- Journal of Refractive Surgery
- August 2012 - Volume 28 · Issue 8: 575-586
Click here to read Letter to the Editor about this article
To describe the etiology, diagnosis, clinical course, and management of LASIK interface complications.
Primary interface complications include infectious keratitis, diffuse lamellar keratitis, central toxic keratopathy, pressure-induced stromal keratopathy (PISK), and epithelial ingrowth. Infectious keratitis is most commonly caused by Methicillin-resistant Staphylococcus aureus (early onset) or atypical Mycobacterium (late onset) postoperatively, and immediate treatment includes flap lift and irrigation, cultures, and initiation of broad-spectrum topical antibiotics, with possible flap amputation for recalcitrant cases. Diffuse lamellar keratitis is a white blood cell infiltrate that appears within the first 5 days postoperatively and is acutely responsive to aggressive topical and oral steroid use in the early stages, but may require flap lift and irrigation to prevent flap necrosis if inflammation worsens. In contrast, PISK is caused by acute steroid response and resolves only with cessation of steroid use and intraocular pressure lowering. Without appropriate therapy PISK can result in severe optic nerve damage. Central toxic keratopathy mimics stage 4 diffuse lamellar keratitis, but occurs early in the postoperative period and is noninflammatory. Observation is the only effective treatment, and flap lift is usually not warranted. Epithelial ingrowth is easily distinguishable from other interface complications and may be self-limited or require flap lift to treat irregular astigmatism and prevent flap melt.
Differentiating between interface entities is critical to rapid appropriate diagnosis, treatment, and ultimate visual outcome. Although initial presentations may overlap significantly, the conditions can be readily distinguished with close follow-up, and most complications can resolve without significant visual sequelae when treated appropriately.
From the Department of Ophthalmology, Emory University School of Medicine, Atlanta, Georgia (Randleman, Shah); and Case Western Reserve University, Cleveland, Ohio (Shah).
Supported in part by NIH NEI P30EY06360 and an unrestricted departmental grant from Research to Prevent Blindness Inc, New York, New York.
The authors have no financial interest in the materials presented herein.
Study concept and design (J.B.R.); data collection (J.B.R., R.D.S.); analysis and interpretation of data (J.B.R., R.D.S.); drafting of the manuscript (J.B.R., R.D.S.); critical revision of the manuscript (J.B.R.)
Correspondence: J. Bradley Randleman, MD, Emory Eye Center, 875 Johnson Ferry Rd, Ste 100, Atlanta, GA 30342. E-mail: firstname.lastname@example.org
Received: May 25, 2012
Accepted: July 16, 2012