Background: Early-onset sepsis, occurring within 72 hours of birth, and late-onset sepsis, occurring after this time period, present serious risks for neonates. While culture-based screening and intrapartum antibiotics have decreased the number of early-onset cases, sepsis remains a top cause of neonatal morbidity and mortality in the United States. Purpose: To provide a review of neonatal sepsis by identifying its associated risk factors and most common causative pathogens, reviewing features of the term and preterm neonatal immune systems that increase vulnerability to infection, describing previous and the most current management recommendations, and discussing relevant implications for the neonatal nurse and novice neonatal nurse practitioner. Methods/Search Strategy: An integrative review of literature was conducted using key words in CINAHL, Google Scholar, and PubMed. Findings/Results: Group B streptococcus and Escherichia coli are the most common pathogens in early-onset sepsis, while Coagulase–negative staphylococci comprise the majority of cases in late-onset. The neonatal immune system is vulnerable due to characteristics including decreased cellular activity, underdeveloped complement systems, preferential anti-inflammatory responses, and insufficient pathogenic memory. Blood cultures remain the criterion standard of diagnosis, with several other adjunct tests under investigation for clinical use. The recent development of the sepsis calculator has been a useful tool in the management of early-onset cases. Implications for Practice: It is vital to understand the mechanisms behind the neonate's elevated risk for infection and to implement evidence-based management. Implications for Research: Research needs exist for diagnostic methods that deliver timely and sensitive results. A tool similar to the sepsis calculator does not exist for preterm infants or late-onset sepsis, groups for which antibiotic stewardship is not as well practiced. Video Abstract available at https://journals.lww.com/advancesinneonatalcare/Pages/videogallery.aspx?autoPlay=false&videoId=40

Background: Patent ductus arteriosus (PDA) is the persistence of a fetal shunt between the pulmonary artery and the aorta. This structure normally closes in the first 3 days after birth; however, closure is delayed in up to 80% of infants born at 25 to 28 weeks of gestation. Persistent PDA results in pulmonary overcirculation and systemic hypoperfusion. Purpose: The purpose of this article is to review pathophysiology and treatment options for PDA. Methods: A literature review was conducted using PubMed, CINAHL, and Google Scholar (2013-2018). Search terms included neonate, PDA, pathophysiology, pharmacotherapy, nursing, ligation, indomethacin, ibuprofen, and acetaminophen (paracetamol). Results: Optimal treatment remains contentious. Options include conservative/medical, pharmacologic, and surgical management. Conservative/medical management includes mild fluid restriction, increased airway pressures, and supportive care. Pharmacologic treatment is accomplished using indomethacin, ibuprofen, or acetaminophen. Surgical intervention is by direct closure or by percutaneous ligation. Treatment may be prophylactic, presymptomatic, or symptomatic. Long-term morbidities associated with PDA include chronic lung disease, retinopathy of prematurity, and neurodevelopmental delay. Implications for Research: Absence of a universal scoring system for severity of PDA limits accuracy of comparisons among research studies. Lack of a consistent definition also makes it difficult to aggregate data for meta-analyses. Adoption of a consistent scoring system for hemodynamic significance would facilitate comparisons of outcomes among research studies. Implications for Practice: Clinicians should be aware of treatment options for PDA and their implications on neonatal outcomes. For nurses, anticipation of possible side effects is important for performance of focused assessments.

The paucity of research, which focuses on CS, is most likely due to ethical concerns related to infants as research participants and provides an opportunity for future research. Future research could focus on factors that focus on maternal-fetal/maternal-child transmission of CS.

Methods to prevent readmission and ensure successful discharge from hospital to home is indicated. Standardization of a discharge process of infants of technology dependence combining medical team, family, outpatient coordinators, and primary care providers.

Further research is needed regarding the prevention of blood culture contamination, especially in vaginally delivered placentas. Institutions that adopt this procedure should perform quality improvement initiatives to monitor outcomes and add to the growing body of literature on the utilization of placental blood for neonatal admission laboratory tests.

Investigation of consumption of time and nursing personnel required to perform TcB testing, compared with TSB testing, is indicated. Cost analyses comparing TcB-driven screening protocols and interval TSB measurements, among premature infants, are indicated. As newer generations of TcB devices are approved for use, additional studies using mixed-race populations of premature infants will be necessary to continue to evaluate the reliability and validity of this screening tool within the everyday neonatal intensive care unit.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common enzymopathy worldwide, is an insufficient amount of the G6PD enzyme, which is vital to the protection of the erythrocyte. Deficient enzyme levels lead to oxidative damage, hemolysis, and resultant severe hyperbilirubinemia. If not promptly recognized and treated, G6PD deficiency can potentially lead to bilirubin-induced neurologic dysfunction, acute bilirubin encephalopathy, and kernicterus. Glucose-6-phosphate dehydrogenase deficiency is one of the three most common causes for pathologic hyperbilirubinemia. A change in migration patterns and intercultural marriages have created an increased incidence of G6PD deficiency in the United States. Currently, there is no universally mandated metabolic screening or clinical risk assessment tool for G6PD deficiency in the United States. Mandatory universal screening for G6PD deficiency, which includes surveillance and hospital-based risk assessment tools, can identify the at-risk infant and foster early identification, diagnosis, and treatment to eliminate neurotoxicity.

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