KTP激光联合透明质酸钠留置治疗泪道阻塞

目的 研究KTP激光联合透明质酸钠留置治疗泪道阻塞的效果。方法 用带针芯的泪道探针探察泪道至阻塞处，拔出针芯，将KTP激光导光纤维插至泪道阻塞处，发射激光至泪道阻塞处疏通为止，并注入透明质酸钠。术后随访2周－6月，观察效果。结果 采用此方法治疗各种泪道阻塞118眼，112眼治愈，6眼无效，治愈率为94．92％。结论 KTP激光联合透明质酸钠留置是治疗泪道阻塞的有效方法。     

KTP激光泪道成形术的临床研究

目的 探討KTP激光泪道成形術治療泪道阻塞的臨床效果。方法 用帶針芯的泪道探針探至泪道阻塞處,拔出針芯,將KTP激光導光纖維插至泪道阻塞處,激發激光至泪道阻塞處疏通為止。结果 采用此方法治療各種泪道阻塞116例(138眼),均為一次性疏通(100％),135眼治愈、3眼無效,治愈率為97.8％。結論 KTP激光泪道成形術是目前治療泪道阻塞的最有效方法。     

Nd：YAG激光联合置管术治疗泪道阻塞

目的探讨Nd：YAG激光联合置管术治疗泪道阻塞的效果。方法用带针芯的泪道探针探查泪道至阻塞处,拔出针芯,将Nd：YAG激光导光纤维插至泪道阻塞处,发射激光至疏通为止,采用直径1mm硅胶管自下或上泪点经鼻泪管固定于鼻腔中。结果采用此方法治疗各种泪道阻塞96眼。治愈92眼,好转3眼,1眼无效,治愈率为95．83％。结论Nd：YAG激光联合置管术是治疗泪道阻塞的有效方法。     

激光泪道成形术

目的　探讨倍频 YAG激光及 Nd:YAG泪道激光行泪道成形术的疗效。方法　将带针芯的泪道探针按常规泪道探通方法探至泪道阻塞处 ,拔出针芯 ,将倍频 YAG或N d:YAG激光的光纤插入泪道探针达到泪道阻塞处 ,反复击射至击通为止。然后注入生理盐水及抗生素 ,术后泪道冲洗或进一步扩张 1wk～ 3mo不等。结果　共治疗 5 5 4眼 ,随访496眼 ,随访时间 3～ 2 2 m o,单纯性泪道阻塞经 1～ 2次治疗泪道通畅者 412眼。17眼外伤性泪道断裂吻合术后阻塞病例全部再通 ,慢性泪囊炎 5 6眼中 5 0眼治愈 ,复发者有 6例 ,其中再次激光治愈 3例 ,3例术后又发生阻塞。 11例泪囊鼻腔吻合术失败者 ,经激光治疗 8眼症状完全消失。结论　泪道激光治疗泪道阻塞性疾病安全有效 ,并发症少     

532nm激光泪道成形术治疗泪道阻塞的临床研究

目的:研究532nm激光泪道成形术治疗各种泪道阻塞的临床效果。方法:采用532nm激光泪道治疗机,患眼局部常规消毒后,充分扩张泪小点,用带针芯的泪道探针由泪小点插至泪道阻塞处,拔出针芯,将532nm激光导光纤维插至泪道阻塞处,激发激光至泪道阻塞处疏通,并同时接冲左氧氟沙星液,术后隔日泪道冲洗。结果:采用此方法治疗各种泪道阻塞630例(717眼),5眼未疏通,疏通率为99.3%。术后0.5a再阻塞;复打激光者32例(32眼),复打率为4.5%。680眼一次性治愈,治愈率为94.8%。结论:532nm激光泪道成形术是目前治疗泪道阻塞效果快捷有效的治疗方法。     

泪小管阻塞的KTP激光治疗

目的 观察磷酸钛氧钾[Kalium(potassium)titanyl phosphate，KTP]激光治疗泪小管阻塞的效果。方法 采用国产KTP激光治疗仪。用带针芯的泪道套管针按常规泪道探通法从下泪点插至泪道阻塞处，拔出针芯，插人光纤，发射激光，气化疏通泪道。结果 在各种原因所致的泪小管阻塞489例，516眼中，激光治疗有效478眼(92．64％)，无效38眼(7．36％)。结论 KTP激光治疗泪小管阻塞有较好的效果。适应证广，组织损伤小。     

Nd:YAG激光泪道成形术的临床体会

目的 探讨Nd：YAG泪道激光行泪道成形术后的临床疗效。方法 将带针芯的泪道探针按常规泪道探通方法探至泪道阻塞处,拔出针芯,将Nd：YAG激光的光纤插入泪道探针达到泪道阻塞处,反复击射至击通为止。然后注入生理盐水及抗生素,术后泪道冲洗或进一步扩张1周～3月不等。结果 共治疗93例（93只眼）,随访89只眼,随访时间6～24月,单纯性泪道阻塞经1～2次治疗泪道通畅者46只眼。慢性泪囊炎39只眼中37只眼治愈,复发者6只眼,其中再次激光治愈5只眼,2只眼术后又发生阻塞。3只眼泪囊鼻腔吻合术失败者,经激光治疗症状完全消失,1例上颌窦肿瘤术后泪道阻塞激光治疗失败。结论 Nd：YAG泪道激光治疗泪道阻塞性疾病安全有效,并发症少,且创伤小,无痛苦,易为患者接受。再联合多种药物治疗效果更好。     

KTP泪道激光成形术治疗泪道阻塞10a回顾分析

目的:回顾研究10a来KTP激光泪道成形术治疗各种泪道阻塞的临床效果。方法:采用KTP激光泪道治疗机,患眼局部常规消毒后,充分扩张泪小点,用带针芯的泪道探针由泪小点插至泪道阻塞处,拔出针芯,将KTP激光导光纤维插至泪道阻塞处,激发激光至泪道阻塞处疏通,并同时接冲左氧氟沙星液,术后隔日泪道冲洗。结果:采用此方法治疗各种泪道阻塞766例870眼,9眼未疏通,疏通率为99.0%。42例溢泪症状再现,泪道冲洗不通畅术后6mo后再阻塞,复打激光者42例42眼,复打率为4.8%;其中36例36眼再次激光无效。825眼一次性疏通,术后泪道冲洗通畅,溢泪症状消失或明显减轻,治愈率为94.8%。结论:KTP激光泪道成形术是目前治疗泪道阻塞损伤性小、治愈率高、效果快捷的治疗方法。     

KTP激光联合新型泪道引流管治疗泪道阻塞

目的:观察KTP激光联合新型泪道引流管治疗各种原因所致的泪道阻塞。方法:用带针芯的泪道探针探察泪道阻塞处,拨出针芯,再插入KTP激光纤维,发射激光,消除阻塞,疏通泪道,冲洗通畅,用泪道引流管两端分别自上下泪点进入,疏通泪道至鼻腔,两端稍拉紧至鼻孔,至此处打死结,减除多余软管,管结弹回鼻腔。术后点抗生素眼液,3mo后取管。结果:各种原因所致泪道阻塞426例482眼,手术成功445眼(92.3%),失败37眼(7.7%)。结论:KTP激光联合泪道引流管治疗泪道阻塞,操作简便,适应证广,组织损伤小,术后无瘢痕,患者无痛苦,门诊即可手术,时间在5min左右即可完成。     

磷酸钛氧钾激光治疗泪道阻塞

目的 观察磷酸钛氧钾（KTP）激光性治疗各种原因所致泪道阻塞的效果。方法 用带针芯的9号泪道探针探查泪道阻塞处，拔出针芯，再插入KTP激光纤维，发射激光，疏通泪道。结果 治疗各种原因引起的泪道阻塞256眼，成功196眼，失败60眼。结论 KTP激光治疗各种原因所致泪道阻塞操作简单、适应证广、组织损伤小，是泪道阻塞的首选治疗方法，但目前尚不能完全取代传统的泪囊鼻腔吻合术。     

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.