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

The serum-ascites albumin difference is reported to be superior to ascitic total protein, ascitic-to-serum total protein ratio, lactic dehydrogenase, and ascitic-to-serum lactic dehydrogenase ratio in differentiating between ascites from liver disease and malignant ascites, S-A greater than 1.1 reflecting portal hypertension. We analyzed ascitic fluid from 46 consecutive patients with chronic liver disease, 28 patients with ascites associated with malignancy, 10 patients with right-sided heart failure, 4 patients with hypothyroidism, and 6 patients with miscellaneous causes of ascites to determine if this albumin difference is indeed a more valuable parameter. Analysis of our data confirms with a larger number of patients that the serum-ascites albumin difference is a more reliable indicator of transudative ascites, better termed portal hypertensive ascites. Malignant ascites without liver metastases had features of nonportal hypertensive ascites, and the serum-ascites albumin difference confirms this. The characteristics of malignant ascites associated with liver metastases, however, resemble those of the portal hypertensive ascites complicating liver disease. This new parameter is also helpful in distinguishing congestive heart failure with high protein ascites and portal hypertensive ascitic features from malignant ascites without liver metastases. Of particular note, myxedematous ascitic fluid, classically categorized as exudative, had an S-A greater than 1.1, indicating the possible role of portal hypertension in the development of ascites in these patients.
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PMID:Usefulness of serum-ascites albumin difference in separating transudative from exudative ascites. Another look. 316 91

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

In a case of traumatic superior mesenteric arteriovenous fistula resulting from a stab wound in the abdomen clinical signs of high-output cardiac failure or portal hypertension were absent. Selective angiography was useful in confirming and locating the fistula. The patient made a good recovery after resection of the aneurysm and fistula and insertion of a prosthetic graft.
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PMID:Traumatic superior mesenteric arteriovenous fistula. A case report. 357 9

The vascular lesions, angiomas, and arteriovenous malformations are known to be associated with a number of complications. These lesions, when present in the liver, may precipitate heart failure in infants. Recent reports suggest that although the prognosis is good for the majority of infants who survive the neonatal period, the lesions are capable of causing portal hypertension later in life. We have encountered three patients whose vascular lesions were in continuity with the portal circulation who subsequently went on to develop portal hypertension. One patient had angiomas of the liver, one splenic and colonic angiomas, and the third had diffuse arteriovenous malformations of the intestine. Data are presented and literature is reviewed, which suggest that any vascular lesion that is capable of substantially increasing portal blood flow may lead to the development of portal hypertension. The treatment of such lesions should be aggressive. If surgical management is not possible, alternative treatments such as embolization should be attempted early in order to increase the chance for successful therapy.
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PMID:Splanchnic bed vascular malformations and the development of portal hypertension. 370 54

Arteriovenous fistulas of the mesentery are rare sequelae of abdominal injuries or operations. Symptoms, when present, are most often due to intestinal ischemia or portal hypertension. Cardiac failure is less common, and the case described in this report is, to our knowledge, the first in which the patient presented with duodenal obstruction--the superior mesenteric artery syndrome. A bruit is an expected finding and a thrill is pathognomonic of an arteriovenous fistula. With rare exception, operation is indicated to dismantle the fistula.
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PMID:Traumatic mesenteric arteriovenous fistula presenting as the superior mesenteric artery syndrome. 376 53

A case of an aorto-mesenteric fistula presenting with portal hypertension and cardiac failure is presented. Both the computed tomographic and angiographic features proved valuable in the diagnosis of this unusual condition.
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PMID:Traumatic arterio-venous fistula involving the portal venous system. 381 72

Between October, 1976 and December, 1982, 176 patients with full-blown liver cirrhosis were referred to us either with Acute oesophageal variceal bleeding, or after having had such a haemorrhage. Eight of these patients died of a haemorrhage that did not respond to conservative treatment, or of hepatic failure after emergency surgery. After receiving initial conservative treatment, 168 patients were classified in accordance with clinical, biochemical and haemodynamic selection criteria, particular importance being attached to the haemodynamic criteria. One-hundred-and-one of these patients in whom a shunt operation was not justifiable, were treated conservatively by means of repeated sclerotherapy. In the cases of acute bleeding, a balloon tamponade was performed in 3, an emergency shunt procedure in 1 and palliative dissection surgery in 4. Twenty-three patients in a non-bleeding state were treated conservatively without sclerotherapy. Shunt surgery was performed in 44 patients; out of the 42 patients shown by our selection criteria to be suitable for shunt surgery, only 1 patient died, 5 days after the operation, of cardiac failure with underlying toxic cardiomyopathy. In view of the low early mortality rate in selectively operated patients, a major argument against the use of the shunt for the treatment of portal hypertension is no longer valid, and it should again be considered whether the surgical procedure might not provide better long-term results than does conservative sclerotherapy alone.
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PMID:Stricter selection criteria improve the results of shunt surgery. 387 35

The hypersplenism associated with portal hypertension usually resolves with a successful shunting procedure. Recurrent hypersplenism has been associated with shunt thrombosis. We describe a patient with pancytopenia, jaundice, and diffuse edema after a distal splenorenal shunt. His shunt was angiographically proved patent. Extensive evaluation revealed severe alcoholic cardiomyopathy with passive splenic congestion. He died of cardiac failure. Alcohol is a systemic toxin that affects other organs, as well as the liver.
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PMID:Recurrent hypersplenism caused by alcoholic cardiomyopathy after distal splenorenal shunt. 395 75

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

This paper presents a review of the literature on hepatic circulation and circulatory disorders of the liver in the dog and cat, and also includes a number of our own not previously published data. Circulatory disorders of the liver are frequently observed in dogs and cats. These disorders can be divided into congenital portosystemic shunts, disorders associated with outflow disturbances, and disorders associated with portal hypertension. Outflow disturbances result in passive congestion of the liver and in both species are mainly due to cardiac failure. Portal hypertension with resultant portosystemic collateral circulation and ascites mainly results from chronic liver disease, particularly cirrhosis. The main vascular disorder resulting in portal hypertension and ascites in the dog is primary hypoplasia of the portal vein.
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PMID:Circulatory disorders of the liver in dogs and cats. 757 Dec 84


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