视网膜中央动脉阻塞选择性溶栓与常规治疗前后眼底荧光血管造影对比

目的 通过对比选择性眼动脉溶栓及传统常规治疗视网膜中央动脉阻塞.治疗前后眼底荧光血管造影,了解两种治疗方法对视网膜中央动脉血供改善效果.方法 收集病人为非随机对照,根据患者是否同意溶栓或有溶栓禁忌证分为介入溶栓组及常规治疗组,记录所有患者年龄、性别、全身病、发病到治疗时间、患眼眼底检查、治疗前眼底荧光血管造影、治疗48h及1月后的眼底及荧光血管造影结果.对比治疗前后荧光血管造影臂-视网膜显影时间、视网膜动-静脉显影时间.结果 溶栓治疗组发病时臂-视网膜显影时间及视网膜动-静脉显影时间明显延长分别为(28.76±6.81)s及(40.44±8.48)s,治疗48h及1m后复查显示臂-视网膜显影时间(15.36±4.03)s和(15.84±3.42)s,视网膜动-静脉显影时间(22.28±4.63)s和(21.72 4±3.55)s,与治疗前对比显著缩短,差异有统计学意义.常规治疗组发病时臂-视网膜显影时间及视网膜动一静-脉显影时间亦明显延长分别为(29.81±6.08)s及(38.33±7.41)s,治疗48h后臂-视网膜显影时间及视网膜动-静脉显影时间(29.19±6.27)s及(37.85±7.79)s,与治疗前对比差异无统计学意义,治疗1月后臂-视网膜显影时间及视网膜动-静脉显影时间(24.38±6.69)s及(33.56±6.43)s,较治疗前缩短差异有统计学意义,但仍较溶栓组显影时间延长.眼底检查1月复查时均出现视网膜神经纤维层及视盘不同程度萎缩,但常规治疗组损害更重.结论 选择性眼动脉溶栓治疗视网膜中央动脉阻塞可较常规治疗方法更及时有效恢复视网膜血供,缩短眼底荧光血管造影的臂-视网膜显影及视网膜动-静脉充盈时间,但即使迅速恢复了视网膜中央动脉血供,仍可会出现视网膜神经组织不同程度的组织形态学损害.     

视网膜中央动脉阻塞介入溶栓治疗前后视网膜组织形态学改变

目的通过对视网膜中央动脉阻塞患者行选择性眼动脉溶栓治疗,观察治疗前后眼底彩照、荧光血管造影及黄斑OCT改变,了解溶栓前后视网膜组织形态学改变。方法收集在我科行选择性眼动脉溶栓治疗的视网膜中央动脉阻塞患者17例,溶栓前、溶栓后48h行眼底彩照、黄斑OCT及眼底荧光血管造影检查,记录溶栓前、溶栓后48h眼底荧光血管造影后臂-视网膜显影时间及视网膜动-静脉显影时间;术后1个月复查眼底彩照和OCT改变。结果患眼溶栓前及溶栓后48h,OCT显示黄斑明显增厚,黄斑中心凹平均厚度分别为(265.00±105.93)μm及(269.00±99.04)μm,与对侧健眼的(161.00±18.06)μm相比,差异有显著统计学意义(均为P<0.01);治疗后1个月黄斑变薄,黄斑中心凹平均厚度为(139.00±34.11)μm,与治疗前、治疗后48h及对侧健眼比较差异有统计学意义。眼底彩照显示,溶栓前视网膜中央动脉明显变细,后极部视网膜灰白色水肿,黄斑樱桃红;溶栓后48h视网膜中央动脉血流恢复,视网膜水肿仍同前;溶栓后1个月,视网膜水肿逐渐减轻,但视盘及视网膜神经纤维层出现不同程度萎缩。眼底荧光血管造影示溶栓前臂-视网膜动脉显影时间及视网膜动-静脉显影时间明显延长,分别为(30.65±7.11)s及(39.82±7.06)s;溶栓后48h则显著缩短,分别为(14.58±2.79)s及(22.76±4.84)s,溶栓前后差异均有显著统计学意义(均为P<0.01)。结论选择性介入溶栓治疗视网膜中央动脉阻塞,可及时有效恢复视网膜血供,缩短臂-视网膜显影及视网膜动-静脉充盈时间,但即使迅速恢复了视网膜中央动脉血供,仍可出现视网膜神经组织不同程度的组织形态学损害。     

视网膜中央动脉阻塞早期眼动脉溶栓治疗前后视力改变

目的 选择性眼动脉溶栓治疗早期视网膜中央动脉阻塞患者治疗前后视力变化的临床研究.方法 收集2006年9月至2009年7月经确诊并在发病12h内进行溶栓的视网膜中央动脉阻塞患者.所有患者均记录年龄、性别、全身病史、发病至溶栓时间、眼底镜检查、眼底荧光血管造影(fundus fluorescein angiography,FFA)、术后48 h复查视力、眼底镜检查、眼底荧光血管造影,术后1月复查,记录视力及眼底检查,并进行对比.结果 24例患者发病至溶栓的平均时间(8.39±3.24)h,溶栓治疗前臂一视网膜动脉显影时间明显延长,平均(29.34±7.83)s,治疗48 h后眼底血管造影显示,臂一视网膜动脉充盈时间明显缩短,平均(15.48±4.33)s,与治疗前对比差异显著有统计学意义;治疗后1月,复查荧光血管造影,臂一视网膜动脉显影时间平均为(15.76±3.12)s,与治疗48 h对比无差异.发病时视力低于0.05患者20例占83.3％,0.05～0.1者4例占16.7％,治疗48 h后视力低于0.05患者7例29.2％,0.05～0.1,6例占25％,高于0.1者11例占45.8％,其中2例高于0.5,占8.3％;治疗前及治疗后48 h患眼视力获得提高的病人数量对比变化显著有统计学意义P＜0.01,治疗后1月视力低于0.05患者5例占20.8％,0.05～0.1者6例占25％,超过0.1患者13例占54.2％,与治疗前患者视力相比差异显著有统计学意义.结论 局部动脉溶栓治疗视网膜中央动脉阻塞,可及时有效恢复早期阻塞的视网膜神经组织的血流灌注,改善早期视网膜中央动脉阻塞患者的视力,但此研究缺乏与传统治疗方法对照研究,同时该治疗方法还需要多中心大样本的临床对比.     

超选择眼动脉溶栓介入治疗视网膜中央动脉阻塞

目的评价超选择动脉介入溶栓治疗视网膜中央动脉阻塞的初步疗效。设计回顾性病例系列。研究对象21例(21眼)视网膜中央动脉阻塞患者。主要指标视力及手术并发症。方法经检眼镜检查及荧光素眼底血管造影检查证实为视网膜中央动脉阻塞患者21例,通过Seldinger技术经微导管超选择眼动脉推注尿激酶溶栓治疗。结果21例患者中10例经超选颈内动脉造影显示眼动脉主干狭窄和阻塞,11例眼动脉主干显影,全部患者均成功进行了溶栓治疗。溶栓治疗前、治疗后3天视网膜中央动脉显影时间分别为(38.18±10.86)秒、(12.65±3.30)秒(t=-11.89,P=0.000)。平均随访(3.23±1.26)个月。治疗后4例患者视力>0.25,9例视力不同程度改善,8例视力无变化。结论超选择眼动脉溶栓介入治疗视网膜动脉阻塞可改善患者视力,但需迅速完成内科、神经科及眼科诊断.尽快治疗。     

眼球缺血综合征临床特点观察

目的探讨眼球缺血综合征(OcularischemicsyndromeOIS)患者眼部表现、眼底荧光血管造影临床特点及血流动力学改变。方法OIS患者眼部检查、眼底荧光素血管造影检查,彩色多谱勒超声检查对比研究OIS患者组和正常对照组颈总动脉、颈内动脉、眼动脉、视网膜中央动脉收缩期血流峰速(PSV)值。结果①共观察OIS患者22例22眼。21例(95%)患者以不同程度的视力下降为主要表现。6眼(27%)出现虹膜新生血管。眼底改变:16眼(73%)视网膜静脉扩张,20眼(90%)有中周部视网膜点状出血。2眼(9%)见到视网膜动脉搏动。②眼底荧光素血管造影臂-视网膜循环时间、视网膜动-静脉循环时间延长,15例(68%)视网膜血管着染,有2只眼发现视网膜动-静脉交通支形成。③OIS患者患侧眼动脉、视网膜中央动脉PSV降低。结论①眼球缺血综合征临床表现复杂,FFA及彩色多谱勒超声检查是诊断该病的重要手段。     

尿激酶动脉溶栓对非动脉炎性视网膜中央动脉阻塞患者的疗效和安全性

目的 探讨尿激酶动脉溶栓治疗非动脉炎性视网膜中央动脉阻塞(NA-CRAO)患者的有效性和安全性。方法 回顾性研究。577例(577眼)NA-CRAO患者纳入研究,其中,男424例,女153例,年龄21～80(58.04±12.68)岁,发病时间2～240(89.88±76.51)h。治疗前均行荧光素眼底血管造影(FFA)检查,记录臂-视网膜循环时间(A-Rct)及视网膜主干-末梢充盈时间。所有患者均行尿激酶动脉溶栓治疗,24 h后复查FFA,记录并对比治疗前及治疗后30 d最佳矫正视力(BCVA)。观察治疗中及治疗后并发症发生情况。结果 577例NA-CRAO患者治疗前及治疗后24 h的A-Rct分别为(31.48±0.99)s、(20.99±0.55)s,差异具有统计学意义(P=0.000);治疗前及治疗后24 h主干-末梢充盈时间分别为(73.32±8.05)s、(20.74±3.28)s,差异具有统计学意义(P=0.001);治疗后30 d的BCVA(logMAR)为1.46±0.14,较治疗前2.19±0.32明显改善,差异具有统计学意义(P=0.037)。577例NA-CRA...     

视网膜中央动脉阻塞患者视网膜循环时间与中心视力损害的关系

目的探讨视网膜中央动脉阻塞（CRAO） 患者中心视力损害与病程、视网膜循环时间的关系。方法对99例99只眼CRAO患者的中心视力、发病病程、荧光素眼底血管造影 (FFA)检查视网膜循环时间等量化数值进行统计学分析。结果CRAO 患者不同病程时间(2~21 d)与中心视力损害程度差异无统计学意义（P＞0.05），视网膜循环时间中视网膜动脉荧光充盈间期与中心视力损害的关系差异有统计学意义（P＜0.05），臂 视网膜循环时间与中心视力损害差异无统计学意义（P＞0.05）。结论视网膜循环时间指标中视网膜动脉荧光充盈间期与中心视力损害相关，时间愈长视力损害愈重，值得关注。(中华眼底病杂志，2007，23：177-179)     

视网膜中央动脉阻塞的颈内动脉造影检查和 介入溶栓治疗

目的观察超选择性动脉插管溶栓治疗视网膜中央动脉阻塞（CRAO）的治疗效果。方法回顾分析16例从股动脉插管行主动脉弓造影观察双侧颈动脉、再行选择性颈内动脉造影的CRAO患者以及其中12例患者应用尿激酶进行溶栓治疗的临床资料。结果16例患者中，颈内动脉严重狭窄3例和眼动脉开口处阻塞1例未进行溶栓治疗。眼动脉主干阻塞和视网膜中央动脉阻塞的12例患者，成功地进行了溶栓治疗。手术后患者视力有不同程度改善，治疗过程中未见全身不良反应。结论超选择性眼动脉插管溶栓治疗CRAO，可恢复患者部分视力。由于病例较少，对其确切疗效以及危险性尚有待于进一步评估。(中华眼底病杂志,2005,21:20-21)     

以尿激酶静脉溶栓为主治疗视网膜中央动脉阻塞115例临床疗效观察

目的 观察尿激酶静脉溶栓为主的治疗方法对视网膜中央动脉阻塞(CRAO)的疗效.方法 115例经眼底和荧光素眼底血管造影(FFA)检查确诊且临床资料完整的CRAO患者纳入研究.其中,男性61例,女性54例.年龄41～75岁,平均年龄(56.7±15.2)岁.均为单眼发病,病程1～30 d.静脉溶栓治疗为3000 U/kg尿激酶静脉滴注,2次/d,连续治疗6～7 d;地塞米松2.5 mg球后注射,1次/2 d,连续治疗14d.后续治疗为1.2 mg/kg脑蛋白水解物、360 mg曲克芦丁静脉滴注,1次/d,连续治疗14d.观察静脉溶栓治疗以及后续治疗对视力的影响以及静脉溶栓治疗对视网膜动脉充盈时间的影响.治疗后视力较治疗前提高3行以上为显效;较治疗前提高2行为有效;无变化或变化在1行内或下降为无效.以FFA作为视网膜循环恢复的判定指标,分为显效、有效、无效3种情况.其中,臂视网膜循环时间(A Rct)≤15s和视网膜中央动脉各分支在2 s内全部充盈为显效;A Rct较治疗前缩短但在15～20 s,其各分支动脉充盈时间3～8 s为有效;A-Rct虽较治疗前缩短但仍≥21s,其各分支动脉充盈时间≥9 s为无效.分析年龄、性别、病程以及后续治疗时间与疗效的关系.结果 尿激酶静脉内溶栓治疗后FFA复查的79例患者中,11例治疗前为完全阻塞,溶栓治疗后其中8只眼显示视盘表面的血管逆行充盈消失,A-Rct 28～54 s,视网膜动脉主干末梢充盈时间18～55 s;3只眼造影3～4 min内仍显示视盘表面的血管逆行充盈.68例不完全阻塞者A Rct恢复正常35例,占51.5％;有效18例,占26.5％;无效15例,占22.0％;溶栓治疗后视网膜循环时间短于治疗前,差异有统计学意义(x2 =11.4,P＜0.05).尿激酶静脉内溶栓治疗前后视力分布比较,差异有统计学意义(x2＝12.1,P＜0.05).后续治疗后最终视力与尿激酶静脉内溶栓治疗后视力分布比较,差异有统计学意义(x2＝14.6,P＜0.05);其中,48只眼视力提高2行甚至2行以上,占41.7％.后续治疗后最终视力与治疗前视力分布比较,差异有统计学意义(x2 =44.5,P＜0.05).其中,视力改变为显效者58只眼,占 50.4％;有效者35只眼,占30.4％;无效者22只眼,占19.2％.不同年龄段患者有效率比较,差异无统计学意义(x2=4.8,P＞0.05).男性患者与女性患者有效率比较,差异无统计学意义(x2 ＝2.6,P＞0.05).病程7d内者76例,显效者43例,有效者22例,有效率85.5％;病程8～15 d者25例,显效者11例,有效者8例,有效率76.0％;病程超过15d者14例,显效者4例,有效者5例,有效率64.3％.后续治疗7d者30例,显效13例,有效8例,有效率70.0％;后续治疗8～14 d者34例,显效18例,有效9例,有效率79.4％;后续治疗15～21 d者51例,显效27例,有效者18例,有效率88.2％.结论 以尿激酶静脉溶栓为主的治疗方法可有效治疗CRAO.     

重组葡激酶和尿激酶在治疗实验性视网膜中央动脉阻塞中的比较

目的 观察重组葡激酶(recombinant staphylokinase,r-Sak)治疗实验性视网膜中央动脉阻塞(central retinal artery occlusion,CRAO)的效果及其对全身的影响。 方法 15只猫(30只眼)静脉注射光化学药物3%孟加拉红后,用氩绿激光照射视网膜动脉形成阻塞模型,静脉给予r-Sak和尿激酶（erokinase,UK)溶栓,通过荧光素眼底血管造影判断动脉再通情况,同时作血液生化指标的检查。 结果 成功地建立了CRAO模型,实验用药给药4h后,r-Sak组CRAO的完全再通率为100%,而UK组的完全再通率仅为60%。使用r-Sak后血液中凝血、纤溶、抗纤溶指标与空白对照组比较均差异无显著意义。 结论 光化学法可建立和临床相似的CRAO模型,R-Sak是一种高效安全、特异性强的溶栓药,在临床治疗CRAO上有较好的应用前景。（中华眼底病杂志,2000,16：71-138）     

Iatrogenic ophthalmic artery occlusion and retinal artery occlusion

Iatrogenic ophthalmic artery occlusion (IOAO) is a rare but devastating ophthalmic disease that may cause sudden and permanent visual loss. Understanding the possible etiologic modalities and pathogenic mechanisms of IOAO may prevent its occurrence. There are numerous medical etiologies of IOAO, including cosmetic facial filler injection, intravascular procedures, intravitreal gas or drug injection, retrobulbar anesthesia, intraarterial chemotherapy in retinoblastoma. Non-ocular surgeries and vascular events in arteries that are not directly associated with the ophthalmic artery, can also cause IOAO. Since IOAO has a limited number of treatment modalities, which lead to poor final visual prognosis, it is imperative to acknowledge the information regarding medical procedures that are etiologically associated with IOAO. We accumulated all searchable and available IOAO case reports (our cases and previous reported cases from the literature), classified them according to their mechanisms of pathogenesis, and summarized treatment options and responses of each of the causes. Various sporadic cases of IOAO can be categorized into three mechanisms as follows: intravascular event, orbital compartment syndrome, and increased intraocular pressure. Embolic IOAO, which is considered the primary cause of the condition, was classified into three subgroups according to the pathway of embolic movement (retrograde pathway, anterograde pathway, pathway through collateral channels). Despite the practical limitations of treating spontaneous (non-iatrogenic) retinal artery occlusion, this article will contribute in predicting and improving the prognosis of IOAO by recognizing the treatable factors. Furthermore, it is expected to provide clues to future research associated with the treatment of retinal artery occlusion.     

Branch retinal artery occlusion and carotid artery stenosis

A patient who presented with a branch retinal artery occlusion (BRAO) of the left eye was discovered to have severe carotid artery stenosis bilaterally. A case report and a discussion of the optometrist's role in diagnosis and management of retinal artery occlusion and carotid stenosis are presented.     

Embolic cilioretinal artery occlusion due to carotid artery dissection

PURPOSE: To report a case of embolic cilioretinal artery occlusion caused by carotid artery dissection. DESIGN: Interventional case report. METHODS: A 38-year-old woman presented with acute visual loss in her right eye. Funduscopy showed a cilioretinal artery occlusion, which was confirmed by a fluorescein angiography. An embolus was found in the distal segment of the vessel. RESULTS: Color Doppler images of right internal carotid artery (ICA) disclosed a pseudolumen, suggesting a diagnosis of carotid dissection. Retrobulbar color Doppler image showed relative low flow velocity in the ophthalmic artery without flow reversal. Magnetic resonance angiography and cerebral angiogram showed total occlusion of the right ICA. Follow-up visual field examination revealed an inferior central defect fed by the cilioretinal artery. CONCLUSION: The pathogenesis of retinal artery occlusion caused by carotid dissection may be embolic or hemodynamic. In our case, a permanent visual defect was related to embolic occlusion of the cilioretinal artery.     

Branch retinal artery occlusion after thyroid artery interventional embolization

PURPOSE: To report a case of branch retinal artery occlusion after thyroid artery interventional embolization. METHODS: A 33-year-old man with hyperthyroidism complained of visual loss and scotoma in the left eye after thyroid artery interventional embolization. He underwent a full ophthalmologic examination, including fluorescein angiography. RESULTS: Visual acuity was 20/25, with inferior and superior scotomas present in the left eye. Fluorescein angiography of the left eye revealed delayed filling of a superotemporal branch retinal artery and nonfilling of an inferotemporal branch retinal artery. CONCLUSION: A small, but definite risk of retinal artery occlusion after thyroid artery interventional embolization should be considered.     

Cilioretinal artery occlusions following embolization of an artery to an intracranial meningioma

Purpose To report a case in which a prophylactic embolization of a feeder artery to an intarcranial meningioma led to an occlusion of a cilioretinal artery. Design A case report. Methods A 48-year-old man with an intracranial meningioma presented with ocular pain and visual loss in his right eye following embolization of a feeder artery to the meningioma with polyvinyl alcohol. Results Ophthalmoscopy 1 month later showed a cilioretinal artery occlusion which was confirmed by fluorescein angiography. His visual acuity was 0.01 in the right eye. The patient was not treated for his ocular symptoms, and his visual acuity 9 month postoperatively improved slightly to 0.1. Conclusions Our case demonstrated that an occlusion of a retinal artery can be a complication of preoperative embolization of an artery to an intracranial tumor and can lead to severe visual loss.     

Acute insufficiency of the ophthalmic artery during occlusion of the internal carotid artery

The authors present a case of a patients aged 41 years in whom the acute insufficiency of the ophthalmic artery was the first and single sign of an internal carotid occlusion. Doppler's pulsating focused ultrasonography showed to be an indispensable method which rendered possible a prompt diagnosis. Besides--this methods enables us to evaluate the dynamics of changes--the regeneration of the ciliary circulation with a compensatory perfusion of blood in some branches of the posterior ciliary arteries, the creation of collateral circulation from the ipsilateral external carotid artery through the ophthalmic artery with a reverse direction of perfusion in its extent and creation of a collateral circulation from the contralateral internal carotid through the anterior cerebral artery.