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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-one infants with respiratory failure secondary to primary pulmonary disease and with a birth weight of 1000 g. or over have been managed in a negative-pressure respirator (Air-Shields) over a three-year period. Of these the failure in 87 was due to respiratory distress syndrome (RDS) and in four it resulted from massive meconium aspiration. Respiratory failure was indicated initially by arterial blood gas tensions (while breathing 100% O(2)) of Po(2) <40 mm. Hg, pH <7.10 and Pco(2) >75 mm. Hg in the initial 47 cases; these levels were subsequently raised to Po(2) < 50 mm. Hg, pH <7.20 and Pco(2) >70 mm. Hg for the remainder. Fifty-four (59.3%) of the infants survived the use of the respirator and 47 of these (51.6%) were subsequently discharged alive and well. Mean time in hours to normalization of blood gas values while on the respirator were as follows: for Po(2), 10.5; for pH, 11.6; and for Pco(2), 22.6. These values indicate that the respirator is more efficient in promoting oxygenation (raising Po(2)) than ventilation (lowering Pco(2)). They also suggest that the observed acidosis is in large part secondary to the hypoxia rather than the result of co(2) retention. For the survivors the average time of total respirator dependency before commencement of weaning was 53.7 hours. All the infants were managed without the use of endotracheal tubes although the use of the respirator and/or administration of 100% oxygen were either continuous or intermittent for periods of up to two weeks. There have been no instances of so-called respirator lung disease in the survivors or in those who died, which suggests that the use of high oxygen concentration by itself is not the major factor in the pathogenesis of this complication.
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PMID:Negative pressure artificial respiration: use in treatment of respiratory failure of the newborn. 526 97

Two patients with small cell carcinoma of the lung treated by chemoradiotherapy developed, diffuse interstitial pneumonitis after 7 and 21 months of treatment while in complete remission of their malignant disease. One patient died after an acute respiratory distress syndrome, but the second improved after steroid therapy and discontinuation of cytotoxic therapy. Pulmonary toxicity appeared to be related to cyclophosphamide therapy, but radiation therapy could have potentiated cyclophosphamide toxicity as it has been shown in bleomycin lung disease.
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PMID:[Drug induced pulmonary disease. Diffuse interstitial pneumonitis during chemoradiotherapy for small cell carcinoma of the lung. Two cases (author's transl)]. 628 5

This study quantifies apnoea and assesses the response to xanthine derivatives amongst 172 consecutively born, surviving very low birth weight (VLBW) infants, 136 appropriate weight for gestational age (AGA), 36 small for gestational age (SGA). All babies had electronic monitoring of heart and respiratory rates and nursing staff recorded episodes of apnoea (greater than 10 s), bradycardia (less than 100) and cyanosis. Only 42 (24.2%) babies had no episodes recorded. (25 AGA, 17 SGA). Sixty-four (37.2%) received active resuscitation on at least one occasion with six babies ventilated by bag and mask on more than 10 occasions. Apnoea had commenced by day 10 of life in all the babies who had apnoea and persisted beyond day 50 in only six; however four of these infants were still requiring active resuscitation. Apnoea had ceased by 37 weeks post-conceptual age in 88% and by 40 weeks in all but three babies. Risk factor analysis revealed a strong correlation (P less than 0.005) with lower gestational ages and birth weights, respiratory distress syndrome (RDS) and the problems associated with it, such as mechanical ventilation, patency of the ductus arteriosus (PDA) and chronic neonatal lung disease. A single, reversible cause for apnoea was rarely demonstrated. Care must be exercised with feeding, physiotherapy and suctioning the pharynx and trachea of 'at risk' infants. Xanthine derivatives were highly effective in decreasing the frequency of recurrent apnoea from a mean of 10.08 episodes one day before, to 1.83 two days after commencement of treatment.
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PMID:Clinical spectrum of neonatal apnoea in very low birthweight infants. 646 30

Plasma concentrations of retinol and retinol-binding protein were measured at birth in 91 preterm infants. In 64% of these babies retinol values were less than 20 micrograms/dl, suggestive of vitamin A deficiency. Forty-seven of these infants were observed with sequential measurements of retinol and retinol binding protein through 21 days of age. In babies with respiratory distress syndrome retinol values were similar to those in babies without respiratory distress syndrome. The retinol binding protein levels were lower on the third day of life in babies with respiratory distress syndrome. Babies who developed bronchopulmonary dysplasia had lower concentrations of retinol at birth (P less than 0.05) and on day 21 (P less than 0.05) than did babies who did not develop bronchopulmonary dysplasia, despite receiving recommended intakes of vitamin A. Many preterm infants are deficient in vitamin A at birth, and failure to correct this deficiency may contribute to the development of chronic lung disease.
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PMID:Relationship of vitamin A (retinol) status to lung disease in the preterm infant. 648 38

The pulmonary course and respiratory management of 65 asphyxiated infants with at least one arterial pH less than or equal to 7.00 within the first 2 hours of life was determined. Asphyxia in the preterm and term infants in the absence of respiratory distress syndrome or meconium aspiration syndrome was associated with a transient respiratory insufficiency requiring assisted ventilation which markedly improved in the first 24 hours of life. In contrast, infants with asphyxia complicated by respiratory distress syndrome or meconium aspiration syndrome developed profound lung disease including pulmonary hemorrhage and persistence of the fetal circulation. The course of their illness was significantly worse than control infants without asphyxia. Ineffective neonatal resuscitation allowing for the development of meconium aspiration syndrome and persistent respiratory acidosis contributed to the severity of illness in more than 50% of the infants. Central nervous system pathologic conditions were present in asphyxiated infants with and without severe pulmonary disease. We conclude that severe asphyxia in the absence of underlying lung disease results in a predictable postasphyxial transient respiratory insufficiency, with marked improvement in the first 24 hours of life.
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PMID:Postasphyxial lung disease in newborn infants with severe perinatal acidosis. 648 2

Increased synthesis of type I collagen, leading to increased ratios of type I to type III collagen in the lungs, has been observed in the lungs of animals with experimental pulmonary fibrosis. Similar changes in collagen type ratios have been observed in lungs of humans dying of idiopathic pulmonary fibrosis and of adult respiratory distress syndrome. In this study, lung collagen type ratios were examined in infants with acute and chronic lung disease. Tissue from the right lower lobes of neonates was obtained post mortem. Specific collagen types were quantitated by solubilization of lung collagen with CNBr and fractionation of the resulting mixture of peptides by column chromatography and polyacrylamide gel electrophoresis. Ratios of type I/III collagen were calculated for each lung sample using two independent pairs of marker peptides for these determinations. In some cases the ratio of type V to type III collagen in these same lung samples was also quantitated. We observed a significant increase in the ratio of type I/III collagen in infants with a premortem diagnosis of chronic lung disease, usually preceded by respiratory distress syndrome. We also observed two infants with large changes in collagen type ratios who might have had pulmonary fibroplasia secondary to intrauterine lung disease. These data suggest that there may be several subsets of infants with respiratory distress syndrome, each having a different prognosis.
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PMID:Elevated ratios of type I/III collagen in the lungs of chronically ventilated neonates with respiratory distress. 651 44

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 effluent samples were obtained from 26 preterm or term infants throughout the period of endotracheal intubation. Infants with respiratory distress syndrome, infants with this disorder developing bronchopulmonary dysplasia, and intubated infants without lung disease were compared daily in terms of lung effluent cellularity, albumin, elastase activity, alpha 1-proteinase content and activity, and elastase inhibitory capacity. The elastase activity was determined to be neutrophilic in origin. Polyacrylamide gel electrophoresis of pulmonary effluents from two infants with respiratory distress syndrome and exposed to FiO2 greater than or equal to 0.6 up to 6 d revealed cleavage of alpha 1-proteinase inhibitor to a 47,000-mol weight fragment suggestive of oxidation. Pulmonary effluent neutrophils, macrophages, and elastase activity were increased by day 3 of life in infants with respiratory distress syndrome eventually developing bronchopulmonary dysplasia. Elastase inhibitory capacity and alpha 1-proteinase inhibitor activity were reduced in infants developing chronic lung disease. Bronchopulmonary dysplasia developed in infants with enhanced inflammatory response, but with less or inhibited antiprotease activity.
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PMID:Elastase and alpha 1-proteinase inhibitor activity in tracheal aspirates during respiratory distress syndrome. Role of inflammation in the pathogenesis of bronchopulmonary dysplasia. 660 78

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

It is well recognized that the lung has its own hormonally responsive endogenous metabolism. Less well recognized is the potential of the lung to influence and, in turn, be influenced by the homeostatic mechanisms of the body. It is suggested that the lung could modulate concentrations of circulating hormones and thereby play an indirect exogenous metabolic role in whole-body metabolism. Investigations of patients undergoing cardiopulmonary bypass as well as studies with the perfused rat lung suggest that the lung could make an important direct contribution to whole-body lactate and perhaps alanine production. The control of the endogenous and exogenous metabolism of the lung may be exerted through circulating hormones, substrates, blood gases and lung movement. Disorders of the lung or the whole body may disturb these relationships. In patients with chronic lung disease circulating blood metabolites are affected and conversely in diabetes there are effects on lung metabolism. The unified concept of lung/whole-body metabolism is discussed in relation to therapeutic approaches for the prevention and investigation of neonatal and adult respiratory distress syndromes.
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PMID:The lung, whole-body metabolism and disease. 678 28


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