Pathophysiology of Transient Corneal Edema and Pseudophakic Cystoid Macular Edema

Dear Editor,

We read with interest the article titled "Transient corneal edema is a predictive factor for pseudophakic cystoid macular edema after uncomplicated cataract surgery" [1], in which the authors found that transient corneal edema (TCE) following cataract surgery is a predictive factor of pseudophakic cystoid macular edema (PCME). The study was well designed and conducted and answered a question that we thought we might know but never really studied.

However, although the authors suggested that TCE and PCME may partly share the same etiologies of inflammation, we would like to point out that TCE and PCME may have different pathophysiologies. As the authors described, PCME may be caused by disruption of the blood-aqueous and blood-retinal barriers due to postoperative inflammation [2]. Postoperative anterior chamber (AC) reaction is also caused by destruction of the blood-aqueous barrier and reflects the degree of inflammation; thus, increased AC reaction is associated with development of PCME [3]. However, TCE is caused by endothelial cell damage due to ultrasound energy, direct mechanical trauma or toxicity of the irrigating solution [4], rather than by disruption of the blood barriers. TCE tends to occur more frequently in cases with increased surgical difficulty, such as advanced age, increased nuclear density, narrower AC, small pupil, floppy iris syndrome and pseudoexfoliation syndrome, in which a larger amount of ultrasound energy is used, mechanical trauma to corneal endothelial cells is frequent and the toxic effect of the irrigation solution increases with operation time. The authors also demonstrated that patients with TCE had significantly smaller AC volume compared to those without TCE and also tended to have older age, shorter AC depth and longer surgical duration, although the differences were not statistically significant [1]. These conditions also tend to increase the severity of postoperative inflammation as higher ultrasound energy, increased manipulation of surgical instruments and longer surgical duration result in increased damage to tissues including iris, ciliary body and trabecular meshwork. This exacerbates the breakdown of blood-aqueous and blood-retinal barriers, consequently leading to PCME and AC reaction. Taken together, therefore, although TCE and PCME may have basically the same cause, the mechanisms leading to the two conditions appear to be different. Nevertheless, we agree with the authors that TCE in an early postoperative period can be a valuable predictor of later development of PCME because they successfully showed the significant association between the two conditions.

In addition, we suggest that the results would be even more interesting if the authors included information about the degree of AC reaction. As AC reaction is a marker of postoperative inflammation and does share, at least in part, the pathogenesis of CME [3], we expect that there is a close relationship among TCE, PCME and AC reaction. We understand that the authors had difficulty obtaining data on AC reaction, as well as nuclear density and cumulative ultrasound energy [1]. The authors previously showed that TCE and PCME can be quantified using spectral domain optical coherence tomography, and AC reaction can be quantified using laser photometry [3]. We believe analyses of the quantified data on TCE, PCME and AC reaction in further studies will provide more detailed information that will be helpful in clinical practice.