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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between April 1985 and July 1989, 125 cases with pleural effusion were admitted to our department. The causes of pleural effusion were carcinomatous pleurisy in 47 cases, infection without tuberculosis in 34 cases, tuberculous pleurisy in 17 cases, cardiac insufficiency and hypoproteinemia in 11 cases, trauma and pneumothorax in nine cases, collagen disease in two cases and unknown origin in five cases. Carcinomatous pleurisy and tuberculous pleurisy, the differential diagnosis of which is very important, comprised 37% and 14% of all cases, respectively. These diseases can be definitively diagnosed by pleural biopsy, effusion cytology and/or effusion culture. In July 1987, we introduced thoracoscopy to improve the ratio of definitive diagnoses. The ratio for carcinomatous pleurisy in the previous term, when thoracoscopy was not being used, was 59%, while that in the latter term, when it was used, was 73%. The ratio for all cases with tuberculous pleurisy was 47%. Prior to June 1987, pleural biopsies in our department were performed with a Cope needle. Using that procedure, a low positive ratio of 50% was obtained. For thoracoscopic pleural biopsies, a high positive ratio of 84% was achieved (in carcinomatous pleurisy, 13 out of 15 cases; in tuberculous pleurisy, three out of four cases). This procedure was performed with minimal patient discomfort and no serious complications. Therefore, thoracoscopic pleural biopsy is recommended as a diagnostic procedure for cases with pleural effusion.
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PMID:[The role of thoracoscopy in pleural biopsy in cases with pleural effusion]. 221 27

A 57-year-old patient presented with periorbital and lower limb edema. The physical examination revealed no signs of cardiac insufficiency or chronic liver disease. Initial laboratory values showed significant hypoproteinemia and hyperlipidemia. Renal function was normal. Urinary protein excretion was 5.5 g/d. Thus, the patient was diagnosed to have nephrotic syndrome. The patient's history, the physical examination and further laboratory work-up suggested a primary glomerulopathy. Percutaneous renal biopsy was performed. The biopsy was diagnostic of minimal change glomerulonephritis. A therapy with steroids was initiated which induced a complete remission of the nephrotic syndrome. The patient has been relapse-free for the entire follow-up period.
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PMID:[Eyelid and ankle edema]. 231 82

The clinical background relating to edema in elderly inpatients was investigated, in terms of various items in elderly (aged greater than or equal to 65) cases with edema (n = 96) and without edema (controls, n = 95). Both groups were matched for sex, age, and underlying diseases. As compared with the control patients, the patients with edema had longer hospital stays with more disabled status, and showed less activity of daily living (ADL). The rates of bed-restricted patients, dementia patients, and patients with decubitus, muscle atrophy, or incontinence were found to be significantly higher in the patients with edema. The measurement of biochemical parameters revealed that the patients with edema had significantly lower levels of serum albumin, Na, Cl, creatinine, and uric acid, in contrast to higher levels of C-reactive protein. According to the classification of the assumed causes of edema, we divided the patients with edema into five groups; group 1 (n = 33): edema associated with immobilization, group 2 (n = 18): edema due to heart failure, group 3 (n = 15): edema on paretic limbs, group 4 (n = 6): edema due to hypoproteinemia, group 5 (n = 5): edema associated with liver cirrhosis. Both group 1 and group 4 patients had lower levels of hemoglobin and albumin, whereas group 3 patients had higher scores of ADL, higher blood pressure, and higher levels of hemoglobin and albumin. These results suggest that immobilization and restriction in bed, as well as malnutrition, were important factors in causing edema in elderly inpatients.
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PMID:[A controlled study on edema in elderly inpatients]. 238 89

Application of isolated ultrafiltration (IUF) of blood in 70 out of 100 patients with refractory heart failure (HF) made it possible, acting on some mechanisms of water excretion disorders, to attain the compensation for the HF signs. At the same time the correction of the manifestations of secondary hyperaldosteronism, hypoproteinemia, hyperbilirubinemia, and azotemia was attained only thanks to the presence of the functional reserves of the liver and kidneys. In 35 patients with cachectic HF, IUF failure was determined by marked cardial liver cirrhosis together with depletion of the functional reserves of the cardiovascular system. The lack of sufficient diuresis, hyponatremia, hypoproteinemia, and hyperbilirubinemia may be unfavourable prognostic signs despite the reduction of HF intensity consequent on IUF.
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PMID:[The efficacy of isolated ultrafiltration of the blood in patients with refractory heart failure]. 276 1

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the newborn lung. 676 Oct 39

Twenty cases of sonographically visualized thickening of the gallbladder wall were reviewed and the clinical diagnoses compiled. In only eight of these patients was cholecystitis considered responsible for the finding. The rest had hepatitis, alcoholic liver disease with hypoproteinemia, heart failure, renal disease, and multiple myeloma; however, all lacked clinical evidence of gallbladder disease. Because of these findings, caution is urged in making the diagnosis of cholecystitis on the basis of wall thickening alone.
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PMID:Sonography of the thickened gallbladder wall: a nonspecific finding. 678 Dec 56

We report the case of a 9 month-old infant in whom acute heart failure was the presenting symptom of cystic fibrosis. Post-mortem examination showed lesions of myocardial fibrosis associated with typical lesions of cystic fibrosis in the pancreas. Hypoproteinemia and anemia were present and earlier could have suggested the correct diagnosis before the episode of acute heart failure. The analogy of the histologic myocardial changes in cystic fibrosis and in congenital lipomatosis of the pancreas suggests a common pathogeny related to the deficiency of the exocrine secretion of the pancreas.
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PMID:[Myocardial fibrosis in cystic fibrosis. A new case report (author's transl)]. 706 17

A retrospective study of all perinatal autopsies done during 11 years at hospital SBA showed 33 cases of nonimmunologic fetal hydrops (1.83% of all perinatal autopsies). The incidence was 1/3624 liveborn babies. Intrauterine fetal infections and chromosome genetic abnormalities accounted for 27.3% each; and in 15.2% of the cases some pathology of pregnancy was identified (including twining). All the cases showed severe anemia and in 58% of them pulmonary hypoplasia was identified. Moreover 31% of the cases showed renal hypoplasia. A placenta megaly was identified in 100% of the cases studied. The three most important mechanisms associate with the genesis of nonimmune fetal hydrops are: chronic intrauterine anemia, hypoproteinemia and intrauterine fetal heart failure.
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PMID:[Nonimmunological hydrops fetalis. Experience with 33 cases]. 756 65

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in an uremic patient without evidence for a causative (specific) underlying disease. The incidence is not known. Contributing mechanisms may include peritoneal membrane changes, fluid overload, hyperparathyroidism, reduced lymphatic drainage, heart failure and hypoproteinemia. Rigid fluid control, intensive hemodialysis, high-protein diet, intravenous albumin infusion, intraperitoneal steroid injections and paracenteses as well as implantation of a peritoneatrial pump have all been found ineffective as treatment. Peritoneal dialysis has been shown to resolve ascites, however, the only effective treatment is so far renal transplantation. The development of nephrogenic ascites is associated with a poor prognosis. Thus, one year after the development of nephrogenic ascites 1/3 had died.
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PMID:Nephrogenic ascites. Case report and review of the literature. 781 79


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