眼挫伤后房角后退青光眼的临床分析

眼球挫伤的发病率占眼外伤的34％，甚者可造成眼球的复合伤致解剖结构变形而引发各种并发症，而前房角结构的改变和前房角后退是眼球挫伤的严重并发症。临床上对外伤后继发性青光眼病因分析往往倾向于房角后退的结构改变。本文回顾1990～2003年我院治疗的眼球钝挫伤房角后退患者153眼的临床资料，探讨眼球挫伤后继发高眼压的原因。     

眼球穿孔伤后继发性青光眼的临床调查分析

目的探讨眼球穿孔伤后继发性青光眼的病因及早期诊断方法。方法回顾性分析36例(36眼)眼球穿孔伤后继发性青光眼的临床资料，探讨继发性青光眼的原因、发生时间及与眼外伤的关系。结果穿孔性眼外伤后继发青光眼与粘连性角膜白斑、晶状体损伤和晶状体异位有关，集中于晶状体虹膜隔的损伤，而引起小梁网明显的功能损伤。结论眼球穿孔伤的正确处理，长时间密切随访观察和及早预防对视力的损害。     

挫伤性青光眼的危险因素及治疗对策

目的 探讨挫伤继发青光眼的危险因素及治疗对策。方法 回顾分析３７例发生青光眼的原因、治疗方法及治疗后的情况。结果 原因：眼内出血占６７．５７％，其中以前房出血更为多见占６４．８６％；房角挫伤占２１．６２％；晶状体脱位占１８．９２％。经药物治疗和手术治疗，眼压控制正常占８９．１９％。结论 ⒈前房出血是挫伤后发生继发性青光眼的主要原因。⒉手术时机是影响治疗的重要因素，不同原因的眼挫伤所继发的青光眼应根     

眼挫伤继发青光眼105例临床分析

目的:探讨眼挫伤继发性青光眼的病因及治疗.方法:对105例眼挫伤继发性青光眼进行回顾性分析.结果:不同类型的眼挫伤继发性青光眼有不同的病因,其治疗也不同.105例眼挫伤继发性青光眼经治疗后79.5%视力有提高.89例眼压恢复正常,治愈率84.8%.结论:眼挫伤继发性青光眼应及时发现,根据病因及时治疗,避免视功能进一步的损害.     

手术治疗挫伤性前房积血所致继发性青光眼的疗效及安全性分析

目的：探讨手术治疗挫伤性前房积血所致继发性青光眼的疗效及安全性分析。方法：选取2014－11／2015－11我院收治的挫伤性前房积血继发性青光眼患者70例70眼，所有患者均行手术治疗，对比患者手术前后的视力、前房深度、平均眼压及术后并发症情况。结果：与治疗前相比，挫伤性前房积血所致继发性青光眼患者治疗后视力明显改善，差异有统计学意义（t＝42.471，P＜0．001）。与治疗前相比，挫伤性前房积血所致继发性青光眼患者治疗后前房深度较深，平均眼压较低，差异有统计学意义（ t＝9．726、26．041， P＜0．001）。2例继发性青光眼患者手术治疗后出现前房积血，经治疗后症状缓解，未出现角膜血染、眼球肿胀疼痛等并发症。结论：手术治疗挫伤性前房积血所致继发性青光眼患者的疗效佳，安全性高，能提高患者的视力、加深前房角深度以及降低眼压。     

睫状体切除术—治疗外伤性青光眼的新方法

外伤性青光眼的治疗是很困难的,无论是古典式滤过性手术和最流行的虹膜睫状体退缩术都是无效的。具有重要意义的是Sautter和Demeler提出了一种新的手术-睫状体切除术,该种手术主要用于治疗继发性无晶体性青光眼。本文作者采用该种手术对25个病人25只眼施行了此种手术,其中16只眼是角膜穿通伤后继发青光眼,有9只眼是眼球挫伤后继发青光眼。考虑到手术损伤和睫状体出血的可能性,对于睫状体切除术仅选择了晚期和终末期青光眼及有明显组织变化的病人。     

眼外伤继发青光眼调查分析

目的　探讨眼外伤继发青光眼的病因及其在外伤青光眼中的发生率 ,作为外伤后继发青光眼的早期诊断依据。方法　回顾性分析了1 1 2例眼外伤后继发青光眼的临床资料 ,探讨继发青光眼的原因、发生时间及与眼外伤的关系。结果　眼挫伤后继发青光眼与外伤性白内障、超过 1 80°范围的前房角后退、虹膜明显损伤和晶状体异位有高度一致性。 4种原因中的 2种存在于所有病例中。穿孔性眼外伤后继发青光眼与粘连性角膜白斑、可见的晶状体损伤或晶状体异位有关 ,集中于晶状体虹膜隔的损伤 ,而引起小梁网明显的功能损伤。结论　眼外伤的正确处理 ,密切随访 ,观察眼压 ,尽可能早的预防不必要的视力损害     

儿童眼外伤继发青光眼临床分析

目的 探讨儿童眼外伤继发青光眼的病因及其在外伤青光眼中的发生率，作为外伤后继发青光眼的早期诊断依据。方法 回顾分析了89例儿童眼外伤后继发青光眼的临床资料，探讨了继发育光眼的原因、发生时间及与眼外伤的关系。结果 儿童眼球顿挫伤后继发青光眼与外伤性白内障，超过180。范围的房角后退，虹膜明显损伤和晶状体异位有高度一致性。四种原因中的二种存在于所有病例中。儿童眼球穿通伤后继发青光眼与粘连性角膜白斑，可见的晶状体损伤或晶状体异位有关，集中于晶状体虹膜膈的损伤，而引起小梁网明显的功能损伤。结论 儿童眼外伤的正确处理。密切随访，观察眼压，尽可能早的预防不必要的视力损害。     

眼挫伤继发青光眼的临床分析与治疗

目的探讨眼钝挫伤继发青光眼的原因和治疗方法。方法对61例（61眼）眼挫伤继发性青光眼的原因及治疗等临床资料进行回顾性分析。结果本组61例中由眼内积血所致青光眼26例,由房角挫伤所致青光眼20例,由晶状体所致青光眼14例,由眼内炎所致青光眼1例。根据眼压升高原因分别通过单纯药物治疗15例（24．59％）,药物治疗加前房冲洗14例（22．95％）,药物治疗加抗青光眼手术治疗32例（52．46％）。经治疗后眼压恢复正常57例（93．44％）,视力不同程度提高。结论眼挫伤后不同原因引起眼压升高,应针对其原因,采取及时和正确的治疗。     

外伤性白内障继发性青光眼伴前房消失的临床研究

目的 探讨眼球穿孔伤伴外伤性白内障后继发性青光眼引起前房消失的治疗方法.方法 对12例(12眼)眼球穿孔伤后外伤性白内障后继发青光眼伴前房消失,立即施行晶状体超声乳化和(或)前部玻璃体切除术,手术细心操作.术后随访6～ 24个月.结果 所有术眼术后前房形成良好,眼压控制理想,术后视力较术前明显提高,无角膜内皮失代偿等并发症.结论 眼球穿孔伤伴外伤性白内障后继发青光眼及前房消失,及时行白内障超声乳化手术,解除瞳孔阻滞,是前房形成的关键,从而可获得较好的结果.     

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.

---

     

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.