Late-onset diffuse lamellar keratitis following laser in situ keratomileusis

Objective

To analyze 12 cases of late-onset diffuse lamellar keratitis (DLK) following uncomplicated LASIK and propose a method of management.

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。     

Bilateral marginal sterile infiltrates and diffuse lamellar keratitis after laser in situ keratomileusis

PURPOSE: To report cases of acute bilateral catarrhal infiltrates in the early postoperative period after laser in situ keratomileusis (LASIK). METHODS: Retrospective review of both eyes of two patients. RESULTS: Two patients developed acute bilateral, marginal, catarrhal infiltrates in the early postoperative period after LASIK. Both patients had moderate to severe chronic meibomian gland dysfunction preoperatively. One patient (both eyes) developed grade 3 diffuse lamellar keratitis (DLK) that required both flaps to be lifted for irrigation and cleaning on postoperative day 5. Fungal and bacterial cultures were negative in both eyes of both patients. The condition resolved with intensive topical corticosteroids and fortified antibiotics. Regression of refractive error and the need for enhancement was encountered in all eyes. There was mild recurrence in one eye of each patient with pretreatment with topical corticosteroids prior to enhancement. CONCLUSIONS: Endogenous factors such as chronic blepharitis and meibomian gland dysfunction may trigger inflammation resulting in sporadic cases of catarrhal infiltrates after LASIK. These patients may have chronic inflammatory milieus that can trigger sporadic cases of catarrhal infiltrates after LASIK, with accompanying diffuse lamellar keratitis.     

Delayed diffuse lamellar keratitis after laser in situ keratomileusis

Two cases are reported of delayed diffuse lamellar keratitis after uneventful laser in situ keratomileusis. The first patient presented with an epithelial defect 6 weeks after laser in situ keratomileusis. Three days later the defect was healed but diffuse lamellar keratitis was noted. This was treated with topical dexamethasone and ketorolac with complete resolution of the diffuse lamellar keratitis over 3 weeks. The second patient presented with an epithelial defect and gross diffuse lamellar keratitis 10 weeks after laser in situ keratomileusis. Treatment was with topical dexamethasone and ciprofloxacin with gradual resolution of the diffuse lamellar keratitis. Common to both patients was a background of rosacea, implanted debris with no initial reaction, and epithelial defects leading to diffuse lamellar keratitis. It is suggested that these two cases represent epithelial defect associated corneal infiltration, which resembles classical diffuse lamellar keratitis with the spread of inflammatory cells through a path of least resistance.     

Multifocal lamellar keratitis following laser in situ keratomileusis

Over a period of approximately 7 months, multiple subepithelial spots were noted in one or both corneas of some patients examined 2 to 6 months after laser in situ keratomileusis (LASIK). The lesions appeared identical to adenovirus keratitis. The eyes were quiet, had good vision, and no patient had a history of adenoviral keratoconjunctivitis. In all eyes, the lesions resolved spontaneously or with topical steroid eyedrops. All investigations were negative for adenovirus. Corneal laser scanning in vivo confocal microscopy revealed Langerhans cells in the epithelium, which disappeared after the lesions resolved.     

Late-onset idiopathic diffuse lamellar keratitis after laser in situ keratomileusis

We report a case of late-onset diffuse lamellar keratitis (DLK) in the left eye of a 56-year-old white woman 3 years after uneventful bilateral laser in situ keratomileusis (LASIK). Slitlamp examination revealed stage 3 DLK with diffuse, multifocal, dot-like, and granular haze in the interface. The DLK did not have an obvious causative agent such as trauma or epithelial defects and responded rapidly to topical corticosteroid therapy. Surgery was performed to relift the flap, remove cellular infiltrates, and obtain cultures. The microbiology culture was negative. This case indicates that DLK can occur several years after LASIK without an obvious cause.     

准分子激光原位角膜磨镶术后DLK的临床治疗

目的:探讨准分子激光原位角膜磨镶术后弥漫性层间角膜炎的临床分级治疗。方法:收集2008-04/2009-09我院的准分子激光原位角膜磨镶术后弥漫性层间角膜炎患者19例21眼,根据角膜层间炎性细胞浸润程度和浸润范围,制定分级标准,予以相应分级治疗方案。观察其治疗前和治疗后1,3,5,7,10d及1mo时临床症状,角膜浸润程度和范围,视力,屈光度数及眼压等情况。结果:19例21眼准分子激光原位角膜磨镶术后弥漫性层间角膜炎病例多为轻度,其中Ⅰ度18眼,Ⅱ度2眼,Ⅲ度1眼,经过相应分级糖皮质激素治疗,角膜瓣下炎性细胞浸润灶多在1wk内消退,随访至治疗后1mo,裸眼视力显著提高,达术前最佳矫正视力。角膜体征,视力及屈光不正恢复程度在各分级DLK之间,及在接受不同分级治疗方案的病例之间,差异均无统计学意义。无糖皮质激素性高眼压发生。结论:弥漫性层间角膜炎的临床综合分级对糖皮质激素分级治疗准分子激光原位角膜磨镶术后弥漫性层间角膜炎具有治疗指导作用。     

准分子激光原位角膜磨镶术后弥漫性层间角膜炎的临床分析

目的 探讨准分子激光原位角膜磨镶术后弥漫性层间角膜炎的临床综合分级标准,指导临床分级治疗.方法 前瞻性系列病例研究.收集2004年12月至2005年5月于复旦大学附属眼耳鼻喉科医院就诊的准分子激光原位角膜磨镶术后弥漫性层间角膜炎患者29例(35只眼),根据角膜层间炎性细胞浸润程度和浸润范围制定分级标准,依照综合分级诊断,予以相应分级治疗方案.观察其治疗前和治疗后1 d、3 d、5 d、7 d、10 d及1个月时临床症状、角膜浸润程度和范围、视力、屈光度数及眼压等情况.测得的小数视力转换为logMAR单位进行统计分析,配对t检验比较LASIK术前、DLK确诊时和治疗后1月的视力及屈光不正变化情况.以炎性细胞浸润程度、浸润范围和治疗方案作为研究因素,对炎性细胞浸润灶消退时间、视力、屈光不正及眼压变化情况进行方差分析或t检验.方差不齐时采用非参数检验方法Kruskal-wallis检验.以P<0.05作为差异有统计学意义.结果 29例(35只眼)准分子激光原位角膜磨镶术后弥漫性层间角膜炎病例多为轻度,其中Ⅰ度30只眼.Ⅱ度3只眼,Ⅲ度和Ⅳ度各1只眼;20只眼侵及周边1区,11只眼侵及中周2区,4只眼侵及中央3区;19只眼为Ⅰ度1区.33只眼在术后1～3 d内确诊.确诊时裸眼视力低于术前最佳矫正视力.经过相应分级糖皮质激素治疗,角膜瓣下炎性细胞浸润灶平均在(6.06 ±2.04)d内消退.随访至治疗后1个月,裸眼视力显著提高,达术前最佳矫正视力水平,30只眼最佳矫正视力优于或同术前.等效球镜平均为(-0.21±1.16)D.角膜体征、视力及屈光不正恢复程度在各分级弥漫性层间角膜炎之间,及在接受不同分级治疗方案的病例之间,差异均无统计学意义.无糖皮质激素性高眼压发生.结论 弥漫性层间角膜炎的临床综合分级对糖皮质激素分级治疗准分子激光原位角膜磨镶术后弥漫性层间角膜炎具有治疗指导作用.(中华眼科杂志,2009.45:601-606)     

Surgical-glove-related diffuse lamellar keratitis after laser in situ keratomileusis: long-term outcomes

PURPOSE: To study the long-term refractive results in eyes that developed surgical-glove-related diffuse lamellar keratitis (DLK) after laser in situ keratomileusis (LASIK). SETTING: Department of Ophthalmology, Hospital Provincial, Toledo, Spain. METHODS: This retrospective review analyzed an epidemic of surgical-glove-related DLK over a 5-month period at a single hospital. Twenty-four eyes (24 patients) that developed DLK (DLK group) were compared to 30 eyes (30 consecutive patients) that had surgery during the same time but had an uneventful postoperative course (control group). Follow-up was 12 months in all cases. RESULTS: Twelve months after LASIK, the mean spherical equivalent was 0.14 diopter (D) +/- 0.36 (SD) in the DLK group and -0.07 +/- 0.33 D in the control group (P=.03). The mean uncorrected visual acuity was 0.91 +/- 0.18 and 0.90 +/- 0.17, respectively (P = .81). The mean best spectacle-corrected visual acuity (BSCVA) was 0.97 +/- 0.08 in the DLK group and 0.99 +/- 0.06 in the control group (P = .42). At 1 year, 91.7% of eyes in the DLK group and 93.3% of eyes in the control group were within +/-0.50 D of the attempted correction (P = .82). The BSCVA was 1.0 or better in 87.5% and 93.3%, respectively (P =.46). CONCLUSIONS: Early diagnosis and appropriate treatment of glove-related DLK provided visual outcomes that were similar to those in eyes with an uneventful postoperative course. These good results are consistent with those in studies of classic DLK.     

Confocal microscopic findings in a case of delayed-onset bilateral diffuse lamellar keratitis after laser in situ keratomileusis

We report a case of bilateral diffuse lamellar keratitis (DLK) with delayed onset after a bilateral laser in situ keratomileusis (LASIK) procedure. A thorough history, review of systems, and laboratory evaluation revealed no pertinent medical history or risk factors for delayed-onset DLK after LASIK. Confocal microscopic examination of both corneas demonstrated a large number of activated keratocytes in the flap interface, particulate debris of variable size distributed throughout the interface, and scattered inflammatory cells. It was then decided to lift and wash both corneal flaps and interfaces. Scrapings for stains and cultures were also taken from both flap beds and were negative. After treatment with prednisolone acetate 1% and topical cyclosporin A 0.5%, the DLK resolved in both eyes with residual faint, diffuse, corneal haze. The patient developed a steroid-induced elevation in intraocular pressure that resolved after the topical corticosteroids were stopped.     

Traumatic flap displacement and subsequent diffuse lamellar keratitis after laser in situ keratomileusis

A 45-year-old man was struck in the left eye by the edge of a paper shopping bag 3 weeks after having laser in situ keratomileusis (LASIK). The injury resulted in partial displacement of the LASIK flap. The patient developed diffuse lamellar keratitis (DLK) the day after the flap was repositioned. By day 4, visual acuity diminished to 20/60. By day 9, the clinical evidence of the DLK had resolved, and by day 15, uncorrected visual acuity was 20/20. Eye trauma 3 weeks after LASIK can result in displacement of the LASIK flap, and DLK can develop following flap replacement. Long-term anatomic and visual results are usually good.     

Risk factors for development of diffuse lamellar keratitis after laser in situ keratomileusis

PURPOSE: To investigate the risk factors and mechanisms of diffuse lamellar keratitis (DLK) after laser in situ keratomileusis (LASIK). METHODS: In 5708 eyes of 2927 patients who underwent LASIK, the patient's background, clinical findings, and surgical data were retrospectively evaluated and compared with patients who had DLK and those who did not (non-DLK group). RESULTS: DLK occurred in 46 of 5708 eyes (0.81%). DLK occurred more frequently in eyes operated with the MK-2000 microkeratome (1.1%) than with the LSK-One microkeratome (0.6%; P = .039). Corneal endothelial cell density (2686.8 +/- 235.3/mm2) was significantly lower in eyes that developed DLK than in eyes without DLK (2783.8 +/- 275.5/mm2; P = .017). The width of palpebral fissure in a normal state and the maximum opening position were significantly larger in the DLK group (10.3 +/- 1.9 mm and 18.1 +/- 7.2 mm, respectively) than the non-DLK group (8.3 +/- 1.6 mm with P < .001; 11.5 +/- 2.0 mm with P = .012). CONCLUSIONS: The type of microkeratome, lower corneal endothelial cell density, and larger palpebral fissure were potential risk factors for DLK after LASIK. These factors may be associated with delayed wound healing of the corneal flap margin, resulting in poor sealing of the flap, which may induce the influx of inflammatory cells.     

Severe late-onset recurrent epithelial erosion with diffuse lamellar keratitis after laser in situ keratomileusis

A 39-year-old woman had laser in situ keratomileusis that was complicated by intraoperative epithelial erosion in both eyes. Seven months after surgery, the patient returned, complaining of pain and blurred vision in the left eye. Slitlamp examination revealed corneal epithelial erosion with severe diffuse lamellar keratitis (DLK). Reepithelialization was complete in several days. However, severe inflammation remained until systemic steroids were administered. Recurrent erosions can lead to a serious inflammatory reaction such as DLK because of the presence of the flap-stroma interface.     

LASIK术后弥漫性板层角膜炎

弥漫性板层角膜炎(diffuse lamellar keratitis,DLK),为非感染性弥漫性板层界面角膜炎症反应,发生于准分子激光原位角膜磨镶术(laser in situ keratomileusis,LASIK)之后。我们综述了本病的病因、发病机制、临床症状、诊断和治疗,特别强调对LASIK术后DLK的预防应给予充分的关注。     

Peripheral keratitis following laser in situ keratomileusis

PURPOSE: To report two different cases of sterile, peripheral keratitis following laser in situ keratomileusis (LASIK). METHODS: A report of two cases (two eyes of two patients). RESULTS: In two patients, peripheral infiltrates appeared 1 day after LASIK. One patient had a history of rheumatoid arthritis and both had peripheral corneal changes that may have represented prior inflammatory events. The presentations were quite different, with one occurring in association with an epithelial defect at the edge of the flap and the other occurring without an epithelial defect peripheral to the microkeratome cut. In the second case a similar infiltrate showed up in the unoperated fellow eye. Both patients were treated with aggressive antibiotic and corticosteroid therapy. Both patients recovered well with no loss of best spectacle-corrected visual acuity. CONCLUSION: Peripheral keratitis can occur in patients following LASIK; preoperative evidence of previous inflammation may be a marker for patients at higher risk. Rheumatoid arthritis patients may be at increased risk for this complication. With careful and aggressive management excellent visual outcomes are still possible.