prospective trials. 8,9 However, the incidence of hemorrhage The incidence and the risk factors of hemorrhage from from FV has not been fully investigated. 3,7 Although several gastric fundal varices (FV) have not been fully evaluauthors have mentioned the incidence of hemorrhage from ated. We therefore conducted a retrospective and pro-FV, 3,7 to our knowledge, there has been no prospective study spective study to define the incidence and risk factors documenting the cumulative risk for FV hemorrhage in a for such episodes. We investigated 132 patients with cirlarge number of patients. The aim of this study was to define rhosis and gastric FV. Of these 132 patients, 15 patients the incidence and the risk factors for hemorrhage from FV. had hemorrhagic FV at the time of enrollment. The clinical characteristics were compared between these pa-PATIENTS AND METHODS tients and those without a first hemorrhage from FV. In Baseline Clinical Assessment. From January 1985 through Decemthe patients who had never previously bled, the inciber 1995, a total of 1,392 cirrhotic patients consecutively underwent dence and risk factors were prospectively investigated.upper gastrointestinal endoscopy at our institute. Of these patients, The size of FV was greater and red-spot on the FV were 540 patients had esophageal varices, 96 patients had gastric varices, more prevalent in patients with hemorrhagic FV. Child's and 253 patients had both esophageal and gastric varices. In the status was also more severe in these patients. In the 117 patients with gastric varices, 143 patients had FV, while the repatients who had never bled, 34 hemorrhages from FV maining 206 patients had varices in the cardia. In the 143 patients occurred during the follow-up period. The cumulative with FV, 11 patients were subsequently excluded from further evaluation because of their refusal to participate in the study. We thus risk for such hemorrhage at 1, 3, and 5 years was 16%, investigated a total of 132 patients with FV in the current study. 36%, and 44%, respectively. A multiple regression analy-The subjects consisted of 89 men and 43 women ranging in age from 1 The blood flow of such collaterals is abundant, 2 and apy. All patients were informed of the scientific nature of the investihemorrhage from FV is more serious than that of esophageal gation and gave their informed consent. The study protocol was apvarices. [3][4][5][6] The treatment of hemorrhagic FV by endoscopic proved by the Hospital Ethics Committee. procedures sometimes fails to cease the bleeding, and surgiAssessment of Endoscopic Findings. The diagnosis of FV was made cal modalities are thus often required for hemostasis.3-6 As a based on endoscopy with the agreement of two experienced endoscoresult, the mortality rate is high in patients with hemor-pists when one or more distinct venous channels were found in the rhagic FV. [3][4][5][6] In addition, because hemorrhagic esophageal gastric fundus. In patients with hemorrhagic FV, the endoscopic findings were analyzed after the cessation o...

We investigated the effects of nifedipine on splanchnic haemodynamics in 13 patients with cirrhosis and portal hypertension, and in 10 control subjects using hepatic venous catheterization and pulsed Doppler ultrasound. There were no significant changes in systemic or splanchnic haemodynamics in control patients. In contrast, systemic vasodilatation, evidenced by significant decreases in mean arterial pressure and systemic vascular resistance, was observed in patients 20 min after sublingual application of 10 mg nifedipine. Moreover, hepatic venous pressure gradient and portal vein blood flow significantly increased after nifedipine administration. There was a significant correlation between the percentage increases in portal vein blood flow and in hepatic venous pressure gradient. However, no correlation was found between the percentage change in cardiac output and that in portal vein blood flow. Thus the increase in portal vein blood flow appears to be related to splanchnic arterial vasodilatation by nifedipine. Consequently, nifedipine has deleterious effects on portal haemodynamics in patients with cirrhosis. As nifedipine may potentially increase the risk of variceal haemorrhage in patients with less advanced varices, this drug should be used with caution in patients with chronic liver disease.

Duodenal varices are a rare site of hemorrhage in patients with portal hypertension, but their rupture is a serious and often fatal event. We report a 65-year-old woman who presented with hematemesis and melena. She was admitted to our department because of prolonged shock, despite having received transfusion of a large volume of blood. Upper gastrointestinal endoscopy revealed nodular varices with active bleeding in the second portion of the duodenum. Endoscopic injection sclerotherapy (EIS) was performed using a tissue adhesive agent, alpha-cyanoacrylate monomer, with only temporary benefit. However, anemia continued to progress after the procedure. Therefore, we combined transileocolic vein obliteration (TIO) with balloon-occluded retrograde transvenous obliteration (B-RIO), using 5% ethanolamine oleate with iopamidol to obliterate the varices. Complete hemostasis was achieved without complications. Neither recurrence of varices nor further bleeding has occurred for over 3 years. We conclude that combined TIO and B-RTO, which can obstruct both the feeding and the draining vessels of duodenal varices to retain the sclerosing agent completely in the varices, is a safe and effective hemostatic measure for ruptured duodenal varices, when EIS has failed to accomplish complete hemostasis.

BACKGROUND The current study was designed to determine the usefulness of pretreatment tumor pressure as a new prognostic factor in patients with small hepatocellular carcinoma (HCC; 3 cm or smaller in diameter). METHODS The study included 39 patients with small HCC in whom tumor pressure was determined. They underwent percutaneous ethanol (with Lipiodol) injection therapy (Lp‐PEI) or transcatheter arterial embolization (TAE) of the hepatic artery. Tumor pressure was determined percutaneously under ultrasonographic guidance. The factors analyzed were age, gender, mean blood pressure, the presence/absence of antibody to hepatitis C virus (anti‐HCV), alcohol abuse, Child's classification, the presence/absence of esophagogastric varices, serum α‐fetoprotein (AFP) level, tumor size, number of tumors, degree of tumor differentiation, the presence/absence of tumor capsule, tumor pressure, and the method of treatment. Multivariate analysis using Cox proportional hazards model was conducted on the factors that may have affected prognosis (P < 0.25) according to the univariate analysis using a proportional hazards model. RESULTS The rates of local and distant recurrence were higher (P < 0.01, P < 0.01, respectively) and the survival rate was lower (P = 0.03) in patients with high tumor pressure than in those with low tumor pressure. Multivariate analysis revealed that tumor pressure (P < 0.01), AFP level (P = 0.01), and age (P = 0.01) were significant predictive factors associated with local recurrence. Tumor pressure (P < 0.01) and AFP level (P < 0.01) were both significantly associated with distant recurrence. The only significant predictive factor associated with survival rate was tumor pressure (P < 0.04). CONCLUSIONS The current study revealed that tumor pressure was associated significantly with survival rates after Lp‐PEI or TAE in patients with small HCC. There were also significant predictive factors associated with local recurrence, these being tumor pressure, AFP level, and age, and with distant recurrence, namely, tumor pressure and AFP level. Tumor pressure measured before the initial treatment of patients with small HCC may be a useful new prognostic factor. Cancer 2002;95:596–604. © 2002 American Cancer Society. DOI 10.1002/cncr.10690

The aim of this study was to determine whether endoscopic variceal sclerotherapy affects systemic or splanchnic hemodynamics.Wemeasured hemodynamic parameters before and after the first course of sclerotherapy in 35 patients with cirrhosis. Following sclerotherapy, there was a significant decrease in cardiac index and a significant increase in systemic vascular resistance. Changes in hepatic venous pressure gradient varied from patient to patient with no statistically significant change in the group overall. However, all 20 patients with a decline in the hepatic venous pressure gradient had a concomitant decrease in cardiac index and/or a large extravariceal shunt. The multivariate analysis disclosed that the decrease in cardiac index was a statistically significant contributor for the decline in hepatic venous pressure gradient. Weconclude that the obliteration ofesophageal varices by sclerotherapy significantly reverses the hyperdynamic circulatory state in patients with cirrhosis. Spontaneous changes in systemic hemodynamicsand the interaction with hepatic hemodynamics must be taken into account when evaluating hepatic hemodynamics in patients undergoing variceal sclerotherapy.

The present study was designed to determine the systemic haemodynamic effects of obliterating oesophageal varices by endoscopic sclerotherapy. We evaluated systemic and splanchnic haemodynamics before and after the first course of sclerotherapy in cirrhotic patients. The baseline cardiac index was significantly correlated with baseline azygos vein blood flow (r = 0.64; P < 0.01) and the azygos vein blood flow and cardiac index significantly decreased (-33% and -16%, respectively; P < 0.01) following sclerotherapy. The systemic vascular resistance index was also increased significantly (+ 20%; P < 0.01) in these patients. Moreover, the per cent change in azygos vein blood flow was directly correlated with that of the cardiac index (r = 0.51; P < 0.03). We conclude from these findings that the obliteration of portosystemic collaterals by sclerotherapy significantly reverses hyperdynamic circulation in such patients via a decrease in cardiac preload. The blood flow of the portosystemic shunt per se is a leading contributor to the hyperdynamic circulation observed in patients with well-developed portal systemic collateral vessels.

a critical role in the arteriolar vasodilation and high cardiac The effects of endoscopic variceal ligation (EVL) on output of cirrhosis. 10 It has been documented that cirrhotic systemic hemodynamics are unknown. This study was patients have a significant increase in the concentration of conducted to determine whether the obliteration of porserum nitrate/nitrite, metabolites of NO, 11 compared with tal-systemic collaterals by EVL affects systemic hemodycontrol subjects. 12,13 The role of NO in the regulation of sysnamics and serum nitrate concentrations in patients temic hemodynamics in cirrhosis, however, is unclear. cate that EVL decreased cardiac output via a reductionProphylactic EVL was administered when the patients had esopha- in cardiac preload (central venous return). Blood flowgeal varices with endoscopic findings predictive of a high risk of through portal-systemic collaterals has an important bleeding, such as enlarged tortuous varices (F2) or largest sized varirole in the enhanced cardiac preload of cirrhotic pa-ces (F3) with a severe red-color sign.14 The patients were a subgroup tients. The sudden decrease in serum nitrate concentra-of a prospective trial comparing the effectiveness of EVL in the pretions suggests that endogenous nitric oxide may be in-vention of first bleeding and reduction of mortality in patients with volved in the regulation of systemic hemodynamics in high-risk esophageal varices. Patients with alcoholic cirrhosis (n Å 2) were excluded from the study to avoid the potential effects of patients with compensated cirrhosis. (HEPATOLOGY abstinence on systemic and splanchnic hemodynamics. 15 In addition, 1996;24:47-52.)patients were also excluded because of inadequate cardiac imaging preventing echocardiographic assessment (n Å 1) and renal failure Portal hypertension and arteriolar vasodilation are im-(n Å 1). Thus, 17 patients were enrolled in this study. To evaluate portant hemodynamic alterations that lead to a high cardiac the possible hemodynamic effects of endoscopy, a control group of cirrhotic patients receiving gastroscopy were matched by systemic output and stroke volume, associated with a low peripheral hemodynamics, age, severity of liver damage, and grade of varices. vascular resistance, in patients with cirrhosis.1-3 Recent inAll subjects had histologically proven cirrhosis of the liver and were vestigations have shown an enhanced left ventricular diamefree of edema and ascites ascertained by ultrasonography.ter and cardiac output together with a direct correlation be-EVL. Endoscopic variceal ligation was carried out through flexible tween both parameters in cirrhotic patients. [4][5][6] These findings endoscopy (GIF Q-20, Olympus Corp., Tokyo, Japan), a plastic endosuggest that an increased cardiac preload may play an im-scopic esophageal overtube and an endoscopic ligation device (Varioportant role in the increased cardiac output of cirrhosis. In-ligator, Top Corp., Tokyo, Japan). To avoid the hemodynamic effects creased circulating blood volume and portal-syst...

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