挫伤性前房积血56例临床分析

目的探讨挫伤性前房积血的治疗时机和治疗措施。方法对挫伤性前房积血56例患者进行回顾性分析,其中I级33眼,II级17眼,III级6眼,给予相应的药物保守治疗及手术治疗,观察其前房积血吸收时间、视力预后及相关并发症等。结果积血吸收时间:2d内吸收者36眼,3～7d内吸收者14眼,8～14d内吸收者5眼,14d以上仍未吸收者1眼。I级和II级前房积血的视力恢复较满意,III级前房积血视力恢复欠佳。继发青光眼15眼,晶状体脱位1眼,玻璃体积血合并视网膜脱离1眼,角膜血染1眼。结论挫伤性前房积血视力预后与治疗是否及时、出血量多少、出血部位、就诊时间及并发症有密切关系。     

外伤性前房积血56例临床治疗分析

目的:探讨眼球钝挫伤引起的前房积血的治疗方法。方法:对56例眼球钝挫伤前房积血患者的临床资料进行回顾性分析,采用保守治疗和手术治疗。结果:39例患者通过保守治疗,前房积血3～10d吸收;17例手术治疗,行前房穿刺冲洗术14例,行小梁切除术3例。眼压恢复正常,前房积血吸收,Ⅱ级以下原发性前房积血无并发症,视力恢复良好;Ⅱ级以上挫伤性前房积血,伴有继发性出血及并发症者,及时手术等综合治疗,视力恢复。结论:挫伤性前房积血早期治疗选择好手术方法可获得良好治疗效果。     

挫伤性前房积血临床分析

目的 分析挫伤性前房积血的治疗方法和临床疗效。方法 对我院2000年1月-2004年6月78例挫伤性前房积血进行治疗，方法 是双眼包扎，半卧位，休息，应用止血剂，根据病情应用甘露醇、皮质类固醇激素，有的做前房冲洗。观察积血吸收时间、并发症和视力。结果 积血吸收时间：Ⅰ级前房积血吸收时间1-5天，Ⅱ级积血吸收时间6～10天，Ⅲ级积血吸收时间11-19天。前房积血吸收后视力：0．1以下者5例，0．1～0．3者11例，0．4～0．9者23例，1．0以上者39例。结论 挫伤性前房积血的视力恢复程度与积血量多少有关，也与挫伤程度有关。并发症少和治疗早者，视力恢复较好。     

挫伤性前房积血128例临床分析

目的 探讨挫伤性前房积血的治疗时机和方案。方法 挫伤性前房积血 128例,其中Ⅰ级64例,Ⅱ级28例,Ⅲ级36例,运用相应的中西医疗法治疗。结果 出血吸收时间:1～3天内吸收41例,占32％;4～6天35例,占27％;7～10天23例,占19％;11～15天17例,占13％;15天以上的 12例,占 9％。视力恢复较满意。结论 中西医结合治疗挫伤性前房积血疗效较好,但愈后视力恢复与治疗是否及时,出血量多少及并发症有一定关系。     

挫伤性前房积血112例临床分析

目的 分析挫伤性前房积血的治疗方法。方法 对我院1993年10月～2003年10月收治的112例(112眼)挫伤性前房积血进行治疗，方法 是双眼包扎，半卧位，制动休息，止血剂、甘露醇、皮质类固醇等的应用，有的作前房冲洗。观察积血吸收时间、并发症和视力。结果 积血吸收时间：Ⅰ级1～5天，Ⅱ级6～10天，Ⅲ级和Ⅳ级11—20天。积血吸收后视力：0．05以下6例，0．05～0．111例，0．2．0．39例，0．4～0．610例，0．7～0．925例，1．0以上51例。结论 挫伤性前房积血的视力恢复程度与积血量多少有关，也与挫伤的程度有关。并发症少和治疗早者，视力恢复较好。     

挫伤性前房积血42例临床分析

目的分析挫伤性前房积血治疗方法和效果。方法对我院2007年1月至2009年10月收治的42例（42眼）挫伤性前房积血患者进行回顾性分析。结果经保守治疗和前房冲洗（7例）前房积血完全吸收37例（88.1%）,视力大于0.3者37例（88.1%）。结论挫伤性前房积血及时合理治疗视力恢复良好,并与出血量眼球挫伤程度及有无并发症有关。     

儿童挫伤性前房积血78例临床分析

目的 探讨儿童挫伤性前房积血的治疗方法及结果。方法 对78例（78只眼）儿童挫伤性前房积血患者的临床资料进行回顾性分析。结果 78例中71例经保守治疗后积血吸收,视力恢复;7例须手术治疗。其并发症主要为外伤性瞳孔散大、虹膜根部离断、继发性青光眼、视网膜震荡、晶状体半脱位及角膜血染。结论 儿童挫伤性前房积血经早期止血、降眼压、抗炎及促进积血吸收等治疗后多数患者在较短时间内前房积血吸收,视力恢复。对保守治疗无效者应根据病情及时手术以恢复视力、减少及预防并发症。     

挫伤性前房积血128例临床分析

目的 探讨挫伤性前房积血的治疗时机和方案。方法 挫伤性前房积血128例，其中I级64例，Ⅱ级28例，Ⅲ级36例，运用相应的中西医疗法治疗。结果 出血吸收时间：1－3天内吸收41例，占32％；4－6天35例，占27％；7－10天23例，占19％；11－15天17例，占13％；15天以上的12例，占9％。视力恢复较满意。结论 中西医结合治疗拾零务性前房积血疗效较好，但愈后视力恢复与治疗是否及时，出血量多少及并发症有一定关系。     

早期前房穿刺放液治疗重度外伤性前房积血

目的评价早期前房穿刺放液治疗重度外伤性前房积血的效果。方法对60例（60眼）重度外伤性前房积血,按年龄进行分层随机分为两组,分别行早期前房穿刺放液及保守治疗,观察前房积血后眼压变化、积血吸收时间、瞳孔大小变化及视力恢复情况。结果重度外伤性前房积血伤后早期83．3％出现眼压升高,早期前房穿刺放液组眼压下降明显,与保守治疗组相比差异有统计学意义（P〈0．05）。早期前房穿刺放液组积血平均吸收时间为（5．57±1．28）d,与保守治疗组的平均（10．00±1．91）d相比差异有统计学意义（P〈0．05）。早期前房穿刺放液组有3例出现瞳孔散大,保守治疗组有11例出现瞳孔散大,两组差异有统计学意义（P〈0．01）。早期前房穿刺放液组治疗后平均视力0．84±0．45,保守治疗组愈后平均视力0．61±0．46,两组差异有统计学意义（P〈0．05）。结论重度前房积血早期行前房穿刺放液可加快积血吸收,减少并发症,获得较好的视力恢复。     

外伤性前房积血90例临床分析

目的:探讨外伤性前房积血的治疗方法和临床疗效。方法:回顾性分析我院2000-01/2007-12外伤性前房积血90例进行治疗及其效果。治疗方法是双眼包扎,半卧位,休息,应用止血剂、甘露醇、皮质类固醇激素、神经营养剂,必要的行手术治疗。观察积血吸收时间、并发症和视力。结果:前房积血88例在3～16d吸收,2例发生角膜血染。前房积血吸收后视力<0.1者6例,0.1～0.3者9例,0.4～0.9者29例,≥1.0者46例。结论:外伤性前房积血的视力恢复程度与积血量多少、挫伤程度、并发症的多少及治疗有关。     

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.