LASIK术后弥漫性板层角膜炎的药物预防

目的探讨糖皮质激素对准分子激光原位角膜磨镶术(LASIK)后弥漫性板层角膜炎(DLK)的预防作用。设计前瞻性随机对照临床研究。研究对象接受双眼LASIK手术的近视患者101例(202眼),按眼别分为处理组(101眼)和对照组(101眼)。方法 LASIK术中,处理组局部用糖皮质激素(0．001％地塞米松)进行角膜瓣层间冲洗,对照组则用平衡盐液进行冲洗。主要指标术前、术后第1、3、7天及1个月的裸眼视力、最佳矫正视力、屈光度、眼压,术后DLK的发病率及临床分期。结果 LASIK术后各时期,处理组和对照组的裸眼视力、最佳矫正视力、平均屈光度、眼压差异均无统计学意义(P>0．05)。术后第1天,处理组DLK发病率为4．0％(4眼),全部为Ⅰ期,对照组17．8％(18眼),其中Ⅰ期占88．9％,Ⅱ期占11．1％;术后第 3天,处理组DLK发病率为5．0％(5眼),全部为Ⅰ期,对照组为21．8％(22眼),其中Ⅰ期占86．4％,Ⅱ期占13.6％。两组间比较, DLK的发病率差异有显著统计学意义(P<0．01)。结论 LASIK术中应用O．001％的地塞米松进行角膜瓣层间冲洗,能够明显降低DLK的发病率,是一种安全、有效的预防方法。     

LASIK术中粗大水流冲洗对弥漫性板层角膜炎的影响

目的探讨粗大水流冲洗方法对准分子激光原位角膜磨镶术（laser in situ keratomileusis,LASIK）后弥漫性板层角膜炎（diffuse lamellar keratitis,DLK）的预防作用。方法接受双眼LASIK手术的近视患者120例（240眼）,按眼别分为处理组（左眼）和对照组（右眼）。在IASIK术中,以乳酸钠林格注射液．处理组采用粗大水流冲洗方法进行角膜瓣基质面和角膜基质床冲洗,对照组则进行角膜瓣层间冲洗。术前,术后第1、第3、第7天及第1个月,检查患者的裸眼视力、最佳矫正视力、屈光度、眼压．以及术后DLK的发病率及临床分期。采用SPSS11．0统计软件对术后视力、屈光度、眼压进行配对t检验,对术后DLK的发病率进行χ^2检验。结果术后各时期．处理组和对照组的裸眼视力、最佳矫正视力、平均屈光度、眼压等差异均无统计学意义（P〉0．05）。术后第1天,处理组DLK发病率为1．6％（2眼）．全部为Ⅰ期;对照组为9.2％（11眼）,其中Ⅰ期占90．9％,Ⅱ期占9．1％。术后第3天,处理组没有DLK发生;对照组为8.3％（10眼）,全部为Ⅰ期。两组间比较．术后第1、第3天DLK的发病率差异均有显著统计学意义（P〈0．01）。术后第7天,两组DLK均消退,差异无统计学意义。结论术中应用粗大水流冲洗方法进行角膜瓣基质面和角膜基质床冲洗,能够明显降低DLK发病率,是一种安全、有效的预防方法。     

不同糖皮质激素用药方法对准分子激光原位角膜磨镶术后弥漫性板层角膜炎的预防作用

目的探讨糖皮质激素对准分子激光原位角膜磨镶术（laser in situ keratomileusis,LASIK）后弥漫性板层角膜炎（diffuse lamellar keratitis,DLK）的预防作用及不同用药方法的效果。方法设计前瞻性研究,对接受LASIK手术的近视患者208例（416眼）根据术后用药不同,随机分为实验组和对照组各104例。实验组术后使用碘必殊滴眼液4次/d,用药1周,再用0.1%氟美瞳滴眼液3次/d、2次/d、1次/d,用药各1周。对照组术后用0.1%氟美瞳滴眼液4次/d、3次/d、2次/d、1次/d,用药各1周,加托百士滴眼液1周。观察指标：在术后第1周、第1个月进行眼压检测,用裂隙灯观察术眼,统计DLK发生率并进行临床分期。结果LASIK术后第1周和第1个月,实验组与对照组比较,眼压差异无统计学意义,个别眼压增高者停用激素眼药后眼压很快恢复正常。术后第3天,实验组有7眼（3.3%）发生DLK,全为Ⅰ期;对照组有25眼（12.0%）发生DLK,其中Ⅰ期20眼（80.0%）,Ⅱ期5眼（20.0%）。术后第7天,实验组有1眼发生DLK,对照组有18眼（8.6%）发生DLK,其中Ⅰ期15眼（83.3%）,Ⅱ期3眼（16.7%）。对两组的DLK发生率进行比较,差异有显著统计学意义。结论LASIK术后短期应用强效糖皮质激素可明显降低DLK的发生率并缩短病程,眼压升高作用不明显,是一种安全有效的预防方法。     

LASIK术后弥漫性板层角膜炎的研究现状

随着准分子激光原位角膜磨镶术(LASIK)日益普及,与其相关的并发症越来越受到人们重视。LASIK术后弥漫性板层角膜炎是其并发症之一,且近几年越来越受到重视。本文通过检索近年来国内外的有关文献,对其流行病学、发病机制、临床特点、诊断及治疗作一综述。     

滑石粉对LASIK术后发生弥漫性板层角膜炎的影响观察

目的：观察是否戴无菌滑石粉手套影响准分子激光原位角膜磨镶术（ laser in situ keratomileusis,LASIK）术后弥漫性板层角膜炎（ diffuse lamellar keratitis,DLK）的发生率,证实残留滑石粉对DLK发生起重要作用。 方法：收集单纯手消毒法行 LASIK 手术的患者563例1126眼作为观察组,采用手消毒戴无菌手套法行手术的患者592例1184眼作为对照组。术后第1,7d复查,观察DLK的发生情况。采用卡方检验及秩和检验对DLK的发生情况进行统计分析。 结果：术后第1d,观察组DLK发病率为7.4%（83眼）,其中Ⅰ期为4.6%（52眼）,Ⅱ期为2.8%（31眼）;对照组为12.2%（144眼）,其中Ⅰ期为7.7%（91眼）,Ⅱ期为4.5%（53眼）。术后第7d,两组DLK均消退。对照组2例3眼（术后第8d首次复查,未按时行氟米龙点眼治疗）出现Ⅳ期DLK。观察组DLK的发生率（ P〈0.01）及严重程度（P〈0.01）明显低于对照组。 结论：滑石粉是LASIK术后DLK发生的一个重要因素,采用单纯手消毒法可以去除滑石粉的刺激作用,明显降低DLK的发生率。     

LASIK术后弥漫性板层角膜炎的发病机制及药物调控

弥漫性板层角膜炎（DLK）为准分子激光原位角膜磨镶术（LASIK）术后的一种非感染性炎症。其发病机制可分为内源性、外源性及宿主特异性,其中IL-1、IL-8、TNF-α、内毒素、遗传过敏症、角膜内皮细胞密度及功能等分别参与了不同发病机制的过程。目前的药物治疗及预防主要包括糖皮质激素、LAU0901、非甾体抗炎药及0．5％羧甲基纤维素钠,其中糖皮质激素的术中使用在预防方面具有其独特的优越性。就LASIK术后DLK的发病机制及药物控制进行综述。     

准分子激光原位角膜磨镶术术后弥漫性板层角膜炎研究进展

准分子激光原位角膜磨镶术是目前治疗屈光不正的主要手术方法。随着技术和设备的改进,术后并发症现已比较少见,其并发症之一的弥漫性板层角膜炎因其本身所具有的特殊性而时有报道。本文对其病因、临床表现、分期及分型、病理和治疗的研究进行综述。     

LASIK术后弥漫性板层角膜炎1例

患者男性,18岁。因“双眼近视”于2008年我院行准分子激光原位角膜磨镶术（laser in situ keratomileusis,LASIK）,术后第8天来院复诊。主诉：双眼视物不清4d,异物感2d。查体：全身检查未见明显异常。专科检查：视力：右眼0．25,左眼0．4。双眼球结膜混合充血（＋）,角膜上皮轻度水肿,双眼角膜瓣中央部见直径4mm大小灰白色较浓密混浊,略隆起,边界清楚。角膜后KP（-）,房水清,虹膜晶状体、玻璃体、眼底检查均未见异常。     

原位角膜磨镶术后迟发性弥漫性板层角膜炎

目的：报告1例LASIK术后11mo由于角膜损伤引起的弥漫性板层角膜炎（diffuse lamellar keratitis，DLK）。 方法：22岁女患者应用laser Sight SLX准分子激光机和MoriaII角膜板层刀行双眼原位角膜磨镶术（1aser in situ keratomileusis，LASIK），术中和术后早期未见并发症发生。 结果：LASIK术后11mo，由于书页损伤角膜上皮，右眼诊断为I级DLK。经局部应用皮质类固醇激素，2wk后DLK很快治愈，没有并发症发生。 结论：DLK经常发生于术后早期，但也可发生于术后数月，一旦确诊应迅速治疗，效果良好。     

准分子激光原位角膜磨镶术后弥漫性板层角膜炎

弥漫性板层角膜炎是准分子激光原位角膜磨镶术或相关板层角膜屈光手术后出现的一种非感染性炎症。其发病率不高，但如处理不当，对病人视力的恢复将会产生严重的不良影响。本文对其临床表现、分期、病理、发病机制、治疗和预防等进行综述。     

LASIK术后迟发性弥漫性板层角膜炎

目的:回顾性分析LASIK术后迟发性弥漫性板层角膜炎的病因。方法:2005-01/2007-10到我院行LASIK手术治疗并连续进行观察的近视患者,分为甲、乙两组。LASIK术中所用板层角膜刀、刀头甲组用诗乐氏消毒,乙组采用高压消毒。结果:LASIK术后各时期,甲、乙组的裸眼视力、眼压差异无统计学意义(P>0.05)。甲组患者术后1mo4眼(0.25%)发生弥漫性板层角膜炎(diffuse lamellar keratitis,DLK),全部为Ⅰ期;术后3mo56眼(3.54%)发生DLK,其中Ⅰ期41眼(73.21%),Ⅱ期15眼(26.79%);术后6mo10眼(0.63%)发生DLK,全部为Ⅰ期;术后1a3眼(0.19%)发生DLK,全部为Ⅰ期。乙组患者各时期均未见DLK发生。结论:诗乐氏可能导致LASIK术后迟发性弥漫性板层角膜炎。     

Idiopathic recurrence of diffuse lamellar keratitis after LASIK

PURPOSE: To report a case of late recurrence of bilateral diffuse lamellar keratitis (DLK) after LASIK. METHODS: A 39-year-old woman presented in the early postoperative period with bilateral DLK after hyperopic LASIK and was treated with topical steroids. One year after and with no obvious cause (idiopathic), recurrence of the same stage (stage III) of disease was observed. RESULTS: Slit-lamp examination revealed diffuse, multifocal, and granular haze in the interface. The microbiology culture was negative. Confocal microscopy demonstrated multiple activated keratocytes, debris, and inflammatory cells adjacent to the flap interface. After intense treatment with topical corticosteroids, DLK resolved and corneal transparency was achieved with complete restoration of visual acuity. CONCLUSIONS: Diffuse lamellar keratitis may recur in LASIK patients with previous episodes without an obvious cause (idiopathic). Early diagnosis and treatment with topical corticosteroids can achieve complete resolution without visual loss--even in advanced stages of DLK.     

准分子激光原位角膜磨镶术后弥漫性板层角膜炎的共焦显微镜观察

目的探讨准分子激光原位角膜磨镶术（LASIK）后弥漫性板层角膜炎（DLK）的临床病理学特征及发病机制。方法LASIK术后DLK患者30例（39只眼）（Ⅰ～Ⅳ期）,术后1、3、5、7d及1个月进行裂隙灯显微镜检查,术后3、7d及1个月进行共焦显微镜检查。结果Ⅰ期及Ⅱ期DLK的典型表现出现在术后3d,共焦显微镜观察所见：角膜板层切口前基质及层间可见大量直径12～20μm的圆形或卵圆形细胞,反光较强,散在分布或排列成行,细胞内可见偏心的高反光的核和低反光的细胞内结构。层间还可见大量直径8～12μm的圆形细胞,强反光,多聚集成簇或排列成行,细胞核形态不规则。术后7d上述细胞几乎消失。Ⅲ期DLK出现于术后3～5d,表现为前基质中的细胞浸润更浓密,层间无定形的高反光物质较明显。Ⅳ期DLK在术后5～7d出现明显的前基质结构模糊,高反光,角膜瓣全层皱褶,晚期形成大量高反光的瘢痕组织。结论LASIK术后弥漫性板层角膜炎是角膜瓣层间的炎性反应,主要病理学特征为角膜瓣层间的炎性细胞浸润,其发病是多种因素通过内源性途径和外源性途径共同作用的结果。     

Delayed onset diffuse lamellar keratitis following enhancement LASIK surgery

Background: Diffuse lamellar keratitis (DLK) is a relatively uncommon complication of the refractive procedure, laser‐assisted in situ keratomileusis (LASIK). If detected and diagnosed in a timely fashion, it can be treated and should resolve with minimal sequelae. If untreated, or misdiagnosed and treated incorrectly, there may be loss of visual acuity. Optometrists should be familiar with this condition, its signs, symptoms and correct treatment protocol. Case history: A 58‐year‐old male Caucasian developed delayed onset diffuse lamellar keratitis, seemingly in the absence of an epithelial defect, 25 days following an enhancement LASIK procedure to his right eye. The DLK in this patient is delayed longer than typically reported in the literature. Subsequent management with topical steroids was complicated as the patient was a steroid responder and developed a markedly raised intraocular pressure that was managed with a topical anti‐glaucoma agent. The diagnosis, pathogenesis and issues relevant to the treatment of this condition are discussed. Conclusion: Optometrists, particularly those actively participating in the shared care of refractive surgery patients, must be familiar with diffuse lamellar keratitis so that diagnosis is not delayed. As the number of cases of refractive surgery in Australia increases, optometrists will encounter this condition more frequently.     

Sporadic diffuse lamellar keratitis (DLK) after LASIK

PURPOSE: To examine the incidence of sporadic diffuse lamellar keratitis (DLK) in a large series of LASIK eyes and to suggest the hypothesis that the etiology of sporadic DLK differs from that of epidemic DLK. METHODS: The incidence and severity of DLK was noted in 1352 consecutive eyes that had primary LASIK for myopia or hyperopia and 217 consecutive eyes that had LASIK enhancement. RESULTS: Twelve of the eyes having primary LASIK had stage 1 DLK and 5 had stage 2 DLK (.9% total). No eyes had stage 3 or stage 4 DLK. Three of the 217 eyes (1.4%) that had LASIK enhancement had stage 1 DLK. The difference in the rate of DLK for primary LASIK compared with LASIK enhancement was not statistically significant (p = 0.69). All eyes responded to intensive corticosteroid therapy, with the addition of flap lifting and irrigation for the eyes with stage 2 DLK. Two of the eyes (one primary LASIK and one LASIK-enhancement) had implanted epithelial nests associated with the DLK. None of the cases of DLK occurred in eyes of patients who had surgery on the same operating day in this series. Two other eyes that had epithelial abrasions more than 3 months after LASIK or LASIK enhancement developed stage 1 DLK. CONCLUSIONS: Many cases of sporadic DLK, including cases associated with epithelial trauma after LASIK, are likely attributable to endogenous factors that trigger inflammation. One trigger is the release of epithelium-derived cytokines such as interleukin-1 that stimulate keratocytes to produce chemokines that are chemotactic to inflammatory cells. Cells likely accumulate at the interface because it is potential space, representing a path of least resistance for cell movement. Some sporadic cases may also be related to exogenous factors such as Betadine. Epidemic DLK is likely associated with exogenous factors that stimulate inflammation, such as endotoxin contaminating sterilizer reservoirs or detergents on instruments.     

Late-onset diffuse lamellar keratitis

BACKGROUND: Diffuse lamellar keratitis (DLK) is marked by the presence of diffuse or multifocal infiltrates confined to the laser in situ keratomileusis (LASIK) interface. These infiltrates are culture-negative, and the etiology is thought to be noninfectious. Most cases of DLK occur within the first week or 2 following surgery. CASES: We described 2 cases of DLK that occurred 3 months after LASIK. These patients were treated with intensive topical corticosteroids. RESULTS: Treatment with topical corticosteroid was instituted, with rapid improvement in patient symptoms, visual acuity, and slit-lamp biomicroscopic findings. CONCLUSION: DLK may occur as late as 3 months after LASIK.