晶状体、虹膜及脉络膜缺损、病理性近视合并白内障独眼患者手术治疗一例

患者,男,42岁,因“左眼视力下降并逐渐加重1年”收住入院。既往史：右眼失明30余年,病因不详。30年前左眼近视,30 年来至今度数逐渐缓慢增加。否认眼部手术及外伤史。父母非近亲婚配,否认家族遗传病史。入院时全身查体未见异常,专科检查：右眼视力无光感;左眼0.02,-13.0 DS=0.1;右眼眼压<5 mmHg（1 mmHg=0.133 kPa）,左眼眼压16 mmHg;右眼球萎缩,角膜变性,眼内结构窥不见;左眼角膜透明,前房深、清,虹膜无粘连;左眼6-7点位部分虹膜缺损,7点位根部见扁圆形全层孔,其面积约2 mm×1 mm;左眼瞳孔下移,呈倒梨型,直径4～5 mm,对光反应迟钝;晶状体核性混浊,其赤道部5-7点位有切迹样缺损,相应范围内悬韧带缺失;玻璃体及眼底窥不清（见图1）。眼部B超提示左眼后巩膜葡萄肿。入院诊断：左眼白内障;左眼晶状体缺损;左眼虹膜缺损;左眼脉络膜缺损;左眼病理性近视;右眼眼球萎缩。入院后患者行各项相关检查,在局麻下行“左眼白内障超声乳化摘除联合人工晶状体植入术”。     

先天性晶状体及虹膜缺损并发白内障一例

患者,男,47岁,维吾尔族,因右眼视力下降1年,加重1个月就诊.患者无眼部手术及外伤史,无其他疾病史,父母非近亲婚配,家族中无类似疾病史.患者发育正常,全身检查未见异常.眼部检查:视力:右眼0.02,左眼0.2,均不能矫正;眼压:右眼12.5 mmHg(1 mmHg=0.133 kPa),左眼13.5 mmHg.双眼外眼未见异常,结膜无充血,角膜透明,前房正常,瞳孔呈倒梨形.右眼6:00处虹膜缺损,左眼6:30处虹膜缺损.双眼晶状体混浊.散瞳后见右眼虹膜缺损处晶状体下方边缘呈切迹状缺损,该部位无悬韧带,其附近皮质较其他区域明显混浊;左眼虹膜缺损处晶状体皮质较其他区域明显混浊.右眼玻璃体及眼底均窥不清.左眼玻璃体轻度混浊,眼底未见明显异常.诊断:双眼并发性白内障;右眼先天性晶状体缺损;双眼先天性虹膜缺损.患者因个人原因,放弃进一步检查和治疗.     

长期视网膜脱离并脉络膜脱离的眼部表现

患者女性, 71岁。因右眼视物不清10余年, 加重1个月就诊。既往高度近视眼50余年。眼部检查:视力右眼为无光感, 左眼为0.4;眼压右眼为7 mmHg(1 mmHg=0.133 kPa), 左眼为15 mmHg;右眼球结膜充血, 角膜水肿, 角膜后大量结晶样沉积物, 前房深, 下方钙化物沉积(精粹图片1), 虹膜后粘连, 晶状体混浊, 其余窥不清;左眼晶状体混浊, 左眼视盘边界不清, 颞侧可见近视萎缩弧, 后极部视网膜可见巩膜露白, 黄斑中心凹反光未见。眼部B超检查:右眼360°脉络膜和视网膜脱离(精粹图片2)。临床诊断:右眼脉络膜脱离型视网膜脱离;双眼病理性近视眼。     

人工晶状体混浊置换术1例

1病例报告患者,男,74岁,于2009-03来我院,以“左眼视力下降2a”之主诉入院,入院诊断:左眼人工晶状体混浊,右眼义眼。患者于2001年在外院行左眼白内障摘除+人工晶状体植入术,术后视力恢复良好,近2a来视力逐渐下降;于1957年行右眼球摘除术(外伤原因);否认左眼部外伤史和全身疾病史。入院时眼部情况:左眼视力0.05。右眼上睑塌陷,结膜囊内置一义眼薄壳。左眼角膜清,前房(-),虹膜9∶30～11∶00缺损,瞳孔欠圆且向鼻上方轻度移位,约4mm×6mm,光反射存在,人工晶状体位正,呈灰白色致密混浊(图1),眼底窥不进。左眼B超提示眼轴22.9mm,人工晶状体眼,玻璃体混浊,视网膜平伏在位     

先天性双视乳头合并脉络膜与部分虹膜缺损一例

患儿男性, 8岁,自幼左眼视力不佳伴内斜视,近 6个月左眼视物不清,于 2003年 10月来我院就诊。患儿为第 3胎足月顺产。家族中无类似疾病,父母非近亲联姻。其母怀孕2至 4个月时曾多次发生上呼吸道感染。体检未见异常。眼部检查:右眼视力 0 4 , 戴 +1 25DS () 0 75DC×75°=0 7;左眼视力眼前手动。眼压:右眼 18 86mmHg(1mmHg=0 133kPa),左眼 13 35mmHg。左眼内斜 30°,外转轻度受限,水平性眼球震颤。双眼角膜透明。裂隙灯显微镜检查:可见左眼鼻下方虹膜部分缺损并有少许后粘连 (图 1),右眼瞳孔鼻下方部分虹膜缺损 (图 2 )。左眼晶状体…     

眼球摘除术后交感性眼炎一例

患者,男,74岁,因左眼球穿通伤缝合术后8年,疼痛、流泪3个月就诊。入院时检查：右眼视力4．8,左眼无光感;右眼晶状体轻度混浊,余未见异常。左眼球结膜睫状充血,角膜混浊、水肿,角膜内皮色素样KP,前房暗红色积血约5mm,虹膜可见新生血管,瞳孔不规则形,直径约2mm,后粘连,晶状体混浊,眼底窥不见。B型超声提示左眼球萎缩,有眼眼压16mmHg,左眼2mmHg（1mmHg=0．133kPa）。     

角膜外伤后眼内炎一例

患者,女,46岁,因左眼被黄豆崩伤视力下降2d入院.眼部检查：视力右眼0.8,左眼手动/眼前,左眼球结膜混合性充血,角膜颞下方可见长度4 mm全层裂伤,伤口稍隆起,已闭合,伤口处虹膜前粘连.角膜后沉着物（KP）（-）,前房轴深3个角膜厚度（CT）,前房无积脓,瞳孔直径约3 mm,对光反射消失.瞳孔区可见大片白色渗出物,隐见晶状体混浊,其后窥不入.右眼球前后段未见异常.眼压右眼15 mmHg（1 mmHg=0.133kPa）,左眼12 mmHg.眼眶SCT检查：未见球内异物.入院诊断：（1）左眼角膜挫裂伤.     

白内障摘除术中假驱逐性脉络膜上腔出血(附一例报告)

患者女87岁因左眼视力渐进性下降5年,加重2年,于2004年6月24日以左眼老年性白内障入院。既往高血压史30年,冠心病史6年。全身检查:血压130/70mmHg(1mmHg=0.133kPa),心电图示心肌缺血。眼科检查:视力右眼0.2,不能矫正:左眼眼前手动。右眼结膜、角膜、前房、虹膜、瞳孔检查均未见异常。晶状体核浅黄色混浊,眼底检查:视盘正常,动脉细,动脉壁反光强,动脉:静脉=1:2,黄斑区未能窥清。左眼晶状体核棕黄色混浊,眼底不能窥入,其余检查同右眼。右眼眼压20mmHg,左眼20mmHg。B超检查:左眼玻璃体内探及散在细小点状回声。左眼角膜内皮细胞计数3355/mm2…     

急性闭角型青光眼伴先天性小角膜、眼球震颤一家系

例1:先症者,女,30岁。因左眼红痛、视物模糊伴头痛、恶心3天于2004年10月7日入院。神志清楚,发育正常,体格检查未见异常。眼部检查:角膜映光正位,双眼眼球水平震颤,眼球运动未见异常。右眼视力:指数／60cm,结膜正常, 角膜透明,角膜直径8mm,前房普遍浅,周边1／5CT,虹膜纹理清,瞳孔3mm,光反应存在,晶状体核白色混浊,眼底未能窥入,眼压16mmHg。左眼视力:眼前手动,结膜混合充血,角膜上皮水肿,角膜直径8mm,前房普遍浅,周边<1／5CT,虹膜     

Rieger综合征二例

例1,男,23岁,因双眼视物模糊2年,胀痛近半年入院.入院检查:右眼视力0.12,眼压30.39 mmHg(1 mmHg＝0.133 kPa);角膜垂直径8.5 mm,水平径7.5 mm,前房轴深3 CT,瞳孔呈裂隙状移至9点位,虹膜根部与该处角膜前粘连,鼻侧虹膜有一5.5 mm×2 mm横椭圆形破孔,其余虹膜色淡,基质层可见组织稀薄及部分萎缩;晶状体混浊,眼底窥视不清.颞侧前房角虹膜前粘连,余各区均有不同程度的周边虹膜前粘连,部分Schwalbe线呈前突状;视野弥散缺损,不规则暗点.左眼视力手动,眼压50.62 mmHg,角膜水肿,垂直径8.5 mm,水平径8.0 mm,12点虹膜根部"V"字形破孔,颞侧虹膜有5.8 mm×3.5 mm破孔.患者面部鼻梁扁宽,面颊平坦,下颌前突.牙齿尖小,齿缝宽.肚脐皮肤残留长7 mm.无类似病家族史.入院诊断:(1)双眼Rieger综合征.(2)双眼继发性青光眼.入院药物治疗后,眼压右眼17.30 mmHg,左眼28.01 mmHg.左眼在局部麻醉下行小梁切除术+MMC,术后眼压7.10 mmHg.右眼药物保守治疗,随访观察眼压.     

Thick corneas,large pupils,and a giant problem

An 87-year-old woman presented 1 month after uneventful cataract surgery with ipsilateral corneal edema. She was diagnosed with pseudophakic bullous keratopathy and scheduled for endothelial transplantation. A few days later, however, she presented with bilateral corneal edema, dilated pupils, and further reduction of visual acuity. Neuro-ophthalmic evaluation disclosed a bilateral ocular ischemic syndrome causing complete visual loss. Temporal artery biopsy was consistent with giant cell arteritis. Corneal decompensation should be considered as a rare presentation of giant cell arteritis, a diagnosis that ophthalmologists should suspect in any case of unilateral or bilateral ocular ischemic syndrome.     

Destructive ophthalmic procedures,a comparison between a developed and a developing country

Summary The causes for enucleation, evisceration, and exenteration were compared between Malawi and Israel. Differences in etiology, age, and sex were found due to the medical facilities, standard of living, and cultural background of each country.     

Cytokines and uveitis, a review.

Although the exact pathogenic mechanisms underlying uveitis are unknown, cytokines appear to be involved in this inflammatory disorder. This review describes the studies in which the uveitogenic properties of several cytokines, including tumor necrosis factor (TNF), interleukin 1 (IL-1), IL-6, IL-8 and interferon gamma (IFN-gamma), were investigated and the reports on intraocular expression of cytokines, such as TNF, IL-2, IL-6 and IFN-gamma, during uveitis. The exact contribution of these mediators to uveitis remains to be determined. This may provide new clues in the treatment of uveitis.     

Pseudoxanthoma elasticum: a clinical,histopathological, and molecular update

Pseudoxanthoma elasticum is an autosomally inherited disorder that is associated with the accumulation of mineralized and fragmented elastic fibers in the skin, Bruch's membrane in the retina, and vessel walls. The ophthalmic and dermatologic expression of pseudoxanthoma elasticum and its vascular complications are heterogeneous, with considerable variation in phenotype, progression, and mode of inheritance. Using linkage analysis and mutation detection techniques, mutations in the ABCC6 gene were recently implicated in the etiology of pseudoxanthoma elasticum. ABCC6 encodes the sixth member of the ATP-binding cassette transporter and multidrug resistance protein family (MRP6). In humans, this transmembrane protein is highly expressed in the liver and kidney. Lower expression was found in tissues affected by pseudoxanthoma elasticum, including skin, retina, and vessel walls. So far, the substrates transported by the ABCC6 protein and its physiological role in the etiology of pseudoxanthoma elasticum are not known. A functional transport study of rat MRP6 suggests that small peptides such as the endothelin receptor antagonist BQ123 are transported by MRP6. Similar molecules transported by ABCC6 in humans may be essential for extracellular matrix deposition or turnover of connective tissue at specific sites in the body. One of these sites is Bruch's membrane. This review is an update on etiology of pseudoxanthoma elasticum, including its clinical and genetic features, pathogenesis, and biomolecular basis.     

Corneal biopsy. Indications, techniques, and a report of a series of 87 cases

Corneal biopsy can be an effective aid in establishing diagnoses in a variety of infections, dystrophic and degenerative conditions, corneal manifestations of systemic diseases, and drug-induced changes. Preoperative planning and proper preparation of the tissue are stressed. In a series of 87 cases, the indications for biopsy were ulcerative keratitis in 42 cases, nonulcerative lesions in 25 cases, dystrophic and degenerative processes in 15 cases, and corneal manifestations of systemic diseases in 5 cases. Of the 42 cases of ulcerative keratitis, the presence of bacteria, fungi, and Acanthamoeba organisms was excluded in 33 instances (79%). Organisms observed in 9 (21%) of the 42 ulcerative cases included 4 with bacteria, 3 with fungi, and 1 each with Acanthamoeba organisms and virus.