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

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

Causes of death of 260 tumorous patients autopsied in 1974 were analyzed. Most common causes were inflammation and tumorous and non-tumorous organ insufficiencies; the others, in order of decreasing incidence, massive tumorous dissemination, infarct and haemorrhage. Pneumonia was predominating over the inflammatory causes although peritonitis and sepsis were also not rarely encountered. Death due to inflammation occurred most frequently in cases of myeloid-lymphoid, urogenital and gastro-intestinal tumours and in postoperative states. The incidence of insufficiencies due to tumorous or non-tumorous origin differed but slightly. Of the various organ insufficiencies, massive hepatic metastases, occlusion of the biliary duct and cardiac failure were the most common. In cases of tumors of the small pelvis, compression of the ureters led most often to death. Massive dissemination was observed most of all in breast and ovarian carcinomas. Myeloid-lymphoid tumors led to death through extensive organ infiltration in about one thirds of the cases. After hearth infarction, venous thrombosis was often followed by pulmonary embolism, however, coronary occlusion was also not rare. Death due to haemorrhage originated from acute or chronic ulcers of the gastrointestinal tract or from vascular invasion of tumors in the head and neck regions or from thrombocytopaenia induced by cytostatics.
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PMID:[Causes of death in cancer patients]. 92 45

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

Twenty-eight women with severe pre-eclampsia were misdiagnosed and initially thought to have disorders unrelated to pregnancy. Their chief complaints included failing vision, liver or gallbladder dysfunction, renal failure, hemorrhage, seizures, and heart failure. Laboratory studies usually demonstrated thrombocytopenia and high hematocrit values. The development of these symptoms appears to begin with failure of the primigravida to appropriately increase her blood volume commensurate with the increase in size of her uterus. Expanding the severly pre-eclamptic patient's blood volume with intravenous albumin appears to be an effective and appropriate therapy.
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PMID:Severe pre-eclampsia: another great imitator. 94 95

In 395 consecutively investigated patients with cardiac failure of varying aetiologythe platelet ocurt in venous blood was less than 100 000/mm(3) in 5.3% and below the 2s devaition (less than 136 000/mm (3)) in 19.2. The average platelet count of the whole group was 197 500 +/- 70 800/mm (3) which was significantly lower (P less than 0.001) than in normal controls (n = 128). In 6 patients a (51)Cr study of platelet kinetics was performed; the results support the conclusion that the faculatative thrombocytopenia in cardiac failure is mainly,but not exclusively, due to an increased uptake of platelets in the congested spleen.
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PMID:[Frequency and pathogenis of thrombocytopenia in cardiac failure]. 95 98

Since April 1973 we have treated nine patients with extracorporeal membrane oxygenation (ECMO), utilizing the spiral coil membrane lung. One patient is a long-term survivor. All patients except one showed substantial improvement in peripheral arterial oxygen tension. Four adults and two neonates were treated for critical hypoxia. Two patients were treated for cardiac failure but failed to show improved myocardial function. Complications involving perfusion circuitry, cannulation, chronic systemic heparinization, thrombocytopenia, and renal failure have been managed with minimal difficulty. However, irreversible pulmonary, neurologic, hepatic, or gastrointestinal damage due to hypoxia present before the institution of ECMO was associated with lethal complications. The ECMO has supplied adequate oxygenation to this group of nine critically hypoxic patients. Institution of ECMO at an earlier date in patients with critical hypoxia would provide a higher likelihood of survival.
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PMID:Clinical use of the membrane oxygenator. 109 13

Clinical records of 30 neonates with aortic coarctation admitted to neonate ICU from January 1985 to June 1990 are reviewed. We analyzed perioperative data to search for adverse prognostic signs. Patients weights were 2,970 +/- 500 grams and gestational age 38.5 +/- 1.7 weeks. Mean age at admission was 10.5 +/- 10 and mean age of surgery 13 +/- 11 days. 70% had associated congenital heart defects. Surgical technique was patch angioplasty in 86% and subclavian flap in 14%. Early or late mortality among patients with isolated aortic coarctation was nonexistent, and it was 28.5% in patients with other congenital heart defects. 13% has postoperative hypertension and 3.3% recoarctation. Adverse prognosis signs were preoperative (associated congenital heart defects, especially ventricular septal defect and interrupted aortic arch, greater dose of catecholamines and mechanical ventilation), intraoperative (pulmonary artery banding), and postoperative (hypotension, cardiac failure, arrhythmia, oligoanuria, metabolic acidosis, greater need of mechanical ventilation, bleeding and thrombopenia). Date are compared with other neonatal series.
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PMID:[The perioperative management of aortic coarctation in the neonatal period]. 159 63

The Kasabach-Merritt syndrome is characterized by thrombocytopenia and localized coagulopathy associated with a hemangioma. Most techniques applied to eradicate the tumor or accelerate its involution (surgery, radiation therapy, embolization) are invasive and require transfusion of large amounts of blood products. In some cases, medical treatment is the only alternative. Efficacy of steroids and antifibronolytic agents has already been described, but even this approach is associated with the administration of blood products. We report two cases of infants with Kasabach-Merritt syndrome associated with cardiac and hepatic hemangiomas. At admission, both had signs of cardiac failure. They were successfully treated with prednisone and epsilon-aminocaproic acid (EACA). Blood products were not required once the diagnosis was made. These observations have important implications for the management of patients with Kasabach-Merritt syndrome because they show that even in severe cases blood transfusions can be avoided by the use of prednisone and EACA.
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PMID:Successful treatment of Kasabach-Merritt syndrome with prednisone and epsilon-aminocaproic acid. 831 77

A 4-month-old infant with cardiac hemangioendothelioma presented with thrombocytopenia, and pericardial effusion, as well as signs and symptoms of heart failure. This is the first reported case of infantile cardiac hemangioma successfully treated with steroids.
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PMID:Infantile cardiac hemangioendothelioma. 173 71

An analysis of 4 cases of the thrombotic thrombocytopenia in children of 4 to 10 years of age is performed. The disease was characterized by fever, purpura, headache and abdominal pains, arterial hypertension, microangiopathic haemolytic anemia, thrombocytopenia, increase of blood urea and serum creatinine, micro-haematuria and proteinuria. The duration of the disease was from 4 days to 7 months. Anuria, gangrene of the ears, scrotum, penis and soft tissues of legs and feet were registered in a 5-year-old patient with a fulminant disease. The cause of death of other patients was heart failure with acute lung oedema, brain haemorrhages and haemorrhagic pancreonecrosis. The diagnosis of the thrombotic thrombocytopenia was confirmed by the finding in the autopsy material of thrombotic microangiopathy of small arteries, veins, arterioles, venules and capillaries in kidneys and other organs and tissues. Kidney damage in fulminant disease is complicated by segmentary cortical necrosis, in a more prolonged disease--by glomerulosclerosis or mesangio-capillary glomerulonephritis.
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PMID:[Thrombotic thrombocytopenic purpura in children]. 180 69


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