Nitric oxide for respiratory failure in infants born at or near term Review question: Is inhaled nitric oxide gas, in addition to standard therapy, beneficial for babies born at full term who have lung disease leading to low levels of oxygen in the blood? Specifically, does it reduce the death rate or the number of babies who require highly invasive ECMO treatment? Background: Nitric oxide is a naturally occurring molecule that relaxes blood vessels and is active in the lungs when mixed with the gases that a patient is breathing. Study characteristics: In a search updated to February 2016, review authors identified a total of 17 studies for inclusion in the review. Most of the results reported in this review were obtained from 10 studies of moderate to high quality, which compared inhaled nitric oxide (iNO) versus standard therapy without iNO. Six studies compared iNO started when babies were less sick against waiting to see if they deteriorated, then treating them later. These studies were smaller, and only one was a high-quality trial. Key results: Inhaled nitric oxide is safe and can help some full-term babies with respiratory failure who have not responded to other methods of support. Inhaled nitric oxide increases levels of oxygen in babies' blood, and babies are more likely to survive without needing ECMO, a highly invasive therapy with many complications. Unfortunately, benefits of iNO are not clear in babies whose respiratory failure is due to a diaphragmatic hernia. Inhaled nitric oxide has shown no short-term or long-term adverse e ects. No signs suggest that iNO given earlier is more beneficial or results in more babies treated, and the number who die or who need ECMO is not significantly reduced.

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CDH newborns have evidence of biventricular dysfunction and decreased cardiac output. Abnormal function may be a factor in the non-response to pulmonary arterial vasodilators in CDH patients. A two-pronged management strategy aimed at improving cardiac function, as well as reducing pulmonary artery pressure in CDH newborns, may be warranted.

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Screening for PH in BPD, and subsequent evaluation and management is highly variable.

Pulmonary vascular disease and resultant pulmonary hypertension (PH) have been increasingly recognized in the preterm population, particularly among patients with bronchopulmonary dysplasia (BPD). Limited data exist on the impact of PH severity and right ventricular (RV) dysfunction at PH diagnosis on outcome. The purpose of this study was to evaluate if echocardiography measures of cardiac dysfunction and PH severity in BPD-PH were associated with mortality. The study is a retrospective analysis of the echocardiography at three months or less from time of PH diagnosis. Survival analysis using a univariate Cox proportional hazard model is presented and expressed using hazard ratios (HR). We included 52 patients with BPD and PH of which 16 (31%) died at follow-up. Average gestational age at birth was 26.3 ± 2.3 weeks. Echocardiography was performed at a median of 43.3 weeks (IQR: 39.0–54.7). The median time between PH diagnosis and death was 117 days (range: 49–262 days). Multiple measures of PH severity and RV performance were associated with mortality (sPAP/sBP: HR 1.02, eccentricity index: HR 2.02, tricuspid annular plane systolic excursion Z-score: HR 0.65, fractional area change: HR 0.88, peak longitudinal strain: HR 1.22). Hence, PH severity and underlying RV dysfunction at PH diagnosis were associated with mortality in BPD-PH patients. While absolute estimation of pulmonary pressures is not feasible in every screening echocardiography, thorough evaluation of RV function and other markers of PH may allow to discriminate the most at-risk population and should be considered as standard add-ons to the current screening at 36 weeks.