视网膜中央动脉阻塞的动物模型及介入治疗研究进展

视网膜中央动脉阻塞（central retinal artery occl usion, CRAO )是致盲的眼科急症之一。通过玻璃体腔内注射药物、视网膜中央动脉球后夹持、颈动脉或眼动脉注入动脉粥样硬化颗粒或血小板凝集物等方法可建立CRAO模型并有助于研究该病的转归及治疗。目前临床应用局部介入溶栓的方法治疗CRAO取得了较为显著的效果，由于受导管本身和介入技术等因素限制，微导管只能放在眼动脉近端，而不能直接放入视网膜中央动脉内。通过玻璃体切割手术，超微导管能直接插入视网膜中央动脉内，使介入溶栓的疗效更加可靠。现就CRAO的动物模型建立及介入治疗的最新进展加以综述。（中华眼底病杂志，2003，19：269-332）     

视网膜中央动脉阻塞的治疗进展

视网膜中央动脉(CRA)是视网膜神经上皮层内五层组织的血供来源。若CRA发生阻塞，可导致患眼视力骤降甚至永久性视力丧失。视网膜中央动脉阻塞(CRAO)患者的自然视力预后通常较差。虽然可用于CRAO治疗的手段多样，如眼球按摩、前房穿刺术、高压氧治疗(HBOT)以及组织型纤溶酶原激活剂(tPA)动脉内溶栓等，但尚未有基于循证医学证据的CRAO治疗指南被应用于临床。而这些治疗手段对于CRAO的疗效均存在争议或存在治疗风险。本文将对目前可应用于CRAO治疗的措施予以综述，并对其各自的安全性及有效性进行探讨。     

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)     

介入溶栓治疗视网膜中央动脉阻塞

目的评价对视网膜中央动脉阻塞(central retinal artery occlusion，CRAO)7例7眼采用介入溶栓的疗效。方法导管介入颈内动脉(internal carotid artery，ICA)或眼动脉(ophthalmic artery，OA)行造影后，用尿激酶10～30万u直接灌注行溶栓治疗。结果7眼术后视力均明显提高，术中及术后无并发症发生，荧光造影示视网膜动脉再通。结论介入溶栓是治疗CRAO的有效方法，视力恢复与阻塞部位、程度、时间有关。     

评价临床上完全性视网膜中央动脉阻塞行选择性动脉溶栓微创治疗和原理的前瞻性随机验证

目的：确定对于临床完全性非动脉炎性的视网膜中央动脉阻塞(CRAO)普遍应用微创治疗的效果，并设计一项评价选择性动脉溶栓治疗此疾病的前瞻性随机实验。     

视网膜中央动脉阻塞治愈1例

0引言视网膜中央血管属于终末血管,一旦阻塞后引起视网膜急性缺血,视网膜功能障碍,视力严重受损。视网膜中央动脉阻塞(CRAO)是一种严重影响视功能的急性眼疾,发病急、预后差,现报告1例近期收治的CRAO患者的治疗情况。     

视网膜中央动脉阻塞的溶栓疗法

视网膜中央动脉阻塞 (CRAO)是一种眼科急症 ,起病急 ,视力损害严重 ,常规治疗疗效差。 1991年Schumacham cherm〔1〕等首次报道了经眼动脉溶栓的方法治疗视网膜中央动脉阻塞 ,取得了明显疗效。近年来 ,随着微导管技术及溶栓的发展和应用 ,超选择眼动脉溶栓相继报道 ,为视网膜中央动脉阻塞开辟了一条新的治疗途径 ,国内尚未见相关报道。本文就超选择眼动脉溶栓进行初步探讨。临床资料 :我们从 2 0 0 1年 9月～ 2 0 0 2年 3月收治了 5例该病患者 ,其中男性 4人 ,女性 1人 ,年龄 3 4～ 5 6岁 (平均44 4岁 ) ,从发病到接受溶栓治疗的时间为 1…     

视网膜中央动脉阻塞150分钟视力恢复正常1例

视网膜中央动脉阻塞(CRAO)是一种严重影响视功能的急性眼病，发病急，预后差。我院收治一例视网膜中央动脉阻塞150分钟经积极救治后视力恢复到1．0患者，现报告如下：     

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）     

急性视网膜坏死伴视网膜中央动脉阻塞的临床观察

目的:观察急性视网膜坏死(acute retinal necrosis,ARN)并视网膜中央动脉阻塞(central retinal artery occlusion,CRAO)的临床特征并进行文献复习。方法:回顾云南省第二人民医院于2015年1月至2019年9月确诊的ARN合并视网膜中央动脉的患者6例(8眼),结合病史、病情发展、转归及影像学检查表现进行分析,并结合以往相关文献报道,对ARN合并视网膜中央动脉这一少见病例的临床表现进行总结。结果:眼底彩色照相及超广角照相可见玻璃体轻至中度混浊,视网膜苍白水肿,以周边视网膜明显,后极部视网膜动脉白线,周边视网膜血管闭塞,伴动脉走行可见大量出血,视网膜大片斑状黄白色渗出;眼底荧光造影可见荧光素充盈不同程度延迟,视网膜散在少许斑状出血遮蔽荧光,视网膜动脉管径细,各方向周边视网膜血管闭塞,大片低荧光无灌注区形成。眼底(optical coherence tomography,OCT)结果显示后极部视网膜水肿增厚,以内层视网膜水肿危重,层次结构欠清晰。部分区域可见神经上皮下液。结论:ARN合并CRAO虽然较为少见,但会进一步严重破坏患者视功能,因此CRAO应该被知晓为一类ARN严重并发症,在对ARN患者诊断和治疗的过程中应加强对CRAO的风险认识和评估。     

Ophthalmic Artery Aneurysm: Potential Culprit of Central Retinal Artery Occlusion

Central retinal artery occlusion (CRAO) is one of the most devastating ophthalmic emergencies, causing acute painless visual loss in the affected eye. We describe the first case of acute non-arteritic CRAO associated with peripheral ophthalmic artery aneurysm and its clinical course after intra-arterial thrombolysis therapy. This case suggests that ophthalmic artery aneurysm can be the cause of CRAO and should be included in the differential diagnosis of CRAO.     

Central retinal artery occlusion—A new,provisional treatment approach

The retinal ganglion cells infarcted in central retinal artery occlusion (CRAO) are the somata of the optic nerve axons, part of the central nervous system. Consequently, CRAO with inner retinal infarction is a small vessel stroke, usually with the devastating consequence of severe visual loss in the affected eye. At present, there is no generally accepted, evidence-based therapy of nonarteritic CRAO in contrast to ischemic cerebral stroke that has well-accepted treatment protocols. Widely divergent and controversial therapeutic options for CRAO reflect the desperation of treating physicians and disparate conflicting studies. We examine reasons why treatment of nonarteritic CRAO remains problematic and then suggest a provisional new approach to treatment based on updated understanding of CRAO pathophysiology and analysis of current therapeutic options and their rationales.     

A review of central retinal artery occlusion: clinical presentation and management

Central retinal artery occlusion (CRAO) is an ophthalmic emergency and the ocular analogue of cerebral stroke. Best evidence reflects that over three-quarters of patients suffer profound acute visual loss with a visual acuity of 20/400 or worse. This results in a reduced functional capacity and quality of life. There is also an increased risk of subsequent cerebral stroke and ischaemic heart disease. There are no current guideline-endorsed therapies, although the use of tissue plasminogen activator (tPA) has been investigated in two randomized controlled trials. This review will describe the pathophysiology, epidemiology, and clinical features of CRAO, and discuss current and future treatments, including the use of tPA in further clinical trials.     

A case of Churg–Strauss syndrome and central retinal artery occlusion with good visual recovery

Here we report a case of Churg–Strauss syndrome (CSS) and central retinal artery occlusion (CRAO), with good visual recovery. A 58-year-old Japanese man with CSS experienced acute painless loss of vision in his right eye. CRAO was diagnosed by fundoscopic findings (retinal whitening with a cherry-red spot). Steroid pulse therapy (methylprednisolone at 1 g daily for 3 days) followed by combined treatment with prednisolone (30 mg/day) and cyclophosphamide (150 mg/day) was administered; his visual acuity recovered to 20/30 in 1 month, and no recurrence has occurred for 1 year. Steroid pulse therapy may be effective for CRAO in CSS patients.     

Acute retinal arterial occlusive disorders

The initial section deals with basic sciences; among the various topics briefly discussed are the anatomical features of ophthalmic, central retinal and cilioretinal arteries which may play a role in acute retinal arterial ischemic disorders. Crucial information required in the management of central retinal artery occlusion (CRAO) is the length of time the retina can survive following that. An experimental study shows that CRAO for 97 min produces no detectable permanent retinal damage but there is a progressive ischemic damage thereafter, and by 4 h the retina has suffered irreversible damage. In the clinical section, I discuss at length various controversies on acute retinal arterial ischemic disorders.Classification of acute retinal arterial ischemic disorders: These are of 4 types: CRAO, branch retinal artery occlusion (BRAO), cotton wool spots and amaurosis fugax. Both CRAO and BRAO further comprise multiple clinical entities. Contrary to the universal belief, pathogenetically, clinically and for management, CRAO is not one clinical entity but 4 distinct clinical entities – non-arteritic CRAO, non-arteritic CRAO with cilioretinal artery sparing, arteritic CRAO associated with giant cell arteritis (GCA) and transient non-arteritic CRAO. Similarly, BRAO comprises permanent BRAO, transient BRAO and cilioretinal artery occlusion (CLRAO), and the latter further consists of 3 distinct clinical entities – non-arteritic CLRAO alone, non-arteritic CLRAO associated with central retinal vein occlusion and arteritic CLRAO associated with GCA. Understanding these classifications is essential to comprehend fully various aspects of these disorders.Central retinal artery occlusion: The pathogeneses, clinical features and management of the various types of CRAO are discussed in detail. Contrary to the prevalent belief, spontaneous improvement in both visual acuity and visual fields does occur, mainly during the first 7 days. The incidence of spontaneous visual acuity improvement during the first 7 days differs significantly (p < 0.001) among the 4 types of CRAO; among them, in eyes with initial visual acuity of counting finger or worse, visual acuity improved, remained stable or deteriorated in non-arteritic CRAO in 22%, 66% and 12% respectively; in non-arteritic CRAO with cilioretinal artery sparing in 67%, 33% and none respectively; and in transient non-arteritic CRAO in 82%, 18% and none respectively. Arteritic CRAO shows no change. Recent studies have shown that administration of local intra-arterial thrombolytic agent not only has no beneficial effect but also can be harmful. Prevalent multiple misconceptions on CRAO are discussed.Branch retinal artery occlusion: Pathogeneses, clinical features and management of various types of BRAO are discussed at length. The natural history of visual acuity outcome shows a final visual acuity of 20/40 or better in 89% of permanent BRAO cases, 100% of transient BRAO and 100% of non-arteritic CLRAO alone.Cotton wools spots: These are common, non-specific acute focal retinal ischemic lesions, seen in many retinopathies. Their pathogenesis and clinical features are discussed in detail.Amaurosis fugax: Its pathogenesis, clinical features and management are described.     

Prevalent misconceptions about acute retinal vascular occlusive disorders

Acute retinal vascular occlusive disorders collectively constitute one of the major causes of blindness or seriously impaired vision, and yet there is marked controversy on their pathogeneses, clinical features and particularly their management. This is because the subject is plagued by multiple misconceptions. These include that: (i) various acute retinal vascular occlusions represent a single disease; (ii) estimation of visual acuity alone provides all the information necessary to evaluate visual function; (iii) retinal venous occlusions are a single clinical entity; (iv) retinal vein occlusion is essentially a disease of the elderly and is not seen in the young; (v) central retinal vein occlusion (CRVO) is one disease; (vi) fluorescein fundus angiography is the best test to differentiate ischemic from nonischemic CRVO; (vii) the site of occlusion in CRVO is invariably at the lamina cribrosa; (viii) clinical picture of CRVO is often due to compression or strangulation of the central retinal vein (CRV) in the lamina cribrosa and not its occlusion; (ix) an eye can develop both CRVO and central retinal artery occlusion (CRAO) simultaneously; (x) every eye with CRVO is at risk of developing neovascular glaucoma; (xi) lowering intraocular pressure (IOP) helps to improve retinal circulation in an eye with CRVO; (xii) every patient with retinal vein occlusion should have complete hematologic and coagulation evaluation; (xiii) the natural history of CRVO does not usually involve spontaneous visual improvement; (xiv) management of CRVO is similar to that of venous thrombosis anywhere else in the body, i.e. with aspirin and/or anti-coagulants; (xv) fibrinolytic agents can dissolve an organized thrombus in the CRV; (xvi) it is beneficial to lower blood pressure in patients with CRVO; (xvii) panretinal photocoagulation used in ischemic retinal venous occlusive disorders has no deleterious side-effects; (xviii) glaucoma or ocular hypertension can cause branch retinal vein occlusion; (xix) branch retinal vein occlusion can cause neovascular glaucoma; (xx) in eyes with CRAO, the artery is usually not completely occluded; (xxi) CRAO is always either embolic or thrombotic in origin; (xxii) amaurosis fugax is always due to retinal ischemia secondary to transient retinal arterial embolism; (xxiii) asymptomatic plaque(s) in retinal arteries do not require a detailed evaluation; (xxiv) retinal function can improve even when acute retinal ischemia due to CRAO has lasted for 20h or more; (xxv) CRAO, like ischemic CRVO, can result in development of ocular neovascularization; (xxvi) panretinal photocoagulation is needed for "disc neovascularization" in CRAO; (xxvii) fibrinolytic agents are the treatment of choice in CRAO; (xxviii) there is no chance of an eye with retinal arterial occlusion having spontaneous visual improvement; (xxix) absence of any abnormality on Doppler evaluation of the carotid artery or echography of the heart always rules out those sites as the source of embolism; and (xxx) absence of an embolus in the retinal artery means the occlusion was not caused by an embolus. The major cause of all these misconceptions is the lack of a proper understanding of basic scientific facts related to the various diseases. The objective of this paper is to discuss these misconceptions, based on these scientific facts, to clarify the understanding of these blinding disorders, and to place their management on a rational, scientific basis.     

Scanning laser polarimetry of the retinal nerve fiber layer in central retinal artery occlusion

PURPOSE: To report the results of scanning laser polarimetry (NFA/GDx; Laser Diagnostic Technologies, San Diego, CA). DESIGN: Prospective, consecutive observational case series. PARTICIPANTS: Ten consecutive patients with central retinal artery occlusion (CRAO). METHODS: Neuro-ophthalmic examination and scanning laser polarimetry of the retinal nerve fiber layer (RNFL) of 10 patients with CRAO. MAIN OUTCOME MEASURES: Duration of visual loss, visual acuity, funduscopy, and scanning laser polarimetry of the RNFL in 10 eyes of 10 patients with CRAO. RESULTS: The duration of visual loss before examination and scanning laser polarimetry ranged from 1 to 7 days. Visual acuity was counting fingers at 1 foot or worse in all 10 eyes with CRAO, and funduscopy revealed pallid retinal edema accompanied by a cherry red spot in all affected eyes. Funduscopy of the fellow eyes in all but one patient, who had anterior ischemic optic neuropathy and was subsequently diagnosed with giant cell arteritis, revealed no acute changes. Scanning laser polarimetry of all eyes with CRAO revealed diffuse attenuation of the retardation of the RNFL. Scanning laser polarimetry of the fellow eye revealed a normal bimodal distribution in the eight patients in whom it could be measured. In one patient who was examined 1 day after the onset of visual loss, repeat nerve fiber analysis 6 weeks later revealed further depression of the RNFL compared with the initial scan. Repeat analysis of the RNFL in four other patients showed persistence of the diffuse depression noted during their initial examinations. CONCLUSIONS: Scanning laser polarimetry in CRAO reveals diffuse depression of the retardation of the RNFL, which occurs acutely after the onset of visual loss. To our knowledge these patients represent the first reports of scanning laser polarimetry of the RNFL in acute CRAO.     

A case of central retinal vein occlusion accompanied by central retinal artery occlusion

A 81-year-old woman developed central retinal vein occlusion (CRVO) in her left eye subsequent to central retinal artery occlusion (CRAO). She noticed sudden visual loss in the left eye. At initial examination, her left visual acuity was 0.03, and only a small visual field was preserved at temporal area. The left fundus showed findings of mild non-ischemic CRVO. In addition white clouded retina was recognized at the left posterior pole which indicated CRAO. FAG showed remarkably prolonged arterial circulation, but no retinal capillary obliteration. Then retinal hemorrhage increased rapidly and her left eye developed hemorrhagic retinopathy. Two weeks after initial examination, FAG showed extensive retinal capillary obliteration. In this case it was supposed that central retinal artery occlusion due to arteriosclerosis produced ischemic capillaropathy and venous thrombosis, after which restoration of arterial circulation caused hemorrhagic retinopathy.     

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)