玻璃体腔内注射曲安奈德治疗黄斑水肿的疗效探讨

目的:观察玻璃体腔注射曲安奈德治疗黄斑水肿的疗效。方法:对38例(40眼)黄斑水肿患者行玻璃体腔内注射曲安奈德后定期随访6mo,观察治疗前后视力、眼压及眼底FFA黄斑区改变情况。结果:全部患者玻璃体腔内注射曲安奈德后视力比术前提高,黄斑水肿消退或减轻。结论:玻璃体腔内注射曲安奈德可消除黄斑水肿,提高视力,但一过性高眼压及远期效果有待进一步研究     

玻璃体腔注射曲安奈德治疗白内障术后黄斑囊样水肿疗效观察

目的:观察玻璃体腔注射曲安奈德(triamcinoloneacetonide,TA)治疗白内障术后黄斑囊样水肿(cystoid macular ede-ma,CME)的疗效。方法:对21例22眼经间接检眼镜、荧光素眼底血管造影(FFA)以及光学相干断层扫描(OCT)检查确诊的CME患者行TA玻璃体腔注射,治疗后随访0.5a,对比分析术前术后不同时期的视力、眼底、FFA表现,观察OCT显示黄斑水肿高度。结果:术前视力平均0.25±0.23,术后3mo平均0.58±0.27,差异有显著性(P<0.01);经OCT随访检查,术后所有病例患眼黄斑中心凹厚度均有下降,术前平均为(482.37±102.54)μm,术后3mo平均为(205.46±113.35)μm,差异有显著性(P<0.01)。结论:玻璃体腔注射TA是一种安全有效的治疗白内障术后黄斑囊样水肿的方法。     

玻璃体腔注射曲安奈德联合激光治疗视网膜黄斑分支静脉阻塞黄斑水肿

目的:观察玻璃体腔注射曲安奈德(triamcinolone ace-tonide,TA)联合激光治疗视网膜黄斑分支静脉阻塞黄斑水肿的临床疗效。方法:将经过视力、眼压、眼底检查、眼底彩色照相、荧光素眼底血管造影(FFA)、光相干断层扫描(OCT)检查确诊的164例164眼视网膜黄斑分支静脉阻塞伴黄斑水肿患者纳入治疗。男90例90眼,女74例74眼,年龄20～80(平均59.7)岁。矫正视力0.02～0.6,logMAR视力为0.778±0.347。病程3d～2a。平均眼压15.22mmHg(1mmHg=0.133kPa)。FFA检查黄斑区晚期均有荧光素蓄积;OCT示平均黄斑中心凹视网膜厚度442.41±74.07μm。表面麻醉下给予4mgTA玻璃体腔注射,2wk后进行黄斑区光凝治疗。治疗后第1,3,6mo随访。结果:164例患者治疗后1,3,6mo的平均logMAR最佳矫正视力(BCVA)分别提高至0.49±0.34,0.44±0.34,0.43±0.33,与治疗前比较,差异均有统计学意义。治疗后6mo视力提高135眼(82.3%),其中视力提高≥2者103眼(62.8%);治疗后1,3,6moFFA检查黄斑区晚期荧光素蓄积均有减轻或消失,治疗后1,3,6mo,OCT检查平均黄斑中心凹视网膜厚度分别为253.99±63.99μm,239.84±53.74μm,234.55±51.32μm;与治疗前比较,差异均有统计学意义。治疗后6mo,黄斑水肿改善者147眼(89.6%)。玻璃体腔注药后3d之内有4眼发生假性眼内炎,观察及治疗后恢复至可行激光治疗,治疗后3mo时有11眼眼压高于正常,用药后均恢复至正常范围。结论:玻璃体腔注射TA联合激光治疗视网膜黄斑分支静脉阻塞引起的黄斑水肿疗效较好,明显提高视力,改善视功能,促使黄斑水肿消退或减轻。     

玻璃体腔注射不同药物联合激光治疗视网膜静脉阻塞合并黄斑水肿的疗效比较

目的:观察和分析玻璃体腔注射曲安奈德或康柏西普联合激光治疗视网膜静脉阻塞合并黄斑水肿的疗效.方法:视网膜静脉阻塞合并黄斑水肿患者50例50眼,分为两组,分别注射曲安奈德和康柏西普,术后7d眼底激光对黄斑区进行局部光凝或格栅样光凝,分别在注药术后14d,1、3mo行最佳矫正视力、眼压、眼底检查、光学相干断层扫描检查,术后3 mo行荧光素眼底血管造影检查,将各组各时间点术后检测结果与术前值进行比较,做出客观评价.结果:两种治疗方式与治疗前相比,在注药术后14d,激光治疗后1、3 mo视力均有不同程度的提高,其中曲安奈德组视力提高者分别为76%、80%、68%,康柏西普组视力提高者分别为88%、92%、88%;两组治疗方式在各个时间段最佳矫正视力均有不同程度的提高,治疗后1 mo最佳矫正视力最好;与术前相比,两组治疗方式黄斑区厚度均有不同程度地降低,术前、术后14d,1、3mo黄斑区平均视网膜厚度曲安奈德组分别为557.5±150.9、301.7±120.1、262.7±131.2、338.1±146.5μm,术前黄斑区厚度与术后有显著差异性,康柏西普组分别为569.4±135.9、282.3±133.5、259.5±116.4、307.8±122.6μm,术前黄斑区厚度与术后有统计学差异.结论:曲安奈德或康柏西普玻璃体腔注射联合激光治疗视网膜静脉阻塞合并黄斑水肿疗效好,但康柏西普治疗效果更优、更安全、更有效.     

玻璃体腔内注射曲安奈德治疗糖尿病性弥漫性黄斑水肿

目的:观察玻璃体腔内注射曲安奈德治疗糖尿病性弥漫性黄斑水肿的疗效。方法:经检眼镜、光相干断层扫描及荧光素眼底血管造影检查证实的糖尿病性弥漫性黄斑水肿患者25例(25眼),玻璃体腔内注射40g/L的曲安奈德0.1mL,随访6mo,对比观察治疗前后视力、眼压及黄斑区视网膜厚度变化。结果:治疗后1,3,6mo,平均视力分别为0.20±0.15,0.35±0.20,0.21±0.18,与治疗前的0.08±0.04相比,其差异具有统计学意义;黄斑区视网膜厚度分别为360.7±50.2,263.2±60.1,313.5±86.4μm,与治疗前的463.4±105.1μm相比,其差异具有统计学意义。结论:玻璃体腔内注射曲安奈德治疗糖尿病性弥漫性黄斑水肿短期内能有效改善黄斑水肿,提高视力,但其长期疗效和安全性需进一步研究。     

TA联合激光治疗视网膜静脉阻塞黄斑水肿的临床观察

目的:观察玻璃体腔内注射曲安奈德联合激光光凝治疗视网膜静脉阻塞引起的黄斑水肿的有效性和安全性。方法:患者38例38眼经眼底镜检查、眼底荧光素血管造影(fundus fluorescein angiography,FFA)及光学相干断层扫描(optical coherence tomography,OCT)检查明确诊断的视网膜静脉阻塞引起的黄斑水肿,玻璃体腔内注入曲安奈德4mg(0.1mL),术后1～2mo时行视网膜激光光凝,随访3～9mo,观察视力、眼压、眼底情况及视网膜厚度变化。结果:视力提高36眼,视力无变化2眼。视力<0.1者3眼,0.1～0.3者11眼,0.3～0.5者17眼,>0.5者7眼。4例患者眼压不同程度升高,予以局部降眼压药物治疗后,术后2～5mo眼压恢复正常,未发生1例视网膜毒性反应。结论:曲安奈德联合激光可以安全、有效治疗视网膜静脉阻塞引起的黄斑水肿,提高患者视功能。     

曲安奈德玻璃体腔注射治疗视网膜分支静脉阻塞继发黄斑水肿

目的:观察玻璃体腔注射曲安奈德(tviamcinolone ace-tonide,TA)治疗视网膜分支静脉阻塞(branch retinal vein occusion,BRVO)继发黄斑水肿的疗效。方法:经眼底检查、荧光眼底血管造影(FFA)、光学相干断层扫描(OCT)检查确诊的BRVO继发黄斑水肿22例(22眼)行玻璃体腔曲安奈德注射,治疗后随访(4.2±0.4)mo,对比治疗前及治疗后1,3mo视力、眼压、眼底、FFA表现、OCT所显示黄斑水肿高度以及黄斑中心凹阈值。结果:治疗的22眼中19眼(82%)视力明显提高,3眼(14%)视力不变,治疗前平均视力0.10±0.06,治疗后1,3mo平均视力分别为0.25±0.12、0.28±0.13,黄斑中心凹厚度(OCT)治疗前平均厚度(519.0±137.5)μm,治疗后1,3mo平均厚度分别为(256.4±68.3)μm、(239.4±52.2)μm,黄斑中心凹阈值(dB):治疗前(18.8±4.2)dB,治疗后1,3mo分别为(24.0±6.0)dB、(24.6±5.2)dB,治疗前后比较差异有统计学意义(P<0.01)。22眼中有6眼(27%)治疗后暂时性眼压升高,经局部抗青光眼药物治疗后恢复正常。5例(23%)患者2次注药。结论:玻璃体腔注射TA在短期内可有效改善BRVO继发黄斑水肿,但也要注意对原发病治疗。     

曲安奈德眼内注射联合格栅样光凝治疗视网膜静脉阻塞黄斑囊样水肿短期疗效观察

目的:观察曲安奈德玻璃体腔注射联合黄斑区格栅样光凝治疗视网膜静脉阻塞黄斑囊样水肿的效果.方法:视网膜静脉阻塞合并黄斑囊样水肿的患者40例40眼,其中治疗组20例20眼给予曲安奈德2mg玻璃体腔注射,lwk后行黄斑区格栅样光凝治疗;另外对照组20例20眼行单纯曲安奈德2mg眼内注射.通过OCT测量黄斑区视网膜的厚度以分析治疗前后黄斑囊样水肿的吸收情况和视力的改善情况.结果:治疗组患者治疗前黄斑区视网膜平均厚度为412.67±133.04μm,治疗后3mo为281.63±59.39μm;对照组治疗前黄斑区视网膜的平均厚度为409.58±131.96μm,治疗后3mo为358.72±116.17μm,治疗后两组患者间黄斑区的视网膜厚度变化差异有统计学意义(t=8.97,P=0.003 ＜0.05).治疗组3mo后有4眼患者黄斑囊样水肿复发,再次行曲安奈德眼内注射;对照组3 mo后有12眼黄斑水肿复发,再次行眼内曲安奈德注射治疗.卡方检验比较两组患者间复发病例,差异有统计学意义(x2=6.50,P=0.022＜0.05).结论:曲安奈德玻璃体腔注射联合黄斑区格栅样光凝治疗静脉阻塞黄斑囊样水肿疗效显著,患者视力有所提高,并且较少复发.     

玻璃体腔注射曲安奈德治疗糖尿病性视网膜病变引起的弥漫性黄斑水肿

目的:通过对糖尿病性视网膜病变引起的弥漫性黄斑水肿患者玻璃体腔注射曲安奈德,以减轻黄斑部水肿,增进视力.方法:选择视网膜静脉阻塞患者13例17眼,向玻璃体腔注射曲安奈德4mg/0.1mL,术前、术后及术后,1,2,3,6mo分别进行最佳矫正视力、OCT、HRT-Ⅱ检查.结果:术后6mo各随访时间点平均视力均较术前显著提高(P＜0.001),术后6mo与术后3mo比较,视力显著回退(P=0.033);术后6mo内黄斑中心凹1mm范围内神经感觉层平均厚度与术前比较,显著降低(P＜0.001),术后6mo较术后3mo有显著增厚(P=0.001);术后3mo各随访时间点e值较术前显著降低(P=0.000).结论:玻璃体腔注射曲安奈德在短期内能够有效减轻由糖尿病性视网膜病变引起的弥漫性黄斑水肿,恢复视力,但随后疗效会逐渐减退.     

玻璃体腔注射Bevacizumab(Avastin)治疗湿性ARMD临床观察

目的:观察玻璃体腔注射bevacizumab(avastin)治疗湿性年龄相关性黄斑变性(age-related macular degeneration,ARMD)的疗效和安全性。方法:对22例22眼湿性ARMD患者行玻璃体腔注射bevacizumab1.25mg,间隔6wk再注射1次,第12wk对检查发现黄斑区水肿或渗漏明显的再注射1次。随访6mo,术后第1wk;1,3,6mo行视力、眼压、裂隙灯、间接检眼镜及光学相干断层扫描(optical coherence tomography,OCT)检查,第3,6mo行荧光素眼底血管造影(fundusfluorescence angiography,FFA)、彩色眼底照相检查,分析治疗前后患者平均视力及黄斑中心视网膜厚度(centralmacular thickness,CMT)的改变。结果:至第6mo随访,平均视力较治疗前有所提高,平均CMT比治疗前减少92.59μm,均有显著意义;FFA显示黄斑区渗漏均消失或明显减轻。除4例局部球结膜下出血,没有观察到其他不良反应。结论:玻璃体腔注射bevacizumab能够提高湿性ARMD患者的视力,减轻黄斑水肿;重复注射可以巩固疗效,减少复发。长期效果和安全性还需要更多病例和更长随访观察时间来评估。     

米诺环素对糖尿病视网膜病变的作用机制研究进展

糖尿病视网膜病变（ｄｉａｂｅｔｉｃｒｅｔｉｎｏｐａｔｈｙ,ＤＲ）是糖尿病最常见且最严重的眼部并发症之一,现已成为２０～７４岁人群致盲的首要原因。其病理改变主要包括早期的神经细胞凋亡以及后期新生血管形成。米诺环素作为一种半合成四环素类抗生素,除了具有抗菌、抗炎症反应外还有抗新生血管、保护神经细胞的作用,越来越多的研究着重于米诺环素对ＤＲ的抑制作用,本文通过文献回顾,对米诺环素抑制ＤＲ的作用机制及研究进展进行综述,并对米诺环素在ＤＲ的研究方向进行展望。     

眼位对主动追踪效果的实验影响

目的研究眼位对主动追踪效果的影响。方法以金属环模拟虹膜及瞳孔,其上置3.5 mm厚透明PMMA板模拟角膜,将该模拟装置置于MEL-70准分子激光主动追踪系统下,分别标记模拟装置在中央位置及位置偏移5 mm及10 mm后主动追踪系统所指示切削中心位置,观测两种位置偏移引起的追踪效果偏差量。结果偏差量分别为0.15mm及0.25 mm。结论眼位对主动追踪有影响,这种影响对常规屈光手术是可接受的,对高阶像差的影响则不容忽视。     

屈光不正对微扫视性眼球运动的影响

目的观察屈光不正对人眼微扫视性眼球运动的影响。方法前瞻性病例对照研究。收集2010年10月至2011年3月在天津市眼科医院就诊的屈光不正患者17例和无屈光不正的受试者17例,按照屈光状态与眼别进行分组。屈光不正者未戴镜矫正条件下17只主导眼为ADa组,17只非主导眼为ANa组;屈光不正者戴镜矫正条件下17只主导眼为ADb组,非主导眼为ANb组;正常受试者主导眼为ND组,非主导眼为NN组。采用高速眼球运动记录系统对受试者双眼分别进行注视性眼球运动记录。采用自编的Matlab程序对微扫视性眼球运动成分进行识别、提取和分析。对各组微扫视幅度、峰值速度、发生频率、微扫视间隔时间等量化指标的组间比较采用单因素方差分析（ANOVA）,两两比较采用Turkey检验,以P〈0．05为差异有统计学意义。结果6组间平均微扫视幅度的差异无统计学意义,但ADa组（5．42％±0．26％）、ANa组（5．48％±0．25％）较ADb组、ANb组、ND组、NN组幅度变异度大,差异有统计学意义（F=38．67,P〈0．01）;ADa组[（55．25±2．40）°／s]、ANa组[（54．51±1．77）°／s]微扫视峰值速度较ADb组、ANb组、ND组、NN组小（F=311．84,P〈0．01）;ADa组[（1．56±0．03）Hz]、ANa组[（1．57±0．05）Hz]微扫视发生频率较ADb组、ANb组、ND组、NN组低（F=155．25,P〈0．01）;ADa组[（558±23）ms]、ANa组[（555±22）ms]微扫视间隔时间较ADb组、ANb组、ND组、NN组长（聘102．12,P〈0．01）;屈光不正者戴镜或不戴镜及正常受试者主导眼与非主导眼比较,各项指标差异无统计学意义。屈光不正者戴镜条件下与正常受试者比较,各项指标差异也无统计学意义。结论屈光不正可影响人眼微扫视性眼球运动的行为,表现为微扫视幅度变异度增加、峰值速度降低、发生频率降低及微扫视间隔时间延长。戴镜可矫正屈光不正患者微扫视的异常。     

ET-1的眼科研究进展

内皮素1(ET-1)是体内已知的作用力最强、持续时间最长的缩血管肽,目前在眼科有了较广泛深入的研究,本文就其在糖尿病视网膜病变等眼底疾病、青光眼、角膜疾病中的作用研究作一阐述.     

改良型抗青光眼滤过手术疗效观察

目的:探讨改良型抗青光眼手术的临床疗效。方法:2004-01/2006-01在我科住院的双眼慢性闭角型青光眼20例40眼,每位患者一侧眼行传统的小梁切除虹膜周切术(传统术),另一侧行改良型抗青光眼手术(改良术),将两组疗效对照,随访观察18mo以上。结果:改良术组远期眼压控制与传统术组相比,P<0.05,具有统计学差异。结论:改良型抗青光眼手术是常用抗青光眼手术的联合,较易掌握,且远期疗效较理想。     

红细胞增多症影响早产儿视网膜病变的临床观察

目的 观察红细胞增多症对早产儿视网膜病变(ROP)的影响.方法 回顾分析262例早产儿的临床资料.患儿中红细胞增多症46例,占17.56%;其中,男性27例,女性19例.无红细胞增多症216例,占82.46%;其中,男性155例,女性61例.有无红细胞增多症两组患儿在出生体重(t=0.730,P=0.466)、胎龄(t=1.603,P=0.110)、吸氧人数(χ1=0.04,P>0.90)、吸氧时间(t=1.225,P=0.223)、吸氧浓度(t=1.823,P=0.071)之间比较,差异均无统计学意义.所有受检早产儿均由有经验的服科医生采用双目间接检眼镜检查眼底,确定有无ROP并进行分期.回顾分析时,着重分析有无红细胞增多症与ROP发生和分期之间的相互关系.结果 262例早产儿中发生ROP 120例,占45.80%.其中,红细胞增多症组发生ROP 25例,占红细胞增多症患儿的54.34%;无红细胞增多症组发生ROP 95例,占无红细胞增多症患儿的43.98%.有无红细胞增多症两组ROP发生率比较,差异无统计学意义(χ2=1.64,P>0.1).120例ROP患儿中,ROP<3期者104例,占86.67%;≥3期者16例,占13.33%.25例发生ROP的红细胞增多症患儿中,ROP<3期者18例,占发生ROP的红细胞增多症患儿的72.00%;≥3期者7例,占发生ROP的红细胞增多症患儿的28.00%.95例发生ROP无红细胞增多症患儿中,ROP<3期者的86例,占发生ROP的无红细胞增多症患儿的90.53%;≥3期者9例,占发生ROP的无红细胞增多症患儿的9.47%.有无红细胞增多症两组间在<3期和≥3期ROP发生率之间比较,差异有统计学意义(x2=4.38P<0.05).120例ROP患儿中,阈值前病变106例,占88.33%;阈值及以上病变14例,占11.67%.25例发生ROP的红细胞增多症患儿中,阈值前病变19例,占发生ROP的红细胞增多症患儿的76.00%;阈值及以上病变6例,占发生ROP的红细胞增多症患儿的24.00%.95例发生ROP无红细胞增多症患儿中,阈值前病变87例,占发生ROP的无红细胞增多症息儿的91.58%;阈值及以上病变8例,占发生ROP的无红细胞增多症患儿的8.42%.有无红细胞增多症两组间阈值前病变和阈值及以上病变ROP发生率比较,差异无统计学意义(χ2=3.27,P>0.05).结论 红细胞增多症不影响ROP发生率,但可能影响ROP的严重程度.     

Studies on the mechanism of action of timolol and on the effects of suppression and redirection of aqueous flow on outflow facility

Long-term use of drugs that suppress aqueous humor formation, such as timolol and dorzolamide, or that redirect aqueous humor outflow from the trabecular meshwork, such as prostaglandin F2alpha analogues, could cause underperfusion of the trabecular meshwork and a secondary decrease in outflow facility. We investigated the mechanism of suppression of aqueous humor formation by timolol in monkey eyes by measuring aqueous humor ascorbate levels. We also determined whether suppression of aqueous humor formation with and without redirection of aqueous humor away from the trabecular meshwork could lead to a subsequent reduction in outflow facility, and whether this reduction was correlated with increased fibronectin levels in anterior chamber aqueous humor. In cynomolgus monkeys, unilateral dose/aqueous humor formation response curves were generated for timolol, dorzolamide, and a combination of timolol + dorzolamide. Aqueous humor formation and/or outflow facility were measured in both eyes after approximately four days, four weeks and seven weeks of twice daily treatment with 3.5 microg timolol + 1.0 mg dorzolamide to one eye and 30% DMSO to the other. In some monkeys, 5 microg prostaglandin F2alpha-isopropyl ester (PG) was added to timolol + dorzolamide for 4-week treatments. Intraocular pressure and corneal endothelial transfer coefficients (k(a)) were also measured at four weeks. Aqueous humor fibronectin levels were determined in four monkeys after approximately 9.5 weeks of timolol + dorzolamide treatment. Aqueous humor formation, intraocular pressure, and aqueous humor ascorbate levels were also determined in rhesus monkeys at baseline and after a single unilateral topical administration of 25 microg timolol. Compared to baseline for the same eye, aqueous humor formation was significantly decreased in treated eyes at all doses of timolol and at 1.8 and 4 mg dorzolamide. Compared to the opposite control eye, aqueous humor formation was lower in treated eyes after 3.5 and 5 microg timolol and after all doses of dorzolamide. Aqueous humor formation after treatment with 3.5 microg timolol + 1.0 mg dorzolamide was decreased in treated vs. control eyes, after four days and was suppressed in both treated and control eyes after four weeks of treatment, but not when PG was added. There was no difference in k(a) values with or without the addition of PG. Intraocular pressure was significantly lower in both treated and control eyes vs. baseline after approximately 6.5 weeks treatment with timolol + dorzolamide when taken 2 hr after the last dose and after approximately 3.5 weeks treatment with timolol + dorzolamide + PG when measured 6 hr after the last dose. Outflow facility after treatment with timolol + dorzolamide was unchanged after four days, tended to be lower in the treated vs. control eyes after four and seven weeks, and was significantly lower in treated vs. control eyes after four weeks treatment with timolol + dorzolamide + PG (0.352 +/- 0.052 vs. 0.515 +/- 0.096 microl min(-1) mmHg(-1), p < or = 0.02). Both treated vs. control eye aqueous humor fibronectin levels were below the level of detection for our assay (0.01 microg ml(-1)). The 25 microg timolol dose decreased ipsilateral, but not contralateral intraocular pressure (12.6 +/- 1.7 vs. 15.2 +/- 0.9; p < 0.05) and aqueous humor formation (1.40 +/- 0.08 vs. 2.03 +/- 0.09 microg ml(-1), p < or = 0.01). There was no difference in anterior chamber ascorbate levels in treated vs. control eyes or compared to their respective baselines. Our findings indicate that timolol affects neither ciliary epithelial transport of ascorbate nor aqueous fibronectin levels. Our data also indicate that decreasing aqueous humor formation over a period of time can lead to reduction in outflow facility, particularly when combined with therapy that redirects aqueous from the trabecular meshwork. Future intraocular pressure-lowering therapies for glaucoma may better be directed at enhancing flow through the trabecular pathway as opposed to decreasing aqueous humor formation or rerouting aqueous humor away from the trabecular meshwork.     

Exoerimental Study on the Effect of Perfluorodecalin on Rabbit Corneas

Purpose: To study the effects of perfluorodecalin on the cornea of the rabbit eyes. Methods: Perfluorodecalin (0. 05 ml/each) was injected into the anterior chambers of eighteen rabbit eyes. Corneal morphology and endothelial cells were monitored clinically by slit-lamp biomicroscope and specular microscope for 26 weeks. Animals were sacrificed in 1st, 2nd, 4th, 10th, 16th, 22nd, and 26th week after injection, respectively, and the corneas were examined under the light microscope.Results: Perfluorodecalin droplets looking like "fish eggs" were found at about 1 /4 ~ 1/2 of the corneal height in the inferior anterior chamber. Corneal opacification on the area contacted with perfluorodecalin was observed in five eyes five weeks after injection, and all in the 22nd week. Mutton fat KPs in one eye were seen in the 6th week firstly, and in all eyes in the 7th week. Corneal pannus formation in one eye was present in the 4th week, two eyes in the 5th week and three eyes in the 6th week. Retrocorneal fibrous me     

Assessment of the quality of information on treatment of keratoconus on YouTube

International Ophthalmology - To evaluate the reliability, quality and effectiveness of YouTube videos addressing treatment of keratoconus. This is a retrospective, cross-sectional and...     

干眼对生活质量影响的相关研究进展

干眼是一种日益严重的公共卫生问题,临床常见的干眼引起的眼部不适包括眼部干涩、视疲劳、眼异物感、烧灼感及畏光等,进一步可导致视觉损害和对比敏感度降低.这些不适很大程度上影响了干眼患者的身体功能、社会功能、心理功能、日常活动及工作生产力等情况.但干眼的视觉障碍对患者生活质量的影响不易量化,本文中笔者结合现有相关文献,对干眼视觉障碍的评估方法 及其对生活质量的影响进行综述.旨在为临床工作提供指导.