Posterior capsule opacification (PCO) referred to as 'secondary cataract' or 'after cataract', develops over the clear posterior capsule a few months to a few years after an uneventful cataract surgery. PCO results from the growth and abnormal proliferation of lens epithelial cells (LECs) on the posterior capsule.
The PCO has two forms, fibrous and pearl, or a combination of both is also found. Clinically, it is seen as a wrinkling on the posterior capsule at the site of fusion of the anterior and posterior capsules. The development of PCO involves three basic phenomena: proliferation, migration and differentiation of residual LECs.
The incidence of PCO is known to range from as high as 50% to as low as <5% in eyes undergoing cataract surgery for uncomplicated senile cataracts.
Age remains a confounding factor, with younger individuals at a higher risk. At the 1-year follow-up, diabetic patients had significantly severe PCO after cataract surgery when compared with nondiabetic patients. However, among the diabetics, the stage of diabetic retinopathy and the systemic status of diabetes did not seem to correlate with the degree of PCO. The incidence of PCO is also high in eyes with uveitis. In these eyes, hydrophobic acrylic intraocular lens (IOL) have been seen to provide a better visual outcome and lower incidence of PCO than silicone, polymethyl methacrylate (PMMA) or heparin-surface-modified PMMA IOLs. Patients with myotonic dystrophy have required multiple capsulotomies following cataract surgery. Patients with retinitis pigmentosa showed a significantly higher incidence and density of PCO. In traumatic cataracts, the incidence of PCO is significantly higher and has been quoted to be as high as 92% at the 3-year follow-up.
Modifiable Surgical Techniques
Continuous Curvilinear Capsulorhexis:
It was found to delay the development of central visual obscuration by facilitating the mechanism of fusion between the edge of the continuous curvilinear capsulorhexis to the posterior capsule, forming a Soemmering's ring. (Figure 1) This ring provides a closed environment, which restricts the migration of the LECs toward the central posterior capsule. The ring contains residual LECs, residual cortical fibers and differentiated LECs. Excessive proliferation of residual LECs or migration of LECs across this ring has been reported at longer follow-up.
Fixation of the optic and the haptic functions primarily to enhance the IOL optic barrier effect, reducing the incidence of central PCO. Tan and Chee noticed an increased incidence of fibrosis-type PCO in cases of ciliary sulcus fixation.
Anterior Capsule Overlap of IOL Optic:
It is believed that with a capsulorhexis smaller than the IOL optic, the adhesion between the anterior capsule and the IOL optic keeps the anterior lens epithelium away from the posterior capsule. This would decrease the incidence of migration of the anterior LECs behind the IOL optic. It has also been postulated that a capsulorhexis larger than the IOL optic allows adhesion of the anterior and posterior capsules, forming a Soemmering's ring. This could contain the cells and regenerative cortical matter, preventing LEC migration onto the visual axis. Probable mechanisms of anterior capsule overlap over the IOL optic that help in delaying the development of central PCO include the 'shrink wrap' effect, the concept of the barrier effect of an IOL optic edge and the creation of a discontinuous capsular bend by an IOL with a sharp optic edge. Different IOL materials show different PCO rates due to the variations in the overlap of the anterior capsule with the IOL optic.
Cortical Cleaving Hydrodissection:
The hydraulic force exerted by cortical cleaving hydrodissection causes a cleavage between the lens capsule and the cortex, which could cleave mitotically active LECs from the capsule.
Hydrodissection Combined With Rotation:
In an experimental laboratory study of fresh human cadaver eyes, cortical cleaving hydrodissection combined with rotation removed significant quantities of LECs and residual cortical fibers by way of friction.
Cortical Clean Up:
Bimanual irrigation and aspiration for cortical clean up facilitates access to the deep fornices of the capsular bag, especially in the subincisional quadrants. The thorough removal of residual cortical fibers reduces the number of mitotically active cells that have the potential to proliferate and migrate across the central visual axis.
This technique has been shown to limit LEC proliferation. Anterior and posterior capsule flaps of similar sizes are inserted in a flange of the IOL. The LEC proliferation is restricted within the space of the remaining lens bag and does not approach the visual axis. It is cautioned that this prevents PCO only if the anterior and posterior capsules have been secured properly in the peripheral groove of the IOL.
Polishing (Scraping) the Anterior Capsule:
Has been effective in reducing fibrotic opacification but ineffective in reducing regeneratory opacification.
Plate-haptic versus Loop-haptic IOLs: with the plate haptic design IOLs, a high rate of anterior capsule opacification (ACO) as well a high rate of PCO (up to 65% in standard plate design) has been reported. This may lead to various forms of LEC fibrosis. The cellular processes that may wrap around the haptics cause conditions such as lens tilt, Z syndrome and decentration, as well as CCC syndrome (capsular phimosis).
Single-piece versus Multipiece IOL Design: no statistical difference has been reported in the rate of development of PCO in the AcrySof three-piece versus the single-piece design. Optic edge design is known to influence the migration of LECs on the posterior capsule. The discontinuous sharp bend created by the sharp optic edges of the IOL appeared to induce contact inhibition of migrating LECs (it creates a mechanical barrier), it was found to be more effective in the prevention of formation of PCO compared with IOLs with round optic edges.
Haptic Designs & Angulation: haptic angulation also reduces the incidence of PCO by inducing a pressure gradient over the posterior capsule.
Biocompatibility: should be assessed in terms of uveal biocompatibility as well as in terms of capsular biocompatibility. Uveal biocompatibility is related to the inflammatory foreign-body reaction of the eye against the implant. In a study comparing three IOLs: a PMMA IOL, silicone IOL and acrylic IOL, it was found that all three IOLs were sufficiently biocompatible. However, acrylic IOLs were associated with lower giant cell counts and may produce better results in eyes with pre-existing blood–aqueous barrier damage. Capsular biocompatibility is determined by the relationship of the IOL with remaining LECs within the capsular bag; for example, ACO, PCO and LEC growth on the anterior surface of the IOL. ACO occurs as a result of myofibroblastic differentiation of the residual anterior LECs.
Bioadhesive IOL Materials: bioactive materials are those that allow a single LEC to bond both to the IOL and the posterior capsule. This would produce a sandwich pattern including the IOL, the cell monolayer and the posterior capsule. This sealed sandwich structure may prevent further epithelial ingrowth and prevent PCO. Theoretically, a bioactive material such as hydrophobic acrylic would prevent PCO more than PMMA and silicone IOLs, which are biocompatible but also bioinert. The degree of bioactivity can explain the difference in PCO and Nd:Yag capsulotomy rates with different IOL materials.
Central PCO obscuring the visual axis can be treated with either surgical intervention, such as posterior capsule scraping or with a nonsurgical Nd:YAG laser capsulotomy. The need for performing capsulotomy depends on the patient's functional impairment of vision, discomfort, demand and the presence of associated risk factors such as high myopia, history of retinal detachment, high risk of cystoid macular edema and only functioning eye. A size that is larger than the pupil diameter under scotopic conditions may prevent disturbances of vision such as monocular diplopia. The clinical complications from Nd:YAG laser capsulotomy include a rise in intraocular pressure, glaucoma, cystoid macular edema and retinal detachment.
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