晶状体超声乳化联合人工晶状体植入术后迟发型葡萄膜炎临床分析

目的探讨晶状体超声乳化联合人工晶状体植入术后迟发型葡萄膜炎发病机制。方法回顾性分析18例19眼老年性白内障行晶状体超声乳化联合人工晶状体植入术后迟发型葡萄膜炎的发病、表现、治疗及治疗结果。结果晶状体超声乳化联合人工晶状体植入术后迟发型葡萄膜炎高发期为术后2-8周,发生率为7.85%,均表现为急性前葡萄膜炎症状,部分病例于过度劳累后及皮质类固醇类眼药过早停药或突然停药后发病。局部及全身皮质类固醇治疗效果明显,预后良好。结论晶状体超声乳化联合人工晶状体植入术后迟发型葡萄膜炎发病机制可能为晶状体皮质残留、人工晶状体材料所含可溶性化学物质及人工晶状体本身引起的免疫反应等多因素所致。过度劳累、过早或突然停用含激素类眼药可为其诱发因素。     

晶状体超声乳化及人工晶状体植人术后迟发性葡萄膜炎

目的探讨晶状体超声乳化及人工晶状体植入术后迟发性葡萄膜炎发病的相关因素及治疗方法。方法回顾分析白内障35例（36眼）超声乳化人工晶状体植入术术后迟发性葡萄膜炎的临床资料及随访情况。结果32例（33眼）经1～4周的治疗好转，2例（2眼）经治疗60d好转，1例（1眼）放弃治疗。治疗后均无复发。结论迟发性葡萄膜炎的发生与糖尿病、高血压、外伤、手术操作、晶状体材料等有关。皮质类固醇治疗有效。一旦延误治疗对视力影响很大，须高度重视。     

白内障人工晶状体植入术后迟发性葡萄膜炎

目的探讨白内障人工晶状体植入术后迟发性葡萄膜炎的发病机制和治疗方法。方法本组白内障术后迟发性葡萄膜炎10例12眼，年龄45～79岁，平均67岁。全部行白内障囊外摘出联合后房型人工晶状体植入术，术后早期（5～10d）眼内葡萄膜炎反应基本消失后，突然发生急性葡萄膜炎反应，发病时间为术后13～37d．平均18.75d。全部患者局部及全身应用皮质类固醇、消炎痛及散瞳剂治疗。结果眼部炎症10d左右基本消失。除1眼视力下降外，其余视力均达反应前水平，无严重并发症。随访3～6个月，平均4.5个月，无1例复发。结论白内障术后迟发性葡萄膜炎是由免疫复合物介导的急性前葡萄膜炎症反应，用皮质类固醇及早治疗可预防严重并发症，恢复良好视力。     

后房型人工晶体植入术后迟发性葡萄膜炎

目的：探讨白内障摘除后房型人工晶体植入术后迟发性葡萄膜炎的发病机制。方法;对白内障超声乳化吸除后房型人工晶体植入术后12例13眼迟发性葡萄膜炎患者资料进行回顾性总结分析。本组老年性白内障患者,男4例5眼,女8例8眼,平均年龄62岁（43-72岁）。常规完成白内障超声乳化吸除后房型人工晶体植入,在术后早期（7-10天）眼内炎症完全消失或基本消失的情况下,突然发生急性葡萄膜炎症反应,发病时间最早在术后第12天,最迟34天,平均17.93天。结果：经局部及全身皮质类固醇、消炎痛治疗,6-15天眼部炎症完全消失,视力恢复良好,无严重并发症与后遗症,随访6-24个月,平均18.6个月,无一例复发,视力稳定。结论：后房型人工晶体植入术后迟发性葡萄膜炎是由免疫复合物介导的急性葡萄膜炎症反应,及时正确处理,可获得较好的效果随着手术后时间的推移。免疫复合物逐渐清除及人工晶体在眼内耐受,其发病率会逐渐降低。     

超声乳化白内障吸除治疗葡萄膜炎并发白内障

目的观察超声乳化白内障吸除人工晶状体植入术治疗葡萄膜炎并发白内障的临床效果。方法对25例（29只眼）葡萄膜炎并发白内障行超声乳化白内障患者吸除人工晶状体植入术,同时用非切开方式对粘连性小瞳孔进行扩张。结果白内障术后患者视力均得到提高,术后6个月最佳矫正视力≥0．5者24只眼占82.8％,术后恢复生理性小圆瞳孔25只眼占86．2％。结论对葡萄膜炎并发白内障施行超声乳化白内障吸除人工晶状体植入术可提高视力,恢复生理性圆瞳孔。     

人工晶状体植入术后的迟发性葡萄膜炎

目的探讨人工晶状体植入术后的迟发性葡萄膜炎的发病原因及预防方法。方法对不同类型的白内障囊外摘出联合人工晶状体植入术后所发生的迟发性葡萄膜炎11例(11眼)进行回顾性总结,分析其发病原因、发病时间、临床特点及预防方法。结果术后迟发性葡萄膜炎发生率为1.65%;自身免疫反应和术后抗生素、皮质类固醇用量不足是发病的主要原因;本病对皮质类固醇治疗敏感,只要及时治疗,一般预后良好。结论本病是由自身免疫变态反应引起的葡萄膜炎,术中尽量清理残余皮质,术后抗生素、皮质类固醇不可过早停药是降低本病的发生率的关键。     

人工晶状体植入术后迟发性葡萄膜炎及t-PA治疗

目的 探讨白内障摘出人工晶状体植入术后迟发性葡萄膜炎的发病机制和tPA治疗效果。方法 回顾性分析12眼人工晶状体植入术后迟发性葡萄膜炎的临床资料。结果 人工晶状体植入术后迟发性葡萄膜炎的发生率为3．29％，经过t-PA 10μg前房内注射，5～10天前房内纤维蛋白完全吸收，视力恢复良好，无后遗症。随访9～12月，无1眼复发，视力稳定。结论 白内障摘出人工晶状体植入术后迟发性葡萄膜炎是由免疫复合物介导的急性葡萄膜炎症反应，前房内注射t-PA治疗白内障摘出人工晶状体植入术后迟发性葡萄膜炎是一种简单安全可靠的方法。     

人工晶状体植入术后迟发性葡萄膜炎38例分析

目的探讨人工晶状体植入术后迟发性葡萄膜炎的发病机制及影响因素。方法总结分析1027例，人工晶状体植入术后迟发性葡萄膜炎38例（38眼）临床资料。结果本组术后迟发性葡萄膜炎的发生率为3．70％，其发病因素与术后过早停药、糖尿病、眼部术前并发症等有关，本病对皮质类固醇治疗敏感，及时治疗，预后良好。结论人工晶状体植入术后迟发性葡萄膜炎是免疫复合物介导的急性葡萄膜炎，术前严格掌握手术适应症，术中尽量清除干净晶体皮质，术后不过早停药，并注意控制糖尿病人的血糖水平，应可降低其发生率。     

人工晶状体植入术后迟发性葡萄膜炎14例分析

目的：探讨白内障囊外摘除后房型人工晶体状植入术后迟发性葡萄膜炎的发病机制、诱因及防治。方法：对14例人工晶状体植入术后迟发性葡萄膜炎患者的发病时间、诱因、眼部表现及治疗结果等临床资料进行总结分析。结果：人工晶状体植入术后迟发性葡萄炎的发病率为3.1%。发病时间最早在术后第二周，最迟在术后1年。糖尿病及风湿病患者的发病率较高。术后用药不规则及局部过早停药、早期过度用眼、过度疲劳可诱发本病。全部病体经局部及全身应用激素治疗后，炎症在一周内完全消退，视力恢复。结论：人工晶状体植入术后迟发性葡萄膜炎是一种由免疫复合物介导的葡萄膜炎症反应，正确治疗，预后良好。随着术后时间的推移，其发病率会逐渐降低。术后定期复查及规则用药，炎症消退后局部常规用药1个月，避免早期过度用眼及过度疲劳可降低本病的发病率。     

人工晶体植入术后迟发性葡萄膜炎及影响因素

目的：探讨人工晶体植入术后迟发性葡萄膜炎的发病机制及影响因素。方法：回顾性分析11例18眼白内障超声乳化人工晶体植入术后迟发性葡萄膜炎的临床资料及随访结果。结果：①术后迟发性葡萄膜炎的发病率为3．3％；②糖尿病、眼部合并症、劳累和早期过度用眼为发病主要影响因素；③本病对皮质类激素治疗敏感，只要治疗及时，一般预后良好。结论：本病可能是由免疫复合物介导的急性葡萄膜炎症反应。术前严格掌握适应症；术中尽可能彻底清除晶体皮质；术后局部不可过早停药、监控糖尿病人血糖变化、早期避免劳累和过度用眼可降低其发生率。     

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.