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PubMed1980

High pulmonary vascular resistance after birth: I. Pathophysiologic considerations and etiologic classification.

The clinical syndrome known as persistent fetal circulation, or persistent pulmonary hypertension of the newborn, is characterized by maintenance of a high pulmonary vascular resistance after birth. The small pulmonary arteries of the fetus have a thick muscular medial layer; they are very reactive, being actively constricted by the low PO2 levels normally present during fetal life. The pulmonary vascular smooth muscle layer is hypertrophied in conditions that result in chronic fetal hypoxia, or a maintained increase in pulmonary arterial pressure. Normally, pulmonary vasodilation occurs rapidly after birth, partly related to physical expansion with gas, but mainly due to the increased PO2 associated with ventilation with air. Based on these developmental considerations, the factors responsible for an increased pulmonary vascular resistance after birth may be classified in three main groups: (A) Acute vasoconstriction due to postnatal hypoxia and aggravated by acidemia; (B) Prenatal increase in pulmonary vascular smooth muscle development; and (C) Decreased cross sectional area of the pulmonary vascular bed due to inadequate numbers of vessels. The various mechanisms that may promote these responses are presented.

Animals↗
PubMed2001

Steroids in full term infants with respiratory failure and pulmonary hypertension due to meconium aspiration syndrome.

Persistent pulmonary hypertension of the newborn (PPHN) due to meconium aspiration syndrome (MAS), has a high morbidity and mortality especially in centres with limited access to extra-corporeal membrane oxygenation or nitric oxide therapy. In such a setting, we conducted a pilot study to evaluate the effect of dexamethasone on severe respiratory failure with PPHN due to MAS with a view to exploring possible justification for randomised controlled trials in similar patients. We prospectively managed a consecutive case series of 14 infants over a 3-year period with the above mentioned diagnosis, who were ventilated and with an oxygenation index >25. Dexamethasone was commenced in a dose of 0.5 mg/kg per day and given for up to a maximum of 9 days in a reducing schedule. Differences between time points were analysed using analysis of variance for repeated measures. The mean age of commencing dexamethasone was 79.9 h. There was a rapid, significant improvement (P < 0.05) in the respiratory status in 13 of these infants after commencing dexamethasone, allowing weaning from the ventilator and eventual extubation at a mean age of 8.7 days. One infant died. Two infants had infective episodes. Conclusion. Dexamethasone, if started early in infants with respiratory failure and persistent pulmonary hypertension of the newborn due to meconium aspiration syndrome may be effective in improving gas exchange, and possibly avoiding extra-corporeal membrane oxygenation. A randomised controlled trial of using dexamethasone early in similar patients and setting is warranted.

Analysis of Variance↗
PubMed1994

Failure of acute perinatal asphyxia or meconium aspiration to produce persistent pulmonary hypertension in a neonatal baboon model.

OBJECTIVE: Our purpose was to determine whether perinatal asphyxia or meconium aspiration, or both, can produce the physiologic and histologic pulmonary vascular changes associated with the meconium aspiration syndrome. STUDY DESIGN: Twenty neonatal baboons were studied in four groups: 1, control; 2, meconium aspiration; 3, asphyxia (intermittent cord compression); and 4, asphyxia with meconium aspiration. Animals were ventilated for 24 hours under ketamine, diazepam, and pancuronium. Data were analyzed by means of mixed model analysis of measures. RESULTS: Meconium significantly impaired oxygenation (p < 0.001), whereas concurrent asphyxia moderated this effect (p < 0.034). Meconium also increased the need for ventilatory support (p < 0.002). No animal had persistent pulmonary hypertension; neither systemic nor pulmonary systolic pressures differed statistically between the groups. No animal showed evidence of abnormal pulmonary arteriolar muscularization. CONCLUSION: Sublethal perinatal asphyxia or meconium aspiration were insufficient to produce either the physiologic or histologic changes of severe meconium aspiration syndrome. It is unlikely that intrapartum fetal distress alone can produce this syndrome in human neonates.

Acute Disease↗
PubMed1999

[Two cases of newborns with persistent pulmonary hypertension syndrome -- difficulties in diagnosis and treatment].

The persistent pulmonary hypertension syndrome is a heavy and very often a lethal complication in the neonatal period. It is more common in full-term infants with perinatal asphyxia, meconium aspiration or inborn infection. We discuss two clinical cases of newborns, delivered by Caesarian section in the 38th week of gestation without history of prenatal asphyxia or inborn infection. The main clinical symptom was a progressive lung failure that finally lead to mechanical ventilation. Both infants had clinical symptoms of pulmonary hypertension and intracranial hemorrhages (proved by ultrasound). During autopsy, bilateral pneumonia and intracranial hemorrhages were found in both infants and in one of them meconium aspiration and suprarenal gland hemorrhages were proven. In conclusion we may say that the diagnosis of persistent pulmonary hypertension is often very difficult and the conventional methods of mechanical ventilation and medicament treatment cannot always prevent the infant's lethal outcome.

Adrenal Gland Diseases↗
PubMed1991

Plasma prostanoids in neonatal extracorporeal membrane oxygenation. Influence of meconium aspiration.

Thromboxane B2 may be a mediator of neonatal persistent pulmonary hypertension. Elevated levels of plasma thromboxane and prostacyclin have been described previously in hypoxic newborn infants with neonatal pulmonary hypertension. We measured serial plasma levels of thromboxane B2 and 6-keto-prostaglandin F1 alpha (stable metabolite of prostacyclin) in 21 newborn infants with severe respiratory failure and pulmonary hypertension who required extracorporeal membrane oxygenation support. We sought to study (1) the evolution of plasma prostanoids in pulmonary hypertensive infants treated with extracorporeal membrane oxygenation and (2) whether different pulmonary hypertensive diagnostic subgroups have distinctive prostanoid profiles. Our data indicated that infants with meconium aspiration had significantly lower levels of plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha while receiving extracorporeal membrane oxygenation than did infants with persistent pulmonary hypertension but no meconium aspiration. Levels of all infants decreased progressively as extracorporeal membrane oxygenation support continued.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Venovenous compares favorably with venoarterial access for extracorporeal membrane oxygenation in neonatal respiratory failure.

Traditional extracorporeal membrane oxygenation via the venoarterial route requires cannulation and ligation of the internal jugular vein and common carotid artery. Concerns about ligation of the common carotid artery prompted development of a 14F double-lumen internal jugular vein cannula for venovenous oxygenation for neonates with respiratory failure. We retrospectively compared 22 patients supported by venovenous bypass and 20 patients supported with traditional venoarterial bypass. The two groups of patients were selected to be comparable in terms of diagnosis and severity of respiratory insufficiency. The diagnoses in both groups were limited to meconium aspiration syndrome or persistent pulmonary hypertension of the newborn. The average oxygenation indexes in the two groups were similar (46.6 venovenous, 47.2 venoarterial, p = not significant). Venovenous access allowed flow rates of more than 100 ml/kg per minute, which were adequate for gas exchange support. One patient required conversion from venovenous to venoarterial bypass because of hemodynamic instability. The average time of bypass support was 115 hours (range 24 to 338 hours) for venovenous bypass and 134 hours (range 47 to 361 hours) for venoarterial bypass (p < 0.05). The time to extubation after decannulation from extracorporeal membrane oxygenation was 133 hours (range 38 to 720 hours) for venovenous support and 100 hours (range 27 to 192 hours) for venoarterial support (p = not significant). One patient supported with venoarterial bypass had an intracranial hemorrhage. There were no documented neurologic injuries in the patients managed with venovenous bypass. There were no deaths in either group. Venovenous extracorporeal membrane oxygenation through a double-lumen cannula can adequately provide respiratory support for neonates with pulmonary failure and effectively avoids ligation of the common carotid artery.

Carotid Artery, Common↗
PubMed1988

High-frequency oscillatory ventilation combined with intermittent mandatory ventilation in critically ill neonates: 3 years of experience.

A heterogeneous group of 45 neonates with severe pulmonary disease and inadequate gas exchange on conventional intermittent mandatory ventilation (IMV) was treated with a high-frequency oscillator combined with an IMV (HFO-IMV) system (Emerson Airway Vibrator connected to a BABYBird 1 ventilator). The mean gestational age was 33 weeks (25.5-43) and mean birth weight 2.02 kg (0.66-4.24). Primary diagnoses included respiratory distress syndrome (RDS; 23), pneumonia (12), persistent fetal circulation (PFC; 6), diaphragmatic hernia/hypoplastic lungs (4). The IMV rate was reduced from 78 to 29 BPM (P less than or equal to 0.0005), while maintaining lower partial pressure of carbon dioxide (PaCO2) (P less than 0.005) and higher partial pressure of oxygen (PaO2) (P less than or equal to 0.0025). Active air leaks were present in 20 infants and these infants responded most favourably to HFO-IMV. HFO-IMV failed to improve ventilation in neonates with diaphragmatic hernia/hypoplastic lungs. Complications during HFO-IMV were increased pulmonary secretions (11), worsening or recurrence of pre-existing air leaks (11), or occurrence of new air leaks (10). In 4 patients death was related to major air leak complications. Twenty-four infants died, 18 of them of a respiratory cause. Twenty-one infants finally survived. We assembled a well-tolerated system to provide HFO-IMV and to successfully ventilate neonates with severe respiratory disease, who failed to respond to conventional IMV. Initiation of HFO-IMV earlier in the course of the disease in this type of infant may improve survival.

Female↗
PubMed2001

Pharmacologic therapy of persistent pulmonary hypertension of the newborn.

Persistent pulmonary hypertension of the newborn (PPHN) is a potentially life-threatening condition characterized by a failure of pulmonary vascular resistance to decrease adequately during the transition to extrauterine life. Inhaled nitric oxide, a vasodilator that acts selectively on the pulmonary circulation, has revolutionized the treatment of this condition. However, inhaled nitric oxide has not proven effective in all patients, particularly those with congenital diaphragmatic hernias or meconium aspiration syndrome. Furthermore, large clinical trials of inhaled nitric oxide have failed to demonstrate significant differences in mortality between nitric oxide-treated and control infants with PPHN. Other therapeutic approaches to PPHN have been limited by a relative lack of specificity for the pulmonary circulation, and have received much less attention. Pharmacologic approaches, including pulmonary surfactants, prostacyclin, endothelin antagonists, Ca(2+)-channel blockers, magnesium sulfate, and tolazoline, have exhibited varying degrees of efficacy in lowering pulmonary vascular pressures in humans and/or animals. A number of these agents are also effective when used in combination. For example, phosphodiesterase inhibitors have been reported to act synergistically with inhaled nitric oxide. Surfactants also appear to be useful in PPHN, particularly in patients with congenital diaphragmatic hernia, when used in combination with other therapies. Surfactant lavage and other novel therapies may also be effective in combination therapy of meconium aspiration syndrome. Further studies should be directed at defining the optimal therapies in specific clinical settings. Validation of multiple therapeutic modalities for PPHN, including inhaled nitric oxide, will allow for rational, combined vasodilator strategies that are specific for the underlying pathophysiology in each patient.

Anti-Inflammatory Agents↗
PubMed2000

Advances in management of meconium aspiration syndrome.

Meconium Aspiration Syndrome (MAS) is a leading cause of respiratory distress in the newborn. Antenatal diagnosis of meconium stained amniotic fluid and fetal distress is important to reduce morbidity and mortality in the neonates. Amnioinfusion of saline and tracheal suctioning of meconium are preventive interventions. Babies with MAS who continue to have respiratory distress need to be put on conventional ventilators. Increasing hypoxia, hypercarbia and barotrauma warrants changing to high frequency oscillatory ventilation. Pulmonary hypertension is an important complication which should be promptly recognized. Nitric oxide therapy used with high frequency ventilation has improved the outcome of babies with severe MAS and pulmonary hypertension. Some of these babies who continue to worsen clinically need to be put on ECMO circuit. Surfactant infusion in babies with MAS has been shown to improve gas exchange, resolve pulmonary hypertension and decrease oxygenation index. Total and partial liquid ventilation with perflurocarbon improves oxygenation, increases lung expansion and increases pulmonary blood flow in model studies of animals with MAS. Surfactant infusion and liquid ventilation are newer promising modes of therapeutic interventions in babies with severe MAS.

Extracorporeal Membrane Oxygenation↗
PubMed1998

Inhaled nitric oxide and high frequency oscillatory ventilation in persistent pulmonary hypertension of the newborn.

UNLABELLED: Inhaled nitric oxide (iNO) improves oxygenation in near-term and term newborns with persistent pulmonary hypertension of the newborn (PPHN), and decreases the need for treatment with extracorporeal membrane oxygenation. However, some patients with PPHN either do not respond or have only transient improvements in oxygenation during iNO therapy. Extrapulmonary shunting associated with high pulmonary vascular resistance in PPHN can cause critical hypoxaemia; however, the syndrome of PPHN is often associated with severe parenchymal lung disease (e.g., meconium aspiration pneumonitis, bacterial pneumonia, and surfactant deficiency) which causes intrapulmonary shunting. It is increasingly recognized that the effective use of iNO requires adequate lung inflation to optimize delivery of the drug within the lung. High frequency oscillatory ventilation (HFOV) causes safe and effective lung recruitment when an appropriate strategy is applied and has recently been shown to improve the response to iNO when parenchymal lung disease occurs in association with PPHN. CONCLUSION: Recent studies have shown that HFOV augments the response to iNO in PPHN associated with meconium aspiration syndrome or diffuse parenchymal lung disease (pneumonia, respiratory distress syndrome). Suboptimal lung inflation compromises the efficacy of iNO in PPHN, and may in part explain the reported differences in iNO response rates.

Administration, Inhalation↗
PubMed2005

Hypoxic respiratory failure in term newborns: clinical indicators for inhaled nitric oxide and extracorporeal membrane oxygenation therapy.

PURPOSE: The criteria for starting extracorporeal membrane oxygenation (ECMO) therapy in term newborn patients with hypoxemic respiratory failure consist of an oxygenation index (OI) of 25 or higher and alveolar-arterial oxygen (Aao(2)) gradient of more than 600 at sea level. In such conditions, inhaled nitric oxide (iNO) may improve oxygenation and reduce the need for ECMO therapy. We studied early changes in OI and Aao(2) gradients in response to iNO treatment that may indicate a need to continue iNO treatment or the necessity to start an ECMO therapy. MATERIALS AND METHODS: In this prospective study, we used 34 outborn neonatal patients that were referred to our pediatric critical care unit in a children's hospital for ECMO therapy with diagnosis of hypoxemic respiratory failure. In all patients, iNO therapy, starting at 80 ppm, was instituted either during transport or on arrival to hospital. Response to iNO was assessed after 1 hour, at which time, iNO concentration was reduced to 40 ppm, provided there was more than 20% improvement in either or both oxygenation indices. Patients who did not respond positively to continuous iNO therapy and met ECMO criteria were given ECMO therapy. RESULTS: Inhaled nitric oxide therapy alone was successful in 10 (29%) of 34 patients. Eighteen patients (53%) required ECMO therapy within the first 10 hours of iNO treatment (early ECMO therapy), whereas 6 other neonates (18%) became eligible for ECMO therapy after prolonged (2-4 days) iNO treatment (late ECMO therapy). No mortality occurred with any treatment. Within 4 hours after iNO therapy, patients who required early ECMO therapy had significantly higher OI and Aao(2) gradients than patients who were treated with iNO therapy alone (P<.01, analysis of variance followed by Tukey-Kramer multiple comparison test). Six of 34 patients (18%), categorized as late ECMO therapy, on the average, had initially higher levels of OI and mean airway pressure than neonates in iNO treatment and early ECMO therapy. CONCLUSION: Persisting levels of OI of more than 20 or Aao(2) gradients of more than 600 after 4 hours of iNO therapy could be indicative of an immediate need for ECMO therapy.

Extracorporeal Membrane Oxygenation↗
PubMed2006

Surfactant phosphatidylcholine metabolism in neonates with meconium aspiration syndrome.

OBJECTIVE: Because meconium directly inhibits surfactant function, we sought to determine the effect of meconium on endogenous surfactant synthesis and clearance. STUDY DESIGN: We studied surfactant phosphatidylcholine kinetics with the use of stable isotopes in 11 newborn infants with meconium aspiration syndrome (MAS) who required extracorporeal membrane oxygenation (ECMO). For comparison we studied 6 neonates with persistent pulmonary hypertension (PPHN) on ECMO and 10 term neonates ventilated for non-pulmonary indications and not on ECMO. All patients received a 24-hour [U- 13C]glucose infusion as precursor for the palmitic acid in surfactant phosphatidylcholine. RESULTS: In the meconium group, the maximal 13C-incorporation in phosphatidylcholine (PC) was half of that in controls (0.09 +/- 0.01 vs 0.18 +/- 0.03 atom percent excess [APE], P = .027). There was a trend toward lower surfactant synthesis in the MAS group (3.3 +/- 0.7%/day) and PPHN group (2.6 +/- 0.3%/day) compared with controls 8.0 +/- 2.4%/day, P = .058). Significantly lower PC concentrations in tracheal aspirates were found in the MAS group (4.4 +/- 2.6 mg/mL) and PPHN group (3.6 +/- 2.0 mg/mL) compared with controls (12.8 +/- 2.6 mg/mL, P = .01). Endogenously synthesized surfactant had a similar half-life in all groups, ranging from 63 to 98 hours. CONCLUSION: We conclude that surfactant synthesis is disturbed and that surfactant PC concentrations are low in infants with MAS on ECMO.

Analysis of Variance↗
PubMed2002

Intravenous sildenafil lowers pulmonary vascular resistance in a model of neonatal pulmonary hypertension.

Persistent pulmonary hypertension secondary to meconium aspiration syndrome is an important cause of morbidity and mortality in the neonatal population. We investigated the use of the phosphodiesterase-5 inhibitor sildenafil, in its intravenous form, as a pulmonary vasodilator in a model of meconium aspiration syndrome. Pulmonary hypertension was induced in 18 piglets, by endotracheal instillation of human meconium, 6 piglets subsequently received an infusion of intravenous sildenafil for 2 hours, 6 received inhaled nitric oxide for 2 hours, and 6 control animals received no additional intervention. Meconium aspiration increased pulmonary vascular resistance by 70%, and increased oxygenation index by over 100%. Pulmonary vascular resistance remained elevated for the remainder of the study period in control animals. Inhaled nitric oxide reduced the pulmonary vascular resistance by 40% after 2 hours of treatment; intravenous sildenafil completely reversed the increase in pulmonary vascular resistance within 1 hour of commencing the infusion. Neither agent had an effect on systemic hemodynamics. Sildenafil also increased cardiac output by 30%, but while doing so did not adversely influence oxygenation. Intravenous sildenafil is a selective and highly effective pulmonary vasodilator, which is at least as effective as inhaled nitric oxide, in this model of neonatal persistent pulmonary hypertension.

Administration, Inhalation↗
PubMed1998

[Nitric oxide inhalation in newborn infants with pulmonary hypertension].

Nitric oxide (NO) is an important endogenous vasodilator. NO, produced in the endothelial cell, causes vasodilation by relaxation of the vascular smooth muscle cell. Inhalation of NO plays a role in the treatment of persistent pulmonary hypertension of the newborn, a syndrome with considerable morbidity and mortality. NO inhalation specifically leads to pulmonary vasodilation without systemic hypotension, since NO binds avidly to haemoglobin. Neonates with pulmonary hypertension associated with lung hypoplasia, meconium aspiration syndrome, infantile inspiratory distress syndrome due to surfactant deficiency, and sepsis have been treated with inhaled NO. Literature data on NO inhalation and experience in our units with NO inhalation show an improvement in arterial oxygen tension and a decreased need for extracorporeal membrane oxygenation, but no reduction in mortality. NO toxicity as a result of NO inhalation in the newborn has not been reported yet.

Administration, Inhalation↗
PubMed1991

Fertility, pregnancies and offspring complications after bone marrow transplantation.

Hormonal assessment including luteotropic hormone (LH), follicle stimulating hormone (FSH), testosterone (T), oestradiol and sex hormone binding globulin was performed 1-6 years after allogeneic, syngeneic and autologous bone marrow transplantation in nine patients with severe aplastic anaemia (SAA) and 14 patients with haematological malignancy (HM). Among nine allografted SAA patients, seven aged less than 26 years showed normal gonadal function while two women above 26 years had premature ovarian failure. All eight female patients transplanted for HM had premature ovarian failure. Among six male patients transplanted for HM, four have elevated FSH but normal LH and T levels, while two have normal LH, FSH and T levels or elevated LH and FSH levels but decreased T levels, respectively. Three patients transplanted for SAA (two female, one male), but none of those transplanted for HM, parented four healthy children. A high incidence of offspring complications was noticed, including (i) persistence of fetal circulation syndrome, (ii) erythroblastosis fetalis, and (iii) prolonged newborn icterus. One female patient transplanted for SAA had an abortion in the 25th week of gestation. These observations confirm previous reports on recovery of fertility, mainly in younger patients transplanted for SAA; there was, however, an unexpectedly high incidence of pre-, peri- and postpartum complications in the offspring of bone marrow graft recipients.

Adolescent↗