Preexisting Posterior Capsule Defects
Abhay R. Vasavada
Sajani K. Shah
Mamidipudi R. Praveen
Posterior capsule defect (PCD) is associated quite frequently in cases of traumatic cataract in both adults and children.1,2 Occurrences of preexisting PCD have also been well documented in adults with posterior polar cataract, and such cases are easily recognized owing to their characteristic appearance.3,4 Preexisting PCD also manifests in infants and small children in association with cataract. In children, the presence of preexisting PCD is not easily recognized, because the defect is hidden behind a dense central nuclear or combined nuclear/cortical cataract when viewed through a normal-sized, undilated pupil. This difficulty in recognizing the presence of preexisting PCD in pediatric eyes can pose a challenge to pediatric cataract surgeons.
INCIDENCE
While evaluating 400 consecutive eyes with pediatric cataract surgery at our centre, we observed that 27 eyes (20 children) had preexisting PCD. Thus, the incidence of preexisting PCD was 6.75%, which is significant for pediatric cataract surgeons.5 Singh and coauthors6 found chalky white spots in a cluster or a rough circle at the level of the posterior capsule before or during surgery. Vajpayee and Sandramouli7 observed preexisting PCD in an eye of a 2-year-old patient with congenital cataract. Wilson and Trivedi8 reported preexisting PCD in 8/364 (2.2%) eyes implanted with an intraocular lens (IOL) at the time of surgery for nontraumatic cataracts. Six of the eight eyes presented with leukocoria.
LATERALITY
THEORIES AND HYPOTHESIS
Based on our clinical experience, we speculate that the defect perhaps begins at birth as a posterior lentiglobus with herniation of the lens substance through an intact, but developmentally weak, posterior capsule. Many theories have been proposed to explain the development of posterior lentiglobus. These include subepithelial capsule hyperplasia, embryologic hyaloid artery traction,11 inherent weakness of the posterior capsule wall, and the excessive strain of accommodation, which results in posterior herniation of the lens.9,10 Franceschetti and Rickli12 also noted overgrowth or aberrant hypertrophy of the posterior lens cortex. This overgrowth of lens fibers forces backward displacement of a thin and defective posterior capsule.
When the barrier of the posterior capsule is breached, the elements of the crystalline lens are exposed to outside
fluids. The ingress of even scanty previtreous fluid into the crystalline lens triggers a chain of events. There is local hydration, opacification, liquefaction, absorption, and posterior migration of the lens material toward the Berger space. There may also be changes in the rest of the lens and in the anterior capsule. Thus, a break in the posterior capsule has the potential to trigger myriad lenticular changes. Unlike classical posterior lentiglobus, PCD develops at an accelerated pace until a fully thickened defect is seen.6
fluids. The ingress of even scanty previtreous fluid into the crystalline lens triggers a chain of events. There is local hydration, opacification, liquefaction, absorption, and posterior migration of the lens material toward the Berger space. There may also be changes in the rest of the lens and in the anterior capsule. Thus, a break in the posterior capsule has the potential to trigger myriad lenticular changes. Unlike classical posterior lentiglobus, PCD develops at an accelerated pace until a fully thickened defect is seen.6
CLINICAL PRESENTATION
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