We read with great interest the original article by Noda and associates regarding the long-term increase in subfoveal choroidal thickness after surgery for senile cataracts. In this study, the authors reported that cataract surgery increased the subfoveal choroidal thickness and this increment persisted as long as 6 months postoperatively. The authors also revealed that thicker baseline choroid and male sex predicted a larger amplitude of increase in subfoveal choroidal thickness after cataract surgery.
Choroidal thickness increment is especially important for our understanding the association of cataract surgery with age-related macular degeneration or cystoid macular edema that the deterioration of the choroid is thought to play a role for onset. Speculated mechanisms of this increment in choroidal thickness after cataract surgery in Noda and associates’ study were inflammatory reactions associated with the surgery and increased light exposure during surgery.
However, inflammatory mechanism alone seems to be incapable of causing significant morphologic choroidal changes after cataract surgery in the long term. As it can be understood from the study design, in Noda and associates’ study all patients were treated with anti-inflammatory drops, and these treatments are known to lower postcataract inflammation and thus to diminish the postcataract retinal inflammatory response. So, we can speculate that they could have lowered the choroidal response as well.
It is well known that intraocular pressure (IOP) decreases after cataract surgery. Strikingly, Ohsugi and associates reported that choroidal thickness increased after cataract surgery and the changes in choroidal thickness were negatively correlated with IOP changes (early after surgery) and the axial length (in the late postoperative period). We also conducted research about choroidal thickness changes after cataract surgery and, consistent with Ohsugi and associates’ findings, we found that phacoemulsification surgery causes a significant increase in the choroidal thickness, which is correlated with surgery-induced IOP change in the short term ( www.escrs.org/abstracts/details.asp?confid=18&sessid=559&type=PresentedP&paperid=22201 ). It is known that the decrease in IOP is associated with an increase in ocular perfusion pressure. This increment in ocular perfusion pressure attributable to decreased IOP might have been the reason for increased choroidal thickness in these studies. Also, the surgical procedure releases inflammatory mediators, such as prostaglandins (albeit limited by anti-inflammatory medications), which lead to an increase in uveoscleral outflow. Because the choroid is part of the uveoscleral outflow pathway, increased fluid drainage from the anterior chamber might have also contributed to the increase in the choroidal thickness.
Therefore, we think that choroidal thickness changes 6 months after the surgery in Noda and associates’ study might also be attributable to IOP changes induced by surgery. Thus we would like to ask the authors if they have any knowledge about the IOP changes after the surgery and the correlation between IOP changes and choroidal thickness changes in their study population.