Although the cause is unknown, central toxic keratitis may occur after PRK or femtosecond laser-created flaps, within 3-9 days. DLK usually precedes CTK. Since CTK is noninflammatory, it’s important that ODs recognize it as soon as possible, to avoid unnecessary topical steroids.
Laser vision correction has progressed in many ways since its U.S. Food and Drug Administration (FDA) approval. The outcomes are improved, and the complications are reduced.1 Technology has made improvements in the ability to identify good candidates, and in the hands of a skilled surgeon patients are as happy as ever.
Therefore, it is interesting when ODs see complications that they do not completely understand, such as central toxic keratitis (CTK). The good news is that incidence is rare with studies estimating its occurrence from 0.0076 percent to 0.016 percent.2
Related: Refractive surgery in 2020: From minimally invasive LASIK to light adjustable lenses
Central toxic keratitis has occurred in laser-assisted in situ keratomileusis (LASIK), photorefractive keratectomy (PRK), corneal collagen cross-linking (CXL), and even contact lenses patients, but LASIK is the most common surgery leading to the condition.3
Interestingly, CTK has not been observed in enhancement procedures4—the thinking is the condition may be intrinsic to each individual. It is an acute, self-limited, non-inflammatory reaction of the central cornea. It usually appears on Day 3 to Day 9 after surgery but is often preceded by diffuse lamellar keratitis (DLK) on Day 1.3
Differential diagnosis includes Grade 3 to Grade 4 DLK, pressure-induced stromal keratitis (PISK), and infectious keratitis. CTK often results in opacification of the central corneal along with a significant hyperopic shift in the patient’s refraction.5 Confounding early diagnosis of CTK is the fact that it is often preceded by DLK on postop Day 1 and Day 2, and the two have overlapping features.6
DLK is defined by infiltrative white cells at the interface of the LASIK flap. These infiltrative cells are diffuse in the central or peripheral flap interface and respond to increased topical steroids. DLK will typically resolve in 5 to 8 days and only rarely has any impact on the final refractive outcome.7
1. Chua D, Htoon HM, Lim L, et al. Eighteen-year prospective audit of LASIK outcomes for myopia in 53 731 eyes. Br J Ophthalmol. 2019 Sep;103(9):1228-1234
2. Hainline BC, Price MO, Choi DM, Price FW. Central flap necrosis after LASIK with microkeratome and femtosecond laser created flaps. J Refract Surg. 2007 Mar;23(3):233-42.
3. Sonmez B, Maloney RK. Central toxic keratopathy: description of a syndrome in laser refractive surgery. Am J Ophthalmol. 2007 Mar;143(3):420-7.
4. Mari Cotino JF, Suriano MM, et al. Central toxic keratopathy: a clinical case series. Br J Ophthalmol. 2013 Jun;97(6):701-3.
5. Liu A, Maloney RK, Manche EE. Toxic peripheral kera-topathy: a syndrome in laser refractive surgery. J Cataract Refract Surg. 2012 Sep;38(9):1684-9.
6. Galal A, Artola A, et al. Interface corneal edema secondary to steroid-induced elevation of intraocular pressure simulating diffuse lamellar keratitis. J Refract Surg. 2006 May;22(5):441-7.
7. Linebarger EJ, et al. Diffuse lamellar keratitis: diagnosis and management. J Cataract Refract Surg. 2000 Jul;26(7):1072-7.
8. De Paula FH, Khairallah CG, et al. Diffuse lamellar keratitis after laser in situ keratomileusis with femtosecond laser flap creation. J Cataract Refract Surg. 2012 Jun;38(6):1014-1019.
9. Hau SC, Allan BD. In vivo confocal microscopy findings in central toxic keratopathy. J Cataract Refract Surg. 2012 Apr;38(4):710-2.