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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report 22 cases of hepatic necrosis following catheterization of the umbilical vein. The morphology of the necrotic lesions, which were confined to the left lobe in 21 patients, was that of an anemic infarct. Their causes are multiple and include intimal damage during the insertion of the catheter with consecutive thrombosis of portal vein branches, the postpartum immaturity of the arterial hepatic oxygen supply, postpartum hypoxia due to respiratory failure of cerebral or pulmonary origin, obstruction of portal venous flow through the catheter as such, the postpartum involution of the left hepatic lobe, and prolonged periods of catheterization. Toxic damage of the hepatic parenchyma due to an infusion of Tris buffer through the catheter into the portal venous system is a potential additional factor.
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PMID:Anemic necrosis of the liver after umbilical vein catheterization. 42 93

To determine the influence of body position on chest wall and pulmonary function, we studied the ventilatory, pulmonary mechanics, and thoracoabdominal motion profiles in 20 preterm infants recovering from respiratory disease who were positioned in both the supine and prone position. Thoracoabdominal motion was assessed from measurements of relative rib cage and abdominal movement and the calculated phase angle (an index of thoracoabdominal synchrony) of the rib and abdomen Lissajous figures. The ventilatory and pulmonary function profiles were assessed from simultaneous measurements of transpulmonary pressure, airflow, and tidal volume. The infants were studied in quiet sleep, and the order of positioning was randomized across patients. The results demonstrated no significant difference in ventilatory and pulmonary function measurements as a function of position. In contrast, there was a significant reduction (-49%) in the phase angle of the Lissajous figures and an increase (+66%) in rib cage motion in prone compared with the supine position. In addition, the degree of improvement in phase angle in the prone position was correlated to the severity of asynchrony in the supine position. We speculate that the improvement in thoracoabdominal synchrony in the prone position is related to alterations of chest wall mechanics and respiratory muscle tone mediated by a posturally related shift in the area of apposition of the diaphragm to the anterior inner rib cage wall and increase in passive tension of the muscles of the rib cage. This study suggests that the mechanical advantage associated with prone positioning may confer a useful alternative breathing pattern to the preterm infant in whom elevated respiratory work loads and respiratory musculoskeletal immaturity may predispose to respiratory failure.
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PMID:Effect of position on the mechanical interaction between the rib cage and abdomen in preterm infants. 153 9

Respiratory failure in the preterm results from not only surfactant deficiency but also the immaturity of a number of other elements that have a structural basis. Airway, alveolar, fluid clearance, and epithelial and endothelial barrier functions also are important to lung function. Immaturities in these lung elements have identifiable adverse consequences for lung function such as pulmonary interstitial emphysema and pulmonary edema. The maturation of each of these elements appears to be achievable by agents such as corticosteroids, and maturation will result in an improved response to surfactant treatments. While surfactant treatments can improve respiratory failure by minimizing lung injury, other aspects of lung immaturity continue to contribute to respiratory compromise in the preterm. A thorough understanding of respiratory failure in the newborn depends on a better appreciation of the contribution of immaturity of the different structural elements of the lung on lung function.
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PMID:Pathogenesis of respiratory failure in the preterm infant. 177 25

We studied urine excretion of free and conjugated aldosterone by 12 control infants and 14 infants with hyaline membrane disease (HMD) on the first and seventh days after birth. Both groups had a mean gestational age of 29 weeks. Total urine aldosterone excretion (UAE) and percent excreted as conjugate were similar for both groups on both study days, and did not relate to the severity of respiratory failure in infants with HMD. Sodium intake was higher for infants with HMD on both study days (p less than 0.02), but their urine sodium excretion was only significantly (p less than 0.01) higher on day 7. For total UAE values greater than 3 nmol/kg/d, there was no significant difference between estimated sodium-potassium exchange by control (22 +/- 5%, n = 8) and HMD (31 +/- 5%, n = 10) groups. These data suggest that neither the magnitude of excretion of aldosterone in the urine, the ability to conjugate aldosterone nor the degree of relative distal tubular unresponsiveness to aldosterone are related to the severity of pulmonary immaturity in preterm infants.
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PMID:Hyaline membrane disease and early neonatal aldosterone metabolism in infants of less than 33 weeks gestation. 186 79

The Pierre Robin Syndrome is characterized by three defects (8,9): micrognathia, cleft palate and glossoptosis responsible for respiratory failure. The new definition of this syndrome associates retrognathia, cleft palate and respiratory distress. This respiratory distress is mixed: obstructive due to glossoptosis, and central, secondary to brainstem immaturity (1,2). The main ocular manifestations associated with the syndrome are congenital glaucoma, high congenital myopia and retinal detachment. Microphtalmia has already been reported, but is infrequent. We present a clinical case of a major microphthalmia in a Pierre Robin Syndrome, confirmed by CT scan exploration.
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PMID:[Microphthalmos in Pierre Robin syndrome. Clinical and x-ray computed tomographic study]. 269 74

Intrauterine exposure to the potent lung toxicant OOS-TMP was found to result in neonatal lethality attributed to immature lungs (Koizumi et al. 1988). The present study was initiated to investigate biological/pathological profiles of such pulmonary immaturity. OOS-TMP was given p.o. to five pregnant female Sprague-Dawley rats on gestation day (G) 19 at 2.5, 7 or 20 mg/kg. Control (N = 6) or pair-fed dams (N = 5: pair-fed to 20 mg/kg dams) received 2 ml/kg corn oil. On G 22, fetuses were delivered by Cesarean section. The biochemical maturity of lungs was assessed by glycogen content and production of disaturated phosphatidylcholine (DSPC), a major component of pulmonary surfactant. Mean DSPC content was significantly lower in fetuses from dams dosed at 7 or 20 mg/kg while mean glycogen concentration, in contrast, was 3- to 6-fold higher in those fetuses than fetuses from control or pair-fed dams. Pathological examination revealed that in fetuses delivered from dams dosed at 7 mg/kg or 20 mg/kg, glycogen-rich cuboidal epithelial cells completely covered the terminal air space and alveolar/blood barriers stayed at the poorly developed stage. The stage of the pulmonary development in those fetuses was similar to those in fetuses on G19. Therefore it was concluded that intrauterine exposure to OOS-TMP delayed pulmonary development, thereby causing respiratory failure after birth.
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PMID:Immature alveolar/blood barrier and low disaturated phosphatidylcholine in fetal lung after intrauterine exposure to O,O,S-trimethylphosphorothioate. 276 22

The main pathology leading to mortinatality has been determined. It is shown that in 57.8% of cases mortinatality is associated with placental insufficiency, the reason for which can be found out by the pathoanatomical study of the afterbirth. It is proposed to differentiate afterbirth disorders of implantation, placentation, circulation and inflammatory changes. Fifty per cent of neonates are shown to die from the respiratory failure associated with the formation of atelectasis, hyaline membranes and edema with pulmonary hemorrhages. Next in frequency are cephalic ventricle extravasations. The main pathogenetic factor of both neonatal pathologies is prematurity with functional and morphological tissue immaturity.
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PMID:[The nature of the major pathology in the perinatal period at the present time]. 353 67

Prenatal starvation causes pulmonary hypoplasia in newborn guinea pigs, and is associated with postnatal cyanosis, hypothermia, and respiratory failure. To determine the effects of such starvation on ventilation, neonates from litters either fed ad libitum throughout gestation (control) or given 50% rations in the last trimester of pregnancy (starved) were studied at 29 degrees C by plethysmography in 21, 11, and 5% O2. After 15 min (steady-state) in 11% and then 5% O2, 13 of 14 controls (mean = 95 g) sustained increases in weight-specific minute ventilation of 46 and 75% compared to values in air (p less than 0.01), due to increases in respiratory frequency. Seven of 11 starved neonates (mean = 76 g) also sustained increases in respiratory frequency and weight-specific minute ventilation in 11 and 5% O2 similar in magnitude to those of the normal controls, although at higher weight-specific tidal volumes. One abnormal control (85 g) and four starved neonates (mean = 70 g) hyperventilated in air, did not respond to 11% O2, and then hypoventilated in 5% O2 due to a reduced weight-specific tidal volume. Neonates with normal ventilatory patterns did not alter weight-specific minute ventilation in 100% O2 and did not show a biphasic response in acute (1-5 min) exposures to moderate hypoxia, as noted for newborn of other species. Thus, hypoxia identified those starved neonates in which pulmonary immaturity or other starvation-induced pathologies necessitated a maximal ventilatory effect in air. The sustainable hyperventilation among normal guinea pigs during hypoxia emphasizes the precocial development in this species at birth, which may be compromised by intrauterine starvation.
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PMID:Prenatal starvation retards development of the ventilatory response to hypoxia in newborn guinea pigs. 377 4

A clinical classification of perinatal morbidity and mortality should be based upon the pathophysiological mechanisms which affect the fetus and newborn infant, resulting in this morbidity and mortality. Each mechanism is a distinctive disturbance which may be regarded as the common pathway for expression of insults to the fetus and newborn infant arising from a wide variety of obstetric abnormalities and specific disease entities. The following classification of mechanisms incorporating the whole spectrum of perinatal problems is proposed: (1) developmental abnormality; (2) immaturity and prematurity; (3) chronic fetal insufficiency; (4) acute fetal insufficiency; (5) newborn respiratory failure; (6) blood group incompatibility; (7) infection, and (8) trauma.
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PMID:A clinical classification of the mechanisms of perinatal wastage. 541 22

Renal tubular dysgenesis is a rarely recognized condition characterized by oligohydramnios, Potter's sequence and congenital anuria leading to stillbirth or neonatal death from respiratory failure. It is thought to be inherited in an autosomal recessive manner. Definitive diagnosis is based on renal histology, revealing the lack of proximal tubule differentiation. Two additional cases of affected sibs in a family with parental consanguinity are reported. Lectin and immunohistochemical studies confirmed structural and functional immaturity of the proximal tubule. Further findings include bilateral renal vein thrombosis. The clinical and morphological parameters defining this disorder and the possible mechanisms of pathogenesis are discussed.
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PMID:[Renal tubular dysgenesis with fetal renal vein thrombosis]. 776 60


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