黄斑下脉络膜新生血管膜的手术治疗及随访观察

目的探讨黄斑下脉络膜新生血管膜手术治疗后的远期效果。方法经睫状体平部行闭路式玻璃体切除术后，切开视网膜，取出黄斑下脉络膜新生血管膜瘢痕组织。７例（７只眼）手术前、后均行视力、矫正视力、眼底及眼底血管荧光素造影检查，并进行长期随诊观察。结果随诊观察１年以上，６只眼黄斑下脉络膜新生血管膜消失，１只眼脉络膜新生血管膜复发。６只眼手术后视力均有不同程度增进，其中２只眼视力提高到０．５以上；１只眼视力减退，黄斑机化组织形成；１只眼发生继发性黄斑前膜。结论黄斑下脉络膜新生血管膜手术切除后，大多数眼视力有所提高，视力提高大小与黄斑下脉络膜新生血管膜瘢痕组织对色素上皮及神经上皮的损害程度有关，手术操作对色素上皮及神经上皮的影响亦有一定关系。     

TTT治疗息肉状脉络膜血管病变的疗效观察

目的观察经瞳孔温热疗法(transpupillarythermotherapy,TTT)治疗息肉状脉络膜血科病变(phlypoidalchoroidalvasculopathy)的临床疗效。方法经荧光血管造影(FFA)、吲哚菁脉络膜血管造影(ICGA)和光相干断层成像术(OCT)检查确诊的16例19眼PCV患者,进行TTT治疗,患者年龄43岁～76岁,平均59.4岁,男10例11眼,女6例8眼,有4眼行两次治疗,有1眼行3次治疗。有5眼为玻璃体出血玻璃体切割术后,有2眼联合PDT治疗。术前和术后均行视力,眼底检查,彩色眼底像,荧光血管造影(FFA)和吲哚菁绿脉络膜血管造影(ICGA),光学相干断层成像术(OCT)检查,随诊3m～24m。结果TTT治疗后视力提高2行以上4眼(21.1%),视力不变15眼(78.9%)。TTT治疗后ICGA显示息肉状脉络膜血管扩张减少和消失16眼(84.2%),1(5.3%)眼扩大,2眼(10.5%)在别处复发,未见明显的并发症。结论TTT治疗息肉状脉络膜血管病变是有效和安全的,可稳定病变的进展及患者的视力,需要更多的病例和更长的随诊时间来验证。     

经瞳孔温热疗法治疗黄斑部脉络膜新生血管

目的探讨经瞳孔温热疗法(transpupillary thermotherapy,TTT)治疗黄斑部脉络膜新生血管膜(choroidal neovascularization,CNV)的疗效.方法经眼底荧光血管检查证实的各原因所致的黄斑部CNV患者27例30眼,其中老年黄斑变性9例11眼,高度近视12例12眼,中心性渗出性脉络膜视网膜炎(简称"中渗")5例5眼,血管条纹症1例,双眼.于2000年6月～2001年9月行TTT治疗,治疗采用IRIS半导体激光,波长810nm,光斑根据CNV病灶大小0.5～3.0 mm,能量180～350 mW,时间60s,治疗后病灶颜色不变或呈淡灰色.随访期8～24个月.结果视力提高2行以上者6眼,占20%,均为中渗或高度近视眼;21眼视力改变不超过2行,占70%;3眼视力下降2行,占10%.19眼于术后复查荧光血管造影,CNV有不同程度的减小或闭塞.结论TTT对多种原因所致的黄斑部CNV均有稳定作用,其作用可持续较长时间.治疗参数因患者眼底色素含量不同而有所差异.最终治疗效果与治疗前病程、CNW的位置及治疗参数的适度有关.     

脉络膜新生血管伴自发性脉络膜上腔出血的临床分析

目的:描述脉络膜新生血管(choroidal neovascularization,CNV)伴自发性脉络膜上腔出血患者的临床特征,探讨其发生的高危因素以及玻璃体视网膜手术的疗效。方法:CNV伴自发性脉络膜上腔出血3例3眼,男性,年龄58~75(平均62岁)。玻璃体脉络膜积血病程6~12d(平均8±4.3d)。术前视力2眼手动,1眼无光感。眼压16~28mmHg(平均19±4.8mmHg)。2眼伴前房红褐色积血,3眼伴重度玻璃体混浊。FFA显示既往均有黄斑区CNV,其中1例健眼有玻璃膜疣。屈光力正常。眼轴22~24mm,双眼无显著性差异(P>0.05)。B超均显示玻璃体积血、出血性视网膜脱离并脉络膜脱离。所有患者均接受常规脉络膜上腔放血、巩膜外环扎、玻璃体切割、视网膜切开、血管膜和积血块清除、视网膜复位及眼内硅油充填术。追踪观察6~34mo。结果:所有患者均为一次手术即成功引流脉络膜上腔积血,术中发现脉络膜下液为黑红色血性积液,玻璃体积血呈灰黑色,术毕脉络膜和视网膜平复。术后2眼发生前部增殖性玻璃体视网膜病变(anterior proliferative vitreoreti-nopathy,aPVR),1眼再次手术。最终在取出硅油后,2眼(67%)视网膜获得解剖复位,术后视力0.05~0.1,1眼无光感。结论:CNV所致的自发性脉络膜上腔出血伴出血性视网膜脱离非常少见,这类患者眼部病变发展迅速,脉络膜上腔积血可渗透到前房,眼压正常或偏高。玻璃体视网膜手术可取得较好的效果。     

黄斑中心脉络膜新生血管的手术治疗

黄斑中心脉络膜新生血管形成通常视力预后较差。根据黄斑光凝研究组(MPS)的随机对照治疗观察,视网膜光凝对某些黄斑中心脉络膜新生血管膜,尤其是复发膜有一定疗效,但视力不可避免地下降。因此作者们探索应用玻璃体视网膜切割技术切除黄斑中心脉络膜新生血管(CNV)。共切除或分离了92眼的 CNV,其中病因为老年性黄斑变性者42眼,组织胞浆菌病综合征者35眼,其它病因5眼。通过短期随诊观察,由老年性黄斑变性引起的黄斑中心CNV 48例中12例视力明显提高(以提高二行或二行以上为标准);病因为组织胞浆菌病综合征者31例中14例视力明显提高;其它病因5例中2例视力明显提高。玻璃体视网膜切割技术切除 CNV 在技术上的可行性为研究 CNV 提供了机会,并为许多黄斑疾病无法恢复视功能者提供了手术治疗的前景。     

玻璃体视网膜联合手术治疗湿性老年性黄斑变性疗效的探讨

目的 分析研究手术治疗湿性老年性黄斑变性(AMD)伴玻璃体积血、出血性视网膜脱离的价值及疗效.方法 对28只眼湿性AMD伴玻璃体积血及黄斑下视网膜出血患者:其中12只眼单纯行闭合式玻璃体切除术;16只眼行玻璃体切除联合视网膜切开视网膜下积血冲洗+黄斑下脉络膜新生血管膜取出术(联合术).观察比较手术前与手术3个月后的视力和眼底情况,随访时间3～12个月.结果 手术3个月后22只眼视力不同程度提高占78.6%(22/28);14只眼视力≥0.02占50.0%(14/28);7只眼视力≥0.05占25.0%(7/28).12只眼单纯玻璃体切除术5只眼视网膜下出血吸收,7只眼出血未全吸收或出现视网下再出血.首选行单纯玻璃体切除手术眼随访中有5只眼玻璃体再出血而行联合手术.16只眼联合术视网膜下出血全部吸收.结论 玻璃体切除手术可使AMD玻璃体积血的清除获得很好效果;湿性 AMD伴玻璃体积血及出血性视网膜脱离患者术后视力恢复效果不好;玻璃体切除联合手术也不能较好提高术眼视力,但可减少玻璃体积血的再发生.     

年龄相关性黄斑变性中隐匿性脉络膜新生血管 伴色素上皮脱离的光动力学疗法

目的：研究新生血管性年龄相关性黄斑变性(AMD)伴有色素上皮脱离(PED)采用光动力学疗法后的视力和血管造影的结果。方法：回顾自2000年1月1日-002年8月31日，患有AMD伴脉络膜新生血管和至少一个视盘直径的浆液性PED，接受过光动力学疗法所有连续患者的荧光素和吲哚青绿血管造影照片和医疗图表。结果：30例(34只眼)符合研究标准。每例进行了1—8次治疗(平均4次)；随访12—36个月(平均19个月)。19只眼(56％)丧失了Snellen表3行或3行以上视力，7只眼(21％)丧失1—2行视力，6只眼(18％)保持原有视力，2只眼(6％)增进1—2行视力。5只眼发生了视网膜下出血，4只眼视网膜色素上皮破裂。有4只眼视力下降至数指、手动或光感。结论：在AMD和PED的34只眼中，尽管有44％丧失了少于3行的Snellen视力，但视力严重丧失至数指或更少的有4只眼，其中3只眼PED内有脉络膜新生血管形成。需要进一步的研究和治疗程式以改善新生血管性AMD伴浆液性PED的预后。     

眼弓形体病晚期并发症—脉络膜新生血管膜

眼弓形体病常表现为前色素膜炎、视网膜脉络膜炎、玻璃体炎等。作者报告3例视力突然障碍是由静止性视网膜脉络膜疤痕附近的脉络膜新生血管膜所致的黄斑脱离而引起。其中1例新生血管膜成功地用氩激光光凝治疗。例1:13岁女孩,以往视力6/6,后降至6/7.5,视网膜有炎症。Sabin-Feldman染色试验阳性,效价1∶128,证实了临床疑为弓形体性视网膜脉络膜炎,用乙嘧啶(Pyrimethamine)、磺胺嘧啶及全身类固醇治疗,炎症静止而停药。右中心凹下方留有视网膜脉络膜疤痕。1年后发现疤痕附近有青灰色脉络膜新生血管膜引起黄斑部浆液性脱离。荧光血管造影显示新生血管膜位于中心凹后方而未予治疗。又1年后视力6/15。例2:53岁女患者,12岁开始双侧黄斑部有脉络膜视网膜疤痕,诊断为先天性弓形体病。视     

激光光凝治疗增殖期糖尿病视网膜病变

目的探讨全视网膜光凝术(panretinalphotocoagulationPRP)对增殖期糖尿病性视网膜病变(proliferativediabeticretinopathy,PDR)的治疗效果。方法对我院438例603眼PDR患者行PRP术,3m后进行眼底荧光血管造影,复查眼底新生血管及玻璃体出血等情况。患者每2w～4w复查,观察期为6m～5y,并记录视力及眼底。结果285眼视力提高≥2行,占47.26%,206眼视力无变化,占34.16%,112眼视力下降,占18.57%(其中71眼因白内障发展而视力下降)。16眼新生血管未消退,占2.65%。14眼发生玻璃体出血,2.32%,后行玻璃体切割手术,术中补激光。新生血管性青光眼9眼中,8眼虹膜新生血管消退,眼压恢复至正常,占88.89%。结论PRP通过抑制新生血管生成及玻璃体出血,是治疗PDR的有效手段。     

鼻咽癌放疗术后眼部并发症的临床分析

目的：探讨鼻咽癌放疗术后眼部并发症的临床特点、荧光素及吲哚菁绿血管造影特征、影响因素及其诊治方法。

方法：回顾性分析2007-03/2012-03我院眼科收治的因鼻咽癌放疗后视力下降的患者33例63眼的临床资料。

结果：所有患者均以进行性、无痛性单眼或双眼视力下降为主要临床表现。放射性视网膜病变48眼,其中视网膜中央动脉阻塞2眼,视网膜中央静脉阻塞3眼,色素上皮改变2眼,黄斑前膜1眼,其余40眼均出现后极部棉絮斑及出血。放射性视神经病变36眼,其中视神经边界清晰27眼,视神经边界不清9眼。黄斑区典型性脉络膜新生血管2眼,脉络膜转移灶1眼,脉络膜循环异常4眼,前部葡萄膜炎2眼,玻璃体积血7眼。

结论：鼻咽癌放疗术后眼部并发症复杂多样,最常见放射性视网膜病变和放射性视神经病变,少数表现为黄斑部脉络膜新生血管、动静脉阻塞、脉络膜循环异常等。     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.