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

Lesional pulmonary edema caused by substances which are directly caustic for the gastrointestinal pathways (strong acids and bases, inhaled vomit) are opposed by their immediate and long-term gravity with those due to cardiotropic medicamentatous toxins or volemic overloading which lead to curable pulmonary edema. Material and human factors, in favour of accidental intoxication are compensated for by the fact that many toxins produce vapours which are strongly irritant for the upper respiratory pathways: this prevents prolonged exposure and therefore wards off edema. Drug intoxication by ingestion can lead to pulmonary edema by relative or absolute volemic overload, by allergic accidents or by immaturity of the enzyme degradation systems. It seems to us that the notions of "neurological" and "metabolic" toxic edema should be abandoned. In lesional edema the treatment is that of the acute respiratory failure. The combination of pethidine, promethazine, and chlorpromazine gives good immediate results. Owing to careful follow-up, hemodynamic pulmonary edema should most frequently be avoided.
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PMID:[Nonhemodynamic pulmonary edema due to toxins]. 0 74

The authors report 6 cases of acute respiratory failure complicating chronic bronchial and lung disease admitted to hospital with the diagnosis of: heart disease, 3 cases, pulmonary oedema, pulmonary embolism, atrial flutter; status asthmaticus : one case; neuro-psychiatric disease : 2 cases (toxic coma and agitation). The authors emphasize the frequency of chronic bronchial disease and recall the signs of acute decompensation discussing the possible difficulties in diagnosis and the therapeutic implications.
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PMID:[Deceptive and revealing clinical forms of acute respiratory insufficience in chronic bronchopneumopathies]. 19 94

Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
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PMID:Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome. 37 80

The ability of the portable chest x-ray film to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in thirty-seven observations of eleven patients. Ten of the eleven patients were suffering from acute respiratory failure. The radiologic assessment of the amount of pulmonary edema and the severity of left ventricular failure were compared with the physiologic shunt fraction, tracer-measured lung water, and pulmonary arterial wedge pressure. The radiologic scores for edema did not predict the shunt fraction or tracer measurements of lung water. The radiologic score for congestive failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the x-ray results were false-positive and 11 per cent false-negative. Results indicate that the portable chest x-ray technic does not provide quantitative information regarding cardiopulmonary function. It is especially hazardous to accept an x-ray diagnosis of congestive failure as the cause of pulmonary edema.
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PMID:Diagnostic value of the portable chest x-ray technic in pulmonary edema. 63 9

The ability of the portable roentgenography of the chest to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in 37 observations of 11 patients. Ten of the 11 patients had acute respiratory failure. The roentgenologic assessment of the amount of pulmonary edema and the severity of left ventricular failure was compared with the physiologic shunt fraction, tracer measured lung water and the pulmonary arterial wedge pressure. The roentgenologic scores for edema did not predict the shunt fraction or tracer measured lung water. The roentgenologic score for congestive heart failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the roentgenograms were false-positive and 11 per cent were false-negative. Roentgenologic findings lagged behind physiologic derangements. Thus, the roentgenogram could predict the shunt value of the preceding day. Results indicate that it is hazardous to accept a portable roentgenographic diagnosis of congestive heart failure as a cause of pulmonary edema.
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PMID:Limitations of portable roentgenography of the chest in patients with acute respiratory failure. 64 29

In patients with fulminating pulmonary edema not responsive to conventional therapy, venoarterial membrane lung bypass can provide assistance if decreased systemic blood pressure prevents use of high-level positive end-expiratory pressure ventilation. In 10 patients with acute respiratory failure, partial venoarterial bypass provided a rapid and marked improvement of systemic oxygenation. Measurement of pulmonary blood flow (PBF) and intrapulmonary shunting (QS/QP) during bypass via prolonged left heart catheterization showed that left ventricular PaO2 was increased through a rapid and profound reduction of QS/QP. During the first days of bypass, derecruitment of pulmonary vessels is probably the mechanism of improved pulmonary oxygenation. When low pulmonary arterial pressures (PAP) are sustained, resorption of pulmonary edema is favored. Despite the beneficial effects of bypass, death occurred in every case due to diffuse interstitial fibrosis and/or parenchymal damage. The absence of healing, due to prolonged circulatory exclusion, may be detrimental despite immediate improvement. Because of this possibility, venovenous or mixed perfusion should be more extensively explored.
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PMID:Pulmonary gas exchange during venoarterial bypass with a membrane lung for acute respiratory failure. 66 54

Noncardiogenic pulmonary edema and acute respiratory failure were found to develop after blood transfusion. Pulmonary antiographic studies and hemodynamic measurements were performed in the presence of pulmonary edema. Normal wedge pressure was observed at the time of angiographic studies, and contrast material appeared to extravasate across the alveolocapillary membrane into the alveoli. The mechanisms of acute injury to the alveolocapillary membranes and of pulmonary edema secondary to reactions to transfusion are discussed.
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PMID:Noncardiogenic pulmonary edema following blood transfusion. 68 93

Acute respiratory failure evolved in five patients following hypovolemic shock related to trauma or surgical operation, or both. A reduction in colloid osmotic pressure, increases in pulmonary artery wedge pressure and reductions in colloid osmotic pressure-pulmonary artery wedge pressure gradient to levels which are likely to account for pulmonary edema were observed. Accordingly, reduction in the colloid hydrostatic pressure gradient may, in part, explain the development of acute respiratory failure after acute blood loss. In one instance, however, the absence of such reduction in the colloid osmotic pressure-pulmonary artery wedge pressure gradient together with increases in pulmonary vascular resistance showed that colloid osmotic pressure and pulmonary artery wedge pressure are not exclusively operative in the pathogenesis of the clinical syndrome of acute respiratory failure.
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PMID:Colloid osmotic and pulmonary wedge pressures in acute respiratory failure following hemorrhage. 70 73

The possible association between acute respiratory failure and disseminated intravascular coagulation was examined in eight patients with severe acute respiratory failure--a condition characterized by tachypnea, right to left intrapulmonary shunting of blood greater than 30 per cent of cardiac output, increased pulmonary artery pressure with low or normal pulmonary artery wedge pressure and roentgenologic interstitial pulmonary edema. Treatment consisted of mechanical ventilation with positive end expiratory pressure sufficient to minimize intrapulmonary shunting. There was no abnormality in platelet concentration fibrin split product concentration, fibrinogen concentration, prothrombin time or activated partial thromboplastin time during the period of most severe respiratory failure in any patient. However, mean platelet concentration fell to 90,000+/-9,000 per cubic millimeter, less than 0.001, and mean fibrin split product levels rose to 60+/-10 micrograms per milliliter, p less than 0.05, the fourth day after the onset of acute respiratory failure. No significant change occurred in other coagulation parameters. Disseminated intravascular coagulation developed in none of the patients nor was there any correlation between coagulation abnormalities and severity of acute respiratory failure that would suggest a cause and effect relationship.
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PMID:Acute respiratory failure and intravascular coagulation. 78 44

Patients with shock lung syndrome were identified as those who developed acute respiratory failure after a profound episode of hypotension secondary to hemorrhagic, gram-negative, or endotoxic shock. In this study, each of the 10 patients with shock lung syndrome received methylprednisolone sodium succinate, 30 mg. per kilogram, intravenously every 6 hours for 48 hours. In addition, all patients were supported with mechanical ventilation, with or without positive end-expiratory pressure (PEEP). Arterial oxygenation improved markedly, and pulmonary edema resolved in all patients. Nine were discharged from the hospital and one died subsequently of disseminated intravascular coagulation. This study demonstrated a significant improvement in mortality rate with repeated pharmacologic doses of methylprednisolone compared to previously reported mortality rates of 60 to 90 per cent in patients with shock lung syndrome treated without repeated pharmacologic doses of steroid therapy.
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PMID:Methylprednisolone. Pharmacologic doses in shock lung syndrome. 126 66


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