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Results for “Persistent Fetal Circulation Syndrome”

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PubMed1982

beta-hemolytic streptococcal infection appearing as persistent fetal circulation.

Sixty neonates who were transferred to a neonatal intensive care unit during a four-year period had diagnoses of persistent fetal circulation (PFC). Six of these 60 neonates had beta-hemolytic streptococcal infection. The clinical appearance of these six neonates included respiratory distress, cyanosis, and/or apnea. The chest roentgenograms showed mild to moderate lung disease. All six neonates had progressive acidosis with hypoxemia. The diagnosis of PFC was made by cardiac catheterization or contrast echoangiography. The neonates were treated with mechanical ventilation, antibodies, and supportive therapy, including tolazoline hydrochloride. Mortality was high; only one of the six neonates survived. Streptococcal infection should be added to the growing list of conditions associated with PFC.

Apnea↗
PubMed1984

Persistent pulmonary hypertension of the newborn. Trends in incidence, diagnosis, and management.

Persistent pulmonary hypertension of the newborn ( PPHN ) has become a more commonly recognized problem in neonatal intensive care nurseries. In 62 neonates, 27 from 1980 and 35 from 1981, we compared classification, methods of diagnosis, modes of therapy, and survival. Thirty neonates (48%) had primary and 32 (52%) had secondary PPHN . Overall survival was 71% with significant differences in primary v secondary PPHN . Survival was also higher in 1981 than 1980 and was related to earlier diagnosis and to the more rapid initiation of therapy.

Humans↗
PubMed1985

Persistent fetal circulation. Neurodevelopmental outcome.

Forty children who had persistent fetal circulation (PFC) were followed up for one to four years. At the most recent examination, 16 (40%) were normal, eight (20%) had neurosensory hearing loss, three (7.5%) were profoundly impaired, six (15.0%) had suspect or abnormal results of neurologic examinations exclusive of hearing loss, three (7.5%) had speech impairment and normal hearing, and one had a delay in motor development. The remaining three had clinically suspect speech. Neurosensory hearing loss correlated only with having a mother with insulin-dependent diabetes, hand-to-mouth facility on the Brazelton scale, and eight-month neurologic status. Earlier diagnosis of hearing loss may be facilitated by testing of neonatal auditory behavioral responses, neurologic status at eight months, and by attention to parental concern about abnormal speech development. Neonatal and infancy auditory screening are recommended in children who have PFC in the neonatal period.

Child Development↗
PubMed1987

Cerebral infarction in persistent pulmonary hypertension of the newborn.

Persistent pulmonary hypertension of the newborn and its attendant hypoxemia may place the infant at high risk for hypoxic-ischemic injury. In 19 infants with persistent pulmonary hypertension of the newborn, 16 of whom suffered intrapartum asphyxia, we evaluated a series of electroencephalograms (EEGs) for evidence of major focal cerebral injury, ie, persistent voltage attenuation and/or focal electrical-seizure activity. Of the 15 infants (78.9%) with such EEG findings, nine infants (47% of the total population) had cerebral infarction documented by cranial sonograms, computed tomographic scans, or autopsy findings. In eight (89%) of the nine infants with infarction, electrical seizures were noted during periods of muscle paralysis. We recommend (1) the use of electroencephalography in this population, particularly during periods of muscle paralysis, to detect underlying cerebrovascular lesions and (2) the use of cranial computed tomography if persistent, focal EEG abnormalities are noted.

Cerebral Infarction↗
PubMed1988

Outcome of persistent pulmonary hypertension in relation to severity of presentation.

Since the initial description of persistent pulmonary hypertension of the newborn (PPHN), the management of these infants has been controversial. A variety of therapeutic modalities, such as extracorporeal membrane oxygenation, have been utilized. Early recognition of a group of patients with PPHN who might require aggressive therapy would be clinically useful. Highest alveolar-arterial oxygen gradient at or near diagnosis was evaluated retrospectively in 53 patients with PPHN in relation to survival, aggressiveness of management, and frequency of pulmonary complications (air leak and broncho-pulmonary dysplasia). Highest alveolar-arterial oxygen gradient was a good early predictor of nonsurvival and was significantly higher in nonsurvivors compared with survivors (mean [+/- SD], 618 +/- 23 mm Hg vs 521 +/- 128 mm Hg). Values of 600 mm Hg or greater were more frequent in the nonsurvivors compared with the survivors (92% vs 37%). Air leak also proved to be a good predictor of nonsurvival.

Humans↗
PubMed1988

Hypoxic vs septic pulmonary hypertension. Selective role of thromboxane mediation.

Pulmonary hypertension was generated in 11 newborn piglets, via either infusion of group B beta-hemolytic streptococci (n = 5) or induction of isocapnic hypoxia (n = 6), to study the contributions of thromboxane metabolite thromboxane B2 levels to different types of pulmonary hypertension. After 30 minutes of stable pulmonary hypertension, mean (+/- SD) pulmonary artery pressure increased similarly from 16 +/- 4 to 33 +/- 5 mm Hg (hypoxic), and from 14 +/- 2 to 34 +/- 6 mm Hg (septic). All other measured hemodynamic variables were similar. Despite these hemodynamic similarities, there were significant differences in thromboxane B2 levels. After 60 minutes of pulmonary hypertension, thromboxane B2 levels were 760 +/- 253 pg/mL (hypoxic), and 3103 +/- 1083 pg/mL (septic). These data demonstrate that, while thromboxane appears to be crucial in mediating septic pulmonary hypertension in the piglet, it is not associated with hypoxic pulmonary hypertension, implying that different types of pulmonary hypertension are probably mediated by different biochemical agents.

Animals↗
PubMed1989

High-frequency jet ventilation in neonatal pulmonary hypertension.

To determine if high-frequency jet ventilation is beneficial in neonates with persistent pulmonary hypertension, we compared the ventilator settings, blood gas concentrations, and outcome of infants who met established criteria for a high predictive mortality. During a six-year period, 14 neonates who had severe respiratory failure and hypoxemia while receiving conventional ventilation were treated with high-frequency jet ventilation. Twenty-three comparable infants meeting the same criteria were treated exclusively with conventional ventilation. After initiation of high-frequency jet ventilation there was a significant reduction in mean airway pressure and partial pressure of arterial carbon dioxide (PaCO2). In contrast, neonates treated exclusively with conventional ventilation continued to have higher airway pressures and PaCO2. However, there was no difference in the alveolar-to-arterial oxygen gradient, air leakage, incidence of bronchopulmonary dysplasia, or duration of assisted ventilation or oxygen supplementation. Furthermore, mortality was comparable in both groups of infants. These preliminary observations suggest that high-frequency jet ventilation can reduce airway pressure and PaCO2 in neonates with persistent pulmonary hypertension but does not appear to improve outcome.

Carbon Dioxide↗
PubMed1980

Pulsed Doppler echocardiographic findings in total anomalous pulmonary venous drainage to the coronary sinus.

The pulsed doppler echocardiographic (PDE) findings in a premature cyanotic infant with total anomalous pulmonary venous return to the coronary sinus are reported. Features that suggested the diagnosis of total anomalous pulmonary venous return were 1) an area of systolic-diastolic turbulent flow posterior to the apparent left atrial border, which was interpreted as representing the convergence of pulmonary venous return to a common pulmonary vein, and 2) systolic and diastolic turbulent flow within the right atrium suggesting pulmonary venous return through the coronary sinus. We suggest that PDE should be included as part of the evaluation of cyanotic infants in whom the diagnosis of total anomalous pulmonary venous return is considered.

Diagnosis, Differential↗
PubMed2005

Endothelin receptor expression in human lungs of newborns with congenital diaphragmatic hernia.

Congenital diaphragmatic hernia (CDH) is a major cause of refractory respiratory failure in the neonatal period and is characterized by persistent pulmonary hypertension of the newborn (PPHN) and pulmonary hypoplasia. Endothelin-1 (ET-1) dysregulation may play a significant role in the pathophysiology of PPHN and ET-1 acts through binding to type A (ETA) and type B (ETB) receptors. Therefore, ETA and ETB receptor protein expression was studied using immunohistochemistry in 10 lung specimens obtained from newborns with CDH, and 4 normal lung specimens, in order to explore whether dysregulation of ETA and ETB expression contributes to PPHN. ETA and ETB mRNAs were then quantified using real-time RT-PCR in laser-microdissected pulmonary resistive arteries. In the lungs of newborns with CDH, immunohistochemistry of both ETA and ETB receptors demonstrated over-expression in the thickened media of pulmonary arteries. Using laser microdissection and real-time RT-PCR, higher levels of ETA and ETB mRNA were found in CDH pulmonary arteries than in controls: this increase was more pronounced for ETA mRNA. This study provides the first demonstration of ET-1 receptor dysregulation in association with structural alteration of pulmonary arteries in newborns with CDH and PPHN. This dysregulation preferentially affects the ETA receptor. These results suggest that dysregulation of ET-1 receptors may contribute to PPHN associated with CDH.

Body Weight↗
PubMed2003

Acinar arterial changes with chronic lung disease of prematurity in the surfactant era.

Because echocardiographic studies on infants with chronic lung disease (CLD) suggest that pulmonary hypertension (PH) may contribute to its severity, we studied acinar arterial walls in the following surfactant-era infants: controls (n=38): 22-41 weeks of gestational age (GA), exposed briefly to oxygen and positive pressure ventilation, died within 48 hr of birth; prolonged rupture of fetal membranes (PROM) and persistent pulmonary hypertension (PPHN) (n=17); and SCORE (integrated area under curve of average daily FiO2 x average daily MAP) groups (<20, 20-69, and 70-500; mild, moderate, and severe clinical lung disease, respectively, n=35): 23-30 weeks GA, lived 7-79 days. Lungs were stained for elastic tissue and smooth muscle actin. Vessels were assessed for percent of vessel circumference with smooth muscle, extent of elastic laminae in the walls, and percent arterial wall thickness (%AWT) at three levels: terminal to respiratory bronchiole transition (TRB), alveolar duct, and saccule. At the alveolar ductal and saccular levels, percent arterial wall thickness (%AWT) in mild CLD (SCORE < 20) was less than controls (P < 0.05) and those with more severe CLD (SCORE 70-500), indicating that normal postnatal arterial wall thinning may be delayed, or there is remodeling associated with increased %AWT. Severe CLD infants also had a significantly higher percent of circumferential actin than those with milder disease (SCORE < or = 69) and controls. In moderate and severe CLD, there was an increase in extent of the elastic laminae compared to controls and mild CLD. These changes were also significantly greater in PROM and PPHN infants compared to even severe CLD. We conclude that PH is a real possibility in severe CLD infants after discharge at 36 weeks. Grading the severity of CLD at discharge, and echocardiographic studies, may guide subsequent oxygen therapy.

Actins↗
PubMed1988

Predicting survival in infants with persistent pulmonary hypertension of the newborn.

Since persistent pulmonary hypertension of the newborn (PPHN) often occurs as a life-threatening illness, it would be advantageous to identify the highest-risk infants within the first 24 hours of life so that transfer to centers with extracorporeal membrane oxygenation (ECMO) or high-frequency ventilation can be facilitated. Fifty-three infants with PPHN were evaluated retrospectively. A multivariate discriminant analysis of risk factors determined that lowest pH, critical PaCO2, highest inspiratory pressure (PI), maximum ventilator rate, and 5-minute Apgar score were significantly different between the 35 survivors (66%) and the 18 infants (34%) who had died when examined within the first 24 hours of life. A clinical scoring system was designed based on these five criteria, which predicted outcome accurately in 93% of infants. A logistic regression analysis was performed as a check on these results and found that lowest pH, critical PaCO2, and PI predicted outcome with great accuracy. These results suggest that the use of these scoring systems within the first 24 hours of age may help predict outcome in infants with PPHN.

Apgar Score↗
PubMed2005

Pathophysiologic mechanisms of persistent pulmonary hypertension of the newborn.

Persistent pulmonary hypertension of the newborn (PPHN), among the most rapidly progressive and potentially fatal of vasculopathies, is a disorder of vascular transition from fetal to neonatal circulation, manifesting as hypoxemic respiratory failure. PPHN represents a common pathway of vascular injury activated by numerous perinatal stresses: hypoxia, hypoglycemia, cold stress, sepsis, and direct lung injury. As with other multifactorial diseases, a single inciting event may be augmented by multiple concurrent/subsequent phenomena that result in differing courses of disease progression. I review the various mechanisms of vascular injury involved in neonatal pulmonary hypertension: endothelial dysfunction, inflammation, hypoxia, and mechanical strain, in the context of downstream effects on pulmonary vascular endothelial-myocyte interactions and myocyte phenotypic plasticity.

Endothelium, Vascular↗