利用前囊膜为依托的后房型人工晶体植入术

利用前囊膜为依托的后房型人工晶体植入术施汉彬，邹召中，袁俊由于白内障囊袋内摘除术在前囊处理方式上首先采用上方水平截囊，故一旦发生后囊破裂而无法施行人工晶体囊袋内植入时，可利用下方的前囊膜为依托，改行睫状沟固定￣［１］。我院自１９８７年开展人工晶体囊袋...     

无晶体后囊膜支持的后房型人工晶体植入术（一）

无晶体后囊膜支持的后房型人工晶体植入术（一）北京三○四医院眼科周朝军综述当晶体后囊膜完整无损时，可安全的将人工晶体植入在奖袋内或睫状沟，然而对一些外伤性白内障或晶体脱位，预期囊外术中后囊膜破裂或晶体小带大范围损伤松解，以及白内障囊内摘除术后等致后游膜...     

后房型人工晶体偏心的讨论

后房型人工晶体植入术，无理是继白内障囊外摘出术或超声乳化摘出术后，术后人工晶体常发生不同程度的偏心。根据尸体眼及临床研究，发现影响偏心的因素很多，主要为前囊孔的形状，后房型人工晶体的位置、大小和设计，还有因术后炎症机化膜形成造成囊膜不对称收缩。提出位于中心的不小于５ｍｍ直径的、连续圆形撕囊法可以预防囊膜收缩综合征，人工晶体的最佳位置是对称性囊袋内植入，大直径视部优于小直径视部。推荐囊袋对称性植入袢－袢直径１２ｍｍ的后房型人工晶体，或睫状沟对称性植入袢－袢直径１４ｍｍ的后房型人工晶体。要避免不对称的囊袋－睫状沟植入。     

白内障囊外摘除术后囊破裂类型分析及处理

作者对１０６例现代囊外白内障摘除术中发生后囊破裂的原因，临床特片及术中处理进行了分析，其中外伤性白内障２２例术前已存在后囊的裂孔、裂孔边缘较厚，在晶体皮质抽吸过程中无扩大或玻璃体脱出，并顺利植入了后房人工晶体。８４例为老年性白内障术中新鲜形成的后囊破裂，其边缘较薄，术中有扩大的趋势，其中４７例（５６％）经处理后植入了后房人工晶体，术中后囊破裂的主要原因是机械性损伤，本文对后囊破裂的术中处理，粘弹剂     

环形撕囊囊袋内人工晶体植入术

环形撕囊囊袋内人工晶体植入术季建，许瀛海，张福昆现代显微镜下的白内障囊外摘除术及后房型人工晶体植入术，初期多数采用开罐式截前囊，后房型人工晶体多固定在睫状沟内或囊袋内，多呈不对称植入，效果尚可，但有一定的弊病￣［１］。以后许多学者提倡采用囊袋内植入人...     

外伤性白内障后囊缺损的后房型人工晶体植入术

眼球穿通伤所致的外伤性白内障，临床表现错综复杂，常致晶体后囊缺损。有关采用非睫状沟缝线固定法，利用残余晶体囊膜做支撑，植人后房型人工晶体报道甚少卜一。本文观察7例外伤性白内障中，后囊缺损直径最大8．ofnm，最小o．smfn，均在手术显微镜下成功地植入后房型人工晶体，术中及术后无明显并发症，水后视力恢复满意。材料与方法l一股资料：本组7例外伤性白内障均为男性，最大把岁，最小4岁，全身一般检查正常04例外伤性白内障合并限内异物（后路搞出术后），B型超声检查显示玻璃体轻度混浊23例外伤性白内障囊外摘除术后无晶体眼，虹…     

白内障术中后囊破裂的Ⅰ期后房型人工晶状体植入术

目的评价白内障囊外摘出术中后囊破裂行前段玻璃体切割联合Ⅰ期后房型人工晶状体植入的手术效果。方法对１４８０例白内障囊外摘出联合后房型人工晶状体植入术中４９例后囊破裂,行前段玻璃体切割联合Ⅰ期后房型人工晶状体植入的手术技巧、术后并发症和术后视力等进行分析。结果手术后囊破裂率为３．３％,７０％患者人工晶状体植入囊袋内,３０％患者为睫状沟,８９．９％患者出院时裸眼视力≥０．５。结论白内障囊外摘出术中后囊破裂,行前段玻璃体切割联合Ⅰ期后房型人工晶状体植入是安全有效的。     

外伤性膜性白内障人工晶体植入的临床观察

目的探讨膜性白内障后房型人工晶体植入的方法。方法３８例外伤性膜性白内障病人，采取长２．０ｍｍ宽６．７ｍｍ的短巩膜隧道切口；充分使用粘弹剂，虹膜粘连者用整复器分离或剪刀剪开，充分暴露睫状沟；机化膜中央区做直径３．０～４．０ｍｍ的部分切除，有玻璃体脱出时采取前段玻切；最后植入睫状沟固定型后房型人工晶体。结果术后一周视力０．１～０．３者６例，０．４～０．８者１５例，＞０．８者１７例；视轴区透明，随访半年后视力＞０．８者２５例。结论膜性白内障由于形成的膜坚韧，激光治疗难以奏效，单纯膜切开又不能自动张开，更谈不上后囊连续性撕囊术了。选择膜性白内障部分切除并植入睫状沟固定型后房型人工晶体是治疗外伤性膜性白内障的理想方法。     

白内障囊外摘除术中后囊破裂类型分析及处理

作者对106例现代囊外白内障摘除术中发生后囊破裂的原因、临床特征及术中处理进行了分析.其中外伤性白内障22例术前已存在后囊的裂孔,裂孔边缘较厚,在晶体皮质抽吸过程中无扩大或玻璃体脱出,并顺利植入了后房人工晶体.84例为老年性白内障术中新鲜形成的后囊破裂,其边缘较薄,术中有扩大的趋势.其中47例(56%)经处理后植入了后房人工晶体.术中后囊破裂的主要原因是机械性损伤.本文对后囊破裂的术中处理,粘弹剂及玻璃体切除在术中的应用进行了讨论.     

42例(43眼)后房型人工晶体缝线固定术观察

目的探讨人工晶体睫状沟缝合固定术在晶体囊内摘除术后、囊外术中囊膜破裂或晶体小带大范围的松解、以及外伤性白内障、晶状体脱位、玻璃体切割术后等无晶体囊膜的患眼中的应用。方法我院1997年1月～2004年8月间采用后房型IOL缝线固定术完成了42例(43眼)，均获得满意效果。其中：1．晶体后囊膜破损在2个象限残存后囊膜者，以此为依托将一侧人工晶体襻置于其上，另侧襻睫状沟缝线固定，即“一点固定法”实施了7例。2．因严重外伤或晶体囊内摘除术后而无晶体后囊者，施行双襻睫状沟缝线固定，即“二点固定法”实施了35例(36眼)。结果随访4～54个月，平均随访24个月复查时矫正视力最佳1．2，最低0．2，视力在0．6以上者22眼(占53．6％)，视力偏低者多为角膜瘢痕或眼底病变所致。二期植入者术后视力均高于术前最佳矫正视力。眼压均在正常范围。43眼中，术后均无明显并发症发生。结论IOL睫状沟缝线固定术是无晶体囊膜及晶体后囊膜破裂或晶体小带大范围松解的首选。     

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.