Posterior Capsule Opacification After Lens Implantation

Incidence, Risk Factors and Management

Abhay R Vasavada; Shetal M Raj; Gauri D Shah; Mayank A Nanavaty

Disclosures

Expert Rev Ophthalmol. 2013;8(2):141-149. 

In This Article

Abstract and Introduction

Abstract

Postoperative capsular opacification is a multifactorial physiological consequence of cataract surgery. Opacification involving the central posterior capsule has a significant impact on high- and low-contrast acuity and low-contrast sensitivity. The proliferation, migration and abnormal differentiation of residual lens epithelial cells and fibers in the capsular bag have been implicated in the pathogenesis of posterior capsule opacification (PCO). The incidence and severity of PCO correlates to the use of surgical techniques, intraocular lens optic edge designs and intraocular lens materials. This article summarizes the clinical studies with recommendations for retarding the development of central PCO. These studies will remain critical for future endeavors undertaken for the eradication of PCO.

Introduction

Posterior capsule opacification (PCO) is a physiological postoperative consequence of an uneventful uncomplicated extracapsular cataract surgery. Capsular opacification is different from the intraoperative opacification that takes place in the intact lenses. It is known as a plaque that can either be in the anterior and/or posterior capsule.[1] 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. Figure 1 shows various forms of capsular opacification. PCO results from the growth and abnormal proliferation of lens epithelial cells (LECs) on the capsule at the time of cataract surgery. These cells migrate to the posterior capsule, where they approach the central visual axis and cause visual-axis obscuration, resulting in dimness of vision. The PCO has two forms, fibrous and pearl. Sometimes, 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. A histological examination of the fibrous PCO shows extracellular matrix accumulation and the presence of elongated myofibroblast cells positive to vimentin and α-smooth muscle actin.[2] Examination of the proliferative PCO shows clusters of swollen, opacified, differentiated LECs called bladder or Wedl cells.[3] The development of PCO is a very dynamic process and involves three basic phenomena: proliferation,[4–6] migration[7–9] and differentiation[10–12] of residual LECs.

Figure 1.

Eyes showing various forms of capsular opacification. (A) Extensive anterior capsule opacification (arrows). (B) Mixed type of posterior capsule opacification with fibrous (arrow) and pearl type areas (asterisk). (C) Fibrous form of posterior capsule opacification (arrow). (D) Proliferative or pearl form of posterior capsule opacification (asterisk). (E) Linear posterior capsule opacification (arrows).

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