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Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition that occurs after birth. It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia and right-to-left extra-pulmonary shunting of blood. In the treatment of persistent pulmonary hypertension of the newborn, the goal is to increase oxygen flow to the baby's organs to prevent serious health problems. Treatment may include medication, mechanical ventilation and respiratory therapy. We performed a retrospective, descriptive and transversal study to investigate the prevalence and treatment of neonatal patients with persistent pulmonary hypertension who were admitted at the Hospital del Niño DIF from 2004 to 2008. Data, collected from hospital charts, included demographic, clinical course and use of medication. A total of 38 patients were included (prevalence of 5.7%). The average age of patients was 8.4 +/- 1.4 days. The mortality rate was 42.1%. Data were collected and 45 different drugs were given to the pediatric patients. The median number of drugs/inpatient was 8.3 (1-18). The therapeutic class most prescribed was anti-infective (29.9% of all the prescriptions), followed by cardiovascular and renal drugs (26.4% of all the prescriptions) and gastrointestinal agents (14.6% of all the prescriptions). Ranitidine was the drug most commonly used, followed by ampicillin and midazolam. We found a high mortality rate and as in many studies, the therapeutic class most used were anti-infectives.

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OBJECTIVE: To determine the cardiovascular outcome of a group of term newborns treated with inhaled nitric oxide (iNO) for severe hypoxemic respiratory failure with associated persistent pulmonary hypertension. STUDY DESIGN: We performed echocardiographic evaluations in 40 survivors treated for severe neonatal hypoxemic respiratory failure. Each of the 40 had at least 2 follow-up echocardiograms at 3 or 6 and 24 months. These studies were compared with echocardiograms done in infants in a normal, age-matched control group. RESULTS: Three of 31 infants met echocardiographic criteria for pulmonary hypertension at the 3-month examination. Two of the 3 had associated structural heart disease (1 with an atrial septal defect and 1 with a ventricular septal defect). At 24 months only 1 patient had pulmonary hypertension. This infant had an atrial septal defect that was surgically closed shortly after the 24-month echocardiogram because of the pulmonary hypertension. Group comparisons of 3- and 24-month echocardiographic variables showed no differences between the study and control groups. In the 31 infants in whom serial studies were completed, expected age-related changes were demonstrated between the 3- and 24-month examinations. CONCLUSIONS: The incidence of residual pulmonary hypertension in infants treated as newborns for severe hypoxemic respiratory failure is low. The group at highest risk is those with structural heart disease.

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To define the course of neonatal circulatory transition and to identify clinically relevant echocardiographic measurements in the diagnosis of persistent pulmonary hypertension, we prospectively studied 32 healthy term infants from 30 minutes to 24 hours after birth with color and quantitative Doppler echocardiography on the first day of life, and compared them with 33 term infants supported by mechanical ventilation for respiratory failure. Color Doppler imaging included measurements of cardiac output, left pulmonary artery flow, aortopulmonary pressure difference, ductal flow, left-to-right color-flow jet area of the ductus arteriosus, and ductal flow characteristics. In healthy infants the majority of measurable changes in cardiopulmonary hemodynamics had occurred by 8 hours after birth, although some degree of right-to-left ductal shunting was found up to 12 hours after birth. In the infants with respiratory failure, ductal flow and maximum aortopulmonary pressure difference measurements at 8, 12, and 24 hours showed a significant delay in ductal closure and a high incidence of persistent pulmonary hypertension, which correlated well with the severity of their respiratory failure. Factors such as aortopulmonary pressure difference, prolonged right-to-left shunting with decreased left pulmonary artery flow, and failure to develop a left-to-right ductal color-flow jet were found to be practical markers for assessing the course of neonatal circulatory transition in sick term infants.

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To study the potential role of endothelin-1, a potent endothelium-derived vasoconstrictor peptide, in the pathophysiology of persistent pulmonary hypertension of the newborn (PPHN), we measured arterial concentrations of immunoreactive endothelin-1 (irET-1) in 24 neonates with PPHN. Secondary diagnoses included meconium aspiration syndrome (13 patients), sepsis (2), congenital diaphragmatic hernia (1), asphyxia (1), pulmonary hemorrhage (1), aspiration of blood (1), and respiratory distress syndrome (1). Compared with irET-1 levels in umbilical cord blood in normal infants (15.1 +/- 4.1 pg/ml; mean +/- SEM) and in newborn infants with hyaline membrane disease who were supported by mechanical ventilation (11.8 +/- 1.2 pg/ml), infants with PPHN had markedly elevated circulating irET-1 levels (27.6 +/- 3.6 pg/ml; p < 0.01 vs cord blood, hyaline membrane disease). Infants with severe PPHN requiring extracorporeal membrane oxygenation (ECMO) therapy had higher irET-1 levels than infants with milder disease (31.0 +/- 4.7 for ECMO-treated infants vs 21.2 +/- 2.0 for non-ECMO-treated infants; p < 0.05). In patients treated without ECMO, irET-1 progressively decreased during the following 3 to 5 days, paralleling clinical improvement. In contrast, irET-1 concentrations remained elevated in infants with severe PPHN during ECMO therapy. We conclude that circulating irET-1 levels are elevated in newborn infants with PPHN, are positively correlated with disease severity, and decline with resolution of disease in patients who do not require ECMO therapy. Whether endothelin-1 contributes directly to the pathophysiology of PPHN or is simply a marker of disease activity remains speculative.

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The purpose of this study was to determine the frequency of patients with congenital heart disease who were given extracorporeal life support (ECLS) for respiratory failure. Underlying congenital heart disease "masked" by respiratory failure occurred in 2%. The most frequent pre-ECLS diagnosis that "masked" congenital heart disease was persistent fetal circulation. Of neonates with a pre-ECLS diagnosis of persistent fetal circulation, congenital heart disease was found in 56 (9%) of 623 patients.

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