Inhaled nitric oxide for oligohydramnios-induced pulmonary hypoplasia: A report of two cases and review of the literature
ABSTRACT We describe the clinical courses of two premature infants, a male born at 29(4/7) weeks' gestational age after an 8-week period of rupture of membranes (ROM) and severe oligohydramnios, and a female infant born at 31 weeks' gestational age after an 18-week period of ROM and severe oligohydramnios. Within hours after birth, despite intubation and aggressive ventilation, both infants developed fulminant hypoxic respiratory failure. Their clinical courses were consistent with pulmonary hypertension and both infants were transferred for trials of inhaled nitric oxide (iNO). Both infants had dramatic responses to iNO, suggesting that the pulmonary disease seen after prolonged oligohydramnios may have a component of nitric oxide-sensitive pulmonary hypertension. The goals of this article are to (1) review oligohydramnios-induced pulmonary hypoplasia, (2) discuss patients at highest mortality risk, and (3) describe the effects of iNO on pulmonary hypertension in infants with hypoxemia following prolonged ROM and severe oligohydramnios.
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- "Gestational age at PPROM and the latency period between rupture of membranes and delivery are significant risk factors for the development of pulmonary hypoplasia, which is associated with a poor neonatal outcome . However, it is increasingly recognised, that many infants with pulmonary hypoplasia have an element of reversible pulmonary hypertension that is sensitive to inhaled nitric oxide (iNO) therapy   . Furthermore, animal data suggest that iNO therapy enhances distal lung growth and promotes pulmonary vascular angiogenesis . "
ABSTRACT: Second trimester preterm premature rupture of the membranes (PPROM) before 24 weeks of gestation is associated with a high morbidity and mortality rate. To demonstrate the efficacy of early continuous positive airway pressure (CPAP) combined with inhaled nitric oxide (iNO) for treatment of preterm infants with lung hypoplasia and persistent foetal circulation (PFC) due to very early PPROM and prolonged severe oligohydramnios. Seven infants with prolonged PPROM, lung hypoplasia, respiratory distress and persistent foetal circulation were intubated in the delivery room for subsequent surfactant and iNO application. As our new treatment strategy was to keep the period of mechanical ventilation as short as possible, all infants were switched on nasal CPAP combined with iNO within the first 24 hours. Mean gestational age at PPROM was 19+6 weeks (range 14+2 to 23+6 weeks) and the average latency period between rupture of membranes and delivery was 10+3 weeks (7+3 to 16+4 weeks). Infants were born at 30+3 weeks of gestation (28+3 to 33+1 weeks) with an average birth weight of 1468g (884 to 2200g). In all neonates CPAP combined with iNO reversed PFC and 6 patients stabilised without the need for reintubation and mechanical ventilation. One infant had to be reintubated following 12 hours of CPAP combined with iNO due to respiratory insufficiency. All seven infants survived to discharge. CPAP combined with iNO might be a promising approach for therapy of preterm infants with lung hypoplasia and persistent foetal circulation due to very early PPROM.Early human development 10/2010; 87(1):17-20. DOI:10.1016/j.earlhumdev.2010.09.004 · 1.93 Impact Factor
- Journal of Perinatology 10/2002; 22(6):510. DOI:10.1038/sj.jp.7210767 · 2.35 Impact Factor
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ABSTRACT: Pulmonary hypertension is an uncommon, yet devastating, syndrome with a complex underlying pathobiology. Hypoxia, inflammation, and increased shear stress appear to be the primary pathogenic events; however, mechanisms by which these processes lead to pulmonary hypertension remain incompletely understood. The ultimate increase in pulmonary vascular resistance is attributed to remodelling of the walls of resistance vessels, which can lead to encroachment on and reduction of the vascular lumen. The number of blood vessels per unit of cross-sectional area in the hypertensive lung is also reduced, which can contribute to increased vascular resistance. Regardless of its etiology, endothelial dysfunction underlies pulmonary hypertension, one manifestation of which is the attenuated production of bioactive nitric oxide. Nitric oxide administration can exert beneficial effects at various stages of the disease. Here we review the known pathobiology of pulmonary hypertension, with a principal focus on endothelial nitric oxide, and also summarize the data on nitric oxide replacement therapy and other novel therapies that relate to nitric oxide as one approach to treatment.Journal of Cardiovascular Pharmacology and Therapeutics 04/2004; 9(1):1-8. DOI:10.1177/107424840400900i101 · 3.07 Impact Factor