A36 Persistent pulmonary hypertension secondary to MAS and early onset GBS sepsis

2012 ◽  
Vol 88 ◽  
pp. S112
Author(s):  
M. Bedetta ◽  
S. Picone ◽  
P. Paolillo
Keyword(s):  
Pulmonary Hypertension ◽  
Early Onset ◽  
Persistent Pulmonary Hypertension

scholarly journals Neonatal pulmonary hypertension after severe early-onset fetal growth restriction: post hoc reflections on the Dutch STRIDER study

2022 ◽  
Author(s):  
Anouk Pels ◽  
Wes Onland ◽  
Rolf M. F. Berger ◽  
Arno F. J. van Heijst ◽  
Enrico Lopriore ◽  
...  
Keyword(s):  
At Risk ◽  
Pulmonary Hypertension ◽  
Bronchopulmonary Dysplasia ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Early Onset ◽  
Growth Restriction ◽  
Persistent Pulmonary Hypertension ◽  
Pathophysiological Mechanism ◽  
Co Morbidity

AbstractThe aim was to reflect on the unexpected finding of persistent pulmonary hypertension of the neonate (PPHN) and pulmonary hypertension in infants born within the Dutch STRIDER trial, its definition and possible pathophysiological mechanisms. The trial randomly assigned pregnant women with severe early-onset fetal growth restriction to sildenafil 25 mg three times a day versus placebo. Sildenafil use did not reduce perinatal mortality and morbidity, but did result in a higher rate of neonatal pulmonary hypertension (PH). The current paper reflects on the used definition, prevalence, and possible pathophysiology of the data on pulmonary hypertension. Twenty infants were diagnosed with pulmonary hypertension (12% of 163 live born infants). Of these, 16 infants had PPHN shortly after birth, and four had pulmonary hypertension associated with sepsis or bronchopulmonary dysplasia. Four infants with PPHN in the early neonatal period subsequently developed pulmonary hypertension associated with bronchopulmonary dysplasia in later life. Infants with pulmonary hypertension were at lower gestational age at delivery, had a lower birth weight and a higher rate of neonatal co-morbidity. The infants in the sildenafil group showed a significant increase in pulmonary hypertension compared to the placebo group (relative risk 3.67; 95% confidence interval 1.28 to 10.51, P = 0.02).Conclusion: Pulmonary hypertension occurred more frequent among infants of mothers allocated to antenatal sildenafil compared with placebo. A possible pathophysiological mechanism could be a “rebound” vasoconstriction after cessation of sildenafil. Additional studies and data are necessary to understand the mechanism of action. What is Known:• In the Dutch STRIDER trial, persistent pulmonary hypertension in the neonate (PPHN) was more frequent among infants after antenatal sildenafil exposure versus placebo. What is New:• The current analysis focuses on the distinction between PPHN and pulmonary hypertension associated with sepsis or bronchopulmonary dysplasia and on timing of diagnosis and aims to identify the infants at risk for developing pulmonary hypertension.• The diagnosis pulmonary hypertension is complex, especially in infants born after severe early-onset fetal growth restriction. The research field could benefit from an unambiguous consensus definition and standardized screening in infants at risk is proposed.

Congenital Alveolar Capillary Dysplasia: Rare Cause of Persistent Pulmonary Hypertension

1997 ◽  
Vol 17 (6) ◽  
pp. 959-975 ◽  
Author(s):  
Sibylle Haraida ◽  
Hannelore Lochbuhler ◽  
A. Heger ◽  
A. Nerlich ◽  
J. Diebold ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Persistent Pulmonary Hypertension ◽  
Alveolar Capillary Dysplasia ◽  
Alveolar Capillary

scholarly journals Inhaled Nitric Oxide at Birth Reduces Pulmonary Vascular Resistance and Improves Oxygenation in Preterm Lambs

Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 378
Author(s):  
Satyan Lakshminrusimha ◽  
Sylvia F. Gugino ◽  
Krishnamurthy Sekar ◽  
Stephen Wedgwood ◽  
Carmon Koenigsknecht ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Preterm Infants ◽  
Vascular Resistance ◽  
Inhaled Nitric Oxide ◽  
Persistent Pulmonary Hypertension ◽  
Inhaled No ◽  
Birth Preterm

Resuscitation with 21% O2 may not achieve target oxygenation in preterm infants and in neonates with persistent pulmonary hypertension of the newborn (PPHN). Inhaled nitric oxide (iNO) at birth can reduce pulmonary vascular resistance (PVR) and improve PaO2. We studied the effect of iNO on oxygenation and changes in PVR in preterm lambs with and without PPHN during resuscitation and stabilization at birth. Preterm lambs with and without PPHN (induced by antenatal ductal ligation) were delivered at 134 d gestation (term is 147–150 d). Lambs without PPHN were ventilated with 21% O2, titrated O2 to maintain target oxygenation or 21% O2 + iNO (20 ppm) at birth for 30 min. Preterm lambs with PPHN were ventilated with 50% O2, titrated O2 or 50% O2 + iNO. Resuscitation with 21% O2 in preterm lambs and 50%O2 in PPHN lambs did not achieve target oxygenation. Inhaled NO significantly decreased PVR in all lambs and increased PaO2 in preterm lambs ventilated with 21% O2 similar to that achieved by titrated O2 (41 ± 9% at 30 min). Inhaled NO increased PaO2 to 45 ± 13, 45 ± 20 and 76 ± 11 mmHg with 50% O2, titrated O2 up to 100% and 50% O2 + iNO, respectively, in PPHN lambs. We concluded that iNO at birth reduces PVR and FiO2 required to achieve target PaO2.

Methemoglobin and the response to inhaled nitric oxide in persistent pulmonary hypertension of the newborn

2020 ◽  
Vol 13 (2) ◽  
pp. 175-182
Author(s):  
R. Dadiz ◽  
J. Nair ◽  
C.T. D’Angio ◽  
R.M. Ryan ◽  
S. Lakshminrusimha
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Inhaled Nitric Oxide ◽  
Persistent Pulmonary Hypertension

scholarly journals Maternal tobacco smoke exposure and persistent pulmonary hypertension of the newborn.

1997 ◽  
Vol 105 (2) ◽  
pp. 202-206 ◽  
Author(s):  
C Bearer ◽  
R K Emerson ◽  
M A O'Riordan ◽  
E Roitman ◽  
C Shackleton
Keyword(s):  
Pulmonary Hypertension ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Persistent Pulmonary Hypertension

Persistent Pulmonary Hypertension of the Newborn

1991 ◽  
Vol 7 (S1) ◽  
pp. 66-69
Author(s):  
George Lister
Keyword(s):  
Pulmonary Hypertension ◽  
Diaphragmatic Hernia ◽  
Vascular Development ◽  
Clinical Syndrome ◽  
Persistent Pulmonary Hypertension ◽  
Maternal Infection ◽  
Fetal Circulation ◽  
Cns Disease ◽  
Persistent Fetal Circulation

Persistent pulmonary hypertension of the newborn or persistent fetal circulation is a clinical syndrome that is usually apparent within the first 2 days after birth because of the presence of hypoxemia (2;12;19). The syndrome was first described in an abstract by Gersony, Due, and Sinclair (6) in 1969. Two infants were reported who had “RV decompensation, cyanosis and clear lung fields… in the absence of recognizable cardiac, pulmonary, hematologic or CNS disease.” The syndrome has been associated with aspiration of meconium, diaphragmatic hernia, asphyxia, hemorrhage, shock, and maternal infection (4;18). In other cases, there is no clear antecedent event. Despite considerable interest in the problem and a wealth of research related to pulmonary vasoregulation and vascular development in the fetus and newborn, the etiology of the syndrome remains obscure 20 years since its recognition.

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