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

Lung water homeostasis and the subsequent prevention of pulmonary edema involve a balance of many forces and safety factors. Malnutrition and its effects on fluid distribution within body compartments and on oncotic pressure gradients can play a crucial role in this balance of forces. These forces are discussed, with emphasis on the complications of superimposed malnutrition.
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PMID:Nutrition and lung water. 363 74

A 20-year-old woman presented with malignant hypertension, pulmonary edema, anemia, and azotemia. Blood pressure was adequately controlled only after progressively more intensive drug regimens, finally including minoxidil, nadolol, and furosemide. On these drugs, the patient developed progressive left and right heart failure, anasarca, and malnutrition. The control of hypertension, heart failure, and fluid retention, was accomplished by administration of captopril and furosemide. Captopril is a logical alternative to vasodilators in refractory hypertension complicated by congestive heart failure.
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PMID:Efficacy of captopril in relieving congestive heart failure developing during management of hypertension. Case report. 634 Dec 22

Re-expansion pulmonary edema (RPE) due to pneumothorax aspiration can lead to a fatal outcome, as in the case reported, the chronic nutritional deficiency and hypoproteinemia that it provokes probably playing a contributing role. Pathogenesis and factors affecting prognosis of RPE are discussed. These include the duration of the pulmonary collapse, though this is not an essential factor, the alterations in alveolar surfactant activity possibly related to the chronicity of the collapse, and the abruptness of aspiration which is, in contrast, a determining mechanical factor. Finally, the hypoproteinemia present in certain cases could facilitate fluid extravasation towards the alveolus. It is concluded that aspiration should be a gentle procedure in all cases, and should be conducted with extreme caution in the presence of hypoproteinemia.
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PMID:[Re-expansion pulmonary edema after iatrogenic pneumothorax. A propos of 1 case]. 686 92

Pulmonary oedema is an important problem in premature neonates with surfactant deficiency because of fluid accumulation in the lung interstitium and reduced urine output. Some retrospective reports suggest that excessive early hydration might increase the risk of bronchopulmonary dysplasia (BPD). Only three prospective studies evaluating low or conventional fluid administration regimens to very low birth weight infants have been published. According to their results no significant differences in the incidence of BPD have been shown. However, fluid restriction seems to improve the outcome of the infants because of decreased incidence of haemodynamically significant patent ductus arteriosus, necrotizing enterocolitis, pulmonary air leaks and decreased mortality. The appropriate amount of sodium in the intravenous fluids during the first days of life needs further evaluation. In tiny infants with birth weights from 500 to 800g intensive monitoring of fluid balance is essential to control the extremely high fluid losses due to evaporation. Undernutrition is a risk factor of BPD and therefore it is important to start parenteral nutrition early. The benefit of the use of colloids as volume expanders is controversial. According to some retrospective reports there might be an association with increased use of colloidal fluids during the first days of life and the development of BPD. Early excessive fluid administration might constitute a potential risk for low birth weight infants with hyaline membrane disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Appropriate fluid regimens to prevent bronchopulmonary dysplasia. 758 83

The autopsy records of 115 children with severe protein-energy malnutrition were reviewed. Sections of the lung histology showed evidence of bacterial pneumonia in 49% of cases. An additional 18% showed bronchitis, bronchiolitis or interstitial pneumonitis. Aspiration of gastric contents was evident in 10% of cases; 6% showed pulmonary oedema and congestion. In the remaining cases, no lung pathology was identified (17%). In 8 cases, rapid autopsy examination permitted fixation of lung tissue for electron microscopy. These included 4 cases of bronchopneumonia, one of which was associated with viral pneumonia. Another interstitial pneumonitis, probably of viral aetiology, was also studied. Both these virus-associated cases showed loss of type I pneumocytes and hyperplasia of type II pneumocytes. Another patient with herpes simplex hepatitis showed necrotic emboli in pulmonary capillaries with virions, as well as colonies of interstitial bacteria. One patient with acute pulmonary oedema displayed severe endothelial cell swelling on electron microscopy. In one case, there was no evidence of respiratory changes, apart from desquamation of type I pneumocytes. Useful information can be obtained on the fine structure of the lung, using samples taken soon after death.
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PMID:Pathology of the lungs in childhood malnutrition in Jamaica. Light and electron microscopy. 794 98

A twenty-year-old woman with anorexia nervosa (body mass index=11) suffered from severe liver dysfunction (aspartate aminotransferase 5,000 IU/l, alanine aminotransferase 3,980 IU/l, prothrombin time 32%), hypoglycemia (serum glucose 27 mg/dl), and pancreatic dysfunction (amylase 820 IU/l, lipase 558 IU/l). She fell into a depressive state with irritability, which was not improved by intravenous glucose. Despite treatment with plasmapheresis for the liver dysfunction, she subsequently developed pulmonary edema, acute renal failure, gastrointestinal bleeding, and disseminated intravascular coagulation. Hemodialysis, mechanical ventilation and drug therapy including prednisolone, prostaglandin E1, and branched-chain amino acid, improved her critical condition. In this case, malnutrition may have been the cause for the liver dysfunction and subsequent complications.
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PMID:Anorexia nervosa with severe liver dysfunction and subsequent critical complications. 1043 64

Pleuropulmonary amebiasis is the common and pericardial amebiasis the rare form of thoracic amebiasis. Low socioeconomic conditions, malnutrition, chronic alcoholism, and ASD with left to right shunt are contributing factors to the development of pulmonary amebiasis. Although no age is exempt, it commonly occurs in patients aged 20 to 40 years, with an adult male to female ratio of 10:1. Children rarely develop thoracic amebiasis: when it does occur there is an equal sex distribution. The infection usually spreads to the lungs by extension of an amebic liver abscess. Infection may pass to the thorax directly from the primary intestinal lesion through hematogenous spread, however. Lymphatic spread is one possible route. Inhalation of dust containing cysts and aspiration of cysts or trophozoites of E histolytica in the lungs are some other hypothetical routes. The lung is the second most common extraintestinal site of amebic involvement after the liver. Usually the lower lobe, and sometimes the middle lobe of the right lung, are affected, but it may affect any lobe of the lungs. The patient develops fever and right upper quadrant pain that is referred to the tip of the right shoulder or in between the scapula. Hemophtysis is common. The diagnosis of thoracic amebiasis is suggested by the combination of an elevated hemidiaphragm (usually right), hepatomegaly, pleural effusion, and involvement of the right lung base in the form of haziness and obliteration of costophrenic and costodiaphragmatic angles. Infection is usually extended to the thorax by perforation of a hepatic abscess through the diaphragm and across an obliterated pleural space, producing pulmonary consolidation, abscesses, or broncho-hepatic fistula. Empyema develops when a liver abscess ruptures into the pleural space. Rarely, a posterior amebic liver abscess can burst into the inferior vena cava and develop an embolism of the inferior vena cava and thromboembolic disease of the lungs with congestive cardiac failure or corpulmonale. Diagnosis by finding E histolytica in stool specimens is of limited value. In a limited number of cases amebae might be found in aspirated pus or expectorated sputum. "Anchovy sauce-like" pus or sputum may be found. Presence of bile in sputum indicates that the pus is of liver origin. Serological tests are of immense value in diagnosis. Liver enzymes are usually normal and neutrophilic leucocytosis may or may not be found. ESR is invariably elevated. Anti-amebic antibodies can be detected by ELISA, IFAT, and IHA. Amebic antigen can be detected from serum and pus by ELISA. Detection of Entamoeba DNA in pus or sputum may be a sensitive and specific method. Pleuropulmonary amebiasis is easily confused with other illnesses and is treated as pulmonary TB, bacterial lung abscesses, and carcinoma of the lung. A single drug regimen with metronidazole with supportive therapy usually cures patients without residual anomalies. Aspiration of pus from empyema thoracis may be needed for confirmation and therapeutic purposes. The pericardium is usually involved by direct extension from the amebic abscess of the left lobe of the liver, sometimes from the right lobe of the liver, and rarely from the lungs or pleura. An initial accumulation of serous fluid due to reactive pericarditis followed by intrapericardial rupture may develop either (1) acute onset of severe symptoms with chest pain, dyspnea, and cardiac tamponade, shock, and death, or (2) progressive effusion with thoracic cage pain, progressive dyspnea, and fever. Chest radiograph, ultrasound examination, and CT scan usually confirm the presence of a liver abscess in continuity with the pericardium and fluid within the pericardial sac with or without the fistulous tract. Echocardiography may demonstrate fluid in the pericardial cavity. Patients should be cared for in the ICU and ambecides should be started without delay. Pericardiocentesis usually confirms the diagnosis and improves the general condition of the patient. Aspiration of the accumulated fluid should be performed urgently in cardiac tamponade; repeated aspiration may be needed. Surgical drainage should be done if needed. Acanthamoeba, a free-living ameba, may also infect the lungs in the form of pulmonary nodular infiltration and pulmonary edema in association with amebic meningoencephalitis in immunocompromised patients. It usually spreads to the meninges of the brain by way of the blood from its primary lesion in the lung or skin. Early diagnosis and institution of treatment may be life saving for these patients. A literature review shows that HIV/AIDS patients are not prone to infection with E histolytica. It is now clear that there are an increasing number of HIV-seropositive patients among amebic liver abscess patients, however, which suggests that although the incidence of intestinal infection is not high among HIV-seropositive or AIDS patients they are more susceptible to an invasive form of the disease.
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PMID:Thoracic amebiasis. 1209 41

Inadequate nutrition complicates the clinical course of critically ill patients, and many of these patients develop pulmonary edema. However, little is known about the effect of malnutrition on the mechanisms that resolve alveolar edema. Therefore, we studied the mechanisms responsible for the decrease in alveolar fluid clearance in rats exposed to malnutrition. Rats were allowed access to water, but not to food, for 120 h. Then, the left and right lungs were isolated for the measurement of lung water volume and alveolar fluid clearance, respectively. The rate of alveolar fluid clearance was measured by the progressive increase in the concentration of Evans blue dye that was instilled into the distal air spaces with an isosmolar 5% albumin solution over 1 h. Malnutrition decreased alveolar fluid clearance by 38% compared with controls. Amiloride (10(-3) M) abolished alveolar fluid clearance in malnourished rats. Either refeeding for 120 h following nutritional deprivation for 120 h or an oral supply of sodium glutamate during nutritional deprivation for 120 h restored alveolar fluid clearance to 91 and 86% of normal, respectively. Dibutyryl-cGMP, a cyclic nucleotide-gated cation channel agonist, increased alveolar fluid clearance in malnourished rats supplied with sodium glutamate. Terbutaline, a beta(2)-adrenergic agonist, increased alveolar fluid clearance in rats under all conditions (control, malnutrition, refeeding, and glutamate-treated). These results indicate that malnutrition impairs primarily amiloride-insensitive and dibutyryl-cGMP-sensitive alveolar fluid clearance, but this effect is partially reversible by refeeding, treatment with sodium glutamate, or beta-adrenergic agonist therapy.
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PMID:Malnutrition impairs alveolar fluid clearance in rat lungs. 1497 28

Inducible nitric oxide synthase (iNOS) has been implicated in the pathophysiology of congestive heart failure (CHF). Given the extensive evidence supporting this concept, we hypothesized that iNOS deficiency (iNOS(-/-)) would attenuate the severity of CHF in mice. Mice were subjected to permanent occlusion [myocardial infarction (MI)] of the proximal left anterior descending coronary artery to produce CHF. Cardiac function was assessed in vivo using echocardiography and ultraminiature ventricular pressure catheters. Sham wild-type (n = 17), sham iNOS(-/-) (n = 8), MI wild-type (n = 56), and MI iNOS(-/-) (n = 48) mice were subjected to MI (or sham MI) and followed for 1 mo. Deficiency of iNOS did not alter survival during CHF compared with wild type (35% vs. 32%, P = not significant). Furthermore, fractional shortening and cardiac output were not significantly different between wild-type (9.6 +/- 2.0% and 441 +/- 20 microl.min(-1).g(-1)) and iNOS(-/-) (9.8 +/- 1.3% and 471 +/- 26 microl.min(-1).g(-1)) mice. The extent of cardiac hypertrophy and pulmonary edema was also similar between wild-type and iNOS(-/-) mice. None of the indexes demonstrated any significant differences between iNOS(-/-) and wild-type mice subjected to MI. These findings indicate that deficiency of iNOS does not significantly affect severe CHF in mice after MI.
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PMID:Deficiency of iNOS does not attenuate severe congestive heart failure in mice. 1531 10

Hypoalbuminemia is common in patients with heart failure, and this condition becomes more prevalent with increasing age and illness. Hypoalbuminemia is thought to result mainly from malnutrition, inflammation and cachexia. Other causal factors include hemodilution, liver dysfunction, protein-losing enteropathy, increased transcapillary escape rate, and nephrotic syndrome. According to Starling's law, low plasma oncotic pressure related to hypoalbuminemia induces a fluid shift from the intravascular to the interstitial space, and there is now clinical evidence that hypoalbuminemia facilitates the onset of cardiogenic pulmonary edema. Hypoalbuminemia has emerged as an independent predictor of incident heart failure in end-stage renal disease and elderly patients. Recent data also suggest that hypoalbuminemia provides prognostic information incremental to the usual clinical and biochemical variables in patients with heart failure regardless of clinical presentation. The presence of hypoalbuminemia in patients with heart failure may have potential therapeutic consequence in clinical practice. If present, subclinical excess of fluid must be removed. A dietary survey should also be performed, and renutrition may be indicated. It is unknown whether targeted nutritional intervention and albumin administration confer benefits to hypoalbuminemic patients with heart failure, and further research is warranted in this setting.
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PMID:Human serum albumin in the clinical syndrome of heart failure. 2162 32


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