Abstract and Introduction
Abstract
Retinopathy of prematurity (ROP) is a disorder of retinal–blood vessel development that is potentially blinding. ROP is the number one cause of blindness in infancy and the second leading cause of childhood blindness in the Unites States. The exact etiology is not completely understood and many factors appear to contribute to the pathogenesis and progression of the disease. These factors may include prematurity, low birth weight, genetic predisposition, oxygen, hypoxia, ischemia, insulin-like growth factor, vascular endothelial growth factor and sepsis. This article reviews the process of retinal development, the pathogenesis of ROP and how oxidative stress, infection and inflammation may contribute this pathogenesis.
Introduction
Retinopathy of prematurity (ROP) is a disorder of retinal–blood vessel development and is the second leading cause of childhood blindness in the United States behind cortical visual impairment.[1] The National Center for Health Statistics report has listed the incidence of infants born at risk for developing this eye disease (≤ 32 weeks' gestation) to be at 2% of all live births. In 2008, 84,224 babies were born at or less than 32 weeks' gestation in the United States.[2] The National Eye Institute has estimated that 14,000–16,000 of these infants are affected by some degree of ROP and that 1100–1500 infants in the United States develop ROP that is severe enough to require medical treatment on an annual basis. Of these, 400–600 become legally blind from ROP each year.[3]
Retinopathy of prematurity (ROP) is a potentially blinding disorder caused as abnormal new blood vessels develop in the immature retina. In 1942, an ophthalmologist from Boston named Theodore Terry was the first to recognize a previously undescribed form of blindness in children born prematurely and of low birth weight. He named the condition based on the eye examination finding that showed a white fibrous mass behind the lens which obliterated the retinal vessels—"retrolental fibroplasia."[4] The name was later changed in 1984 by consensus of an international group of pediatric ophthalmologists to retinopathy of prematurity.[5]
Despite efforts to avoid the development of ROP since it was first recognized in the 1940s by Terry, ROP continues to be a challenging problem in the care of premature infants. The exact etiology of ROP is not completely understood and many factors appear to contribute to the pathogenesis and progression of the disease. Prematurity, genetic predisposition, oxygen, hypoxia, ischemia, insulin-like growth factor 1 (IGF-1) and VEGF all have been shown to be important in the development of ROP.[6] Severity of illness, sepsis, acidosis, blood transfusions and light have also been associated with ROP.[7] The degree of prematurity itself remains the most significant risk factor, with the avascular retina of premature babies being at the highest risk.[8,9] High oxygen saturations, oxygen fluctuation and hypoxia are known to significantly contribute to the development of ROP.[8,10-16]