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PubMed1986

Increased arterial pH, not decreased PaCO2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs.

Mechanically induced hyperventilation is used in the treatment of newborn infants with persistent pulmonary hypertension syndrome to induce respiratory alkalosis, which may attenuate their pulmonary vasoconstriction. Whether this treatment is effective because of the increase in arterial pH or the decrease in Paco2 was investigated in nine sedated, mechanically ventilated newborn lambs with hypoxia-induced pulmonary vasoconstriction. We found that respiratory alkalosis and metabolic alkalosis were equally effective in attenuating hypoxia-induced pulmonary vasoconstriction, but that hypocapnia (low Paco2 with a normal arterial pH) was ineffective. These results indicate that increased arterial pH, not decreased Paco2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs and possibly the pulmonary vasoconstriction in newborn infants with persistent pulmonary hypertension syndrome.

Alkalosis↗
PubMed1985

Fatal meconium aspiration syndrome occurring despite airway management considered appropriate.

A combined obstetric-pediatric approach to tracheal toilet is said to prevent serious cases of the potentially fatal meconium aspiration syndrome. After delivery of the head a DeLee trap is used to suction the oropharynx and nasopharynx. Immediately following delivery, endotracheal suction is performed in an effort to remove any remaining meconium-stained amniotic fluid. Although routinely using this approach, we continue to have occasional cases of fatal meconium aspiration syndrome. Therefore, we reviewed the outcome of infants born through meconium-stained fluid. During a 5-year period, 1420 (15%) of 9299 live-born infants had meconium-stained fluid. Thirty (2.1%) of these 1420 developed meconium aspiration syndrome and 12 (40%) died; eight received a postmortem examination. Four had unequivocal evidence of meconium aspiration, two had large numbers of intra-alveolar squamous cells, and two had no evidence of aspiration. We conclude that aggressive airway management during and immediately after delivery does not always prevent fatal meconium aspiration syndrome.

Amniotic Fluid↗
PubMed1997

The role of nitric oxide in respiratory disease.

Nitric oxide (NO) is found in both the upper and lower airways of man. In the lower airways it is found at concentrations less than 3 ppb, and in the upper airways at about 400 ppb. The NO found in the upper airways is thought to play a role in maintaining the sterility of the paranasal sinuses. NO is also produced by the endothelium of the pulmonary vasculature. Endothelium-derived NO is a potent vasodilator involved in maintaining low pulmonary tone. Impaired endothelial NO production is thought to be involved in some types of pulmonary hypertension. When inhaled, NO acts as a selective pulmonary vasodilator which is used to treat respiratory diseases. One area in which NO has proven to be particularly effective is in the treatment of persistent pulmonary hypertension of the newborn. Inhaled NO therapy can be used in the treatment of adult respiratory distress syndrome, primary pulmonary hypertension and chronic obstructive pulmonary disease.

Adult↗
PubMed2001

[Persistent pulmonary hypertension of the newborn].

Persistent pulmonary hypertension of the newborn (PPHN) is a cardiopulmonary disorder characterized by systemic arterial hypoxemia secondary to elevated pulmonary vascular resistance with resultant shunting of pulmonary blood flow to the systemic circulation. This disorder can be classified into four forms dependent on the etiology of the pulmonary hypertension: (1) Hypoplastic lung associated with congenital diaphragmatic hernia and oligohydramnions. (2) Primary PPHN (without known causative factor), such as preterm PPHN. (3) Secondary PPHN (with known causative factor), such as meconium aspiration syndrome, birth asphyxia or respiratory distress syndrome. (4) Relative PPHN associated with heart failure of hydrops fetalis or ischemic myocardial dysfunction. Inhalation of nitric oxide, which previously known as endothelial-derived-relaxation-factor, has been studied intensively as therapy for PPHN.

Administration, Inhalation↗
PubMed1994

Respiratory disorders of the neonate.

This paper presents recently published literature linking current understanding of neonatal respiratory physiology and pathophysiology to current therapy. Respiratory development is a continuum. The persistence of a fetal breathing pattern into the neonatal period may explain idiopathic neonatal apnea and the pattern of breathing seen with asphyxial apnea. Discussion with the obstetrician will focus more on prenatal diagnosis and on ensuring that prenatal corticosteroids are given. The advent of inhaled nitric oxide therapy for persistent pulmonary hypertension of the newborn offers a viable method of avoiding extracorporeal membrane oxygenation. New insights into the management of respiratory distress syndrome are derived from studies of how lung mechanics are altered by surfactant therapy. Lung injury due to capillary stress is highlighted as is attention to the way in which artificial ventilation is performed. Finally, the development of optimal guidelines for care in respiratory distress syndrome must involve consideration of multiple, interacting factors and their impact on associated conditions, especially periventricular hemorrhage.

Adrenal Cortex Hormones↗
PubMed1983

Left ventricular function in persistent pulmonary hypertension of the newborn. Computer analysis of the echocardiogram.

Regional and global left ventricular function was assessed in 23 neonates with persistent pulmonary hypertension using computer assisted analysis of their left ventricular echocardiograms and compared with that in 50 healthy neonates. End diastolic left ventricular dimension was normal and end systolic dimension increased while percentage left ventricular shortening and peak velocity of circumferential fibre shortening decreased indicating impaired systolic performance. The peak rate of increase in left ventricular diameter in early diastole was significantly decreased and the durations of the rapid filling and isovolumic relaxation periods were prolonged suggesting resistance to left ventricular filling due to changes in diastolic myocardial properties. This abnormal left ventricular cavity function may have been due to a combination of increased diastolic wall thickness, reduced percentage systolic wall thickening, increased relative wall thickness, and pronounced reduction in peak rates of systolic wall thickening and diastolic wall thinning Seven neonates with persistent pulmonary hypertension died, and of the three examined at necropsy all had left ventricular hypertrophy and two extensive subendocardial haemorrhage and infarction affecting the right and left ventricular papillary muscles. Thus left ventricular dysfunction appears to be a common feature in neonates with this disorder and may be readily detected using computer analysis of left ventricular echocardiograms. Unfortunately, no single echo measurement was useful prognostically. Left ventricular dysfunction in persistent pulmonary hypertension probably results from a combination of hypoxaemia, acidaemia, and pulmonary hypertension, and although it may contribute to the high mortality in this syndrome, a correlation between the severity of left ventricular dysfunction and clinical outcome could not be shown.

Computers↗
PubMed1997

[Inhaled nitric oxide: a physiologic treatment of persistent pulmonary arterial hypertension in the newborn].

Fetal pulmonary circulation is characterized by high resistance and low pulmonary blood flow. Right-to-left shunting through the foramen ovale and/or patent ductus arteriosus is necessary to perfuse the placenta and insure fetal life. At birth, pulmonary arterial blood flow increases immediately by 8- to 10-fold, and allows pulmonary gas exchange and postnatal life. In some circumstances, this adaptation to extra-uterine life is inadequate, because of persistent high pulmonary resistance (PPHN). Due to the lack of a selective pulmonary vasodilator, the treatment of this syndrome remained purely symptomatic using high oxygen levels and barotraumatic mechanical hyperventilation. When this medical treatment failed, the only alternative was extracorporeal membrane oxygenation (ECMO). The discovery of the major role of various endothelium-derived factors including nitric oxide (NO) in the control of vascular reactivity led to dramatic switches in the concepts of severe neonatal respiratory failure and the therapeutic approach of PPHN. It was shown, first in experimental animals then in a few infants with hypoxemic respiratory failure, that NO inhalation selectively vasodilated the vasoconstricted pulmonary vessels, and reversed right-to-left shunting and refractory hypoxemia. Whether inhaled NO also reduces mortality and/or morbidity in hypoxic infants remains to be proven by appropriate randomized clinical trials. However, not only PPHN is associated with pulmonary diseases of various etiologies and underlying pathophysiologic mechanisms, but also inhaled NO is used in conjunction with other validated therapeutic strategies including ante- or postnatal steroids, exogenous surfactants, and high-frequency oscillatory ventilation. Thus, the relevant primary endpoint might be not only crude survival but the most physiological and economical way of obtaining it.

Administration, Inhalation↗
PubMed1989

Misalignment of lung vessels and alveolar capillary dysplasia: a cause of persistent pulmonary hypertension.

Two infants with fatal persistent pulmonary hypertension are described. Morphologically there was misalignment of the lung vessels, with the veins and the arterioles anomalously related, often sharing the same adventitial sheet. The capillaries did not make contact with the alveolar epithelium. The arterioles had increased medial muscle, and there was extension of the arteriolar muscularization to the precapillary level. The fraction of the parenchyma that was septal and connective tissue was increased. The acini had a decreased complexity, with immature alveoli and with a decreased radial alveolar count. The cause appeared to be related to abnormal capillary and venous plexus formation and migration. This syndrome seems to be identical with that described in three previous reports and probably represents a specific cause of persistent pulmonary hypertension.

Arterioles↗
PubMed1993

Inhaled nitric oxide: its effects on pulmonary circulation and airway smooth muscle cells.

Nitric oxide (NO), an endothelium-derived relaxing factor synthesized from L-arginine by the enzyme NO synthase, has been identified as an important, short-acting, endogenous vasodilator. In patients with pulmonary hypertension, inhaling a low dose of NO as a gaseous vasodilator has been shown to induce selective vasodilation in ventilated lung areas. It achieves this without the disadvantages attributed to systemically infused vasodilators e.g. systemic vasodilation and an increase in pulmonary right-to-left shunt with a consecutive fall in PaO2. Thus, inhaled NO reduces pulmonary hypertension in the severe adult respiratory distress syndrome and in persistent pulmonary hypertension of the newborn, and improves arterial oxygenation by redistributing pulmonary blood flow away from the shunt and towards areas with almost normal ventilation/perfusion ratios. The bronchodilatory effect of NO may be an alternative therapy for treating asthma and bronchospasm.

Administration, Inhalation↗
PubMed1979

Primary pulmonary hypoplasia in the neonate.

Infants with primary pulmonary hypoplasia with respiratory distress immediately after birth, but usually elude early diagnosis. They have no other abnormalities, but frequently develop signs and symptoms of the PFC syndrome. Roentgenographically, they show small, clear lungs and are prone to develop complicating pneumothoraces. The clinical, roentgenographic, and pathologic features of eight infants with primary pulmonary hypoplasia are presented.

Humans↗
PubMed2004

Maternal, neonatal, and placental features associated with diffuse chorioamniotic hemosiderosis, with special reference to neonatal morbidity and mortality.

OBJECTIVE: Our purpose was to examine the significance of diffuse chorioamniotic hemosiderosis (DCH) on neonatal morbidity and mortality. METHODS: Using data from a retrospective case-control study, we analyzed 46 singleton placentas with DCH from infants who were delivered and/or admitted to the neonatal intensive care unit of Kanagawa Children's Medical Center during 1987-2001 and 92 control placentas without DCH from infants of comparable gestational age, birth weight, and duration. RESULTS: Mean and standard deviation of gestational age and infants' birth weight at delivery from the DCH group were 27 +/- 3 weeks and 939 +/- 342 g, respectively. Macroscopically, the placentas with DCH were more likely to show old peripheral blood clots (46% in the DCH group vs 8% in control group), subchorionic hematoma (20% vs 1%), and circumvallation (13% vs 1%). Histologically, amniotic necrosis was significantly more frequent in the DCH group (63% vs 24%). Of the obstetric factors, incidence of recurrent episodes of vaginal bleeding (70% vs 11%), oligohydramnios (59% vs 8%), and chronic abruption-oligohydramnios sequence (57% vs 5%) were significantly higher in the DCH group. Of the neonatal factors, persistent pulmonary hypertension of the newborn (29% vs 8%) and dry lung and/or pulmonary hypoplasia (20% vs 4%) were more common. However, respiratory distress syndrome was rare (15% vs 45%) in the DCH group. Neonatal death including stillbirth was increased in the DCH group but was not significant (24% vs 15%). Of infants who survived beyond day 28, chronic lung disease (CLD) was more frequent in the DCH group (51% vs 22%). The association of DCH, especially accompanied by amniotic necrosis, with CLD was still evident using likelihood ratio test. CONCLUSION: DCH is closely associated with preterm delivery, pulmonary hypertension of the newborn, and dry lung syndrome and is a significant risk factor for CLD.

Abruptio Placentae↗
PubMed2004

High frequency oscillatory ventilation in acute respiratory failure.

High frequency oscillatory ventilation (HFOV) has emerged over the past 20 years as a safe and effective means of mechanical ventilatory support in patients with acute respiratory failure. During HFOV, lung recruitment is maintained by application of a relatively high mean airway pressure with superimposed pressure oscillations at a frequency of 3 to 15Hz, creating adequate ventilation using tidal volumes less than or equal to the patient's dead space volume. The physiologic rationale for the application of HFOV in the clinical arena comes from its ability to preserve end-expiratory lung volume while avoiding parenchymal overdistension at end-inspiration and theoretically limiting the potential for ventilator-associated lung injury. Data in the neonatal population suggests significant benefits in pulmonary outcomes when HFOV is applied with a recruitment strategy in preterm infants with respiratory distress syndrome (RDS). Use of HFOV in the paediatric and adult populations has not as yet been associated with significant improvements in clinically important outcome measures.

Acute Disease↗
PubMed2004

Bench-to-bedside review: Ventilator strategies to reduce lung injury -- lessons from pediatric and neonatal intensive care.

As in the adult with acute lung injury and acute respiratory distress syndrome, the use of lung-protective ventilation has improved outcomes for neonatal lung diseases. Animal models of neonatal respiratory distress syndrome and congenital diaphragmatic hernia have provided evidence that 'gentle ventilation' with low tidal volumes and 'open-lung' strategies of using positive end-expiratory pressure or high-frequency oscillatory ventilation result in less lung injury than do the traditional modes of mechanical ventilation with high inflating pressures and volumes. Although findings of retrospective studies in infants with respiratory distress syndrome, congenital diaphragmatic hernia, and persistent pulmonary hypertension of the newborn have been similar to those of the animal studies, prospective, randomized, controlled trials have yielded conflicting results. Successful clinical trial design in these infants and in children with acute lung injury/acute respiratory distress syndrome will require an appreciation of the data supporting the modern ventilator management strategies for infants with lung disease.

Adult↗
PubMed1998

Clinical response to inhaled nitric oxide in persistent pulmonary hypertension of the newborn.

We observed clinical response to inhaled nitric oxide (iNO) in 12 neonates with persistent pulmonary hypertension of the newborn (PPHN). Clinical response was defined as a decrease in oxygenation index (OI) by 40%. Ten of 12 neonates had response to iNO showing decrease OI from 46.1+/-7.6 to 14.4+/-6.8 at 1 hour after inhalation. Sustained improvement of OI was achieved in 8 neonates and two neonates were relapsed. In the group of neonates who had OI above 40 (n=7), 6 of them showed the decrease of OI from 66.1+/-4.8 to 18.3+/-8.0 at 1 hour. In two groups, one had OI of 40 or greater, and the other OI of 40 or less, there were no differences in pattern of response and early death rate. The response rates according to underlying diseases were as follows; idiopathic PPHN 100%, respiratory distress syndrome 100%, and diaphragmatic hernia 66.7%. Relapse was observed in one neonate with sepsis caused by pneumonia and in one infant with meconium aspiration syndrome. Two infants showed no response to iNO (one diaphragmatic hernia and one suspected pulmonary hypoplasia). We conclude that iNO therapy could improve oxygenation in high percentage of newborn infants with severe PPHN of various underlying conditions except pulmonary hypoplasia.

Administration, Inhalation↗
PubMed1998

The use of inhaled nitric oxide in a wide variety of clinical problems.

Inhaled nitric oxide (NO) clearly decreased pulmonary vascular resistance in pediatric patients with pulmonary hypertension, regardless of the underlying origin of the pulmonary hypertension. In persistent pulmonary hypertension of the neonate (PPHN) and CHD, the use of inhaled NO appears to improve the outcome of these patients. In acute respiratory distress syndrome (ARDS) and surfactant deficiency the role of inhaled NO therapy remains unclear. The use of inhaled NO is safe in a carefully monitored setting with a delivery system designed to minimize the generation of NO2.

Administration, Inhalation↗