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Parenteral nutrition (PN) in the neonatal intensive care unit (NICU) involves a succession of risky processes. The objective was to identify and prioritize the risks associated with PN in order to improve the quality of the pathway. A failure modes, effects, and criticality analysis (FMECA) was used to identify potential PN pathway failure modes. A multidisciplinary working group conducted a functional analysis of the processes, then listed the failure modes (FM). The FM criticality was assessed on a scale from 1 to 5 for occurrence (O), severity (S), and detection (D). The risk priority number (RPN), ranging from 1 to 125, was calculated. The FMECA identified 99 FM (prescription (n=28), preparation (n=48), and administration (n=23)). The median RPN was 12, with scores ranging from 3 to 48. 25 % of the scores had an RPN>21.75.

Infant and family centered development care reduces infant distress and supports the parent and infant's individual abilities. However, a new environmental factor is daily encountered: the radiofrequency electromagnetic fields (RF EMFs) with the most recent fifth-generation (5G) technology. Currently, the effects of RF EMF during development are discussed in animal models. The neonatal intensive care units are not spared from this stressor. The objective of this study was to evaluate the efficacy of a novel, electromagnetically insulating incubator cover to prevent the preterm infant from RF EMF exposure. A personal dosimeter was placed on the mattress of a closed incubator. Periods of exposure to low, medium, and high levels of 5G RF were delivered in the presence or absence of the incubator cover. The use of a silver-copper cover reduced the intensity of 5G radiofrequency levels from 52% to 57% (p < 0.0001), allowing to easily apply the precautionary principle. [ABSTRACT FROM AUTHOR]

Newborns are prone to hypothermia immediately following birth. Hypothermia is associated with increased morbidity and mortality rates. We sought to assess the thermal environment and metabolic costs associated with exposure to various situations in the delivery room when skin-to-skin care (SSC) has to be curtailed. Environmental variables (air temperature: Ta; relative humidity: RH; radiative temperature: Tr; and air convection velocity) were recorded during sequences reproducing SSC, in the maternity unit's various rooms ("passive environments") and in incubators ("active environments"). Analytical calorimetry was then used to calculate the body heat loss (BHL) from these data. The analysis of 1280 measurements of Ta, RH, Tr, and air convection velocity in SSC, passive and active environments revealed that (i) the thermohygrometric environment during SSC was optimal (Ta: 32.7 ± 3.2 °C; RH: 50.9 ± 5.6%), (ii) BHL rose when SSC had to be interrupted, and (iii) the use of a radiant incubator prevented hypothermia and reduced dry BHL but not humid BHL (9.4 ± 1.5 kcal/kg/h; p <.001), relative to SSC (5.8 ± 2.0 kcal/kg/h; p <.001). The newborn infant's thermohygrometric environment is optimal during SSC in the delivery room. When SSC was interrupted, Ta and RH always decreased, and BHL increased in all passive environments. [ABSTRACT FROM AUTHOR]

Aim: Thermal instability is harmful on the newborn infant. We sought to draw up practical guidelines on maintaining homeothermy alongside skin‐to‐skin contact. Methods: A systematic analysis of the literature identified relevant studies between 2000 and 2021 in the PubMed database. Selected publications were evaluated, and their level of evidence was graded, in order to underpin the development of clinical guidelines. Results: We identified 7 meta‐analyses and 64 clinical studies with a focus on newborn infants homeothermy. Skin‐to‐skin contact is the easiest and most rapidly implementable method to prevent body heat loss. Alongside skin‐to‐skin contact, monitoring the newborn infant's body temperature with a target of 37.0°C is essential. For newborn infants <32 weeks of gestation, a skullcap and a polyethylene bag should be used in the delivery room or during transport. To limit water loss, inhaled gases humidification and warming is recommended, and preterm infants weighing less than 1600 g should be nursed in a closed, convective incubator. With regard to incubators, there are no clear benefits for single‐ versus double‐wall incubators as well as for air versus skin servo control. Conclusion: Alongside skin‐to‐skin contact, a bundle of practical guidelines could improve the maintenance of homeothermy in the newborn infant. [ABSTRACT FROM AUTHOR]

Tourneux P, Markham N, Seedorf G, Balasubramaniam V, Abman SH. Inhaled nitric oxide improves lung structure and pulmonary hypertension in a model of Neomycin-induced bronchopulmonary dysplasia in neonatal rats. Am J Physiol Lung Cell Mol Physiol 297:L1103-L1111, 2009. First published October 16, 2009; doi: 10.1152/ajplung.00293.2009.--Whether inhaled nitric oxide (iNO) prevents the development of bronchopulmonary dysplasia (BPD) in premature infants is controversial. In adult rats, Neomycin (Bleo) induces lung fibrosis and pulmonary hypertension, but the effects of Bleo on the developing lung and iNO treatment on Bleo-induced neonatal lung injury are uncertain. Therefore, we sought to determine whether early and prolonged iNO therapy attenuates changes of pulmonary vascular and alveolar structure in a model of BPD induced by Bleo treatment of neonatal rats. Sprague-Dawley rat pups were treated with Bleo (1 mg/kg ip daily) or vehicle (controls) from day 2 to 10, followed by recovery from day 11 to 19. Treatment groups received early (days 2-10), late (days 11-19), or prolonged iNO therapy (10 ppm; days 2-19). We found that compared with controls, Bleo increased fight ventricular hypertrophy (RVH), and pulmonary arterial wall thickness, and reduced vessel density alveolarization. In each iNO treatment group, iNO decreased RVH (P < 0.01) and wall thickness (P < 0.01) and restored vessel density after Bleo (P < 0.05). iNO therapy improved alveolarization for each treatment group after Bleo; however, the values remained abnormal compared with controls. Prolonged iNO treatment had greater effects on lung structure after bleomycin than late treatment alone. We conclude that Bleo induces lung structural changes that mimic BPD in neonatal rats, and that early and prolonged iNO therapy prevents right ventricle hypertrophy and pulmonary vascular remodeling and partially improves lung structure. lung development; nitric oxide; alveolarization doi: 10.1152/ajplung.00293.2009

Impaired nitric oxide-cGMP signaling contributes to severe pulmonary hypertension after birth, which may in part be due to decreased soluble gnanylate cyclase (sGC) activity. Cinacignat (BAY 58-2667) is a novel sGC activator that causes vasodilation, even in the presence of oxidized heine or heine-free sGC, but its hemodynamic effects have not been studied in the perinatal lung. We performed surgery on eight fetal (126 [+ or -] 2 days gestation) lambs (full term = 147 days) and placed catheters in the main pulmonary artery, aorta, and left atrium to measure pressures. An ultrasonic flow transducer was placed on the left pulmonary artery to measure blood flow, and a catheter was placed in the left pulmonary artery for drug infusion. Cinaciguat (0.1-100 [micro]g over 10 rain) caused dose-related increases in pulmonary blood flow greater than fourfold above baseline and reduced pulmonary vascular resistance by 80%. Treatment with IH-[l,2,4]oxadiazolo[4,3-a]quinoxalin-l-one (ODQ), an sGC-oxidizing inhibitor, enhanced cinacignat-induced pulmonary vasodilation by > 120%. The pulmonary vasodilator effect of cinacignat was prolonged, decreasing pulmonary vascular resistance for > 1.5 h after brief infusion. In vitro stimulation of ovine fetal pulmonary artery smooth muscle cells with cinacignat after ODQ treatment resulted in a 14-fold increase in cGMP compared with non-ODQ-treated cells. We conclude that cinaciguat causes potent and sustained fetal pulmonary vasodilation that is augmented in the presence of oxidized sGC and speculate that cinacignat may have therapeutic potential for severe neonatal pulmonary hypertension. BAY 58-2667; cGMP; nitric oxide; persistent pulmonary hypertension of the newborn; pulmonary hypertension

In addition to high pulmonary vascular resistance (PVR) and low pulmonary blood flow, the fetal pulmonary circulation is characterized by mechanisms that oppose vasodilation. Past work suggests that high myogenic tone contributes to high PVR and may contribute to autoregulation of blood flow in the fetal lung. Rho-kinase (ROCK) can mediate the myogenic response in the adult systemic circulation, but whether high ROCK activity contributes to the myogenic response and modulates time-dependent vasodilation in the developing lung circulation are unknown. We studied the effects of fasudil, a ROCK inhibitor, on the hemodynamic response during acute compression of the ductus arteriosus (DA) in chronically prepared, late-gestation fetal sheep. Acute DA compression simultaneously induces two opposing responses: 1) blood flow-induced vasodilation through increased shear stress that is mediated by NO release and 2) stretch-induced vasoconstriction (i.e., the myogenic response). The myogenic response was assessed during acute DA compression after treatment with [N.sup.[omega]]-nitro-L-arginine, an inhibitor of nitric oxide synthase, to block flow-induced vasodilation and unmask the myogenic response. Intrapulmonary fasudil infusion (100 [micro]g over 10 min) did not enhance flow-induced vasodilation during brief DA compression but reduced the myogenic response by 90% (P < 0.05). During prolonged DA compression, fasudil prevented the time-dependent decline in left pulmonary artery blood flow at 2 h (183 [+ or -] 29 vs. 110 [+ or -] 11 ml/min with and without fasudil, respectively; P < 0.001). We conclude that high ROCK activity opposes pulmonary vasodilation in utero and that the myogenic response maintains high PVR in the normal fetal lung through ROCK activation. calcium sensitization; persistent pulmonary hypertension of the newborn; pulmonary vascular resistances; lung development