恶性青光眼的预防及处理

目的:探讨恶性青光眼的预防措施和治疗方法。方法:回顾性分析2001-03/2006-06我院经治的15例17眼恶性青光眼的临床资料,采用综合药物治疗和手术治疗,手术方法包括单纯经睫状体扁平部玻璃体腔穿刺抽液术或联合前房重建术;晶状体摘除、部分晶状体后囊膜、玻璃体前界膜、前部玻璃体切除术及再滤过术。结果:术后随访1~63(平均17.2±4.1)mo。术后眼压平均15.1±3.5mmHg(1mmHg=0.133kPa),全部前房深度恢复且稳定,视力保持,无严重并发症。结论:对药物治疗无效的恶性青光眼应及时采用手术疗法。单纯经睫状体扁平部玻璃体腔穿刺抽液术或联合前房重建术能有效缓解部分早期恶性青光眼,且能防止严重并发症的发生。晶状体超声乳化、人工晶状体植入、部分晶状体后囊膜及玻璃体前界膜和前部玻璃体切除、再滤过术的多种联合手术,能有效治疗各种恶性青光眼。     

晶状体超声乳化摘除联合前段玻璃体切割治疗恶性青光眼

目的：评价超声乳化摘除晶状体联合前段玻璃体切割治疗恶性青光眼的疗效，并对具体操作手法作一介绍。方法：对23例青光眼术后恶性青光眼患者行联合手术，回顾分析其临床资料。结果：全部病例术后前房形成，其中20例眼压控制良好，1例需加用抗青光眼药物治疗，2例再行阀门管植入术以控制眼压。22例视功能得到不同程度的改善。结论：超声乳化摘除晶状体联合前段玻璃体切割是治疗恶性青光眼的有效手段。     

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。     

恶性青光眼18例综合治疗的临床分析

目的:探讨恶性青光眼综合治疗方法的治疗效果。方法:对12例14眼小梁切除术后的恶性青光眼,6例6眼白内障囊外摘除+人工晶状体植入术后的恶性青光眼进行药物及玻璃体腔水囊抽吸术治疗。结果:白内障囊外摘除+人工晶状体植入术后的4例4眼恶性青光眼患者在术中发现并及时行玻璃体腔水囊抽吸联合前房形成术;其余14例16眼先用药物治疗2d无效后,行玻璃体腔水囊抽吸术1～2次,其中1例1眼(小梁切除术后)在行2次玻璃体腔水囊抽吸术后未能控制眼压、恢复前房,经行白内障囊外摘除+人工晶状体植入+玻璃体水囊抽吸术,全部成功。眼压控制理想,前房正常,随访平均21mo期间未复发。结论:恶性青光眼治疗中,抽吸玻璃体腔水囊、解除睫状环阻滞、建立前房是成功的关键。     

恶性青光眼的临床特点与防治方法

目的探讨恶性青光眼的临床特点与防治方法。方法回顾分析12例（13只眼）恶性青光眼的临床资料及治疗方法。本组病例角膜直径9．5—11mm,平均10．8mm。眼轴长17．8～22．5mm,平均21．9mm,发生于慢性闭角型青光眼小梁切除术后11只眼,占84．6％。6只眼行药物治疗,其中2只眼联合YAG激光治疗;5只眼行晶状体摘除联合人工晶状体植入、后囊截开、前部玻璃体切除术;2只眼行晶状体摘除联合人工晶状体植入、小粱切除术,再次经睫状体平部行前部玻璃体切除、晶状体后囊膜部分切除术。结果出院时患者眼压在10-15mm Hg,中央及周边前房形成。随访观察10个月至5年,平均20个月,前房稳定,眼压15—21mm Hg,平均18．7mm Hg。结论恶性青光眼好发于小角膜、短眼轴的慢性闭角型青光眼小梁切除术后,药物治疗、无晶状体眼联合Y-AG激光治疗可以控制部分恶性青光眼,晶状体摘除联合人工晶状体植入、后囊截开、前部玻璃体切除手术可以治愈药物不能控制的恶性青光眼。     

恶性青光眼12例手术治疗分析

目的:探讨两种手术方法对恶性青光眼的治疗效果。方法:对12例16眼小梁切除术后的恶性青光眼患者,晶状体核硬度≤2级,视力≥0.1者采取抽吸玻璃体水囊联合前房注气重建(A术)。晶状体核硬度≥3级,视力<0.1者采取抽吸玻璃体水囊、联合白内障囊外摘除+人工晶状体植入+晶状体后囊膜、玻璃体前界膜切开(B术)。结果:所有病例经4～5d药物治疗均无效,其中5例7眼采取A术,有2眼前房形成后又消失,再次行A术后获成功,余均一次性成功。7例9眼采取B术者均全部成功,随访5～13(平均9)mo,全部病例眼压得到控制,前房深度恢复正常,视力得到有效保护,无严重并发症。结论:恶性青光眼采取A,B两种术式可以有效的控制眼压,保护视功能。     

前段玻璃体切除-超声乳化-人工晶状体植入联合手术治疗恶性青光眼

目的:评价经睫状体平部中央玻璃体切除-超声乳化-人工晶状体植入-前段玻璃体切除联合手术治疗有晶状体眼恶性青光眼的疗效,并对具体操作手法作一介绍。方法:对10例11眼青光眼术后恶性青光眼患者行联合手术,回顾分析其临床资料。结果:全部病例术后前房形成,眼压稳定在21mmHg以下,视功能得到不同程度的改善。结论:经睫状体平部中央玻璃体切除-超声乳化-人工晶状体植入-前段玻璃体切除联合手术是治疗有晶状体眼恶性青光眼的有效手段。     

联合手术治疗晶状体脱位继发性青光眼疗效分析

目的 回顾性评价晶状体摘除术联合玻璃体切割术和／或抗青光眼手术治疗晶状体脱位继发性青光眼的临床疗效。方法 34例(34只眼)晶状体脱位继发性青光眼患者分别行晶状体摘除术联合前部或全部玻璃体切割术、单纯小梁切除术、房水引流物植入术或多种联合手术。结果 26例患者(26只眼)成功摘除脱位晶状体；30例患者(88．24％)眼压恢复正常，21例(61．76％)患者矫正视力提高。结论 晶状体摘除术、玻璃体切割术联合抗青光眼手术是治疗晶状体脱位继发性青光眼的有效手段，但应根据患者具体情况，选择适当的手术；确诊为晶状体脱位继发性青光眼患者。尽早手术有利于保存和恢复视功白色。     

睫状环阻塞性青光眼治疗的临床分析

目的探讨睫状环阻塞性青光眼的联合治疗方法并评介其疗效。方法回顾性分析2002年11月至2008年10月经治的11例（11眼）睫状环阻塞性青光眼的临床资料,4例药物治疗;其余7例采用不同的手术治疗：对于青光眼手术后发生的睫状环阻塞性青光眼4例行前段玻璃体切除、前房形成、房角分离联合品状体超声乳化人工晶状体植入术;对于白内障摘出联合抗青光眼术后发生的3例,其中1例行部分晶状体后囊切开、玻璃体前界膜及前部玻璃体切除：另2例行人工晶状体摘出,后囊连续环行撕囊联合前段玻璃体切除术,其中1例摘出人工晶状体稳定半年后行人工晶状体二期植人。结果11例前房均恢复并保持良好,视力提高,平均眼压（15．3±2．7）mmHg,未发生严重的并发症。结论睫状环阻塞性青光眼是一种有多种因素造成的难治性青光眼,早期药物治疗有效,如药物治疗无效,需行手术治疗。     

复杂外伤性青光眼的联合手术治疗

目的：观察复杂外伤性青光眼联合手术治疗的临床疗效，探讨手术方法及并发症。方法：对28例继发于钝挫伤、穿通伤的复杂外伤性青光眼行联合手术治疗，其中行晶状体摘除、前部玻璃体切除联合青光眼阀前房植入术10例，保留晶状体、前部玻璃体切除联合青光眼阀前房植入术3例，无晶状体眼行前部玻璃体切除、人造瞳孔术联合青光眼阀前房植入术4例及睫状体扁平部植入术5例，人工晶状体眼行可调整缝线小梁切除联合前部玻璃体切除术4例，恶性青光眼行前房成形术，前部玻璃体切除联合青光阀扁平部植入术2例，以上眼其中7例同时行人工晶状体缝线固定术。结果：术后随诊9～40个月，平均18．6个月，手术成功(眼压：6～21mmHg)21只眼(75％)视力提高15只眼(53．5％)。并发症：早期低眼压18例，脉络膜脱离12例，眼压失控7例，玻璃体出血4例，引流管内口阻塞5例，驱逐性出血1例，视网膜脱离1例。结论：联合手术是治疗复杂外伤性青光眼的一种有效方法。     

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.

---

     

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.