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.     

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     

复合式小梁切除术联合睫状体冷凝治疗晚期新生血管性青光眼

目的探讨复合式小梁切除术联合睫状体冷凝治疗晚期新生血管性青光眼的疗效。方法晚期新生血管性青光眼16例（16眼）．一次性施行180°睫状体冷凝联合复合式小梁切除术．观察术后眼压、新生血管消退情况及手术并发症。结果术后随访6—48个月,视力均无明显改善,平均眼压自（57．48±10．00）mmHg降至（12．46±4．36）mmHg,控制在21mmHg以下者13眼（占80．12％）,手术眼压控制较好。结论一次性施行复合式小梁切除术联合睫状体冷凝对晚期新生血管性青光眼有较好的长期疗效。     

综合手术治疗晚期新生血管性青光眼的临床观察

目的：：观察综合手术治疗晚期新生血管性青光眼的疗效。方法：对2010-10/2013-10期间在我院住院的39例39眼晚期新生血管性青光眼患者使用视网膜及睫状体冷凝联合小梁切除术及前部玻璃体切除术治疗的临床资料进行回顾性分析。结果：所有患者出院后随访6~12 mo。39例术后第1 wk眼压(12.94±2.33mmHg)较术前眼压(57.31±6.72mmHg)明显降低,患者疼痛明显缓解。随访12 mo时35例不用降眼压药物眼压为17.25±2.24mmHg,4例用1~2种降眼压药物治疗眼压<21 mmHg。39例虹膜及房角新生血管均有不同程度回退。34例结膜滤过泡弥散隆起,5例较扁平。术后无浅前房或眼球萎缩。结论：视网膜及睫状体冷凝联合小梁切除术及前部玻璃体切除术治疗晚期新生血管性青光眼,能有效降低眼压,改善患者临床症状,为一种较安全而有效的综合性治疗方法。     

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。     

激光虹膜光凝术联合粘弹剂在新生血管性青光眼治疗中的应用

目的:探讨532 nm激光行虹膜新生血管光凝术联合粘弹剂在小梁切除术中治疗新生血管性青光眼的作用.方法:对18例新生血管性青光眼先用532 nm激光封闭虹膜表面血管,1 wk后行小梁切除术,术中应用粘弹剂,观察降眼压效果,观察前房和滤过泡,随诊10 mo.结果:术中18例前房均无大量出血,术后滤泡均呈弥散隆起.眼压:第1 wk内1～5 mmHg.2～4 wk 2～10 mmHg,随诊期间眼压为6～12 mmHg.结论:采用532 nm激光直接封闭虹膜新生血管后再行小梁切除术,同时术中应用粘弹剂能避免发生前房大量出血,避免出血阻塞滤过口.提高了新生血管性青光眼手术治疗的成功率.为新生血管性青光眼治疗提供了一种经济有效的综合治疗方法.     

小梁切除术联合视网膜光凝术治疗新生血管性青光眼

目的 探讨复合小梁切除术联合视网膜光凝术治疗新生血管性青光眼的疗效.方法 回顾性分析视网膜中央静脉阻塞继发新生血管性青光眼患者9例,行复合小梁切除术,术后1周予全视网膜光凝术.记录术前及术后3个月、12个月患者视力、眼压、虹膜及房角新生血管检查,眼底视网膜新生血管消退及无灌注区情况.结果 术后12个月患者视力提高8眼,1眼无明显提高.术后眼压：5例患者眼压控制在21mmHg以下;4例眼压控制欠佳,需要局部使用降眼压药物,其中2例使用一种局部降眼压药物后眼压控制在21mmHg以下,另外2例眼压不能控制.虹膜及房角新生血管消退.眼底3个月和12个月后行荧光血管造影显示新生血管消退,无水肿,毛细血管无灌注区消失.结论 复合小梁切除术联合全视网膜光凝术是一种治疗视网膜中央静脉阻塞继发的新生血管性青光眼的有效的方法.     

新生血管性青光眼综合手术治疗疗效观察

目的 评价全视网膜冷凝术(PRC)联合小梁切除、自体巩膜条翻转固定引流，并应用丝裂霉素C(MMC)治疗新生血管性青光眼的效果。方法 回顾21例PRC联合小梁切除、自体巩膜条翻转固定引流，并应用MMC治疗新生血管性青光眼的病例。结果 术后随访4月～2年，18例眼压控制在1．46～2．6个kPa(10．94～19．55mmHg)。结论 PRC联合小梁切除、自体巩膜条翻转固定引流，并应用MMC治疗新生血管性青光眼疗效理想。     

小梁切除联合巩膜条反折术治疗NVG的疗效

目的：评价小梁切除术联合巩膜反折术治疗新生血管性青光眼的临床疗效。 方法：回顾48例48眼小梁切除联合巩膜条反折进入前房引流治疗新生血管性青光眼的病例。观察术后视力、眼压、前房、出血、虹膜新生血管及滤过情况。 结果：术后6～12mo,40例眼压控制在21mmHg以下,6例症状缓解,加用盐酸卡替洛尔滴眼液治疗后眼压控制在21mmHg以下。 结论：小梁切除联合巩膜条反折术治疗新生血管性青光眼疗效理想。     

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.     

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.