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1.
目的:观察急性闭角型青光眼急性发作缓解后继发睫状体脉络膜脱离时眼压、前房深度的变化,探讨继发性睫状体脱离的原因、临床特征及治疗效果。方法:回顾性分析我院2011-08/11住院治疗的84例急性闭角型青光眼急性发作的患者,发作缓解后,经超声生物显微镜(UBM)及B超发现,19例出现睫状体脉络膜脱离,用非接触式眼压计及UBM测量急性发作前后和睫状体脉络膜脱离时的眼压和前房深度,并进行统计学分析。结果:急性发作期眼压50.4±6.5mmHg,中央前房深度1.65±0.12mm;发作缓解继发睫状体脉络膜脱离时眼压7.93±4.3mmHg,中央前房深度1.29±0.1mm。UBM及B超检查显示:继发单纯脉络膜脱离10例,单纯睫状体脱离4例,睫状体脉络膜脱离5例,给予常规抗青光眼手术联合适量糖皮质激素治疗,全部睫状体脉络膜脱离均复位。结论:急性闭角型青光眼急性发作缓解后常可合并睫状体及脉络膜脱离,且治疗前眼压越高,缓解时间越短,缓解后发生睫状体、脉络膜脱离的几率越高,其直接征象为眼压过低、前房更浅,UBM为其最可靠的检查方法,常规抗青光眼手术联合适量糖皮质激素为该类患者的有效治疗方法。  相似文献   

2.
急性闭角型青光眼并发睫状体脱离的观察与分析   总被引:1,自引:0,他引:1  
目的分析原发性急性闭角型青光眼并发睫状体脱离的特点及治疗转归。方法对2006年5月至2008年5月治疗的163例(186眼)原发性急性闭角型青光眼,72h内经药物控制眼压后行超声生物显微镜(ultrasound biomicroscope,UBM)检查,并对这些病例的年龄、性别、UBM表现、中央前房深度及治疗结果进行分析。结果186眼中有26眼(13.98%)并发睫状体脱离,此类患者就诊时大多眼压较高(〉50mmHg,1mmHg=0.133kPa),经治疗后迅速下降至正常甚至更低。脱离范围有全周也有部分,中央前房深度变浅。治疗后眼压控制良好,睫状体脱离复位。结论并发睫状体脱离是原发性急性闭角型青光眼的体征之一,UBM检查对其具有较高的诊断价值,并可为临床提供可靠依据。  相似文献   

3.
闭角型青光眼急性发作合并睫状体脱离的UBM图像分析   总被引:1,自引:1,他引:1  
目的探讨闭角型青光眼急性发作患者合并睫状体脱离的超声生物显微镜(UBM)图像特征。方法利用UBM对高眼压状态下的急性闭角型青光眼患者作前房角、前房深度、睫状体检查,对合并睫状体脱离UBM图像的形态进行分析。结果21例(29只眼)患者合并睫状体脱离,平均眼压为(34.84±9.37)mmHg,中央前房深度为(1.67±0.18)mm,眼轴长度为(23.10±1.25)mm。UBM图像分析示睫状体脱离双眼8例、单眼13例;脱离分级,1级11只眼、2级12只眼、3级6只眼;脱离范围2象限6只眼、3象限4只眼、全周脱离19只眼。结论UBM检查显示原发性急性闭角型青光眼高眼压状态的患者可合并睫状体上腔脱离,对该类患者的临床初期治疗,需重视降眼压药物及适量的皮质激素联合应用。  相似文献   

4.
曹鎏  王林农 《国际眼科杂志》2010,10(10):1900-1902
目的:应用超声生物显微镜观察急性闭角型青光眼小梁切除术的有效性和安全性。方法:选取80例80眼急性闭角型青光眼病例按手术前眼压水平分为高眼压组(30例30眼,眼压≥30mmHg)和对照组(50例50眼,眼压<30mmHg),对两组病例小梁切除术后眼压、视力以及超声生物显微镜(ultrasound biomicroscopy,UBM)情况等进行统计比较。结果:高眼压组术后大多数保留了较好的视力;两组病例术后眼压大多控制在8~15mmHg;UBM检测结果,高眼压组术后发生1例睫状体脱离,1例恶性青光眼,1例浅前房,对照组术后发生1例浅前房,两组比较差异无显著性(P>0.05);两组患者手术后ACD,AOD,TCPD术前术后比较差异均无显著性。结论:急性闭角型青光眼高眼压下小梁切除术是有效、安全的,在充分药物治疗后,应及时采取手术治疗。UBM检查可发现小梁切除术后睫状体脱离、恶性青光眼等严重并发症,在急性闭角型青光眼诊治过程中发挥重要作用。  相似文献   

5.
目的量化观察急性闭角型青光眼降眼压治疗中继发脉络膜脱离的眼压和前房深度的变化,总结临床特点。方法回顾分析2005年1月至2006年4月,107例114只眼急性闭角型青光眼在降眼压治疗中,34例36只眼(31.8%)经超声生物显微镜(UBM)检查诊断继发脉络膜脱离,用Goldmann压平眼压计和UBM分别测量这组病例降眼压治疗前和发现脉络膜脱离时的眼压和前房深度,观察总结其临床特点。结果降眼压治疗前眼压平均(51.6±7.5)mmHg(1mmHg=0.133kPa),前房中央深度平均(1.763±0.285)mm;脉络膜脱离时眼压平均(7.6±3.2)mmHg,前房中央深度平均(1.547±0.334)mm;眼压变化平均(42.9±6.7)mmHg,前房中央深度变化平均(0.162±0.136)mm。继发脉络膜脱离无须特殊治疗,予减少或停用降眼压药物(尤其是缩瞳剂),2-7(3.5±1.4)天自愈,给予皮质类固醇类药物可缩短疗程。结论急性闭角型青光眼降眼压抢救治疗时,继发性脉络膜脱离的发生与眼压降低过快过低有关;UBM具有较高的诊断价值,并可为临床提供可靠依据。  相似文献   

6.
急性闭角型青光眼合并睫状体脉络膜脱离22例   总被引:2,自引:1,他引:2  
目的分析原发性急性闭角型青光眼(acute prima-ry angle-closure glaucoma,APACG)高眼压状态患者并发睫状体脉络膜脱离的临床特征及治疗结果。方法回顾性研究经超声生物显微镜(ultrasound biomicroscopy,UBM)、B超等检查证实22例31眼高眼压状态合并睫状体、脉络膜上腔积液与脱离的APACG患者,对该组患者的眼前部结构、UBM、B超图像特征及治疗结果进行分析与评价。结果22例31眼首诊时眼压(37.61±10.94)mmHg(1kPa=7.5mmHg),中央前房深度(1.68±0.10)mm,眼轴长度(22.80±0.67)mm。UBM显示:睫状体脱离双眼9例、单眼13例;脱离分级:1级15眼,2级10眼,3级6眼;脱离范围:1/2象限6眼,3/4象限7眼,4个象限脱离18眼。4例(7眼)合并脉络膜脱离。临床治疗10眼作YAG激光虹膜切开术,21眼行巩膜瓣松解缝线小梁切除术,随访所有病例眼压控制良好。结论APACG高眼压患者可合并睫状体脉络膜脱离,常规抗青光眼及联合适量糖皮质激素治疗能有效控制该类患者眼压。  相似文献   

7.
原发性视网膜色素变性并发急性闭角型青光眼临床分析   总被引:1,自引:0,他引:1  
目的探讨原复性视网膜色素变性(PRP)并发急性闭角型青光眼的治疗。方法对8例PRP并发急性闭角型青光眼(单眼发作5例、双眼发作3例)患者行常规眼部检查,部分患者行视野、A型和B型超声波检查、超声生物显微镜检查(UBM)检查、角膜内皮细胞镜检查及眼部电生理检查。结果男女发病比例1:3。青光眼发作期11只眼,其中1只眼并发自发性晶状体半脱位,临床前期5只眼。发作眼平均眼压(52.63±11.22)mmHg,临床前期平均眼压(15.75±2.43)mmHg。A型超声波检查:眼轴长度平均(22.28±1.04)mm。UBM检查:前房中轴部深度平均(1.50±0.46)mm。手术治疗11只眼,其中小梁切除术7只眼,白内障摘除联合小粱切除术3只眼,二极管激光经巩膜睫状体光凝术1眼。术后并发症:前房葡萄膜炎性反应絮状渗出多见于青光眼自内障联合手术,小梁切除术后浅前房发生率为57.14%。结论PRP并发急性闭角型青光眼患者具有与原发性闭角型青光眼一致的解剖结构,小梁切除术术后浅前房发生率较高。并发自发性晶状体脱位者较为少见。  相似文献   

8.
原发性急性闭角型青光眼并发睫状体脉络膜脱离   总被引:4,自引:2,他引:4  
原发性急性闭角型青光眼是眼科急症 ,急性发作期通过典型的临床症状与体征即可作出正确的诊断 ,如能及时进行药物和激光或手术治疗 ,眼压可以下降并获得良好的治疗效果。由于急性闭角型青光眼患者前房往往很浅 ,因此临床上较难观察到是否存在睫状体脉络膜脱离。最近我们对一组原发性急性闭角型青光眼患者行眼前段超声生物显微镜 (ultrasoundbiomicroscopy,UBM)检查 ,发现一些患者伴有睫状体脉络膜脱离 ,现报告如下。资料和方法一、临床资料 :病人来源于 2 0 0 0年 3~ 4月在我中心确诊的急性闭角型青光眼患者 ,共 16例 31眼。其中男 4例 ,…  相似文献   

9.
目的观察原发性急性闭角型青光眼患者高眼压状态下行复合式小梁切除术的远期疗效。方法回顾性研究。收集2008年1月至2015年12月惠州市中心人民医院收治的原发性急性闭角型青光眼大发作期患者26例(26眼)的临床资料。所有患者均行局部及全身降眼压治疗后眼压仍控制欠佳,对急性大发作眼行复合式小梁切除术。术后随访4~11年,观察远期疗效。结果随访期间均未见葡萄膜炎、前房积血或睫状体环阻塞性青光眼等严重并发症。入院眼压为(46.65±18.08)mmHg,出院眼压为(11.58±4.20)mmHg,末次随访眼压为(16.07±10.01)mmHg(1 mmHg=0.133 kPa)。末次随访时滤过泡Ⅰ级者18眼、Ⅱ级者1眼、Ⅲ级者7眼。滤过泡等级与末次随访眼压呈正相关(r=3.350,P=0.009)。随访期间视网膜神经纤维层厚度、视野指数及视野平均偏差逐渐降低(P<0.001)。结论复合式小梁切除术治疗持续性高眼压状态的急性闭角型青光眼患者有效且安全。  相似文献   

10.
目的:探讨激光周边虹膜成形术(laser peripheral iridoplasty,LPIP)治疗急性闭角型青光眼(acute angle-closure glaucoma,AACG)急性发作期药物不能控制的高眼压持续状态中的疗效。方法:原发性急性闭角型青光眼67例69眼发作期药物治疗3~6h后眼压仍>30mmHg时,行LPIP治疗。监测术前和术后30,60min和2h眼压、视力变化。应用UBM测量术前、术后2h房角宽度和虹膜厚度,并应用房角镜观察前房角粘连情况。结果:LPIP后2h,房角开放距离(AOD)较术前明显增大(P<0.01),小梁虹膜夹角(TIA)增宽、部分患者周边虹膜前粘连(PAS)减少、周边虹膜变薄。所有患者眼压在激光虹膜成形术后不同时间均有不同程度下降。术前平均眼压53.81±10.22mmHg,术后30min平均眼压33.81±9.22mmHg,术后60min为21.93±7.19mmHg,2h后眼压下降至15.16±3.07mmHg,治疗前后差异有显著统计学意义(F=151.79,P<0.01)。同时所有患者视力都有所提高。结论:LPIP可以明显加深患者的周边前房,增宽房角入口,降低患者眼压,是治疗AACG急性发作期药物不能控制高眼压持续状态的重要辅助措施,为青光眼的进一步治疗创造了条件,并且能够改善预后。  相似文献   

11.

Purpose

To report a case of bilateral acute angle-closure glaucoma after oral administration of cabergoline for the treatment of galactorrhea.

Methods

A diagnosis of secondary drug-induced angle-closure glaucoma was made in a patient with elevated intraocular pressure (IOP) and myopic refractive shift, which was confirmed by ultrasound biomicroscopy (UBM) of the ciliary body and anterior segment, sonography, and optical coherence tomography. The treatment included the discontinuation of the culprit drug and the administration of topical anti-glaucoma drops. The treatment course was followed with serial measurements of the IOP and refraction, and with performing UBM.

Results

Five hours after he received a single 0.5-mg oral cabergoline tablet, the patient suffered from acute secondary angle-closure glaucoma and myopic refractive error. UBM demonstrated both effusion of the ciliary body and an anterior rotation of the iris-ciliary body. IOP was reduced 8 h after cessation of the causative agent and administration of anti-glaucoma drops. Refractive errors returned to normal levels after 8 days.

Conclusion

Secondary acute angle-closure glaucoma has been reported to occur after the administration of some drugs. In this report, an attempt has been made to describe this adverse reaction after oral cabergoline intake.Key Words: Bilateral angle-closure glaucoma, Cabergoline, Galactorrhea  相似文献   

12.
PURPOSE: To present an unusual case of simultaneous bilateral acute angle-closure (AAC) glaucoma in a patient with subarachnoid hemorrhage due to an aneurysm involving the right middle cerebral artery. METHODS: A 60-year-old woman with a clinically inexplicable bilateral nonreacting mydriasis after brain surgery underwent an ophthalmologic consultancy. The bilateral mydriasis was diagnosed as an unusual clinical presentation of simultaneous bilateral AAC glaucoma. One week after the AAC was bilaterally resolved, the patient underwent echographic examination because of the outbreak of a unilateral relapsed ocular hypertensive attack that required an ultrasound biomicroscopy (UBM) to be accurately diagnosed and treated. RESULTS: The bilateral AAC regressed completely after pharmacologic therapy. UBM evaluation of the eye with recurrence of the angle-closure glaucoma attack was necessary to confirm the diagnosis of unilateral relapsed angle-closure glaucoma due to an unresolved pupillary block. A viscoelastic-aided opening of the angle and peripheral surgical iridectomy were performed. UBM and tonometry were performed intraoperatively to confirm the success of the surgical treatment. CONCLUSIONS: The UBM allowed us to identify the pupillary block as the main mechanism involved in the pathogenesis of this unusual case of simultaneous bilateral AAC glaucoma. Despite the fact that drug-induced supraciliary uveal effusion and mydriasis due to surgical anesthesia have been frequently reported to contribute to this complication, we presumed that simultaneous intravenous administration of sedative drugs and adrenergic agonists, in a patient with individual biometric predisposing factors to the angle-closure, created the anatomic conditions which induced the pupillary block with obliteration of the trabeculum.  相似文献   

13.
BACKGROUND: We report a patient with acute angle-closure glaucoma secondary to annular ciliochoroidal detachment after unsutured cataract surgery. CASE: An 82-year-old man was diagnosed with bilateral shallow central anterior chamber depth, flat peripheral anterior chamber, and elevated intraocular pressure. One day previously he had undergone uncomplicated unsutured cataract surgery in the right eye and eight days previously, in the left eye. Ultrasound biomicroscopy revealed annular ciliochoroidal detachment in both eyes. Treatment with intravenous methyl prednisolone deepened the anterior chamber and reduced intraocular pressure. CONCLUSION: Annular ciliochoroidal detachment may lead to anterior rotation of the ciliary body and angle-closure. This clinical entity is indistinguishable from malignant glaucoma when the fundus cannot be visualized.  相似文献   

14.
PURPOSE: To describe the pathophysiology of angle-closure glaucoma secondary to idiopathic inflammatory orbital pseudotumor. DESIGN: Retrospective, small noncomparative case series. PARTICIPANTS: Three patients with angle-closure glaucoma and orbital pseudotumor. METHODS: The pathophysiology of this entity was investigated using magnetic resonant imaging (MRI) and ultrasound biomicroscopy (UBM). MAIN OUTCOMES MEASURES: Clinical features, anterior chamber angle configuration, and intraocular pressure. RESULTS: Angle closure from anterior rotation of the ciliary body caused by choroidal effusions secondary to pseudotumor was demonstrated using MRI and UBM. Two of the three cases resolved after treatment for orbital pseudotumor. CONCLUSIONS: Idiopathic orbital pseudotumor is a cause of secondary angle-closure glaucoma. The mechanism of angle closure is anterior rotation of the ciliary body secondary to choroidal effusions resulting from the orbital inflammation.  相似文献   

15.
Presumed topiramate-induced bilateral acute angle-closure glaucoma.   总被引:1,自引:0,他引:1  
PURPOSE: We describe a case of bilateral angle-closure glaucoma associated with oral topiramate therapy. METHODS: Interventional case report. Case report with echographic illustration. RESULTS: A 51-year-old man developed bilateral acute angle-closure glaucoma 2 weeks after beginning topiramate therapy for bipolar affective disorder. Laser peripheral iridotomy was performed in the right eye without resolution of the acute attack. Echography revealed lens thickening and ciliochoroidal detachments in both eyes. Visual acuity, intraocular pressure, and anterior and posterior segment anatomy normalized 2 weeks after cessation of topiramate therapy. CONCLUSION: Topiramate, a new sulfa-derivative antiepileptic medication, may cause idiosyncratic ciliochoroidal detachments and ciliary body edema leading to anterior displacement of the lens-iris diaphragm, lens thickening, and acute angle-closure glaucoma.  相似文献   

16.
BACKGROUND: We report a patient with persistent hyperplastic primary vitreous(PHPV) who presented with acute angle-closure glaucoma in his adult life. CASE: A 30-year-old man had an attack of acute angle-closure glaucoma associated with retrolenticular fibrous tissue, atrophic retina, and elongated cilliary process in his right eye. RESULT: Ultrasound biomicroscopy(UBM) study showed iris bowing, shallow anterior chamber, and elongated cilliary body which were being pulled by the retrolenticular mass. The posterior chamber was normal. CONCLUSION: Although the mechanisms of secondary angle-closure glaucoma in PHPV are complicated, we suspected pupillary block resulting from constriction by the retrolenticular mass in this case.  相似文献   

17.
目的:观察闭角型青光眼中虹膜睫状体囊肿的发病情况,虹膜睫状体囊肿与前房轴深、房角的关系。方法:利用超声生物显微镜(UBM)对闭角型青光眼患者740例1057眼进行眼前节检查。结果:闭角型青光眼740例1057眼中检出合并虹膜睫状体囊肿者42例60眼,占被检眼数的5.68%。60眼虹膜睫状体囊肿中虹膜睫状沟囊肿56眼(93.33%),睫状冠囊肿4眼(6.67%);其中单发囊肿33眼(55.00%),多发囊肿27眼(45.00%)。不伴有虹膜睫状体囊肿的患者前房轴深1.16~2.37(平均1.843)mm;合并有虹膜睫状体囊肿的患者前房轴深1.67~2.78(平均2.297)mm。伴有及不伴有虹膜睫状体囊肿的闭角型青光眼患者房角粘连>2个象限的比率分别为66.67%和44.59%。结论:虹膜睫状体囊肿在闭角型青光眼中的发病率较高,多为虹膜睫状沟囊肿,对前房轴深影响不大,但可以增加房角粘连范围,引起闭角型青光眼。  相似文献   

18.
Two homosexual men, 35 and 42 years old, had bilateral acute angle-closure glaucoma in association with the acquired immune deficiency syndrome. In one patient, the angle-closure attack was the initial manifestation of AIDS. Choroidal effusion with secondary anterior rotation of the ciliary body at the scleral spur appeared to be the pathophysiologic mechanism. Pupillary block, angle crowding, and inflammatory synechial angle closure must be differentiated from anterior rotation of the ciliary body as the mechanism of the angle closure to provide optimal treatment. Whereas primary angle closures are treated with miotics and iridectomy, secondary angle closure may be worsened with this treatment. Cycloplegics and, if necessary, drainage of suprachoroidal fluid may be curative in AIDS-related angle closure associated with a choroidal detachment. Both patients died before the long-term efficacy of this treatment could be assessed.  相似文献   

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