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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of the unusual clinical course of a patient with hepatic cirrhosis, refractory ascites, and hepatorenal syndrome, we were able to examine the complex interrelationships between massive ascites, renin-aldosterone activity, and renal and hepatic function before and after placement of a peritoneojugular vein (LeVeen) shunt. Measurements indicated that when the shunt was functioning, renin-aldosterone production was suppressed, the hepatorenal syndrome was reversed, and ascites remitted. These data suggest that hyperreninemia, hyperaldosteronism, and functional renal abnormalities of this disorder are potentially reversible and arise primarily from the imbalance between formation and drainage of hepatosplanchnic lymph rather than from hepatocellular dysfunction, lowered plasma oncotic pressure, or portal hypertension.
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PMID:Peritoneovenous (LeVeen) shunt. Control of renin-aldosterone system in cirrhotic ascites. 57 28

Techniques of hepatic vein catheterization, hepatic venous pressure measurement, and occlusion phlebography using a balloon catheter are described. Hepatic venous pressure measurements (n=95) and hepatic occlusion phlebography were combined in 32 cases. In patients with liver cirrhosis (n=63) a significant elevation of hepatic venous pressure gradients was found. A decrease of the pressure gradient was seen after portacaval and splenorenal shunt operations. Hepatic occlusion phlebography showed alterations of hepatic veins only in patients with cirrhosis. A rough correlation between pressure gradients and the extent of changes in the liver veins was found. Hepatic occlusion phlebography, in patients who had undergone shunt procedure, demonstrated various collaterals. Combined hepatic vein pressure measurements and hepatic occlusion phlebography using a balloon catheter are proposed as a very suitable method for the evaluation of chronic liver disease and portal hypertension.
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PMID:Clinical value of hepatic vein catheterization. Improved pracability by balloon catheter technique. 61 18

A new operation for selective or total decompression of the portal venous system in cases of intrahepatic portal hypertension is described. It involves interposition of a large-caliber Dacron graft between the splenic vein and the inferior vena cava. The graft-interposition splenocaval shunt is performed readily and quickly, satisfying the variable hemodynamic needs of patients with portal hypertension. It can be either selective (S-SCS) or total (T-SCS) from the beginning, or a T-SCS may be converted subsequently to a S-SCS should surgically induced hepatic decompensation supervene. It is less demanding technically than distal splenorenal shunt (D-SRS). The S-SCS conserves portal venous perfusion of the liver, preserves hepatocellular function and architecture at the preoperative levels, avoids precipitation of postshunt portal-systemic encephalopathy, and decompresses gastric-esophageal varices with prevention of further variceal bleeding even better than D-SRS. One hundred percent graft patency has been obtained, and the surgical results have been superior to those following portacaval shunt in patients with large liver blood flow and relative benignity of the liver disease, be it cirrhosis or noncirrhotic portal fibrosis. In patients with advanced cirrhosis, variceal bleeding, and small liver blood flows, T-SCS would be indicated. Patients of this category obtained inferior surgical results and had operative deaths (16.7%) following S-SCS. The concept of the operation has merits and deserves further evaluation.
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PMID:Graft interposition splenocaval shunt for total or selective decompression of portal hypertension. 62 91

Thirty consecutive cases of portal hypertension seen in a surgical unit in Lusaka, Zambia, are reported. Of these cases 70% were due to portal fibrosis caused by Schistosoma mansoni infestation. Portacaval shunting was undertaken in most cases. Patients with portal fibrosis responded more favourably to portal decompression than did patients with cirrhosis. It is probable that the condition is more common than is generally reconigzed in areas where S. mansoni infestation is endemic.
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PMID:Bilharzial portal fibrosis: an important cause of portal hypertension. 62 72

Renal handling of sodium was studied in five dogs where an end-to-side portacaval fistula was constructed prior to the induction of cirrhosis with DMN. Such a model permits the effects of cirrhosis to be studied separately from the consequences of portal hypertension. Three control animals without cirrhosis maintained normal liver and kidney function and remained in sodium balance for as long as 8 weeks following surgery. In the five cirrhotic dogs, urinary sodium retention preceded ascites formation and was independent of hyperaldosteronism, hypoalbuminemia, hepatic ischemia, or decreased renal perfusion. Portal venous pressure remained normal in all cirrhotic dogs, and the splanchnic area remained free of venous collaterals. Plasma volume expansion also preceded ascites formation, and this variable increased by 8.4% (p less than 0.05) following 6 days of sodium retention. These temporal relationships between sodium retention, expanded plasma volume, and ascites formation are similar to those observed in ordinary cirrhotic dogs previously studied in this laboratory. Total plasma volume increased by 13.2% (p less than 0.05) when measured during the ascitic phase of cirrhosis. However, when the splanchnic and nonsplanchnic ("effective") components of plasma volume were measured by an exclusion technique, the ratio of these components to total plasma volume was not different from that observed in normal dogs. Thus no preferential consignment of retained salt and water had occurred. We conclude that urinary sodium retention in cirrhotic dogs occurs independently of portal hypertension or augmented splanchnic vascular capacity and is associated with expansion of the effective plasma volume, even though ascites is present.
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PMID:Renal sodium retention and ascites formation in dogs with experimental cirrhosis but without portal hypertension or increased splanchnic vascular capacity. 62 53

In examinations of 72 patients with liver cirrhosis and chronic hepatitis the transaminase activity of the urine (T-uria) was found in 55.6% of the cases, above all in liver cirrhosis. The T-uria increases parallel to the progressing portal hypertension to the hepatocellular insufficiency and to the hepatorenal syndrome. It is reduced in positive dynamics of the hepatic process. The T-uria has an essential prognostic value. In the terminal phase of the liver cirrhosis the T-uria is perhaps connected with disturbances of the hepatic haemodynamics.
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PMID:[Urinary transaminase in the diagnosis of kidney disorders in liver cirrhosis]. 63 78

Hyperkinetic portal hypertension is caused by pathological arterioportal shunts. Clinical differentiation is necessary between extrahepatic fistulas, splenoportal hypertension (arteriovenous anastomoses at the level of the pre-penicilary arteries) and intrahepatic fistulas in "active" cirrhosis and malignant tumors. This paper reports the clinical and angiographic features of eight patients with this type of fistula. A review of the literature is also presented (144 cases). Because of the severity of this disease, surgical intervention is necessary. The surgical technique depends on the organ-related necessity of vascular preservation.
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PMID:[Hyperkinetic portal hypertension. Arterioportal fistula: problems--case reports--review of the literature]. 64 68

The notorious predilection for rupture of splenic artery aneurysms in women of childbearing age is once more stressed by this case report. Although such ruptures usually result in a catastrophic interabdominal bleeding, in rare instances they lead to the formation of an arteriovenous fistula and consequent portal hypertension. Arterialization of the portal vein results in a progressive development of intrinsic hepatic morphologic changes and hepatoportal sclerosis, which further elevate the pressure in the portal system. This combination of pathophysiologic hemodynamic features closely resembles the original concept of Banti. He postulated that portal hypertension began with pathologic changes within the spleen which were associated with an increased blood flow through this organ. This led to increased flow and pressure in the portal venous system and ultimately cumulated in cirrhosis of the liver. This concept of the pathophysiology of portal hypertension has been universally abandoned, but it could serve as a model of the sequelae of an arteriovenous communication within the portal system.
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PMID:Arteriovenous fistula and forward hypertension in the portal circulation. 65 66

Two canine models of cirrhosis induced by administration of dimethyl-nitrosamine (DMNA) alone or in combination with hepatic vein ligation, were studied. The criteria used for development of cirrhosis were not only the appearance of portal hypertension, ascites, biochemical disorders or retention of BSP but also the formation of histological lesions such as sclerotic transformation of the liver lobules together with nodular regeneration. According to these criteria, the experimental protocol consisting in hepatic vein ligation and prolonged administration of DMNA was successful in inducing in animals liver cirrhosis similar to human conditions.
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PMID:Comparative study of two models for experimental cirrhosis in the dog. 65 65

A successfully operated case of neonatal common bile duct cyst is described. Cystoduodenostomy was employed. Whether or not this condition is attributable to obstruction dysembryogenesis or aganglia is discussed. Assessment of the anatomopathological features leads to the establishment of three clinical types: cyst properly so called, hernia and diverticulum. True choledochus cyst has three main symptoms: mass, icterus and pain. The other two forms constitute only 5% of the reported cases. They have no distinct signs and the few cases described have been encountered during surgery or necropsy. Diagnosis is complicated by cholostatic cirrhosis and portal hypertension. Treatment is necessarily surgical: excission of the cyst, reconstruction of the main duct by direct anastomosis of the hepatic duct to the duodenum or a jejunal loop prepared according to Roux; anastomosis by means of cystoduodenostomy.
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PMID:[Choledochal cysts. Clinico-radiological considerations and surgical technical notes]. 66 7


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