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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Assessing the short-term prognosis of bronchopulmonary dysplasia (BPD) (duration of mechanical ventilation, of O2 therapy, and risk of death) is often uncertain at the early stages of the disease. From a retrospective study of 124 cases of BPD, we made a search for factors of poor prognosis which could be recognized early. Among the 124 BPD, 56 (45%) had a severe disease (mechanical ventilation for greater than 3 months and/or O2 for greater than 4 months), and 24 of them (20%) died. Two types of factors have been identified as linked to a poor prognosis (risk of evolution towards a severe disease in a proportion of 70 to 90%): some respiratory events (refractory hypoxemia, recurrent pneumothorax, interstitial emphysema, no improvement of hyaline membrane disease at 3-4 days of life in babies less than 32 weeks gestational age) and hemodynamic failures (cardiac failure due to persistent ductus arteriosus, collapse following infection or anoxia). We have also defined different values of a ventilatory index (I = mean airway pressure x FiO2) which allows the neonatologists to estimate the final prognosis of BPD during the first two months of life.
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PMID:[Evaluation of short term prognosis of bronchopulmonary dysplasia]. 207 7

We examined two groups of fetuses in which echocardiography had been performed and in which ventricular volume overload eventually led to fetal hydrops. The first group (18 fetuses) had atrioventricular valve regurgitation and almost all of the fetuses had structural heart disease. No fetus in this group survived the neonatal period; only two of the pregnancies in this first group were terminated. A second group of three fetuses had ventricular volume overload from sacrococcygeal teratomas at 21 to 24 weeks' gestation. These fetuses also had nonimmune hydrops (or it developed), but they did not have structural heart disease or atrioventricular valve regurgitation. Combined ventricular output in this group was calculated by Doppler ultrasound to be greater than twice the normal output for fetuses of the expected gestational weight. The proportion of the combined output to the lower body and the placenta was increased with the increase to the teratoma, exceeding the increase to the placenta. In one fetus, serial study demonstrated increasing output and the development of hydrops. Intrauterine surgery was undertaken to control the high output failure. The abnormal variables tended to revert to normal after replacement of blood loss, and the hydrops disappeared. The pregnancy continued until the spontaneous rupture of membranes at 26 weeks' gestation forced delivery by cesarean section. The infant died from severe hyaline membrane disease. These findings suggest that, in some circumstances, fetal hydrops is a late sign of cardiac failure and heralds incipient death.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventricular volume overload in the human fetus: observations from fetal echocardiography. 231 May 88

Tracheal agenesis is described in a premature infant. Absent cry, failure of tracheal intubation despite adequate ventilation with a face mask, and ventilation of both lungs after oesophageal intubation suggested the diagnosis. The infant's condition deteriorated rapidly because of severe pulmonary hyaline membrane disease 12 h later due to intractable cardiac failure. At post-mortem examination, large bilateral broncho-oesophageal fistulae were found.
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PMID:Tracheal agenesis: a case report. 261 9

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the newborn lung. 676 Oct 39

The findings at autopsy in 99 cases of perinatal deaths in a ten-year period and on pathologic examination of the accompanying placentas in 39 cases were analyzed clinicopathologically. Also reviewed were the pathologic diagnoses of 225 placentas that were examined for causes other than neonatal death. Cardiovascular and pulmonary problems, particularly hyaline membrane disease, atelectasis and cardiac anomalies were most common. Asphyxia, heart failure and premature placental separation were the most frequent causes of death. In slightly more than half of the cases a reasonable final diagnosis was established by autopsy, and if the placenta was examined, nearly two-thirds could be properly classified. In the remaining 37 per cent, as previously reported in larger series, neither the autopsy nor placental examinations disclosed a satisfactory explanation of the perinatal death.
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PMID:PERINATAL DEATH. A CLINICOPATHOLOGICAL ANALYSIS OF 99 CASES. 1414 66