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• W1998726711 abstract "The immature retinas of preterm neonates are susceptible to insults that disrupt neurovascular growth, leading to retinopathy of prematurity. Suppression of growth factors due to hyperoxia and loss of the maternal–fetal interaction result in an arrest of retinal vascularisation (phase 1). Subsequently, the increasingly metabolically active, yet poorly vascularised, retina becomes hypoxic, stimulating growth factor-induced vasoproliferation (phase 2), which can cause retinal detachment. In very premature infants, controlled oxygen administration reduces but does not eliminate retinopathy of prematurity. Identification and control of factors that contribute to development of retinopathy of prematurity is essential to prevent progression to severe sight-threatening disease and to limit comorbidities with which the disease shares modifiable risk factors. Strategies to prevent retinopathy of prematurity will depend on optimisation of oxygen saturation, nutrition, and normalisation of concentrations of essential factors such as insulin-like growth factor 1 and ω-3 polyunsaturated fatty acids, as well as curbing of the effects of infection and inflammation to promote normal growth and limit suppression of neurovascular development. The immature retinas of preterm neonates are susceptible to insults that disrupt neurovascular growth, leading to retinopathy of prematurity. Suppression of growth factors due to hyperoxia and loss of the maternal–fetal interaction result in an arrest of retinal vascularisation (phase 1). Subsequently, the increasingly metabolically active, yet poorly vascularised, retina becomes hypoxic, stimulating growth factor-induced vasoproliferation (phase 2), which can cause retinal detachment. In very premature infants, controlled oxygen administration reduces but does not eliminate retinopathy of prematurity. Identification and control of factors that contribute to development of retinopathy of prematurity is essential to prevent progression to severe sight-threatening disease and to limit comorbidities with which the disease shares modifiable risk factors. Strategies to prevent retinopathy of prematurity will depend on optimisation of oxygen saturation, nutrition, and normalisation of concentrations of essential factors such as insulin-like growth factor 1 and ω-3 polyunsaturated fatty acids, as well as curbing of the effects of infection and inflammation to promote normal growth and limit suppression of neurovascular development. In the late 1940s, retinopathy of prematurity appeared suddenly in preterm infants. The disorder, initially called retrolental fibroplasia, was characterised by a complete retinal detachment behind the lens. The cause of this first wave of retinopathy of prematurity was the use of supplemental oxygen in closed incubators, which helped to improve the survival of preterm infants,1Silverman WA Retrolental fibroplasia: a modern parable. Grune & Stratton, New York1980Google Scholar but also contributed to blindness.2Campbell K Intensive oxygen therapy as a possible cause of retrolental fibroplasias: a clinical approach.Med J Aust. 1951; 2: 48-50PubMed Google Scholar Optimum oxygenation to balance risk of retinopathy of prematurity against improved survival is still unknown. Studies3Carlo WA Finer NN Walsh MC et al.Target ranges of oxygen saturation in extremely preterm infants.N Engl J Med. 2010; 362: 1959-1969Crossref PubMed Scopus (115) Google Scholar, 4Stenson B Brocklehurst P Tarnow-Mordi W Increased 36-week survival with high oxygen saturation target in extremely preterm infants.N Engl J Med. 2011; 364: 1680-1682Crossref PubMed Scopus (83) Google Scholar have compared various oxygen saturation targets, but not actual patient oxygen saturation levels. Low oxygenation targets are associated with increased mortality, but the optimum timing and target concentration of oxygen treatment remain unanswered questions. Oxygen administration is better controlled nowadays than in the past in developed countries, but retinopathy of prematurity persists, partly because of the increased survival of infants with extremely low gestational ages and birthweights4Stenson B Brocklehurst P Tarnow-Mordi W Increased 36-week survival with high oxygen saturation target in extremely preterm infants.N Engl J Med. 2011; 364: 1680-1682Crossref PubMed Scopus (83) Google Scholar who are at high risk for the disease. In some developing countries unmonitored treatment with 100% oxygen is still used, which can even cause more mature babies to develop severe retinopathy of prematurity. Where advanced care in neonatal intensive care units is available, most cases of retinopathy of prematurity occur in extremely low-gestational-age neonates (gestational age of less than 28 weeks at birth). The low concentrations of factors important for development that are normally provided in utero prevent the very immature retinas of extremely preterm infants from vascularising normally, which can precipitate the disease,5Chen J Smith LE Retinopathy of prematurity.Angiogenesis. 2007; 10: 133-140Crossref PubMed Scopus (282) Google Scholar, 6Heidary G Vanderveen D Smith LE Retinopathy of prematurity: current concepts in molecular pathogenesis.Semin Ophthalmol. 2009; 24: 77-81Crossref PubMed Scopus (42) Google Scholar, 7Rivera JC Sapieha P Joyal JS et al.Understanding retinopathy of prematurity: update on pathogenesis.Neonatology. 2011; 100: 343-353Crossref PubMed Scopus (32) Google Scholar, 8Raghuveer TS Bloom BT A paradigm shift in the prevention of retinopathy of prematurity.Neonatology. 2011; 100: 116-129Crossref PubMed Scopus (25) Google Scholar, 9Mataftsi A Dimitrakos SA Adams GG Mediators involved in retinopathy of prematurity and emerging therapeutic targets.Early Hum Dev. 2011; 87: 683-690Summary Full Text Full Text PDF PubMed Scopus (6) Google Scholar, 10Lee J Dammann O Perinatal infection, inflammation, and retinopathy of prematurity.Semin Fetal Neonatal Med. 2012; 17: 26-29Summary Full Text Full Text PDF PubMed Scopus (22) Google Scholar, 11Hartnett ME Penn JS Mechanisms and management of retinopathy of prematurity.N Engl J Med. 2012; 367: 2515-2526Crossref PubMed Scopus (56) Google Scholar possibly with different effects during different developmental stages. Identification of postnatal factors that affect the risk for and the course of retinopathy of prematurity might allow neonatologists and ophthalmologists to attempt to prevent the disease and to limit comorbidities with which it shares modifiable risk factors. Worldwide about 10% of births occur preterm (before gestational age 37 full weeks).12Goldenberg RL Culhane JF Iams JD Romero R Epidemiology and causes of preterm birth.Lancet. 2008; 371: 75-84Summary Full Text Full Text PDF PubMed Scopus (1737) Google Scholar Preterm birth is the most common cause of neonatal death,13Lawn JE Gravett MG Nunes TM Rubens CE Stanton C GAPPS Review GroupGlobal report on preterm birth and stillbirth (1 of 7): definitions, description of the burden and opportunities to improve data.BMC Pregnancy Childbirth. 2010; 10: S1Crossref PubMed Google Scholar and the second most common cause of death in children younger than 5 years.14Liu L Johnson HL Cousens S et al.for the Child Health Epidemiology Reference Group of WHO and UNICEFGlobal, regional, and national causes of child mortality: an updated systematic analysis for 2010 with time trends since 2000.Lancet. 2012; 379: 2151-2161Summary Full Text Full Text PDF PubMed Scopus (768) Google Scholar Comparisons of the incidence of retinopathy of prematurity from population-based studies is difficult because of substantial variability in study designs, gestational ages of included infants, survival rates, and treatments used. In a prospective study from Sweden15Austeng D Källen KB Ewald UW Jakobsson PG Holmström GE Incidence of retinopathy of prematurity in infants born before 27 weeks gestation in Sweden.Arch Ophthalmol. 2009; 127: 1315-1319Crossref PubMed Scopus (42) Google Scholar in infants with a gestational age of less than 27 weeks at birth, retinopathy of prematurity (at any stage) was reported in 73% (368/506) and severe retinopathy of prematurity was reported in 35% (176/506). In a study in Norway16Markestad T Kaaresen PI Rønnestad A et al.Early death, morbidity, and need of treatment among extremely premature infants.Pediatrics. 2005; 115: 1289-1298Crossref PubMed Scopus (189) Google Scholar of infants with a gestational age of less than 28 weeks at birth, retinopathy of prematurity (at any stage) was reported in 33% (95/290). Investigators of a study in Belgium17Allegaert K de Coen K Devlieger H for the EpiBel Study groupThreshold retinopathy at threshold of viability: the EpiBel study.Br J Ophthalmol. 2004; 88: 239-242Crossref PubMed Scopus (33) Google Scholar in which infants with a gestational age of less than 27 weeks at birth were included reported severe retinopathy of prematurity in 26% (45/175). A study from Australia and New Zealand18Darlow BA Hutchinson JL Henderson-Smart DJ Donoghue DA Simpson JM Evans NJ for the Australian and New Zealand Neonatal NetworkPrenatal risk factors for severe retinopathy of prematurity among very preterm infants of the Australian and New Zealand Neonatal Network.Pediatrics. 2005; 115: 990-996Crossref PubMed Scopus (97) Google Scholar of infants with a gestational age of less than 29 weeks at birth reported severe retinopathy of prematurity in 10% (203/2105). In a study in Austria,19Weber C Weninger M Klebermass K et al.Mortality and morbidity in extremely preterm infants (22 to 26 weeks of gestation): Austria 1999–2001.Wien Klin Wochenschr. 2005; 117: 740-746Crossref PubMed Scopus (22) Google Scholar severe disease was reported in 16% (50/316) of babies with a gestational age of less than 27 weeks at birth. In a Finnish study20Tommiska V Heinonen K Lehtonen L et al.No improvement in outcome of nationwide extremely low birth weight infant populations between 1996–1997 and 1999–2000.Pediatrics. 2007; 119: 29-36Crossref PubMed Scopus (106) Google Scholar in infants with birthweights of less than 1000 g, severe retinopathy of prematurity was seen in only 5–10% (no numbers reported). Thus, prevalence estimates from population-based studies vary even among countries with similar neonatal intensive care facilities. This variation might be partly accounted for by differences in the proportions of infants at high risk of retinopathy of prematurity who survive when born at an early gestational age—in Sweden 11·5% of survivors were born in weeks 22–23,15Austeng D Källen KB Ewald UW Jakobsson PG Holmström GE Incidence of retinopathy of prematurity in infants born before 27 weeks gestation in Sweden.Arch Ophthalmol. 2009; 127: 1315-1319Crossref PubMed Scopus (42) Google Scholar compared with 0–6% in the other studies.16Markestad T Kaaresen PI Rønnestad A et al.Early death, morbidity, and need of treatment among extremely premature infants.Pediatrics. 2005; 115: 1289-1298Crossref PubMed Scopus (189) Google Scholar, 17Allegaert K de Coen K Devlieger H for the EpiBel Study groupThreshold retinopathy at threshold of viability: the EpiBel study.Br J Ophthalmol. 2004; 88: 239-242Crossref PubMed Scopus (33) Google Scholar, 18Darlow BA Hutchinson JL Henderson-Smart DJ Donoghue DA Simpson JM Evans NJ for the Australian and New Zealand Neonatal NetworkPrenatal risk factors for severe retinopathy of prematurity among very preterm infants of the Australian and New Zealand Neonatal Network.Pediatrics. 2005; 115: 990-996Crossref PubMed Scopus (97) Google Scholar, 19Weber C Weninger M Klebermass K et al.Mortality and morbidity in extremely preterm infants (22 to 26 weeks of gestation): Austria 1999–2001.Wien Klin Wochenschr. 2005; 117: 740-746Crossref PubMed Scopus (22) Google Scholar, 20Tommiska V Heinonen K Lehtonen L et al.No improvement in outcome of nationwide extremely low birth weight infant populations between 1996–1997 and 1999–2000.Pediatrics. 2007; 119: 29-36Crossref PubMed Scopus (106) Google Scholar, 21Fledelius HC Dahl H Retinopathy of prematurity, a decrease in frequency and severity. Trends over 16 years in a Danish county.Acta Ophthalmol Scand. 2000; 78: 359-361Crossref PubMed Scopus (32) Google Scholar, 22Lundqvist P Källen K Hallström I Westas LH Trends in outcomes for very preterm infants in the southern region of Sweden over a 10-year period.Acta Paediatr. 2009; 98: 648-653Crossref PubMed Scopus (22) Google Scholar An alternative to non-uniform and intermittent data collections in many countries or regions would be occasional snapshots of the burden of severe disease in one geographical area with uniform care.23Haines L Fielder AR Scrivener R Wilkinson AR Pollock JI for the Royal College of Paediatrics and Child Healththe Royal College of Ophthalmologists and British Association of Perinatal MedicineRetinopathy of prematurity in the UK I: the organisation of services for screening and treatment.Eye (Lond). 2002; 16: 33-38Crossref PubMed Scopus (36) Google Scholar, 24Haines L Fielder AR Baker H Wilkinson AR UK population based study of severe retinopathy of prematurity: screening, treatment, and outcome.Arch Dis Child Fetal Neonatal Ed. 2005; 90: F240-F244Crossref PubMed Scopus (35) Google Scholar Sweden now has a register (SWEDROP) for all children screened for retinopathy of prematurity, which is used to measure incidence.25Holmström GE Hellström A Jakobsson PG Lundgren P Tornqvist K Wallin A Swedish national register for retinopathy of prematurity (SWEDROP) and the evaluation of screening in Sweden.Arch Ophthalmol. 2012; 130: 1418-1424Crossref PubMed Scopus (9) Google Scholar Taken as a whole, the data do not suggest that incidence has changed substantially over time.7Rivera JC Sapieha P Joyal JS et al.Understanding retinopathy of prematurity: update on pathogenesis.Neonatology. 2011; 100: 343-353Crossref PubMed Scopus (32) Google Scholar, 26Tan SZ Dhaliwal C Becher JC Fleck B Trends in the incidence of retinopathy of prematurity in Lothian, south-east Scotland, from 1990 to 2009.Arch Dis Child Fetal Neonatal Ed. 2012; 97: F310-F311Crossref PubMed Scopus (3) Google Scholar, 27Hameed B Shyamanur K Kotecha S et al.Trends in the incidence of severe retinopathy of prematurity in a geographically defined population over a 10-year period.Pediatrics. 2004; 113: 1653-1657Crossref PubMed Scopus (26) Google Scholar, 28Lad EM Nguyen TC Morton JM Moshfeghi DM Retinopathy of prematurity in the United States.Br J Ophthalmol. 2008; 92: 320-325Crossref PubMed Scopus (60) Google Scholar, 29Lad EM Hernandez-Boussard T Morton JM Moshfeghi DM Incidence of retinopathy of prematurity in the United States: 1997 through 2005.Am J Ophthalmol. 2009; 148: 451-458Summary Full Text Full Text PDF PubMed Scopus (50) Google Scholar, 30Gunn DJ Cartwright DW Gole GA Incidence of retinopathy of prematurity in extremely premature infants over an 18-year period.Clin Experiment Ophthalmol. 2012; 40: 93-99Crossref PubMed Scopus (10) Google Scholar Perhaps increased survival of very immature infants at high risk for the disease balanced against improved neonatal intensive care can account for this finding. Incidence can also increase when neonatal care is sufficient to save the babies' lives but insufficient to prevent disease—eg, through use of uncontrolled oxygen delivery.31Zin AA Moreira ME Bunce C Darlow BA Gilbert CE Retinopathy of prematurity in 7 neonatal units in Rio de Janeiro: screening criteria and workload implications.Pediatrics. 2010; 126: e410-e417Crossref PubMed Scopus (24) Google Scholar, 32Darlow BA Zin AA Beecroft G Moreira ME Gilbert CE Capacity building of nurses providing neonatal care in Rio de Janeiro, Brazil: methods for the POINTS of care project to enhance nursing education and reduce adverse neonatal outcomes.BMC Nurs. 2012; 11: 3Crossref PubMed Scopus (4) Google Scholar Retinopathy of prematurity can be viewed as an arrest of normal retinal neuronal and vascular development in the preterm infant, with ultimately pathological compensatory mechanisms that result in aberrant vascularisation of the retina. The more profound the immaturity at birth and the persistence of developmental arrest due to exposure of the retina to harmful factors, coupled with deficiencies of factors normally provided in utero, the more aggressive the later pathological response. The disease has two postnatal phases (figure 1),5Chen J Smith LE Retinopathy of prematurity.Angiogenesis. 2007; 10: 133-140Crossref PubMed Scopus (282) Google Scholar, 6Heidary G Vanderveen D Smith LE Retinopathy of prematurity: current concepts in molecular pathogenesis.Semin Ophthalmol. 2009; 24: 77-81Crossref PubMed Scopus (42) Google Scholar, 11Hartnett ME Penn JS Mechanisms and management of retinopathy of prematurity.N Engl J Med. 2012; 367: 2515-2526Crossref PubMed Scopus (56) Google Scholar possibly preceded by a prephase10Lee J Dammann O Perinatal infection, inflammation, and retinopathy of prematurity.Semin Fetal Neonatal Med. 2012; 17: 26-29Summary Full Text Full Text PDF PubMed Scopus (22) Google Scholar of antenatal sensitisation via inflammation (figure 2). Understanding these phases and their causes might allow the identification of the optimum postnatal environment for these immature babies.Figure 2Infection, inflammation, and retinopathy of prematurityShow full captionExposure to infection and inflammation seems to modify risk of retinopathy of prematurity, especially before (prephase) and a few weeks after birth (phase 2), when oxygen concentrations are relatively low compared with phase 1 (immediately after birth). Whereas prenatal inflammation seems to exert a sensitising effect without directly increasing risk, postnatal infection and inflammation are associated with an increased risk, perhaps most prominently in phase 2. Adapted from 10Lee J Dammann O Perinatal infection, inflammation, and retinopathy of prematurity.Semin Fetal Neonatal Med. 2012; 17: 26-29Summary Full Text Full Text PDF PubMed Scopus (22) Google Scholar, by permission of Elsevier.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Exposure to infection and inflammation seems to modify risk of retinopathy of prematurity, especially before (prephase) and a few weeks after birth (phase 2), when oxygen concentrations are relatively low compared with phase 1 (immediately after birth). Whereas prenatal inflammation seems to exert a sensitising effect without directly increasing risk, postnatal infection and inflammation are associated with an increased risk, perhaps most prominently in phase 2. Adapted from 10Lee J Dammann O Perinatal infection, inflammation, and retinopathy of prematurity.Semin Fetal Neonatal Med. 2012; 17: 26-29Summary Full Text Full Text PDF PubMed Scopus (22) Google Scholar, by permission of Elsevier. In 1952, Patz and coworkers34Patz A Hoeck LE De la Cruz E Studies on the effect of high oxygen administration in retrolental fibroplasia, I: nursery observations.Am J Ophthalmol. 1952; 35: 1248-1253Summary Full Text PDF PubMed Google Scholar showed in a clinical study the association between administration of very high concentrations of oxygen and retinopathy of prematurity. Ashton35Ashton N Pathological basis of retrolental fibroplasia.Br J Ophthalmol. 1954; 38: 385-396Crossref PubMed Scopus (21) Google Scholar then established the notion of oxygen toxicity (phase 1) followed by hypoxia-mediated vasoproliferation (phase 2) through work in cats. In both animal and human studies,11Hartnett ME Penn JS Mechanisms and management of retinopathy of prematurity.N Engl J Med. 2012; 367: 2515-2526Crossref PubMed Scopus (56) Google Scholar, 36Smith LE Wesolowski E McLellan A et al.Oxygen-induced retinopathy in the mouse.Invest Ophthalmol Vis Sci. 1994; 35: 101-111PubMed Google Scholar, 37Connor KM Krah NM Dennison RJ et al.Quantification of oxygen-induced retinopathy in the mouse: a model of vessel loss, vessel regrowth and pathological angiogenesis.Nat Protoc. 2009; 4: 1565-1573Crossref PubMed Scopus (149) Google Scholar hyperoxia is an important driver for the arrest of vascular growth in phase 1. Even room air can lead to hyperoxia compared with the intrauterine environment, where mean oxygen pressure is less than 50 mm Hg during the second half of pregnancy.38Nicolaides KH Economides DL Soothill PW Blood gases, pH, and lactate in appropriate- and small-for-gestational-age fetuses.Am J Obstet Gynecol. 1989; 161: 996-1001Summary Full Text PDF PubMed Scopus (214) Google Scholar More importantly, supplemental oxygen given to premature infants with respiratory distress can lead to abnormally high oxygen saturation. Hyperoxia leads to suppression of oxygen-regulated angiogenic growth factors, particularly erythropoietin39Chen J Connor KM Aderman CM Smith LE Erythropoietin deficiency decreases vascular stability in mice.J Clin Invest. 2008; 118: 526-533PubMed Google Scholar, 40Chen J Connor KM Aderman CM Willett KL Aspegren OP Smith LE Suppression of retinal neovascularization by erythropoietin siRNA in a mouse model of proliferative retinopathy.Invest Ophthalmol Vis Sci. 2009; 50: 1329-1335Crossref PubMed Scopus (79) Google Scholar and vascular endothelial growth factor (VEGF),41Pierce EA Avery RL Foley ED Aiello LP Smith LE Vascular endothelial growth factor/vascular permeability factor expression in a mouse model of retinal neovascularization.Proc Natl Acad Sci USA. 1995; 92: 905-909Crossref PubMed Scopus (770) Google Scholar which in turn causes both cessation of retinal vessel growth and loss of some existing retinal vessels42Pierce EA Foley ED Smith LE Regulation of vascular endothelial growth factor by oxygen in a model of retinopathy of prematurity.Arch Ophthalmol. 1996; 114: 1219-1228Crossref PubMed Google Scholar (a process that has been partly reversed in mice with the replacement of VEGF and erythropoietin).39Chen J Connor KM Aderman CM Smith LE Erythropoietin deficiency decreases vascular stability in mice.J Clin Invest. 2008; 118: 526-533PubMed Google Scholar, 40Chen J Connor KM Aderman CM Willett KL Aspegren OP Smith LE Suppression of retinal neovascularization by erythropoietin siRNA in a mouse model of proliferative retinopathy.Invest Ophthalmol Vis Sci. 2009; 50: 1329-1335Crossref PubMed Scopus (79) Google Scholar, 41Pierce EA Avery RL Foley ED Aiello LP Smith LE Vascular endothelial growth factor/vascular permeability factor expression in a mouse model of retinal neovascularization.Proc Natl Acad Sci USA. 1995; 92: 905-909Crossref PubMed Scopus (770) Google Scholar, 42Pierce EA Foley ED Smith LE Regulation of vascular endothelial growth factor by oxygen in a model of retinopathy of prematurity.Arch Ophthalmol. 1996; 114: 1219-1228Crossref PubMed Google Scholar Some investigators43Shah PK Narendran V Kalpana N Aggressive posterior retinopathy of prematurity in large preterm babies in South India.Arch Dis Child Fetal Neonatal Ed. 2012; 97: F371-F375Crossref PubMed Scopus (16) Google Scholar speculate that in more mature infants, exposure to high oxygen concentrations causes loss of existing vessels not seen with controlled oxygen delivery, which mainly causes cessation of vessel growth. Like preterm infants, newborn cats,34Patz A Hoeck LE De la Cruz E Studies on the effect of high oxygen administration in retrolental fibroplasia, I: nursery observations.Am J Ophthalmol. 1952; 35: 1248-1253Summary Full Text PDF PubMed Google Scholar rats,44Penn JS Tolman BL Lowery LA Variable oxygen exposure causes preretinal neovascularization in the newborn rat.Invest Ophthalmol Vis Sci. 1993; 34: 576-585PubMed Google Scholar and mice36Smith LE Wesolowski E McLellan A et al.Oxygen-induced retinopathy in the mouse.Invest Ophthalmol Vis Sci. 1994; 35: 101-111PubMed Google Scholar have incomplete retinal vascularisation at birth and oxygen can be used to induce retinal vessel loss. However, unlike premature infants, the developmental stage at delivery of these animals is appropriate for their species. In human infants born before completion of the third trimester of pregnancy, factors such as insulin-like growth factor 1 (IGF-1),45Hellström A Engström E Hård AL et al.Postnatal serum insulin-like growth factor I deficiency is associated with retinopathy of prematurity and other complications of premature birth.Pediatrics. 2003; 112: 1016-1020Crossref PubMed Scopus (227) Google Scholar normally present at optimum concentrations in utero, are missing, which can also contribute to arrest of vascular growth. IGF-1 is crucial for normal growth and development of many tissues, including brain and blood vessels. Moreover, the loss of maternally-provided ω long-chain polyunsaturated fatty acids seems to have a role in pathogenesis of retinopathy of prematurity (figure 1).46Connor KM Sangiovanni JP Löfqvist C et al.Increased dietary intake of omega-3-polyunsaturated fatty acids reduces pathological retinal angiogenesis.Nat Med. 2007; 13: 868-873Crossref PubMed Scopus (316) Google Scholar, 47Pawlik D Lauterbach R Turyk E Fish-oil fat emulsion supplementation may reduce the risk of severe retinopathy in VLBW infants.Pediatrics. 2011; 127: 223-228Crossref PubMed Scopus (35) Google Scholar In severe disease, phase 2 begins when the increasingly metabolically active yet poorly vascularised retina (caused by suppression of vessel growth in phase 1) becomes hypoxic. Phase 2 is characterised by proliferation of blood vessels largely in response to hypoxia-driven increases in VEGF and erythropoietin.48Aiello LP Pierce EA Foley ED et al.Suppression of retinal neovascularization in vivo by inhibition of vascular endothelial growth factor (VEGF) using soluble VEGF-receptor chimeric proteins.Proc Natl Acad Sci USA. 1995; 92: 10457-10461Crossref PubMed Scopus (968) Google Scholar, 49Watanabe D Suzuma K Matsui S et al.Erythropoietin as a retinal angiogenic factor in proliferative diabetic retinopathy.N Engl J Med. 2005; 353: 782-792Crossref PubMed Scopus (312) Google Scholar The new vessels poorly perfuse the retina and are leaky, which leads to fibrous scar formation and retinal detachment. In most infants retinopathy of prematurity regresses spontaneously and the retina vascularises fairly normally, although neural deficits (loss of photoreceptor function) can remain even in mild cases.50Fulton AB Hansen RM Moskowitz A Akula JD The neurovascular retina in retinopathy of prematurity.Prog Retin Eye Res. 2009; 28: 452-482Crossref PubMed Scopus (47) Google Scholar The transition between phase 1 and 2 seems to depend on the postmenstrual age of the infant rather than the postnatal age. In a study of infants with birthweights of less than 1251 g, disease onset began at roughly 30 weeks' postmenstrual age and peaked at 36–38 weeks' postmenstrual age, irrespective of gestational age at birth. This important finding suggests that onset of retinopathy of prematurity corresponds more closely with postmenstrual age than with postnatal age,51Palmer EA Flynn JT Hardy RJ et al.The Cryotherapy for Retinopathy of Prematurity Cooperative GroupIncidence and early course of retinopathy of prematurity.Ophthalmology. 1991; 98: 1628-1640Summary Full Text PDF PubMed Google Scholar which points to an association between programmed timing of development and disease pathogenesis. However, this association might not be evident in extreme prematurity. In a study of infants with gestational ages at birth from 22 weeks to 26 weeks and 6 days, the onset of retinal vascular events corresponded more closely with postnatal age (mean range 8·6–9·6 weeks) than with postmenstrual age, which suggests that extreme prematurity confers additional risk for the development of retinopathy of prematurity since vascular events occurred earlier in more immature infants.52Austeng D Källen KB Hellström A et al.Screening for retinopathy of prematurity in infants born before 27 weeks' gestation in Sweden.Arch Ophthalmol. 2011; 129: 167-172Crossref PubMed Scopus (9) Google Scholar The timing of the phases of retinopathy of prematurity can be also be modified by exposure to very high concentrations of oxygen. In one study,43Shah PK Narendran V Kalpana N Aggressive posterior retinopathy of prematurity in large preterm babies in South India.Arch Dis Child Fetal Neonatal Ed. 2012; 97: F371-F375Crossref PubMed Scopus (16) Google Scholar even relatively mature preterm infants (gestational age at birth of 31·7 weeks [range 28–35 weeks]) lost retinal vessels (phase 1) and progressed to severe zone-1 neovascularisation (phase 2) when exposed to 100% oxygen after birth. In some cases factors that cause preterm birth might also affect intrauterine retinal neurovascular development. Antenatal factors such as placental infection and inflammation53Chen ML Allred EN Hecht JL et al.Placenta microbiology and histology and the risk for severe retinopathy of prematurity.Invest Ophthalmol Vis Sci. 2011; 52: 7052-7058Crossref PubMed Scopus (17) Google Scholar might predispose the fetal retina to severe retinopathy of prematurity, and such a sensitisation effect might constitute a prephase of the disease.10Lee J Dammann O Perinatal infection, inflammation, and retinopathy of prematurity.Semin Fetal Neonatal Med. 2012; 17: 26-29Summary Full Text Full Text PDF PubMed Scopus (22) Google Scholar The question of the correct balance between high oxygen supplementation in the early postnatal period to prevent death and lower oxygen to prevent vessel loss in phase 1 of retinopathy of prematurity remains unsettled, and remains crucially important in neonatology. After the first wave of retinopathy of prematurity, when the use of 100% oxygen made even some mature preterm babies blind, oxygen was restricted to 50% of inspired O2, which resulted in about 16 dea" @default.
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• W1998726711 title "Retinopathy of prematurity" @default.
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