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

A prospective study in 76 newborn with perinatal asphyxia searching for myocardial ischemia was carried out. The disease was found in 51% of the patients. With electrocardiogram, myocardial enzymes, X ray and clinical manifestations the diagnosis was elaborated. No difference in the sex was present, the mean of gestational age was 35 weeks, and with mean birth weight 2,216 g, respiratory distress was present in all the people; only 20.5% developed heart failure and two had heart murmurs; 61.5% showed cardiomegaly. The creatine kinase MB isoenzyme at twelve hours after birth was raised in most of the patients. Respiratory distress syndrome was the principal diagnosis in 38%; hypoxic ischemic encephalopathy and peri-intraventricular hemorrhage was present in 50 and 33% of the patients, respectively. Mortality rate was 33%. Also a comparative study in the infants with and without myocardial ischemia was carried out appearing significative difference in: 1. Cardiomegaly, 2. Hypoxic-ischemic encephalopathy and 3. Creatine kinase MB isoenzyme.
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PMID:[Transient myocardial ischemia in newborn babies with perinatal asphyxia (hypoxic cardiomyopathy)]. 209 33

Spontaneous bacterial peritonitis rarely complicates high-protein (greater than 2.5 g/dl) ascites. The relatively high endogenous antimicrobial (opsonic) activity of the ascitic fluid in this setting appears to protect the patient from infection. We report two patients with high-protein, noncirrhotic ascites complicated by spontaneous peritonitis due to Salmonella species. One patient had ascites due to heart failure, whereas the other patient's ascites was due to peritoneal carcinomatosis. The ascitic fluid total protein concentrations were 3.1 and 3.3 g/dl, respectively, and the opsonic activity of the ascitic fluid specimens were 2.03 and 2.00 log kill, respectively, indicating a high degree of bacterial killing. We hypothesize that the virulence of the Salmonella species was able to overcome the high opsonic activity in the ascitic fluid, resulting in infection in these two patients. Fever, abdominal pain, or encephalopathy in a patient with high-protein ascites may suggest the presence of an unusual organism causing spontaneous bacterial peritonitis.
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PMID:Spontaneous Salmonella infection of high-protein noncirrhotic ascites. 220 53

The case of a patient developing hypomagnesemic encephalopathy and coma secondary to intensive treatment for severe cardiac failure, is reported. Following an early improvement of symptoms and signs of cardiac failure, a rapidly developing neurologic disorder appeared. This was characterized by insomnia, agitation, mental derangement and, finally, sopor and I-II degree coma. Serum magnesium concentration was 1.0 mEq/l. Magnesium sulfate iv infusion was followed by a immediate and complete recovery from the neurological disorder. Patients with cardiac failure undergoing prolonged intensive therapy are prone to develop hypomagnesemia. This electrolyte alteration may be responsible for symptoms and signs of central nervous system involvement (metabolic encephalopathy) that need to be differentiated from those of organic origin.
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PMID:[Hypomagnesemic coma in heart failure: description of a case]. 237 57

We have retrospectively evaluated 24 sepsis episodes caused by viridans streptococci in 23 neutropenic children during a 21 months period at the Pediatric Hematology Unit of St. Louis Hospital. The underlying malignancies included acute lymphoblastic leukemia, acute non lymphoblastic leukemia, aplastic anemia and solid tumor. In 17 children neutropenia, defined as a neutrophil count of less than 500 per cubic millimeter, was caused by cytotoxic chemotherapy. For 6 other children neutropenia was consequential to pretransplant treatment regimen for autologous bone marrow transplantation including cytotoxic chemotherapy and total body irradiation. All patients had a silicone rubber atrial catheter. In 9 patients sepsis was associated only with fever for less than 48 hours. In 5 other children fever was prolonged more than 72 hours in spite of specific antimicrobial therapy. No other organism was isolated. In 10 patients, however, the infectious syndrome was severe and the features included cardiac failure (7 patients), pneumonia (7 patients) resembling adult respiratory distress syndrome, encephalopathy (3 patients) without meningitis and proteinuria, 7 of these patients needed a management in a pediatric intensive care unit and 2 died in spite of adapted antibiotics. Streptococci were isolated in blood cultures in 23 children.
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PMID:[Frequency and severity of systemic infections caused by Streptococcus mitis and sanguis II in neutropenic children]. 278 Jan 2

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

Fifty-seven cirrhotic patients with intractable ascites had a portosystemic shunt. In 35 patients, a peritoneovenous shunt had previously failed. Forty-six patients were in Pugh's class B and 11 were in class C. There were three operative deaths (5.3%). Fifty-three (98.2%) of the 54 survivors were cleared of ascites. In one patient, ascites persisted because of postshunt heart failure that resulted in a marked increase of caval pressure. Twenty-seven patients (50%) had late encephalopathy, which was severe and disabling in 12 (22%). One- and three-year survival rates were 72% and 36%, respectively. These results suggest that although portosystemic shunts are remarkably effective in dealing with ascites, the high rate of postoperative encephalopathy is a strong argument against their routine use in the management of intractable ascites in cirrhosis.
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PMID:Should portosystemic shunt be reconsidered in the treatment of intractable ascites in cirrhosis? 339 43

The liver in an infant or child is as liable to the same pathologies afflicting the adult liver but with certain differences in prevalence and causes. Genetic disorders are more likely to present in the paediatric age group where many involve metabolic processes such as galactosemia, phenylketonuria, glycogen storage disease and others. Many of these present in the newborn period. However, neoplasms and hamartomas also present in the newborn period, such as congenital neuroblastoma with an enormously enlarged liver, hepatoblastoma and haemangioma. The latter may present with intractable cardiac failure as a result of considerable shunting of blood. Acquired liver lesions often present in the newborn period or early infancy and this includes hepatitis and biliary atresia. The difficulties in the differentiation of the two lesions will be discussed together with the management of biliary atresia. As the child grows older, Reyes encephalopathy with microvesicular fat in the liver is not uncommon. The pathophysiology of Reyes encephalopathy as seen locally will be described. The choledochal cyst with direct (Caroli's disease) or indirect effect on the liver will be described. Problems of childhood portal hypertension as well as congenital hepatic fibrosis will be described. Hemosiderosis of the liver is chiefly seen in homozygous beta-thalassaemia patients who have been kept alive with repeated blood transfusions. Amoebic and pyogenic hepatitis, fatty liver due to protein malnutrition, biliary ascariasis, etc, which are common in tropical and subtropical countries are rarely seen now in Singapore children.
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PMID:Paediatric liver disorders in Singapore. 346 38

Hypertension in childhood is diagnosed according to age-adjusted values for each sex. It is more commonly diagnosed now than it was 2 decades ago because blood pressure is more frequently measured in children today. Surgically curable forms of hypertension are not common but usually present as moderate or severe hypertension (diastolic blood pressure greater than or equal to 110 mm Hg). Although many patients in this group are asymptomatic, some present with Bell's palsy, enlarged hearts, heart failure, encephalopathy, or stroke. Newer imaging techniques have proved particularly useful for localizing tumors, such as pheochromocytoma. Many antihypertensive drugs are now available, and therapy should be tailored to the patient's needs, with as few adverse or side effects as possible.
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PMID:Evaluation and management of childhood hypertension. 407 63

Eighteen patients with severe symptoms of the carcinoid syndrome were assessed for hepatic embolisation. Four were too ill, and one had mild symptoms; thus 13 received a periembolisation regimen of cyproheptadine, fenclonine, aprotinin, methylprednisolone, tobramycin, flucloxacillin, and metronidazole. Embolisation was not performed in one patient with an occluded portal vein and was unsatisfactory in two others, in one because she was moribund and in the other because the hepatic artery had been ligated. Dramatic improvement in symptoms occurred in the nine patients in whom embolisation was successfully carried out, with abolition of flushing, severe abdominal pain, and wheeze and reduction in diarrhoea from 10.5 (SD 7.6) to 1.6 (0.9) stools/day. Urinary excretion of 5-hydroxyindole acetic acid fell from 1048 (716) to 289 (184) mumol/24 h (200 (137) to 55 (35) mg/24 h). Complications included one death from septicaemia, a hepatic abscess requiring surgical drainage, abdominal pain in three patients, pleural effusion in two, and transient encephalopathy in one. Relief of symptoms lasted for one to 24 months, and second embolisation in two patients produced further remissions of four to six months. Five patients died, one to 40 months after embolisation, in four cases because of metastases or heart failure. Hepatic embolisation is the treatment of choice for symptoms of the carcinoid syndrome resistant to medical treatment.
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PMID:Role of hepatic arterial embolisation in the carcinoid syndrome. 641 93

Malignant hypertension still constitutes a medical emergency, particularly when complicated by renal failure, encephalopathy, or left ventricular failure. A shift to the right of the autoregulatory curve of cerebral blood flow (and probably of renal blood flow) is known to occur in patients with hypertension. Local cerebral edema, complicating the malignant phase, is likely to aggravate this trend. While inadequate or tardy treatment leads to encephalopathy, renal and cardiac failure, over aggressive treatment may also result in damage to brain, heart, and kidney. Recent reports of neurological damage, sometimes fatal, following aggressive hypotensive treatment suggests the need for a reappraisal of current practices. More investigation is needed to determine the effects of the various classes of antihypertensive drugs on organ perfusion, particularly of brain, heart, and kidney, in both normal and hypertensive humans. Other hypertensive crises include raised arterial pressure in association with acute dissection of the aorta and in the presence of stroke or subarachnoid hemorrhage. While there is agreement about the need for urgent hypotensive treatment in patients with aortic dissection, there is no information with which to base rational decisions in the management of high arterial pressure in the acute phase of stroke or subarachnoid hemorrhage.
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PMID:Management of hypertensive crises. 662 56


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