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D. M. Skale, B. R. Will, S. Lee, H. A. Saad; Keratocyte Induced Corneal Microedema (KME)-A Novel Pathophysiologic Model describing the Etiology, Physiology and Management of Diffuse Lamellar Keratitis (DLK), Central Toxic Keratopathy (CTK), Central Flap Necrosis (CFN), Flap Necrosis Syndrome (FNS) and Central Lamellar Keratitis (CLK). Invest. Ophthalmol. Vis. Sci. 2010;51(13):2861.
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To describe 8 cases of Stage 4 Diffuse Lamellar Keratitis (DLK) and to propose a unifying comprehensive model describing the pathophysiology of this disorder in order to better understand the relationship between Stage 4 DLK, CTK, CFN, FNS and CLK. In addition, to further discuss the implications of this model on strategies for prevention and management of this disease process.
A retrospective review of 8 eyes between 8/02 and 4/04 that developed central opacities and interface infiltrates consistent with Stage 4 DLK following LASIK. All patients had manifest refraction, keratometry, corneal topography, pachymetry, slit-lamp examination, and fundoscopic examination prior to surgery. All flaps were created using the IntralaseTM FS laser operating at 15 kHz and non-wavefront excimer laser treatment.
6 eyes were myopic, the remaining 2 eyes were mixed astigmats. Best spectacle corrected visual acuity (BSCVA) at time of presentation of Stage 4 DLK ranged from 20/50 to 20/400. All eyes demonstrated marked hyperopic shifts combined with induced astigmatism that were rapidly reversed using topical hyperosmotic agents. In all cases, topical steroid dosing was discontinued at presentation of Stage 4 DLK. 7 of 8 eyes underwent some form of flap lift procedure. 4 of 8 eyes underwent laser enhancement. All eyes recovered BSCVA of 20/20 or better. No patient had complaints of untoward visual disturbances at completion of therapy. No patients exhibited residual corneal scarring or visually significant flap microstriae.
We propose a model for Stage 4 DLK, CTK, CFN, FNS and CLK that postulates all are caused by a loss of control of factors regulating interstitial fluid pressures within the cornea. Disruption of these interactions leads to matrix relaxation and creates a cascade of physiologic processes that reorder corneal fluid dynamics, alter tissue compliance, redistribute tissue tension across the cornea and initiate reversible biologically mediated mechanical processes. Reversible biomechanical forces cause marked shifts in refraction, transient opacification of central flap stroma and tissue macrofolds. Appropriate therapy is directed at managing corneal edema acutely and limiting loss of BSCVA through timely management of flap macrostriae.
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