白内障小切口囊外摘除联合小梁切除治疗PACG合并白内障

目的：观察白内障小切口囊外摘除联合小梁切除术治疗原发性急性、慢性闭角型青光眼的疗效。

方法：急性闭角型青光眼合并白内障23例24眼,慢性闭角型青光眼合并白内障11例12眼,进行白内障小切口囊外摘除联合小梁切除术,均一期植入人工晶状体。

结果：术后随访1mo,急性闭角型青光眼组术前平均眼压30.68±7.60mmHg,术后17.83±5.95mmHg,差异有统计学意义(P<0.05); 慢性闭角型青光眼组术前平均眼压29.27±5.55mmHg,术后18.12±1.88mmHg,差异有统计学意义(P<0.05)。术前、术后两组间平均眼压差异无统计学意义。术后眼压控制良好者(6～21mmHg)者26眼(72%),局部使用抗青光眼药物后眼压控制良好者8眼(22%),总体有效控制率94%,眼压不能控制者(22～30mmHg)2眼(6%); 术后视力提高者32眼(89%),没有发生严重并发症。

结论：白内障小切口囊外摘除联合小梁切除术对于原发性闭角型青光眼(PACG)合并白内障的治疗可以有效控制眼压、提高视力,并发症少; 其在控制眼压方面对于原发性急/慢性闭角型青光眼无差异。     

青光眼术后继发恶性青光眼19例手术疗效观察

目的:评估前部玻璃体切除晶状体摘除联合小梁切除手术治疗恶性青光眼的临床效果。方法:我们回顾了19例(19眼)恶性青光眼患者接受前部玻璃体切除晶状体摘除联合小梁切除手术治疗的病例。恶性青光眼发生前青光眼包括急性闭角型青光眼4眼,慢性闭角型青光眼11眼,开角型青光眼2眼,先天性青光眼2眼。曾行手术包括虹膜周边切除术3眼,小梁切除术16眼。手术前后均进行最佳矫正视力、眼压和裂隙灯显微镜检查。结果:有15眼术后最佳矫正视力较术前均有不同程度提高。患者术前眼压为41.33±13.85mmHg;术后眼压降低为14.23±4.88mmHg。术后患者前房形成,术后早期炎症反应较重,术后4d减轻。术后常见的并发症包括角膜内皮水肿、皱褶和少量玻璃体脱入前房。结论:前部玻璃体切除晶状体摘除联合小梁切除手术是治疗恶性青光眼的有效方法。     

超声乳化白内障吸除联合小梁切除术治疗闭角型青光眼合并白内障

目的：探讨双切口白内障超声乳化吸除人工晶状体植入联合小梁切除术治疗闭角型青光眼合并白内障的临床疗效。方法：回顾分析双切口白内障超声乳化吸除人工晶状体植入联合小梁切除术治疗闭角型青光眼合并白内障患者65例70眼,术后随访3~12mo,观察视力、眼压及并发症的发生。
　　结果：术后患者视力≤0.1者2眼,>0.1~0.3者6眼,0.4~0.8者60眼,≥1.0者2眼,术后眼压在正常范围内(<21mmHg)者69眼,1眼术后出现浅前房,经治疗改善。
　　结论：双切口白内障超声乳化吸除人工晶状体植入联合小梁切除术治疗闭角型青光眼合并白内障手术成功率高,疗效佳,是一种理想的手术方式。     

玻璃体抽吸术在药物难控制性急性闭角型青光眼治疗中的应用

目的:探讨玻璃体抽吸术在药物难控制性急性闭角型青光眼治疗中的作用。方法:回顾分析我院住院患者共60例60眼,男28例,女32例,入院诊断符合急性闭角型青光眼发作期临床特征,且药物治疗24h后眼压仍>21mmHg的急性闭角型青光眼患者,其中控制眼压为21～35mmHg者26眼(43%),眼压～50mmHg者18眼(30%),50mmHg以上者16眼(27%)。视力范围为光感～0.3。所有患者行局部麻醉下睫状体平坦部玻璃体抽吸术治疗,吸出玻璃体液0.4～1.0mL,术后继续观察眼压、视力、前房深度变化,眼压控制稳定后分别进行单纯抗青光眼术、青光眼白内障联合人工晶状体置换术,或白内障摘除人工晶状体植入术。出院后门诊观察,随访6～12mo。结果:患者60例60眼急性闭角性青光眼行玻璃体抽吸术后,第3d检测眼压≤21mmHg者14眼(23%),眼压为～35mmHg者29眼(48%),眼压～50mmHg者13眼(22%),眼压>50mmHg者4眼(7%);抽吸术后视力增加2行的为28眼(47%),视力增加1行的24眼(40%),视力不增加的8眼(13%);58眼前房深度增加(97%);抽吸术后并发前房出血16眼(27%)。眼压控制稳定后分别进行单纯抗青光眼术14眼,青光眼白内障联合人工晶状体置换术28眼,白内障摘除人工晶状体植入术18眼。观察随访6～12mo,眼压控制≤17mmHg者54眼,眼压≤21mmHg者4眼,眼压为～35mmHg者2眼,未见视网膜脱离、黄斑囊样水肿等并发症。结论:玻璃体抽吸术应用在药物难控制性急性闭角型青光眼能明显降低眼压,为各种青光眼手术的治疗实施提供安全可靠的条件,有助于视功能保护和恢复,提高疗效。     

白内障囊外摘除并小梁切除治疗青光眼合并白内障疗效观察

目的：探讨小切口白内障囊外摘除并人工晶状体植入联合小梁切除术治疗青光眼合并白内障的临床疗效。方法：选择我院2007-09/2011-10原发性闭角型青光眼合并白内障患者80例86眼。本组患者均行小切口白内障囊外摘除联合小梁切除术。术后观察患者的视力和眼压情况。结果：术后视力：〈0.1共5眼,0.1～0.2共11眼,0.3～0.5共53眼,0.6以上17眼。术后患者眼压均降到临床统计正常范围（10～21）mmHg。结论：小切口白内障囊外摘除并人工晶状体植入联合小梁切除术治疗青光眼合并白内障减轻了患者多次手术的负担,临床有显著效果,是治疗青光眼合并白内障较佳术式,值得临床推广应用。     

先天性小眼球的眼部表现与合并症的治疗

目的探讨先天性小眼球眼部表现特点与合并症的治疗。方法回顾性分析在北京协和医院眼科诊断为先天性小眼球的11例(20眼)患者的临床资料,眼部检查包括视力、眼压、裂隙灯显微镜、眼底、A型和B型超声波及超声活体显微镜等。平均随访33个月。结果初诊视力无光感者2眼,光感～0.1者12眼,0.2～0.5者2眼,0.6～1.0者3眼,1.2者1眼。初诊眼压:8～21mmHg(1kPa=7.5mmHg)者7眼,22～40mmHg者4眼,40mmHg以上者9眼。裂隙灯显微镜检查:20眼小睑裂,9眼小角膜,20眼浅前房。20眼均合并闭角型青光眼及白内障。眼底检查:12眼因屈光间质混浊眼底不能窥入;8眼视盘C/D为0.3～0.9,1眼合并先天性视网膜劈裂。20眼眼轴长度为15.87～20.38mm,平均18.00mm。13眼施行小梁切除术,术后眼压控制在23mmHg以下9眼。11眼行白内障摘出术,其中5眼联合人工晶状体植入术。术后矫正视力提高7眼,其中提高至0.9～1.0者3眼,0.05～0.10者4眼。结论先天性小眼球眼轴短(眼轴长度≤20.50mm)、晶状体大及巩膜厚,多合并闭角型青光眼和白内障等。合并症的手术风险高,术前充分降低眼压,术中酌情先行后巩膜切开术,可降低术中或术后风险,有望提高手术成功率。     

儿童晶状体异常合并青光眼的联合手术

目的　对先天性青光眼合并晶状体异常的病例进行手术效果的评价 ,以探讨先天性白内障合并青光眼的最佳治疗方法和手术时机。方法　 1 998年 4月～ 2 0 0 1年 2月对 7例 1 3眼先天性青光眼合并晶状体异常的病例进行了手术 ,其中 1 0眼行小梁切开 +小切口晶状体摘除 ;1眼行小梁切除 +小切口晶状体摘除 ;1人 2眼为白内障术后半年发现青光眼 ,行小梁切除术。结果　术前眼压 1 1眼(84 6% ) >40mmHg ,平均 46 5mmHg。术后平均随访 1 4 9月 ,有 1 0眼 (76 9% )于手术近期都有一过性眼压高 ,一般发生在术后 0 5～ 1月后 ,随访终末期有 4眼 (3 6 4% )眼压在 2 5～ 3 0mmHg ,眼压控制不好的主要为眼球扩张合并晶状体脱位病例。术后并发症中 1人 2眼有术后前房出血 ,1～ 2日吸收 ,无其他近期及远期并发症发生。结论　对先天性青光眼合并晶状体异常的儿童可以实施青光眼白内障联合手术。大部分病例一次手术可以完全控制眼压 ,小部分需加抗青光眼药物。手术并发症少。     

小梁切除联合小切口白内障摘除人工晶状体植入术疗效观察

目的探讨小梁切除联合小切口白内障摘除人工晶状体植入术的临床疗效。方法对26例31眼闭角型青光眼合并白内障患者行小梁切除联合小切口白内障摘除人工晶状体植入术,术后对视力、眼压、结膜滤过泡、并发症等情况观察,术后随访6～27月,平均3个月。结果术前平均眼压25.64±4.23mmHg,术后最终平均眼压13.68±3.7OmmHg,<0.0l;术后最终矫正视力0.2～1.0者27眼,0.1～0.15者3眼,0.02者1眼;术后早期并发症:角膜水肿及弹力层皱褶5眼,脉络膜脱离l眼,前房及瞳孔区纤维渗出6眼;晚期并发症:瞳孔欠圆7眼,人工晶状体夹持2眼,后发障4眼。结论小梁切除联合小切口白内障摘除及人工晶状体植入术治疗闭角型青光眼合并白内障患者,具有有效控制眼压、恢复视力,并发症少等效果。     

小切口非超声乳化青光眼白内障联合手术疗效观察

目的:探讨小切口非超声乳化白内障摘出人工晶状体植入联合小梁切除术治疗青光眼并发白内障的疗效。方法:回顾分析32例32眼行小切口非超声乳化白内障摘除人工晶状体植入联合小梁切除术治疗慢性闭角型青光眼并发白内障患者的临床资料。结果:术后随访6～9(平均7.3)mo,患者术后最佳矫正视力≥0.3者27眼(84%),术后所有患者眼压控制正常,平均13.50±5.30mmHg,功能性滤泡者28眼(88%),术中术后均无严重并发症。结论:小切口非超声乳化白内障囊外摘除人工晶状体植入联合青光眼小梁切除术是治疗慢性闭角型青光眼并发白内障的一种安全、有效、经济的方法。     

小切口白内障摘除联合小梁切除术治疗开角型青光眼

目的:观察小切口白内障囊外摘除、后房型人工晶状体植入联合小梁切除术治疗合并白内障的开角型青光眼的疗效。方法:回顾分析2004-01/2010-06在我院住院行小切口白内障囊外摘除、后房型人工晶状体植入联合小梁切除术且资料完整的32例56眼开角型青光眼的疗效,根据患者年龄、眼球筋膜情况、视神经受损程度及术后要求达到的靶眼压确定术中用或不用丝裂霉素C(MMC),其中29眼术中使用MMC,27眼不使用MMC,患者均有明显的晶状体混浊。随访6～24(平均14.2±6.7)mo。结果:术中使用MMC组29眼,术前眼压(39.2±10.6)mmHg,术后眼压(13.2±5.5)mmHg,仅1眼需辅助1种局部降眼压药。不使用MMC组27眼,术前眼压(30.1±9.2)mmHg,术后眼压(17.5±8.1)mmHg,有4眼需辅助1种局部降眼压药,1眼需辅助2种局部降眼压药,1眼再手术。术后不需使用降眼压药者49眼(88%)。术后47眼(84%)最佳矫正视力提高。结论:小切口白内障囊外摘除、后房型人工晶状体植入联合小梁切除术可有效治疗合并白内障的开角型青光眼。     

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.