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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared four treatment protocols in 57 patients with presumed pre-hospital pulmonary edema. Group A patients were treated with nitroglycerin and furosemide, group B patients with morphine sulfate and furosemide, group C with all three agents, and group D with nitroglycerin and morphine, but without furosemide. Twenty-three percent of our patients were ultimately found not to have pulmonary edema, with pneumonia and/or exacerbations of chronic lung disease the most frequent alternate diagnoses. Group A patients had significantly greater improvement, both subjectively and objectively, than group B patients, a substantial number of whom failed to improve, or even worsened. There was no evident synergistic effect of any of the drugs, and some indication that furosemide might have caused clinically important problems with fluid and electrolyte management in some of the patients. Our data suggest that nitroglycerin is beneficial in the management of presumed pre-hospital pulmonary edema, while morphine and furosemide may not add anything to its efficacy, and may be potentially deleterious in some of these patients.
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PMID:Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema. 311 87

Acute bovine pulmonary edema is a naturally occurring lung disease caused by 3-methylindole (3MI), a ruminal fermentation product of tryptophan. Morphological and in vitro studies have suggested that 3MI causes abnormalities in phospholipid synthesis. The present study was designed to investigate the effect of 3MI on the quantity and functional quality of surfactant using the goat as an experimental model. Following intravenous infusion of 3MI, goats were killed at 6-, 18-, and 30-h intervals. The lungs were removed and intracellular surfactant, in the form of lamellar bodies, and extracellular surfactant from alveolar lavage were quantified. 3MI treatment did cause modest changes in the lamellar body phospholipid pools, decreasing the quantity of phosphatidylcholine and the proportion of palmitate in this fraction. The quantity of lavage phospholipids was not significantly affected. There was an increase in the protein content of the lavage, reflecting the presence of edema. The functional quality of the surfactant isolated from the lavage fraction was tested in vitro using a pulsating bubble surfactometer. 3MI infusion decreased the ability of surfactant to lower the surface tension of an air bubble at maximum radius and during compression.
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PMID:The effect of 3-methylindole on the quantity and functional quality of lung surfactant. 321 1

Adult respiratory distress syndrome, a clinical syndrome of respiratory failure that follows many kinds of insults, often in patients with no previous pulmonary disease, occurs in pediatric patients. This group of disorders has a typical clinical, pathologic, and pathophysiologic course, the hallmark of which is injury to the alveolar-capillary membrane with increased permeability of the pulmonary vasculature and pulmonary edema. Resolution may occur at any stage, but most patients die and many develop chronic lung disease requiring respiratory support for weeks or months. Multiple organ system failure, secondary infection, and irreversible respiratory dysfunction are responsible for the poor outcome. The underlying mechanisms that relate injury to the development of pulmonary disease are unclear. In some cases there may be direct injury to the lung, but in others, such as septic shock, there are mediators that link the initial insult to the subsequent lung injury. The leukocyte may have a central role in this process, although this is uncertain. Therapeutic measures needed to support the patient, especially increased inspired oxygen, are additional factors in the progression of lung disease. Current therapy, as summarized in Table II, is primarily supportive. Efforts to treat ARDS after it is clinically apparent have been disappointing. The pathogenic mechanisms that lead to ARDS are probably well advanced by the time the syndrome is diagnosed on the basis of the usual clinical signs. Therefore an emphasis on understanding the mechanisms of lung injury so that specific markers can be used to predict which patients will develop ARDS, allowing intervention in the early stages of the process, may prove rewarding.
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PMID:Adult respiratory distress syndrome in pediatric patients. II. Management. 327 74

Six cases of leptospirosis with pulmonary complications are reported. Three cases were accompanying an hepato-nephritis due to L. icterohaemorrhagiae. The first patient died with massive hemoptysis. The second, presenting a bilateral pneumopathy predominant on the left side, recovered after plasma exchange and hemofiltration. The third case concerned a pulmonary edema complicating a vascular refilling in a shock syndrome it simply recovered. The three other cases were observed in an anicteric leptospirosis: in two cases, L. Australis was responsible; in the last, L. icterohaemorrhagiae was involved. The first patient had a radiologic picture simulating miliary tuberculosis. The second had pulmonary edema complicating a vascular refilling in a shock syndrome. The last was an acute respiratory distress syndrome, treated with artificial ventilation with penicillin therapy and corticotherapy. All these 3 patients recovered. The diagnostic, physiopathologic and therapeutic problems of these pulmonary complications of leptospirosis are discussed. The lesional nature of the pulmonary edema is proved by the low pulmonary wedge pressures observed with the Swan-Ganz Catheter.
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PMID:[Respiratory complications of leptospirosis. Apropos of 6 cases, 3 of which show hemodynamic studies]. 340 72

Lung disease may result from a persisting proteinase excess or a depletion of antiproteinase in pulmonary parenchyma. We investigated the in vivo effect of a 48-hr exposure to ozone at 0.5, 1.0, or 1.5 ppm on proteinase and antiproteinase activity of rat lungs. Elastase inhibitory capacities of serum, lung tissue, and airway washings were measured as indicators of antielastase activity. Trypsin inhibitory capacity was measured using an esterolytic procedure. Proteinase was measured as radioactive release from a 14C-globin substrate. The 48-hr exposures to O3 at levels up to 1 ppm produced concentration-dependent decreases of 35-80% of antiproteinase activities in serum and in lung tissue. However, exposure to 1.5 ppm O3 resulted in no decrease in antiproteinase activities. Acid proteinase activities (pH 4.2) were increased 65-120% by exposure to 1 or 1.5 ppm O3, which correlated with inflammatory cells noted histologically. At 1.5 ppm O3, pulmonary edema and hemorrhage were noted in histologic sections. These changes led to a flooding of the alveoli with up to 40 times normal protein levels and a greater than fivefold increase in airway antiproteinase. These data suggest that serum and soluble lung tissue antiproteinase activity decreased upon exposure to low levels of ozone. However, if O3 exposure is high enough to produce pulmonary hemorrhage, antiproteinase may increase following serum exudation. These changes may be important in the development of ozone-induced lung diseases, especially emphysema.
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PMID:Effect of acute ozone exposure on the proteinase-antiproteinase balance in the rat lung. 354 51

Impedance pneumography, electrical impedance measurements of the lung, is a technique which has been widely used to monitor respiration non-invasively and more recently, the onset of pulmonary oedema. Attempts have been made to try to localise the changes in impedance using electrode arrays and electrode guarding. These techniques allow localisation to a particular hemithorax, but the resolution of the majority of the systems remains poor. To assess the performance and possible clinical applications of APT, measurements have been made following increases in lung volume and pulmonary blood volume. During inspiration an increase in both the area and the magnitude of the impedance changes over the area of the lungs was observed. Numerical analysis of the impedance changes in normal subjects reveals a consistently high correlation between the volume of air inspired and the magnitude of the impedance changes. The resolution of the system is sufficient to monitor differences in ventilation in the right and left lung and to measure variations in these levels with posture. Preliminary clinical work suggests that APT may be used to detect ventilatory defects in certain types of lung disease. APT measurements show a decrease in resistivity over the area of the lungs when the pulmonary blood volume is increased by the intravenous infusion of 1.5 litres of isotonic saline. Similar changes in the volume of fluid in the lungs are known to occur in pulmonary oedema. APT measurements of lung impedance may detect the onset of pulmonary oedema in high risk patients.
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PMID:Applications of applied potential tomography (APT) in respiratory medicine. 356 65

The pathological findings in the lungs and related organs of 26 patients (21 female, 5 male) with systemic lupus erythematosus (SLE), with onset of disease before age 20 years, were reviewed. Several categories of lung lesions were found. Chronic interstitial pneumonitis was present in all 26 patients and was severe in 5. Acute pneumonia was present in 20, mild in 13, moderate in 2, and severe in 5. Alveolar hemorrhage, massive enough to cause death in 5, was seen in 18 patients, and pulmonary edema was found in 13. Fourteen patients had hyaline membranes indicative of acute alveolar damage (DAD), 12 had alveolitis obliterans, indicative of prior episodes of DAD, and 9 had bronchiolitis obliterans. Other parenchymal lesions were mild interstitial fibrosis in 12, alveolar hemosiderosis and alveolar overinflation in 10 each, and alveolar septal calcinosis with chronic renal insufficiency in 3. Pleural effusion, pleuritis, or pleural thickening were noted in 15 of 26, 6 of 23, and 7 of 23 evaluable patients, respectively. Vascular lesions were present in 16 as intimal thickening (9), thromboemboli (8), medial hypertrophy (6), calcinosis (3), and vasculitis (2). A previously unreported lesion was chronic (proliferative) peribronchitis, noted in 11 patients. Diaphragmatic lesions included mild variation in fiber size in 7, mild fibrosis in 2, and calcinosis in 1 of 13 evaluable patients. Correlation of the above lesions with previously described lung syndromes in SLE such as lupus pneumonitis, hemorrhagic lung disease, chronic interstitial fibrosis, lupus cor pulmonale, pleurisy, and "shrinking lung syndrome" are discussed.
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PMID:Pulmonary lesions in childhood onset systemic lupus erythematosus: analysis of 26 cases, and summary of literature. 360 12

In the present study we investigated the phospholipid composition of small-volume (up to 20 ml) in vivo bronchoalveolar lavage and that of quantitative ex vivo bronchoalveolar lavage. Furthermore, the accuracy of the small-volume lavage in predicting lung disease was evaluated. There was a positive linear correlation (r approximately equal to 0.87-0.91) between the amount of saturated phosphatidylcholine and the saturated phosphatidylcholine/sphingomyelin ratio in quantitative bronchoalveolar lavage. The phospholipid distributions in the small-volume lavage and the quantitative lavage were similar (r approximately equal to 0.78-0.94, n = 14). The overall accuracy of phosphatidylcholine/sphingomyelin ratio and phosphatidylglycerol/total phospholipid ratio in predicting the presence or absence of respiratory failure was 85-87% in newborns, children, and adults. In respiratory diseases without respiratory failure, the abnormalities in the phospholipids were frequent, although less distinct. According to animal experiments the surfactant system is inhibited at the onset of high permeability lung edema. Soon thereafter, the lavageable surfactant pool is decreased. Present findings support the view that surfactant defects are of importance in the pathogenesis of respiratory disease, and that surfactant-oriented therapy may be effective in the treatment and prevention of respiratory failure.
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PMID:Endobronchial surface active phospholipids in various pulmonary diseases. 386 Mar 95

Acute lung disease is commonly associated with interstitial pulmonary edema and a tendency towards partial or total alveolar collapse. To counteract this tendency mechanical ventilation is successfully used in most cases. Mechanical ventilation, however, leads to a harmful retention of water and salt, which may worsen interstitial pulmonary edema and further impair gas exchange. This problem seems to be less known. A survey of the effects of currently used modes of mechanical ventilation on excretory function and hemodynamics of the kidneys is given together with a short review of the possible afferent and efferent mechanisms which mediate the renal response to mechanical ventilation. Some clinical suggestions are made to break through the vicious cycle between mechanical ventilation and kidney function.
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PMID:[Artificial respiration and kidney function disorder--a vicious circle?]. 389 Jun 7

A study was conducted to determine the dose of lasalocid that would effectively reduce ruminal conversion of tryptophan (TRP) to 3-methylindole (3MI) and prevent the development of acute bovine pulmonary edema and emphysema (ABPE). After adaptation to a maintenance diet for 3 wk, 20 mature beef cows were randomly divided into four groups of five cows each and fed 0, 200, 400 or 600 mg lasalocid X head-1 X d-1 in .5 kg ground barley for the 12-d experimental period. In vitro conversion of TRP to 3MI and indole by ruminal fluid and volatile fatty acid (VFA) concentrations were determined on d 0, 2, 4, 6 and 12. On d 6, an oral dose of .35 g TRP/kg body weight was given to induce ABPE, and ruminal production of 3MI and indole was determined at intervals thereafter. Formation of 3MI was sharply reduced (P less than .01) both in vitro and in vivo by lasalocid treatment at 200 mg X head-1 X d-1. Further suppression of 3MI production occurred as the lasalocid dose was increased (P less than .05). Linear (P less than .0001) and quadratic (P less than .002) components were determined for the relationship between lasalocid dose and 3MI production. Indole formation was variable, but tended to increase (P less than .05) with increasing lasalocid dose. Cows that received no lasalocid developed moderate to severe clinical signs of ABPE and three cows died of acute lung disease. Lasalocid treatment at all levels prevented ABPE. Lasalocid decreased ruminal acetate and butyrate, and increased propionate concentration (P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of 3-methylindole production and prevention of acute bovine pulmonary edema and emphysema with lasalocid. 397 44


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