Search

The results of a prospective randomized controlled trial of elective endoscopic intravariceal sclerotherapy carried out over a 36-mo period in comparison with elective percutaneous transhepatic obliteration of varices (PTO) are presented. Sixty-six patients with nonalcoholic cirrhosis were randomized after they had stabilized, usually between 7 and 14 days after variceal bleeding had stopped following medical treatment (balloon tamponade and vasopressin infusion). Thirty-three patients were assigned to the sclerotherapy group and the other 33 patients were assigned to the PTO group. The mean follow-up period was similar in both groups. There was no significant difference in demographic, clinical, and laboratory data between the two groups. Six patients (18%) in the sclerotherapy group and 21 (64%) in the PTO group had at least one episode of gastrointestinal bleeding during the follow-up period (p less than 0.005). Three patients in the sclerotherapy group and 1 patient in the PTO group bled from lesions other than varices; therefore the incidence of variceal bleeding was 9% in the former and 61% in the latter (p less than 0.005). The cumulative variceal bleeding rate was significantly lower in the sclerotherapy group than the PTO group (p less than 0.05). Five patients in the sclerotherapy group died during the follow-up period but none died of recurrent variceal bleeding. Nineteen patients in the PTO group died and 10 of them died of bleeding from varices. The cumulative survival rate was significantly better in the sclerotherapy group (p less than 0.05). These results indicate that elective endoscopic intravariceal sclerotherapy is superior to elective PTO in the prevention of recurrent variceal hemorrhage and mortality in nonalcoholic cirrhosis.

We studied the direction of blood flow in the splenic vein, using a combined ultrasonic system consisting of an electronic sector scanner and a pulsed Doppler flowmeter, in 21 patients with a large spontaneous splenorenal shunt demonstrated by angiography. Pulsed Doppler flowmetry revealed hepatofugal flow in the splenic vein in all 11 patients with chronic spontaneous hepatic encephalopathy, and hepatopetal flow in 10 patients without encephalopathy. In the former, hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt was corroborated by the venogram obtained after superior mesenteric arteriography. In 5 patients without a history of hepatic encephalopathy, superior mesenteric arteriography demonstrated hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt. Pulsed Doppler flowmetry, however, revealed hepatopetal flow in all of these patients, suggesting that the angiographic finding of hepatofugal flow may have represented an artifact.

A 58-yr-old woman with biopsy-proven idiopathic portal hypertension presented with ascites and pretibial pitting edema. On admission, ultrasonic Doppler flowmetry demonstrated hepatopetal flow of a markedly reduced velocity in the portal vein, hepatofugal flow in the splenic vein, and a large spontaneous splenorenal shunt. The patient spontaneously developed hepatic encephalopathy 1 mo later. Percutaneous transhepatic portography demonstrated mural thrombi at the porta hepatis after the catheter had penetrated the mural thrombi without resistance; there was also a long retention of contrast medium in the portal vein. 99mTc-Macroaggregated albumin instilled into the superior mesenteric vein was caught in the lungs, and no activity entered the liver. Measurements of ammonia and immunoreactive insulin clearly indicated that superior mesenteric venous blood was shunted through the splenic vein and the splenorenal shunt. Subsequent ultrasonic examination with Doppler flowmetry suggested further growth of the thrombi and lack of blood flow in the portal vein. Although the procedure of percutaneous transhepatic catheterization could have contributed to the growth of thrombi, it is more likely that the thrombosis in the portal vein was a sequela to idiopathic portal hypertension, and was growing at the time of catheterization. This case may be of significance in the understanding of the relationship between idiopathic portal hypertension and extrahepatic portal obstruction.

A comparative study of portal hemodynamics was made in 17 patients with idiopathic portal hypertension, 5 patients with chronic persistent hepatitis having no portal hypertension, and 21 healthy adults who served as the control for certain measurements. Venous pressures were measured by portal and hepatic vein catheterizations, blood flow by the pulsed Doppler flowmeter, organ volume by computed tomography, and intrahepatic shunt index by 99mTc-macroaggregated albumin instilled in the portal vein. The patients with idiopathic portal hypertension were divided into two groups: group A (n = 8) and group B (n = 9), consisting of those who respectively had portal venous flow per liver volume above and below the mean + 2 SD of healthy adults. In group A, portal vein pressure was moderately elevated, portal venous flow was significantly increased compared with the control, and portal vascular resistance was not much altered. In group B, portal vein pressure was markedly elevated above that of control, portal venous flow was comparable, and portal vascular resistance was significantly elevated. Splenic venous flow measured in the splenic vein between the left and short gastric veins was markedly increased in groups A and B, the increase being greater in the former. It was concluded that in some patients with idiopathic portal hypertension, increased portal venous flow, partly a result of increased splenic venous flow secondary to splenomegaly of an undetermined process, is the main contributor initially to the elevation of portal vein pressure; in others, possibly later, increased portal vascular resistance plays an important role.

Two patients in whom real-time ultrasonography and percutaneous transhepatic portography or the venous phase of the arteriogram of the superior mesenteric artery demonstrated a localized saccular dilation of a peripheral branch of the portal vein are described. One patient subsequently died, and autopsy confirmed the diagnosis. A hypoechoic lesion continuous with a branch of the portal vein seems to be the characteristic sonographic picture. Radiologic evidence for portal vein aneurysm was obtained in only 2 of 300 patients with portal hypertension in whom percutaneous transhepatic portography was performed, and in 2 of 3000 patients who visited our unit and in whom ultrasonography for the liver was performed. Thus, aneurysm of the intrahepatic portal vein does occur, but very rarely.

To estimate vascular changes in chronic liver disease, we quantitated intrahepatic arteriovenous and portal-systemic shunts in 12 patients with cirrhosis and arteriovenous shunts alone in 4 patients with cirrhosis. An index was obtained for intrahepatic arteriovenous shunts by instilling technetium 99m-macroaggregated albumin into the proper hepatic artery and portal-systemic shunts, by the same procedure done in the portal trunk, near the porta hepatis on different days. Counts were taken over the liver and both lungs in the anterior as well as the posterior view for calculation of the shunt index: cpm in lungs divided by cpm in liver and lungs X 100%. In the 12 patients with cirrhosis in whom both shunts were measured, intrahepatic arteriovenous shunting was significantly lower compared with intrahepatic portal-systemic shunting (1.4% +/- 1.1% vs. 36.0% +/- 29.0%, p less than 0.001). Thus, it seems that in patients with cirrhosis, the development of intrahepatic arteriovenous shunts is not as great as that of portal-systemic shunts, which were found in this study to be considerable and variable in degree.

Portal hemodynamics were studied in 55 patients with hepatocellular carcinoma in comparison with 41 normal subjects, using the duplex system that consists of an electronic sector scanner and a pulsed Doppler velocitometer. Changes of portal hemodynamics after transcatheter hepatic artery embolization were also investigated in 15 of the patients with hepatocellular carcinoma. The duplex system showed that 9 of the 55 had no Doppler signal in the portal trunk, suggesting portal vein thrombosis, 2 had hepatofugal flow in the portal trunk indicative of arterioportal shunts, and 44 had hepatopetal flow in the portal trunk. One of the 9 patients with no significant portal venous flow showed hepatopetal flow in collateral veins at the porta hepatis, suggesting cavernous transformation of the portal vein. All of these ultrasound findings were confirmed by subsequent celiac-mesenteric angiography. In 44 of the 55 patients there was no tumor invasion in the portal trunk, and portal venous flow was found to be close to that of normal subjects regardless of the stage or size of tumor, and tumor invasion into relatively large portal branches. After transcatheter hepatic artery embolization, portal venous flow was increased, even on the next day, and it remained increased for at least 2 wk. Thus, the duplex system is useful to study qualitative and quantitative changes of portal hemodynamics in hepatocellular carcinoma. Our observations suggest that the portal venous flow is kept relatively constant by some homeostatic mechanism even in advanced hepatocellular carcinoma until the tumor invades into the portal trunk, and that it increases when hepatic arterial flow is occluded.

One hundred fifty-four liver lesions, including 63 hepatocellular carcinomas, were studied to determine the value of duplex ultrasound in the diagnosis of small hepatocellular carcinomas. Arterial Doppler signals were obtained either within the body of the tumor, at its periphery, or in both locations, from 28 to 37 hepatocellular carcinomas less than or equal to 3 cm in diameter and from all 26 hepatocellular carcinomas with a diameter greater than 3 cm. Arterial Doppler signals were obtained at the periphery of 5 of 7 cholangiocarcinomas, 4 of 11 liver metastatic tumors, and 5 of 23 hemangiomas. No such signals were obtained from 29 regenerative nodules, 10 hepatic pseudotumors, and 11 liver cysts. The mean peak systolic frequency seen in hepatocellular carcinoma (1.2 kHz) was significantly greater than in cholangiocarcinoma (0.6 kHz), metastatic tumors (0.5 kHz), or hemangiomas (0.3 kHz). A peak systolic frequency of greater than 3 kHz was found in 6 of 8 hepatocellular carcinomas greater than or equal to 4 cm in diameter with angiographically proven arterioportal shunting, whereas the value in other hepatocellular carcinomas or other hepatic focal lesions was less than 2.6 kHz. This study showed that the peak systolic shift was related to the degree of arterioportal shunting. Because shunting is either minor or nonexistent in small hepatocellular carcinomas, the value of duplex Doppler ultrasound in the diagnosis of these lesions appears to be limited.

A 24-yr-old woman with hemolytic anemia developed multiple thrombosis of the hepatic vein and inferior vena cava. She was found to have circulating lupus anticoagulant that could have been causally related to the thrombosis and hence the Budd-Chiari syndrome. On her first admission to the hospital vena cava and hepatic vein catheterizations revealed partial thrombotic occlusion of the cava at the level of the diaphragm, which was subsequently transformed into complete membranous obstruction. The right hepatic vein, which was patent on the first admission, was also completely occluded. These observations support the theory that membranous obstruction of the inferior vena cava is a sequela to inferior vena caval thrombosis rather than a congenital anomaly.