坐位裂隙灯下前房穿刺处理有晶状体眼硅油进入前房中的应用

目的探讨坐位裂隙灯下进行前房穿刺处理有晶状体眼前房硅油的临床效果。方法对6例（6只眼）有晶状体眼硅油进入前房并继发青光眼的患者,采取坐位在裂隙灯下进行前房穿刺术。术者双手操作,一手固定眼球,一手持7号针头,由助手协助抽取前房内硅油。结果 2例术中前房硅油完全抽出,4例部分抽出,仅有小于1/3前房容积的硅油滴存留。手术后观察：1例前房硅油完全消失,眼压正常,角膜透明;1例术中完全抽出,术后又有硅油滴进入前房,但小于1/3前房容积,眼压正常,角膜透明;3例术中部分抽出,术后未见明显增多,眼压正常,角膜透明;1例术中部分抽出,术后前房硅油又增多,再次行前房穿刺抽取后前房又充满硅油,眼压超过30 mmHg,角膜轻度雾状水肿,后行玻璃体及前房内硅油完全取出并注入长效气体（C3F8）,术后视网膜脱离复发,行晶状体切除并硅油再次填充后视网膜复位,眼压正常,角膜透明。最终6例患者中5例3个月内行玻璃体及前房内硅油取出,保留晶状体,术后稳定;1例硅油取出后视网膜脱离复发再次硅油填充后稳定。结论对于有晶状体眼硅油进入前房患者,采取坐位在裂隙灯下进行前房穿刺抽出部分或全部硅油是可行的,该术式操作简便,效果可靠。     

人工晶状体眼硅油入前房继发青光眼的预防与处理

目的探讨人工晶状体眼硅油入前房继发青光眼的预防与处理方法。方法对人工晶状体眼视网膜脱离患者12例，在行玻璃体切割硅油填充术后，有硅油入前房继发青光眼者，行Healon注入前房、硅油排出，常规作6点位虹膜周边切除术。结果12眼眼压恢复正常，人工晶状体位正，硅油及视网膜在位，未见不良并发症。结论采用Healon注入、硅油排出联合6点位虹膜周边切除术是治疗人工晶状体眼硅油入前房继发青光眼的有效方法，应采取积极措施预防该并发症的发生。     

有晶体眼硅油入前房继发青光眼的手术处理

目的：总结前房硅油排出术治疗有晶体眼硅油入前房继发青光眼的临床效果。方法：对６例玻璃体切除,硅油填充术后有晶体眼硅油入前房者,行１２点位角膜缘穿刺注入Ｈｅａｌｏｎ,６点位角膜缘切开排除硅油,悬韧带断裂超过２点钟同时行６点位虹膜周边切除术。结果６眼术后眼压控制正常、硅油在位、视网膜在位、除１例角膜轻度混浊外无其他并发症。结论：采用Ｈｅａｌｏｎ注入硅油排出虹膜周边切除术治疗有晶体眼硅油入前房继发青光眼     

玻璃体切除术后无晶状体眼硅油进入前房的原因及处理

目的 探讨无晶状体眼硅油进入前房的原因及治疗方法.设计 回顾性病例系列.研究对象 2007年3月至2009年12月沈阳爱尔眼视光医院收治的玻璃体切除术后无晶状体眼,出现硅油进入前房患者14例(14眼).方法 根据术中及术后情况、术后有无晶状体囊膜及虹膜根部切除孔(根切孔)的状态分析硅油进入前房的原因并采取相应治疗.治疗...     

有晶状体眼前房型人工晶状体植入治疗高度近视疗效观察

目的 观察有晶状体眼前房型虹膜固定人工晶状体植入治疗高度近视的临床疗效.方法 对11例(17只眼)高度近视患者进行术前虹膜YAG激光周边切除,1周后接受有晶状体眼Verisyse前房虹膜固定型人工晶状体植入手术,观察术后的裸眼视力、最好矫正视力、眼压、角膜及前房内炎症变化情况.结果 11例(17只眼)均顺利在前房内植入虹膜固定的人工晶状体,其中1只眼术后第3天发现人工晶状体单侧脱位再次手术固定.术后所有患者视力较术前均增加,裸眼≤0.5者3只眼,>0.5者14只眼.16只眼眼压术后检查正常,1只眼术后眼压升高至25 mm Hg,局部加用0.5%噻吗心胺点眼,2 d后眼压恢复正常.术后所有患者角膜透明,无内皮水肿的情况.13只眼出现前房轻度闪辉,4只眼前房可见较多的炎性细胞,用药后很快控制.结论 高度近视患者有晶状体眼前房植入虹膜固定型人工晶状体是一种较好的矫正视力方法,但其远期疗效及并发症有待进一步观察.     

玻璃体切割硅油注入术后无晶体眼青光眼的临床分析

为分析玻璃体切割硅油注入术后无晶体眼青光眼临床特点和防治方法，１９９２．１１－９７．６期间１８例此类青光眼的住院病人的临床资料进行回顾性分析。结果：行预防性虹膜周边切除者未发生瞳孔阻滞。行硅油取出术控制眼压成功率８８．９％，其中２７．８％需合并使用降眼压药。术后平均眼压２．５９±１．３１ｋＰａ，术后视力稳定占３８．９％，视力提高占３８．９％。结论：虹膜周边切除应列为无晶体眼硅油注入时的常规。及时的硅油取出术是防治玻璃体切割硅油注入术后无晶体青光眼的有效方法。     

无晶体眼蛙油填充术后硅油入前房的原因分析及处理

目的 对１５２例无晶体体眼硅油填充术后出现硅油入前房的原因进行统计学分析并提出了处理意见。方法：１９９３年９月至１９９６年３月我院进行的１５２只无晶体眼硅油填充术后，随诊至少半年或至硅油取出，详细记录眼压、虹膜和下方周边虹膜切除情况、硅油位置以及视网膜情况。用卡方检验对相关因素进行统计学分析。结果 １５２只无晶体硅油填充术眼中有２１只眼硅油前称入前房（１３．８％），由于ＩＰＩ关闭所致者１４只眼（占     

硅油填充术后前房硅油分析

目的：评估硅油填充术后前房硅油及其对眼压的影响。方法：对110例112眼行硅油填充术的患者的临床资料进行回顾性分析。结果：术后1－21月随访发现19眼（17％）前房硅油,其中16眼（84％）为无晶体眼：12眼下方6点虹膜周切闭锁,4眼周切大于2mm。前房硅油中继发青光眼的发生率为53％（10／19）,角膜混浊21％（4／19）。结论：虹膜周发闭锁为无晶体眼中硅油入前房的首要原因。前房硅油继发性青光眼发生率率,应予及早取出。     

玻璃体切除术后无晶状体眼的硅油取出联合人工晶状体植入

0引言对玻璃体切除硅油填充手术后的无晶状体眼,我们通常分期手术,取出硅油后3mo后再植入人工晶状体[1]。分期手术对患者来说增加了一定的经济负担和思想压力,也增加了一定的手术风险。我院对2007-01/2007-10的15例矫正视力≥0.1且眼底视网膜复位较好的无晶状体硅油填充眼行硅油取出与人工晶状体植入联合手术,现将结果报告如下。1临床资料硅油填充眼共15例15眼,男9例9眼,女6例6眼。所有患眼首次行玻璃体视网膜手术硅油填充时已行晶状体切除,硅油取出术前检查视网膜复位良好,无继发青光眼和角膜变性,无明显视神经萎缩。硅油填充原因为眼外伤10眼,复杂性视网膜脱离5眼。手术时间为硅油填充术后3~     

硅油填充术后前房硅油的原因探讨

目的 探讨硅油填充术后前房硅油的发生原因。方法 对55例(57只眼)行硅油填充术的病例的临床资料进行回顾性分析。结果 术后1—18个月随访发现13只眼前房硅油。其中8只眼为无晶状体眼，3只有晶状体眼者悬韧带断裂，2只眼为人工晶状体眼。结论 无晶状体眼和有晶状体眼晶状体悬韧带断裂为前房硅油的主要原因。     

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.