眼挫伤致隐匿性巩膜破裂伤的手术治疗

隐匿性巩膜破裂伤由于球结膜水肿、瘀血而易被漏诊。我院1998年1月-2002年12月收治15例(15眼)隐匿性巩膜破裂伤，报告如下。     

隐匿性巩膜破裂伤的临床分析(附10例临床报告)

目的 探讨隐匿巩膜破裂伤的诊断要点及手术方式。方法 回顾分析了10例隐匿性巩膜破裂伤临床资料。结果 手术后视力提高3例，保持眼球形态6例。结论 眼挫伤后低眼压或形态改变要排除巩膜破裂。影像检查有参考价值。疑有后部巩膜破裂时应及早进行手术探查，是避免漏诊或误诊的关键。     

隐匿性巩膜破裂伤的临床观察

目的 分析讨论隐匿性巩膜破裂伤的临床表现、诊断、治疗、远期疗效及并发症。方法 回顾分析了1985年-2001年间收治的56例56眼隐匿性巩膜破裂伤的临床资料。结果 该病均由严重钝器损伤所致，结膜完整，伤口隐蔽，诊断困难易漏诊，并发症多，预后差。结论 拟为隐匿性巩膜破裂伤者即行B超扫描及手术探查。术后需用大剂量皮质类固醇联合抗生素，定期随访。     

隐匿性巩膜破裂伤临床分析

目的探讨诊治隐匿性巩膜破裂伤的方法。方法回顾分析26例(26只眼)隐匿性巩膜破裂伤的临床资料。结果26只眼均行术中探查,其中23只眼行巩膜显微缝合术。术后视力提高8只眼,保持眼球形态23只眼。一期眼球摘除3只眼。结论隐匿性巩膜破裂伤的诊断无绝对依据,对疑似病例应及时手术探查。视力无光感不应作为眼球摘除的唯一指征。     

隐匿性巩膜破裂伤临床分析

探求隐匿性巩膜破裂的诊断标准。方法：回顾总结我院１９８９年１月－１９９９年１月间收治２４例隐匿性巩膜破裂伤。结果：隐匿性巩膜破裂伤占同期眼破裂伤４．８％。本组病例球结膜均完整,前房出血发生率１００％,视力严重下降,巩膜破裂伤跨双象限１３例占５４．２％。     

隐匿性巩膜破裂伤的诊断与治疗

严重眼球钝挫伤导致后部巩膜破裂 ,由于球结膜及眼前段巩膜相对完整 ,直视检查不易发现伤口 ,临床上称为隐匿性巩膜破裂伤 ,容易造成漏诊。 1998年 1月至 2 0 0 0年 1月 ,我院共收治隐匿性巩膜破裂伤 2 6眼 ,现将结果报告如下。一般资料 :2 6例 ( 2 6眼 )中 ,男 2 3眼 ,女 3眼 ,年龄 8～6 1岁 ,平均 34 3岁。术后随访 3月～ 13月 ,平均为 6 4月。致伤原因 :致伤原因均为硬物击伤 (包括铁锤 ,石块 ,木块 ,拳击伤等 )或车祸伤 ,就诊时间 :伤后就诊时间最短 1天 ,最长 2月 ,平均 12 3天 ;术后随访 3～ 17月 ,平均 6 5月。眼部检查 :经常规眼…     

隐匿性巩膜破裂伤病例分析

对于一些巩膜破裂性外伤，因其损伤部位靠后，球结膜完整或结膜小伤口已愈合、及救结膜下出血掩盖巩膜伤口，致直视检查不易发现，故称为“隐匿性巩膜破裂伤”。一旦漏诊将导致严重后果。现将我院近年来收治的14例报告如下：一般资料：1985年10月至1995年6月期间我院眼科共收治隐匿性巩膜破裂伤住院病人14例，占同期限外伤总住院人数的8．45％。其中男11例、女3例，均为单眼受伤，左眼8眼，右眼6眼，年龄最小20岁，最大52岁（平均引．34岁）。受伤患者中工人4例，农民6例，干部2例，职员1例，学生1例。致伤原因：锐器伤9例，其中锐利金属刺…     

隐匿性巩膜破裂的临床分析

目的　探讨隐匿性巩膜破裂的诊断要点及手术方法。方法　分析了 15例 (15眼 )隐匿性巩膜破裂的临床资料。结果　手术后视力提高 6眼 (4 0 0 0 % ) ,除 1眼行二期眼球摘除外 ,其余眼球得以保留 ,为以后争取复明提供了机会。结论　视力光感以下、低眼压、球结膜下大量出血、结膜水肿及前房积血为隐匿性巩膜破裂的诊断依据。眼球某一方向运动受限、眼球塌陷变形及角膜横形皱纹对诊断有重要的参考价值。对疑有巩膜破裂的患者早期行手术探查是避免漏诊和误诊的关键。     

隐匿性巩膜破裂伤的临床分析

隐匿性巩膜破裂伤因其伤口隐匿,临床上可能引起误诊或漏诊。我院1996年5月至2001年4月共收治10例(10眼)隐匿性巩膜破裂伤,经及时正确诊治,获得满意效果。现报告如下。 临床资料:本组共10例,男7例,女3例。右眼6例,左眼4例。年龄12～68岁,平均39.2岁。伤后就诊时间:最短半小时,最长6天。致伤原因:拳、掌击伤3例,车祸伤2例,工具崩伤3     

隐匿性巩膜破裂伤的临床分析

目的 探讨隐匿性巩膜破裂伤的诊断要点及手术方法。方法 回顾分析了１３例隐匿性巩膜破裂伤的临床资料。结果 视力进步５眼（３８．５％），除１眼二期行眼球摘除外，其余１２眼眼球得以保留，为以后争取复明提供了机会。结论 视力光感以下、球结膜水肿、结膜下大量出血、眼压低及前房积血为隐匿性巩膜破裂伤的诊断依据。眼球运动某一方向受限、眼球塌陷变形及角膜横形皱纹对诊断有重要的参考价值。对疑有巩膜破裂的患者早期行手     

隐匿性巩膜裂伤47例临床分析

目的:探讨隐匿性巩膜裂伤临床表现和手术方法方法:总结2000-05/2004-05因隐匿性巩膜裂伤而行手术治疗的47例(47眼),分析其致伤原因、临床表现、手术方法及结果。结果:术后视力≥0.05者20眼,视力<0.05者12眼,眼球萎缩10眼,眼球摘除5眼。结论:隐匿性巩膜裂伤主要由眼挫伤引起,应及时根据临床表现进行手术探查,缝合伤口,预防并发症发生。     

超声乳化人工晶状体植入术的临床研究

目的探讨超声乳化白内障摘出及人工晶状体植入术的方法、技巧及术中术后并发症的防治。方法对73例（78眼）白内障行超声乳化摘出及人工晶状体植入。结果术后1周矫正视力1．0以上51眼（65．7％），术后3月矫正视力1．0以上60眼（77％），0．5以上72眼（92％）。术中主要并发症为后囊破裂和虹膜损伤，术后为角膜内皮水肿。结论超声乳化术成功的关键在于手术者的手术方法和操作技巧。     

睫状上皮撕裂并发视网膜脱离的临床特点和手术疗效观察

目的探讨睫状上皮撕裂并发视网膜脱离的临床特点和手术疗效。方法回顾性分析16例（17只眼）睫状上皮撕裂并发视网膜脱离患者的临床资料,包括患者临床特征、治疗方法及病情转归。结果16例（17只眼）患者均有眼部钝挫伤史、睫状上皮撕裂并发视网膜脱离,均行巩膜外冷冻-硅胶外加压-环扎术,其中13只眼放视网膜下液,4只眼联合行玻璃体腔注气,术后视网膜全部复位,视力均有不同程度的提高。结论睫状上皮撕裂并发视网膜脱离多发生于眼球钝挫伤后,多位于鼻上象限,超声活体显微镜、前房角镜及间接检眼镜结合巩膜压迫法检查有利于诊断,巩膜扣带术治疗成功率高。     

反眉状隧道小切口白内障摘除人工晶体植入术在复明工程中的应用

目的了解开展反眉状隧道小切口白内障摘除人工晶体植入术在复明工程中的应用效果。方法2006～2007两年为复明工程收治白内障患者400例为治疗组,施行反眉状隧道小切口白内障摘除人工晶体植入术。结果本组病人随访,术后一周,矫正视力0.05～0.1者5眼,占1.25%;0.12～0.25者27眼,占6.75%;0.3～0.6者255眼,占63.75%;0.8～1.0者87眼,占21.75%;1.2～1.5者26眼,占6.5%。并发症有中、重度角膜水肿12眼（3%）;虹膜损伤10眼（2.5%）;角膜后弹力层脱离5眼（1.25%）;后囊膜破裂15眼（3.75%）。结论反眉状隧道小切口白内障摘除人工晶体植入术在复明工程中可以达到治盲脱残的目的。     

非穿透性小梁手术联合丝裂霉素及深层巩膜反折疗效观察

目的:观察非穿透性小梁手术联合丝裂霉素及深层巩膜反折引流治疗开角型青光眼的临床效果。方法:对14例(18眼)开角型青光眼患者进行非穿透性小梁切除手术,术中联合应用丝裂霉素C及深层巩膜反折引流。观察手术前、后的眼压、视力、视野、前房(前房角)变化及手术后滤过泡情况。随访3~18mo。结果:术前平均眼压(33.96±8.16)mmHg(1mmHg=0.133kPa),术后眼压为(14.62±3.53)mmHg,手术前后眼压差异有显著意义(t=11.82,P<0.01)。手术前、后视力及视野无明显改变。术后16眼均形成滤过泡,其中I型6眼,Ⅱ型11眼,Ⅲ型1眼。结论:非穿透性小梁切除联合应用丝裂霉素及深层巩膜反折引流术是治疗开角型青光眼的一种安全、有效、便宜和具有可重复性的新治疗方式。     

自体前板层角巩膜缘移植治疗角膜重度碱烧伤

目的:探讨自体前板层角巩膜缘移植治疗角膜周边部小面积重度碱烧伤的临床疗效及安全性。方法:对39例39眼角膜周边部小面积重度碱烧伤患者,行局部清创,切除病灶处前板层角膜及邻近板层巩膜、部分结膜,取健眼相对应处的前板层角巩膜及结膜移植,术后观察患者主观症状(疼痛、畏光、流泪)、视力、角膜上皮修复时间及复发情况,健眼的视力、伤口恢复及并发症。结果:术后随访2～12mo,所有患者角膜上皮全部愈合,患者主观症状恢复快,均未发生视力下降,无1例复发;健眼角巩膜缘伤口愈合良好,未出现并发症。结论:自体前板层角巩膜缘移植治疗角膜周边小面积重度碱烧伤,手术操作简单,可有效缩短角膜碱烧伤的愈合时间,促进角膜上皮修复,健眼(供体眼)恢复良好,无严重并发症发生。     

Pirenzepine affects scleral metabolic changes in myopia through a non-toxic mechanism

Whilst the precise mechanism regulating ocular growth is unknown, it has been shown that various pharmacological agents, including the muscarinic receptor antagonists, atropine and pirenzepine, are effective at preventing the development of myopia. A recent study, which demonstrated that muscarinic antagonists reduce the synthesis of glycosaminoglycans and DNA in chick sclera in vitro, led to the suggestion that such drugs may act directly on the sclera, possibly through a toxic mechanism. Accepted markers of scleral metabolism and cell viability were used in conjunction with a non-invasive, physiological method of ocular growth regulation to determine whether the selective muscarinic antagonist pirenzepine inhibits the development of myopia via toxicity to the sclera. Chicks were monocularly deprived (MD) of pattern vision and given daily intravitreal injections of either pirenzepine (700 microg) or saline vehicle into the deprived eye over 5 days. Unoccluded animals also received intravitreal injections of either pirenzepine or saline into one eye (n=6, all groups). The contralateral eye of all animals was left untreated for comparison. Optical and ocular biometric measures were collected on the final experimental day. Following in vivo delivery of [(35)S] labelled sulphate, levels of sulphate incorporation into scleral glycosaminoglycans were measured in proteinase K digests following selective precipitation with alcian blue dye. The DNA content was also assessed through luminescence spectrometry after binding to Hoechst 33258 dye. To allow comparison with an accepted non-invasive, physiological method of ocular growth regulation, myopia was prevented in additional groups of MD animals by allowing 3hr of unoccluded vision each day, over 5 days, before levels of sulphate incorporation were measured. Scleral DNA content, a marker of cell viability, was not significantly altered between treated and control eyes in any injected group. Relative levels of sulphate incorporation (% difference between treated and contralateral control eyes) were significantly lower in the cartilaginous sclera of pirenzepine-MD animals, compared to saline-MD controls (+35.9 +/- 10.1% vs +121.2 +/- 28.6%, P<0.05), after 2hr of incorporation. However, after 6hr incorporation, there was no significant difference in sulphate incorporation in the cartilaginous sclera between the two groups (+87.2 +/- 33.1% vs +111.0 +/- 14.4%, P=0.53). No significant change was found in the levels of glycosaminoglycan synthesis in the fibrous sclera of any pirenzepine treated group, when compared to the appropriate saline control. Relative patterns of sulphate incorporation, between treatment and control groups, were essentially identical at both time points examined, regardless of whether myopia was prevented through pirenzepine injection or periods of unoccluded vision. The present study shows that, at a dose of pirenzepine sufficient to prevent experimentally-induced axial myopia, glycosaminoglycan synthesis in the cartilaginous sclera was significantly reduced for a transient period following the injection. These pirenzepine-induced reductions in glycosaminoglycan synthesis were not caused by direct drug toxicity to scleral cells as these changes were reversible and no significant reduction in DNA content was observed in pirenzepine treated eyes. Similar patterns of scleral glycosaminoglycan synthesis changes were found following the provision of brief periods of unoccluded vision further demonstrating that pirenzepine is effective in myopia prevention via a non-toxic mechanism. Consequently, the prevention of myopia development in chicks, with either pirenzepine or brief periods of unoccluded vision, is associated with the transient modulation of scleral glycosaminoglycan synthesis in the cartilaginous sclera.     

Scleral changes in chicks with form-deprivation myopia

The sclera in myopic regions of chick eyes was studied histologically and compared to the sclera in corresponding regions of normal fellow eyes. Chicks had been monocularly deprived of form vision in the nasal half of the retina from hatching. The fellow control eye and the temporal retina of the deprived eye had normal vision. With this treatment, the resulting form-deprivation myopia and eye enlargement are restricted to the retinal region that had been form deprived. We found that the cartilaginous sclera in the myopic nasal region exhibited several differences from that in the corresponding non-myopic region: it was thicker, its cell density was lower, and the number of chondrocytes and binucleate cells was higher. In contrast, the fibrous sclera was thinner. These changes suggest that form-deprivation myopia causes an increased production of extracellular matrix and an increased level of mitotic activity in the cartilaginous sclera. As expected, the non-myopic temporal regions of experimental and control eyes did not differ in any of these parameters. The findings of the present study suggest that the eye enlargement accompanying form-deprivation myopia is not the consequence of scleral stretching but of abnormal growth.     

隱匿性鞏膜破裂傷的臨床分析

目的探討隠匿性鞏膜破裂傷的臨床診斷要點及手術方法.方法同顧分析了21例隱匿性鞏膜破裂傷的臨床資料.結果視力術後随訪半年～2年,視力0.1～04者3眼,0.02～0.1者7眼,眼前手動5眼,光感2眼,無光感4眼.1眼脱殘,20眼眼球保持了正常外形,1眼行二期眼球摘除外.結論視力光感以下、球結膜水腫、結膜下大量出血、眼壓低及前房積血爲隱匿性鞏膜破裂傷的診斷依據.眼球蓮動某一方向受限、眼球塌陷變形及角膜横形皺紋對診斷有重要的参考價值.對疑有鞏膜破裂的患者早期行手術探查是避免漏診和誤診的關鍵,視力無光感已不再作爲眼球摘除的唯一指徵,適時行玻璃體手術可以獲得較好效果.