Pediatric cataracts, including congenital cataracts, represent the most common cause of treatable blindness in early infancy.1
However, there remain challenging questions to be addressed in relation to the optimal timing of cataract surgery and postoperative optical management, both of which may affect visual outcomes and eye growth.
The human eye undergoes extensive growth over the first few years of life, being only ~70% of its adult size at birth.2
This period is important for emmetropization, with neonatal refractive errors normally being reduced or eliminated through the coordinated growth of the critical ocular components— cornea, crystalline lens, and vitreous chamber. This emmetropization process also has implications for the management of cataracts in infants. For example, form deprivation may be caused by the cataract before surgery or by subcapsular opacification occurring after surgery as a complication.3,4
The likely consequence in both cases is accelerated eye growth, and a similar response is expected to refractive errors left uncorrected after surgery.5,6
Emmetropization may also be disrupted by amblyopia, another possible consequence of early cataracts.7
Studies of pediatric subjects undergoing cataract surgery are inconclusive with respect to the effects of early surgical intervention on postoperative eye growth. For example, greater than normal eye elongation and myopic shifts in refraction have been described in pseudophakic eyes of infants (<1 year old) and older children.8,9
However, there are also reports of reduced eye growth after cataract surgery10
and minimal effects of cataract surgery on eye growth.11,12
Studies using the infant monkey as an animal model to study the effects of early cataract surgery on eye growth mostly report reduced eye growth after the removal of the crystalline lens, irrespective of whether the surgical eye is left aphakic or corrected optically.13-15
However, many of these studies involve one or more postoperative manipulations, including implantation of monofocal or multifocal intraocular lenses (IOLs), the use of contact lens optical corrections, surgical intervention to remove opaque membranes, and part-time occlusion of fellow eyes, confounding study results and making interstudy comparisons difficult.
Various explanations for growth retardation in young aphakic eyes have been considered in the studies reporting this phenomenon, with most having some credibility. An exception is the attribution of growth retardation to a reduction in IOP, which, to the contrary, is generally reported to be within normal range or higher in aphakic monkey eyes.13,14
The involvement of inflammatory mediators, released in response to the surgical manipulation, has not been ruled out.16,17
Other explanations rest on the assumption that the lens is a source of critical growth-enhancing trophic factors13
and/or exerts a critical biomechanical influence during early ocular development. Finally, as an explanation for why uncorrected young aphakic eyes do not show increased growth in compensation for surgically-induced hyperopia, it is possible that the operating range for such defocus-driven changes in eye growth is exceeded.18
In seeking further insight into the effects of early lensectomy on eye growth, we built on our experience with the young chick as an animal model for emmetropization, using them to study the effects of lensectomy alone or within combination with various postoperative optical correction strategies. We found evidence of active emmetropization in young aphakic chick eyes: Uncorrected aphakic eyes grew faster than their fellows, this growth enhancement being attenuated by partial or full optical correction of surgically induced refractive errors.
Some of the data described herein were included in a conference abstract (Ai L, et al. IOVS. 2007;48:ARVO E-Abstract 1529).