新生血管性青光眼睫状体及视网膜冷凝联合复合式小梁切除术

目的 评价睫状体及周边视网膜冷凝联合复合式小梁切除术治疗新生血管性青光眼的效果.方法 对53例(53眼)新生血管性青光眼施行睫状体及周边视网膜冷凝联合复合式小梁切除术,术中应用丝裂霉素C 0.33 mg/mL及可调整缝线.术后观察眼压、结膜滤过泡及眼前段反应等,随访6～12个月.结果 53例术后第1周眼压(10.36±2.53)mmHg(1 mmHg=0.133 kPa),较术前眼压(47.89±6.74)mmHg明显降低;随访时47例不用降眼压药物眼压(18.41±2.16)mmHg(88.68%);5例用1～2种降眼压药物治疗眼压＜30 mmHg;1例手术失败.47例结膜滤过泡弥散隆起,6例较扁平.术中有4例前房少量积血.术后浅前房2例,无前房继发性积血或眼球萎缩等.结论 睫状体及周边视网膜冷凝联合复合式小梁切除术治疗新生血管性青光眼,经随访证明能有效降低眼压,痛苦小,为一种较安全而有效的综合性治疗新生血管性青光眼的方法.     

小梁切除术后早期前房出血危险因素的临床分析

目的 探讨小梁切除术后早期前房出血的发生率、出血原因及预防处理.方法 回顾分析249例（355眼）青光眼小梁切除术后早期前房出血的情况,对各类型青光眼小梁切除术后前房出血发生率、出血量及术后积血吸收情况,全身相关因素等进行总结、分析.结果 355眼小梁切除术后,前房出血37眼（10.42％）,其中新生血管性青光眼术后发生率为55.55％,急性闭角型青光眼小梁切除术后发生率为8.87％,慢性闭角型青光眼术后发生率为11.49％,原发性开角型青光眼术后发生率为9.24％.14.34％术前高眼压患者术后发生前房出血,伴有高血压病的小梁切除患者术后前房出血发生率为30.43％,伴有糖尿病的术后发生率为26.32％,术前有口服抗凝药物史的术后发生率为31.25％.卡方检验结果显示新生血管性青光眼,术前高眼压,伴有高血压、糖尿病以及术前有抗凝药物服用史的患者,前房出血发生率高.进一步回归分析发现新生血管性青光眼和术前高眼压是小梁切除术后前房出血的独立危险因子.前房出血量1级者19眼,2级者11眼,达3级者7眼,出血后眼压分别为（10.93±2.46）mm Hg（1 mm Hg =0.133 kPa）、（9.33±1.63）mm Hg、（24.75±12.76）mm Hg,出血量达3级者眼压显著性增高.前房出血组术前平均眼压（32.92±7.32） mm Hg,与未发生前房出血者眼压（28.10±7.70） mm Hg相比,差异有统计学意义.结论 前房出血是小梁切除术后常见并发症,术前高眼压、新生血管性青光眼是术后发生前房出血的危险因素;合并高血压、糖尿病和口服抗凝药物患者较无合并全身疾病者,术后前房出血发生率高.少量前房出血对术后眼压无明显影响.     

改良小梁切除术治疗Ⅱ期新生血管性青光眼

目的 探讨改良小梁切除术治疗Ⅱ期新生血管性青光眼的疗效.方法 取30例(30只眼)Ⅱ期新生血管性青光眼行术中应用丝裂霉素C和可拆缝线的小梁切除术.术后早期,术眼眼压≥15mmHg和滤过泡扁平,拆除可拆缝线.术后观察眼压、滤过泡、并发症.随访12～48个月.结果 术前平均眼压(26.1±3.2)mmHg,最后一次随访时平均眼压(18.2 4±2.1)mmHg,两者之间差异有统计学意义(t=7.51,P<0.01).17只眼眼压<21mmHg,眼压控制成功率为56.7%.6只眼眼压>21mmHg,经局部应用降眼压药物后,眼压<21mmHg.17只眼术后有Ⅰ型或Ⅱ型功能性滤过泡.术后4只眼(13.3%)在一周内有Ⅰ度浅前房,未经处理,自行恢复.术后12只眼(40.0%)有前房积血,10只眼前房积血在术后7d内吸收.2只眼在术后15d内吸收.无其他并发症.结论 改良小梁切除术能有效控制Ⅱ期新生血管性青光眼的眼压,术后无严重并发症,是一种安全、有效地Ⅱ期新生血管性青光眼的降眼压方法.     

玻璃体腔注射雷珠单抗联合小梁切除术治疗新生血管性青光眼疗效观察

目的观察玻璃体腔注射雷珠单抗（Lucentis）联合复合式小梁切除术治疗新生血管性青光眼的疗效。方法对17例（17只眼）新生血管性青光眼行玻璃体腔注射Lucentis 0.50 mg/0.05 ml,8~14 d后行复合式小梁切除术。观察玻璃体腔注射Lucentis后虹膜及房角新生血管消退的时间、眼压的变化以及复合式小梁切除术后视力和眼压的变化。术后随访8~12个月。结果玻璃体腔注射Lucentis后,13只眼虹膜新生血管1周内完全消退,4只眼2二周内完全消退。注药前平均眼压（39.56±10.12）mm Hg,注药后1周平均眼压（38.62±8.35）mm Hg与注药前比较眼压变化无统计学意义（t=0.951,P〉0.05）。小梁切除术后1周眼压（10.43±6.12）mm Hg,最后一次随访眼压（13.61±4.31）mm Hg,与术前比较差异均有统计学意义（t=21.362、19.817,P均﹤0.01）。末次随访时12只眼视力提高,5只眼视力未变。结论玻璃体腔注射雷珠单抗联合复合式小梁切除术能有效地控制眼压,保护视功能。     

小梁切除术联合硅胶片填充治疗新生血管性青光眼

目的　观察小梁切除术联合硅胶片巩膜层间填充治疗新生血管性青光眼的临床效果。方法　28 例(28 眼)新生血管性青光眼作小梁切除并用3m m ×5m m 硅胶片填充于巩膜层间,观察其术后降眼压效果。结果　28 眼新生血管性青光眼术后随访9～14 个月(平均12.3 个月),最后一次随访时眼压为17.3～28.97m m Hg,病人眼部疼痛症状均消失。未出现严重并发症。结论　小梁切除术联合薄硅胶片填充是治疗新生血管性青光眼的较为理想的方法     

睫状体冷冻联合小梁切除治疗晚期新生血管性青光眼

目的：分析睫状体冷冻联合小梁切除治疗晚期新生血管性青光眼疗效。方法：晚期新生血管性青光眼37例37眼,行睫状体冷冻联合小梁切除术,术后随访12mo,观察术后眼压、前房反应及疼痛程度和并发症等。结果：术前平均眼压52.34mmHg,术后1,3d;1wk;1,3,12mo平均眼压分别为17.30±9.35,17.98±7.69,17.38±5.31,17.22±3.82,16.45±4.82,16.76±4.52mmHg,与手术前平均眼压比较,差异均有统计学意义（P〈0.05）。术后前房反应较轻,疼痛缓解明显,无严重并发症。结论：睫状体冷冻联合小梁切除术能有效治疗晚期新生血管性青光眼。     

新生血管性青光眼的联合手术治疗观察

目的:探讨视网膜光凝或视网膜冷凝联合小梁切除术治疗新生血管性青光眼的疗效。方法:新生血管性青光眼64例64眼,首先行视网膜光凝或视网膜冷凝,再行小梁切除术,术后观察视力、眼压、虹膜新生血管、球结膜滤过泡及手术并发症等。结果:术后随访6～12mo,视力均无明显改善,平均眼压自术前47.89±6.74mmHg随访末降至18.41±2.16mmHg,控制在21mmHg以下者53眼(73%)。结论:视网膜光凝或视网膜冷凝联合小梁切除术治疗新生血管性青光眼有较好的长期疗效。     

虹膜氪激光联合小梁切除术治疗新生血管性青光眼临床观察

目的评价氪激光虹膜新生血管光凝联合小梁切除术治疗新生血管性青光眼的效果。方法对22例(男15例、女7例)药物难于控制的新生血管性青光眼患者,首先应用氪-绿激光器对虹膜新生血管进行直接覆盖光凝,观察虹膜新生血管闭塞、萎缩后,施行巩膜瓣下小梁切除与虹膜周边切除,术中应用丝裂霉素C(MMC0.4mg/ml)。术后处理同常规小梁切除术。术后观察项目:眼压、结膜滤过泡、眼前段反应等,随访时间6～12个月。结果22例术后第1周眼压(11.42±2.61)mmHg较术前(43.42±6.46)mmHg明显降低(t=15.06,p=0.000):随访时眼压控制良好(18.17±2.04mmHg),其中仅2例接受局部应用β-受体阻滞剂。20例结膜滤过泡弥散隆起,2例较为扁平。术中有1例前房少量出血,不影响手术操作。术后前房无继发性出血发生。结论采用氪-绿激光直接覆盖光凝虹膜新生血管及小梁切除术的“二步”法,即首先利用氪-绿激光器对虹膜新生血管进行激光光凝,待虹膜新生血管闭塞、萎缩后,继之施行巩膜瓣下小梁切除联合MMC治疗新生血管性青光眼,经随访能有效降低眼压,控制病情进展。减少与避免常规滤过性手术中、术后因虹膜新生血管出血而导致的前房出血并发症,提高了新生血管性青光眼手术治疗的成功率。为一种较安全及有效的综合性治疗新生血管性青光眼的方法     

改良小梁切除术联合羊膜移植治疗难治性青光眼

目的 探讨改良小梁切除术联合羊膜移植治疗难治性青光眼的临床疗效.方法 难治性青光眼患者32例(42眼),采用改良小梁切除术联合羊膜移植治疗,术后随访3 ～12个月,观察患者术后3个月、6个月的眼压、滤过泡、视力及并发症等情况.结果 术后3个月、12个月眼压分别为(13.4±2.8) mmHg(1 kPa=7.5 mmHg)、(15.8±3.7) mmHg,与术前(35.6±6.3)mmHg相比,差异均有显著统计学意义(均为P＜0.01).术后3个月、6个月功能性滤过泡分别占90.5％、95.2％.术后3个月、6个月视力较术前均有不同程度提高,差异均有统计学意义(均为P＜0.05).术后仅4眼新生血管性青光眼由于滤过泡瘢痕化,经局部加用抗青光眼药物后眼压仍大于21 mmHg;所有患眼均无明显并发症和羊膜移植排斥反应.结论 改良小梁切除术联合羊膜移植治疗难治性青光眼疗效确切,并发症较少.     

改良小梁切除术联合睫状体视网膜冷凝治疗新生血管性青光眼

目的 观察改良小梁切除术联合睫状体视网膜冷凝治疗新生血管性青光眼的临床疗效.方法 2008年1月至2011年6月我院共收治新生血管性青光眼患者46例(46眼),均采用改良小梁切除术联合睫状体视网膜冷凝治疗,术后随访6 ～12个月,观察患者术后一般疗效、视力、眼压及并发症等情况.结果 46眼中手术完全成功38眼,条件成功6眼,失败2眼,手术成功率为95.7％.与术前比较,术后1周、1个月、6个月视力均有不同程度提高,差异均有统计学意义(均为P＜0.05).术前眼压(38.9±3.2)mmHg(1 kPa =7.5 mmHg),术后1周、1个月、6个月眼压分别为(18.2±1.2) mmHg、(17.8±1.6) mmHg、(17.2±1.5)mmHg,与术前比较,差异均有显著统计学意义(均为P＜0.01).术后1周形成功能性滤过泡39眼(84.8％),非功能性滤过泡7眼(15.2％);术后6个月形成功能性滤过泡42眼(91.3％),非功能性滤过泡4眼(8.7％).术后并发症主要包括前房积血、浅前房、前部葡萄膜炎、玻璃体出血等.结论 改良小梁切除术联合睫状体视网膜冷凝治疗新生血管性青光眼能显著控制眼压,改善视力.     

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.