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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Understanding of the causes of pulmonary oedema must be based on knowledge of the mechanism responsible for fluid exchange between the several compartments of the normal lung. Recent physiological studies have clarified the main features of these mechanisms. However in three areas knowledge is still incomplete--the magnitude of the hydrostatic and oncotic forces responsible for fluid movement within the lung, the means by which protein leaks across the wall of small pulmonary vessels and the routes by which fluid and protein pass between the interstitial tissues of the lung and the alveolar space. Further work is needed in these areas. On the basis of this physiological knowledge the mode of development of hydrostatic oedema, the role of lymphatics in pulmonary oedema, and the several stages of pulmonary oedema development that may culminate in alveolar flooding are now clearly understood. Knowledge is less complete about oedema due to increased vascular permeability. In some experimental models, such as alloxan, leakage is due to irreversible injury to the alveolar wall; in other models, including ANTU, oedema formation has been shown to depend upon minor and reversible changes in pulmonary vascular endothelium similar to those that cause exudate formation in areas of acute inflammation. In no instance is detailed information available of both the rate and magnitude of protein leakage and of the morphological basis of increased vascular permeability. Further work is required in this area. Present knowledge allows an adequate explanation of the changes that occur in many clinically important types of pulmonary oedema, including cardiac failure and neurogenic pulmonary oedema. Other types of oedema, notably that which may complicate traumatic shock or extrapulmonary sepsis and high altitude pulmonary oedema, are more complex and the details of their pathogenesis are still obscure.
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PMID:Current views on the mechanisms of pulmonary oedema. 36 92

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

During a 1 yr period, 19 infants less than 2 mo of age were fed intravenously with an infusate composed of glucose, amino acids, electrolytes, and vitamins. The solution was infused at a rate of 200 ml/kg/day or more for periods ranging from 5-247 days. No central venous catheters were utilized; the solutions were always administered through a needle in a peripheral vein. Weight gains similar to those seen with other techniques of intravenous nutrition were observed in all of the patients studied. No instance of fluid overload in the form of pulmonary edema, peripheral edema, or congestive heart failure was seen, and osmotic diuresis was not observed because of the lower tonicity of the infusate. Phlebitis was seen in 1/5 of the infusions, but was reversed by stopping the infusion and applying warm soaks. Three cases of skin slough were observed and two of these healed spontaneously without the need of skin grafting. The advantages of this technique over central venous nutrition are the elimination of the complications related to the central venous catheter, namely, sepsis and superior vena cava thrombosis.
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PMID:Peripheral intravenous nutrition without fat in neonatal surgery. 40 75

The first home dialysis was carried out from Guy's Hospital in London in 1968. Since then, 141 patients have been treated in this manner. The age of the patients ranged from 4 to 64 years. 24 patients have died (cerebrovascular accidents, myocardial infarction, pulmonary edema, sepsis, peritonitis, hyperkalemia etc.). Some of the deaths were due to a slackening of discipline on the part of the patients and nursing staff during the years of constant dialysis. Of 60 adults 52 were able to start work again; full rehabilitation still seems possible in 6 cases. Nevertheless, many patients cannot lead a normal life because their social and sexual activity is greatly restricted. The present economic crisis led to financial limitations in the National Health Service. In future, home dialysis may have to be reduced and more transplantations performed.
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PMID:[Guy's Hospital home dialysis program (author's transl)]. 41 3

Current evidence suggests that pulmonary edema accompanying human sepsis may result either from changes in the serum oncotic and hydrostatic pressures or an increase in the permeability of the pulmonary microvasculature. In this study, we compared the "clearance" of injected 131I-labeled human serum albumin from blood to bronchoalveolar secretions in intubated patients with pulmonary edema secondary to sepsis or myocardial infarction. A significantly increased mean +/- SE clearance of the radionuclide was seen in patients with sepsis (0.34 +/- 0.03 ml per hour) compared to those with myocardial infarction (0.043 +/- 0.008 ml per hour) (P less than 0.001), although both groups had similar degrees of edema on chest radiographs. Because the patients with sepsis had no severe decrease in serum oncotic pressure (18.4 +/- 5.0 mm Hg) or evidence of left heart failure, as determined by the pulmonary wedge pressure (11.0 +/- 6.8 mm Hg), we concluded that the genesis of the pulmonary edema in sepsis was due to an increase in pulmonary microvascular permeability, as measured by the increased clearance of 131I-labeled human serum albumin.
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PMID:Documentation of pulmonary capillary permeability in the adult respiratory distress syndrome accompanying human sepsis. 45 8

Eleven cases of renal failure associated with resection of ruptured abdominal aortic aneurysm and requiring hemodialysis are reported. Previously described series have emphasized the extremely high mortality rate in such patients. In our clinical experience, however, 8 of 11 consecutively treated patients with this clinical problem survived and recovered adequate renal function. We believe that these favorable results can be largely explained by the low incidence of pulmonary infection in our patients as opposed to the frequent occurrence of pulmonary sepsis in other reported series. The reduction in the incidence of pulmonary infection can probably be attributed to the early discontinuance of artificial ventilation after prompt removal of pulmonary edema fluid by intensive hemodialysis ultrafiltration. These survival figures demonstrate that, with appropriate intensive management, full recovery is possible in the majority of patients with acute renal failure complicating ruptured aortic abdominal aneurysm. Our experience serves as a stimulus to render full intensive care support to such patients.
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PMID:Acute renal failure after ruptured abdominal aortic aneurysm: an improved clinical prognosis. 45

Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.
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PMID:Hemodynamic and alveolar protein studies in noncardiac pulmonary edema. 98 76

Fifteen critically ill patients with sepsis, 12 of whom had significant pulmonary dysfunction develop, were investigated with regard to changes in pulmonary capillary pressure, in serum oncotic pressure and on roentgenograms of the chest. It could not be shown that the pulmonary edema, which is a major characteristic of the septic lung lesion, was due to changes only in oncotic and hydrostatic pressures. Nor was there evidence that increased capillary permeability was the sole explanation of the edema. A significant relationship was found which consisted of increasing severity of the lung lesion, decreasing serum oncotic pressure and increasing pulmonary pressure. When patients with sepsis require resuscitation with fluids, the administration of moderate amounts of albumin along with monitoring of pulmonary capillary pressure appears to be a rational approach to therapy.
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PMID:Pulmonary edema in patients with sepsis. 112 75

Hemodynamic data were collected in 42 patients with pulmonary edema (P.E.) due to altered permeability of various causes. Pulmonary artery wedge pressure (PWP) was normal, whatever the time of the study and the severity of the P.E. Pulmonary artery hypertension was present in the cases with severe hypoxemia, but disappeared with hypoxemia correction. In some cases, a hyperkinetic or a hypovolemic syndrome was found, being induced by the cause of P.E. Although within normal limits, PWP was significantly higher at the first hours of P.E. than after the 6th hour. Perfusion of colloid solutes worsened P.E., although increasing PWP by only a few mmHg. Dehydration using diuretics markedly improved the venous admixture, although PWP was previously normal. These data document the production of P.E. in many causes-such as severe sepsis, drowning, fat embolism, barbiturate overdose-by impaired alveolo-capillary permeability, PWP and blood protein content remaining within normal limits. They also demonstrate the noxious effects of overperfusion and the efficiency of dehydration in such pulmonary edemas.
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PMID:[Hemodynamic study of pulmonary edemas due to the increase of alveolo-capillary permeability]. 119 58

The complications encountered in caring for 185 patients intoxicated with barbiturates were reviewed. The population consisted of 142 patients with long-acting barbiturate concentrations of 8 mg per 100 ml or greater, 20 patients with short-acting barbiturate concentrations of 3 mg per 100 ml or greater and 23 consecutive patients with short-acting barbiturate intoxication referred for monitoring. Pneumonia was the major cause of morbidity and mortality and correlated best with the initial depth of coma and the use of an endotracheal tube in treatment. Cardiovascular instability manifested by pulmonary edema was the next leading cause of morbidity and mortality and correlated best with the initial depth of coma and the quantity of intravenous fluid administered. In retrospect, use of eliminative measures such as dialysis would probably not have altered the outcome in most of the patients who died and attempts at forced diuresis may have contributed to several deaths. Particular emphasis should be placed on the problems of sepsis and fluid therapy in the management of these patients.
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PMID:Barbiturate intoxication. Morbidity and mortality. 125 66


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