Korean J Ophthalmol > Volume 29(3); 2015 > Article
Han, Kim, Lee, and Yang: 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.

Conflicts of interest

Conflict of Interest: No potential conflict of interest relevant to this article was reported.

REFERENCES

1. Do JR, Oh JH, Chuck RS, Park CY. Transient corneal edema is a predictive factor for pseudophakic cystoid macular edema after uncomplicated cataract surgery. Korean J Ophthalmol 2015;29:14-22.
2. Flach AJ. The incidence, pathogenesis and treatment of cystoid macular edema following cataract surgery. Trans Am Ophthalmol Soc 1998;96:557-634.
3. Ersoy L, Caramoy A, Ristau T, et al. Aqueous flare is increased in patients with clinically significant cystoid macular oedema after cataract surgery. Br J Ophthalmol 2013;97:862-865.
crossref pmid pmc
4. Behndig A, Lundberg B. Transient corneal edema after phacoemulsification: comparison of 3 viscoelastic regimens. J Cataract Refract Surg 2002;28:1551-1556.
pmid pmc
Dear Editor,
Thank you very much for this opportunity to discuss our recent paper titled "Transient corneal edema is a predictive factor for pseudophakic cystoid macular edema after uncomplicated cataract surgery" [1]. In this paper, we concentrated on very subtle transient corneal edema (TCE) after routine uncomplicated cataract surgery. Such subtle TCE is occasionally overlooked on slit-lamp examination (4 of 17 eyes in our study). Although TCE occurs with relatively high frequency (11.3% in our paper and 50% in Tao et al. [2]), little is known about the etiology and clinical relevance of subtle TCE. TCE in our study should be differentiated from prominent corneal edema caused by mechanical endothelial damage during difficult or inadvertent phacoemulsification. In the setting of mechanical damage, serial tracing of endothelial cell count shows a marked decrease in final cell density. In our study, although preoperative endothelial density in TCE eyes was slightly lower than that in control eyes, the serial tracing and comparison of endothelial cell density did not show any significantly increased loss compared to that in control eyes. Because postoperative endothelial count was not performed in all study eyes, this result was omitted from the original paper. Therefore, we suggest inflammation and transient functional dysfunction as the main etiology of TCE, although mechanical effects cannot be excluded. The finding that diabetes mellitus increased the risk of TCE also supports the greater role of dysfunction compared to mechanical cell death. Inflammatory material released from damaged tissue during cataract surgery can fill the anterior chamber during the immediate postoperative period. The small volume of the anterior chamber can greatly increase the concentration of inflammatory mediators and result in frequent TCE, as shown in our paper. The lack of quantitative analysis of anterior chamber reaction during the postoperative course and then cumulative ultrasound energy delivered are the major limitations of our study. We agree that including these two parameters in the analysis will provide better understanding of TCE and pseudophakic cystoid macular edema in future study.

REFERENCES

1. Do JR, Oh JH, Chuck RS, Park CY. Transient corneal edema is a predictive factor for pseudophakic cystoid macular edema after uncomplicated cataract surgery. Korean J Ophthalmol 2015;29:14-22.
crossref pmid
2. Flach AJ. The incidence, pathogenesis and treatment of cystoid macular edema following cataract surgery. Trans Am Ophthalmol Soc 1998;96:557-634.
crossref pmid
3. Ersoy L, Caramoy A, Ristau T, et al. Aqueous flare is increased in patients with clinically significant cystoid macular oedema after cataract surgery. Br J Ophthalmol 2013;97:862-865.
crossref pmid pmc
4. Behndig A, Lundberg B. Transient corneal edema after phacoemulsification: comparison of 3 viscoelastic regimens. J Cataract Refract Surg 2002;28:1551-1556.
crossref pmid pmc


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