Retinopathy of prematurity (ROP), a proliferative retinopathy affecting premature infants of low birth weight (BW) and young gestational age (GA), remains a leading cause of lifelong visual impairment among children in developed countries. ROP causes visual loss in 1300 children and severe visual impairment in 500 children each year in the United States alone. Terry described ROP in 1942. Initially termed “retrolental fibroplasia” (RLF), a detailed nomenclature has evolved to describe the various stages of ROP (see “ROP Classification and Findings”).
The earliest cases of ROP were noted to occur as a consequence of introducing oxygen therapy into the newborn nursery to improve the survival rates of premature infants. Though more premature infants survived, some went on to develop retrolenticular membranes in one or both eyes that progressed to blindness. Campbell, Kinsey, and Patz were credited with identifying oxygen as an agent that could aggravate this process and lead to retinal detachment.
As a result of the work of Patz and others, oxygen use was curtailed in newborn nurseries, and the incidence of ROP declined. The use of oxygen is now closely monitored and no longer implicated as the sole or even the primary — factor in the pathogenesis of ROP (see “ROP Pathogenesis”). In the last 20 years, the survival rate for high-risk neonates has improved yet the incidence of ROP has remained constant, although posterior ROP is more prevalent.
Terry TL. Extreme prematurity and fibroblastic overgrowth of persistent vascular sheath behind each crystalline lens: (1) preliminary report. Am J Ophthalmol 1942;25:203-204.
Patz A. Clinical and experimental studies on retinal neovascularization. XXXIX Edward Jackson Memorial Lecture. Am J Ophthalmol 1982;94:715-743.
Kinsey VE. Cooperative study of retrolental fibroplasia and the use of oxygen. Arch Ophthalmol 1956;56:481-543.
Campbell K. Intensive oxygen therapy as a possible cause of retrolental fibroplasia. A clinical approach. Med J Aust 1951;2:48.