Refraction and keratometry in premature infants.

A bnormalities of emmetropisation, resulting most often in myopia, have long been independently associated by numerous authors from nearly every corner of the globe with increasing prematurity, increasing severity of retinopathy of prematurity (ROP), and retinal ablative therapy. This topic has also been the subject of an editorial in the BJO in 1997, the substance of which remains true today. These refractive error abnormalities of prematurity and of ROP have been found to present early in infancy and persist into adulthood. It is not clear whether the mechanism for the development of myopia of prematurity is the same or different from the mechanism for the development of myopia of ROP. It appears that an alteration in the normal growth patterns of the eye is caused by the prematurity, the retinal ablative therapy, or probably both factors, leading to the refractive error. This disruption in growth results in structural abnormalities of parts of the eye which affect refractive development. These structures might include corneal curvature, axial length, lens thickness, and anterior chamber depth. Most authors of studies involving myopia of prematurity have had only refractive error data available, which makes it impossible to directly determine which ocular structures have had their development altered before term. Furthermore, most studies have dealt with patients examined well beyond the expected due date, after which other environmental and disease factors could affect the observed outcome. 3 There has been until recently few biometric data available for these premature patients to explain the refractive error findings, and essentially no such data during infancy. Donzis and coworkers reported a dramatic flattening in the corneal curvature of six premature patients with very steep corneas between 28–34 weeks gestation and term, which they associated with a change in refractive status. No comparison data to term infants were available, but these data can be used to support the idea that there is substantial, rapid corneal growth throughout this period. Cook and colleagues found, in premature infants without evidence of ROP (mean post-menstrual age at birth 29.4 weeks), or complex pattern of rapid growth between 30 and 50 weeks postmenstrual age. They noted a significant correlation between corneal curvature growth and refractive status resulting in less hypermetropia when compared to published data from term infants. Cook and her coworkers did not include comparison data for eyes of children delivered at term in their nursery or information concerning eyes with ROP.