Ординатура / Офтальмология / Английские материалы / Jaypee Gold Standard mini Atlas Series Lasik_Aragawal, Jacob_2009

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Figure 3.10E

Figure 3.10F

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Figure 3.10G

Figure 3.10H

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Figure 3.10I

Figures 3.10A to I: (A) Diffuse lamellar keratitis (Courtesy: Ronald J Smith); (B) DLK in a 44 year M 3 days after LASIK (performed in 1995 when astigmatic keratotomy, AK, was performed under the flap to correct astigmatism). Fine granular punctate infiltrates are diffusely scattered in the lamellar interface. Smith RJ, Maloney RK. Diffuse lamellar keratitis: A new syndrome in lamellar refractive surgery. Ophthalmology 1998; 105:172126; (C and D) DLK in a 33 year M 2 days after LASIK (combined with AK under the flap). (C) Fine infiltrates are diffusely scattered through the interface and best seen at the pupillary margin.

(D) Slit-lamp exam localizes the pathology to the flap interface. Smith RJ, Maloney RK. Diffuse Lamellar Keratitis: A new syndrome in lamellar refractive surgery. Ophthalmology 1998;

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105:1721-26; (E) Central haze, hyperopia and folds. Central Toxic Keratopathy after DLK. Corneal flattening with hyperopia on topography and central haze and folds on slit lamp exam. Corneal stromal healing takes place of the course of months to years like PRK haze. Courtesy Dr. David R Hardten and Dr. Richard Lindstrom; (F) Staph. aureus infection after LASIK. Dominant focus with extension anteriorly posteriorly and peripherally. The infiltrate does not respect the flap margins. Redness and irritation were present on the first postoperative day, and fluffy white infiltrates appeared on the second day after LASIK. (Photographed 2 weeks postoperatively) Hovanesian JA, Faktorovich EG, Hoffbauer JD, Shah SS, Maloney RK. Bilateral bacterial keratitis after laser in situ keratomileusis in a patient with human immunodeficiency virus infection. Arch Ophthalmol. 1999 Jul;117(7): 968-70; (G) Epithelial ingrowth from the flap edge. A demarcation line is seen at the edge of the ingrowth. In this eye, epithelial pearls are also prominently visible. Wang MY, Maloney RK. Epithelial ingrowth after laser in situ keratomileusis. Am J Ophthalmol 2000;129(6):746-51;

(H) Mycobacterial keratitis 20 days after LASIK. Focal round corneal opacities at the interface. History was positive for intense topical and oral prednisone for DLK during the first postoperative week, and the patient was on a corticosteroid taper at the time of presentation. Chandra NS, Torres MF, Winthrop KL, Bruckner DA, Heidemann DG, Calvet HM, Yakrus M, Mondino BJ, Holland GN. Cluster of Mycobacterium chelonae keratitis cases following laser in situ keratomileusis. Am J Ophthalmol 2001;132(6):81930; (I) Multiple focal intrastromal infiltrates 49 days after LASIK. The patient was receiving a long course of topical corticosteroids and already had undergone a flap lift with antibiotic and corticosteroid irrigation of the interface 3 weeks earlier. A 1 mm

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the flap without posterior extension into the bed nor anterior extension into the flap, nor extension peripherally beyond the flap margin.

Linebarger and coworkers published a clinical staging system to describe the severity of DLK. Stage 1 is defined as a diffuse scattering of fine infiltrates in the periphery of the flap interface outside of the visual axis. In Stage 2, the diffuse interface infiltrates are also seen within the visual axis involving the center of the flap interface. In Stage 3, there is some clumping of the interface infiltrates in addition to the diffuse infiltrates involving the visual axis. In stage 4 there is an increased density of the interface infiltrates forming several roughly parallel curves which may appear like waves.

Within stage 4 DLK, they also described a rare syndrome of central haze extending into the stromal bed, flattening with hyperopia and deep stromal folds which persist long after the infiltrates are gone. This syndrome probably represents a sequelae of DLK or an unrelated comorbidity following surgery, but should not be called DLK, since the three primary characteristics of diffuse lamellar keratitis are absent or not prominent in the syndrome of haze, hyperopia and folds is a composite of the slit-lamp photograph and topography of the condition

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be questioned, and the pathology may not be representative of DLK. Animal models, confocal microscopy, tearfilm analysis, and epidemiology in addition to clinical examination have improved the understanding of DLK.

Endotoxin is a potent inflammatory agent that has been useful in developing animal models for corneal inflammation, and has recently been implicated in toxic anterior segment syndrome in cataract surgery. The ability of heat stable bacterial endotoxin to incite a vigorous inflammatory response has been observed years before the advent of LASIK. In 1977 Mondino et al demonstrated that intracorneal injection of bacterial endotoxin into rabbit corneas stimulates the alternative complement pathway leading to a rapid polymorphonuclear neutrophil response that presents within the first few days after the initial insult. Holzer and coworkers have developed an elegant model for DLK that involves applying endotoxin to the interface of surgically created corneal flaps in rabbits to reliably cause DLK. Direct histopathology and immunohistopathology studies have confirmed that the predominant cells within the interface in DLK are indeed neutrophils and that corticosteroids significantly reduce the incidence of DLK while NSAIDs do not. Esquenazi also found that the

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Prevention of Diffuse Lamellar Keratitis

Postoperative prophylactic topical corticosteroids, usually four times per day, during the first few days can help prevent DLK. The most useful measure to prevent epidemic DLK has been attention to the sterilization system and instrument cleaning protocol. Standing fluids enable bacteria to proliferate and leave a heat stable endotoxin biofilm before being sterilized. Holland et al described the findings of an in depth investigation of a DLK outbreak that occurred in their center between October 1998 and January 1999. They studied microbial cultures for bacteria, limulas assay for endotoxin and electron microscopy for biofilm, and all were positive. Cultures of the sterilizer reservoir grew Burkholderia picketti. Endotoxin was found on the ultrasonic instrument cleaner, the surgical instruments at the end of the sterilization cycle, in the distilled water, and on the ocular surface of a patient with DLK. Biofilm was detected in the sterilizer. They controlled the outbreak by instituting a protocol that involved draining the sterilizer at the end of each surgical day and using mechanical scrubbing and 70% isopropyl alcohol in the sterilizer at the end of each surgical day and allowing it to evaporate. Boiling water treatments were then performed in the morning before and at the end of each