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PubMed1997

Randomized, multicenter trial of inhaled nitric oxide and high-frequency oscillatory ventilation in severe, persistent pulmonary hypertension of the newborn.

BACKGROUND: Although inhaled nitric oxide (iNO) causes selective pulmonary vasodilation and improves oxygenation in newborn infants with persistent pulmonary hypertension, its effects are variable. We hypothesized (1) that the response to iNO therapy is dependent on the primary disease associated with persistent pulmonary hypertension of the newborn (PPHN) and (2) that the combination of high-frequency oscillatory ventilation (HFOV) with iNO would be efficacious in patients for whom either therapy alone had failed. METHODS: To determine the relative roles of iNO and HFOV in the treatment of severe PPHN, we enrolled 205 neonates in a randomized, multicenter clinical trial. Patients were stratified by predominant disease category: respiratory distress syndrome (n = 70), meconium aspiration syndrome (n = 58), idiopathic PPHN or pulmonary hypoplasia (excluding congenital diaphragmatic hernia) ("other": n = 43), and congenital diaphragmatic hernia (n = 34); they were then randomly assigned to treatment with iNO and conventional ventilation or to HFOV without iNO. Treatment failure (partial pressure of arterial oxygen [PaO2] < 60 mm Hg) resulted in crossover to the alternative treatment; treatment failure after crossover led to combination treatment with HFOV plus iNO. Treatment response with the assigned therapy was defined as sustained PaO2 of 60 mm Hg or greater. RESULTS: Baseline oxygenation index and PaO2 were 48 +/- 2 and 41 +/- 1 mm Hg, respectively, during treatment with conventional ventilation. Ninety-eight patients were randomly assigned to initial treatment with HFOV, and 107 patients to iNO. Fifty-three patients (26%) recovered with the initially assigned therapy without crossover (30 with iNO [28%] and 23 with HFOV [23%]; p = 0.33). Within this group, survival was 100% and there were no differences in days of mechanical ventilation, air leak, or supplemental oxygen requirement at 28 days. Of patients whose initial treatment failed, crossover treatment with the alternate therapy was successful in 21% and 14% for iNO and HFOV, respectively (p = not significant). Of 125 patients in whom both treatment strategies failed, 32% responded to combination treatment with HFOV plus iNO. Overall, 123 patients (60%) responded to either treatment alone or combination therapy. By disease category, response rates for HFOV plus iNO in the group with respiratory syndrome and the group with meconium aspiration syndrome were better than for HFOV alone or iNO with conventional ventilation (p < 0.05). Marked differences in outcomes were noted among centers (percent death or treatment with extracorporeal membrane oxygenation = 29% to 75%). CONCLUSIONS: We conclude that treatment with HFOV plus iNO is often more successful than treatment with HFOV or iNO alone in severe PPHN. Differences in responses are partly related to the specific disease associated with PPHN.

Administration, Inhalation↗
PubMed1992

ECMO in newborn infants: the New South Wales experience.

Extracorporeal membrane oxygenation (ECMO) has been used at the Prince of Wales Children's Hospital, Sydney for the treatment of newborn infants with life-threatening respiratory or cardiac failure since August 1989. The main indications are that the disease is reversible, the surviving infant is likely to be normal and there is an 80% likelihood of death without ECMO. Eighteen of 19 newborn infants have survived at least 2 months after ECMO. The 15 infants receiving ECMO (nine with meconium aspiration, six with persisting pulmonary hypertension) who did not have a congenital diaphragmatic hernia were normal survivors. One death occurred at 5 months of age from chronic lung disease. Three of four infants with congenital diaphragmatic hernia were discharged following ECMO and appeared normal at 6, 9 and 18 months of age. These results are similar to results from other centres internationally. It appears that ECMO is a useful therapy for near-term newborn infants with otherwise fatal cardiorespiratory failure.

Extracorporeal Membrane Oxygenation↗
PubMed2002

A 16-year neonatal/pediatric extracorporeal membrane oxygenation transport experience.

OBJECTIVE: To characterize the population and survival of neonatal and pediatric patients transported by Wilford Hall Medical Center (WHMC) on extracorporeal membrane oxygenation (ECMO) since 1985. STUDY DESIGN: A retrospective chart, literature, and database review of pediatric and neonatal patients transported on ECMO by the WHMC ECMO transport team. In addition, a subpopulation analysis was performed comparing neonates with meconium aspiration syndrome (MAS) placed on ECMO at WHMC with those infants with MAS transported on ECMO. Characteristics of interest for this comparison included disease severity before ECMO, age at initiation of ECMO, survival, ECMO-related complications, and duration of ECMO support. RESULTS: Forty-two patients transported on ECMO were identified: 23 neonatal respiratory cases (survival 57%), 7 pediatric respiratory cases (survival 71%), 4 cardiac cases (survival 50%), and 8 extra-institutional ECMO transports (survival 63%). In the MAS subpopulation, there was significantly greater survival in the in-house group--97% (31/32)--than in the ECMO transport group--75% (9/12); there were no other significant differences between these groups. Overall, no ECMO-related complications leading to patient demise could be identified in the ECMO transport group. CONCLUSIONS: ECMO transport, although demonstrating acceptable survival, is a risk-laden modality that should not replace early referral to an ECMO center.

Extracorporeal Membrane Oxygenation↗
PubMed1998

Disease-related response to inhaled nitric oxide in newborns with severe hypoxaemic respiratory failure. French Paediatric Study Group of Inhaled NO.

Inhaled nitric oxide (iNO) has been shown to improve oxygenation in severe persistent pulmonary hypertension of the newborn (PPHN). However, PPHN is often associated with various lung diseases. Thus, response to iNO may depend upon the aetiology of neonatal acute respiratory failure. A total of 150 (29 preterm and 121 term) newborns with PPHN were prospectively enrolled on the basis of oxygenation index (OI) higher than 30 and 40, respectively. NO dosage was stepwise increased (10-80 ppm) during conventional mechanical or high-frequency oscillatory ventilation while monitoring the oxygenation. Effective dosages ranged from 5 to 20 ppm in the responders, whereas iNO levels were unsuccessfully increased up to 80 ppm in the nonresponders. Within 30 min of iNO therapy, OI was significantly reduced in either preterm neonates (51+/-21 vs 23+/-17, P < .0001) or term infants with idiopathic or acute respiratory distress syndrome (45+/-20 vs 20+/-17, P < .0001), 'idiopathic' PPHN (39+/-14 vs 14+/-9, P < .0001), and sepsis (55+/-25 vs 26+/-20, P < .0001) provided there was no associated refractory shock. Improvement in oxygenation was less significant and sustained (OI=41+/-16 vs 28+/-18, P < .001) in term neonates with meconium aspiration syndrome and much less (OI=58+/-25 vs 46+/-32, P < .01) in those with congenital diaphragmatic hernia. Only 21 of the 129 term newborns (16%) required extracorporeal membrane oxygenation (57% survival). Survival was significantly associated with the magnitude in the reduction in OI at 30 min of iNO therapy, a gestational age > or =34 weeks, and associated diagnosis other than congenital diaphragmatic hernia. Conclusion, iNO improves the oxygenation in most newborns with severe hypoxaemic respiratory failure including preterm neonates. However, response to iNO is disease-specific. Furthermore, iNO when combined with adequate alveolar recruitment and limited barotrauma using exogenous surfactant and HFOV may obviate the need for extracorporeal membrane oxygenation in many term infants.

Administration, Inhalation↗
PubMed1986

Misalignment of lung vessels: a syndrome causing persistent neonatal pulmonary hypertension.

The cases of two female infants with persistent neonatal pulmonary hypertension are described. Combinations of pulmonary parenchymal lesions were present, including underdevelopment of alveoli and interstitial fibrosis as well as misalignment of lung vessels. As a result of the misalignment, the pulmonary veins joined the pulmonary arteries, rather than following a course away from them. One of the infants had additional congenital malformations. This syndrome should be considered in the evaluation of infants with persistent fetal circulation.

Female↗
PubMed1992

ECMO in newborn infants: the Melbourne experience.

At the Royal Children's Hospital, Melbourne, extracorporeal membrane oxygenation (ECMO) has been used in the treatment of newborn infants with life-threatening respiratory or cardiac failure since May 1989. The main indications for the use of ECMO are that the disease is reversible, the surviving infant is likely to be normal and there is an 80% likelihood of death without ECMO. Sixteen of 22 (73%) newborn infants have survived at least 6 months after ECMO. Fourteen of 16 (87.5%) infants receiving ECMO (who did not have a congenital diaphragmatic hernia) were functionally normal survivors; the other two infants died. Two of six infants with congenital diaphragmatic hernia who received ECMO were discharged and survived to have normal neurological and respiratory function at 6 month follow up. These results are similar to results from other centres internationally. It would appear that ECMO is a useful therapy for near-term newborn infants with otherwise fatal cardiorespiratory failure.

Australia↗
PubMed2005

Neonatal persistent pulmonary hypertension treated with milrinone: four case reports.

Current standard therapy for persistent pulmonary hypertension of the newborn (PPHN) consists of optimal lung inflation, hemodynamic support and selective vasodilation with inhaled nitric oxide (iNO). However, not all infants will respond. Milrinone, a phosphodiesterase (PDE) III inhibitor, is routinely used in pediatric cardiac intensive care units to improve inotropy and reduce afterload. Although its use in post-operative cardiac failure has been proven in a randomized trial, it has not been reported to be beneficial in PPHN. We report four cases with severe PPHN treated with a combination of iNO and Milrinone. All four cases were unresponsive to therapy including iNO, with a mean oxygenation index (OI) of 40 (standard deviation (SD) 12)) before Milrinone. Substantial improvement in OI (mean of 28; SD 16) was followed by extubation and survival. However, of 4 patients, 2 developed serious intraventricular hemorrhages (IVHs), and 1 had a small IVH. To clarify the risk benefit ratio, of death versus survival with impairment, a randomized controlled trial is needed.

Administration, Inhalation↗
PubMed1982

Eisenmenger syndrome in pregnancy: a possible cause of neonatal polycythemia and persistent fetal circulation.

A 23-year-old white primigravid woman with Eisenmenger syndrome and hypoxemia was delivered of a male infant at 34 weeks' gestation after spontaneous onset of labor. The infant was small for gestational age, weighing 1670 g. He subsequently developed respiratory distress and was found to have a high hematocrit with clinical and echocardiographic evidence of persistent fetal circulation. After partial exchange transfusion with plasma, the hematocrit, pulmonary vascular resistance, and arterial oxygen tension became normal. The authors suggest that chronic maternal hypoxemia during pregnancy may cause polycythemia and increased pulmonary vascular resistance in the newborn, leading to persistent fetal circulation.

Eisenmenger Complex↗
PubMed1989

The pulmonary vasculature in meconium aspiration.

Some studies have suggested that pulmonary hypertension in the newborn with meconium aspiration can be attributed to a primary prenatal increase in pulmonary arterial musculature; but this concept has been controversial. To examine this question, we reviewed 62 infants autopsied at The Johns Hopkins Hospital, 24 of whom demonstrated meconium aspiration, 20 with meconium staining but no aspiration, and 18 with abruptio placentae without meconium aspiration or staining. Clinical and pathologic features were evaluated and cross-sectional arterial medial area was determined at the junction of the conducting and respiratory airways in nondistended lungs. No significant difference in arterial medial area was found between infants with meconium aspiration and those with meconium staining only or abruptio placentae. In addition, circumferentially muscularized intraacinar arteries were present in all infants with meconium aspiration and abruptio placentae, and all but one infant with meconium staining alone. Comparison of lungs with and without arterial injection and fixation in distention showed that injection does not uniformly distend vessels and that formalin distention may remove or mask meconium. The study suggests that meconium aspiration and its complications, not primary structural arterial changes, account for pulmonary hypertension in infants with meconium aspiration.

Arterioles↗
PubMed1991

Possible causes linking asphyxia, thick meconium and respiratory distress.

The cause of fetal distress and neonatal respiratory distress (RD) in association with meconium-stained liquor is not always clear. To clarify this, a prospective study was undertaken in a tertiary referral maternity hospital for 1 year. In all infants born after meconium-stained liquor who developed RD, evidence was sought for 1) fetal distress (from the cardiotocograph (CTG), the cord blood pH, the Apgar score and the asphyxial complications in the neonate) 2) causes of fetal distress (including maternal risk factors, fetal infection and fetal malnutrition) 3) causes of respiratory distress (including meconium aspiration syndrome (MAS), persistent pulmonary hypertension of the newborn (PPHN) and infection). Of 4,026 livebirths, 717 (17.8%) had meconium-stained liquor and 44 term and 5 preterm infants developed RD. In the 44 term infants, there was frequent evidence of fetal distress possibly caused by previously unrecognized factors such as fetal malnutrition with reduced neonatal skinfold thickness in 35% triceps and 41% subscapular measurements, and histological chorioamnionitis (CA) in 74%. The cause for respiratory distress was identified in only 48% of infants, and included clinical evidence of PPHN (41%), MAS (16%) and infection (2%). However in preterm infants, 80% had definite or suspected infection. The findings indicate that fetal distress is common in infants who develop respiratory distress after meconium-stained liquor. A role for histological CA and reduced nutrition in the fetus, as factors contributing to the vulnerability of the term infant to intrapartum fetal distress, is suggested.

Apgar Score↗
PubMedDate not supplied

Neonatal ECMO: Current controversies and trends.

Extracorporeal membrane oxygenation (ECMO), a technique for providing life support to patients with cardiac and/or respiratory dysfunction, allows the heart and lungs to "rest." The neonatal respiratory population has been a major benefactor of ECMO since 1982. Its use for neonatal respiratory disease increased dramatically until the past few years, when the number of neonatal respiratory ECMO cases began a downward trend. Fewer patients with persistent pulmonary hypertension of the newborn (PPHN), meconium aspiration syndrome, respiratory distress syndrome, or sepsis are requiring ECMO support as frequently as in the past. Many attribute this decline to the newer respiratory therapies-mainly, surfactant, high-frequency oscillatory ventilation, and inhaled nitric oxide. Neonates who continue to require ECMO today are sicker than the historic norm and have more complicated and lengthy ECMO runs. Patients with congenital diaphragmatic hernia, PPHN, and sepsis remain the most consistent in their representation among ECMO recipients within this author's institution, suggesting that the newer respiratory therapies have not had the same impact on these patients' needs for ECMO support. Better guidelines for determining which patients would benefit from earlier inititation of ECMO are needed.

Administration, Inhalation↗
PubMed2001

[Persistent pulmonary hypertension in newborn infants].

BACKGROUND: Persistent pulmonary hypertension of the newborn is a clinical syndrome caused by failure in the transition from fetal to neonatal circulation either to achieve or to maintain low pulmonary vascular resistance after birth. The syndrome is a complex condition associated with different cardiopulmonary disorders. METHODS: This article presents a review of the literature and the author's own experience regarding the fetal circulation, the transition to the newborn circulation, and the mechanical and molecular regulatory factors, including a discussion of the pathophysiology, aetiology, diagnostics and main goal of treatment for persistent pulmonary hypertension of the newborn. RESULTS: The pathophysiology of persistent pulmonary hypertension is characterised by high pulmonary vascular resistance and high pulmonary artery pressure. The blood is shunted from the right to the left circuit through the foramen ovale, ductus arteriosus and also by intrapulmonal shunts. The aetiologies can be classified as underdevelopment, maldevelopment and maladaptation of the pulmonary vasculature. The clinical signs are hypoxaemia, higher oxygenation tension and saturation in the upper rather than the lower limbs, respiratory failure, systemic hypotension and systolic cardiac murmur. The differential diagnoses are primarily serious lung disorders without persistent pulmonary hypertension, and congenital cyanotic heart defects. The diagnostic investigations are blood gas analysis, X-ray of the lung, and Doppler echocardiographic examination of the heart. INTERPRETATION: The main treatment goal is good oxygenation, pH in upper normal and pCO2 in lower normal levels. Positive pressure ventilation, sedation, NO gas inhalation and supporting treatment of the systemic blood pressure are usually necessary. Extracorporeal membrane oxygenation is considered as a last option.

Diagnosis, Differential↗
PubMed1981

Extracorporeal membrane oxygenation. Successful treatment of persistent fetal circulation following repair of congenital diaphragmatic hernia.

Four neonates (three having undergone repair of a congenital diaphragmatic hernia and developing a persistent fetal circulatory pattern and one having severe infant respiratory distress syndrome) have been supported with prolonged extracorporeal membrane oxygenation (ECMO) at Children's Hospital of Pittsburgh between December of 1979 and April of 1980. Three have survived. This encouraging experience indicates that the pattern of persistent fetal circulation in the newborn infant who has undergone repair of a diaphragmatic hernia can be successfully managed with ECMO even when efforts to lower pulmonary hypertension and improve oxygenation with vasodilators (tolazoline, phenothiazine, acetylcholine, or prostaglandin E1) and have been ineffective. The effectiveness and safety of ECMO is convincing enough to warrant its consideration as therapy for congenital diaphragmatic hernia and persistent fetal circulation prior to the use of vasodilators.

Blood Flow Velocity↗
PubMedDate not supplied

Persistent pulmonary hypertension of the newborn: experience in a single institution.

Persistent pulmonary hypertension of the newborn (PPHN) remains one of the most challenging situations in the neonatal intensive care unit, and it is associated with high mortality and morbidity. The optimal treatment for PPHN is controversial. We report our 9-year experience in the management of PPHN through a retrospective review of 29 neonates with persistent pulmonary hypertension. The diagnosis of PPHN is made by echocardiography and/or preductal and postductal oxygen tension difference. The treatment modalities include supportive medical care, vasodilator therapy, mechanical ventilation and correction of underlying conditions. The wide diversity of etiologies of PPHN, the complications of vasodilator therapy, the management of assisted ventilation, the mortality and the morbidity are evaluated. There are 29 patients enrolled in this study, including 18 male and 11 female babies. Twenty-two patients (72%) are referred from other hospitals. The mean birth body weight is 2707 +/- 693 grams (range: 1450-4100 grams) and the mean gestational age is 37.1 +/- 3.1 weeks (range: 31-41 weeks). The underlying clinical conditions include meconium aspiration syndrome (n = 8), perinatal asphyxia (n = 7), respiratory distress syndrome (n = 5), sepsis and/or pneumonia (n = 4), congenital diaphragmatic hernia (n = 3) and idiopathic persistent fetal circulation (n = 2). In addition to supportive medical care and correction of underlying clinical conditions, most of the patients receive vasodilator therapy (Tolazoline) and nonhyperventilation respirator management. The overall mortality rate is 27.6% (8/29). The duration on ventilator therapy in the survival group (9.3 +/- 8.6 days) is not significantly different from in the mortality group (6.0 +/- 7.1 days) (p = 0.13). There is also no statistically significant difference between these two groups both in the maximal alveolar-arterial oxygen tension difference (594 +/- 53 mmHg and 613 +/- 37 mmHg, p = 0.145) and in the maximal oxygenation index (49.7 +/- 29.6 and 61.1 +/- 36.9, p = 0.172) before vasodilator therapy. However, twenty-four hours after treatment, these two parameters change significantly with the former changes to 426 +/- 198 mmHg and 643 +/- 7 mmHg, respectively (p < 0.001), and the latter changes to 21.6 +/- 15.8 and 82.3 +/- 54.8, respectively (p < 0.001). Skin rash, gastrointestinal hemorrhage, hypotension and hyponatremia are the most common complications of Tolazoline therapy. Eight patients have pulmonary complications including pneumothorax (n = 5) and pulmonary interstitial emphysema (n = 3). Two patients develop chronic lung disease. Three patients have neurodevelopmental handicap. In conclusion, we achieve a survival rate of nearly 75% in PPHN mainly with the administration of Tolazoline therapy and the nonhyperventilation respirator approach. Further well-controlled and multicenter studies with newer treatment modalities are crucial for the improvement of survival of PPHN in Taiwan.

Arachidonic Acid↗
PubMed2003

Iloprost in persistent pulmonary hypertension of the newborn.

Aerosolized iloprost is now used as a therapeutic option in the treatment of pulmonary hypertension. We report on the administration of this derivative of prostacycline in treating severe pulmonary hypertension of the newborn. The combination of iloprost instilled endotracheally and inhaled was chosen as a last attempt at treatment in a critically ill patient who did not respond to advanced conventional treatments, including high frequency oscillation and inhalation of nitric oxide. The use of iloprost converted permanently the right-to-left shunting, leading to a substantial improvement in oxygenation.

Administration, Inhalation↗
PubMed1997

Inhaled nitric oxide in full-term and nearly full-term infants with hypoxic respiratory failure.

BACKGROUND: Neonates with pulmonary hypertension have been treated with inhaled nitric oxide because of studies suggesting that it is a selective pulmonary vasodilator. We conducted a randomized, multicenter, controlled trial to determine whether inhaled nitric oxide would reduce mortality or the initiation of extracorporeal membrane oxygenation in infants with hypoxic respiratory failure. METHODS: Infants born after a gestation of > or =34 weeks who were 14 days old or less, had no structural heart disease, and required assisted ventilation and whose oxygenation index was 25 or higher on two measurements were eligible for the study. The infants were randomly assigned to receive nitric oxide at a concentration of 20 ppm or 100 percent oxygen (as a control). Infants whose partial pressure of arterial oxygen (PaO2) increased by 20 mm Hg or less after 30 minutes were studied for a response to 80-ppm nitric oxide or control gas. RESULTS: The 121 infants in the control group and the 114 in the nitric oxide group had similar base-line clinical characteristics. Sixty-four percent of the control group and 46 percent of the nitric oxide group died within 120 days or were treated with extracorporeal membrane oxygenation (P=0.006). Seventeen percent of the control group and 14 percent of the nitric oxide group died (P not significant), but significantly fewer in the nitric oxide group received extracorporeal membrane oxygenation (39 percent vs. 54 percent, P=0.014). The nitric oxide group had significantly greater improvement in PaO2 (increase, 58.2+/-85.2 mm Hg, vs. 9.7+/-51.7 mm Hg in the controls; P<0.001) and in the oxygenation index (a decrease of 14.1+/-21.1, vs. an increase of 0.8+/-21.1 in the controls; P<0.001). The study gas was not discontinued in any infant because of toxicity. CONCLUSIONS: Nitric oxide therapy reduced the use of extracorporeal membrane oxygenation, but had no apparent effect on mortality in critically ill infants with hypoxic respiratory failure.

Administration, Inhalation↗