穿透性角膜移植术治疗角膜溃疡穿孔

目的 探讨穿透性角膜移植术治疗角膜溃疡穿孔的效果.方法 对角膜溃疡穿孔42例(42眼)施行穿透性角膜移植术,观察其临床特点及手术效果.随访时间6～18个月.结果 术后31例视力比术前提高,15例发生排斥反应,4例真菌性角膜炎复发,11例继发青光眼.结论 对保守治疗无效者,穿透性角膜移植术是治疗角膜溃疡穿孔的有效方法.     

穿透性角膜移植术治疗真菌性角膜溃疡穿孔

目的 探讨穿透性角膜移植术治疗真菌性角膜溃疡穿孔的临床疗效。方法 对1994年至2003年在青岛眼科医院行穿透性角膜移植术的40例（40只眼）真菌性角膜溃疡穿孔患者进行随访,随访时间为6～24个月,观察术后视力变化和真菌复发、植片排斥、继发性青光眼、并发性白内障等并发症的发生情况。结果 40例患者中,39例（97．5％）成功地保存了眼球,38例（95．0％）不同程度地提高了视力。穿透性角膜移植术后,4例（10．0％）患者真菌复发,其中3例用药物治愈,1例因合并真菌性眼内炎用药物不能控制而摘除眼球;15例（37．5％）患者植片发生排斥,其中12例经抗排斥治疗植片转为透明,3例因药物治疗无效而行二次穿透性角膜移植术;3例（7．5％）患者植片发生溃疡,其中2例治愈,1例因合并角膜内皮功能失代偿而行二次穿透性角膜移植术;5例（12．5％）患者继发青光眼,眼压均得到成功控制;5例（12．5％）患者发生并发性白内障,其中3例行白内障摘除术。其余患者术后随访期间眼部情况稳定,植片保持透明。最终随访时,36例（90．0％）患者角膜植片透明。结论 穿透性角膜移植术是治疗真菌性角膜溃疡穿孔的有效手术方式,是挽救眼球和视力的主要手段。     

用婴儿供体角膜行穿透性角膜移植治疗真菌性角膜溃疡

目的 观察用婴幼儿供体角膜行穿透性角膜治疗真菌性角膜溃疡的效果。方法 采用３岁以下（平均１．６岁）婴幼儿供体角膜行穿透性角膜移植治疗真菌性角膜溃疡２６例２６眼。结果 手术治愈率达９２．３％,植片透明率达８３．３％,视力获不同程度提高者７９．２％。结论 婴幼儿供体角膜具有材料易得及内皮愈合储备能力高的优点,穿透性角膜移植治疗真菌性角膜泪疡可以控制感染、缩短病程、提高视力及保全眼球。     

角膜移植治疗真菌性角膜溃疡的临床观察

探讨角膜移植治疗真菌性角膜溃疡的有效性及影响因素。方法：应用角膜移植治疗真菌性角膜溃疡４４例４４只眼,穿透性角膜移植２９例２９只眼,板层角膜移植１５例１５只眼,３３例为８ｍｍ以上的大植片角膜移植。结果：４１例感染控制并保存了眼球,３２全视力较术前有不同程度提高,１８例获得０．０５以上有用视力,１例穿通性角膜移植术后最佳矫正视力达１．０,１例板层角膜移植术后最佳矫正视力达０．６。３例角膜严重感染者,     

角膜移植治疗严重真菌性角膜溃疡

目的评价角膜移植治疗严重真菌性角膜溃疡的临床效果及影响因素。方法采用穿透性或板层角膜移植治疗穿孔及几近穿孔的真菌性角膜溃疡53人（53眼），临床观察4～40月。结果50眼角膜植片存活，溃疡治愈率94．34％．27眼角膜植片透明，透明率、增视率均为54．00％。结论对药物治疗无效的严重真菌性角膜溃疡、穿孔者及时行治疗性角膜移植术可以治愈感染，挽救眼球，甚至恢复有用视力。     

穿透性角膜移植联合梁切除术的临床观察

２穿透性角膜移植联合小梁切除术治疗溃疡穿孔、角膜瘘或术前合并青光眼的角膜病变３０例。其中联合白内障囊外摘除８例，联合人工晶体取出１例。术后视力提高２５例（８３．３％），２８眼眼压控制在小于２０ｍｍＨｇ（有效率９３．３％），２９眼角膜移植片保持透明（９６．７％），穿透性角膜移植联合小梁切除术是治疗角膜溃疡穿孔、有膜瘘或术前合并青光眼的角膜病主煌有效措施。可以减少术后并发症，中角膜植片透明率，有效地改     

穿透性角膜移植治疗重症真菌性角膜溃疡效果观察

目的探讨穿透性角膜移植治疗重症真菌性角膜溃疡的临床效果。方法对重症真菌性角膜溃疡10例(10眼)行穿透性角膜移植术,随访3~6月。结果术后10眼感染全部得到控制,8眼植片透明,1眼行二次穿透性角膜移植,术后角膜透明。术后视力均比术前提高。结论穿透性角膜移植治疗真菌性角膜溃疡可有效地控制感染,改善视功能,效果较好。     

真菌性角膜炎药物及手术治疗比较

为探讨真菌性角膜炎选择抗真菌药物或角膜移植术治疗的适应症。将８２例按病灶特点分为５组。Ⅰ组药物治疗（３２例），Ⅱ组先药物治疗，待机手术治疗（１１例）。Ⅲ组穿透性角膜移植术治疗（１９例）。Ⅳ、Ⅴ组玻璃体切割联合穿透性角膜移植术（分别１１、９例）。结果：Ⅰ组治愈率７８．１３％，是否伴前房积脓对治愈率的影响无显著性差异。Ⅱ组１１例有２例（２／１１，１８．１８％）药物治愈，９例（９／１１，８１．８２％）需手术治疗，８例治愈。Ⅲ、Ⅳ、Ⅴ组治愈率分别４７．３７％、４５．４５％、５５．５６％。结论无手术适应症的真菌性角膜炎强调药物治疗，只有在发生溃疡穿孔且眼内容物脱出或继发性青光眼时才考虑手术。真菌性角膜炎伴眼内炎采用角膜移植术联合玻璃体切割术及眼内注药术是较理想的方法。     

角膜移植联合玻璃体切除治疗严重眼前段复合伤

目的 观察穿透性角膜移植联合前段玻璃体切除治疗严重角膜穿孔伤的疗法。方法 ２７例严重角膜穿孔伤后有浅前房、继发性青光眼和外伤性白内障的患者行穿透性角膜移植联合前段玻璃体切除术。结果 ２５例术后视力明显提高,角膜移植片保持透明,２７例眼压均得到控制,前房恢复正常。结论 穿透性角膜移植联合前段玻璃体切除对治疗严重角膜穿孔伤伴有合并症的患者,是一种较为理想的手术方法。     

角膜溃疡穿孔的临床治疗

目的:探讨角膜溃疡穿孔的不同临床治疗方法及其疗效评价。方法:收集我院1993-01/2003-06角膜溃疡穿孔病例49例(49眼),进行回顾性分析,对不同病变所采用的不同治疗方法进行比较、评价各种治疗方法的疗效。结果:49例患者中有16例经单纯药物治疗治愈,其中6例患者视力获得不同程度的提高;33例单纯药物治疗效果不佳患者经手术治疗治愈,其中22例穿透性角膜移植患者中有17例患者视力不同程度提高。单纯药物治疗遗留粘连性角膜白斑13例,单纯性角膜白斑3例,结膜瓣掩盖术后遗留粘连性角膜白斑3例。术后继发青光眼2例。角膜移植患者术后有6例发生角膜移植排斥反应。无溃疡复发。结论:药物治疗是有效的方法之一;穿透性角膜移植术是最佳的手术治疗方法。     

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.