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

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
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PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24

Fluid replacement is a major issue in the treatment of patients with diabetic ketoacidosis. During this therapy, development of pulmonary edema has been reported and attributed to an increase in pulmonary microvascular pressure and a decrease in colloid-osmotic pressure (COP). Because clinically apparent pulmonary edema is associated with an increase in extravascular lung water (EVLW) and impairment of pulmonary gas exchange, we studied the effect of fluid replacement on EVLW, COP, pulmonary hemodynamics and gas exchange parameters in 8 patients with diabetic ketoacidosis (blood glucose greater than 300 mg/dl, pH less than 7.1). EVLW was estimated by the thermal-dye technique. All variables were successively determined upon admission (A), after initial fluid replacement (IFR), when glucose had fallen below 180 mg/dl, after 8 h of intravenous glucose treatment (G), and after 24 h of total parenteral nutrition (TPN). Despite a total net fluid intake of 6.0 +/- 1.61, a significant decrease (p less than 0.001) in COP from 29.6 +/- 5.5 at A to 18.8 +/- 2.2 mmHg after TPE and a significant increase (p less than 0.001) in PCWP from 4 +/- 2 at A to 10 +/- 3 mmHg after TPE, EVLW remained almost unchanged. EVLW was 5.1 +/- 2.8 at A, 5.3 +/- 2.1 after IFR, 4.8 +/- 1.4 after G, and 5.3 +/- 1.7 ml/kg after TPN. However, PaO2 decreased from 137 +/- 17 at A to 87 +/- 10 mmHg after TPE (p less than 0.001), while Qs/Qt increased significantly (p less than 0.05). The alterations in gas exchange may be indicative of pulmonary dysfunction but as they were not associated with accumulation of EVLW, they may as well reflect the compensation of metabolic derangements in diabetic ketoacidosis.
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PMID:Influence of fluid replacement on extravascular lung water (EVLW) in patients with diabetic ketoacidosis. 313 89

Heart and lung transplantation has only provided long-term survival for patients with end-stage cardiopulmonary disease. Many more patients of potential recipients cannot receive the transplantation because of a pause of satisfactory donors. One of its reason is difficulty in prolonged heart-lung preservation and this has imposed a significant barrier to donor procurement. Using Autoperfusion of heart and lung, six hours preservation was successfully achieved in six mongrel dogs and an adequate condition for preservation was evaluated. 1. Glucose metabolism, 2. Electrolytes, 3. Acid-base balance, 4. Pulmonary blood flow, 5. Temperature, 6. Ventilation were considered important factors for long hours preservation. Heart and lung preserved for six hours were transplanted in thirteen dogs in heterotopic and orthotopic models and their functions were evaluated two hours after transplantation. The cardiac function was well preserved and pathological changes in cardiac muscle were minimum. But lung preservation was not so stable. Levels of PaO2 were variable and pathological changes of the donor lungs such as pulmonary edema, emphysema, etc were observed. Further studies were needed for lung preservation.
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PMID:[An experimental study on the heart and lung preservation and transplantation. Autoperfusion method and cardiac and pulmonary functions after transplantation]. 314 58

The purpose of this study was to evaluate the mechanism of development of lung edema and to determine adequate components and amounts of transfusion solution after major hepatic resection in normal and Dimethylnitrosamine (DMNA)-induced cirrhotic dogs. The dogs were administered maintenance dose (1-2 ml/kg/h) or large volumes (10-20 ml/kg/h) of lactated Ringer's solution (RL), 10% Dextrose or Dextran 40 (D40) after surgery. 1) In the groups transfused with maintenance dose or large volumes of RL, or large volumes of D40 after 80% and 70% hepatectomy in normal dogs and 40% hepatectomy in DMNA-induced cirrhotic dogs, the extravascular lung water (EVLW) increased with a high incidence of the development of lung edema. On the other hand, in the groups transfused with maintenance dose or large volumes of 10% Dextrose, or maintenance dose of D40, EVLW did not increase, thus preventing the development of lung edema. 2) The lower the functional reserve of the remaining liver and reticuloendothelial function, the more the volume of EVLW increased. The increments in plasma endotoxin titers through the spill over phenomenon, due to the decline of reticuloendothelial function after hepatectomy, caused an increase in the permeability of lung capillaries. Moreover, the decrease of colloid hydrostatic pressure gradient (CHPG) also caused an increase in EVLW. It is clear that both the permeability of lung capillaries and CHPG contribute to the development of lung edema after hepatectomy.
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PMID:[Studies on adequate components and amounts of transfusion solution after hepatectomy from the viewpoint of the development of lung edema]. 343 40

Between July 1981 and June 1985, 49 cases (36 boys (73%) and 13 girls (27%] of mumps meningo-encephalitis confirmed by culture of the virus from the cerebrospinal fluid (CSF) were seen. Patients presented particularly in the late spring and early summer. A CSF cell count greater than 500 X 10(6)/l was obtained in 14 cases (28%), a total CSF protein greater than 0.8 g/l in 6 cases (12%) and a CSF glucose of less than 2.2 mmol/l in 2 cases (4%). Two cases are reported to illustrate the diagnostic problems which the infection may cause, particularly when the CSF changes resemble those of tuberculous meningitis. In 1 case neurogenic pulmonary oedema developed after a convulsion; this caused further diagnostic uncertainty.
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PMID:Mumps meningo-encephalitis. 356 52

It is widely accepted that extravascular lung thermal volume estimated by the double indicator dilution method with heat as a diffusible indicator reliably reflects pulmonary extravascular water volume. Theoretically, as a premise, the indicator should be preserved during its pulmonary circulation. We therefore investigated the thermal conservation during pulmonary circulation; that is, whether there was good agreement in the cardiac outputs "wherever" the thermodilution curves were recorded; for instance, the pulmonary artery trunk (PAT), giving COPAT,heat and the aortic root (Ao), giving COAo,heat. In the present study, we observed a total of 59 pairs of cardiac outputs in dogs (n = 13), including dogs with overt pulmonary edema, produced either by dextran infusion or by alloxan administration. We also studied a total of 23 pairs of cardiac outputs of human subjects (n = 16) with ischemic heart disease or mild mitral stenosis. A mixture of ice-cold 5% glucose solution and indocyanine green was rapidly injected into the right atrium. The thermodilution curve was immediately recorded in the pulmonary artery trunk, and the thermodilution and dye dilution curves were recorded in the aorta using a conventional Swan-Ganz catheter. The cardiac outputs were calculated manually following the Stewart-Hamilton principle. The results were as follows: In dogs, COPAT,heat averaged 2.47 +/- 1.21 L/min (mean +/- SD), COAo,heat averaged 2.44 +/- 1.12 L/min and the difference was not significant (0.3 less than p less than 0.5). The regression equation was COPAT,heat = 1.01 X COAo,heat + 0.02 (n = 59, r = 0.93, p less than 0.001) and the correlation coefficient was excellent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Double indicator dilution method using heat and dye to measure pulmonary extravascular water volume]. 391 10

It is known that reactive oxygen species cause lung injury in association with activation of arachidonate metabolism. Because metabolites of the cyclooxygenase pathway do not appear to mediate the injury, we considered that the 5-lipoxygenase pathway might be activated and that inhibition of the pathway could interfere with the development of the injury. Thus, we sought to induce an oxidant lung injury and to prevent such injury by inhibiting lipoxygenase pathway or by blocking leukotriene action. In isolated rat lungs, glucose oxidase added to a glucose-containing, cell-free perfusate was used to produce the injurious oxygen species. Lung edema occurred and increased with increasing oxygen tension in the inspired air. Light microscopy of the lung showed perivascular fluid cuffs, and electron microscopy showed endothelial cell damage. Measurements in the lung effluent showed that concentrations of 5-hydroxyeicosatetraenoic acid (5-HETE) and of cyclooxygenase metabolites increased after glucose oxidase administration; BW 755C, U60,257, and FPL 55712 inhibited the glucose-oxidase-induced lung edema. And U60,257 also inhibited the glucose-oxidase-induced increase in 5-HETE without concomitant inhibition of cyclooxygenase metabolites. Thus, glucose oxidase via generation of active oxygen species stimulated the lung 5-lipoxygenase pathway, and inhibitors of 5-lipoxygenase protected against the oxidant lung injury. Further, in these experiments, the injury occurred in the absence of circulating blood cells and was augmented by increasing the inspired oxygen concentration.
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PMID:Leukotriene inhibitors attenuate rat lung injury induced by hydrogen peroxide. 392 81

The medical records of 330 patients treated with terbutaline infusion for the inhibition of preterm labor were reviewed over a five-year period. In patients with intact membranes the results were uniformly good, particularly when treatment was instituted before the 30th week. Half these patients had a prolonged labor of six weeks or more; in most cases of treatment failure complications already existed on admission. In only nine patients (2.7%) terbutaline treatment was stopped due to side effects: predominantly maternal tachycardia or vomiting. Two patients had chest symptoms, but in no case was pulmonary edema diagnosed. The results suggested that a low incidence of severe side effects can be obtained if the following precautions are taken: glucose is used as the infusion medium, instead of sodium chloride; concentrated solutions are given to avoid fluid overload; the patients are carefully controlled; and the infusion is immediately reduced or stopped if signs of severe side effects appear.
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PMID:A five-year experience with terbutaline for preterm labor: low rate of severe side effects. 402 80

Despite having implemented rigorous glucose control for women with gestational diabetes early in the third trimester, we found excessive morbidity among the neonates of these women. To accurately assess the risk of newborn complications, we did a five-year review (1977 to 1981) of infants of class A diabetic mothers to determine the incidence and scope of morbidity in these infants. Fifty-one infants of class A mothers were identified (group 1) and randomly matched with 102 infants of nondiabetic mothers (group 2). The distribution of morbidity between the two groups was as follows: hypoglycemia 9/51 (18%) vs 0/102 (P less than .001); birth injuries 4/51 (8%) vs 1/102 (2%) (P less than .05); pulmonary edema 3/51 (6%) vs 0/102 (P less than .05); respiratory distress 4/51 (8%) vs 7/102 (7%) (NS); macrosomia 18/51 (35%) vs 23/102 (23%) (NS); and hyperbilirubinemia 3/51 (6%) vs 8/102 (8%) (NS). There were two fetal deaths and three infants with major congenital anomalies among the diabetic pregnancies compared to none from the nondiabetic pregnancies. Compared to insulin-dependent diabetes, class A diabetes is accompanied by relatively mild metabolic disturbances in the mother. On the other hand, the infant of a mother with class A diabetes appears to be at risk for serious and life-threatening complications, both before and after birth. These results raise the question of whether earlier identification, subsequent meticulous diabetic management, and altered timing of delivery might reduce the complications experienced by these infants.
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PMID:Continuing neonatal morbidity in infants of women with class A diabetes. 649 59

Based on earlier studies in rats, phospholipase C (PLC) seemed to be a very promising prophylactic agent for certain types of thrombo-embolic disease. Recent studies in rabbits have, however, demonstrated that phospholipase C is more toxic than expected from the previous data. To gain more knowledge about its toxicity in larger animals we have studied its effect in sheep. Estimated LD50 for the enzyme in sheep was between 0.4 and 0.2 mg PLC/kg given as a 23 min infusion and below 0.2 mg/kg given as a bolus. Cellular necrosis was a common feature in several tissues of sheep dying from PLC. This explained the pulmonary oedema, decreased oxygen tension and renal failure with haematuria, proteinuria and glucosuria which occurred. PLC was probably filtered out in the glomeruli and totally reabsorbed in the tubuli until they were destroyed by PLC. An increase in different plasma enzymes suggested that PLC exerted a toxic effect on both muscle cells and hepatocytes. The blood glucose level remained about 20% lower in the PLC-treated animals than in the controls for more than 2 weeks. Pulmonary oedema and renal failure were the probable causes of death.
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PMID:The effect of phospholipase C in sheep. 664 29


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