To determine if visuocortical development in premature infants with high bilirubin levels is more adversely affected than that in full-term infants. 57 preterm infants were managed using institutional guidelines for hyperbilirubinemia. At 12-months corrected age, Vernier acuity, contrast sensitivity, and grating acuity measured using the sweep visual evoked potential (sVEP) were correlated to total serum/plasma bilirubin (TSB) levels in the first week of life. As TSB levels increased, Vernier acuity worsened in infants <34 weeks’ gestation compared with those >34 to <37 weeks’ gestation (p < 0.001). Contrast sensitivity varied as a function of TSB levels (Spearman correlation 0.63, p < 0.001). Grating acuity was unaffected. Vernier acuity in preterm infants <34 weeks’ gestation is more vulnerable to the effects of bilirubin, suggesting that the extrastriate visual cortex is primarily affected by bilirubin. Therefore, guidelines for management of hyperbilirubinemia in preterm infants (<34 weeks’ gestation) should be revised.

PURPOSE: There is strong evidence that genetic factors influence retinopathy of prematurity (ROP), a neovascular eye disease. It has been previously suggested that polymorphisms in the genes involved in beta-adrenergic receptor (ADR beta) pathways could protect against ROP. Antagonists for the ADR beta are actively tested in clinical trials for ROP treatment, but not without controversy and safety concerns. This study was designed to assess whether genetic variations in components of the ADR beta signaling pathways associate with risk of developing ROP. DESIGN: An observational case-control targeted genetic analysis. METHODS: A study was carried out in premature participants with (n = 30) or without (n = 34) ROP and full-term controls (n = 20), who were divided into a discovery cohort and a validation cohort. ROP was defined using International Classification of Retinopathy of Prematurity criteria (ICROP). Targeted sequencing of 20 genes in the ADR beta pathways was performed in the discovery cohort. Polymerase chain reaction (PCR)/restriction enzyme analysis for some of the discovered ROP-associated variants was performed for validation of the results using the validation cohort. RESULTS: The discovery cohort revealed 543 bi-allelic variants within 20 genes of the ADR beta pathways. Ten single-nucleotide variants (SNVs) in 5 genes including protein kinase A regulatory subunit 1 alpha (PRKAR1A), rap guanine exchange factor 3 (RAPQEF3), adenylyl cyclase 4 (ADCY4), ADCY7, and ADCY9 were associated with ROP ( P < .05). The most significant SNV was found in PRKAR1A ( P = .001). Multiple variants located in the 3 '-untranslated region (3 ' UTR) of RAPQEF3 were also associated with ROP ( P < .05). PCR/restriction enzyme analysis of the 3 ' UTR of RAPQEF3 methodologically validated these findings. CONCLUSION: SNVs in PRKAR1A may represent protective factors whereas SNVs in RAPQEF3 may represent risk factors for ROP. PRKAR1 alpha has previously been implicated in retinal vascular development whereas the RAPQEF3 product has a role in the maintenance of vascular barrier function, 2 processes important in ROP. Multicenter validation of these newly discovered risk factors could lead to valuable tools for predicting and preventing the development of severe ROP. (c) 2024 Elsevier Inc. All rights reserved.

PURPOSE:To report 2-year ocular and developmental outcomes for infants receiving low doses of intravitreal bevacizumab for type 1 retinopathy of prematurity (ROP).METHODS:A total of 120 premature infants (mean birthweight, 687 g; mean gestational age, 24.8 weeks) with type 1 ROP were enrolled in a multicenter, phase 1 dose de-escalation study. One eye per infant received 0.25 mg, 0.125 mg, 0.063 mg, 0.031 mg, 0.016 mg, 0.008 mg, 0.004 mg, or 0.002 mg of intravitreal bevacizumab; fellow eyes when treated received one dosage level higher. At 2 years, 70 of 120 children (58%) underwent ocular examinations; 51 (43%) were assessed using the Bayley Scale of Infant and Toddler Development.RESULTS:Correlation coefficients for the association of total dosage of bevacizumab with Bayley subscales were -0.20 for cognitive (95% CI, -0.45 to 0.08), -0.15 for motor (95% CI, -0.41 to 0.14), and -0.19 for language (95% CI, -0.44 to 0.10). Fourteen children (21%) had myopia greater than -5.00 D in one or both eyes, 7 (10%) had optic nerve atrophy and/or cupping, 20 (29%) had strabismus, 8 (11%) had manifest nystagmus, and 9 (13%) had amblyopia.CONCLUSIONS:In this study cohort, there was no statistically significant correlation between dosage of bevacizumab and Bayley scores at 2 years. However, the sample size was small and the retention rate relatively low, limiting our conclusions. Rates of high myopia and ocular abnormalities do not differ from those reported after larger bevacizumab doses.

Every year millions of children are exposed to general anesthesia while undergoing surgi-cal and diagnostic procedures. In the field of ophthalmology, 44,000 children are exposed to general anesthesia annually for strabismus surgery alone. While it is clear that general anesthesia is necessary for sedation and pain minimization during surgical procedures, the possibility of neurotoxic impairments from its exposure is of concern. In animals there is strong evidence linking early anesthesia exposure to abnormal neural development. but in humans the effects of anesthesia are debated. In humans many aspects of vision develop within the first year of life, making the visual system vulnerable to early adverse experi-ences and potentially vulnerable to early exposure to general anesthesia. We attempt to address whether the visual system is affected by early postnatal exposure to general anes-thesia. We first summarize key mechanisms that could account for the neurotoxic effects of general anesthesia on the developing brain and review existing literature on the effects of early anesthesia exposure on the visual system in both animals and humans and on neu-rocognitive development in humans. Finally, we conclude by proposing future directions for research that could address unanswered questions regarding the impact of general anes-thesia on visual development. (c) 2022 Elsevier Inc. All rights reserved.

We present the findings of 2 children with neonatal hypoxic ischemic encephalopathy (HIE), who demonstrated ocular neovascularization at birth. While the cerebral effects of HIE have been well described, ocular effects have not. Our cases, combined with recent published laboratory research, demonstrate that significant ocular effects may accompany HIE.

Low-dose and very low-dose intravitreal bevacizumab (IVB) have been reported to be successful in short-term treatment of type 1 retinopathy of prematurity (ROP), down to an initial dose of 0.004 mg. We now report 12-month outcomes for these infants.Masked, multicenter, dose de-escalation study.One hundred twenty prematurely born infants with type 1 ROP.A cohort of 120 infants with type 1 ROP in at least 1 eye from 2 sequential dose de-escalation studies of low-dose IVB (0.25 mg, 0.125 mg, 0.063 mg, and 0.031 mg) or very low-dose IVB (0.016 mg, 0.008 mg, 0.004 mg, and 0.002 mg) to the study eye; the fellow eye (if also type 1) received 1 dose level higher of IVB. After primary success or failure at 4 weeks, clinical management was at investigator discretion, including all additional treatment.Reactivation of severe ROP by 6 months corrected age, additional treatments, retinal and other ocular structural outcomes, and refractive error at 12 months corrected age.Sixty-two of 113 study eyes (55%) and 55 of 98 fellow eyes (56%) received additional treatment. Of the study eyes, 31 (27%) received additional ROP treatment, and 31 (27%) received prophylactic laser therapy for persistent avascular retina. No trend toward a higher risk of additional ROP treatment related to initial IVB doses was found. However, time to reactivation among study eyes was shorter in eyes that received very low-dose IVB (mean, 76.4 days) than in those that received low-dose IVB (mean, 85.7 days). At 12 months, poor retinal outcomes and anterior segment abnormalities both were uncommon (3% and 5%, respectively), optic atrophy was noted in 10%, median refraction was mildly myopic (-0.31 diopter), and strabismus was present in 29% of infants.Retinal structural outcomes were very good after low- and very low-dose IVB as initial treatment for type 1 ROP, although many eyes received additional treatment. The rate of reactivation of severe ROP was not associated with dose; however, a post hoc data-driven analysis suggested that reactivation was sooner with very low doses.

Previously, we reported intravitreous bevacizumab doses as low as 0.004 mg (<1% of BEAT-ROP dose) were effective in treating type 1 ROP. We now report two-year outcomes after low-dose and very low-dose bevacizumab.

Alan B. Scott died after a brief illness on December 16, 2021, leaving behind his wife, Jackie, 5 children (Jennifer, Heidi, Alison, Ann, and Nathaniel), 4 stepdaughters (Suzanne, Mary, Sally, and Phillis Lehmer), 21 grandchildren, and 2 great-grandchildren. Those of us who knew him count ourselves as fortunate and are deeply affected by this loss. He was a generous, highly intelligent, and fun-loving person. Alan was born in Berkeley, California, on July 13, 1932. His father was a dentist, and his mother worked in a laboratory at the University of California, Berkeley. After receiving his bachelor’s degree in medical sciences at the University of California, Berkeley, he trained at the University of California, San Francisco, and received his medical degree in in 1956. He completed his residency training at Stanford. He was married to his first wife, Ruth, for 53 years. He married Jacquelyn Lehmer in 2014. Medical school training was followed by ophthalmology training at Stanford, after which he began working at the Smith-Kettlewell Eye Research Institute, eventually serving as the executive co-director. He had a lifelong affiliation with the California Pacific Medical Center Department of Ophthalmology. He loved teaching and treated residents with kindness and thoughtfulness. He trained many doctors from around the world, particularly from South America. Early in his career he explored the possible uses for botulinum toxin in humans. This research began in the early 1960s, culminating, after years of work and experimentation, in FDA approval for botulinum therapy to treat strabismus and blepharospasm in 1991. Most of his research was self-funded. Botulinum toxin remains an important part of the strabismologist’s armamentarium, but even he could not have anticipated its expanded use in the treatment of dystonias, wrinkles, headaches, hyperhidrosis, and spastic cerebral palsy. At the time of his death, Alan was hard at work investigating the use of bupivacaine to “strengthen” muscles. Most of us had cared for patients who developed diplopia after a retrobulbar injection. Alan imagined the therapeutic use of bupivacaine’s myotoxicity to manage particularly onerous cases of strabismus. He founded the Strabismus Research Foundation to study bupivacaine and to model various forms of strabismus. The interested reader will find much more detail in a forthcoming biography by Eugene Helveston. As I learned through decades of collaboration with Alan, curiosity was the driving force in his scientific life. Even in his last months, he would come to the operating room with me to observe or help with complicated cases. Afterward, he would confide to me where our approaches would have differed. His humility may have been his most remarkable trait. He listened at lectures, hoping to hear something new. When he spoke, a crowded room would crane to hear what he had to say. He praised those whose otherwise seemingly inconsequential lectures nevertheless revived old ideas. His accomplishments were myriad. He was awarded the Howe Medal of the American Ophthalmological Society. His named lectureships are too long to list. He was a gifted lecturer and writer. No one had a better command of the English language. Alan loved golf. No sooner would we arrive in a new city than we would have a tee-time after a morning meeting. Ruth, his first wife, would accompany us, with conversation never involving the practice of medicine. He loved duck hunting, and he took up mushrooming as a hobby. He taught himself Spanish and was conversant in German. I had known about his piano playing abilities—also self-taught—but discovered from his family that he learned to play oboe well enough to play with a local group. Always an optimist, he recently spoke of his remaining few years, during which he wanted to work out specifics of bupivacaine use for strabismus. He planned to join forces with several of us to see patients and talk about strabismus ideas. An article in this edition of J AAPOS is testimony to his constant work on strabismus patterns and to his collaborations. His illness caught us all by surprise. We can only imagine his further contributions to the field, had he had more time. All of us have been touched by his genius, his mastery of litotes, and his camaraderie. We extend our deepest condolences to his family. We have lost a remarkably gifted person, scientist, and doctor.

Perinatal cortical visual impairment (CVI) is a devasting neurologic condition that is ubiquitous in pediatric ophthalmology clinics. 1 Good W.V. Jan J.E. DeSa L. et al. Cortical visual impairment in children. Surv Ophthalmol. 1994; 38: 351-364 Abstract Full Text PDF PubMed Scopus (177) Google Scholar Most cases are attributed to a watershed hypoxic-ischemic injury of the visual cortex at birth. 1 Good W.V. Jan J.E. DeSa L. et al. Cortical visual impairment in children. Surv Ophthalmol. 1994; 38: 351-364 Abstract Full Text PDF PubMed Scopus (177) Google Scholar However, it has been suggested that prenatal cortical malformations that are often genetic in origin can precipitate the hypoxic-ischemic events that give rise to this condition and the cerebral palsy that so often accompanies it. 2 Ho M.L. Mansukhani S.A. Brodsky M.C. Prenatal or perinatal injury: diagnosing the blind infant. Am J Ophthalmol. 2020; 211: 56-62 Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar CVI can be broadly divided into cortical and subcortical variants (manifesting as periventricular leukomalacia), which correspond to term and prenatal visual pathway injury, respectively. 3 Brodsky M.C. Fray K.J. Glasier C.M. Cortical and subcortical visual loss: mechanisms of injury and ophthalmologic signs. Ophthalmology. 2002; 109: 85-94 Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar ,4 Volpe J. Brain injury in premature infants: a complex amalgam of destructive and developmental influences. Lancet Neurol. 2009; 8: 110-124 Abstract Full Text Full Text PDF PubMed Scopus (1658) Google Scholar Subcortical injury to the thalamus, basal ganglia, corpus callosum, and cerebellum are common accompaniments. 4 Volpe J. Brain injury in premature infants: a complex amalgam of destructive and developmental influences. Lancet Neurol. 2009; 8: 110-124 Abstract Full Text Full Text PDF PubMed Scopus (1658) Google Scholar ,5 Barkovich A.J. MR and CT evaluation of profound neonatal asphyxia. AJNR Am J Neuroradiol. 1992; 13: 957-972 Google Scholar Higher attentional centers may also be injured, or their development delayed because of lack of normal visual processing within the cortex. 6 Das M. Bennett D.N. Dutton G.N. Visual attention as an important visual function: an outline of manifestations, diagnosis, and management of impaired visual attention. Brit J Ophthalmol. 2007; 91: 1556-1560 Crossref PubMed Scopus (20) Google Scholar No other condition so challenges our ability to assess vision or provide a visual prognosis.

Purpose: The International Classification of Retinopathy of Prematurity is a consensus statement that creates a standard nomenclature for classification of retinopathy of prematurity (ROP). It was initially published in 1984, expanded in 1987, and revisited in 2005. This article presents a third revision, the International Classification of Retinopathy of Prematurity, Third Edition (ICROP3), which is now required because of challenges such as: (1) concerns about subjectivity in critical elements of disease classification; (2) innovations in ophthalmic imaging; (3) novel pharmacologic therapies (e.g., antievascular endothelial growth factor agents) with unique regression and reactivation features after treatment compared with ablative therapies; and (4) recognition that patterns of ROP in some regions of the world do not fit neatly into the current classification system. Design: Review of evidence-based literature, along with expert consensus opinion. Participants: International ROP expert committee assembled in March 2019 representing 17 countries and comprising 14 pediatric ophthalmologists and 20 retinal specialists, as well as 12 women and 22 men. Methods: The committee was initially divided into 3 subcommittees-acute phase, regression or reactivation, and imaging-each of which used iterative videoconferences and an online message board to identify key challenges and approaches. Subsequently, the entire committee used iterative videoconferences, 2 in-person multiday meetings, and an online message board to develop consensus on classification. Main Outcome Measures: Consensus statement. Results: The ICROP3 retains current definitions such as zone (location of disease), stage (appearance of disease at the avascular-vascular junction), and circumferential extent of disease. Major updates in the ICROP3 include refined classification metrics (e.g., posterior zone II, notch, subcategorization of stage 5, and recognition that a continuous spectrum of vascular abnormality exists from normal to plus disease). Updates also include the definition of aggressive ROP to replace aggressive-posterior ROP because of increasing recognition that aggressive disease may occur in larger preterm infants and beyond the posterior retina, particularly in regions of the world with limited resources. ROP regression and reactivation are described in detail, with additional description of long-term sequelae. Conclusions: These principles may improve the quality and standardization of ROP care worldwide and may provide a foundation to improve research and clinical care. Published by Elsevier on behalf of the American Academy of Ophthalmology

In celebration of the 25th volume of the Journal of AAPOS, its editors in chief are sharing their reflections on the journal's past, present, and future as well as its role in academic and clinical ophthalmology more generally. The American Association for Pediatric Ophthalmology and Strabismus thanks them for their service.

Robert Jackson Hardy died on April 11, 2021, after a brief illness. He was born in 1940 in Alexandria, Louisiana. He is survived by his wife of 57 years, Lydia Waguespack Hardy. Robert and Lydia, lately of San Antonio, Texas, resided for almost 40 years in Missouri City, Texas. He is also survived by his daughters and their families and a large, extended family to whom he was extremely devoted.

Lumpfish (Cyclopterus lumpus), a North Atlantic “cleaner“ fish, is utilized to biocontrol salmon louse (Lepeophtheirus salmonis) in Atlantic salmon (Salmo salar) farms. Lumpfish require excellent vision to scan for and eat louse on salmon skin. The lumpfish eye immune response to infectious diseases has not been explored. We examined the ocular response to a natural parasite infection in wild lumpfish and to an experimental bacterial infection in cultured lumpfish. Cysts associated with natural myxozoan infection in the ocular scleral cartilage of wild adult lumpfish harbored cells expressing cluster of differentiation 10 (CD10) and immunoglobulin M (IgM). Experimental Vibrio anguillarum infection, which led to exophthalmos and disorganization of the retinal tissues was associated with disruption of normal CD10 expression, CD10+ cellular infiltration and IgM expression. We further describe the lumpfish CD10 orthologue and characterize the lumpfish scleral skeleton in the context of myxozoan scleral cysts. We propose that lumpfish develop an intraocular response to pathogens, exemplified herein by myxozoan and V. anguillarum infection involving novel CD10+ cells and IgM+ cells to contain and mitigate damage to eye structures. This work is the first demonstration of CD10 and IgM expressing cells in a novel ocular immune system component in response to disease in a teleost.

Retinopathy of prematurity (ROP) was a leading cause of vision impairment and blindness in children until the multicenter Cryotherapy for Retinopathy of Prematurity of Prematurity Cooperative Group (CRYO-ROP) published its groundbreaking results.1Cryotherapy for Retinopathy of Prematurity Cooperative GroupMulticenter trial of cryotherapy of retinopathy of prematurity: one-year outcome-structure and function.Arch Ophthalmol. 1990; 108: 1408-1416Crossref PubMed Scopus (321) Google Scholar Findings from this landmark research program reduced blindness from ROP by 50%, with subsequent research, predicated on the CRYO-ROP experience, further reducing the incidence of retinal detachments from this condition to less than 10% in high-risk eyes.2Good W.V. 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: 233-248PubMed Google Scholar The CRYO-ROP research team was meticulous, thoughtful, creative, and disciplined. That a team of such disparate disciplines and people could coordinate such an effort is remarkable. The National Eye Institute deserves special mention for its participation in and funding of the study. The editors of Ophthalmology have not chosen any of the results publications for their 2020 supplement, and for good reason. Instead, Ophthalmology is showcasing an article titled, the “Incidence and Course of Retinopathy of Prematurity,” published in 1991 (see page S84).3Palmer E.A. Flynn J.T. Hardy R.J. et al.The Cryotherapy for Retinopathy of Prematurity Group. Incidence and course of retinopathy of prematurity.Ophthalmology. 1991; 98: 1628-1640Abstract Full Text PDF PubMed Scopus (593) Google Scholar This is one of the most intriguing and provocative scientific articles to ever emerge from a clinical trial, and it shows what a careful reading and analysis of data from a study can produce. As billed, the publication describes the incidence of ROP at various birth weights and gestational ages, and this alone would be noteworthy. The findings of incidence of disease at various gestational ages provide a matrix that clinicians can use to time screening examinations. This is obviously the first step toward eliminating ROP, because disease progression is time sensitive. Knowing the incidence of ROP allows researchers to judge whether they have been able to make inroads in reducing the incidence of the disease. Knowing the 1991 incidence makes it particularly perplexing that the incidence has not changed, at least to the time of the Early Treatment for Retinopathy of Prematurity Study (ETROP), 14 years later. The reader who delves deeper into this publication is rewarded with information and knowledge, which to this day offers findings that cannot be explained and yet are clearly important. These findings will eventually lead to the elimination of ROP. Many investigator groups are working with CRYO-ROP data in the hopes of not only treating ROP more effectively but also even eliminating the disease. Two findings from this publication are noteworthy. One, confirmed in the ETROP Study, is that African-American infants have less severe ROP than white infants. A primary hypothesis to explain this finding is that polymorphisms in beta-blocker receptor genes, which are more common in African-Americans than whites, could somehow play a role in ROP prevention.4Good W.V. Hardy R.J. Wallace D.K. et al.β-Blocking and racial variation in the severity of retinopathy of prematurity.Arch Ophthalmol. 2012; 130: 117-118Crossref PubMed Scopus (12) Google Scholar Whether this is true or not is unknown, but the finding of diminished disease in African-Americans is irrefutable. This important “lead” would not have been possible without meticulous records published in the incidence article. A second important finding is that the timing of onset of ROP and its potential need for treatment are based on the gestational age of the infant and not on the chronological age. In short, an infant born at 28 weeks gestational age is most likely to develop ROP requiring treatment at approximately 36 weeks gestational age, and so is the 24-week gestational age infant. Over the years, there have been many explanations offered to explain this finding, which incidentally, was true for the ETROP cohort. The most obvious explanation is that the infant’s endowment, genetic or otherwise, is more important than his/her extrauterine experience after birth. A causative role for extrauterine experience is not dismissed by this observation, but the fact that seemingly identical premature infants, with similar postnatal experience, could have different tendencies to develop ROP argues for constitutional factors in the development of ROP. The article has something for everyone. For the trialist, there is important information on validation of physical findings in ROP. Procedures used to examine infants and timing of treatment of children with threshold ROP can be generalized to other trials. A reading center served to further validate findings. The development of a nomenclature to describe and define ROP preceded the CRYO-ROP trial and served an important requirement for a successful study. For the scientist only marginally interested in ROP, the layout of the article is brilliant. From abstract to conclusion, this article is one of the finest to appear in the medical literature. To this day, we benefit from this article. Much current research relies on clinical findings and observations presented by this study. Incidence and Early Course of Retinopathy of PrematurityOphthalmologyVol. 127Issue 4PreviewIn the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity (ROP), 4099 infants weighing less than 1251 g at birth underwent sequential ophthalmic examinations, beginning at age 4 to 6 weeks, to monitor the incidence and course of ROP. Overall, 65.8% of the infants developed ROP to some degree; 81.6% for infants of less than 1000 g birth weight. As expected, ROP incidence and severity were higher in lower birth weight and gestational age categories. Black infants appeared less susceptible to ROP, of all severity categories, than nonblack infants. Full-Text PDF

Delayed visual maturation (DVM) is diagnosed when a child fails to show normal visual responses and the eye examination is not sufficiently abnormal to explain the poor visual responsiveness. This failure to show visual behavior is seen in the first few weeks and months of life. The etiology of DVM remains obscure. In a most recent careful follow-up study, so-called isolated DVM was associated with minor neurologic abnormalities. This association implies that there may be some underlying neurologic defect that causes DVM, but whether DVM is due to a delay in sensory development or a delay in motor fixation is unknown. Optic nerve hypoplasia, atrophy, and coloboma have all been reported in children exposed to cocaine in utero. Optic nerve hypoplasia is a condition in which the optic nerves fail to develop a normal number of axons. The most common abnormality after in utero cocaine exposure is the development of periorbital edema.

Importance Intravitreous bevacizumab (0.25 mg to 0.625 mg) is commonly used to treat type 1 retinopathy of prematurity (ROP), but there are concerns about systemic toxicity, particularly the risk of neurodevelopmental delay. A much lower dose may be effective for ROP while reducing systemic risk. Previously, after testing doses of 0.25 mg to 0.031 mg, doses as low as 0.031 mg were found to be effective in small cohorts of infants. Objective To find the lowest dose of intravitreous bevacizumab effective for severe ROP. Design, Setting, and Participants Between April 2017 and May 2019, 59 premature infants with type 1 ROP in 1 or both eyes were enrolled in a masked, multicenter, dose de-escalation study. In cohorts of 10 to 14 infants, 1 eye per infant received 0.016 mg, 0.008 mg, 0.004 mg, or 0.002 mg of intravitreous bevacizumab. Diluted bevacizumab was prepared by individual research pharmacies and delivered using 300-µL syringes with 5/16-inch, 30-guage fixed needles. Analysis began July 2019. Interventions Bevacizumab intravitreous injections at 0.016 mg, 0.008 mg, 0.004 mg, or 0.002 mg. Main Outcomes and Measures Success was defined as improvement by 4 days postinjection and no recurrence of type 1 ROP or severe neovascularization requiring additional treatment within 4 weeks. Results Fifty-five of 59 enrolled infants had 4-week outcomes completed; the mean (SD) birth weight was 664 (258) g, and the mean (SD) gestational age was 24.8 (1.6) weeks. A successful 4-week outcome was achieved for 13 of 13 eyes (100%) receiving 0.016 mg, 9 of 9 eyes (100%) receiving 0.008 mg, 9 of 10 eyes (90%) receiving 0.004 mg, but only 17 of 23 eyes (74%) receiving 0.002 mg. Conclusions and Relevance These data suggest that 0.004 mg may be the lowest dose of bevacizumab effective for ROP. Further investigation is warranted to confirm effectiveness of very low-dose intravitreous bevacizumab and its effect on plasma vascular endothelial growth factor levels and peripheral retinal vascularization.

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