LASIK interface complications: etiology, management, and outcomes

Abstract

Purpose: To describe the etiology, diagnosis, clinical course, and management of LASIK interface complications.

Methods: Literature review.

Results: 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.

Conclusions: 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.

Figure 1

Benign interface debris in the LASIK interface. (Reprinted from Randleman JB. Chapter 8: Etiology and clinical presentations of irregular astigmatism after keratorefractive surgery. In: Wang M, ed. Irregular Astigmatism: Diagnosis and Treatment. SLACK Inc., Thorofare, NJ 2007: 79–90)

Figure 2

Infectious keratitis. Note the focal infiltrates interspersed within the somewhat diffuse inflammatory reaction. The causative organism was Mycobacteria.

Figure 3

Diffuse lamellar keratitis (DLK), stage 3. Note the diffuse, granular haze throughout the central cornea.

Figure 4

Pressure induced stromal keratopathy (PISK) with a diffuse, hazy interface but without an obvious fluid layer. (Image courtesy of Theofilos Tourtas, M.D.)

Figure 5

Central toxic keratopathy (CTK). Note the focal corneal haze with a striate appearance within the center of the haze. (Image courtesy of Joung Y. Kim, M.D.)

Figure 6

Epithelial ingrowth, with a nest of epithelial cells notable extending in from the 7 o’clock meridian.

Figure 7

Infectious keratitis. The infection that began in the interface has now extended through the flap anteriorly and posteriorly to become a full-thickness infiltrate with a hypopyon. This cornea perforated the following day, requiring penetrating keratoplasty.

Figure 8

DLK, Stage 4. A) Note the focal corneal haze with a striate appearance within the center of the haze similar to the appearance of CTK. B) Corresponding topography with notable focal flattening corresponding to the focal haze. (Reprinted from Randleman JB. Chapter 8: Etiology and clinical presentations of irregular astigmatism after keratorefractive surgery. In: Wang M, ed. Irregular Astigmatism: Diagnosis and Treatment. SLACK Inc., Thorofare, NJ 2007: 79–90)

Figure 8

DLK, Stage 4. A) Note the focal corneal haze with a striate appearance within the center of the haze similar to the appearance of CTK. B) Corresponding topography with notable focal flattening corresponding to the focal haze. (Reprinted from Randleman JB. Chapter 8: Etiology and clinical presentations of irregular astigmatism after keratorefractive surgery. In: Wang M, ed. Irregular Astigmatism: Diagnosis and Treatment. SLACK Inc., Thorofare, NJ 2007: 79–90)

Figure 9

PISK with an obvious fluid cleft. (Image courtesy of Marc Michelson, M.D. and Matthew J. Fabrizio, M.D.)

Figure 10

Pentacam image of central toxic keratopathy, demonstrating significant focal flattening noted in sagittal curvature map corresponding to focal corneal haze. Note that the corneal thickness (A) and posterior elevation maps (A&B) are also significantly focally altered, likely due to measurement artifact. These changes resolved over time (not shown).

Figure 10

Pentacam image of central toxic keratopathy, demonstrating significant focal flattening noted in sagittal curvature map corresponding to focal corneal haze. Note that the corneal thickness (A) and posterior elevation maps (A&B) are also significantly focally altered, likely due to measurement artifact. These changes resolved over time (not shown).

Figure 11

A) Focal area of epithelial ingrowth noted on slit lamp exam with B) corresponding focal irregular astigmatism noted on topography. (Reprinted from Randleman JB. Chapter 8: Etiology and clinical presentations of irregular astigmatism after keratorefractive surgery. In: Wang M, ed. Irregular Astigmatism: Diagnosis and Treatment. SLACK Inc., Thorofare, NJ 2007: 79–90)

Figure 11

A) Focal area of epithelial ingrowth noted on slit lamp exam with B) corresponding focal irregular astigmatism noted on topography. (Reprinted from Randleman JB. Chapter 8: Etiology and clinical presentations of irregular astigmatism after keratorefractive surgery. In: Wang M, ed. Irregular Astigmatism: Diagnosis and Treatment. SLACK Inc., Thorofare, NJ 2007: 79–90)

Figure 12

Schematic representation of relative onset and severity of the overlapping interface complications. The Y-axis represents that time point by which that relative percentage of cases usually present and the relative severity of each complication; the decline in percentage on the Y-axis for DLK indicates the likelihood that DLK should begin to evolve and resolve with appropriate management over that time course.