Pharmacomodulation in the Treatment of Retinopathy of Prematurity

Abstract

Type I retinopathy of prematurity is increasing in prevalence proportionate to the advancements of neonatal care and remains the most preventable and potentially devastating neonatal retinal disease worldwide. It is distinguished from standard ROP by its posterior location, aggressive tempo, and high vascular activity/VEGF burden. Current treatment for Type 1 retinopathy of prematurity is guided by landmark multicenter prospective studies (CRYO-ROP, STOP-ROP, ET-ROP, and BEAT-ROP) as well as clinical experience and practical considerations using the available treatment modalities; these include ablation with laser or cryotherapy, intravitreal anti-VEGF agents (Bevacizumab or Ranibizumab) and systemic modulation of hemoglobin and oxygen saturation. Ideal treatment is timed to allow maximum growth of the intrinsic retinal vasculature while preventing fibrovascular contraction or retinal detachment and minimizing complications; these include myopia, visual field constriction, and anterior segment ischemia. With anti-VEGF therapy, recurrences well after the due date and consequent smoldering ROP require vigilant and prolonged outpatient monitoring. Herein, a review of retinal vascular development and the role of VEGF in ROP precedes a discussion of the hallmark studies and a systematic strategy to prevent ROP-associated vision loss while minimizing unnecessary treatments and morbidity to the fragile preemie. We argue that laser is most appropriate for ROP anterior to the equator and smoldering ROP, while intravitreal bevacizumab is more appropriate for posterior disease, especially in highly fragile neonates and situations where follow-up will be reliable.