黄斑部视网膜前膜患者手术前后黄斑区结构变化及与视功能预后的关系

目的:探讨黄斑部视网膜前膜患者手术前后黄斑区域结构变化情况,及其与患者术后视功能的关系。方法:对2014年2月-2016年8月间在我院进行手术治疗的黄斑部视网膜前膜患者60例(60眼)的临床资料进行回顾性分析。所有患者均进行光学相干断层扫描(OCT)检查,观察黄斑中心凹及各方位视网膜厚度变化,同时记录患者手术前后最佳矫正视力(BCVA),分析其相关性。结果:术后53例(53眼)患者视力提高,占88.33%,7例(7眼)患者视力不变,占11.67%。术前患者BCVA为(0.18±0.07),术后3个月BCVA为(0.38±0.12),术后3个月BCVA较术前显著提高(P0.05)。患者术后黄斑中心凹厚度、内环颞侧厚度、内环鼻侧厚度、内环上方厚度、内环下方厚度、外环颞侧厚度、外环鼻侧厚度、外环上方厚度、外环下方厚度较术前均显著降低,差异具有统计学意义(P0.05)。经Pearson相关分析显示,患者术前黄斑中心凹厚度、内环颞侧厚度、外环颞侧厚度、术前后黄斑中心凹厚度差值、术前后内环颞侧厚度差值、术前后外环颞侧厚度差值与术后BCVA呈负相关(P0.05)。结论:玻璃体切除术可以显著降低黄斑部视网膜前膜患者黄斑区视网膜厚度,提高患者视功能,术前黄斑区域形态对患者术后视力恢复有一定影响。     

兔眼孔源性视网膜脱离手术复位后视功能以及超微结构的变化

目的对比研究兔眼视网膜脱离后选择不同时期手术复位视功能的变化情况,为临床手术时机的选择及预测术后视功能的恢复情况提供理论与实验依据。方法利用家兔制备孔源性视网膜脱离模型,成模后1 d、7 d1、4 d时经手术达解剖复位,采用多焦视网膜电流图检测复位后视网膜的功能,数据处理应用SPSS软件。制备组织病理学切片。结果多焦视网膜电流图显示1 d、7 d、14 d的RRD手术复位后P1波平均象限反应密度(QAP1,nV/deg2),P1波幅值(AP1,μV),N1波幅值(AN1,μV),P1波潜伏期(TP1,ms),N1波潜伏期(TN1,ms)各项数值差异有显著性(P<0.05)。光镜电镜显示视网膜脱离复位后组织病理学改变。结论视网膜脱离手术复位后视网膜细胞功能的恢复与脱离时间有明显的负相关性;多焦视网膜电流图对于局部视网膜功能的评价有重要意义;组织病理学研究提供了解释视功能变化的重要依据。     

视网膜脱离围手术期的护理

视网膜脱离是视网膜的神经上皮层和它本身的色素上皮层分离。它是一种常见的严重性、致盲性眼底疾病,手术是唯一有效的治疗方法[1]。特别是原发性视网膜脱离应争取早日手术治疗。2003年1月~2005年1月,我院采用巩膜外冷凝外加压环扎术治疗视网膜脱离58例,效果满意。现将护理体会总结如下。1临床资料本组58例患者中,男38例,女20例,年龄最小12岁,最大68岁。全部患者均行冷凝外加压环扎术。术后全部患者视网膜均达到解剖复位,且无感染发生。2护理2·1术前护理(1)术前心理护理。患者因视网膜脱离而视力减退,心理负担很重,既希望尽快手术,又对手术…     

玻璃体切割术治疗角巩膜裂伤的疗效观察

目的:评价、研究玻璃体切割术治疗严重角巩膜裂伤的临床疗效。方法:对我院2011-12/2013-12住院的39例39眼角巩膜裂伤(本组病例一期伤口均≥1.0cm)患者行玻璃体切割术治疗,术中根据视网膜情况酌情辅以视网膜光凝、惰性气体充填、硅油充填。结果:手术后随访3~12个月,随访中行视力、最佳矫正视力、眼压、眼底及B超检查,部分屈光间质透明度较好的患眼进行了OCT和眼底照相检查。患者中39例38眼眼球结构维持良好,视网膜复位良好。术后视力不同程度提高29例29眼,其中0.1者由术前0眼增加到术后的13眼;术后视力无变化4例4眼,其中3例3眼术前术后视力无光感。结论:玻璃体切割术是治疗严重角巩膜裂伤的有效方法。     

玻璃体腔注药联合微创玻璃体切除治疗糖尿病视网膜病变的临床疗效研究

目的:探讨玻璃体腔注药联合微创玻璃体切除治疗糖尿病视网膜病变的临床疗效。方法:选择2014年1月至2016年1月在我院确诊并治疗的增生性糖尿病视网膜病变患者80例,共83只患眼,随机分为A、B两组。A组共42例患眼,接受25 G玻璃体微创手术;B组共41例患眼,在A组治疗的基础上给予玻璃体腔注射康柏西普。比较两组患者的手术情况、治疗前后最佳视力的矫正(Best-corrected visual acuity,BCVA)情况、视网膜厚度以及术后1个月不良反应的发生情况。结果:B组患者的手术时间较A组显著缩短(P0.05),且术中使用电凝的患眼、术中出血以及术中发生医源性裂隙的患眼比例显著低于A组(P0.05),新生血管消失的患眼比例显著高于A组(P0.05)。B组患者术后1个月和3个月的BVCA显著高于A组(P0.05),且术后视网膜的厚度显著薄于A组(P0.05),术后发生玻璃体积血和前方出血的患眼比例显著低于A组(P0.05)。结论:玻璃体腔注射康柏西普联合25G玻璃体微创切除术治疗增生性糖尿病视网膜病变的临床疗效显著,有利于患者术后视力以及视网膜恢复。     

脉络膜脱离型视网膜脱离手术治疗前后眼压及眼轴改变的对比研究

目的：检测脉络膜脱离合并视网膜脱离患者采用不同治疗术式的术前、术后眼压及眼轴的变化,探讨眼压、眼轴与手术的相关性及两者与发病时间之间的关系。方法：收集2006年1月-2006年12月间诊断为脉络膜脱离合并视网膜脱离,并行手术治疗的患者共30例（30眼）,均为首次手术使视网膜成功复位。按照需要分组后分别在确诊后使用糖皮质激素,然后在手术前1天、术后1周、术后1个月、术后3个月及术后6个月时应用A超以及Goldmann眼压计对患者进行眼轴以及眼压的测量,并使用统计学方法进行比较。结果：1．确诊时,患者对测眼压较患侧眼压高,两者差异极显著（P〈0．01）。术前用糖皮质激素治疗7-10天后,患眼眼压值较激素治疗前明显升高（P〈0．01）。两手术组术后（玻璃体视网膜手术复位组为取硅油术后）1周、术后1月、术后3月及术后6月的眼压比术前1天眼压均显著升高（P〈0．01）;术后1月比术后1周的眼压有所降低（P〈0．05）;术后1月、3月及6月眼压之间无统计学差异（P〉0．05）。2．确诊时,患者对侧眼轴较患侧眼轴长,有统计学差异。术前用糖皮质激素治疗7～10天后,患眼眼轴较激素治疗前无统计学差异（P〉0．05）。常规视网膜手术组术后1周、术后1月、术后3月和术后6月均比术前1天延长,差异有极显著统计学意义（P〈0．01）;术后1周（29．46&#177;2．12mm）至术后6月（28．29&#177;2．63mm）的眼轴逐渐回缩（P〈0．01）。玻璃体视网膜手术复位组患者在硅油取出术后1周、1月、3月和6月比复位术前1天眼轴均显著延长（P〈0．01）;硅油取出术后1周（27．74&#177;2．07rnm）至术后6月（27．72&#177;2．17mm）时眼轴无明显改变（P〉0．05）。3．脉脱型视网膜脱离患者在确诊时双眼眼压差值与接受治疗前病程呈直线相关（r=0．833）,病程越长眼压差值越大。结论：1．脉络膜脱离型视网膜脱离患者的患眼确诊时眼压降低、眼轴缩短。2．发病时间越长,患眼眼压越低。3．患者术前应用糖皮质激素,可改善病情,提升患眼眼压。4．常规视网膜手术复位后患者眼压回升、眼轴延长,但在术后1周至术后6月内眼轴长度会有所缩短,眼压值在术后1月内也会有所回落,1个月后趋于稳定;玻璃体视网膜手术复位患者在硅油取出术后,眼压较视网膜复位术前回升、眼轴也较视网膜复位术前延长,硅油取出术后1周至6月间眼轴值无明显改变,眼压值在硅油取出术后最初1个月内有所降低,随着时间的推移趋于平稳。     

康柏西普预防严重后巩膜裂伤玻璃体切除术后增生性玻璃体视网膜病变的临床疗效

摘要 目的：探讨玻璃体腔注射康柏西普对于严重后巩膜裂伤患者玻璃体切除术后增生性玻璃体视网膜病变发生的预防效果。方法：选取从2018年9月至2020年9月我院收治的40例（40眼）严重后巩膜裂伤患者进行研究,随机分为对照组20眼（行常规巩膜裂伤缝合术及经睫状体平坦部玻璃体切除术）和观察组20眼（行巩膜裂伤缝合术及经睫状体平坦部玻璃体切除术的同时联合玻璃体腔注射康柏西普治疗）。比较两组患者术前及术后的视力、眼压,以及术后增生性玻璃体视网膜病变的发生率、视网膜再脱离的发生率。结果：对照组及观察组术后的最佳矫正视力较术前均提高、术后眼压均正常,观察组术后的增生性玻璃体视网膜病变发生率（15.0 %）明显低于对照组（45.0 %, P<0.05）,观察组术后视网膜脱离复发率（5.0 %）低于对照组（30.0 %, P>0.05）。结论：严重后巩膜裂伤患者玻璃体切除术联合玻璃体注射康柏西普治疗能够有效降低增生性玻璃体视网膜病变的发生率和术后视网膜脱离的复发率,还可以改善患者的视力预后。     

复杂性眼外伤患者玻璃体切割围手术期护理体会

目的:玻璃体切割术是眼科手术中比较复杂精细显手术,主要应用于治疗眼外伤导致的玻璃体出血,玻璃体浑浊,复杂性视网膜脱离以及增殖性玻璃体视网膜病变。本文主要探讨玻璃体切割术治疗复杂性眼外伤患者的围手术期护理的临床效应。方法:总结作者所在科室多年来护理眼外伤患者的临床经验,对2013年3月至2013年7月入院的75例(75只眼)复杂性眼外伤患者进行悉心的术前心理护理,完善的用药指导,充分的术前准备,术后特殊卧位的指导,预防并发症的护理及出院指导。结果:术后视力提高57例(76.0%),视力不变13(17.3%)例,视力下降5例(6.7%),28例眼内异物患者均经手术顺利取出异物。相关手术并发症经医护人员的对症治疗后均得到有效控制。患者术后满意度达98%以上,医生满意度达100%。结论:复杂性眼外伤患者玻璃体切割手术围手术期进行全方位的护理服务,对促进病人康复起到至关重要的作用。     

血塞通在23G微创玻切手术治疗糖尿病性玻璃体积血的作用

目的:探讨注射用血塞通(冻干粉)在23G微创玻切手术治疗糖尿病性玻璃体积血中的作用。方法:选取我院收治的2型糖尿病性玻璃体积血70例,将其随机分为两组,均给予常规血糖控制及23G微创玻切手术治疗,实验组于手术前给予注射用血塞通。对比两组患者的手术时间、术后并发症的发生率以及视力恢复情况。结果:实验组的平均手术时间明显短于对照组,术后出血、房性炎症、视网膜脱离、新生血管性青光眼并发症的发生率均明显低于对照组,差异有统计学意义(P0.05);实验组视力恢复的总有效率显著高于与对照组,差异有统计学意义(P0.05)。结论:术前应用注射用血塞通能够明显提高23G微创玻切手术治疗糖尿病性玻璃体积血的临床疗效,值得临床推广。     

26例中国先天性晶状体异位患者的基因诊断及手术初步效果观察

摘要 目的：总结26例中国先天性晶状体异位患者的基因诊断及晶状体异位的手术疗效。方法：回顾性收集2019年3月-2020年3月就诊于北京同仁医院眼科来自不同家系的双眼先天性晶状体异位患者26例共52眼。收集详细临床资料，提取外周静脉血全基因组DNA，应用靶向基因捕获技术筛查晶状体异常相关基因突变对所有患者进行基因诊断，采取微创晶状体-玻璃体切除或白内障超声乳化手术，记录视力、人工晶状体位置及主要并发症，采用配对t检验对术前术后最佳矫正视力进行比较。结果：患者均为汉族，男性14例，女性12例，年龄（21.2±15.2）岁。25例患者存在FBN1突变，1例为GJA8突变。22例（84.6%）可确诊为马凡综合征，3例诊为"潜在马凡综合征"。42眼采取微创晶状体-玻璃体切除类手术，7眼采取白内障超声乳化类手术。有31眼（59.6%）存在视网膜变性行网膜激光光凝。平均随诊时间（15.7±3.7）月，术后6个月及末次随访的最佳矫正视力（最小分辨角对数视力，0.30±0.16及0.21±0.11）均高于术前（0.76±0.31），差异有统计学意义（t=12.492，P＜0.001；t=13.171，P＜0.001）。术后所有眼的人工晶状体位置及稳定性良好，未发生视网膜脱离、黄斑水肿、人工晶状体脱位、人工晶状体偏位、继发性青光眼、眼内炎等并发症。结论：马凡综合征是此26例中国人先天性晶状体异位的主要病因，FBN1基因突变检测可为确诊提供有力证据，微创晶状体-玻璃体切除联合人工晶状体悬吊术效果好。     

Phacoemulsification and silicone oil removal through the planned posterior capsulorhexis

The purpose of the study was to present operative technique and results of a passive hydrodynamic expression of silicone oil through planned posterior capsulorhexis during cataract surgery in patients after pars plana vitrectomy. The retrospective analysis was done on 57 eyes with cataract after a previous pars plana vitrectomy, operated on between 2001 and 2004 at the Clinical hospital "Sestre milosrdnice" Zagreb. Preoperative and postoperative best corrected visual acuity (BCVA), preoperative and postoperative intraocular pressure (IOP), and postoperative complications were reviewed. Visual acuity improved or stabilized in all patients with an attached retina. Retinal detachment occurred in 11 eyes. Transient vitreous hemorrhage, that resolved within 1 week of surgery without treatment, was observed in 4 eyes. Asymptomatic intraocular lens (IOL) decentration occurred in 2 eyes. Our findings suggest that silicone oil removal and cataract surgery can be performed as a single procedure in selected patients in the absence of macular pucker and retinal reproliferation, and in a presence of a stable retina.     

Dissection of Human Vitreous Body Elements for Proteomic Analysis

The vitreous is an optically clear, collagenous extracellular matrix that fills the inside of the eye and overlies the retina. ^1,2 Abnormal interactions between vitreous substructures and the retina underlie several vitreoretinal diseases, including retinal tear and detachment, macular pucker, macular hole, age-related macular degeneration, vitreomacular traction, proliferative vitreoretinopathy, proliferative diabetic retinopathy, and inherited vitreoretinopathies. ^1,2 The molecular composition of the vitreous substructures is not known. Since the vitreous body is transparent with limited surgical access, it has been difficult to study its substructures at the molecular level. We developed a method to separate and preserve these tissues for proteomic and biochemical analysis. The dissection technique in this experimental video shows how to isolate vitreous base, anterior hyaloid, vitreous core, and vitreous cortex from postmortem human eyes. One-dimensional SDS-PAGE analyses of each vitreous component showed that our dissection technique resulted in four unique protein profiles corresponding to each substructure of the human vitreous body. Identification of differentially compartmentalized proteins will reveal candidate molecules underlying various vitreoretinal diseases.     

Evisceration of Mouse Vitreous and Retina for Proteomic Analyses

While the mouse retina has emerged as an important genetic model for inherited retinal disease, the mouse vitreous remains to be explored. The vitreous is a highly aqueous extracellular matrix overlying the retina where intraocular as well as extraocular proteins accumulate during disease.^1-3 Abnormal interactions between vitreous and retina underlie several diseases such as retinal detachment, proliferative diabetic retinopathy, uveitis, and proliferative vitreoretinopathy.^1,4 The relative mouse vitreous volume is significantly smaller than the human vitreous (Figure 1), since the mouse lens occupies nearly 75% of its eye.⁵ This has made biochemical studies of mouse vitreous challenging. In this video article, we present a technique to dissect and isolate the mouse vitreous from the retina, which will allow use of transgenic mouse models to more clearly define the role of this extracellular matrix in the development of vitreoretinal diseases.     

Lack of collagen XVIII/endostatin results in eye abnormalities

Mice lacking collagen XVIII and its proteolytically derived product endostatin show delayed regression of blood vessels in the vitreous along the surface of the retina after birth and lack of or abnormal outgrowth of retinal vessels. This suggests that collagen XVIII/endostatin is critical for normal blood vessel formation in the eye. All basement membranes in wild-type eyes, except Descemet's membrane, showed immunogold labeling with antibodies against collagen XVIII. Labeling at sites where collagen fibrils in the vitreous are connected with the inner limiting membrane and separation of the vitreal matrix from the inner limiting membrane in mutant mice indicate that collagen XVIII is important for anchoring vitreal collagen fibrils to the inner limiting membrane. The findings provide an explanation for high myopia, vitreoretinal degeneration and retinal detachment seen in patients with Knobloch syndrome caused by loss-of-function mutations in collagen XVIII.     

Enhanced Vitreous Imaging in Healthy Eyes Using Swept Source Optical Coherence Tomography

Purpose

To describe enhanced vitreous imaging for visualization of anatomic features and microstructures within the posterior vitreous and vitreoretinal interface in healthy eyes using swept-source optical coherence tomography (SS-OCT). The study hypothesis was that long-wavelength, high-speed, volumetric SS-OCT with software registration motion correction and vitreous window display or high-dynamic-range (HDR) display improves detection sensitivity of posterior vitreous and vitreoretinal features compared to standard OCT logarithmic scale display.

Design

Observational prospective cross-sectional study.

Methods

Multiple wide-field three-dimensional SS-OCT scans (500×500A-scans over 12×12 mm²) were obtained using a prototype instrument in 22 eyes of 22 healthy volunteers. A registration motion-correction algorithm was applied to compensate motion and generate a single volumetric dataset. Each volumetric dataset was displayed in three forms: (1) standard logarithmic scale display, enhanced vitreous imaging using (2) vitreous window display and (3) HDR display. Each dataset was reviewed independently by three readers to identify features of the posterior vitreous and vitreoretinal interface. Detection sensitivities for these features were measured for each display method.

Results

Features observed included the bursa premacularis (BPM), area of Martegiani, Cloquet''s/BPM septum, Bergmeister papilla, posterior cortical vitreous (hyaloid) detachment, papillomacular hyaloid detachment, hyaloid attachment to retinal vessel(s), and granular opacities within vitreous cortex, Cloquet''s canal, and BPM. The detection sensitivity for these features was 75.0% (95%CI: 67.8%–81.1%) using standard logarithmic scale display, 80.6% (95%CI: 73.8%–86.0%) using HDR display, and 91.9% (95%CI: 86.6%–95.2%) using vitreous window display.

Conclusions

SS-OCT provides non-invasive, volumetric and measurable in vivo visualization of the anatomic microstructural features of the posterior vitreous and vitreoretinal interface. The vitreous window display provides the highest sensitivity for posterior vitreous and vitreoretinal interface analysis when compared to HDR and standard OCT logarithmic scale display. Enhanced vitreous imaging with SS-OCT may help assess the natural history and treatment response in vitreoretinal interface diseases.     

A Rabbit Model of Proliferative Vitreoretinopathy Induced by Injection of Astrocytic Cultures

1.The objective of this study was to decipher whether proliferation of astrocytes and invasion of astrocytic processes into the retina could contribute to retinal detachment in a rabbit model.2.Cultures of astrocytes were injected intravitreally into the eyes of albino rabbits.3.Two weeks after injection, proliferation of astrocytes on the retinal surfaces was observed. Vascular endothelial growth factor (VEGF) and proliferative cell nuclear antigen (PCNA) were found by immunohistochemistry to be expressed in the center of the astrocytic growth.4.Using the same immunohistochemical technique to visualize glial fibrillary acidic protein (GFAP), a marker for astrocytes, processes of astrocytes in the growth were observed to penetrate into the host retina.5.Retinal detachment was then confirmed by ultrasound, histologically, and grossly 2 weeks after injection of astrocytes.6.Histochemistry on esterase indicated chloroesterase positive cells inside the growth. The secretion of this form of esterase might soften the vitreous and enhanced retinal detachment.7.Six weeks after injection, VEGF and PCNA decreased in the astrocytic growth but astrocytic processes still attached onto and penetrated the host retina.8.This study suggests that astrocytes could be a major factor in inducing retinal detachment.     

Local production of fibronectin by ectopic human retinal cells

Summary The distribution of fibronectin mRNA and fibronectin in adult human retina and epiretinal membranes was investigated by in situ hybridisation and immunohistochemical techniques. The cells in normal adult retina contained little or no fibronectin mRNA and the retina only showed fibronectin immunoreactivity in retinal vessels. The cells in detached neuroretina did not contain fibronectin message but the vitreoretinal interface of the detached retina exhibited variable fibronectin immunoreactivity. Retinal glia, retinal pigment epithelium and fibroblast-like cells in membranes at the vitreoretinal juncture (epiretinal membranes) showed variable labelling with the fibronectin mRNA probe and all the membranes immunostained for fibronectin. No difference could be detected between membrane cell types in the intensity of labelling with the mRNA probe or for fibronectin immunoreactivity. The results indicate that cells in situ in attached and detached adult human retina do not produce fibronectin. Although fibronectin at the vitreoretinal juncture in retinal detachment is probably partly derived from plasma fibronectin resulting from breakdown of the blood-retinal barrier, ectopic retinal cells produce fibronectin and contribute to the glycoprotein in epiretinal membranes.     

Experimental retinal detachment causes widespread and multilayered degeneration in rabbit retina

Retinal detachment remains one of the most frequent causes of visual impairment in humans, even after ophthalmoscopically successful retinal reattachment. This study was aimed at monitoring (ultra-) structural alterations of retinae of rabbits after experimental detachment. A surgical procedure was used to produce local retinal detachments in rabbit eyes similar to the typical lesions in human patients. At various periods after detachment, the detached retinal area as well as neighbouring attached regions were studied by light and electron microscopy. In addition to the well-known degeneration of photoreceptor cells in the detached retina, the following progressive alterations were observed, (i) in both the detached and the attached regions, an incomplete but severe loss of ganglion cell axons occurs; (ii) there is considerable ganglion cell death, particularly in the detached area; (iii) even in the attached retina distant from the detachment, small adherent groups of photoreceptor cells degenerate; (iv) these photoreceptor cells degenerate in an atypical sequence, with severely destructed somata and inner segments but well-maintained outer segments; and (v) the severe loss of retinal neurons is not accompanied by any significant loss of Müller (glial) cells. It is noteworthy that the described progressive (and probably irreparable) retinal destructions occur also in the attached retina, and may account for visual impairment in strikingly large areas of the visual field, even after retinal reattachment.