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1.
闭角型青光眼合并白内障两种术式的临床比较   总被引:1,自引:0,他引:1  
目的探讨不同手术方法治疗慢性闭角型青光眼合并白内障的临床效果.方法 54例67眼慢性闭角型青光眼合并白内障患者,随机分为2组,观察组39眼和对照组 28眼.观察组行白内障超声乳化吸出人工晶状体植入联合小梁切除术,对照组行单纯白内障超声乳化吸出人工晶状体植入术,术后随访6~12月. 结果术后2组早期视力差异无显著性.6月后因眼压较高引起视力下降者,观察组3眼,对照组8眼,2组差异显著( P< 0.05);眼压控制在正常范围者(<20.55 mmHg,1 kPa=7.5 mmHg)观察组32眼,对照组 20眼.对照组有5眼眼压在30 mmHg以上,需手术治疗.2组间有显著性差异(P<0. 05).术后2组并发症的发生无显著差异(P>0.05). 结论慢性闭角型青光眼合并白内障,术前房角粘连≥3/4象限、眼压不易控制者,应选择青光眼白内障联合术,效果更加确切.  相似文献   

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慢性闭角型青光眼白内障手术治疗临床探讨   总被引:2,自引:0,他引:2  
目的 探讨慢性闭角型青光眼合并白内障的手术方法.方法 慢性闭角型青光眼合并白内障共64例(66眼).其中43例(45眼)施行晶状体超声乳化吸出、人工晶状体植入联合房角分离术,21例(21眼)施行晶状体超声乳化吸出、人工晶状体植入联合小梁切除术.结果 术后视力:晶状体超乳联合房角分离手术组术后视力比术前提高者44眼(97.78%).晶状体超乳联合小梁切除手术组术后视力比术前提高者18眼(85.72%).术后眼压:晶状体超乳联合房角分离手术组术后第1天眼压正常;8周后有2眼眼压>30 mmHg,给予二期行小梁切除术.晶状体超乳联合小梁切除手术组术后第1天19眼(90.48%)眼压正常,有2眼(9.52%)低眼压,4周后均恢复正常.结论 慢性闭角型青光眼合并白内障采用晶状体超声乳化吸出、后房人工晶状体植入联合房角分离术或联合小梁切除术均能有效地提高患者的视力并降低眼压.  相似文献   

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目的观察晶状体超声乳化联合前房角分离术治疗急性及慢性闭角型青光眼伴发白内障的临床效果。方法2012年1月至2014年8月于我院治疗的急性闭角型青光眼伴发白内障30例(30眼),慢性闭角型青光眼伴发白内障19例(27眼)。均进行晶状体超声乳化联合前房角分离术。对两组患者手术前后的眼压、视力、并发症进行观察比较。结果术后随访6~12个月,两组患者术后眼压均明显降低,达到正常范围(P〈0.05),术后视力均有所提高(尸〈0.05),慢性闭角型青光眼组术后并发症发生率明显少于急性组。结论晶状体超声乳化联合前房角分离术治疗伴发白内障的急性与慢性闭角型青光眼同样有效。  相似文献   

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目的探讨晶状体超声乳化吸出人工晶状体植入联合小梁切除术对青光眼伴白内障的疗效。方法开角型青光眼及慢性闭角型青光眼合并白内障共35例(52眼)。行晶状体超声乳化吸出人工晶状体植入联合小梁切除术,比较分析手术前后的视力、眼压控制及术后滤泡形成情况。结果术后矫正视力≥0.3者41眼(78.85%),比术前视力≥0.3者(3眼,5.77%)明显增多。术后随访至少6个月平均眼压(14.71±4.01)mmHg,无需使用降眼压药物。术后功能型滤过泡47眼(90.38%)。无严重并发症发生。结论晶状体超声乳化吸出人工晶状体植入联合小梁切除术是一种安全、有效、便捷的治疗青光眼合并白内障的联合手术。  相似文献   

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超乳治疗慢性闭角型青光眼临床观察   总被引:1,自引:0,他引:1  
目的观察透明角膜切口晶状体超声乳化吸出联合人工晶状体植入治疗慢性闭角型青光眼合并白内障的疗效。方法原发性慢性闭角型青光眼20例(22眼),视力<0.1,晶状体不同程度浑浊,行晶状体超声乳化吸出联合人工晶状体植入术。结果术前用药后眼压(28.63±13.27)mmHg,术后为(15.42±3.86)mmHg(t=4.243,P<0.05);术后房角不同程度开放。结论透明角膜切口晶状体超声乳化吸出联合人工晶状体植入术可有效地治疗因晶状体阻滞合并白内障的慢性闭角型青光眼。  相似文献   

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晶状体超声乳化术治疗急性闭角型青光眼   总被引:2,自引:0,他引:2  
目的探讨晶状体超声乳化吸出联合人工晶状体植入治疗急性闭角型青光眼合并白内障的疗效。方法回顾分析我院2005年2月-2008年3月收治的合并白内障的急性闭角型青光眼46例(48眼),行超声乳化白内障吸出联合囊袋内人工晶状体植入术,术后随访3月-3年。观察术前术后视力、眼压、前房深度及前房角的变化。结果45眼眼压控制正常,3眼需滴降眼压药物。视力均有不同程度提高。结论晶状体超声乳化吸出联合人工晶状体植入能有效治疗合并白内障的急性闭角型青光眼。  相似文献   

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目的:观察超声乳化晶状体吸除加人工晶状体植入治疗闭角型青光眼的临床疗效。方法:对31只闭角型青光眼行白内障吸出加人工晶状体植入术,术前眼压经药物治疗后为21~50mmHg;原发性急性闭角型青光眼27眼,慢性闭角型青光眼1眼,老年性白内障膨胀期继发青光眼3眼,晶状体透明15眼,晶状体不同程度混浊11眼,虹膜节段性萎缩5眼;术后观察患眼压、视力、前房深度,随访1a以上。结果:术后视力31眼均有提高。术后眼压均正常(12~20mmHg)30眼;术后8mo发生恶性青光眼1眼(慢性闭角型青光眼),行小梁切除术加前节玻璃体切割后眼压控制正常。结论:晶状体超声乳化吸出术可使前房加深,房角开放,眼压得到控制,无青光眼小梁切除术的并发症,是治疗某些闭角型青光眼的首选方法。  相似文献   

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目的探讨晶状体超声乳化吸出联合后房人工晶状体植入术,治疗白内障合并原发性闭角型青光眼的疗效。方法本院收治白内障合并原发性闭角型青光眼37例(37眼),术前控制眼压,经视力、眼压、前房角镜和裂隙灯显微镜等检查后,均单独采用晶状体超声乳化吸出联合后房人工晶状体植入。结果术后随访6~18个月,视力较术前提高,视力>0.5者20眼,占54.05%,22例术后眼压<18mmHg,另5例用1种降眼压药物眼压控制在18mmHg以下。结论晶状体超声乳化后房人工晶状体植入可有效地治疗合并白内障的原发性闭角型青光眼。  相似文献   

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晶状体超声乳化人工晶状体植入术治疗闭角型青光眼   总被引:1,自引:0,他引:1  
目的观察分析晶状体超声乳化吸出术联合后房人工晶状体植入术治疗合并白内障的急性闭角型青光眼的疗效。方法对我院治疗的合并白内障的闭角型青光眼48例(48眼),术前查前房角,前房角关闭粘连小于180°范围者行晶状体超声乳化吸出术联合后房型人工晶状体植入术。术前、术后分析比较眼压、视功能及前房深度,随访6~12个月。结果术后48眼眼压全部控制在21.0 mmHg以下,无严重并发症。46眼视力均有不同程度的提高,2眼视力无变化。术前术后视力及眼压差异有统计学意义。结论对于合并有白内障的前房角关闭粘连小于180°的急性闭角型青光眼可行单纯晶状体超声乳化人工晶状体植入术治疗。  相似文献   

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目的观察超声乳化人工晶体植入联合前房角粘连分离术治疗慢性闭角型青光眼合并白内障的效果。方法超声乳化术联合前房角粘连分离术联合人工晶状体植入三联术治疗闭角型青光眼合并白内障26例(33眼)。对其手术前后的视力、眼压、视野、中央前房深度、房角形态进行对照观察。结果术后随访3~36个月,视力均较术前明显提高(P〈0.05)。术后中央前房深度均加深(P〈0.05)。33眼术后眼压明显降低(P〈0.05),术后1个月前房角镜检查房角均较术前开放角度增加。25例(31眼)术后6个月复查视野无明显进展。1例(2眼)眼压正常范围,视野损害加重,用苏为坦滴眼液进一步控制眼压。结论超声乳化前房角分离术可有效治疗合并白内障的慢性闭角型青光眼。  相似文献   

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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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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.  相似文献   

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