Hepatofugal Portal Flow Research Articles

Severe portal hypertension secondary to arterio‐portal fistula: salvage surgical treatment

Arterio-portal fistulas (APFs) are rare vascular disorders of various origins that can lead to severe portal hypertension. Even if surgery was initially the treatment of choice, more recently, interventional radiological procedures have been considered as the first line therapeutic option. A man with no history of liver disease was admitted for abdominal pain and distension. Abdominal ultrasonography with Doppler, magnetic resonance imaging and computed tomography (CT) scan showed ascites, splenomegaly and a probable APF between the left branches of both the hepatic artery and portal vein, associated with hepatofugal portal flow. Upper gastrointestinal endoscopy revealed large oesophageal varices without bleeding. A celiac and mesenteric arteriography and a splenic arteriography were performed and confirmed the existence of multiple intrahepatic APFs. The initial treatment consisted of two sessions of percutaneous transcatheter endovascular embolization. Unfortunately, ascites worsened, and the patient did not respond to diuretic treatment. Therefore, a surgical treatment was considered to be the only suitable treatment because of the absence of improvement after embolization procedures. A left hepatectomy with hepatic artery ligation was performed. Clinical evolution was favourable; an improvement of ascites was obtained; control ultrasonography and CT scan disclosed no residual haemodynamic abnormality; and the portal vein was normal with a hepatopedal flow. Currently, 12 months after surgery, the clinical condition of the patient is good. Percutaneous treatment of portal hypertension by embolizing multiple large APF has been described to be an effective method. Nevertheless, failure of such conservative treatment is possible and must lead to a salvage surgery.

Hepatofugal portal flow due to acute cellular rejection

We describe a case of living donor liver transplantation with hepatofugal portal flow caused by acute cellular rejection. The reversed portal flow was corrected by splenectomy and ligation of the residual collateral veins. Hepatofugal flow causes ischemic damage to the graft, which does not normalize spontaneously. In this particular case, meticulous Doppler ultrasound examination and prompt response to reversed portal flow salvaged the graft.

Ultrasonographic assessment of hemodynamic changes in the portal vein during surgical attenuation of congenital extrahepatic portosystemic shunts in dogs.

To determine portal hemodynamic changes associated with surgical shunt ligation and establish ultrasonographic criteria for determining the optimal degree of shunt narrowing and predicting outcome. Case series. 17 dogs, each with a single congenital extrahepatic portosystemic shunt. Pre- and postligation flow velocities and flow directions were determined by Doppler ultrasonography intraoperatively in the shunt and in the portal vein cranial and caudal to the shunt origin. Outcome was evaluated 1 month after surgery by measuring blood ammonia concentration and performing abdominal ultrasonography. Hepatofugal flow was detected in 9 of 17 dogs before shunt attenuation in the portal segment that was between the shunt origin and the entering point of the gastroduodenal vein. If hepatofugal flow became hepatopetal after shunt ligation, hyperammonemia resolved. Hepatofugal portal flow was caused by blood that flowed from the gastroduodenal vein toward the shunt. Shunt attenuation converted hepatofugal flow to hepatopetal in the shunt in 12 of 17 dogs. Chronic portal hypertension developed or perioperative death occurred when the portal congestion index caudal to the shunt origin increased by > 3.6 times. After hepatopetal flow in the cranial portal vein and the shunt is established, further shunt narrowing is contraindicated. Increase of the portal congestion index caudal to the shunt > 3.5 times should be avoided. Poor outcome because of severe hypoplasia of the portal branches can be expected if the flow direction remains hepatofugal after shunt occlusion cranial to the shunt origin.

Color Doppler sonographic signs of respiration-dependent hepatofugal portal flow.

The role of respiration in modulating blood flow in the portal vein is unclear. The aim of this study was to investigate the phenomenon of respiration-dependent periodic hepatofugal portal venous blood flow as detected on color Doppler sonography. Within 1 year, we identified 13 patients with respiration-dependent reversal of blood flow in the portal vein that was diagnosed on color Doppler sonography. This phenomenon was investigated by color Doppler sonographic examination of the portal venous flow during both mid-inspiration breath-holding and a respiratory cycle including deep inspiration; evaluation of hepatic vein Doppler waveforms as normal (triphasic) or decreased (flattened); and echocardiographic examination to determine the presence or absence of tricuspid regurgitation. The patients' median age was 53 years (range, 26-87 years). Seven of the 13 patients had heart disease (tricuspid regurgitation) with or without liver disease, 3 had liver disease without heart disease, and 3 had other diseases with no evidence of heart or liver disease. On Doppler sonography, 10 of the 13 patients had increased portal venous pulsatility (7 of the 10 had tricuspid regurgitation; the other 3 did not); the remaining 3 patients had neither increased pulsatility nor tricuspid regurgitation. Sonographic follow-up within 4 weeks in 4 of the 13 patients revealed loss of the respiration-dependent hepatofugal portal flow. Respiration-dependent hepatofugal portal flow is a rare finding associated with periodic portal hypertension in patients with right heart insufficiency and liver disease. Its clinical significance is unclear. Among our patients, its occurrence was predominantly associated with an increased venous pulsatility index due to tricuspid regurgitation or venous outflow obstruction. Further study is needed to investigate whether periodic respiration-dependent hepatofugal portal flow is predictive of the occurrence of continuous flow reversal.

Percentage of peak-to-peak pulsatility of portal blood flow can predict right-sided congestive heart failure

To study the change of portal blood flow for the prediction of the status of right-sided heart failure by using non-invasive way. We studied 20 patients with rheumatic and atherosclerotic heart diseases. All the patients had constant systemic blood pressure and body weight 1 week prior to the study. Cardiac index (CI), left ventricular end-diastolic pressure (LVEDP), mean aortic pressure (AOP), pulmonary wedge pressure (PWP), mean pulmonary arterial pressure (PAP), mean right atrial pressure (RAP), right ventricular end-diastolic pressure (RVEDP) were recorded during cardiac catheterization. Ten patients with RAP >10 mmHg were classified as Group 1. The remaining 10 patients with RAP >=10 mmHg were classified as Group 2. Portal blood velocity profiles were studied using an ultrasonic Doppler within 12 h after cardiac catheterization. CI, AOP, and LVEDP had no difference between two groups. Patients in Group 1 had normal PWP (14.6+/-7.3 mmHg), PAP (25.0+/-8.2 mmHg), RAP (4.7+/-2.4 mmHg), and RVEDP (6.4+/-2.7 mmHg). Patients in Group 2 had increased PWP (29.9+/-9.3 mmHg), PAP (46.3+/-13.2 mmHg), RAP (17.5+/-5.7 mmHg), and RVEDP (18.3+/-5.6 mmHg) (P<0.001). Mean values of maximum portal blood velocity (Vmax), mean portal blood velocity (Vmean), cross-sectional area (Area) and portal blood flow volume (PBF) had no difference between 2 groups. All the patients in Group 1 had a continuous antegrade portal flow with a mean percentage of peak-to-peak pulsatility (PP) 27.0+/-8.9 % (range: 17-40 %). All the patients in Group 2 had pulsatile portal flow with a mean PP 86.6+/-45.6 (range: 43-194 %). One patient had a transient stagnant and three patients had a transient hepatofugal portal flow, which occurred mainly during the ventricular systole. Vmax, Vmean and PBF had a positive correlation with CO (P<0.001) but not with AOP, LVEDP, PWP, PAP, RAP, and RVEDP. PP showed a good correlation (P<0.001) with PWP, PAP, RAP, and RVEDP but not with CI, AOP, and LVEDP. All the patients with PP >40 % had a right-sided heart failure with a RAP=10 mmHg. The measurement of PP change is a simple and non-invasive way to identify patients with right heart failure.

Hepatofugal portal flow in advanced liver cirrhosis with spontaneous portosystemic shunts: effects on parenchymal hepatic enhancement at dual-phase helical CT.

We investigated whether spontaneous hepatofugal portal flow in advanced cirrhosis affects hepatic enhancement on dual-phase helical computed tomography. Fifteen patients with hepatofugal portal flow on Doppler sonography and angiography (group 1) and 15 age- and sex-matched patients with hepatopetal portal flow (control; group 2) underwent dual-phase helical computed tomography. Vascular and liver attenuation values were measured on unenhanced scans and scans obtained during hepatic arterial (HAP; 25 s) and portal venous (PVP; 70 s) phases. Portal vein enhancement was lower during PVP in group 1 than in group 2 ( p < 0.0001). Liver enhancement was higher during HAP and lower and delayed during PVP in group 1 versus group 2 ( p < 0.0001). In hepatofugal portal flow, liver enhancement is increased during HAP and compensating for decreased and delayed liver enhancement during PVP, resulting in potential decreased hypervascular tumor conspicuity.

Severe fatty change of the graft liver caused by a portosystemic shunt of mesenteric varices

Abstract Portosystemic shunt is a common complication in patients with portal hypertension. Mesenteric varix is one of the collaterals that can cause post-transplant liver day-function. In this case report, a 45-year-old woman underwent living relative donor liver transplantation for alcoholic cirrhosis. Although the early postoperative course was uneventful, she was readmitted for treatment of liver hypofunction. Fatty change in the graft liver was confirmed by histopathology of the biopsy specimen. The venous phase of a superior mesenteric angiogram revealed large-caliber mesenteric varices comprising portosystemic venous shunts. Surgery was performed to ligate the shunts. The intraoperative color Doppler ultrasonography showed hepatofugal portal blood flow, which was corrected to hepatopetal blood flow by clamping the shunt vessels. The portal pressure was moderately elevated from 13.6 cm to 21.8 cm H2O. Two shunt vessels were ligated and divided. Her liver function returned to nearly normal thereafter. We recommend that descending collatearals be divided during liver transplantation.

Hepatic arterial buffer response in patients with advanced cirrhosis

Hepatic arterial buffer response (HABR) is considered an important compensatory mechanism to maintain perfusion of the liver by hepatic arterial vasodilation on reduction of portal venous perfusion. HABR has been suggested to be impaired in patients with advanced cirrhosis. In patients with hepatopetal portal flow, placement of a transjugular intrahepatic portosystemic shunt (TIPS) reduces portal venous liver perfusion. Accordingly, patients with severe cirrhosis should have impaired HABR after TIPS implantation. Therefore, the aim of this study was to investigate the effect of TIPS on HABR as reflected by changes in resistance index (RI) of the hepatic artery. A total of 366 patients with cirrhosis (Child-Pugh class A, 106; class B, 168; class C, 92) underwent duplex Doppler ultrasonographic examination with determination of RI and maximal flow velocity in the portal vein before and 1 month after TIPS placement. Portosystemic pressure gradient was determined before and after TIPS placement. In 29 patients with hepatofugal portal blood flow, RI was significantly lower than in 337 patients with hepatopetal flow (0.63 ± 0.02 vs. 0.69 ± 0.01; P < .001). TIPS induced a significant decrease of the RI in patients with hepatopetal flow (RI, 0.69 ± 0.01 before vs. 0.64 ± 0.01 after TIPS; P = .001) but not in patients with hepatofugal flow (RI, 0.63 ± 0.02 before vs. 0.63 ± 0.02 after TIPS; NS). This response was not dependent on the Child-Pugh class. In conclusion, our results suggest that some degree of HABR is preserved even in patients with advanced cirrhosis with significant portal hypertension. (HEPATOLOGY 2002;35:630-634.)

Color-doppler evaluation of spontaneous hepatofugal portal flow and correlation with clinical and endoscopic findings in liver cirrhosis

Color-doppler evaluation of spontaneous hepatofugal portal flow and correlation with clinical and endoscopic findings in liver cirrhosis

Hepatic Intraarterial131I Iodized Oil for Treatment of Hepatocellular Carcinoma in Patients with Impeded Portal Venous Flow

To evaluate the efficacy and safety of intraarterial hepatic iodine 131 iodized oil for treatment of hepatocellular carcinoma in patients with impeded portal venous flow. Twenty-four patients (mean age, 61 years) with hepatocellular carcinoma underwent 38 courses of 131I iodized oil (one to three per patient), with a mean dose of 2,146 MBq injected into the proper hepatic artery. Hepatocellular carcinoma manifested as single nodules (n = 8; mean, 7.75 cm), multiple nodules (n = 13; mean, 5.46 cm), or a mass (n = 3) occupying more than two hepatic segments. Portal venous thrombosis was complete (n = 10), right (n = 9), left (n = 2), or multisegmental (n = 1). Two patients had hepatofugal portal flow. Among the 23 patients with evaluable results, response to treatment was partial in three, and disease was stable in 12 and progressive in eight. Estimated actuarial survival rates were 70%, 33%, 12%, and 6% at 3, 6, 9, and 12 months, respectively, with two patients alive at 9 and 11 months. The median survival time was 147 days. Adverse events were the early death of one patient owing to hepatic failure and transient symptomatic hepatic failure after 12 courses in nine patients. In this preliminary experience, intraarterial hepatic 131I iodized oil did not demonstrate high efficacy in the treatment of hepatocellular carcinoma in patients with portal venous thrombosis, as side effects were not rare.

Systemic mastocytosis: CT and US features of abdominal manifestations.

To study the imaging findings in patients with systemic mastocytosis and to correlate the findings with the severity of disease on the basis of an established classification system. Pathologic findings, when available, were correlated with imaging findings. Computed tomographic (CT) and ultrasound (US) scans and corresponding pathologic findings, when available, were retrospectively reviewed in 27 patients with systemic mastocytosis. Only five (19%) of the patients in our series had normal abdominal CT and/or US examination results. Common abdominal imaging findings associated with systemic mastocytosis were hepatosplenomegaly, retroperitoneal adenopathy, periportal adenopathy, mesenteric adenopathy, thickening of the omentum and the mesentery, and ascites. Less common findings included hepatofugal portal venous flow, Budd-Chiari syndrome, cavernous transformation of the portal vein, ovarian mass, and complications such as chloroma. The findings were more common in patients with category II and those with category III disease. Abdominal findings at CT and US are common in patients with systemic mastocytosis. Although the findings in patients with systemic mastocytosis are not specific to the disease, they are useful in directing further studies for diagnostic confirmation and in estimating the extent of systemic involvement.

Surgical Approach for Maintaining Nonischemic Conditions of the Liver in Acute Hepatic Vein Obstruction

To establish a possible surgical approach for preventing warm ischemic injury to the liver followed by hepatic vein occlusion (HVO), the hepatic hemodynamics and energy metabolism were investigated in an acute canine HVO model with and without hepatic arterial blood flow. Arterial blood ketone body ratio (AKBR; acetoacetate/3-hydroxybutyrate) and adenylate energy charge potential (ECP = [ATP + 1/2 ADP]/[ATP + ADP + AMP]) of the liver tissue were measured during and after 60 min of HVO. In the group with hepatic arterial blood flow, in which arterial blood was drained by hepatofugal portal flow via the venovenous bypass, total hepatic blood flow, portal vein pressure, ECP, and AKBR were maintained at almost normal level after the termination of HVO, resulting in the survival of all animals for 3 days or longer. By contrast, in the group without hepatic arterial blood flow (warm ischemic group), total hepatic blood flow was maintained at less than 60% of preischemic value, and portal vein pressure gradually increased up to twice the preischemic value. ECP decreased from 0.81 ± 0.06 to 0.71 ± 0.07 along with increasing portal venous pressure, and AKBR also decreased from 1.23 ± 0.12 to 0.63 ± 0.23, resulting in no survival longer 6 hr. It was concluded that hepatic arterial blood flow during HVO, if drained as hepatofugal portal flow, could maintain nonischemic conditions in the liver, despite vena cava obstruction, by providing an alternate outflow via reversed flow in the portal vein.

Percutaneous transhepatic embolization of a spontaneous mesocaval shunt after liver transplantation

A preoperatively undetected spontaneous mesocaval shunt lead to impairment of organ function after liver transplantation. Ischemia of the graft due to partial hepatofugal portal flow was demonstrated by color-flow Doppler sonography and angiography. The successful catheter embolization of the mesocaval shunt via a transhepatic approach is presented.

Budd-Chiari Syndrome: Recanalization of an Occluded Hepatic Vein with Percutaneous Transluminal Angioplasty and a Metallic Stent

From the First Department of Internal Medicine, Faculty of Medicine, Kyoto University, 54 Shogoin-Kawaharacho, Sakyouku, Kyoto 606 Japan. Received May 19, 1992; revision requested June 12; revision received October 9; accepted November 2. Address reprint requests to M.F. SCVIR, 1993 B u D D c H m I syndrome is a type of portal hypertension with the clinical triad of hepatomegaly, ascites, and right upper quadrant pain. It is caused by obstruction to the hepatic venous outflow, and it consists of acute and chronic forms (1,2). The site and extent of the obstructed lesion are variable. In the Orient, Budd-Chiari syndrome secondary to obstruction of the hepatic ort ti on of the inferior vena cava (IVC) has been commonly reported (1-6); in Japan, membranous obstruction of the vena cava appears to account for approximately 80% of cases (4-6). In the West, most cases are due to thrombotic occlusions of the hepatic veins, which are frequently associated with hypercoagulable states, most commonly including polycythemia Vera and the use of oral contraceptives (1,2,7). We describe a patient with extensive thrombotic occlusion of the IVC and the major hepatic veins. In this patient, hepatic encephalopathy due to the hepatofugal portal flow occurred several times. To relieve obstruction of the hepatic venous outflow, we recanalized the occluded hepatic vein and placed a tantalum wire mesh stent by means of a percutaneous transhepatic approach.

Prevalence of spontaneous hepatofugal portal flow in liver cirrhosis: Clinical and endoscopic correlation in 228 patients

The prevalence of spontaneous reversal of flow in the portal venous system was non invasively evaluated by Doppler ultrasound in 228 patients with liver cirrhosis and portal hypertension. Reversed flow was detected in the portal vein in 7 patients (3.1%), in the splenic vein in 7 patients (3.1%), and in the superior mesenteric vein in 5 patients (2.1%), with an overall prevalence of 8.3% (19/228). This prevalence did not differ in relation to the etiology of liver cirrhosis, whereas hepatofugal flow was found in more patients classified as Child's C (15.4%) and B (12.5%) than those classified as Child's A (2.7%) (P < 0.02) and was associated with a higher frequency of hepatic encephalopathy (21% vs. 7.2%; P < 0.05). Endoscopic evaluation of esophageal varices did not reveal any correlation between the presence and size of varices and hepatofugal flow, whereas red signs were detected more frequently in patients with this hemodynamic pattern (42.1% vs. 24.4%; NS). The rate of previous variceal bleeding was not significantly different in patients with and without hepatofugal flow (30.8% vs. 24.4%; NS). Conversely, the prospective evaluation of 15 patients with hepatofugal flow and 29 matched patients with hepatopetal flow, derived from the group of 228 patients, followed up for a period of 12–18 months, showed that variceal bleeding occurred in 9 of 29 patients with hepatopetal flow and in none of the 15 patients with hepatofugal flow (P < 0.02). However, no statistical difference was found in the survival rates. This study indicates that the actual prevalence of reversed flow in the portal, splenic, and superior mesenteric veins in a nonselected cirrhotic population is 8.3%. From a clinical point of view, the data suggest that this finding might be considered an important prognostic factor because, while occurring in cirrhotic patients with more severe functional impairment, it might play a protective role against the risk of bleeding.

COMPARISON OF TRANSCOLONIC 123I‐IODOAMPHETAMINE AND PORTAL VEIN INJECTION OF 99mTc‐MACROAGGREGATED ALBUMIN SHUNT FRACTION CALCU‐LATIONS IN EXPERIMENTAL DOGS WITH ACQUIRED POR‐TOSYSTEMIC SHUNTS

Shunt fraction was determined using transcolonic 123I‐iodoamphetamine (IMP) and portal vein injection of 99mTc‐macroaggregated albumin (MAA) in a group of eight dogs with chronic cirrhosis and acquired portosystemic shunts subsequent to total common bile duct ligation. Hepatic parenchymal damage was confirmed by alterations in liver function tests and liver histology. Seven of the eight dogs developed portal hypertension and had angiographic evidence of hepatofugal portal blood flow with multiple peripheral portosystemic anastomoses. Shunt fractions determined in the seven dogs with shunts varied from 39 to 100 using IMP and 45 to 93 using MAA. The remaining dog had normal portal pressure, a normal portal angiogram, and normal IMP and MAA scintigraphic studies. There was an excellent correlation between the two methods of shunt fraction calculation (R2= 0.98) and the line of regression was not significantly different from unity (IMP = 1.09 × MAA ‐ 0.03).

Hepatofugal portal flow in cirrhosis: observations on hepatic hemodynamics and the nature of the arterioportal communications.

Six of 85 patients (7%) with alcoholic liver disease undergoing transhepatic portal pressure measurement had either stagnant (3 patients) or reversed (3 patients) portal blood flow documented by gentle hand injection of 1 to 2 ml of angiographic contrast. Portal blood flow was uniformly hepatopetal in 24 patients with nonalcoholic liver disease. Recurrent spontaneous hepatic encephalopathy and sodium retention occurred in 4 of 6 patients with stagnant or reversed portal flow; gastrointestinal bleeding was not seen. Standard laboratory tests of liver function were widely variable. Net portal pressure was lower in this group than in patients with alcoholic liver disease and forward portal flow (9.2 +/- 2.6 vs. 15.6 +/- 4.1 mm Hg, p less than 0.001). Wedged hepatic vein pressure was 1 to 7 mm Hg higher than portal vein pressure in patients with reversed portal flow. The arterioportal extraction of bile acid was calculated from the difference in concentration between artery and portal vein, and total functional hepatic blood flow was calculated from the hepatic extraction and systemic clearance of indocyanine green. Extraction was 0%, and hepatic blood flow was 0.469 liter per min in a patient with hepatofugal portal flow and recurrent encephalopathy. Extraction was 20%, and hepatic blood flow was 4.014 liters per min in a patient who had never had encephalopathy. These data indicate that arterioportal communications may be sinusoidal or presinusoidal in patients who lose forward portal flow and that the amount of flow in the arterioportal circuit, together with its efficiency, largely determine the clinical outcome.

Total hepatofugal portal blood flow in cirrhosis demonstrated by transhepatic portography.

We investigated 108 patients with cirrhosis of the liver and portal hypertension by percutaneous transhepatic portography to demonstrate the occurrence and frequency of total hepatofugal portal blood flow. Sixteen patients (14.8%) had a total hepatofugal portal blood flow. The aetiology of portal hypertension and the portal pressure did not differ from that in the group of patients with hepatopetal portal blood flow. A significantly higher percentage of patients in the group with hepatofugal flow had gastro-oesophageal varices (P less than 0.025). All patients with varices had bled. Half of the patients in the group with hepatofugal blood flow had a false splenoportographic diagnosis of portal vein thrombosis. In conclusion, total hepatofugal postal blood flow exists more often than hitherto assumed. Hepatofugal blood flow does not relieve portal hypertension nor prevent development of gastrooesophageal varices or bleeding.

Hepatoma, arterioportal shunting, and hyperkinetic portal hypertension: therapeutic embolization.

Four patients with hepatocellular carcinoma, shunting of blood from the hepatic artery to the portal vein, and hyperkinetic portal hypertension were treated by transcatheter embolization of the hepatic artery. In three acutely bleeding patients variceal hemorrhage was controlled by the embolization. Following embolization hepatofugal portal venous flow became hepatopetal in all four patients. No serious complications were encountered. When hepatoma is complicated by arterioportal shunting and hyperkinetic portal hypertension, occlusion of the fistula by transcatheter embolotherapy can reduce the portal pressure.

Membranous obstruction of the inferior vena cava in the United States.

The pathogenesis of membranous obstruction of the inferior vena cava (MOVC) is unclear. Although the lesion is rare in the United States compared to Japan, India, and black South Africa, it has been responsible for 23% of cases of hepatic outflow obstruction we have encountered in the ethnically heterogeneous indigent population of Los Angeles. Most patients with MOVC are male. In contrast, recent series of patients with Budd-Chiari Syndrome (BCS) have demonstrated a female predominance. Compared to BCS without involvement of the inferior vena cava (IVC), patients with MOVC have more chronic symptoms. Large truncal collaterals, particularly on the back, strongly suggest MOVC. In patients without this sign, a high index of diagnostic suspicion is required. Chronic hepatitis B infection occurs with increased frequency in these patients. Chest radiograph may show an enlarged azygous shadow. Liver-spleen scan is not helpful, and the liver biopsy is frequently nondiagnostic. A useful screening procedure for hepatic outflow block is transhepatic portal pressure measurement demonstrating aberrant hepatic veins with pressures higher than in the portal vein and, occasionally, hepatofugal portal flow. Transcardiac membranotomy appears to be symptomatically effective in patients with MOVC and at least one patent hepatic vein. It is not known whether this operation will prolong life and prevent the development of hepatocellular cancer, which may occur in up to 48% of these patients. The correct therapeutic approach has not been established for those patients whose lesion is not amenable to surgery because of extensive IVC occlusion or absence of patent hepatic veins.