scholarly journals Treprostinil for persistent pulmonary hypertension of the newborn, with early onset sepsis in preterm infant

Medicine ◽  
2017 ◽  
Vol 96 (26) ◽  
pp. e7303 ◽  
Author(s):  
Bo Young Park ◽  
Sung-Hoon Chung
Author(s):  
Anouk Pels ◽  
Wes Onland ◽  
Rolf M. F. Berger ◽  
Arno F. J. van Heijst ◽  
Enrico Lopriore ◽  
...  

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.


2020 ◽  
Vol 57 (9) ◽  
pp. 864-865
Author(s):  
Ignacio Oulego-Erroz ◽  
Sandra Terroba-Seara ◽  
Leticia Castanon-Lopez ◽  
Antonio Rodriguez-Nunez

Author(s):  
Sunil Pathak ◽  
Deepika Bhil ◽  
Sakshi Prabodh ◽  
Manish Rasania ◽  
Saurabh Kumar ◽  
...  

Background: Persistent pulmonary hypertension of newborn (PPHN) result from failure of normal fall in pulmonary vascular resistance at or shortly after birth. It is associated with high mortality and morbidity. Objectives: To estimate incidence, risk factors; and outcome within limited resources – conventional ventilation, sildenafil, dobutamine and milrinone therapy. Methods: This prospective study was carried out on cases of PPHN admitted between March 2017 to August 2018. PPHN was suspected clinically, and then confirmed by echocardiography. Results: Out of 2811 inborn live births 12 (0.43%) developed PPHN. Out of total 942 NICU admissions, PPHN was diagnosed in 40(4.2%). 32 (80%) were full term, 6 (15%) were late preterm and 2(5%) were post term neonates. 25(62.5%) were male. Major etiological factors were asphyxia 19(47.5%), EOS (early onset sepsis) 18(45%) and MAS (meconium aspiration syndrome)  12(30%). 20(50%) responded to oral sildenafil and dobutamine therapy, 6 more responded with addition of milrinone. The overall survival rate was 26(65%) and poor outcome in 14 (35%) in our study. Median duration of respiratory support was 1.5(1 – 6) days in those with poor outcome and 6(4 – 7) in those survived. Duration of hospital stay was 1.5(1 – 6) days in poor outcome and 17(13 – 22) in those survived. Conclusions: Asphyxia, EOS and MAS are common causes of PPHN. Severity of respiratory distress on admission is correlated with mortality rather than etiological factors. Conventional ventilation, dobutamine, sildenafil and milrinone therapy are mainstay of treatment of PPHN cases in resource limited settings, and helps to reduce mortality to some extent. 


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