To the best of our knowledge, this is the first case report describing patients who developed posterior capsular opacification within two weeks of CE/IOL via ROC technique and silicone intraocular lens placement. A study found that primary ROC helped prevent ND in 21/21 eyes of patients who had ND in their first eye and that secondary ROC treated existing ND in 21/22 eyes.[4] In the present study, primary ROC technique was performed in both patients to prevent the development of ND in the fellow eye.
Previous studies by Adre et al. and Masket et al. have described occurrences of PCO after ROC to treat or prevent NDs.[1, 4] However, the former mentions an increased rate of PCO with no time frame, and the latter mentions the incidence of rapid fibrotic PCO and the use of Nd:YAG laser posterior capsulotomy to treat PCO at 3 months in 21 of 21 patients. In both of our cases the PCO occurred in the first two postoperative weeks and were also successfully managed with Nd:YAG laser capsulotomy.
PCO itself, after ROC or other procedures, is a result of surgical injury promoting a wound-healing response. The pathogenesis of PCO begins with trauma to the anterior surface of the lens and disruption of the barrier that holds the Lens Epithelial Cells (LECs) in place. These leftover cells undergo proliferation and slowly migrate towards the posterior lens thanks to cell-cell adhesion molecules. As they settle, they transform into myofibroblasts while the lens capsule undergoes fibrosis, partly due to TGF-B signaling inhibiting LEC proliferation and favoring transdifferentiation.[7]
It has been determined that using a curvilinear continuous capsulorrhexis (CCC) method to open the anterior capsule results in the lowest amount of PCO.[5, 7] However, at the heart of pathogenesis lies the presence of LECs, whose removal is fundamental to PCO prevention since any amount of leftover LECs can lead to a full response. This is evidenced by previous attempts by X. Liu et al. and Shah et al. at polishing the anterior capsule to eliminate LECs which still led to PCO.[7] There is some evidence by Paik et al. that polishing the posterior capsule can cause a reduction in PCO development, albeit this procedure is not widely adapted due to unknown risks.[8] Similarly, it is theorized that removing the posterior capsule through a posterior CCC can permanently eliminate the possibility of PCO, although this too comes with its own risks such as vitreous loss.[7]
Other factors that can influence the development of PCO are the type of material and "wettability" of the IOL. Although there are multiple studies examining the advantages of hydrophobic vs hydrophilic IOLs for PCO development, there is no conclusive evidence to determine which is recommended. When comparing IOL materials, between PMMA, silicone, and acrylic, the latter has shown lower rates of PCO development. In our cases, silicone IOLs were implanted in both patients which could have contributed to the development of PCO. Hollic et al. evaluated 90 eyes after capsulorrhexis and "in-the-bag" IOL placement, and at 2 years all patients with PMMA and silicone had LECs present on the posterior capsule compared to 62% with polyacrylic lenses. Additionally, in those that showed LECs at 90 days, 83% showed regression with polyacrylic compared to 8% with silicone and 15% with PMMA.[6] Similarly, Auffarth et al. described PCO rates of 28.3%, 21.6%, and 8.9% when using PMMA, silicone, and polyacrylic respectively in a group of 1525 patients.[8] These improved results are thought to be because of acrylate IOLs binding extracellular matrix proteins to the IOL surface and promoting capsular adhesion. These proteins bind to LECs and lens capsule, adhere the IOL to the lens capsule and reduce LEC migration.
Another potential factor that can influence the development of a PCO is the location of the IOL haptics and the optic-haptic design. [9] A previous study by Shah et al., on 500 patients undergoing cataract surgery with a 1-piece IOL found a 13.6% incidence of posterior capsular striae. Additionally, the observed rate of PCO development was lower compared to that reported in the literature on 3-piece IOLs. [9] They hypothesize that the IOL haptics play a critical important role in stretching the capsular bag, which prevents the formation of striae and subsequent formation of a PCO. Further, they believe that the optic-haptic design of a 1-piece IOL and the hydrophobic acrylic biomaterial of the haptics, allows for a greater ability to bend backwards, twist, and contort to evenly stretch the capsular bag along its entire circumference. In our study, we used a 3-piece IOL to cover the anterior capsule and positioned the haptics within the ciliary sulcus. This left the posterior lens capsule empty without IOL haptic support and likely caused the capsule to become more susceptable to striae formation, folding, and opacification.
In terms of causes for early opacification, prior vitrectomy, high myopia, indolent rheumatic disease, and post-surgical inflammation have been reported as risk factors. [8–9] In our study, both cases did not have any prior risk factors for early opacification.
In this report, both patients presented 2 weeks post-surgery with reduced CDVA, much faster than reported in previous literature. We believe that PCO developed so quickly in our cases due to a lack of a barrier between the LECs and the lens capsule epithelium, allowing the migration and transdifferentiation of these cells on the posterior capsule. No other reports have shown such rapid progression of PCO and thus warrants attention due to the need for patient education regarding the post-operative possible complications and expectations after cataract surgery.