼作为对照。结果ACD患者未手术眼共焦显微镜图像特点：基底上皮、Bowman膜及整个角膜基质均可见不同程度的异常反光改变；PK术后复发眼Bowman膜及紧邻其下的前基质可见由细小沉积物组成的不规则混浊；PK术后无复发表现眼角膜各层未见明显异常。GCD I型最显著的共焦显微镜图像特点为角膜基质内以大型沉积物为主。结论首次对经基因检测确诊的Avellino角膜营养不良患者的角膜进行活体共焦显微镜检查。ACD患者基底上皮、Bowman膜及整个角膜基质均可见不同程度的异常反光改变，但较GCD I型患者的沉积物为小。     

角膜内皮炎共焦显微镜形态学分析

目的:观察角膜内皮炎的共焦显微镜下形态学特征。方法:应用Confoscan 4.0共焦显微镜对24例24眼角膜内皮炎患者的角膜进行扫描检查,记录并分析各层角膜图像。结果:所有患者前部基质混浊,角膜深基质层可见基质细胞排列紊乱及条索状高反光结构,深基质层中还可见低反光带为后弹力层皱褶,角膜内皮细胞前可见斑片状大小不等的高反光结构,病变区角膜内皮细胞水肿、变性呈无结构暗区,内皮细胞呈多形性改变。4眼角膜上皮细胞边界不清,排列疏松,细胞较大,细胞核呈高反光结构,其中可见泡状暗区。结论:共焦显微镜可活体检查角膜内皮炎患者角膜组织各层结构,起到类似病理组织切片的作用;角膜内皮炎以深基质层及内皮细胞层损害为特征;共焦显微镜检查对角膜内皮炎具有一定的参考价值。     

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。(     

不同光源共焦显微镜的活体正常角膜图像研究

目的 分别采用卤素灯光源共焦显微镜和激光光源共焦显微镜对中国正常成人活体角膜各层组织结构进行观察,对照研究其图像特征.方法 对35例(70只眼)中国成人(年龄18～55岁)中央部角膜分别采用卤素灯光源共焦显微镜和激光光源共焦显微镜进行检查,研究角膜各层结构的图像特点,并进行对比.结果 共焦显微镜检查的35例(70只眼)中,67只眼95.7％成功获得了角膜上皮翼状细胞层的图像,70只眼100％成功获得角膜上皮基底细胞层、前弹力层、前基质层、后基质层及角膜内皮细胞层的图像.结论 卤素灯光源共焦显微镜的放大倍数是1000倍,细胞放大倍数大,近似于初级电镜的放大倍数,但卤素灯光源的组织穿透力较弱,光源易衰减,所得的角膜各层细胞图像较激光角膜共焦显微镜的略微模糊,所得角膜各层图像总体颜色偏灰、结构偏模糊.激光角膜共焦显微镜的放大倍数是800倍,较卤素灯光源的共焦显微镜略小,但激光光源的组织穿透力强,所得角膜各层细胞图像较卤素灯光源的更清晰,而且在特定角度可获得非常类似角膜组织病理学切片的图像.     

应用共聚焦显微镜观察正常老年人角膜形态学的特点

目的:探讨正常老年人共焦显微镜下角膜各层组织的活体细胞形态学特征。方法:正常老年人19例22眼中央角膜应用共聚焦显微镜(confocal microscope through focus,CMTF)进行观察,记录上皮翼状细胞层、上皮基底细胞层、前基质层、后基质层、内皮层的细胞密度,选取每人上皮基底细胞层下神经丛和中后基质层神经最清晰图像,并记录此幅图像中神经纤维总长度、神经纤维直径、神经纤维数目和每100μm神经纤维包含的念珠状结构(beads)数目,同时比较不同眼别及不同性别之间上述计量和计数资料之间的差别;观察上皮翼状细胞层、上皮基底细胞层、前基质层、后基质层、内皮层及上皮基底细胞层下神经丛(subbasal epithelial nerve plexus)和中后基质层神经(stromal nerves)的组织形态。结果:上皮翼状细胞层、上皮基底细胞层、前基质层、后基质层、内皮层的细胞密度分别为2150±315,5270±539,859±137,627±184,2529±654个/mm2,上皮基底细胞层下神经丛每幅图像中神经纤维总长度、神经纤维直径和数目、每100μm神经纤维包含的念珠状结构分别为944±176μm,2.3±0.5μm,9.0±1.3条,4.9±1.4;中后基质层神经每幅图像中神经纤维总长度、神经纤维直径和数目、每100μm神经纤维包含的念珠状结构分别为306±138μm,5.6±1.7μm,1.8±1.5条,0.0±0.0。上述计量和计数资料左、右眼和男、女之间无统计学差异。同时观察到排列疏松、细胞间夹杂有无结构暗区的表层上皮细胞层,过度形态的翼状上皮细胞层,呈"斑马皮样"外观的基底细胞层,在角膜中后基质层有4眼(18%)可见到微皱褶(microfolds),在排列规则、多呈六边型的角膜内皮层发现有2眼(9%)出现类似滴状赘疣(pseudoguttata-like)结构。结论:共焦显微镜可以在实时、活体和三维空间从细胞水平对角膜各层结构进行定量和定性分析。     

共焦显微镜下虹膜角膜内皮综合征的角膜形态学观察

目的 观察共焦显微镜下虹膜角膜内皮综合征(ICE)的角膜各层组织的形态学特点.方法 观察型系列病例研究.对2000年1月至2007年6月在复旦大学附属眼耳鼻喉科医院眼科就诊的23例(23只眼)ICE患者,行共焦显微镜(NIDEK,Confoscan 3.0)下双眼检查.使用NAVIS软件记录和分析角膜各层组织图像,并使用SPSS 13.0软件对患眼的角膜内皮细胞密度、内皮细胞平均面积、六角形细胞比例及有核细胞比例进行单因素方差分析.结果 ICE患眼的角膜内皮细胞呈"风筝样"或"上皮细胞样",细胞形态失去正常的六角形外观,细胞排列紊乱,胞内可见高反光的细胞核,部分细胞内可见双核或细胞分裂象.随病程时间延长,患眼角膜内皮细胞密度和六角形细胞比例逐渐下降.病程短于1年、1～3年、3～5年及超过5年患者的角膜内皮细胞密度分别为(1687.1±122.6)、(1210.6±168.7)、(947.3±145.2)及(856.8±73.4)个/mm2;六角形细胞比例分别为(51.5±6.3)%、(39.8±9.2)%、(32.7±8.1)%及(24.1±5.6)%.随病程时间延长,患眼角膜内皮细胞平均面积和有核内皮细胞比例逐渐升高.病程短于1年、1～3年、3～5年及超过5年患者的内皮细胞平均面积分别为(678.3±56.3)、(928.7±96.2)、(1188.5±72.6)及(1337.5±60.8)μm2;有核细胞比例分别为(12.6±1.4)%、(56.8±3.7)%、(78.7±5.6)%及(84.3±2.8)%(F=7.158,7.736,6.876,14.452;均P=0.000).患眼基质细胞形态无异常,但是随病程延长,基质神经纤维逐渐增粗并明显扭曲.患眼上皮细胞的形态无异常.对侧眼角膜的各层形态结构无明显异常.结论 共焦显微镜下ICE患眼的角膜内皮细胞表现有一定特点,共焦显微镜对于判断ICE的病程进展有诊断价值.     

三种实验动物角膜活体共焦显微镜检测的比较解剖学研究

背景 海德堡视网膜厚度分析仪和角膜模块的结合实现了对眼表活体组织结构的非侵入性检查,利用共焦显微镜对常用实验动物角膜结构进行比较研究可为相关研究提供依据.目的 利用活体共焦显微镜比较新西兰大白兔、Lewis大鼠、Swiss小鼠的角膜结构,建立实验动物角膜的活体组织图像资料,为共焦显微镜的实验研究提供依据.方法 利用海德堡视网膜厚度分析仪(HRT-Ⅱ)的Rostock角膜模块对新西兰大白兔、Lewis大鼠、Swiss小鼠的角膜进行活体分析,角膜的每一层各采集20张共焦显微镜图片,比较分析实验动物角膜各层的形态学特点及角膜内皮细胞密度.结果 共焦显微镜下3种实验动物角膜表层上皮细胞表现为高反光或低反光的多形细胞,基底上皮细胞表现为暗的细胞质,细胞核不可见,细胞间排列紧密、规则；前弹力层均表现为含有丰富上皮下神经丛的无定形物质.兔角膜基质层在黑色背景中散布着高反光物质,即为角膜基质细胞核,后基质层细胞密度高于前基质层；大鼠和小鼠的角膜基质层仅观察到大量反光的星形结构,无明显的细胞核.3种实验动物的角膜内皮细胞形态相似,均表现为高反光的胞体,边界较暗且细胞排列成蜂窝状.新西兰兔前基质角膜细胞密度中位数为387.5个/mm2,后基质角膜细胞密度中位数为223.5个/mm2,明显少于前基质的细胞密度(U=0.000,P=0.000)；新西兰兔、Lewis大鼠、Swiss小鼠角膜内皮细胞密度中位数分别为2192.5、1936.0、1565.0个/mm2,总体差异有统计学意义(H=49.940,P=0.000),兔角膜内皮细胞密度明显高于大鼠和小鼠,差异均有统计学意义(x2=0.000,P=0.000；x2=0.000,P=0.000),大鼠和小鼠的角膜内皮细胞密度差异亦有统计学意义(x2=0.000,P=0.000).结论 共焦显微镜下新西兰大白兔、Lewis大鼠、Swiss小鼠角膜各层的细胞形态相似,但内皮细胞密度和基质细胞形态之间存在明显差异.HRT-Ⅱ的Rostock角膜模块可为动物实验提供角膜各层次的高分辨率图像.     

共焦显微镜在角膜营养不良诊断中的应用

目的 探讨共焦显微镜在角膜营养不良诊断中的应用价值。设计 病例系列研究。研究对象 6例角膜营养不良，包括4例Reis-Bueckleas角膜营养不良、1例角膜斑点状营养不良、1例。Fuchs角膜内皮营养不良。方法 患者双眼行裂隙灯显微镜及共焦显微镜检查，选择病变在不同角膜层次的共焦显微镜图像，对角膜沉淀进行形态学评价，并与裂隙灯检查比较。主要指标角膜病变的裂隙灯显微镜及共焦显微镜图像。结果 共焦显微镜显示Reis-Bficklers角膜营养不良病变主要累及前部基质，包括角膜上皮、基底细胞及前弹力层；斑点状角膜营养不良病变仅累及基质层，而角膜上皮层及内皮层正常；在Fuchs角膜内皮营养不良中，可直接观察角膜小滴及角膜内皮情况。结论 共焦显微镜检查提供了一种评价角膜病变的方法，较裂隙灯显微镜的分辨率高。     

超高度近视眼角膜的共聚焦显微镜观察

目的利用共聚焦显微镜观察超高度近视眼角膜的超微结构改变。方法 前瞻性病例对照研究。选择拟行准分子激光原位角膜磨镶术（LASIK）的超高度近视患者54例（54眼）作为超高度近视组,屈光度－10.00～－17.00 D,平均（－13.27±3.24）D;同时选择中低度近视患者65例（65眼）,屈光度－1.00～－6.00 D,平均（－3.12±2.32）D作为对照组。于术前行共聚焦显微镜检查角膜上皮、前弹力层、前后基质、内皮细胞及角膜厚度。采用独立样本t检验对数据进行分析。结果 在共聚焦显微镜下超高度近视组6眼（11%）可以看到角膜前弹力层及后基质少量中等反光的点状沉积物,5眼（9%）可见异常基质内神经。角膜前基质细胞、后基质细胞、内皮细胞数及角膜厚度均较中低度近视组低,内皮细胞六角形细胞百分比较中低度近视组低,内皮细胞面积变异系数较中低度近视组高,差异有统计学意义（t=6.41、5.25、2.39、2.67、3.90、4.62,P<0.05）,上皮下神经丛神经纤维与中低度近视组相比,差异无统计学意义（t=0.88,P>0.05）。结论 超高度近视眼角膜与中低度近视眼相比,在超微结构上角膜细胞数减少,内皮细胞形态大小亦有不同,对于角膜功能的影响尚不清楚。     

共焦显微镜对翼状胬肉及其周围角膜的组织病理学观察

目的 探讨角膜共焦显微镜下翼状胬肉及其周围角膜的组织病理学和细胞学特征.方法 前瞻性自身对照研究.单眼初发性翼状胬肉患者40例,应用角膜共焦显微镜观察胬肉形态,对侧无胬肉眼为对照.记录翼状胬肉、中央角膜、翼状胬肉周边角膜各层细胞图像,并对各层细胞形态、密度的结果采用配对t检验进行分析.结果 共焦显微镜下翼状胬肉的表层细胞胞体发亮,边界发暗,胬肉基质中可见毛细血管内血流,有时可见内含小圆形细胞的微囊样结构及Langerhans细胞.翼状胬肉周边角膜翼状上皮细胞、基底上皮细胞形态不规则,部分被拉长并扭曲;中央及周边各层上皮细胞平均密度小于对照眼(t=-3.92、-3.55、-3.36、-2.61、-4.31、-4.11,P均＜0.05);翼状胬肉眼角膜上皮下Langerhans细胞平均密度大于对照眼(t=3.75、4.23,p均＜0.05);角膜上皮基底细胞层下神经纤维比较杂乱,神经弯曲度大(t=5.02,P＜0.01),分支多(t=2.51,P＜0.05).结论 共焦显微镜可观察到翼状胬肉细胞水平的特征.翼状胬肉患者胬肉周边角膜上皮细胞、上皮下Langerhans细胞、上皮基底细胞层下神经、前基质细胞及角膜厚度均有变化.     

In vivo confocal microscopy of patients with corneal recurrent erosion syndrome or epithelial basement membrane dystrophy

OBJECTIVE: To characterize morphologic changes in corneas of patients with recurrent erosion syndrome or epithelial basement membrane dystrophy using in vivo confocal microscopy. DESIGN: Observational case series PARTICIPANTS: Fourteen eyes of eight patients with diagnosed epithelial basement membrane dystrophy and 13 eyes of seven patients with recurrent erosion syndrome were examined. METHODS: Slit-lamp examination and in vivo confocal microscopy. The pathologic findings are presented as digitized images obtained from video tape recorded during the confocal microscopy. MAIN OUTCOME MEASURES: The morphology of corneal surface epithelial cells, basal epithelial cells, subbasal nerve plexus, Bowman's layer, stromal keratocytes, and endothelium was analyzed. RESULTS: The surface epithelium was intact in all but two eyes. One cornea (a basement membrane disorder with clinically visible dots) had multinucleate surface epithelial cells, and one eye with recurrent corneal erosions showed a freely floating surface epithelium sheet in the tear fluid. Patients in both groups showed islets of highly reflective cells with presumed intracellular deposits surrounded by normal cells in the basal epithelial cell layer. The basal epithelial cell area also showed other pathologic changes, including drop-shaped configurations, streaks, or ridges. Folding of the Bowman's layer was also observed in both groups. Anterior keratocytes showed signs of activation (highly reflective nuclei with visible processes) in some of the patients regardless of the clinical diagnosis, and in recurrent erosions even increased deposition of abnormal extracellular matrix in the anterior stroma was suspected. Posterior corneal keratocytes and endothelium appeared normal when examined. The subbasal nerve plexus showed various pathologic changes, such as short or strangely shaped nerve fiber bundles, decreased numbers of long nerve fiber bundles, only faintly visible long nerve fiber bundles (instead of the normally observed long parallel running interconnected bundles), or increased amounts of Langerhans cells, but only one patient (with recurrent erosion syndrome) lacked the subbasal nerve plexus. CONCLUSIONS: In vivo confocal microscopy of corneas with recurrent erosions or epithelial basement membrane dystrophy showed deposits in basal epithelial cells, subbasal microfolds and streaks, damaged subbasal nerves, or altered morphology of the anterior stroma. Confocal microscopy cannot replace biomicroscopy in making a specific diagnosis, but it sometimes helps the diagnosis in corneas that appear normal under a biomicroscope.     

In vivo confocal microscopy of Fleck dystrophy and pre-Descemet's membrane corneal dystrophy

PURPOSE: To assess the value of in vivo confocal microscopy (CM) in the diagnosis of Fleck dystrophy and pre-Descemet's membrane corneal dystrophy. METHODS: Case report of two patients. Standard slit-lamp and ophthalmic examination and in vivo CM were performed on both patients. The thickness of the cornea and the morphology of the corneal epithelium, stroma, endothelium, and subbasal nerves were evaluated by confocal microscopy. RESULTS: Biomicroscopy revealed bilateral, fine, dust-, and flour-like opacities in the corneal stroma for the Fleck dystrophy patient. In the pre-Descemet's membrane corneal dystrophy patient, biomicroscopy showed opacities larger than those in the first patient. Both patients were then examined by in vivo CM. Confocal microscopy of the Fleck dystrophy showed intracellular deposits throughout the stroma. In pre-Descemet's membrane corneal dystrophy, however, these and the extracellular deposits were observed immediately anterior to Descemet's membrane. The thicknesses of the corneas were 560 and 650 microm for Fleck and pre-Descemet's membrane corneal dystrophy, respectively. The surface epithelium, subbasal nerves, and endothelium showed normal morphology in both patients. CONCLUSION: In vivo CM is a valuable tool in diagnosing rare corneal dystrophies when the final diagnosis is difficult to obtain with conventional methods.     

In vivo confocal microscopy of fleck dystrophy

PURPOSE: To use in vivo confocal microscopy to evaluate corneas with fleck dystrophy. METHODS: Both eyes of three patients with corneal fleck dystrophy were examined with a scanning slit confocal microscope. Corneal epithelium, stroma, and endothelium were evaluated, as well as the basal epithelial and stromal nerves. RESULTS: The epithelium did not show any anomalies, but the basal nerves showed hyperreflective inclusions. Throughout the entire stroma, hyperreflective dots of various shapes were seen. These consisted mostly of spherical matter with a diameter of 3-5 microm and were sometimes enclosed in cyst-like structures. The majority of the stromal cells and stromal nerves appeared normal. The endothelial cell layer was unaffected. CONCLUSION: In vivo confocal microscopy demonstrates previously unreported inclusions in the basal nerves of fleck dystrophy corneas. In addition to this new finding, the study confirms earlier histopathologic reports, demonstrating accumulation of pathologic material in the stromal cells.     

In vivo confocal microscopy findings in a patient with posterior amorphous corneal dystrophy

A 21-year-old man, with bilateral posterior amorphous corneal dystrophy, was studied by biomicroscopy, corneal topography and in vivo confocal microscopy. The best-corrected visual acuity was 6/21 in the right eye and 6/6.9 in the left eye. Biomicroscopy revealed bilateral, asymmetric, sheet-like opacification at the deep posterior stromal layer. The corneal topography displayed asymmetric against-the-rule astigmatism in the right eye and prominent steepening at the inferior paracentral cornea in both eyes. In vivo confocal microscopy of the corneas demonstrated microfolds and hyper-reflective layer at the posterior stroma just adjacent to the endothelial layer. The epithelium, Bowman's membrane, anterior stroma and the endothelial layer were normal. In vivo confocal microscopy is useful in evaluating the corneal dystrophies.     

Confocal microscopy in cornea guttata and Fuchs'' endothelial dystrophy

AIMS: To report the appearances of cornea guttata and Fuchs' endothelial dystrophy from white light confocal microscopy. METHODS: Seven eyes of four consecutive patients with cornea guttata were prospectively examined. Of the seven eyes, three also had corneal oedema (Fuchs' dystrophy). In vivo white light tandem scanning confocal microscopy was performed in all eyes. Results were compared with non-contact specular microscopy. RESULTS: Specular microscopy was precluded by corneal oedema in one eye. In the remaining six eyes, it demonstrated typical changes including pleomorphism, polymegathism, and the presence of guttae appearing as dark bodies, some with a central bright reflex. In all seven eyes, confocal microscopy revealed the presence of round hyporeflective images with an occasional central highlight at the level of the endothelium. Changes in cell morphology and size were readily appreciated. CONCLUSION: By comparison with specular microscopy, the hyporeflective images with an occasional central highlight seen on confocal microscopy are consistent with the presence of guttae. Confocal microscopy may confirm the diagnosis of cornea guttata and Fuchs' endothelial dystrophy by demonstrating the presence of guttae. This technique is especially valuable in cases of corneal oedema, where specular microscopy may fail to visualise the endothelium. However, specular microscopy should remain the method of choice to evaluate the endothelium, principally because it is easier to use.     

Confocal microscopy in Bowman and stromal corneal dystrophies.

OBJECTIVE: To use confocal microscopy to demonstrate the similarity among three autosomal-dominant corneal dystrophies and the diversity of the deposit patterns within a single dystrophy. DESIGN: A prospective, comparative case series. PARTICIPANTS: Twenty patients (40 eyes) from 10 families suffering from Bowman or stromal dystrophy agreed to take part: 3 with Reis-Bückler dystrophy, 12 with granular dystrophy, and 5 with lattice type-I dystrophy. Of these, nine had recurrence in their grafts or after phototherapeutic keratectomy before the confocal examination. The confocal images of affected corneas were compared with those of ten normal control eyes (ten subjects). INTERVENTION: All patients were examined by slit-lamp biomicroscopy. Confocal microscopy was performed with Achroplan 40x/numeric aperture (NA) = 0.75 and 63x/NA = 0.9 water immersion objectives. Image analysis was used to identify the corneal epithelial and stromal deposits correlated with each disorder. MAIN OUTCOMES MEASURES: Selected images of the corneal layers were evaluated qualitatively for the size, shape, light scattering, and reflection of the deposits. RESULTS: Slit-lamp biomicroscopy showed stromal involvement in all affected eyes. Confocal microscopy identified epithelial deposits in 30% of the eyes and stromal deposits in all eyes. The deposits within the epithelium were revealed more clearly with the 63x/NA = 0.9 objective (higher numeric aperture). Some of the confocal findings near the Bowman layer were common for all three dystrophies. Normal control eyes showed no epithelial or stromal deposits, either by biomicroscopy or confocal microscopy. CONCLUSIONS: Confocal microscopy provides an in vivo evaluation of the deposits in the cornea, with a higher resolution than biomicroscopy. The confocal findings common to the three dystrophies may agree with previous hypotheses of the same genetic origin. It may be a useful adjunct to slit-lamp biomicroscopy, particularly when histopathologic studies cannot be performed.     

Confocal microscopy of posterior polymorphous endothelial dystrophy

PURPOSE: To report the in vivo confocal microscopic findings of posterior polymorphous endothelial dystrophy (PPED). METHODS: Four patients with PPED from 2 unrelated families and 2 asymptomatic children of an index patient were included in this observational case series. The eyes of the 6 subjects were examined by confocal light microscopy. RESULTS: Confocal microscopy demonstrated craters, streaks, and cracks over the corneal endothelium surface. Pleomorphism and polymegathism were present in eyes with PPED. Guttae and clusters of abnormal endothelial cells were also identified in corneas of these PPED patients. These findings were absent in eyes without clinical manifestations of PPED. CONCLUSIONS: In vivo confocal microscopy is potentially useful for excluding suspected cases of subclinical PPED. Abnormalities in the Descemet membrane and endothelium were observed.     

In vivo confocal microscopy in recurrent granular dystrophy in corneal graft after penetrating keratoplasty

Two case reports of recurrent granular dystrophy in corneal grafts after penetrating keratoplasty are presented. Slit-lamp examination and confocal microscopy (HRT II) were performed in two patients with recurrent granular dystrophy. All confocal microscopic findings of granular dystrophy were evaluated in the graft. Dystrophic lesions of the donor cornea presented the same confocal microscopic aspects in both eyes, and were similar to granular dystrophy lesions. Confocal microscopy is an imaging method that may provide new information on corneal microanatomy in dystrophies. It may be particularly useful in improving the early diagnosis of dystrophic lesions in corneal grafts.     

Occupational corneal argyrosis in art silver solderers

PURPOSE: To determine the value of confocal and specular microscopy in the examination of corneal argyrosis in art silver solderers. METHODS: Six patients with corneal argyrosis underwent a complete physical and ophthalmologic examination. Specular microscopy was performed in three cases, and in vivo confocal microscopy in four cases. Ultrasound biomicroscopy and corneal topography were performed in three cases. A conjunctival specimen of one patient was examined histologically in paraffin sections. RESULTS: Slit-lamp examination showed gray, diffuse opacities in the deep corneal stroma. Confocal microscopy showed highly reflective deposits with a granular pattern anterior to the corneal endothelium and hypereflective keratocyte nuclei with visible cytoplasm in the anterior stroma. Specular microscopy demonstrated round white bodies anterior to the corneal endothelium. Silver deposits were not found histologically. CONCLUSIONS: Silver solderers with long-term exposure to silver compounds are at high risk of developing corneal argyrosis. We conclude that specular microscopy and in vivo confocal microscopy provided important information for the diagnosis of corneal argyrosis.