The diagnosis and management of neonatal hypoglycemia has been widely debated for more than 40 years, with authorities recommending lower¹ and higher² thresholds for intervention and treatment, reflecting the paucity of high-quality evidence to guide management.³ The results of population studies^4,5 have suggested that neonatal hypoglycemia may be one of the most readily preventable causes of neurodevelopmental impairment and learning disorders, but there is also the potential for iatrogenic harm from increased intervention, including decreased breastfeeding and altered cortical development from pain-induced stress with heel lancing.⁶

Neonatal hypoglycemia is common and can cause neurologic impairment, but evidence supporting thresholds for intervention is limited. We performed a prospective cohort study involving 528 neonates with a gestational age of at least 35 weeks who were considered to be at risk for hypoglycemia; all were treated to maintain a blood glucose concentration of at least 47 mg per deciliter (2.6 mmol per liter). We intermittently measured blood glucose for up to 7 days. We continuously monitored interstitial glucose concentrations, which were masked to clinical staff. Assessment at 2 years included Bayley Scales of Infant Development III and tests of executive and visual function. Of 614 children, 528 were eligible, and 404 (77% of eligible children) were assessed; 216 children (53%) had neonatal hypoglycemia (blood glucose concentration, <47 mg per deciliter). Hypoglycemia, when treated to maintain a blood glucose concentration of at least 47 mg per deciliter, was not associated with an increased risk of the primary outcomes of neurosensory impairment (risk ratio, 0.95; 95% confidence interval [CI], 0.75 to 1.20; P=0.67) and processing difficulty, defined as an executive-function score or motion coherence threshold that was more than 1.5 SD from the mean (risk ratio, 0.92; 95% CI, 0.56 to 1.51; P=0.74). Risks were not increased among children with unrecognized hypoglycemia (a low interstitial glucose concentration only). The lowest blood glucose concentration, number of hypoglycemic episodes and events, and negative interstitial increment (area above the interstitial glucose concentration curve and below 47 mg per deciliter) also did not predict the outcome. In this cohort, neonatal hypoglycemia was not associated with an adverse neurologic outcome when treatment was provided to maintain a blood glucose concentration of at least 47 mg per deciliter. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and others.)

Age-related macular degeneration (AMD) is a serious public health issue, representing the leading cause of visual impairment and blindness in high-income countries.¹ Globally, approximately 8.7% of people older than 45 years have some form of AMD, affecting around 200 million individuals. Projections indicate that the number of individuals with any form of AMD will increase to 288 million by 2040.² AMD is a progressive disease of the central retina leading to blurring, distortion, and loss of central vision. Major risk factors associated with AMD are increasing age, smoking, and diet.³ Late-stage AMD presents a higher risk of severe vision impairment compared to early and intermediate stages. The global prevalence of late-stage AMD is 0.37%, affecting around 12 million people, and it is projected that the number of people with the late-stage AMD will increase to 18 million by 2040.² Late-stage AMD can be categorized into 2 types: atrophic (also referred to as geographic atrophy [GA]) and exudative (often referred to as neovascular AMD [nAMD] or wet AMD). GA is the more common form, with early and intermediate stages of AMD typically progressing slowly to the atrophic stage. In contrast, nAMD can develop rapidly from early or intermediate stages. While there are several treatment options available for nAMD, to date, there are 2 US Food and Drug Administration–approved therapies for GA, but neither has been approved by the European Medicines Agency. These therapies have shown anatomic benefits but not visual function improvements across prespecified secondary outcomes. Several other GA treatments are currently in development.^4,5

Visual impairment (VI) has a significant negative impact on quality of life (QoL) amongst older people living in nursing homes. The purpose of this study was to determine the prevalence of VI and blindness and to explore the association between severity of VI and vision-specific QoL among older people living in nursing homes of Kathmandu, Nepal. This cross-sectional study involved 158 residents aged 60 years or older residing in seven nursing homes of Kathmandu Valley, Nepal. Near acuity, presenting and the best corrected distance visual acuity (VA) were assessed in each eye and considered in the better eye after adequate refraction. A complete anterior and posterior segment examination was carried out. Face-to-face interviews were conducted using a 57-item Nursing Home Vision-Targeted Health-Related Quality of Life (NHVQoL) questionnaire. The mean age of residents was 75.60 ± 7.12 years and the majority were female (66.46%). The prevalence of VI and blindness was 45.57% and its leading cause was cataract, which was followed by age-related macular degeneration, corneal opacity, glaucoma and macular scar. The mean composite score of NHVQoL questionnaire was 52.22 ± 12.49. There was a consistent overall deterioration in the mean composite score as well as each subscale score of NHVQoL questionnaire with a worsening of VA. VI and blindness are highly prevalent among older people living in nursing homes. VI has a significant negative impact on vision-specific QoL. Vision-specific QoL is reduced, and the reduction in the QoL bears a positive association with severity of VI among older people living in nursing homes.