改良小切口非超声乳化术治疗高龄硬核白内障

目的探讨改良式小切口非超声乳化白内障摘出人工晶状体植入术在高龄硬核白内障的中的临床应用。方法对82例高龄患者104眼硬核白内障施行改良式小切口非超声乳化白内障摘出人工晶状体植入术,并与同期81例高龄患者103眼硬核白内障施行晶状体超声乳化吸出人工晶状体植入术对比,术后随访12个月,比较两种手术时间、角膜内皮细胞的密度、丢失率,以及术后视力。结果两种手术方式的手术时间差异无统计学意义（P〉0．05）,在角膜内皮细胞密度、丢失率和术后视力的比较差异有统计学意义（P〈0．05）。结论高龄硬核白内障适宜行改良式小切口非超声乳化白内障摘出人工晶状体植入术,且有损伤小、恢复快等优点。     

青光眼术后低角膜内皮细胞密度白内障手术26例临床分析

目的观察抗青光眼小梁切除术后低角膜内皮细胞密度白内障患者行巩膜隧道小切口摘出联合肝素修饰人工晶状体植入术的疗效及并发症。方法选取我院抗青光眼小梁切除术后低角膜内皮细胞密度白内障患者22例(26眼),行巩膜隧道小切口白内障摘出联合肝素修饰人工晶状体植入术,对比观察术前与术后视力、眼压、角膜内皮细胞密度及术后并发症。结果术前与术后3个月矫正视力比较,除1眼患者术后因视神经萎缩明显、视力无明显改善外,余25眼患者术后视力较术前均有不同程度的提高;术前角膜内皮细胞密度(946～520mm-2)与术后3个月(920～499mm-2)比较,差异无统计学意义(P>0.05)。术后3d有2眼出现一过性高眼压,1周后恢复;术后1个月黄斑囊样水肿1眼,2个月后消失;术后3个月视力下降1眼,为视神经萎缩引起。术后随访期间未见角膜内皮失代偿、虹膜粘连、后囊膜破裂等严重并发症发生。结论抗青光眼小梁切除术后低角膜内皮细胞密度白内障患者行巩膜隧道小切口白内障摘出联合肝素修饰人工晶状体植入术是安全、有效的,但术前评估、手术技巧及术后处理是非常重要的。     

小切口非超声乳化囊袋内手法劈核术在硬核性白内障中的应用

目的探讨囊袋内手法劈核术在硬核性白内障手术中的临床效果。方法采用小切口非超声乳化囊袋内的手法劈核术,治疗硬核性白内障117例(159眼),分别于术后1周、1个月、3个月、6个月观察患者术后视力、散光、角膜内皮细胞丢失率、并发症等情况。结果术后1周最佳矫正视力≥0.5者占54.1%,术后散光度数为(2.00±0.75)D,角膜内皮细胞密度为(3327±231)mm-2,角膜内皮细胞丢失率为3.00%;术后1个月最佳矫正视力≥0.5者占86.2%,术后散光度数为(1.50±0.75)D,角膜内皮细胞密度为(3271±253)mm-2,角膜内皮细胞丢失率为4.64%;术后3个月最佳矫正视力≥0.5者占91.2%,术后散光度数为(1.25±0.50)D,角膜内皮细胞密度为(3267±239)mm-2,角膜内皮细胞丢失率为4.75%;术后6个月最佳矫正视力≥0.5者占92.5%,术后散光度数为(1.00±0.50)D,角膜内皮细胞密度为(3257±242)mm-2,角膜内皮细胞丢失率为5.04%,无严重并发症发生。术后视力,散光度差异均有统计学意义(均为P<0.05),角膜内皮细胞丢失率差异均无统计学意义(均为P>0.05)。结论对Ⅳ-Ⅴ级硬核性白内障应用囊袋内手法劈核术,不仅具有小切口的优点,而且角膜相关并发症少,操作更安全,术后视力恢复快。     

低角膜内皮细胞密度白内障行超声乳化术临床效果观察

目的观察低角膜内皮细胞白内障患者行超声乳化摘除联合人工晶体植入术手术效果。方法共收集17例18眼角膜内皮细胞密度<1500/mm^(2)白内障患者,由同一医生行超声乳化白内障摘除联合人工晶状体植入术,术后3个月观察视力、角膜内皮细胞密度变化及术中术后并发症。结果术后3个月所有患者视力均有不同程度提高,角膜内皮细胞丢失率为5.4%-14.3%,平均10.2%±1.6%。无角膜内皮失代偿发生。结论低角膜内皮细胞密度白内障患者,在术前做好评估,术中注意操作,行超声乳化术是安全有效的。     

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。     

无缝线小切口白内障囊外摘出术在硬核白内障中的应用

目的 观察无缝线小切口白内障囊外摘出联合人工晶状体植入术治疗硬核白内障的疗效.方法 观察2组共299例312眼Ⅲ级以上硬核白内障患者,分别应用无缝线小切口白内障囊外摘出联合人工晶状体植入术(小切口组,161眼)和常规超声乳化白内障吸出联合人工晶状体植入术(超乳组,151眼),分别比较手术时间、术后视力、角膜内皮细胞丢失率、术后散光及其他相关并发症发生的差异.结果 手术时间:小切口组平均(691±89)s,超乳组平均(663±97)s,2组比较差异无统计学意义(P＞0.05).术后第1天视力≥0.5者小切口组为142眼,超乳组112眼,2组相比差异有统计学意义(P＜0.05);术后1个月视力≥0.5者小切口组150眼,超乳组140眼,2组相比差异无统计学意义(X2=0.024,P＞0.05).角膜内皮细胞丢失率:术后第1天小切口组(10.03±2.87)%,超乳组(18.31±3.34)%;术后1个月小切口组(8.51±2.62)%,超乳组(16.11±3.76)%;2组相比差异均有统计学意义(P＜0.05).术后散光(＞1.0 DC):小切口组25.47%,超乳组17.22%;角膜水肿:小切口组9.32%,超乳组17.22%,2组比较差异均有统计学意义(P＜0.05).虹膜脱出、后囊膜破裂、切口渗漏等并发症差异无统计学意义.结论 对于Ⅲ级以上硬核白内障,无缝线小切口白内障囊外摘出联合人工晶状体植入术是一种较好的治疗选择,值得基层推广.     

抗青光眼术后低密度角膜内皮细胞白内障患者行超声乳化并人工晶状体植入术的临床观察

目的评价超声乳化技术在抗青光眼术后低密度角膜内皮细胞的白内障患者中应用的可行性、手术技巧及临床效果。方法抗青光眼术后低密度角膜内皮细胞的白内障患者4例（4只眼）,术前角膜内皮细胞密度为348．1—1724．6个／mm^2,均接受超声乳化联合人工晶状体植入术,观察其术前角膜内皮细胞密度及术前、术后视力的改变。结果术后3只眼术后视力均有明显的提高。1只眼视力无明显改善。结论抗青光眼术后低密度角膜内皮细胞的白内障患者在一定程度上可行超声乳化联合人工晶状体植入术。     

无缝线小切口白内障囊外摘除术治疗硬核白内障的临床疗效分析

目的观察无缝线小切口白内障囊外摘除术治疗硬核白内障的临床疗效,总结其临床应用价值。方法选取汉中市中心医院眼科于2007年6月至2009年6月收治的268例(433只眼)白内障患者,均采取无缝线小切口白内障囊外摘除术治疗,术前所有的患者患眼均局部点用妥布霉素滴眼液,术后所有患者局部点用复方妥布霉素滴眼液,观察分析治疗效果,进行统计学分析。结果术后1天球镜矫正视力或裸眼视力≥0.5者397只眼(91.7%),术后1周球镜矫正视力或裸眼视力≥0.5者411只眼(94.9%),术后1个月球镜矫正视力或裸眼视力≥0.5者409只眼(94.5%),基本达到稳定水平,术后1天、1周、1个月、3个月的术后球镜矫正视力或裸眼视力比较差异不显著(P>0.05),无统计学意义;患者术后1天、1周、1个月、3个月与术前的角膜散光度数比较术前存在明显差异(P<0.05),具有统计学意义。术中出现后囊膜破裂22只眼(5.1%),出现悬韧带断离27只眼(6.2%),术中并发症发生率为11.3%;术后出现并发症94只眼,发生率为21.7%。结论无缝线小切口白内障囊外摘除术治疗硬核白内障的临床疗效显著,能有效改善球镜矫正视力或裸眼视力,减少并发症发生,安全可靠,值得在临床上合理推广应用。     

折叠式人工晶状体治疗儿童白内障的初步报告

目的　评价小切口白内障吸除及折叠式人工晶状体囊袋内植入术中采用撕除后囊、切除前段玻璃体技术治疗儿童白内障的临床效果。方法　对 2 8例 (37只眼 )儿童白内障患者行小切口白内障吸除、前后联合撕囊、前段玻璃体皮质切除及折叠式人工晶状体囊袋内植入术 ,其中先天性白内障 2 7只眼 ,外伤性白内障 10只眼。术后随访 3～ 15个月 ,平均 10个月。观察记录并发症发生情况、视力及角膜曲率的变化。结果　先天性白内障患者术后矫正视力均≥ 0 1,16只眼 (5 9 3% )矫正视力≥ 0 5 ;外伤性白内障患者术后矫正视力均≥ 0 3,8只眼 (80 % )矫正视力≥ 0 5。术后 1周 ,1个月和 3个月的手术源性角膜散光度数分别为 (1 18± 0 6 5 )、(0 6 7± 0 5 9)及 (0 6 0± 0 39)D。术后 1个月时 ,手术源性角膜散光度数趋于稳定。随诊中有 5只眼 (13 5 % )出现晶状体后囊膜切开区混浊 ,无其他并发症。结论　小切口白内障吸除及折叠式人工晶状体囊袋内植入术中撕除后囊、切除前段玻璃体治疗儿童白内障具有术后角膜散光小 ,视力恢复快 ,炎性反应轻 ,手术并发症少的优点     

晶状体超声乳化联合玻璃体手术治疗合并白内障的增生性糖尿病视网膜病变

目的分析晶状体超声乳化联合玻璃体手术治疗合并白内障的增生性糖尿病视网膜病变(PDR)的疗效。设计回顾性临床病例系列。研究对象123只合并不同程度白内障的PDR患眼。方法对123只合并不同程度白内障的PDR患眼实施晶状体超声乳化联合玻璃体手术治疗,同时I期植入人工晶状体(IOL),观察术后视力改善程度及术中术后并发症。主要指标术后视力改善程度、术后并发症发生率。结果123眼均实施晶状体超声乳化联合玻璃体手术,并同时一期植入IOL于囊袋内。随访时间3￣21月(平均10个月)。99眼(81%)术后均有不同程度的视力改善。其中93眼(76%)术后视力提高2行或以上。术后无明显角膜水肿和角膜内皮失代偿发生。1例I型糖尿病患者术后6个月发生新生血管性青光眼;1眼术后发生视网膜脱离,再次手术后复位;4眼因玻璃体腔出血再次手术。术后视力无明显改善或视力提高不足2行的病例均合并不同程度的糖尿病黄斑病变。结论晶状体超声乳化联合玻璃体手术是提高合并白内障的PDR患者视力的有效手段。糖尿病黄斑病变是影响术后视力提高的主要因素。(眼科,2006,15:198-201)     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.