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

An elderly female with an acute episode of congestive heart failure, unaccompanied by any periods of hypotension, developed fulminant hepatic failure with an accompanying coagulopathy. Attempts to establish an etiology for her acute hepatic insufficiency, other than cardiac failure, proved negative. Fulminant hepatic failure as a consequence of congestive heart failure, without prolonged periods of hypotension preceding alteration in hepatic function, has not heretofore been described. Liver function is adversely effected in congestive heart failure. Hepatic ammonia clearance is impaired in cardiac failure and may be diminished to the point of resulting in hepatic encephalopathy. Coagulopathy is a frequent concomitant of fulminant hepatic failure. Establishing a clear etiology for a coagulopathy in the face of concomitant liver disease is difficult, thus making any therapeutic intervention fraught with peril.
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PMID:Fulminant hepatic failure secondary to congestive heart failure. 101 98

An 11-month-old girl presented acute episodes of hypoglycaemia and hepatic encephalopathy reminiscent of Reye syndrome and 3-hydroxydicarboxylic aciduria. The patient showed peculiar clinical manifestations of severe sensory-motor neuropathy, pigmentary retinopathy, and cardiomyopathy. She died of cardiac failure. Pathological studies of peripheral nerve showed signs of axonal neuropathy and demyelination. Enzymatic studies in cultured fibroblasts showed a deficiency of mitochondrial long-chain 3-hydroxyacyl-CoA-dehydrogenase. Peripheral nerve involvement and retinal pigmentary degeneration have as yet not been described in patients with proven defects of mitochondrial beta-oxidation.
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PMID:Peripheral sensory-motor polyneuropathy, pigmentary retinopathy, and fatal cardiomyopathy in long-chain 3-hydroxy-acyl-CoA dehydrogenase deficiency. 153 53

Incidence and extent of pulmonary complications were evaluated retrospectively in 101 patients with hepatic coma (34 patients with acute liver failure, 57 patients with hepatic encephalopathy and 10 patients with mixed forms). 76 patients (73.3%) had pulmonary complications (pulmonary edema 57 cases, pneumonia 20 cases, tracheobronchitis 30 cases). Lethality of the group with pulmonary complications was 97% as compared to 16% in the group without pulmonary complications. Pathogenesis of pulmonary complications is not completely clear; different mechanisms are being discussed like central mechanisms, vascular lesions caused by metabolic or toxic factors, cardiac failure, and increased susceptibility to infection. In 9 out of 59 cases (15.3%) with respiratory failure no morphological changes could be observed in the lungs; in these cases intrapulmonary shunts might have been the cause for the pulmonary complications. The incidence of pulmonary complications increased by a factor of 2.4 during intensive care unit treatment of the patients; this increase shows, that intensive care unit treatment still has to be improved.
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PMID:[Pulmonary complications in hepatic coma]. 682 Jun 75

Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequences of which are intermingled with those of cardiac insufficiency in most cases. We report the cases of six patients suffering from chronic heart failure in whom an episode of acute circulatory failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure, ie, hepatic encephalopathy, jaundice, and marked increase in prothrombin time, developed after an interval of one to three days, after the episode of acute circulatory failure, while the patiens' hemodynamic condition had returned to the previous basal status.
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PMID:Fulminant hepatic failure due to transient circulatory failure in patients with chronic heart disease. 735 50

We report the discovery of a congenital intrahepatic portocaval shunt during heart failure in a 68 year-old woman, without cirrhosis or portal hypertension. She had hepatic encephalopathy. Only 17 such cases have been reported. Their physiopathology remains unclear. Reasons for late revelation are debated. Color doppler imaging is very useful for diagnosis following and treatment of these shunts. Therapeutic options are presented.
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PMID:[Late manifestation of congenital intrahepatic portacaval shunt in a healthy liver]. 756 34

From 1975 to 1993, our University Hospital performed 2789 graft procedures. During the same period, 12 poisoned, "brain-dead" patients were considered as organ donors. The toxic substances involved were: methaqualone (n = 1), benzodiazepine alone (n = 1), benzodiazepine plus tricyclic antidepressants (n =1), tricyclic antidepressants alone (n = 1), barbiturates (n = 2), insulin (n = 2), carbon monoxide (n = 1), cyanide (n = 1), methanol (n = 1), and acetaminophen (n = 1). From these intoxicated persons, 32 organ transplants were obtained, but only 23 could be followed for 1 month and only 20 for 1 year. The outcome at 1 month was favorable in 20 of the 23 patients. Two heart transplant patients died with 24h after grafting from stroke and acute heart failure, respectively. Preoperative hepatic encephalopathy was not corrected after grafting and was directly responsible for the death of a liver transplant patient. After 1 year, 15 of the 20 recipients were still alive. Chronic hepatic graft rejection led to a fatal outcome in one recipient and to second grafting in another. Finally, one recipient died from delayed neoplasia. Based on our experience, organ procurement may be considered in a few select cases of acute poisoning. Attention should, however, be drawn to possible graft damage due to some poisons.
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PMID:Outcome following organ removal from poisoned donors: experience with 12 cases and a review of the literature. 762 77

Fulminant hepatic failure is a complication of severe cardiocirculatory failure, with high morbidity and mortality, and is frequently misdiagnosed as fulminant viral hepatitis. We report three cases of patients with chronic severe heart failure who developed cardiogenic shock complicated by elevation of aminotransferase levels above 1,000 soon after the most severe episode of hypotension. All the three patients presented regression of hepatic enzymes 72h after admission. Two patients developed hepatic encephalopathy and renal failure. One underwent the implantation of an artificial left ventricle, followed by orthotopic heart transplantation. One died of systemic multiple organ failure, after he had showed improvement on his hepatic profile, and one was sent to the ward, after 15 days with marked improvement on his clinical status and no signs of hepatic disease.
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PMID:[Acute liver failure secondary to cardiogenic shock in patients with congestive heart failure]. 782 36

Most frequent complications in patients with liver cirrhosis are due to portal hypertension. Beside ascites circumvent vessels formate with vasodilatation. Due to counterregulation a secondary hyperaldosteronism develops with release of vasocontrictive agents. If conservative and endoscopic methods fail, indication for building a portosystemic shunt is given. The TIPSS procedure is less invasive than the surgical method of Warren-Shunt, so the radiological intervention has replaced surgery. Reducing the portal pressure by the shunt, the clinical complications change for the better. Still problems are defined as hepatic encephalopathy and right ventricular heart failure. Regular follow up investigations have to be performed to detect complications in the shunt. Using regular clinical and radiological check up TIPSS is of clinical benefit with good long term results.
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PMID:[Transjugular portosystemic stent shunt (TIPSS) as intervention in clinical complications of portal hypertension]. 1171 78

The development of edematous states is usually due to heart failure, renal failure, hepatic failure, or a combination of these conditions. Although the number of patients with edema and ascites due to hepatic cirrhosis or renal failure is less frequent than with congestive heart failure, the treatment of these conditions is often difficult. Although diuretic therapy is often employed, effective reduction in edema or ascites may be difficult to achieve and is associated with significant side effects including hyponatremia, hypotension, and a further decrease in renal function. Aggressive diuretic therapy of ascites may result in hepatic encephalopathy or hepatorenal syndrome. Each condition needs to be evaluated, and an optimum therapeutic approach needs to be devised. This article provides a review of the challenges and therapeutic approaches for the treatment of these conditions and provides a review of new therapies on the horizon that may be promising.
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PMID:Therapeutic approaches to the treatment of edema and ascites: the use of diuretics. 1914 58

Mild cognitive impairment describes a cognitive decline greater than expected for an individual's age and education level that does not interfere significantly with activities of daily life. In the recent years concepts of "mild cognitive impairment" with divergent definitions have been discussed as potential preclinical forms of dementia. The etiology of cognitive impairment is heterogeneous and it can be promoted or caused by numerous somatic factors. Relevant somatic factors include hypertension, diabetes mellitus, heart failure, chronic obstructive airways disease and bronchial asthma. Cognitive impairment may be facilitated by hypercholesterolemia, chronic renal failure, hypothyroidism, testosterone deficiency, minimal hepatic encephalopathy, HIV- and hepatitis C-infection. Knowledge and diagnosis of these somatic factors is essential in cognitive impairment, as diligent treatment may lead to improve cognitive performance and postpone the manifestation of dementia.
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PMID:[Somatic factors in cognitive impairment]. 1922 69


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