Reply

Abstract

We thank Dr. De Bernardo et al. for their comments regarding our paper on risk factors predicting steroid-induced ocular hypertension after PRK. In our retrospective study, we reviewed the documented IOP values listed in the patient’s electronic medical record. We classified patients as steroid responders if they had an IOP elevation of at least 25% while on topical steroid treatment, to a minimum of 28 mm Hg, followed by an IOP drop of at least 25% when steroid treatment was discontinued. This criterion was chosen because it was similar to that of Chang et al.,1 who studied risk factors for steroid response among cataract patients. Indeed, as pointed out by De Bernardo et al.,2 Goldmann applanation tonometry often underestimates IOP after PRK. It is routine practice in our center to measure IOP with the Goldmann applanation tonometer at all visits other than the first postoperative visit. We wish to add that although not mentioned in our original paper, it is common practice for our physicians and optometrists to also measure IOP with a Tono-Pen or an Ocular Response Analyzer (both Reichert, Inc.) in cases in which the IOP is measured above 21 mm Hg by Goldmann applanation tonometry or if other clinical findings raise suspicion of ocular hypertension (eg, patient complaints, optic disc findings). The highest IOP measurement by any of the modalities was the one documented in the patient’s chart. Therefore, considering that the mean decrease in measured IOP after PRK is approximately 2 to 3 mm Hg,3 it is highly unlikely that cases of steroid-induced ocular hypertension (≥28 mm Hg) after PRK went undetected. In summary, after PRK we identified approximately 3% of steroid-induced ocular hypertension. Significant factors associated with post-PRK ocular hypertension were male sex, a high central corneal thickness, low mean keratometry reading, high myopia, corneal haze, and stronger steroids such as dexamethasone.