ObjectiveTo determine the effectiveness and safety of moderate whole-body hypothermia in newborns with hypoxic-ischemic encephalopathy born in hospitals with and without newborn intensive care facilities or complicated hypothermia equipment.DesignMulticenter, international, randomized controlled trial.SettingNeonatal intensive care units in Australia, New Zealand, Canada, and the United States (N = 28) from February 2001 through July 2007.ParticipantsNewborns of 35 weeks' gestation or more, with indicators of peripartum hypoxia-ischemia and moderate to severe clinical encephalopathy, randomly allocated to hypothermia (n = 110) or standard care (n = 111).InterventionWhole-body hypothermia to 33.5°C for 72 hours or standard care (37°C). Infants who received hypothermia were treated at ambient environmental temperature by turning off the radiant warmer and then applying refrigerated gel packs to maintain rectal temperature at 33°C to 34°C.Main Outcome MeasuresDeath or major sensorineural disability at 2 years of age.ResultsTherapeutic hypothermia reduced the risk of death or major sensorineural disability at 2 years of age: 55 of 107 infants (51.4%) in the hypothermia group and 67 of 101 infants (66.3%) in the control group died or had a major sensorineural disability at 2 years (risk ratio, 0.77 [95% confidence interval, 0.62-0.98]; P = .03). The mortality rate decreased, and the survival rate free of any sensorineural disability increased. Adverse effects of hypothermia were minimal.ConclusionsWhole-body hypothermia is effective and appears to be safe when commenced within 6 hours of birth at the hospital of birth in term and near-term newborns with hypoxic-ischemic encephalopathy. This simple method of hypothermia could be used within strict protocols with appropriate training on correct diagnosis and application of hypothermia in nontertiary neonatal settings while awaiting retrieval and transport to the regional neonatal intensive care unit.Trial Registrationanzctr.org.au Identifier: ACTRN12606000036516

Patent ductus arteriosus (PDA) is common problem, with rates of 40–55% in babies born less than 29 weeks’ gestation,1 2 yet decisions related to management remain highly controversial. Despite numerous studies on the topic there remains uncertainty with respect to diagnosis, assignment of clinical importance, whether treatment is indicated and if so the preferred treatment modality. The most fundamental question remains unanswered: does a PDA cause acute physiological or clinical change that either acutely or chronically leads to organ damage, which further leads to important neonatal morbidities? Put simply is the PDA an “innocent bystander” or is it pathological to the extent that early detection and intervention is warranted to prevent neonatal morbidity?

Persistent pulmonary hypertension of the newborn (PPHN) is a frequent cause for admission to the neonatal intensive care unit and is associated with mortality and variable morbidities. It is primarily a state of oxygenation failure representing a failure of the normal postnatal decline in pulmonary vascular resistance that may be associated with right ventricular dysfunction. Enhanced knowledge of the pathophysiologic contributors to this syndrome helps clinicians understand its phenotypic expression and facilitates more focused intensive care decision-making. The approach to treatment should be based on alleviation of the elevation in pulmonary vascular resistance and should include optimization of lung recruitment and judicious use of pulmonary vasodilators. When response to inhaled nitric oxide is suboptimal, the physiologic contributors to impaired oxygenation need further investigation. Targeted neonatal echocardiography provides novel physiologic insights; in particular, it may help assess the adequacy of right ventricular performance, the relative contribution of the fetal shunts and the magnitude of the overall impairment to cardiac output. This information may facilitate therapeutic next steps and whether adjunctive vasodilators or drugs to augment ventricular function are preferable. This article provides a comprehensive overview of the pathological contributors to PPHN, the physiologic constituents of its phenotypic expression, standard approach to therapeutic intervention, and the role of bedside echocardiography in enhancing the decision-making process.

The role of echocardiography in the neonatal intensive care unit (NICU) has changed over the past few years. Previously, nearly all echocardiographic studies in the NICU were performed by pediatric cardiologists to diagnose or monitor congenital heart disease (CHD) and to screen for patent ductus arteriosus (PDA). More recently, neonatologists have become interested in the echocardiographic assessment of hemodynamic instability in infants. The terms functional echocardiography and point-of-care echocardiography have been introduced to describe the use of echocardiography as an adjunct in the clinical assessment of the hemodynamic status in neonates.^1–4 The increasing availability of echocardiography, with miniaturization of the technology, has resulted in more widespread use of echocardiography in NICUs around the world.⁵ Perhaps the most significant challenge for the application of so-called functional studies is that newborns in the NICU with hemodynamic instability are at a much higher risk for having underlying CHD. In addition, newborns in the NICU are unique in that they are in the process of transition from fetal to postnatal circulation.