巩膜瓣可调整缝线预防小梁切除术后浅前房的作用

目的观察巩膜瓣可调整缝线在预防青光眼小梁切除术后浅前房中的作用。方法对60例(89眼)青光眼患者,在手术显微镜下,做穹隆部或角膜缘为基底结膜瓣,常规的梯形巩膜与小梁切除术。在巩膜瓣两侧做可拆缝线。球结膜切口连续紧密缝合。术后观察眼压、前房深度、结膜滤过泡、眼内组织反应与并发症。当手术后前房形成稳定或眼压回升大于10mmHg时,拆除巩膜调整缝线。术后平均随访时间6个月。结果术后第一天前房形成良好74只眼,术后巩膜瓣缝线松解时间5-30天,平均11天,缝线松解后,结膜滤过泡明显增大。60例患者术后随访眼压3-18mmHg,平均(9.1±2.75)mmHg与术前眼压相比,差异非常显著,所有患者随访中均未应用抗青光眼药物治疗,呈现血管少、弥散而微隆起的功能性结膜滤过泡。结论巩膜瓣可调整缝线能促进青光眼小梁切除术后早期前房的形成,减少前房形成迟缓所致的并发症。有利于小梁切除术后长期滤过作用,提高青光眼手术的安全性和有效性。     

改良复合式小梁切除术临床分析

目的 探讨改良复合式小梁切除术治疗青光眼的效果。方法 86例92眼。做以角膜缘为基底的结膜瓣,制作4mm×4mm的巩膜瓣,将沾有0.25mg/ml丝裂霉素C液的棉片(5mm×5mm)置于巩膜瓣上,用结膜瓣遮盖棉片5分钟后取出。用平衡盐溶液100ml充分冲洗,用2ml一次性注射器针头在角膜缘内0.5mm作1前房穿刺口。作常规小梁切除及虹膜周边切除。10-0尼龙线作改良可拆式缝线缝合巩膜瓣的两个边。术后5～10天视前房及眼压情况拆除巩膜可拆式缝线。结果 92眼术毕前房即形成,拆除缝线后,眼压7.10～18.86mmHg,平均12.53mmHg(1mmHg=0.133kPa)。滤过泡呈弥漫微隆起,术后未见脉络膜脱离或浅前房。结论 改良复合式小梁切除术疗效更确实,手术更安全。     

不同巩膜瓣缝合法在急性闭角型青光眼小梁切除术中的观察

目的:比较改良巩膜瓣可拆除缝线法与传统缝合法在急性闭角型青光眼小梁切除术中的临床效果。方法:42例68眼接受小梁切除术的急性闭角型青光眼患者中,A组16例28眼术中采取改良巩膜瓣可拆除缝线法;B组26例40眼术中施行传统巩膜瓣缝合法。结果:所有患者随访6～12(平均6.7)mo。A组术后拆巩膜缝线时间3～17(平均8.33)d。A、B组术后早期浅前房分别有2眼(7%)和12眼(30%),差异有统计学意义(P<0.05),术后2wkA、B组眼压分别为10～19(平均13.31)mmHg和6～42(平均14.64)mmHg,两组差异无统计学意义;术后6moA、B组眼压分别为10～17.30(平均11.96)mmHg和7～44(平均15.17)mmHg,两组差异无统计学意义;A、B组最终形成功能滤过泡28眼(100%)和36眼(90%),两组差异无统计学意义。结论:改良巩膜瓣可拆除缝线法在急性闭角型青光眼小梁切除术中应用是安全有效的,它较传统方法更能降低术后早期浅前房的发生。     

巩膜瓣可调整缝线在小梁切除术中的应用分析

目的观察巩膜瓣可调整缝线在小梁切除术中的应用效果。方法对60例(80只眼)青光眼患者做常规的三角形巩膜瓣与小梁切除术,在巩膜瓣两侧做可调整缝线,术后观察眼压、前房深度、结膜滤过泡。当手术后前房形成稳定或眼压回升大于10 mm Hg时,拆除巩膜瓣可调整缝线。结果术后第1天全部前房形成良好,术后巩膜瓣可调整缝线2周内拆除,平均7 d,可调整缝线拆除后,结膜滤过泡明显增大。结论巩膜瓣可调整缝线能促进小梁切除术后早期前房的形成,有效预防术后浅前房发生,术后2周内拆线对眼压具有调节作用,提高青光眼小梁切除术的安全性。     

改良巩膜瓣可拆除缝线法在急性闭角型青光眼小梁切除术中的应用

目的:观察一种改良式巩膜瓣可拆除缝线法在急性闭角型青光眼小梁切除术中的临床效果。方法:对16例28眼急性闭角型青光眼患者施行小梁切除联合虹膜周边切除术,术中对巩膜瓣采取改良式可拆除缝合。结果:所有患者随访6～12(平均8.7)mo。可拆除缝线拆线时间3～17(平均8.33)d,拆线前眼压12.23～18.86(平均15.25)mmHg,拆线后眼压为10.00～17.30(平均11.96)mmHg,两者间差异有统计学意义(P<0.05),28眼均无拆线并发症出现和滤过泡渗漏;术后28眼中Ⅰ度浅前房1例,Ⅱ度浅前房1例,浅前房发生率7%;28眼末次随访眼压10.00～17.30(平均12.55)mmHg;28眼最终形成扁平滤过泡20例,微小囊样滤过泡8例,功能滤过泡100%。结论:改良式巩膜瓣可拆除缝线法在急性闭角型青光眼小梁切除术中安全、有效,有利于远期眼压的控制和功能滤过泡的形成。     

青光眼小梁切除联合巩膜瓣下羊膜填充的疗效观察

目的探讨青光眼小梁切除联合巩膜瓣下羊膜填充治疗青光眼的疗效。方法对12例（12眼）青光眼行小梁切除手术，术中联合巩膜瓣下羊膜填充，观察术后并发症的发生和滤过泡的形成以及术后眼压变化。结果（1）眼压：术后3月内，12眼眼压均在10～21mmHg；术后6月，有1眼需用1种降眼压滴眼液使眼压控制在21mmHg以内。（2）滤过泡：滤过泡Ⅰ、Ⅱ型滤过泡10眼；Ⅱ型滤过泡2眼。（3）并发症：术后前房有渗出反应8眼，前房有少量积血1眼，均在1周内恢复。结论小梁切除联合巩膜瓣下羊膜填充，在一定程度上提高了青光眼滤过手术的成功率。     

青光眼滤过性手术后结膜瓣裂开的处理

例1 女16岁住院号492。因右眼角膜粘连性白斑、继发性青光眼入院。眼压34.52mmHg。入院后行巩膜下层间咬切术,术后发现结膜瓣下移,12点处创口裂开5mm,萤光素试验(+),在局部麻下将结膜裂口连续缝合。次日,创口重新哚开,再用褥式间断缝合也未成功。后将巩膜瓣缝合,再连续缝合结膜,一周后,创口愈合。由于巩膜瓣缝合外引流消失而使眼压升高。出院时眼压为24.38mmHg。例2 女67岁住院号714。左眼急性闭角型青光眼,眼压50.62mmHg。眼压控制后,在局麻下行巩膜下层间咬切术。术后7天拆线,鼻侧结膜瓣裂开4mm。用上述同样方法缝合结膜二次均失败。最后改用上     

松解缝线小梁切除术治疗闭角型青光眼147例效果观察

目的评价闭角型青光眼辅助巩膜瓣松解缝线小梁切除术的临床疗效。方法回顾性研究147例(159眼)原发性闭角型青光眼(PACG)施行辅助巩膜瓣松解缝线小梁切除术(简称松解缝线组),同期162例(174眼)PACG行常规小梁切除法(对照组),术后观察两组视力、眼压、前房形成、结膜滤泡、眼内反应等,平均随访时间30个月。结果术后早期前房形成时间(d),松解缝线组短于常规小梁切除组,差异有统计学意义(P<0.001)。松解缝线组出院时眼压(11.77±3.37)mmHg与术前眼压(31.63±9.45)mmHg比较,差异显著(t=25.86,P=0.000)。术后长期随访眼压(14.74±2.71)mmHg低于常规小梁切除组(17.96±2.45)mmHg,差异显著(t=11.22,P=0.000)。随访中无眼部感染与恶性青光眼发生。结论辅助巩膜瓣松解缝线的小梁切除术在闭角型青光眼滤过术中能促进术后早期前房形成。增强长期眼压控制作用。     

小梁睫状体分离造痿术

作者自1986年以来,采用本术式治疗各类青光眼128例,157眼,术后眼压控制占90.7％,效果满意。手术方法:局麻,作以穹窿部为基底的结膜瓣,结膜瓣的大小与小梁切除术相同。切开前房后以虹膜恢复器向前分离周边前房之粘连,向后作睫状体分离4×4mm范围,然后行小梁,前巩膜一并咬切3×3.5mm,虹膜周边切除,巩膜瓣缝合2针,结膜瓣二侧缝合,术毕。结膜下注射庆大霉素2万,氟美松2mg,阿托品0.3ml,术眼加压包扎。前房恢复后解除加压包扎。     

改良的小梁切除术

目的探讨一种改良的小梁切除术的疗效。方法手术员微镜下作以角膜缘为基底的结膜瓣，及4x4mm1／3巩膜厚度的浅层巩膜瓣，然后作一中层巩膜瓣，约3X3mm大小1／3巩膜厚度并切除之。作小梁切除、虹膜周切、巩膜瓣固定、球结膜及筋膜囊分层连续缝合。结果200例（280眼）随访6-24月，近期眼压控制率100％，远期为94％，平均眼压15.90mmHg结论改良的小梁切除术，降眼压效果好，是一种较理想的抗青光眼手术方式。     

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.