Inhaled Nitric Oxide in the Management of a Premature Newborn With Severe Respiratory Distress and Pulmonary Hypertension

Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome, characterized by sustained elevation of pulmonary vascular resistance (PVR) with right-to-left shunting across the ductus arteriosus and/or foramen ovale, causing severe hypoxemia. Although generally associated with diseases of term or near-term newborns, including group B streptococcal sepsis, PPHN has been described in preterm neonates as well. Recent echocardiographic studies have demonstrated increased PVR in preterm neonates with hyaline membrane disease (HMD), which correlated with disease severity and mortality. Severe HMD was associated with lower aortopulmonary pressure gradients and left pulmonary artery blood flow velocities during the first 72 hours after birth, suggesting that high PVR contributes to the mortality of respiratory distress of premature neonates.

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Inhalational Nitric Oxide Therapy for Persistent Pulmonary Hypertension of the Newborn

PEDIATRICS ◽

10.1542/peds.91.5.997 ◽

1993 ◽

Vol 91 (5) ◽

pp. 997-998

Author(s):

JOHN P. KINSELLA ◽

STEVEN H. ABMAN

Keyword(s):

Pulmonary Hypertension ◽

Ductus Arteriosus ◽

Clinical Syndrome ◽

Persistent Pulmonary Hypertension ◽

Current Therapy ◽

Clinical Settings ◽

Group B ◽

Nitric Oxide Therapy ◽

High Pulmonary Vascular Resistance ◽

Vasodilator Drug

Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome associated with various neonatal cardiopulmonary diseases, including meconium aspiration, group B streptococcal sepsis, congenital diaphragmatic hernia, and undetermined causes (idiopathic).12 Despite the diversity of clinical settings of PPHN, marked pulmonary hypertension and altered pulmonary vasoreactivity are its central pathophysiologic features. High pulmonary vascular resistance (PVR) results in right-to-left shunting of blood across the patent ductus arteriosus and foramen ovale, often causing critical hypoxemia. Current therapy to reduce pulmonary hypertension includes mechanical hyperventilation, alkalosis, hyperoxia, and cardiotonic and vasodilator drug therapy.3 Attempts at reducing PVR with hyperventilation and hyperoxia may cause severe lung injury, contributing to further morbidity and mortality of PPHN.

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Newborns With Acute Respiratory Distress: Diagnosis and Management

Pediatrics in Review ◽

10.1542/pir.9.9.279 ◽

1988 ◽

Vol 9 (9) ◽

pp. 279-285

Author(s):

Richard L. Schreiner ◽

Niceta C. Bradburn

Keyword(s):

Pulmonary Hypertension ◽

Respiratory Distress ◽

Newborn Infant ◽

Blood Gases ◽

Indirect Measurement ◽

Chest Roentgenogram ◽

Inborn Errors ◽

Severe Respiratory Distress ◽

Glucose Determination ◽

Arterial Blood

If respiratory distress develops in the newborn after he or she has been normal for more than a few hours, bacterial sepsis, inborn errors of metabolism, cardiac disorders, and intracranial hemorrhage should be suspected. It is virtually impossible to determine whether an infant with mild respiratory distress in the first few hours of life will have rapid resolution of disease or progress to severe respiratory distress. That is, it is difficult to differentiate among transient tachypnea of the newborn, sepsis, and pulmonary hypertension in the infant with mild respiratory distress in the first few hours of life. Transient tachypnea is a diagnosis that can only be made with certainty after the infant's respiratory distress has resolved. The newborn infant with mild respiratory distress of more than a few hours' duration requires a minimum number of laboratory tests including chest roentgenogram, hematocrit or hemoglobin, blood glucose determination, direct or indirect measurement of arterial blood gases, and blood cultures. The liberal use of oxygen in the near-term, term, or post-term vigorous but cyanotic infant in the delivery room may decrease the incidence and/or severity of respiratory distress due to pulmonary hypertension. A newborn infant with respiratory distress for more than a few hours should be considered a candidate for infection.

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X-linked Adrenal Hypoplasia Congenita Due to NR0B1 (DAX1) Deficiency Presenting as Severe Respiratory Distress in Near Term Infants

Pediatrics & Neonatology ◽

10.1016/j.pedneo.2015.10.010 ◽

2016 ◽

Vol 57 (5) ◽

pp. 444-445 ◽

Cited By ~ 2

Author(s):

Tijen Karsli ◽

Jennifer Sutter ◽

Prem S. Shekhawat

Keyword(s):

Respiratory Distress ◽

Term Infants ◽

Severe Respiratory Distress ◽

Adrenal Hypoplasia Congenita ◽

Adrenal Hypoplasia ◽

Near Term

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127 Surfactant Administration by Elective Intubation in Near-Term Infants with Severe Respiratory Distress

Pediatric Research ◽

10.1203/00006450-200508000-00156 ◽

2005 ◽

Vol 58 (2) ◽

pp. 376-376

Author(s):

C Moretti ◽

C Fornari ◽

L Giannini ◽

C Fassi ◽

C Gizzi ◽

...

Keyword(s):

Respiratory Distress ◽

Term Infants ◽

Severe Respiratory Distress ◽

Surfactant Administration ◽

Near Term

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EARLY CPAP-`GENTLE' VENTILATION VERSUS HYPEROXIA-HYPERVENTILATION IN THE TREATMENT OF SEVERE RESPIRATORY DISTRESS AND PERSISTENT PULMONARY HYPERTENSION(PPHN). 1382

Pediatric Research ◽

10.1203/00006450-199604001-01405 ◽

1996 ◽

Vol 39 ◽

pp. 233-233

Author(s):

Simon P Ng ◽

Tsee F Loh ◽

Joseph M Gomez ◽

N K Ho

Keyword(s):

Pulmonary Hypertension ◽

Respiratory Distress ◽

Persistent Pulmonary Hypertension ◽

Severe Respiratory Distress

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Risk factors for patent ductus arteriosus in preterm neonates

Paediatrica Indonesiana ◽

10.14238/pi54.3.2014.132-6 ◽

2014 ◽

Vol 54 (3) ◽

pp. 132 ◽

Cited By ~ 1

Author(s):

Novia Bernati ◽

Ria Nova ◽

Julniar M. Tasli ◽

Theodorus Theodorus

Keyword(s):

Risk Factors ◽

Birth Weight ◽

Patent Ductus Arteriosus ◽

Ductus Arteriosus ◽

Prevalence Ratio ◽

Hyaline Membrane Disease ◽

Preterm Neonates ◽

Antenatal Corticosteroids ◽

Cross Sectional ◽

Patent Ductus

Background The reported prevalences of patent ductus arteriosus(PDA) in preterm neonates vaty, and are currently unknown inPalembang. Birth weight, ges tational age, asphyxia, histoty ofantenatal steroid use, hyaline membrane disease (HMD), raceand ethnicity, are potential risk factors for PDA.Objective To determine the prevalence of PDA and its riskfactors in preterm neonates at Mohammad Hoesin Hospital,Palembang.Methods This cross-sectional study was conducted from October2011 to April 2012. Echocardiographic examinations wereperformed on 242 preterm neonates aged 15 hours to 7 days. Datawas taken from medical records and interviews, and analyzed byChi square and logistic regression analyses.Results Patent ductus arteriosus was found in 142 (58.7%)preterm neonates with a prevalence ratio of 1.43. Neonates withbirthweight ::;;2,000 grams tended to have 1.9 (95% CI 1.17 to3.32) rimes higher risk for PDA (P=0.01). Neonates ::;;JO weeksgestation were also at 1.9 rimes higher risk for PDA (P=0.16).Probabilities for PDA occurrence in neonates with asphyxia,without antenatal corticosteroids and HMD were 1.6 (95%CI 1.13 to 3.36) rimes, 1.3 (95%CI 0.73 to 2.50) times and 2.2(95%CI 1.29 to 3.72) rimes higher risk for PDA, respectively(P=0.22, 0.41, and 0.005, respectively).Conclusion Birth weight and HMD are statistically significantrisk factors of PDA, but the more significant one is HMD.

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Shunts in Patients With Respiratory Distress Syndrome

PEDIATRICS ◽

10.1542/peds.92.5.737 ◽

1993 ◽

Vol 92 (5) ◽

pp. 737-737

Author(s):

NICK EVANS

Keyword(s):

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Preterm Neonates ◽

Published Data ◽

Not Given ◽

Severe Respiratory Distress ◽

Pulmonary Arterial ◽

Severe Respiratory Distress Syndrome ◽

Echocardiographic Findings

To the Editor.— Although I agree with many of the echocardiographic findings of Walther et al1 they have not given us sufficient data to draw their main conclusion: that large right-to-left (R-L) shunts are common in preterm neonates with severe respiratory distress syndrome (RDS). They base this conclusion on two observations. First, they believe that aortopulmonary pressure differences are small in these neonates. Pulmonary arterial pressures in RDS are high2 but, as previously published data have shown,3 they are predominantly subsystemic and therefore not likely to be conducive to a large R-L shunt.

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Brain Type Natriuretic Peptide

Neonatal Network The Journal of Neonatal Nursing ◽

10.1891/0730-0832.27.5.343 ◽

2008 ◽

Vol 27 (5) ◽

pp. 343-346 ◽

Cited By ~ 2

Author(s):

Patricia Nash

Keyword(s):

Heart Failure ◽

Natriuretic Peptide ◽

Transplant Rejection ◽

Ductus Arteriosus ◽

Left Ventricular ◽

Preterm Neonates ◽

Term Infants ◽

End Diastolic Volume ◽

Ventricular Diastolic Dysfunction ◽

Near Term

BRAIN TYPE NATRIURETIC PEPTIDE, also called B-type natriuretic peptide (BNP), has emerged as a valuable diagnostic and prognostic marker in the assessment of heart failure in adults.1–7 Serum BNP levels have also been shown to differentiate pulmonary from cardiac causes of dyspnea and to be useful as a screening tool for ventricular hypertrophy, ventricular diastolic dysfunction, transplant rejection, and risk for sudden death in adult patients with congestive heart failure (CHF).3,7,8 In pediatric patients, BNP levels have been found to increase with a hemodynamically significant ventricular septal defect and to correlate with the volume of the shunt and the left ventricular end diastolic volume.7 Recently, BNP levels have been investigated for use in determining the hemodynamic significance of a patent ductus arteriosus (PDA) in preterm neonates.3,7,9–11 They have also been studied for use in the diagnosis and management of persistent pulmonary hypertension in term and near-term infants.6 This article reviews BNP terminology, structure, physiology, measurement, and potential utility in the NICU.

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