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The impact of a hemodynamically significant patent ductus arteriosus (PDA) in preterm infants. The continuous flow from left-to-right leads to pulmonary overcirculation, protein leak
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![Figure 1. Graphic summary of Nees et al. [17] showing the course of...](publication/349258542/figure/fig1/AS:990569711013889@1613181631603/Graphic-summary-of-Nees-et-al-17-showing-the-course-of-preterm-infants-with_Q320.jpg)
During transition at birth with ventilation of the lungs, pulmonary vascular resistance (PVR) decreases from high fetal values, leading to an 8 to 10-fold increase in pulmonary blood flow (Qp). In some infants, this transition does not occur, resulting in pulmonary hypertension (PH). In infants, PH can present as: (a) primary PH in term neonates (i...
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Citations
... PH in preterm infants after the first few postnatal weeks is associated with higher risk for BPD or death. (44,(50)(51)(52)(53)(54) Late PH, associated with evolving or established BPD at 36 weeks postmenstrual age (PMA), can continue during infancy, childhood, and early adulthood. (Table 1) The American Heart Association/American Thoracic Society Guidelines for pediatric PH recognized that formal diagnostic criteria of PH during the first 3 postnatal months remain poorly defined; specifically, as the pulmonary vascular transition from fetal to neonatal life, especially in preterm infants, represents a very dynamic period of time. ...
Pulmonary hypertension (PH) is associated with significant morbidities and high mortality in preterm infants, yet mechanisms contributing to the pathogenesis of PH, the impact of early pulmonary vascular disease (PVD) on the risk for BPD, the role for PH-targeted drug therapies, and long-term pulmonary vascular sequelae remain poorly understood. PVD is not a homogeneous disease, rather, PVD in the setting of prematurity includes various phenotypes as based on underlying pathophysiology, the severity of associated PH, the timing of disease onset, its contribution to hemodynamic and respiratory status, late outcomes, and other features. As with term newborns, severe hypoxemia with acute respiratory failure (HRF) in preterm infants can be due to marked elevation of pulmonary artery pressure with extrapulmonary shunt, traditionally referred to as persistent pulmonary hypertension of the newborn (PPHN). Transient and less severe levels of PH can also be observed during the early transition after birth without evidence of severe HRF, representing physiologic PH or delayed pulmonary vascular transition in preterm infants. Importantly, echocardiographic evidence of early PH has been strongly associated with the subsequent development of bronchopulmonary dysplasia (BPD), late PH, and chronic respiratory disease during infancy and early childhood. Late PH beyond the first postnatal months in preterm in neonates with established BPD is further associated with poor outcomes, especially as related to BPD severity. In addition, echocardiographic signs of PVD can further persist throughout childhood and may lead to chronic PH of variable severity and cardiac maldevelopment in prematurely born young adults. This review discusses the importance of characterizing diverse pulmonary vascular phenotypes in preterm infants to better guide clinical care and research, and to enhance the development of more precise therapeutic strategies to optimize early and late outcomes of preterm infants.
... Preterm infants<28 weeks of gestation have 50-70% moderate-to-large ductal shunt that can increase pulmonary blood pressure and flow and decrease lung compliance stated as 72.7% in our study. On the other hand the presence of an open ductus can regulate extreme elevations in pulmonary arterial pressure as a pop-off valve (22,23). ...
Cite this article as: Vardar G, Aksoy Okan M, Karadağ N, et al. Controversies in neonatology: The efficacy of inhaled nitric oxide in preterm infants with persistent pulmonary hypertension. ABSTRACT Introduction: There is limited and conflicting information in literature regarding use of inhaled nitric oxide (iNO) in preterm infants. In this study we examined the characteristics of preterm infants with persistent pulmonary hypertension (PHT) who responded and did not respond to iNO therapy. Material and Method: We retrospectively reviewed data of infants <34 weeks of gestational age with hypoxic respiratory failure that received iNO for PHT after being diagnosed with severe respiratory distress syndrome after birth. The data of responders and non-responders to iNO therapy were compared. Results: Twenty-five infants were included in our study. Twelve (48%) had a positive response to iNO administration for PHT. As an antenatal characteristic, oligohydramnios was significantly higher in responders [5 (41.7%) vs 0%, p=0.015] and mortality rate was lower (66% vs. 100%, p=0.039). The SpO2/FiO2 ratio before iNO treatment predicted the response to iNO in preterm neonates with PHT. The ROC analysis yielded an area under curve AUC for SpO2/FiO2 ratio before iNO of AUCSpO2/ FiO2before was 0.756; 95% CI, 0.554-0.959; P=0.03. A cutoff value of 79 point by the SpO2/FiO2 ratio before iNO treatment predicted the response to iNO treatment with 83% sensitivity and 70% specificity. Conclusion: In infants born <34 weeks gestation, response to iNO in PHT has a significant effect on improving survival. The presence of oligohydramnios may be an important factor in prediction of positive response. SpO2/FiO2 ratio can be useful for estimating the effectiveness of iNO.
... Blood flow to the lungs after birth must increase by nearly 8-fold with oxygenation of the alveoli. [1] However, there are several factors (not always identifiable) whose consequence can be persistent pulmonary hypertension of the neonate (PPHN). PPHN is typically secondary to underlying severe Background: Inhaled nitric oxide (iNO) has been in use for several decades now in neonates with hypoxic respiratory failure (HRF) associated with pulmonary hypertension (PH). ...
... HFOV: High frequency oscillatory ventilation; iNO: inhaled nitric oxide; PH: Pulmonary hypertension; SIMV: Synchronised intermittent mandatory ventilation due to acute onset diseases such as MAS, infection (pneumonia/sepsis), hypoxic ischaemic encephalopathy and severe respiratory distress syndrome (RDS). [1] Approximately 0.2% of all neonates >34 weeks develop PPHN characterised by labile arterial saturations and differential cyanosis (higher preductal SpO 2 than in lower limbs) due to bidirectional shunts across the patent ductus arteriosus. In our unit, we relied on an echocardiogram confirmation of PPHN in less than half the cases (40%) before instituting therapy. ...
... 22 Remodeling of the pulmonary vasculature with progressive changes in arteriolar medial hypertrophy, intimal proliferation, and eventually fibrosis of pulmonary capillaries and arterioles can occur, such that ongoing increases in PVR may eventually lead to PDA shunt reversal. 16,17,23 In addition, chronic PDAs increase the incidence of BPD, 8 which is an independent risk factor for pulmonary vascular disease and pulmonary hypertension. Importantly, even with pulmonary hypertension, closure of the PDA can decrease pulmonary pressures 12 provided that the hemodynamics are favorable for closure (ie, test occlusion in the catheterization laboratory to monitor tolerance of PDA closure in the presence of pulmonary vascular disease/pulmonary hypertension). ...
... Promoting pulmonary vasodilation without excessive supplemental oxygen can potentially facilitate the establishment of gas exchange in the lung without exposing the infant to oxygen toxicity. Persistent pulmonary hypertension of the newborn (PPHN) [7] is a disorder characterized by elevated pulmonary vascular resistance (PVR), extra-pulmonary right-to-left shunting and hypoxemia. Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator approved by the Food and Drug Administration in term infants with PPHN and acts by increasing cGMP in pulmonary arterial smooth muscle cells (PASMC). ...
... Persistent pulmonary hypertension of the newborn (PPHN) [7] is a disorder ch terized by elevated pulmonary vascular resistance (PVR), extra-pulmonary rightshunting and hypoxemia. Inhaled nitric oxide (iNO) is a selective pulmonary vasod approved by the Food and Drug Administration in term infants with PPHN and a increasing cGMP in pulmonary arterial smooth muscle cells (PASMC). ...
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.
Bronchopulmonary dysplasia (BPD) is a multifactorial disease occurring as a consequence of premature birth, as well as antenatal and postnatal injury to the developing lung. BPD morbidity and severity depend on a complex interplay between prenatal and postnatal inflammation, mechanical ventilation, and oxygen therapy as well as associated prematurity-related complications. These initial hits result in ill-explored aberrant immune and reparative response, activation of pro-fibrotic and anti-angiogenic factors, which further perpetuate the injury. Histologically, the disease presents primarily by impaired lung development and an arrest in lung microvascular maturation. Consequently, BPD leads to respiratory complications beyond the neonatal period and may result in premature aging of the lung. While the numerous prenatal and postnatal stimuli contributing to BPD pathogenesis are relatively well known, the specific cell populations driving the injury, as well as underlying mechanisms are still not well understood. Recently, an effort to gain a more detailed insight into the cellular composition of the developing lung and its progenitor populations has unfold. Here, we provide an overview of the current knowledge regarding perinatal origin of BPD and discuss underlying mechanisms, as well as novel approaches to study the perturbed lung development.
Pulmonary hypertension in the neonate is associated with cardiopulmonary disturbances and neurodevelopment morbidity. The patent ductus arteriosus is a persistent fetal shunt that can be pathologic vs supportive in the setting of neonatal pulmonary hypertension. Understanding the underlying pathophysiology of pulmonary hypertension and the cardiopulmonary effects of various phenotypes can guide management in this vulnerable population. In this narrative, we will summarize the physiologic principles of pulmonary hypertension, the impact of the patent ductus arteriosus on various phenotypes, and the utility of serial targeted neonatal echocardiography to individualize clinical assessment and management.
