白内障手术后0.1%溴芬酸钠水合物滴眼液的应用研究

目的：探讨0.1%溴芬酸钠水合物滴眼液联合妥布霉素地塞米松眼液应用于控制白内障手术的疗效和安全性。

方法：行白内障超声乳化联合人工晶状体植入术的老年性白内障患者100例120眼,将患者随机分为两组：0.1%溴芬酸钠水合物滴眼液和妥布霉素地塞米松滴眼液联合用药组(试验组)、术后单独滴用妥布霉素地塞米松滴眼液组(对照组)。手术方法采用巩膜隧道切口超声乳化白内障摘除联合人工晶状体植入术。术后第1、7、14d观察症状和体征并进行评分; 并观察眼压变化及黄斑水肿发生情况。

结果：患者100例120眼完成研究,两组患者症状和体征综合评分术后1d无统计学差异(P>0.05),而术后7、14d内有统计学差异(P<0.05),试验组比对照组值低。术前眼压试验组(14.657±2.605mmHg)和对照组(14.415±2.761mmHg)比较,差异无统计学意义(P>0.05)。试验组眼压：在术后1、7、14d眼压均低于对照组,差异有统计学意义(P<0.05)。黄斑水肿发生率：对照组术后1、7、14d黄斑水肿发生率分别为1.7%、1.7%和3.3%,明显高于试验组的 0、0和1.7%,两组比较差异具有统计学意义(P<0.05)。

结论：应用0.1%溴芬酸钠水合物滴眼液和妥布霉素地塞米松滴眼液对白内障超声乳化摘除联合人工晶状体植入术后炎症的治疗效果较佳,是安全有效的,且不易发生高眼压等严重并发症; 同时可显著降低术后黄斑水肿发生率,预防白内障术后黄斑水肿的发生,具有安全可靠性,值得临床推广应用。     

超声乳化人工晶状体植入术后眼压变化的观察

目的观察白内障超声乳化联合人工晶状体植入术对眼压的影响.方法182例218眼行无缝线小切口超声乳化联合人工晶状体植入术,测量术前及术后1周、3周、2月、3月的眼压,进行分析比较.结果术后1周、3周、2月、3月平均眼压分别为(14.7±0.22)mmHg、(14.2±0.23)mmHg、(13.6±0.20)mmHg、(13.8±0.20)mmHg,均与术前(16.0±0.21)mmHg差异有显著性.术前为青光眼者术后1周眼压较术前升高(1.4±2.17)mmHg(P＜0.01),与术前有显著差异.病人年龄、性别、眼别、手术切口、人工晶状体及粘弹剂类型、超乳时间对术后眼压影响差异无显著性.结论无缝线小切口白内障超声乳化联合人工晶状体植入术在眼压方面具有安全性.     

超声乳化联合房角粘连分离术治疗慢性闭角型青光眼合并白内障

目的:探讨白内障超声乳化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临床疗效。方法:分析2008-01/2011-01在我科住院治疗的慢性闭角型青光眼合并白内障患者57例57眼,施行白内障超声乳化后房型人工晶状体植入联合前房角粘连分离术,随访8～15(平均10.8)mo,观察眼压、房角、最佳矫正视力、中央前房深度的变化。结果:术后52眼无需加用降眼压药物,眼压<21mmHg。另4眼随访期内加用1种降眼压药物(10g/L布林佐胺滴眼液)后,眼压<21mmHg,1眼加用2种降眼压药物(10g/L布林佐胺滴眼液和5g/L噻吗洛尔滴眼液)后,眼压<21mmHg;全部患者术后房角开放;除1例术前明显视神经萎缩病例术后视力无提高,其余病例术后视力提高两行或以上;术后中央前房深度3.35±0.54mm,较术前(2.01±0.05mm)明显加深。结论:对于慢性闭角型青光眼合并白内障,白内障超声乳化后房型人工晶状体植入联合前房角粘连分离术是一种安全有效的方法,患者不仅视力明显提高,而且远期眼压也能得到有效控制。     

白内障超声乳化联合IOL植入术治疗晶状体溶解性青光眼

目的: 探讨白内障超声乳化联合人工晶状体植入术治疗晶状体溶解性青光眼的疗效。方法: 对晶状体溶解性青光眼行白内障超声乳化联合人工晶状体植入术,观察术中术后手术并发症,对比入院时及术后的视力及眼压。结果: 手术并发症轻且易于控制;17例术前眼压41.7～62.4mmHg,视力光感,术后眼压平稳于10.7～18.2mmHg,视力≥0.5。结论: 白内障超声乳化联合人工晶状体植入术能够安全、有效地治疗晶状体溶解性青光眼。     

联合手术治疗青光眼合并白内障的临床观察

目的:探讨治疗青光眼合并白内障的手术方法及临床效果。方法:对45例45眼青光眼合并白内障患者施行白内障超声乳化及人工晶状体植入联合隧道内小梁切除术。结果:术前视力<0.1者32眼,0.1～0.3者13眼。术后视力<0.1者6眼(13%),0.1～0.5者22眼(49%),>0.5者17眼(38%)。术前眼压26～60mmHg,术后42例眼压降至正常范围,3例经局部按摩、滴药后降至正常,平均眼压12.78±2.70mmHg。随访6～12mo,无1例眼压再升高。3例视力下降,经戴镜矫正视力提高。并发症主要是角膜水肿和虹膜炎症反应。结论:白内障超声乳化人工晶状体植入联合隧道内小梁切除术是治疗青光眼合并白内障的理想方法。     

透明角膜切口晶状体超声乳化治疗原发性闭角型青光眼合并白内障

目的评价透明角膜切口白内障晶状体超声乳化吸出后房人工晶状体植入术治疗原发性闭角型青光眼合并白内障的疗效。方法回顾性分析闭角型青光眼伴白内障14例(27眼)。单纯行透明角膜切口白内障晶状体超声乳化吸出联合后房型人工晶状体植入术,术后随访8~20个月。结果所有患者术中术后无严重并发症,术后视力较术前明显提高,术后平均眼压(12.64±3.37)mmHg与术前用药后平均眼压(16.72±4.26)mmHg相比差异有统计学意义(配对t检验,P<0.01),周边前房较术前明显加深,前房角均重新开放或部分开放增宽。结论单纯透明角膜切口白内障晶状体超声乳化吸出后房型折叠人工晶状体植入术,可有效治疗合并白内障的闭角型青光眼。     

晶状体超声乳化人工晶状体植入治疗原发性闭角型青光眼

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。     

白内障超声乳化人工晶状体植入联合小梁切除术

目的:探讨局部麻醉下行小梁切除术联合透明角膜切口白内障超声乳化吸除联合折叠人工晶状体植入术(三联术)的临床效果方法:对43例合并有白内障的患者在局部麻醉下采用分切口小梁切除术和透明角膜切口白内障原位超声乳化折叠人工晶状体植入手术,结果:术后视力>0.5者26眼(60%),0.1～0.5者17眼(40%)。43眼术后视力均较术前提高。术后1wk平均眼压15.4±3.8mmHg,较术前眼压降低10～30mmHg,与术前相比有显著性差异(P<0.01)。42眼(98%)形成功能性滤过泡。结论:分切口的青光眼小梁切除术联合透明切口白内障超声乳化折叠人工晶状体植入术可以有效地控制眼压同时提高患者的视力,效果较好,并发症少。     

剥脱综合征并发白内障患者超声乳化术后2a眼压变化的临床研究

目的研究剥脱综合征并发白内障患者和老年性白内障患者在超声乳化术后2a内眼压变化情况。方法选择49例(54眼)剥脱综合征并发白内障的患者作为剥脱组。同期选择单纯老年性白内障患者134例(152眼)作为对照组。两组眼压用药控制正常后行白内障超声乳化联合人工晶状体植入术。比较两组在术后2a内眼压的变化。结果术前剥脱组基础眼压(21.85±2.23)mmHg(1kPa=7.5mmHg)高于对照组(18.62±3.12)mmHg(P=0.002)。在术后2a内,开始时眼压下降,后稍有升高,2a时两组眼压均降低分别为(15.09±0.70)mmHg和(15.19±0.51)mmHg(P=0.0115)。结论在超声乳化联合人工晶状体植入术后2a内,2组术后眼压均降低,剥脱组眼压降低更明显。     

超声乳化人工晶状体植入术治疗抗青光眼术后高眼压

目的:观察抗青光眼术后高眼压合并白内障患者行单纯超声乳化人工晶状体植入术的临床疗效.方法:回顾分析1997-12/2006-09收治的抗青光眼术后高眼压合并白内障患者31例33眼,施行白内障超声乳化人工晶状体植入术,术后随访视力、眼压、眼底情况.结果:术后眼压≤21mmHg者24眼(73%),差异有显著性(t=10.2,P＜0.001);所有病例术后视力均有不同程度提高.结论:单纯白内障超声乳化人工晶状体植入术可有效控制抗青光眼术后高眼压,同时改善患者视力状况.     

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.