Eye Diseases > Retina
Retinopathy of Prematurity
Evidence-based assessment and management of retinopathy of prematurity. Comprehensive guide covering etiology, pathogenesis, international classification, diagnosis, and treatment protocols relevant to optometry practice.
Schematic fundus view: retinal zones I–III, abnormal neovascularisation at the vascular–avascular border, and plus disease (tortuous, dilated posterior vessels). Zone I involvement carries the highest risk of progression.
Retinopathy of prematurity (ROP) is a vasoproliferative disorder of the developing retinal vasculature occurring in premature infants. It results from disrupted retinal vascularisation following premature birth, where exposure to the extrauterine environment — particularly supplemental oxygen — halts normal vessel development and subsequently triggers aberrant neovascularisation. ROP is one of the leading causes of preventable childhood blindness worldwide. With advances in neonatal intensive care increasing survival of very preterm infants, the burden of ROP continues to grow globally, particularly in middle-income countries with expanding neonatal care but inconsistent screening programmes.
Primary Cause
ROP arises from the premature interruption of normal retinal vascular development. The human retina is incompletely vascularised until approximately 40 weeks gestational age. Infants born before this point have an avascular peripheral retina that is susceptible to pathological neovascularisation.
- Premature birth: The earlier the gestation at birth, the greater the area of avascular retina and the higher the ROP risk
- Supplemental oxygen: Hyperoxia suppresses vascular endothelial growth factor (VEGF), causing vessel arrest (Phase 1). On return to relative hypoxia, VEGF surges, driving uncontrolled neovascularisation (Phase 2)
- Relative hypoxia: The metabolically active but avascular peripheral retina becomes hypoxic as the infant grows, providing the stimulus for pathological vessel growth
Contributing Factors
- Low birth weight: Independent risk factor; <1500 g significantly increases risk
- Low gestational age: <32 weeks is the primary threshold for screening eligibility
- Fluctuating oxygen levels: Wide swings in SpO₂ more harmful than sustained stable supplementation
- Sepsis and infection: Systemic inflammation upregulates VEGF and promotes neovascularisation
- Intraventricular haemorrhage: Associated systemic instability worsens ROP risk
- Anaemia and blood transfusions: Alter oxygen delivery to the retina
- Respiratory distress syndrome: Leads to prolonged oxygen dependency
- Lack of maternal antenatal corticosteroids: Reduced lung maturation requiring greater neonatal respiratory support
Biphasic Model of ROP Development
ROP is understood as a two-phase disease driven by oxygen-sensitive growth factor regulation:
Phase 1 — Vaso-obliteration (Vessel Arrest)
- Premature birth exposes the infant to relative hyperoxia compared to the in-utero environment
- Hyperoxia suppresses VEGF (vascular endothelial growth factor) and insulin-like growth factor-1 (IGF-1) production
- Without trophic growth factor support, developing retinal vessels stop growing (vessel arrest) and may undergo regression
- This creates an avascular peripheral retina prone to ischaemia
Phase 2 — Vasoproliferation (Neovascularisation)
- As the infant matures, retinal metabolic demand increases
- The avascular retinal periphery becomes progressively hypoxic
- Hypoxia drives massive VEGF upregulation by retinal Müller cells and astrocytes
- Excess VEGF drives uncontrolled, disorganised neovascularisation into the vitreous rather than along the retinal surface
- These fragile new vessels bleed, contract, and can tractionally detach the retina
Role of Key Mediators
- VEGF-A: Primary driver of pathological neovascularisation; target of anti-VEGF treatments
- IGF-1: Essential for normal retinal vascular development; low postnatal IGF-1 levels correlate with ROP severity
- Angiopoietins (Ang-1, Ang-2): Regulate vessel stability; dysregulation contributes to vessel leakage and proliferation
- Erythropoietin: Has both neuroprotective and pro-angiogenic roles; linked to ROP in some studies
- Oxidative stress: Free radical damage to immature retinal vessels promotes vascular regression
International Classification of Retinopathy of Prematurity (ICROP3, 2021)
ROP is classified by location (zone), extent (clock hours), and severity (stage), with additional descriptors for plus disease and aggressive ROP.
Zone — Location of Disease
| Zone | Definition | Clinical Significance |
|---|---|---|
| Zone I | Circle centred on the optic disc with radius twice the disc-to-fovea distance (posterior pole) | Highest risk; most severe outcomes regardless of stage |
| Zone II | Annular ring from Zone I border to a circle centred on the disc, radius equal to disc-to-nasal ora serrata distance | Moderate risk; most common location for treatable ROP |
| Zone III | Residual temporal crescent anterior to Zone II | Lowest risk; often self-resolves |
Stage — Severity of Disease
| Stage | Description | Fundus Finding |
|---|---|---|
| Stage 1 | Demarcation line | Thin white line separating vascular from avascular retina |
| Stage 2 | Ridge | Demarcation line has height and width; elevated ridge; may have small popcorn neovascularisation |
| Stage 3 | Ridge with extraretinal fibrovascular proliferation | Neovascular tissue growing off the ridge surface into the vitreous |
| Stage 4A | Partial retinal detachment — fovea spared | Tractional or exudative detachment not involving the fovea |
| Stage 4B | Partial retinal detachment — fovea involved | Detachment extending to the macula; significant visual threat |
| Stage 5 | Total retinal detachment | Complete funnel detachment; open or closed funnel configuration; poor visual prognosis |
Plus Disease
Plus disease is defined as dilation and tortuosity of the posterior retinal vessels in at least 2 quadrants, meeting or exceeding a reference standard photograph. It reflects increased retinal blood flow driven by shunting through neovascular tissue.
Pre-plus disease: Vascular changes that are abnormal but insufficient to meet the plus disease threshold. Requires close surveillance as it may progress to plus disease.
Aggressive Posterior ROP (AP-ROP)
AP-ROP (formerly APROP or Rush disease) is a severe, rapidly progressive form located in Zone I or posterior Zone II. It is characterised by prominent plus disease, flat neovascularisation at the ridge (not exophytic), haemorrhages, and shunting. It does not follow the classic orderly progression through stages and can progress to retinal detachment rapidly without treatment. Requires urgent intervention.
Extent
Extent is recorded as the number of clock hours (1–12) involved by the disease at the vascular–avascular junction, separately for each eye.
Infant-Related Risk Factors
- Gestational age <32 weeks: Primary screening criterion; risk increases sharply below 28 weeks
- Birth weight <1500 g: Independent strong predictor; <1000 g (extremely low birth weight) carries highest risk
- Male sex: Slightly higher incidence observed in multiple studies
- Multiple gestation (twins/triplets): Higher likelihood of prematurity and associated complications
- Small for gestational age: Intrauterine growth restriction associated with lower IGF-1 levels
Postnatal / Clinical Risk Factors
- Supplemental oxygen therapy: Duration and variability of oxygen exposure; oxygen saturation target ranges (91–95% preferred)
- Mechanical ventilation / CPAP: Prolonged respiratory support
- Sepsis / necrotising enterocolitis: Systemic inflammation upregulates angiogenic factors
- Intraventricular haemorrhage (grades III–IV): Associated with severe systemic compromise
- Anaemia requiring transfusion: Adult haemoglobin in transfused blood may increase oxygen delivery to retina, paradoxically affecting VEGF
- Parenteral nutrition: Delayed enteral feeds reduce IGF-1 delivery
- Low postnatal IGF-1: Serum IGF-1 may serve as a biomarker; the WINROP algorithm uses IGF-1 trajectories to predict ROP risk
- Lack of antenatal steroid administration: Incomplete lung maturation necessitating greater NICU support
Healthcare System Factors
- Inconsistent oxygen monitoring: Wide SpO₂ fluctuations are more damaging than stable supplementation
- Absence of screening protocols: Late detection leads to worse outcomes
- Limited access to treatment: Particularly in low- and middle-income countries
Clinical note: ROP is diagnosed on indirect ophthalmoscopy under pupillary dilation with a 28D lens or via wide-field retinal imaging. Infants cannot report symptoms; all diagnosis is based on objective fundus findings.
Fundoscopic Signs by Stage
- Stage 1: Flat white demarcation line at the vascular–avascular junction; no elevation
- Stage 2: Ridge — elevated, pink-white structure at the junction; may have small tufts of neovascularisation ("popcorn") on the ridge
- Stage 3: Extraretinal fibrovascular tissue proliferating from the ridge posteriorly into the vitreous; haemorrhage common
- Stage 4A: Peripheral tractional retinal detachment, fovea on; vitreous traction visible
- Stage 4B: Retinal detachment extending to involve the fovea
- Stage 5: Total retinal detachment; retina forms a funnel shape (open or closed) behind the lens; leucocoria may be present
Plus Disease Signs
- Venous dilation and arteriolar tortuosity in the posterior retinal vessels (≥2 quadrants)
- Iris vascular engorgement (rubeosis iridis) in severe cases
- Pupillary rigidity (poor dilation) — reflects severe posterior segment disease
- Vitreous haze
AP-ROP Signs
- Prominent plus disease out of proportion to peripheral ridge
- Flat, ill-defined neovascularisation (not exophytic ridge)
- Haemorrhages near the vascular–avascular border
- Shunting vessels between arteries and veins
Important: Premature infants cannot verbalise symptoms. ROP is clinically silent in early stages. All detection relies on scheduled, systematic screening examinations.
Observable Behaviours / Late Presentations
- Leucocoria (white pupillary reflex): May be visible in Stage 5 from total retinal detachment — an emergency; often noted by caregivers or at routine well-child check
- Strabismus: May develop secondary to unequal vision or amblyopia from undetected ROP sequelae
- Nystagmus: Suggests severe bilateral visual impairment from advanced disease
- Poor visual fixation / lack of visual response: In infants with advanced bilateral disease
- High myopia detected at routine check: A common sequela of ROP picked up in optometry in childhood or adolescence
Later in Life (Sequelae Presenting to Optometry)
- Blurred vision from high myopia or amblyopia
- Reduced visual field from retinal dragging or scarring
- Photopsia or floaters from vitreoretinal traction
- Sudden visual loss from late retinal detachment (rare but recognised)
Ocular Complications
- Retinal detachment: Tractional and/or rhegmatogenous; the most vision-threatening complication
- Macular dragging: Temporal traction distorts macular anatomy, causing pseudoesotropia and eccentric fixation
- High myopia: Extremely common; often exceeds −5.00 D; related to axial elongation and lens changes from ROP and its treatments
- Amblyopia: From anisometropia, strabismus, or deprivation; critical to detect and treat early
- Strabismus: Esotropia most common; may be secondary to macular dragging or anisometropia
- Glaucoma: From angle abnormalities (angle-closure from anterior displacement of lens-iris diaphragm) or neovascular glaucoma
- Cataract: From advanced ROP, retinal detachment surgery, or prolonged steroid use in NICU
- Vitreous haemorrhage: From neovascular membranes
- Corneal changes: Band keratopathy in chronic hypotony from advanced disease
- Phthisis bulbi: End-stage complication of untreated Stage 5 disease
Long-term Visual Outcomes
- Permanent vision loss ranging from mild refractive error to total blindness depending on ROP severity and treatment outcome
- Increased risk of late retinal detachment even after successful early treatment
- Lifelong ophthalmology follow-up required for treated cases
- Neurodevelopmental co-morbidities (cerebral palsy, cognitive delay) may compound visual disability
Associated Systemic Conditions of Prematurity
ROP does not cause systemic disease, but it is a marker for the systemic morbidity of prematurity. Infants with severe ROP are at higher risk for:
- Intraventricular haemorrhage (IVH): Periventricular white matter injury associated with neurodevelopmental impairment; severe IVH correlates with severe ROP
- Bronchopulmonary dysplasia (BPD): Chronic lung disease from prolonged ventilation; same oxygen-exposure pathway as ROP
- Necrotising enterocolitis (NEC): Systemic inflammatory insult worsens ROP risk
- Sepsis: Contributes to ROP progression via inflammatory angiogenesis
- Patent ductus arteriosus (PDA): Haemodynamic instability; treatment with indomethacin may affect retinal vasculature
- Anaemia of prematurity: Altered oxygen delivery
- Neurodevelopmental impairment: Cerebral palsy, cognitive delay, and autism spectrum disorder occur at higher rates in ex-premature infants; visual impairment compounds these
- Hearing loss: Concurrent sensory impairment in premature infants requiring coordinated care
Multidisciplinary Implications
- Coordinated care between neonatology, paediatric ophthalmology, optometry, and allied health is essential
- Developmental assessments should incorporate visual function evaluation
- Family counselling regarding long-term visual and neurodevelopmental risks is a key part of discharge planning
Screening Criteria
Screening guidelines vary by country. Common criteria include:
| Criterion | Threshold |
|---|---|
| Gestational age at birth | <32 weeks (UK, Singapore); <30 or <28 weeks in some countries |
| Birth weight | <1500 g regardless of gestational age |
| Clinical risk factors | Selected infants 32–36 weeks with prolonged supplemental oxygen, sepsis, or other risk factors (at clinician discretion) |
| First examination timing | 31–33 weeks postmenstrual age (PMA) for most infants; 4 weeks chronological age is a common alternative threshold |
Examination Technique
- Pupil dilation: Cyclopentolate 0.5% + phenylephrine 2.5% (neonatal preparations); allow 30–45 minutes
- Indirect ophthalmoscopy: Binocular indirect ophthalmoscope with 28D lens; scleral indentation for peripheral zone III assessment
- Wide-field digital retinal imaging (WFDRI): e.g., RetCam or Optos; allows documentation, remote review (teleophthalmology), and serial comparison; increasingly preferred
- Documentation: Zone, stage, extent (clock hours), plus/pre-plus disease for each eye at each visit
Screening Intervals
| Finding | Recommended Follow-up Interval |
|---|---|
| Type 1 ROP / AP-ROP | Treatment within 48–72 hours |
| Type 2 ROP (high-risk pre-threshold) | Every 1 week |
| Stage 1–2 Zone II without plus | Every 1–2 weeks |
| Immature vessels, Zone II | Every 2 weeks |
| Full vascularisation / Zone III | Discharge from screening |
Ancillary Investigations
- Fluorescein angiography (FA): Not routine in neonates but occasionally used to delineate avascular zones and detect subclinical neovascularisation, particularly when imaging is equivocal
- Ocular ultrasound (B-scan): Useful when media opacity (cataract, vitreous haemorrhage) prevents fundus visualisation; detects retinal detachment
- Electroretinography (ERG): Research tool; not used clinically for ROP diagnosis
- AI-assisted image analysis: Emerging technology (e.g., i-ROP) to quantify plus disease and assist screening in resource-limited settings
Singapore Optometry Scope Note: ROP screening and acute management are exclusively within the domain of paediatric ophthalmology and neonatology in Singapore. Optometrists are not involved in neonatal ROP screening. The optometrist's role is to recognise and manage ROP sequelae presenting later in childhood or adulthood — particularly high myopia, amblyopia, strabismus, and anisometropia — and to refer promptly for ophthalmology review if late retinal detachment, new-onset vitreoretinal traction, or other complications are suspected.
Indications for Treatment — Type 1 ROP
Based on the ETROP (Early Treatment for Retinopathy of Prematurity) study, treatment is indicated for Type 1 ROP:
- Zone I, any stage with plus disease
- Zone I, Stage 3 without plus disease
- Zone II, Stage 2 or 3 with plus disease
Type 2 ROP (Zone I Stage 1–2 without plus; Zone II Stage 3 without plus) is observed closely but not immediately treated unless it progresses to Type 1.
Laser Photocoagulation
- Mechanism: Diode laser ablates the avascular peripheral retina, eliminating the hypoxic stimulus for VEGF production
- Technique: Applied under general anaesthesia or deep sedation; 1500–3000 confluent burns to the avascular zone
- Efficacy: Effective for Zone II–III disease; less reliable for Zone I and AP-ROP
- Complications: Peripheral visual field loss (inevitable); cataract; corneal burns; cardiovascular stress
- Limitation: Destroys peripheral retinal tissue permanently; increasingly supplemented or replaced by anti-VEGF therapy
Intravitreal Anti-VEGF Therapy
- Agents used: Bevacizumab (most widely used off-label), ranibizumab (approved in some countries for ROP), aflibercept
- Mechanism: Binds and neutralises VEGF-A, suppressing neovascularisation and promoting vascular regression
- Advantages: Particularly effective for Zone I disease and AP-ROP; preserves peripheral retina; allows vessels to mature toward the periphery; outpatient procedure without general anaesthesia in many centres
- Limitations: Risk of late recurrence (weeks to months after injection — vigilant follow-up essential); systemic absorption of VEGF inhibitor may affect developing organ systems (brain, lung, kidney — under ongoing study); risk of endophthalmitis; no preserved peripheral visual field loss
- Ranibizumab (Byooviz/Lucentis): The RAINBOW trial demonstrated superior outcomes vs laser for Zone I posterior Zone II Stage 3+ ROP; EMA-approved for ROP
- Post-treatment monitoring: Close follow-up at 1 week, then every 1–2 weeks until retinal vascularisation is complete or recurrence is detected
Surgical Management (Stages 4–5)
- Scleral buckling: Preferred for Stage 4 tractional detachments; good anatomical results; lens-sparing
- Pars plana vitrectomy (PPV): For Stage 4B and 5; technically challenging in neonates; visual outcomes of Stage 5 remain poor despite surgical success
- Lens-sparing vitrectomy: Used in younger infants to preserve the lens and reduce risk of amblyopia from aphakia
- Combined procedures: Scleral buckle + vitrectomy for complex detachments
Management of ROP Sequelae (Optometry-Relevant)
Refractive Management
- Spectacle correction for high myopia, astigmatism, or anisometropia — often high prescriptions required from infancy
- Contact lenses for high anisometropia unacceptable in spectacles (infant CLs possible in select cases)
- Myopia control counselling for progressive high myopia
Amblyopia Treatment
- Occlusion therapy (patching) or penalisation for anisometropic or strabismic amblyopia
- Must be co-managed with ophthalmology given complexity of underlying pathology
Visual Field and Low Vision
- Peripheral visual field loss after laser ablation — assess and document
- Low vision rehabilitation referral for those with permanent visual impairment
Prevention
- Oxygen saturation targeting: Maintaining SpO₂ 91–95% in preterm infants reduces ROP incidence
- Antenatal corticosteroids: Maternal steroids before 34 weeks reduce prematurity complications including ROP
- IGF-1 supplementation: Under clinical trial investigation (ROUTE trial)
- Vitamin E supplementation: Modest antioxidant benefit demonstrated in some studies
- Avoidance of large SpO₂ swings: Consistent oxygen management reduces Phase 2 stimulus
Spontaneous Regression
- Approximately 85–90% of ROP cases (Stages 1–2) regress spontaneously without treatment as vessels mature toward the periphery
- Zone III disease almost universally regresses without treatment
- Regression leaves behind normal or near-normal retinal architecture in mild cases
Visual Outcomes After Treatment
| Disease Stage | Prognosis |
|---|---|
| Stage 1–2 (spontaneous regression) | Generally good; near-normal vision; monitor for myopia and amblyopia |
| Type 1 ROP treated (Zones II–III) | Good; >85% achieve 6/12 or better visual acuity with timely treatment |
| Zone I / AP-ROP treated | Guarded; risk of late recurrence after anti-VEGF; risk of structural sequælæ |
| Stage 4A | Variable; anatomical success in 60–80% with surgery; functional vision depends on macular involvement |
| Stage 4B | Poor to guarded; visual acuity often limited despite anatomical reattachment |
| Stage 5 | Very poor; light perception or no light perception common despite vitrectomy; phthisis bulbi in untreated cases |
Long-term Monitoring Requirements
- Annual refractive assessments throughout childhood — high myopia often progressive
- Fundus surveillance for late retinal detachment (risk persists into adulthood)
- Strabismus and amblyopia management in childhood
- Low vision assessment for those with permanent impairment
- Patients with AP-ROP or Zone I disease require lifelong ophthalmology follow-up
Key prognostic determinant: The single most important factor determining visual outcome is timely detection and treatment. Delay in ROP screening beyond the recommended interval is associated with significantly worse outcomes. The fovea-sparing vs fovea-involving distinction (Stage 4A vs 4B) is the critical surgical watershed for useful vision.
In the neonatal/infant period, ROP must be distinguished from other causes of leucocoria, retinal abnormalities, or neonatal eye disease. In older children presenting with ROP sequelae (high myopia, macular dragging), additional differentials apply.
| Condition | Key Distinguishing Features | Clinical Clue |
|---|---|---|
| Familial Exudative Vitreoretinopathy (FEVR) | Similar peripheral avascularity and fibrovascular proliferation; term infants; family history; autosomal dominant or X-linked | Term gestation, no prematurity history; family members may have milder disease |
| Persistent Fetal Vasculature (PFV) | Unilateral white pupil from persistent hyaloid vasculature; microphthalmos; no vascular ridge | Unilateral, microphthalmia, no prematurity |
| Retinoblastoma | Leucocoria; intralesional calcification on CT; rapidly progressive; potentially bilateral; no vascular ridge | Calcification on imaging; urgent oncology referral required |
| Norrie Disease | X-linked; bilateral leucocoria at birth; associated with hearing loss and intellectual disability; caused by NDP gene mutation | Male, bilateral from birth, sensorineural hearing loss |
| Incontinentia Pigmenti | X-linked dominant; peripheral retinal avascularity and neovascularisation; associated skin lesions (Blaschko lines), dental and CNS anomalies | Female (usually lethal in males); characteristic skin findings |
| Coat's Disease | Exudative retinal detachment; telangiectatic retinal vessels; no fibrovascular ridge; usually unilateral; presents in older children | Older child, unilateral, massive exudation without proliferation |
| Congenital Cataract | Lens opacity causing leucocoria; fundus not visible without treatment; no retinal pathology | Lens opacity on slit-lamp; clear red reflex absent |
| Toxocariasis | Inflammatory granuloma; subretinal or vitreous mass; may cause retinal detachment; history of animal contact or soil ingestion | Older child; unilateral; eosinophilia; serological testing |
- International Committee for the Classification of Retinopathy of Prematurity. The International Classification of Retinopathy of Prematurity revisited. Arch Ophthalmol. 2005;123(7):991–999.
- Chiang MF, Quinn GE, Fielder AR, et al. International Classification of Retinopathy of Prematurity, third edition. Ophthalmology. 2021;128(10):e51–e68.
- Early Treatment for Retinopathy of Prematurity Cooperative Group. Revised indications for the treatment of retinopathy of prematurity: results of the early treatment for retinopathy of prematurity randomized trial. Arch Ophthalmol. 2003;121(12):1684–1694.
- Good WV; Early Treatment for Retinopathy of Prematurity Cooperative Group. Final results of the Early Treatment for Retinopathy of Prematurity (ETROP) randomized trial. Trans Am Ophthalmol Soc. 2004;102:233–250.
- Cryotherapy for Retinopathy of Prematurity Cooperative Group. Multicenter trial of cryotherapy for retinopathy of prematurity: ophthalmological outcomes at 10 years. Arch Ophthalmol. 2001;119(8):1110–1118.
- Hellström A, Smith LE, Dammann O. Retinopathy of prematurity. Lancet. 2013;382(9902):1445–1457.
- Mintz-Hittner HA, Kennedy KA, Chuang AZ; BEAT-ROP Cooperative Group. Efficacy of intravitreal bevacizumab for stage 3+ retinopathy of prematurity. N Engl J Med. 2011;364(7):603–615.
- Stahl A, Lepore D, Fielder A, et al. Ranibizumab versus laser therapy for the treatment of very low birthweight infants with retinopathy of prematurity (RAINBOW): an open-label randomised controlled trial. Lancet. 2019;394(10208):1551–1559.
- Fierson WM; American Academy of Pediatrics Section on Ophthalmology; American Academy of Ophthalmology; American Association for Pediatric Ophthalmology and Strabismus; American Association of Certified Orthoptists. Screening examination of premature infants for retinopathy of prematurity. Pediatrics. 2018;142(6):e20183061.
- Gilbert C. Retinopathy of prematurity: a global perspective of the epidemics, population of babies at risk and implications for control. Early Hum Dev. 2008;84(2):77–82.
- Quinn GE, Barr C, Bremer D, et al. Changes in course of retinopathy of prematurity from 1986 to 2013: comparison of three populations in the United States. Ophthalmology. 2016;123(7):1595–1600.
- Smith LE. Through the eyes of a child: understanding retinopathy through ROP the Smith-Lemli-Opitz mouse. Invest Ophthalmol Vis Sci. 2008;49(12):5177–5182.
- Repka MX, Tung B, Good WV, Shapiro M, Capone A Jr, Baker JD. Outcome of eyes developing retinal detachment during the Early Treatment for Retinopathy of Prematurity Study (ETROP). Arch Ophthalmol. 2006;124(1):24–30.
- Holmström G, Hellström A, Jakobsson PG, Lundgren P, Tornqvist K, Wallin A. Swedish national guidelines for retinopathy of prematurity (ROP): screening, treatment and follow-up. Acta Ophthalmol. 2020;98(1):102–109.
- Vinekar A, Jayadev C, Mangalesh S, Bauer N, Davey PG, Shetty B. Comparing the outcome of single versus multiple intravitreal injections of bevacizumab for aggressive posterior retinopathy of prematurity in zone I. Retina. 2015;35(6):1167–1175.