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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two noninvasive methods of estimating arterial oxygenation were compared in a group of 48 infants ranging in birth weight from 870 to 4,000 gm, with diagnoses including apnea of prematurity, hyaline membrane disease, meconium aspiration, and congenital heart disease. Both transcutaneous oxygen measurements and ear oximetry gave reasonably accurate estimations of arterial oxygen levels within commonly used clinical ranges (PO2 50 to 70 mm Hg, arterial saturation 90 to 98%). Infants with shock demonstrated a wide range of values for transcutaneous oxygen levels, suggesting that this method has limited usefulness in this situation. Ear oximetry had limited ability to distinguish high, but safe, levels of arterial oxygen from excessively elevated levels. While neither method can be recommended for replacement of arterial oxygen sampling, both methods may be useful in a clinical setting if care is exercised in interpretation of the results and if the values obtained are checked against those from arterial blood.
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PMID:Noninvasive estimation of arterial oxygenation in newborn infants. 67 Nov 69

A total of 209 consecutive neonate and infant autopsies were reviewed with special attention to papillary muscle necrosis (PMN) of the heart. Associated major pathological findings were analysed for the evaluation of significant pathological accompaniments of PMN. PMN was found in 52 cases among 171(30.4%) neonates and major pathological accompaniments were bronchopneumonia, hyaline membrane disease, hypoxic neuronal change, sepsis, subarachnoid hemorrhage, disseminated intravascular coagulation (DIC) and acute tubular necrosis, among which hypoxic neuronal change and ATN had a statistically significant higher incidence when compared with the control group. (p < 0.005). PMN was found in 13 cases among 38(34.2%) infants and accompaniments were congenital heart disease, sepsis, bronchopneumonia, DIC and hypoxic neuronal change, all of which showed no difference from the control group in incidence. The results imply that PMN is a kind of organ damage in stressed subjects regardless of age, that it is not a special form of myocardial injury in any specific age group including the newborn period, and is possibly of different pathogenesis and significance.
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PMID:Papillary muscle necrosis in neonates and infants--analysis of 209 autopsies. 129 38

Disseminated intravascular coagulation (DIC) and other clotting abnormalities are common in sick newborn infants who have a variety of conditions. To document evidence of DIC at autopsy, immunoperoxidase staining of fibrin-related antigens (FRA) was used to detect intravascular microthrombi in liver, kidney, and lung from 127 newborns. Patients were selected from seven major disease groups: hyaline membrane disease/bronchopulmonary dysplasia, infection, meconium aspiration, necrotizing enterocolitis, congenital heart disease, other congenital anomalies, and extreme prematurity. Staining for FRA in intravascular microthrombi was seen in 40% of cases studied. The liver showed the highest frequency of intravascular microthrombi, located predominantly in the sinusoids. Unlike the adult kidney, the newborn kidney seldom had evidence of intravascular coagulation. Extravascular staining of FRA was observed in the renal distal tubular epithelium in 48 cases, many of which also had evidence of intravascular FRA staining. No significant differences in FRA staining patterns were seen among the disease groups except for cases of extreme prematurity in which all tissues showed minimal staining. Control tissues from SIDS patients also showed minimal FRA staining. Hepatic sinusoidal staining was the only tissue finding that correlated with thrombocytopenia, a clinical indicator of DIC. Despite the use of this immunohistochemical staining method, discrepancies between the clinical and autopsy diagnosis of DIC remain.
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PMID:Immunohistochemical diagnosis of disseminated intravascular coagulation in newborns. 170 Apr 4

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

Fifty-three newborns with pneumoperitoneum were treated between July 1980 and July 1985. The birth weights of these infants ranged from 600 to 4350 grams; nearly 75 per cent weighed less than 1500 grams. The etiology of the pneumoperitoneum and the hospital survival were reviewed. All operative patients had exploratory surgery through an upper abdominal transverse incision extending across both rectus muscles. All gastric and duodenal perforations were closed primarily; the perforations in the remaining gastrointestinal tract were generally exteriorized through the lateral edge of the wound. The single leading cause of pneumoperitoneum in the newborn is necrotizing enterocolitis, accounting for 60 per cent of the patients in this series; 78 per cent of these infants survived. All infants with ("spontaneous") ileal perforations survived. The two patients with colon perforations (from meconium plug obstruction) died, one of congenital heart disease associated with Down's syndrome and the other of hyaline membrane disease. One patient who had mild hyaline membrane disease, who was not ventilated, and who did not have mediastinal emphysema also had pneumoperitoneum for which no cause was found at laparotomy ("spontaneous"). He survived. In six critically ill infants (11% of the series) pneumoperitoneum developed secondary to mediastinal dissection of air from ventilators. None of these infants was operated on because an intestinal perforation as a source of the pneumoperitoneum could reliably be excluded by the presence of pneumomediastinum and/or a negative paracentesis. This group of infants warrants special attention, because in them "negative" laparotomies performed in search of an intestinal perforation would certainly compromise their already precarious conditions.
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PMID:Pneumoperitoneum in the newborn infant. 357 30

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

This paper reviews the common spectrum of medical diseases of the neonatal chest. Emphasis is on radiographic changes that have been produced by the introduction of new therapeutic maneuvers, particularly the use of artificial surfactant in treating hyaline membrane disease and the survival of profoundly premature newborns (less than 650 g). A discussion of meconium aspiration syndrome, neonatal pneumonia, transient tachypnea of the newborn, congenital lymphangiectasia, and congenital heart disease is also included. The effects on the neonatal chest radiograph of extracorporeal membrane oxygenation and high-frequency ventilation are also mentioned.
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PMID:A radiologic update on medical diseases of the newborn chest. 857 Mar 17

Perinatal changes in myocardial growth have recently evoked considerable interest with regard to cardiac chamber development with congenital cardiac lesions and to myocardial development in preterm infants. It is suggested that cardiac chamber development is influenced by blood flow. Experimental pulmonary stenosis in fetal lambs may induce either greatly reduced or markedly increased right ventricular volume. Ventricular enlargement appears to be associated with a large ventricular volume load resulting from tricuspid valve regurgitation. A small competent tricuspid valve is associated with reduced flow through the ventricle due to outflow obstruction and a small right ventricle. Postnatal growth of the ventricles in congenital heart disease is discussed. Increase in myocardial mass prenatally is achieved by hyperplasia, both during normal development and when myocardial mass is increased by right ventricular outflow obstruction. Postnatally, increases in myocardial mass with normal growth, as well as with ventricular outflow obstruction, are largely due to hypertrophy of myocytes. Myocardial capillary numbers do not increase in proportion with myocyte numbers in ventricular myocardium in association with outflow obstruction. The postnatal effects of these changes in congenital heart lesions are considered. Studies in fetal lambs suggest that the late gestational increase in blood cortisol concentrations is responsible for the change in the pattern of myocardial growth after birth. The concern is raised that prenatal exposure of the premature infant to glucocorticoids, administered to the mother to attempt to prevent hyaline membrane disease in the infant, may inhibit myocyte proliferation and result in a heart with fewer than normal myocytes. This would necessitate that each myocyte would have to hypertrophy abnormally to achieve a normal cardiac mass postnatally.
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PMID:Myocardial growth before and after birth: clinical implications. 1070 76

We report on a female preterm infant with hepatic failure and neonatal tissue siderosis of hemochromatotic type diagnosed by using both histochemistry and atomic absorption spectroscopy. The infant presented with meconium ileus, signs of rapidly progressive hepatic failure, and hyperferritinemia (7132 ng/ml). Despite surgery and intensive care the infant died 32 days after birth. Postmortem examination showed a wrinkled liver with extensive collapse of the hepatic architecture and regenerating nodules as well as hepatic and extrahepatic iron accumulation of hemochromatotic type, sparing the reticuloendothelial system. Atomic absorption spectroscopy confirmed an increase in the iron content of various organs: liver, heart, pancreas, oral salivary gland, kidney, and adrenal gland. The increase in the iron content of various organs was determined by comparing the analysis of the propositus with those of 5 gestationally age-related preterm infants who had died in the intensive care unit: 2 died of meconium aspiration syndrome, the other 3 of hyaline membrane disease, bronchopulmonary dysplasia, and immaturity, respectively. We also compared the analysis of 15 fetuses having a a condition predisposing to iron accumulation (trisomy 21, trisomy 18, cytomegalovirus, amnion infection syndrome, Rhesus- and ABO-incompatibility, congenital hemolysis, anti-phospholipid syndrome, congenital heart disease). Delta F508, the most frequent mutation seen in cystic fibrosis patients, was excluded by gene sequencing. Different noxae causing iron accumulation in the neonatal period have led to the statement that neonatal hemochromatosis may collect different etiologies, such as metabolic disorders, infections, chromosomal aberrations, and immunological disorders. In this study, we report the singular evidence of neonatal iron accumulation of hemochromatotic type in an infant presenting with meconium ileus and propose a classification of the neonatal disorders associated with iron accumulation.
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PMID:Hepatic failure with neonatal tissue siderosis of hemochromatotic type in an infant presenting with meconium ileus. Case report and differential diagnosis of the perinatal iron storage disorders. 1170 Aug 92


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