Intraventricular hemorrhage (IVH) is a common complication of prematurity and continues to represent a considerable threat due to its association with significant short- and long-term morbidity and mortality. Despite the advances in neonatal care, the prevalence of IVH, particularly in the extremely preterm neonates, remains high. Therefore, it is imperative to recognize and implement in clinical practice preventive strategies, non-pharmacological or pharmacological, to reduce IVH effectively. The aim of this narrative review is to provide an overview of novel and debatable preventive measures for IVH that are promising for clinical use and could potentially improve outcomes for very preterm neonates. IVH prevention bundles (IVHPBs) consist of strategies that aim to minimize hemodynamic and cerebral perfusion fluctuations, which are a crucial component of IVH pathogenesis. Early postnatal prophylactic indomethacin, erythropoietin, and insulin-growth factor-1 administration have shown encouraging results on IVH prevention; however, the literature is still inconclusive. Stem-cell-based interventions represent novel and promising techniques with the potential to contribute to the prevention of IVH. The prevention of IVH remains a field of investigation, and there is a requirement for conclusive evidence and recommendations. The necessity for further large-scale prospective studies is therefore evident.

Methicillin-susceptible Staphylococcus aureus (MSSA) remains a major pathogen in neonatal intensive care units (NICUs), with colonization and infection posing significant risks. MSSA colonization occurs in up to 42.8% of neonates, while 12–41% of healthcare personnel also carry MSSA, contributing to nosocomial transmission. MSSA accounts for approximately 12% of neonatal S. aureus bloodstream infections, with mortality rates up to 20.5%, particularly among very-low-birth-weight infants. This review analyzes the molecular attributes, epidemiology, risk factors, clinical presentations, decontamination methods, and treatment alternatives for MSSA infections in newborns. MSSA strains show considerable genetic heterogeneity, being distinguished by a wide variety of sequence types (STs) and Staphylococcal Protein A types (SpA). They harbor several pathogenicity genes—including hemolysins, superantigens, adhesins, and Panton–Valentine leukocidin (PVL)—which are implicated in severe infections, while biofilm-associated genes enhance environmental persistence. Prematurity, low birth weight, prolonged hospitalization, and exposure to invasive devices are key risk factors. Active surveillance and decolonization programs have achieved reductions of up to 73% in MSSA infections. β-lactam antibiotics remain first-line therapy, with adjunctive aminoglycosides reserved for severe cases. Ongoing genomic surveillance and targeted preventive strategies are essential to reduce MSSA-associated morbidity and mortality in this vulnerable population.

Sodium (Na) is essential not only for maintaining extracellular fluid homeostasis as the dominant extracellular cation, but also for supporting the rapid tissue growth characteristic of the neonatal period. Despite its importance, the precise sodium requirements of preterm infants remain insufficiently defined. The immature renal tubules of preterm neonates lead to significant renal sodium losses, making negative sodium balance a common feature in this population. This issue has become increasingly relevant as survival rates improve among extremely preterm infants, while most available data are derived from studies involving more mature preterm or even full-term neonates. Fractional excretion of sodium (FENa) shows a clear inverse correlation with both gestational age and postnatal age, highlighting the developmental limitations in sodium retention among the youngest and most vulnerable infants. Current guidelines on sodium supplementation aim to promote optimal growth and neurodevelopment but vary across organizations. For instance, the most recent ESPGHAN recommendations suggest higher sodium intakes, in the range of 3–8 mEq/kg/day, whereas the American Academy of Pediatrics (AAP) provides more conservative guidance. These discrepancies underscore ongoing uncertainty in determining optimal sodium provision. This narrative review examines both classic and contemporary data on sodium needs in preterm neonates, with the goal of clarifying existing evidence and offering practical insights for clinical care. It also emphasizes unresolved questions and the need for well-designed studies that address the unique physiology of extremely preterm infants. A deeper understanding of sodium metabolism in this population is crucial for improving outcomes and guiding evidence-based supplementation strategies.

Neonatal diabetes mellitus (NDM) is a rare monogenic disorder characterized by persistent hyperglycemia requiring insulin therapy, typically diagnosed within the first six months of life, and may be transient οr permanent. However, hyperglycemia in the neonatal population may be observed outside the NDM range. This narrative review aims to provide an overview of the genetic and molecular mechanisms underlying NDM, including both transient and permanent forms on the one hand and the developmental and regulatory pathways contributing to transient hyperglycemic states in neonates on the other. A comprehensive literature search of PubMed, Scopus, and Google Scholar was conducted, focusing on genetic and molecular mechanisms associated with NDM and transient neonatal hyperglycemia. Mutations in more than 40 genes or chromosomal loci have been implicated in the pathogenesis of NDM, affecting the development and function of pancreatic beta-cells, as well as insulin synthesis and secretion. Abnormalities of the 6q24 locus have been recognized as the most common cause of transient NDM, whereas mutations in genes encoding ATP-sensitive potassium (K_ATP) channels, particularly KCNJ11, are more commonly identified in permanent NDΜ cases. Transient hyperglycemia may occur in preterm and/or critically ill neonates due to immaturity and transient beta-cell dysregulation, insulin resistance, epigenetic modifications, or drug administration. In NDM cases, the clinical course, the presence of extra-pancreatic manifestations, and the optimal treatment depend on the causative gene. Therefore, genetic diagnosis is imperative, as it can facilitate individualized management strategies, long-term follow-up, and genetic counselling.

Neonatal diabetes mellitus (NDM) is a rare monogenic disorder characterized by persistent hyperglycemia requiring insulin therapy, typically diagnosed within the first six months of life and less commonly between six and 12 months. NDM may be transient, with frequent relapses during puberty, or permanent and can be associated with extra-pancreatic manifestations or be part of a syndrome. This monogenic form of diabetes is caused by pathogenic variants in genes or chromosomal loci involved in the development and function of pancreatic beta-cells and in insulin synthesis and secretion. Mutations in more than 40 genes have been identified to be implicated in the pathogenesis of NDM. Abnormalities of the 6q24 locus have been recognized as the most common cause of transient NDM, whereas mutations in genes encoding ATP-sensitive potassium (KATP) channels, particularly KCNJ11, are more commonly identified in permanent NDΜ cases. In NDM cases, the clinical course, the presence of extra-pancreatic manifestations, and the optimal treatment depend on the causative gene. Therefore, genetic diagnosis is imperative, as it can facilitate the individualization of management strategies and long-term follow-up, as well as genetic counselling. However, hyperglycemia in the neonatal population, particularly in preterm and/or critically ill neonates, may be observed outside the NDM range due to immaturity and transient beta-cell dysregulation, insulin resistance, epigenetic modifications, or drug administration. The aim of this narrative review is to provide an overview of the genetic basis of NDM and the mechanisms underlying transient hyperglycemic states in neonates.

Intraventricular hemorrhage (IVH) is a common complication of prematurity and continues to represent a considerable threat due to its association with significant short- and long-term morbidity and mortality. Despite the advances in neonatal care, the prevalence of IVH, particularly in the extremely preterm neonates, remains high. Therefore, it is imperative to recognize and implement in clinical practice preventive strategies, non-pharmacological or pharmacological, to reduce IVH effectively. The aim of this narrative review is to provide an overview of novel and debatable preventive measures for IVH that could be implemented in daily practice to potentially improve outcomes for very preterm neonates. IVH prevention bundles (IVHPBs) consist of strategies that aim to minimize hemodynamic and cerebral perfusion fluctuations, which are a crucial component of IVH pathogenesis. Early postnatal prophylactic indomethacin, erythropoietin, and insulin growth factor-1 administration have shown encouraging results on IVH prevention; however, the literature is still inconclusive. Stem cell-based interventions represent novel and promising techniques with the potential to contribute to the prevention of IVH. The prevention of IVH remains a field of investigation, and there is a requirement for conclusive evidence and recommendations. The necessity for further large-scale prospective studies is therefore evident.