Telfer B. Reynolds

Pathogenesis and Treatment of Hydrothorax Complicating Cirrhosis with Ascites

Excerpt Hydrothorax has long been recognized as a complication of cirrhosis, but there has been much speculation as to its origin. Higgins and his colleagues (1) suggested it forms from the plasma ...

Direct Transhepatic Measurement of Portal Vein Pressure Using a Thin Needle: Comparison with wedged hepatic vein pressure

A technique for the direct measurement of portal vein pressure in fully conscious patients is described. This uses a percutaneous transhepatic approach with a thin Chiba needle and is shown to be simple and safe. The technique has been applied to 123 patients with a variety of liver disorders and the pressure measurements have been compared with those obtained by the indirect technique of wedge hepatic vein catheterization. Close agreement was found between portal vein pressure and wedged hepatic vein pressure in quiescent alcoholic liver disease and alcoholic hepatitis. In chronic active hepatitis, portal vein pressure tended to be higher than wedged hepatic vein pressure, indicating a presinusoidal component to the portal hypertension. This technique is shown to be useful in assessing idiopathic protal hypertension and in demonstrating hepatofugal flow.

Serum alanine aminotransferase in skeletal muscle diseases

Although elevation of the levels of serum alanine aminotransferase (ALT) following liver injury is well known, confusion exists concerning skeletal muscle injury as the cause of this rise. We reviewed the records of 16 patients who had muscle necrosis without evidence of liver disease. The patients were divided into three groups: extreme exercise, polymyositis, and seizures. All patients exhibited markedly elevated creatine kinase and lactate dehydrogenase levels consistent with muscle injury. In acute cases, aspartate aminotransferase (AST) and ALT were both elevated, and the AST/ALT ratio was greater than 3, but this ratio approached 1 after a few days because of a faster decline in AST. In conclusion, this difference in half‐life accounts for the comparable AST and ALT levels in our cases with chronic muscle injury. (HEPATOLOGY 2005;41:380–382.)

Plasma Volume in Cirrhosis of the Liver: Its Relation of Portal Hypertension, Ascites, and Renal Failure

Plasma volume was measured by using albumin-(131)I- and (51)Cr-labeled erythrocytes in 24 control subjects, 140 patients with hepatic cirrhosis, and 10 patients with various portal-systemic shunts for the relief of noncirrhotic portal hypertension. The cirrhotic patients included subgroups with ascites, functional renal failure, and portacaval anastomoses. Elevated values for plasma volume, by both methods, were found in each group of patients.The lymph space drained by the thoracic duct was measured by a radioisotopic technique in six patients with cirrhosis and ascites. The amount of radioactivity in this space was found to be negligible in accounting for the elevated plasma volume. Similar results were obtained when the degree of leakage of albumin-(131)I into the ascites was determined in 10 patients with cirrhosis.The plasma volume was unusually elevated in patients who had bled from esophageal varices, and paired comparisons before and after portacaval shunt normal values. There was a statistically significant correlation between normal values. There was a statistically significant correlation between plasma volume and wedged hepatic venous pressure measured in 36 patients.We concluded that the elevated values for plasma volume in cirrhosis are valid and are not artifacts due to leakage of albumin-(131)I from the circulation during mixing. We also concluded that portal hypertension is responsible for the plasma volume expansion; however, we were unable on this basis to explain the failure of portacaval shunting to return the plasma volume to normal, unless the shunt or some other factor keeps the plasma volume elevated.

Regression of Liver Cell Adenomas Associated with Oral Contraceptives

The regression of liver cell adenomas that follow the use of oral contraceptives when steroids are withdrawn was observed in three patients. At diagnosis by needle biopsy in patients without pain or evidence of hemorrhage, prompt cessation of steriod use is suggested as the preferable form of treatment. The same is true for the diagnosis made at surgery if the tumor or tumors are difficult to remove.

Primary biliary cirrhosis with scleroderma, Raynaud's phenomenon and telangiectasia: New syndrome

Abstract A new syndrome is described consisting of chronic liver disease typical of primary biliary cirrhosis together with scleroderma, Raynauds phenomenon, calcinosis cutis and telangiectasia. Six female patients had pruritus, jaundice and hepatomegaly with marked elevation of serum alkaline phosphatase activity and a positive test for serum mitochondrial antibody. Extrahepatic bile ducts were normal. In addition, they had telangiectasias, resembling those seen in the Rendu-Osler-Weber syndrome, on the finger pads and lips and occasionally on the mucosa of the upper gastrointestinal tract. The other features of the CRST syndrome (calcinosis, Raynauds phenomenon and sclerodactyly) were present to a varying degree. The association of primary biliary cirrhosis with a form of scleroderma suggests an immunologic etiology for the liver disease.

Sclerosing Hyaline Necrosis of the Liver in the Chronic Alcoholic: A Recognizable Clinical Syndrome

Excerpt In recent years we have observed a group of alcoholic patients who present a symptom complex accompanied by a distinctive morphologic lesion in the hepatic cells that has been known as alco...

Measurement of portal pressure and its clinical application

Estimates of portal pressure in unanesthetized man can be obtained by needling the spleen, by cannulating the umbilical vein remnant, by inserting a needle directly into the hepatic parenchyma or by wedging a catheter into an hepatic vein. In recording pressures as low as those in the portal system, it is essential to have an accurate baseline that reflects the pressure in the major hepatic veins. An external zero reference point is not entirely satisfactory since it is not possible to compensate for increase in intra-abdominal pressure that may accompany ascites or bowel distention. Only wedged hepatic vein catheterization allows recording of an accurate internal zero pressure reference point. Using umbilical cannulation for entry into the portal vein, two groups of investigators have recently shown that wedged hepatic vein pressure and portal vein pressure are essentially identical in alcoholic liver disease and probably in cryptogenic cirrhosis and chronic active hepatitis. For these reasons hepatic vein catheterization should be the method of choice for accurate measurement of portal pressure. A high wedged hepatic vein pressure does not indicate that the hepatic vascular resistance increase is all postsinusoidal; this term should be abandoned. Portal pressure measurement is clinically useful in several situations. A high value can be decisive in the diagnosis of chronic liver disease in patients with unexplained bleeding from the upper gastrointestinal tract, splenomegaly or ascites. In chronic liver disease the level of portal pressure can be used to follow the course of the disease and the effects of treatment. It is still uncertain whether portal pressure is useful in predicting variceal bleeding.

Chronic Active and Lupoid Hepatitis Caused by a Laxative, Oxyphenisatin

Abstract In six patients with chronic constipation, chronic active liver disease developed after one to two years of daily ingestion of laxative preparations containing oxyphenisatin; in a seventh liver disease occurred after ingestion of laxatives of unknown composition. Clinical features were jaundice, fatigue, firm hepatomegaly and, occasionally, spider angiomas and splenomegaly. Laboratory abnormalities included an increase in transaminase activity of 10 to 40 times, decreased prothrombin, depressed serum albumin and raised globulin. Two patients had positive LE-cell tests, two others had antinuclear antibody and three had smooth-muscle antibody; none had hepatitis-associated antigen. Liver biopsies showed areas of collapse and fibrosis, with stromal lymphocytic infiltrate and focal areas of hepatocytolysis. All patients improved after changing laxatives. Challenge with oxyphenisatin in three patients caused abrupt rises in transaminase activity. A toxic etiology should be considered, therefore, in al...

Rapid Diuresis in Patients With Ascites From Chronic Liver Disease: The Importance of Peripheral Edema

Serial measurements of plasma volume and ascites volume were made during treatment with large doses of oral diuretics in 14 patients with stable chronic liver disease. Eight patients had pitting edema in addition to ascites. Reproducibility of ascites and plasma volume measurements was verified in 10 control subjects not receiving diuretics. Six patients without edema undergoing rapid diuresis lost a mean of 1.2 +/- 0.2 L of ascites and an equivalent amount of weight (1.3 +/- 0.4 kg) per day. All had a rise in blood urea nitrogen or creatinine, or both, and a fall in creatinine clearance. Eight patients with edema undergoing rapid diuresis lost more weight (1.8 +/- 0.5 kg/day, p = 0.06) but less ascites (0.7 +/- 0.35 L/day, p less than 0.05) than those without edema, and none developed renal insufficiency. After edema disappeared, ascites mobilization increased (1.4 +/- 0.7 L/day) and renal dysfunction occurred. Plasma volume fell an average of 24% +/- 9% in patients without edema but did not change in patients with edema (-0.4% +/- 3%). When edema disappeared, plasma volume fell significantly (28% +/- 8%, p less than 0.001). Electrolyte changes including hyponatremia, hyperkalemia, and hypochloremia were seen only in the group without edema. Patients with ascites and no edema are able to mobilize more than 1 L/day during rapid diuresis, but at the expense of plasma volume contraction and renal insufficiency. Patients with peripheral edema appear to be protected from these effects because of the preferential mobilization of edema and may safely undergo diuresis at a rapid rate (greater than 2 kg/day) until edema disappears.