OBJECTIVES: To determine whether nutritional intake and medical devices are bisphenol A (BPA) exposure sources among premature infants in the NICU. METHODS: Mothers and their premature infants cared for in the NICU for the past 3 days were recruited for this exposure assessment study. Forty-three mothers contributed 1 nutrition sample (breast milk or formula) to characterize the infant’s intake. Two urine samples (before and after feeding) were collected from each of 55 infants. Medical device use was categorized as “low” or “high” based on the number and invasiveness of devices used. BPA urinary concentrations used as a biomarker to estimate BPA exposure were measured by online solid-phase extraction, high performance liquid chromatography, isotope dilution, tandem mass spectrometry. Nonparametric equivalence tests, intraclass correlations, and hierarchical linear mixed-effects models were conducted. RESULTS: Breast milk and formula samples did not differ in total BPA concentration nor did infants’ median urinary concentration of total BPA before or after feedings. However, the median urinary total BPA concentration among infants who required the use of 4 or more medical devices in the past 3 days was significantly higher (36.6 µg/L) than among infants who required the use of 0 to 3 devices (13.9 µg/L). The calculated BPA exposures are lower than the US Environmental Protection Agency reference dose, but considerably higher (16- to 32-fold) than among infants or children from the general population. CONCLUSIONS: The number of medical devices used in the past 3 days, but not nutritional intake, was positively associated with exposure to BPA.
Objectives: To understand retinopathy of prematurity (ROP) follow-up care for preterm very low-birth-weight infants (VLBW; < 1500 g) in the context of the chronic care model and identify opportunities for improvement under accountable care organizations.Methods: We conducted focus groups and interviews with parents (N = 47) of VLBW infants and interviews with neonatal intensive care unit and ophthalmologic providers (N = 28) at 6 sites in Massachusetts and South Carolina. Themes are reported according to consolidated criteria for reporting qualitative research guidelines.Results: Respondents perceived that legal liability and low reimbursement contributed to shortages of ROP providers. Some neonatal intensive care units offered subsidies to attract ophthalmologic providers or delayed transfers to institutions that could not provide ROP examinations and/or treatment. Sites used variable practices for coordinating ROP care. Even at sites with a tracking database and a dedicated ROP coordinator, significant time was required to ensure that examinations and treatment occurred as scheduled. Parents' ability to manage their children's health care was limited by parental understanding of ROP, feeling overwhelmed by the infant's care, and unmet needs for resources to address social stressors.Conclusions: Under accountable care organizations, hospitals and ophthalmology practices should share responsibility for ensuring coordinated ROP care to mitigate liability concerns. To promote integrated care, reimbursement for ROP care should be bundled to include screening, diagnosis, treatment, and appropriate follow-up. Clinical information systems should be enhanced to increase efficiency and limit lapses in care. Self-management tools and connections to community resources could help promote families' attendance of follow-up appointments.
Cerebral blood flow pressure-passivity results when pressure autoregulation is impaired, or overwhelmed, and is thought to underlie cerebrovascular injury in the premature infant. Earlier bedside observations suggested that transient periods of cerebral pressure-passivity occurred in premature infants. However, these transient events cannot be detected reliably by intermittent static measurements of pressure autoregulation. We therefore used continuous bedside recordings of mean arterial pressure (MAP; from an indwelling arterial catheter) and cerebral perfusion [using the near-infrared spectroscopy (NIRS) Hb difference (HbD) signal) to detect cerebral pressure-passivity in the first 5 d after birth in infants with birth weight <1500 g. Because the Hb difference (HbD) signal [HbD = oxyhemoglobin (HbO2) − Hb] correlates with cerebral blood flow (CBF), we used coherence between MAP and HbD to define pressure-passivity. We measured the prevalence of pressure-passivity using a pressure-passive index (PPI), defined as the percentage of 10-min epochs with significant low-frequency coherence between the MAP and HbD signals. Pressure-passivity occurred in 87 of 90 premature infants, with a mean PPI of 20.3%. Cerebral pressure-passivity was significantly associated with low gestational age and birth weight, systemic hypotension, and maternal hemodynamic factors, but not with markers of maternal infection. Future studies using consistent serial brain imaging are needed to define the relationship between PPI and cerebrovascular injury in the sick premature infant.
OBJECTIVE:To assess the role of intrapartum fever in identifying asymptomatic term neonates with early-onset neonatal sepsis.STUDY DESIGN:Retrospective review of all term neonates with sepsis over a 7-year period to evaluate the significance of symptoms at delivery and intrapartum sepsis risks factors in identifying neonates with sepsis.RESULTS:Fifty-three of 90 term neonates with sepsis (59%) were asymptomatic at delivery. Thirty-five of 53 asymptomatic term neonates (66%) met criteria for sepsis evaluations and 18 (34%) were evaluated when symptoms developed after delivery. Among the 35 asymptomatic term neonates meeting criteria for sepsis evaluations, 14 (40%) had evaluations because of intrapartum fever. Thus, 14 of 53 (26%) asymptomatic term neonates with sepsis (30% of GBS sepsis and 11% of non-GBS sepsis) would not have been evaluated if intrapartum fever were ignored.CONCLUSION:Over half of term neonates with sepsis were asymptomatic at delivery. Intrapartum fever was helpful in identifying over a quarter of asymptomatic term neonates with sepsis.
Current vital sign (ICU) monitoring practice is: nurse observes and records the value of oxygen saturation, heart rate, … once an hour; build-in monitor alarms used as indicators between observations. Some physicians make minimum use of monitor data, due to the knowledge that different monitors yield unique results or/and a lack of confidence in the meaning of the values. Physicians use global limits, which are difficult to establish using current sampling procedures. This paper investigates two monitors, their similarities, differences, and the importance of these differences on making clinical decisions.
Introduction: Fatty acids (FA) play an important role in growth and cellular metabolism. The ratio of unsaturated (mono- and polyunsaturated) to saturated fatty acids influences normal growth, brain development and susceptibility to infections. The fetus is entirely dependent on maternal supply for the essential FA (polyunsaturated). Determination of tissue lipid composition is therefore crucial for optimal nutritional support in premature infants.
Ten genomic DNA probes, subcloned from inserts derived from a phage library constructed from the DNA of flow-sorted chromosomes, have now been mapped to locations within 15q11-15q13. By dosage blotting and densitometry, 5 of these probes map to the 15q11.2-15q12 segment missing in one 15 chromosome of a Prader-Willi syndrome (PWS) patient with a prominent cytological deletion. A sixth probe most likely maps to the same region. The other 4 probes map outside of this segment but within 15q11-15q13. Several of the 15q11.2-15q12 probes, and a cDNA probe homologous to one, have been used to test the DNA from 8 patients exhibiting a wide range of the clinical manifestations expected for PWS patients. DNA deletion was observed in all 3 patients with cytological 15q1 deletions as well as in a patient with an unbalanced (Y;15) translocation. DNA from 1 PWS patient with an unbalanced (5;15) translocation and an inverted duplication of the short arm and proximal long arm of 15 showed at least 1 and possibly 2 extra copies of each genomic probe tested. In the other 3 patients with no cytological deletions, no DNA deletions were found. Thus, the molecular probes described can be used in most PWS patients to analyze the region of proximal 15q implicated in this syndrome.