Background Maternal nutrient restriction (MNR) is a widespread cause of fetal growth restriction (FGR), an independent predictor of heart disease and cardiovascular mortality. Our objective was to examine the developmental and long-term impact of MNR-induced FGR on cardiac structure in a model that closely mimics human development. Methods A reduction in total caloric intake spanning pre-gestation through to lactation in guinea pig sows was used to induce FGR. Proliferation, differentiation, and apoptosis of cardiomyocytes were assessed in late-gestation fetal, neonatal, and adult guinea pig hearts. Proteomic analysis and pathway enrichment were performed on fetal hearts. Results Cardiomyocyte proliferation and number of mononucleated cells was enhanced in the MNR-FGR fetal and neonatal heart, suggesting a delay in cardiomyocyte differentiation. In fetal hearts of MNR-FGR animals, apoptosis was markedly elevated and the total number of cardiomyocytes reduced, the latter remaining so throughout neonatal and into adult life. A reduction in total cardiomyocyte number in adult MNR-FGR hearts was accompanied by exaggerated hypertrophy and a disorganized architecture. Pathway analysis identified genes related to cell proliferation, differentiation, and survival. Conclusions FGR influences cardiomyocyte development during critical windows of development, leading to a permanent deficiency in cardiomyocyte number and compensatory hypertrophy in a rodent model that recapitulates human development.

Objective: Viral infections during pregnancy can cause disturbance in normal craniofacial morphogenesis. While some pathogens such as cytomegalovirus and herpes simplex are familiar to us, others remain obscure. This review examines the arbovirus-induced cranial deformities and combines biomechanics with growth dynamics to gain a deeper appreciation of this complex morphogenetic process. Materials and Methods: Using Wolfram Alpha, we analyzed the impact of cell population changes. The growth dynamics of the brain, and thus the size of the calvarium, followed 2 potential logistic curves: compensated and uncompensated. To understand the potential mechanism of cell loss, we performed literature review on maternal immune activation and viral tropism for neurons and glial cells. Results: With arboviral infections such as Zika, uncompensated loss of cells during the critical phases of fetal brain development reduces the intracranial mass and therefore decreases the tensile stress across the cranial sutures. The deflationary effect produces microcephaly by subduction and reduced osteogenesis seen clinically in these infants. Conclusion: Many viral infections cause intense maternal immune activation, some have neurotropism and can result in cell loss within the developing cranium. Unable to overcome this loss, the cranium assumes a new, abnormal shape and volume. Secondary calvarial deformities is due to, and should not cause, changes in brain development.

The use of point‐of‐care sonography in clinical settings such as emergency medicine and intensive care units has increased, but adoption in neonatology has been slow. Unlike the focused assessment with sonography for trauma scan used in adults, a quick bedside scan to rapidly evaluate an acutely deteriorating neonate does not exist. The objective of our article is to introduce a focused bedside ultrasound scan that is easy to learn, rapidly performed, and relatively inexpensive.© 2018 by the American Institute of Ultrasound in Medicine

Coronavirus disease 2019 (COVID-19) was first reported to the World Health Organization (WHO) in December 2019 and has since unleashed a global pandemic, with over 518 million cases as of May 10, 2022. Neonates represent a very small proportion of those patients. Among reported cases of neonates with symptomatic COVID-19 infection, the rates of hospitalization remain low. Most reported cases in infants and neonates are community acquired with mild symptoms, most commonly fever, rhinorrhea and cough. Very few require intensive care or invasive support for acute infection. We present a case of a 2-month-old former 26-week gestation infant with a birthweight of 915 grams and diagnoses of mild bronchopulmonary dysplasia and a small ventricular septal defect who developed acute respiratory decompensation due to COVID-19 infection. He required veno-arterial extracorporeal membrane oxygenation support for 23 days. Complications included liver and renal dysfunction and a head ultrasound notable for lentriculostriate vasculopathy, extra-axial space enlargement and patchy periventricular echogenicity. The patient was successfully decannulated to conventional mechanical ventilation with subsequent extubation to non-invasive respiratory support. He was discharged home at 6 months of age with supplemental oxygen via nasal cannula and gastrostomy tube feedings. He continues to receive outpatient developmental follow-up. To our knowledge, this is the first case report of a preterm infant during their initial hospitalization to survive ECMO for COVID-19.