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World J Gastroenterol. Apr 7, 2007; 13(13): 1912-1927
Published online Apr 7, 2007. doi: 10.3748/wjg.v13.i13.1912
Hepatic venous outflow obstruction: Three similar syndromes
Ulas Darda Bayraktar, Soley Seren, Yusuf Bayraktar
Ulas Darda Bayraktar, Department of Internal Medicine, Interfaith Medical Center, Brooklyn, NY 11230, United States
Soley Seren, Department of Internal Medicine, Wayne State University, Detroit, MI, United States
Yusuf Bayraktar, Division of Gastroenterology, Hacettepe University School of Medicine, Ankara, Turkey
Author contributions: All authors contributed equally to the work.
Correspondence to: Ulas Darda Bayraktar, MD, Department of Internal Medicine, Interfaith Medical Center, 229 Parkville Ave Apt# 4B, Brooklyn, NY 11230, United States.
Telephone: +1-718- 4314657
Received: October 11, 2006
Revised: November 2, 2006
Accepted: November 14, 2007
Published online: April 7, 2007


Our goal is to provide a detailed review of veno-occlusive disease (VOD), Budd-Chiari syndrome (BCS), and congestive hepatopathy (CH), all of which results in hepatic venous outflow obstruction. This is the first article in which all three syndromes have been reviewed, enabling the reader to compare the characteristics of these disorders. The histological findings in VOD, BCS, and CH are almost identical: sinusoidal congestion and cell necrosis mostly in perivenular areas of hepatic acini which eventually leads to bridging fibrosis between adjacent central veins. Tender hepatomegaly with jaundice and ascites is common to all three conditions. However, the clinical presentation depends mostly on the extent and rapidity of the outflow obstruction. Although the etiology and treatment are completely different in VOD, BCS, and CH; the similarities in clinical manifestations and liver histology may suggest a common mechanism of hepatic injury and adaptation in response to increased sinusoidal pressure.

Key Words: Veno-occlusive disease, Sinusoidal obstru-ction syndrome, Budd-Chiari syndrome, Congestive hepatopathy


Although the liver makes up < 3% of the total body weight, it receives one-quarter of the total cardiac output through the hepatic artery and portal vein[1]. Blood is drained from the hepatic acini via central veins into sublobular veins and then into the right, left, and middle hepatic veins, the inferior vena cava and the right atrium[2]. An obstruction to the blood flow out of the liver can result in a spectrum of clinical abnormalities ranging from acute hepatic failure to passive hepatic congestion, depending on the acuity and level of obstruction.

Hepatic venous outflow obstruction (HVOO) can be divided into three categories according to the level of obstruction: (1) Veno-occlusive disease (VOD): at the level of sinusoids and terminal venules, (2) Budd-Chiari syndrome (BCS): from hepatic veins to the superior end of inferior vena cava, and (3) Venous obstruction at the level of heart referred to as congestive hepatopathy (CH) (Figure 1).

Figure 1
Figure 1 Site of venous obstruction in veno-occlusive disease, Budd-Chiari syndrome, and congestive hepatopathy.

The etiology of VOD, BCS, and CH are entirely different (Table 1). It should be noted that VOD develops within three weeks of an acute insult to the sinusoidal endothelial cells while BCS and CH may develop within a few days or may take several years of venous thrombosis and heart failure, respectively. The variations in the ‘acuteness’ of venous obstruction leads to subtle differences in the clinical presentations of VOD, BCS, and CH. Although patients with HVOO generally present with abdominal pain due to hepatomegaly, and jaundice and ascites due to portal hypertension; chronic BCS patients may first present with cirrhosis and its complications. BCS patients with inferior vena cava obstruction may also have leg edema and venous collaterals over the trunk. Additionally, signs and symptoms of heart failure such as jugular venous distention, leg edema, and dyspnea may be seen in patients with CH. Nonetheless, the histological findings in all three syndromes are almost identical and include sinusoidal congestion and hepatocyte necrosis predominating in perivenular areas of hepatic acini which eventually leads to bridging fibrosis between adjacent central veins (Table 1)[1,3,4].

Table 1 Definition, etiology and histology of VOD, BCS, and CH.
Site of venous obstructionHepatic sinusoids and terminal venulesFrom hepatic veins to the superior end of IVCHeart
EtiologySinusoidal endothelial injury due to HSCT, chemotherapy, abdominal radiotherapy, and pyrrolizidine alkaloidsHepatic vein thrombosis, IVC webs, compression of hepatic veins or IVC by tumor, cyst, or abscessIncreased right atrial pressure due to CHF (CAD, cardiomyopathies, valve abnormalities), cor pulmonale (COPD, ILD, pulmonary HTN), and pericardial disease (constrictive pericarditis, pericardial tamponade)
HistologyChanges predominantly in perivenular areasPredominantly in perivenular areas except in presence of concomitant PVT.Predominantly in perivenular areas Sinusoidal congestion and hepatocellular necrosis
Gaps in SEC barrier leading to subendothelial edemaSinusoidal congestion followed by ischemic cell necrosis and bridging fibrosis between central veinsBridging fibrosis between central veins leading to cardiac fibrosis in chronic cases
Narrowing of central veins and sinusoids with sinusoidal congestion and hepatocellular necrosisCaudate lobe hypertrophy, with fibrosis and atrophy in the rest of liver
Collagen accumulation in sinusoids and veins leading to bridging fibrosis between central veins

The laboratory findings in VOD, BCS, and CH are also very similar. Hyperbilirubinemia is universal in HVOO except in patients with constrictive pericarditis[5], and is believed to be due to hepatocellular dysfunction, hemolysis, and biliary canalicular obstruction secondary to distended hepatic veins[6]. Serum aminotransferase levels may be mildly elevated except in fulminant BCS and CH with severe cardiac output impairment causing hepatic ischemia when the levels may exceed 1000 U/L. Alkaline phosphatase levels may also be mildly elevated. New markers for diagnosis of VOD such as plasminogen activator inhibitor-1 are under investigation.

The gold standard for the diagnosis of VOD is liver biopsy. However, because of the risks of liver biopsy in thrombocytopenic patients, the diagnosis is primarily based on clinical criteria. CH is usually diagnosed by routine laboratory tests in patients with symptomatic heart failure. However, physicians may miss the diagnosis of CH in patients with constrictive pericarditis who do not have overt symptoms. Echocardiogram and invasive cardiac hemodynamic evaluation may be necessary in patients with a strong suspicion of CH. Diagnosis of BCS, unlike VOD and CH, is greatly dependant on radiological studies, although a careful history and physical examination is crucial in order not to overlook this protean syndrome. Doppler sonogram followed by venogram are the first line tests in patients with suspected BCS (Table 2).

Table 2 Radiological findings, treatment, and prognosis in VOD, BCS, and CH.
Radiological findingsUltrasonography to rule out other liver disordersDoppler: Abnormal flow in a hepatic vein; large intrahepatic collateral vessels; e nlarged, stenotic, or tortuous hepatic veinsDilatation of all three hepatic veins on sonogram
Doppler may show reverse blood flow in the portal veinMRI: Large intrahepatic comma shaped c ollaterals. Hepatic venography: Spider web venous network patternECHO: Increased pulmonary artery pressure, dilatation of right side of heart, TR, abnormal diastolic ventricular filling due to pericardial disease
Treatment(1) Prevention: UDCA, heparin, LMWH, and defibrotide(1) Prevention of thrombus extension: Anticoagulation with heparin and warfarinTreatment of the underlying heart disease
(2) Treatment: Symptomatic care, defibrotide, tPA, AT-III concentrate(2) Restoration of blood flow: Thrombolytic therapy, percutaneous, angioplasty, TIPS, or shunt surgeryPericardiectomy in constrictive pericarditis
(3)TIPS and liver transplantation in selected cases(3) Liver transplantation
PrognosisMortality rate between 9% to 98% depending on the severityFive-year survival rate 42% to 89% in hepatic vein thrombosis and 25% in IVC obstructionLiver disease rarely contributes to mortality in these patients

The treatment and prognosis of VOD, BCS, and CH are summarized in Table 2. It should be noted that despite new promising therapies, prevention is still the mainstay of VOD management because of its high mortality and the limited efficacy of current therapeutic modalities. Treatment of BCS depends on the site and extent of the obstruction, and varies from sole anticoagulation to TIPS and liver transplantation. Treatment of the underlying heart disease is the basis of the management of CH.

Following are the detailed reviews of VOD, BCS, and CH.


Hepatic VOD is characterized by tender hepatomegaly, fluid retention, weight gain, and jaundice. This condition is seen typically after hematopoietic stem cell transplantation (HSCT)[7], high dose abdominal radiation therapy[8], use of certain chemotherapeutic agents[9], ingestion of pyrrolizidine alkaloids[10,11], and liver transplantation[12]. In 1954, Bras et al[13] first described veno-occlusive disease in Jamaican children who developed occlusion of the tributaries of the hepatic vein with subsequent centrilobular or non-portal fibrosis, associated with poisoning with Senecio type alkaloids. The term, sinusoidal obstruction syndrome was introduced in 2002 by deLeve et al[14] to replace VOD based on their studies identifying the primary site of injury as the sinusoidal endothelial cells, which results in fibrosis and obstruction of hepatic venous outflow. VOD after HSCT will be the focus of our review since it is the most common and studied form of VOD.

Clinical presentation

The reported incidence of VOD after HSCT varies greatly from 5% to 50% largely due to differences in the chemotherapeutic conditioning regimens[15]. Most patients develop signs and symptoms of VOD within the first three weeks after HSCT. The initial signs are sudden weight gain and development of hepatomegaly[16]. Weight gain is believed to be due to renal retention of water and sodium. Hyperbilirubinemia is seen after a few days, sometimes followed by increase in serum transaminase and alkaline phosphatase levels. The first symptom and generally the only one reported by patients with VOD is right upper quadrant pain, likely due to acute congestion of liver[17]. Physical exam reveals tender hepatomegaly and ascites in 83% and 39% patients with histologically proven VOD respectively[18].

Patients with VOD generally require more platelet transfusions than patients without liver disease[19]. This might be because of ongoing thrombotic process in the liver sinusoids or increased splenic sequestration due to portal hypertension[17]. Patients with VOD may develop renal failure as a result of hepatorenal syndrome. The prevalence of renal, cardiac, and pulmonary failure was noted to be higher in patients with VOD than in those without VOD in a report of 355 patients who underwent HSCT[16]. Coagulation factor deficiencies and prolonged prothrombin time can be encountered as the hepatic function declines.

The overall mortality is reported to be between 3% and 67%[20,21]. The severity of VOD can be classified as mild (requiring no treatment and with complete resolution), moderate (requiring treatment with diuretics and pain medications and with complete resolution), and severe (requiring treatment and no resolution before death or by transplant d 100). In one large series, the mortality rate was reported to be 98%, 23%, and 9% in patients with severe, moderate, and mild VOD, respectively[16]. Patients with severe VOD differed from those with mild or moderate VOD in the amount of weight gained, increment speed of total serum bilirubin level, and frequency of edema and ascites. One drawback of this classification is that it can be used only for research purposes because of its retrospective assessment. Therefore, in 1994 Bearman et al[22] formulated a mathematical model to predict the severity of VOD based on alterations in weight and serum bilirubin level.

Risk factors

Several pretransplant and transplant-associated risk factors have been identified in different studies.

One of the most important independent risk factors of VOD is the presence of liver injury prior to HSCT. In a cohort of 1652 patients, the relative risk of VOD in the presence of pre-transplant elevated AST levels and prior radiotherapy to the abdomen were 2.4 and 2.9, respectively[15]. In addition, the presence of hepatic metastases of solid tumors was associated with an increased risk of VOD[21]. Although hepatitis C virus (HCV) infection was reported to increase the risk of VOD in one study[23], in another study on 355 patients the risk for VOD was found not to be increased unless the pretransplant AST levels were elevated[24].

Advanced age[25] and previous HSCT may be associated with higher incidence of VOD[16,17]. Additionally, Factor V Leiden and prothrombin G20210A mutation may be associated with VOD[26,27].

Medications used before, during or after HSCT may increase the risk of VOD. Prior therapy with gemtuzumab ozogamicin, a calicheamicin-conjugated monoclonal CD33 antibody used in the treatment of acute myelogenous leukemia, significantly increases the risk of VOD, regardless of the dose and serum AST levels[28]. The use of vancomycin or acyclovir in the pre-transplant period has been associated with the development of VOD. However, it is unclear whether the increased risk of VOD is due to antibiotics or the underlying infections that necessitated their use. Additionally, women who received norethisterone to prevent menstruation during HSCT have been found to have an increased incidence of VOD[29,30].

One of the most important risk factors for the development of VOD is the type and dose of the conditioning regimens of HSCT. The incidence of VOD was found to be 3 times higher in patients who received cyclophosphamide in combination with busulfan or total body irradiation (TBI) (> 12 Gy) or carmustine and etoposide[15]. The mechanism is thought to involve acrolein, the inactive toxic metabolite of cyclophosphamide[31] which is detoxified by conjugation with glutathione[32]. Hepatic glutathione reserve is decreased by busulfan, carmustine and TBI, thus explaining the increased risk of VOD by these drug combinations.

It is widely believed that the incidence of VOD is higher after allogeneic stem cell transplantation than after autologous stem cell transplantation. However, some studies have failed to show any difference[16,33]. Furthermore, the differences seen in other studies[15] may be due to higher intensity conditioning regimens used in allogeneic transplantation. Additionally, patients receiving stem cells from unrelated or mismatched donors have higher risk of developing VOD[16].


The gold standard for the diagnosis of VOD is liver histology. However, because of the risks of liver biopsy in thrombocytopenic patients, diagnosis is primarily based on clinical findings. The Seattle and Baltimore clinical criteria (Table 3) are generally used for the diagnosis of VOD[33,34]. Carreras et al[18] reported that the diagnosis of VOD could be confirmed histologically in 41%, 91%, and 91% of patients satisfying two and three features of Seattle criteria, and Baltimore criteria, respectively. Sensitivity of latter two was 56%.

Table 3 Diagnostic criteria for veno-occlusive disease.
Seattle criteria
Development of at least 2 of the following 3 clinical features before d 30 after transplantation
Hepatomegaly with right upper quadrant pain
Ascites and/or unexplained weight gain
Baltimore criteria
Development of hyperbilirubinemia with serum bilirubin > 2 mg/dL within 21 d after transplantation and at least 2 of the following clinical signs and symptoms
Hepatomegaly, which may be painful
Weight gain > 5% from baseline

Liver specimens for histological examination can be obtained through percutaneous, laparoscopic, and transvenous (transjugular or femoral) biopsies. The latter method has the advantage of lower risk of bleeding and the opportunity to measure wedge hepatic venous pressures at the same time. Although transvenous liver biopsy specimens tend to be small, with modern techniques and equipment a representative sample can be obtained[35]. Transfemoral approach often results in crush artifact in the tissues obtained so that the transjugular method is generally preferred. It should be noted that the histological abnormalities may be patchy, especially in the early stages and could lead to false negative biopsy results. In one series, 2 of the 29 patients (7%) died due to intraperitoneal bleeding after transvenous liver biopsies[35] whereas Carreras et al[18,36] reported no procedure-related deaths in two series of 71 and 30 patients. Hepatic venous pressure gradient of > 10 mmHg was reported to have > 80 % sensitivity and specificity in these series.

Ultrasonography is useful in excluding other disorders that mimic VOD. Yoshimoto et al[37] suggested that detection of reverse blood flow in a segment of portal vein by color-Doppler sonogram is useful for early diagnosis of VOD.

Plasma plasminogen activator inhibitor-1 (PAI-1) level above 100 ng/mL was found to be 100% sensitive and specific for VOD in a series of 31 posttransplant patients with bilirubin levels > 3 mg/dL[38]. Additionally, serum N-terminal peptide of type III procollagen and hyaluronic acid levels may also have a diagnostic role[39,40].

A variety of clinical conditions can mimic VOD (Table 4) and it is difficult to differentiate these from VOD in the early stages. The main causes of intrahepatic cholestasis after HSCT are acute graft-versus-host disease (GVHD), cholangitis lenta (sepsis related cholestasis), cyclosporine-induced cholestasis, and VOD. Compared to VOD, GVHD generally develops at a later stage after the appearance of intestinal and cutaneous manifestations and moreover does not cause hepatomegaly or ascites. Although hyperbilirubinemia and increased alkaline phosphatase levels can be seen in sepsis, other features of VOD are rare[17,41,42].

Table 4 Differential diagnosis of veno-occlusive disease.
Cholangitis lenta (sepsis-related cholangitis)
Drug/parenteral nutrition induced hepatotoxicity/cholestasis
Acute graft-versus-host disease
Fungal infection
Viral hepatitis
Congestive heart failure
Histology and pathophysiology

DeLeve et al[43] reported that the initial histological change in murine models of VOD was the loss of sinusoidal endothelial cell (SEC) fenestrae and appearance of gaps in SEC barrier. Other early histological findings were narrowing of the sublobular and central veins due to subendothelial edema, likely secondary to disruption of SEC barrier and congestion of hepatic sinusoids surrounded by pale necrotic hepatocytes[3]. Fragmented red blood cells, fibrinogen, and Factor VIII/von Willebrand factor can be demonstrated in the subendothelial space of central veins and perivenular zones of hepatic acini[44]. In the later stages, sinusoidal and venous lumen become obliterated by typeI, III, and IV collagen accompanied by an increase in the stellate cells that line the sinusoids[44,45] (Figure 2). In some cases, fibrous bridges between central venules were observed[14].

Figure 2
Figure 2 Histological examination demonstrates partial central vein occlusion in a patient with veno-occlusive disease.

One hypothesis for the pathogenesis of VOD is depletion of liver glutathione reserve resulting in diminished ability to detoxify acrolein, an inactive but hepatotoxic metabolite of cyclophosphamide. SECs are especially prone to toxic effects of acrolein because of their lower glutathione level compared to hepatocytes[31,46]. Most of the drug metabolism in liver occurs in zone 3 hepatocytes which are rich in p-450 enzymes, explaining why the initial morphological changes are seen in SECs in zone 3. Several findings support this hypothesis. Continuous infusion of glutathione into the portal vein prevents VOD in murine models that were injected with monocrotaline to induce VOD[47]. Additionally, polymorphisms of glutathione S-transferase M1 gene were associated with increased risk of VOD in thalassemic patients undergoing HSCT[48]. Glutathione may also suppress expression of matrix metalloproteinase-9 that was shown to increase in VOD and whose inhibition completely prevents VOD in murine models[14].

Presence of fibrinogen, Factor VIII/von Willebrand factor in the subendothelial space and the finding of low plasma levels of Protein C and antithrombin III suggest involvement of the coagulation system in the pathogenesis of VOD[49]. However, it is unclear if coagulation plays a primary role or is a secondary event. Finally, an immunologic mechanism may have a pathogenetic a role in VOD. Increased risk of VOD in mismatched and unrelated transplants, and decreased risk in T-cell depleted HSCT supports this hypothesis[42,50].


In the absence of an established effective therapy, prevention of VOD is a priority. Non-myeloablative conditioning regimens may be used in eligible patients with a high risk of VOD. In patients who require myeloablation, several measures that may protect against the development of VOD have been recommended. These include: administering busulfan intravenously and adjusting its dose, increasing the interval between cytotoxic drugs and TBI, reducing the total dose and dose-rate of TBI, shielding the liver during TBI, fractionating TBI and carmustine dose, and administering busulfan after the other agents have been given[42].

Administration of ursodeoxycholic acid (UDCA) prior and during the HSCT has been shown to decrease the incidence of VOD in two randomized, prospective, placebo-controlled studies[51,52]. However, two more recent studies showed no decrease in the incidence of VOD in UDCA-treated patients, although one of them reported lower incidence of grade III and IV acute graft-versus-host disease. UDCA is well tolerated, and therefore is used in many transplantation centers for prophylaxis.

Low-dose continuous infusion of heparin is associated with decreased incidence of VOD in a few trials[53,54]. However, other studies have failed to show any beneficial effect[15,29,55]; additionally heparin may increase the risk of bleeding. Low-molecular weight heparin is safer and easier to administer, and may have a preventive role in VOD[56,57], and moreover may accelerate platelet engraftment[58]. However, well designed, randomized controlled studies are needed to confirm its efficacy.

Other agents that have been used in the prevention of VOD with varying results are: glutamine infusion, prostaglandin-E1, and pentoxyfilline[59-63]. Defibrotide, is another promising agent found to be effective in the prevention of VOD[64,65].


In most patients the only treatment needed is the use of diuretics and sodium restriction for the management of water and sodium balance. Repeated paracenteses may be required if ascites causes abdominal discomfort or pulmonary compromise. Renal perfusion and intravascular volume should be maintained while avoiding extravascular fluid accumulation[42]. Hepatotoxic drugs should be avoided and infections should be identified and treated promptly. Further treatment approaches vary greatly in different institutions, both in the choice of intervention and choice of patients to be treated.

A modest response to recombinant human tissue plasminogen activator (γ-tPA) and continuous heparin infusion has been reported in several studies[66,67]. However, thrombolytic therapy is limited by its high risk of fatal bleeding[68,69]. In a series of 42 patients, 12 patients responded to γ-TPA and heparin while 10 patients experienced severe bleeding, at least three of which were fatal[70].

Administration of anti-thrombin III (AT-III) concentrate might decrease the mortality in patients with severe VOD, without any associated serious side effects[71,72]. In one report of 10 patients with severe VOD, clinical improvement was seen in all patients after 5 d of AT-III infusion[73].

There are several reports suggesting a beneficial effect of prostaglandin E1 administration combined with heparin infusion in severe VOD[74-76]. However severe adverse effects limits its routine use. There are anecdotal reports on the successful use of charcoal hemofiltration[77], N-acetylcysteine[78] and glutamine/vitamin E[79,80].

Defibrotide, the most promising drug currently available for the treatment of VOD, is a single-stranded polydeoxyribonucleotide with anti-ischemic, anti-thrombotic and thrombolytic properties. It lacks systemic anticoagulant activity, an advantage in severely thrombocytopenic patients after HSCT[81]. Its mechanism of action is poorly understood but likely involves adenosine receptors[82]. Richardson et al[83] reported that 32 (36%) of 88 patients with VOD with a predicted risk of ≥ 30% of developing severe disease had a complete response to defibrotide treatment. Thirty-one of the 32 patients survived beyond 100 d. Adverse effects were limited to nausea, transient systolic hypotension, fever, abdominal cramping, and vasomotor symptoms such as hot flushes. In another clinical trial of defibrotide, complete response was achieved in 22 (55%) of 40 VOD patients[84].

Isolated case reports have shown benefit of transjugular intrahepatic portosystemic shunt (TIPS) in patients with VOD[85-87]. Although it can control portal hypertension, it is not clear whether TIPS can alter the course of the disease. Orthotopic liver transplantation has been attempted successfully in a few cases, however few institutions are capable of performing it on patients undergoing HSCT[88-90].


Budd-Chiari Syndrome (BCS) is an uncommon but potentially life-threatening disorder caused by obstruction of the hepatic venous outflow at any level from the small hepatic veins to the junction of the inferior vena cava (IVC) with the right atrium[91].


BCS can be classified as primary (due to intrinsic intraluminal thrombosis or webs) or secondary (due to intraluminal invasion by a parasite or malignant tumor or due to extraluminal compression by an abscess, cyst, or solid tumor)[92]. Intravascular thrombosis, mostly seen in primary myeloproliferative disorders, is the most common mechanism leading to the obstruction of the hepatic venous system. At least one hereditary or acquired procoagulative disorder can be identified in 75% of patients with BCS (Table 5)[93]. Polycythemia vera is found in between 10%-40% of patients, whereas essential thrombocythemia and myelofibrosis are less prevalent causes[94,95]. Of note, hepatic vein thrombosis occurs in up to 12% of patients with paroxysmal nocturnal hemoglobinuria and is the leading cause of mortality in this disorder[96,97]. As many as 30% of all cases of BCS are found to have factor V Leiden mutation which is present in the majority of pregnancy- or oral contraceptive-related cases of hepatic vein thrombosis[98,99]. Protein C, Protein S and antithrombin levels may be decreased nonspecifically due to impaired hepatic synthesis in patients with BCS, but levels below 20% of normal suggest inherited deficiency of these proteins[100]. Patients with BCS, as well as their relatives, should be counseled and investigated for hereditary thrombophilias.

Table 5 Causes of the Budd-Chiari Syndrome.
Common causes
Hypercoagulable states
Inherited thrombophilic disorders
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden mutation
Prothrombin gene mutation
Acquired procoagulative disorders
Myeloproliferative disorders (overt and occult)
Paroxysmal nocturnal hemoglobinuria
Antiphospholipid syndrome
Use of oral contraceptives
Uncommon causes
Tumoral invasion
Hepatocellular carcinoma
Renal cell carcinoma
Adrenal carcinoma
Behcet’s syndrome
Inferior vena caval webs
Inflammatory bowel syndrome
Dacarbazine therapy

Although less common in western countries, primary membranous obstruction of the inferior vena cava (IVC) is the most common cause of BCS in South Africa and Asia, and is thought to be a consequence of IVC thrombosis[101]. For unknown reasons, 45-50% patients with known membranous occlusion ultimately develop hepatocellular carcinoma (HCC), even in the absence of cirrhosis[102]. On the other hand, HCC has not been reported to be a complication of hepatic vein thrombosis, except in Behcet’s disease-associated BCS[103].

In about 10% of patients with BCS, an underlying etiology cannot be identified[95]. Recently, endothelial dysfunction and decreased fibrinolytic activity have been suggested as contributing factors in patients with idiopathic BCS[104].


The parenchymal hepatic damage and the histologic abnormalities are variable, depending on the acuity and extent of hepatic venous outflow obstruction. Rapid occlusion of all 3 hepatic veins or 2 veins including the right hepatic vein leads to diffuse hepatic congestion and enlargement. The result is ischemic necrosis followed by fibrosis, predominantly in the perivenular areas (Figure 3). However, in patients with concomitant portal vein thrombosis, fibrosis prevails in the periportal zone[6,105]. In chronic disease, direct blood flow from the caudate lobe to the IVC compensates for hepatic outflow obstruction. Over time, the caudate lobe becomes hypertrophic while cirrhosis and atrophy develops in the rest of the liver[106,107].

Figure 3
Figure 3 Histological examination shows sinusoidal dilatation and congestion.

Compensatory nodular regenerative hyperplasia is common in areas of hepatic parenchyma that have an adequate blood supply, with progression to fibrosis and cirrhosis at a later stage of the disease[6,108]. Also, in the advanced stages, it is common to see areas of infarction secondary to concomitant thrombosis of the intrahepatic and extrahepatic portal veins[109].

Clinical features

There is a wide clinical spectrum, ranging from a fulminant picture to an asymptomatic condition, depending on the location, extent, and rapidity of the obstructive process and on whether the portal vein is thrombosed or not. Obstruction of a single main hepatic vein is clinically silent[110], whereas sudden occlusion of all major hepatic veins may result in fulminant hepatic failure.

BCS is more common in women, and usually presents in the third or fourth decade of life[111]. The most common signs and symptoms are ascites, hepatomegaly, and abdominal pain. In a series of 237 patients, obstruction was found in hepatic veins, IVC or both in 62%, 7%, and 31% patients respectively[112].

For descriptive purposes only, the syndrome can be classified as asymptomatic, fulminant, acute, subacute, or chronic[113]. However, it should be stressed that the correlation between clinical history and the duration of the occlusive process is weak and this classification’s prognostic significance is not clear[114].

Patients with the asymptomatic variant are usually discovered on investigation of abnormal liver function tests. These patients constitute between 5%-20% of BCS cases[112,113]. Absence of ascites and abdominal pain may be attributed to large intrahepatic and portosystemic venous collaterals or patency of one large hepatic vein[93].

Patients with acute BCS develop severe RUQ abdominal pain, hepatomegaly, jaundice, and intractable ascites within a few weeks. The acute form is observed in 20% of BCS patients[113]. Serum aminotransferase levels are elevated due to ischemic hepatocellular damage. Serum alkaline phosphatase level is elevated, usually between 300 and 400 IU/L. Liver functions can deteriorate quickly leading to fulminant hepatic failure.

Fortunately, the fulminant form is uncommon and typically follows rapid and complete occlusion of all major hepatic veins. Patients rapidly develop hepatic encephalopathy, renal failure and coagulopathy. Serum aminotransferase levels are markedly elevated. Unlike the findings in fulminant viral hepatitis, the liver is enlarged and tender[93].

The subacute form has a more insidious presentation, spread over several months. Patients may have minimal ascites, splenomegaly, hepatomegaly, and vague RUQ discomfort. Jaundice is either absent or mild.

The chronic form is seen in 60% of patients with BCS. Patients have signs or symptoms for more than six months and generally present with complications of cirrhosis including variceal bleeding, encephalopathy, coagulopathy, and hepatorenal syndrome. Additionally, hepatopulmonary syndrome has been described in up to 28% patients[115]. Renal impairment is present in one-half of the cases[93].

There is currently no consensus on the association of disease severity with disease duration. Furthermore, the duration of symptoms do not correlate with the degree of histologic damage to the liver. It has been observed that 58% of patients with an acute clinical onset may have marked liver fibrosis, suggesting a long preclinical course. These findings can be explained by the development of recent thrombosis superimposed on previous lesions[110,116].

IVC compression or thrombosis generally presents with less severe symptoms compared with hepatic vein thrombosis and is characterized by leg edema or venous collaterals over the trunk in addition to hepatomegaly, ascites, and abdominal pain. The clinical course is chronic, with repeated acute episodes eventually leading to congestive cirrhosis[117,118].

Portal venous system is usually affected in patients with BCS because: 1) increased sinusoidal pressure decreases flow through the portal system, 2) hypertrophied caudate lobe may compress the main portal branches and the intrahepatic portal venules. These changes can result in stasis and vulnerability to thrombosis in the portal vein, further depleting liver perfusion[119]. However, in our experience the clinical picture in patients with both hepatic and portal vein thrombosis is better compared to that in patients with hepatic vein thrombosis only. This may be due to decreased blood flow to liver resulting in reduced hepatic congestion.

Prognosis and survival

The natural history of BCS is poorly understood, mainly because most patients receive some form of treatment. The spectrum of clinical outcome ranges from progressive deterioration of the general condition to a few reports of spontaneous regression of the acute manifestations[120]. After the institution of anticoagulation therapy and early recognition of asymptomatic cases, mortality rates have decreased over time[113]. In a cohort of 120 patients, survival rates of 77%, 65% and 57% were found at 1, 5 and 10 years, respectively[121]. Murad et al[112] developed a model predicting survival in BCS, classifying patients into three categories with statistically different 5-year survival rates of 89%, 74%, and 42% based on the presence of ascites, encephalopathy, and prothrombin time and serum bilirubin levels.

Histologic abnormalities of the liver were not found to determine the prognosis[112,121,122] except in one study in which advanced fibrosis was associated with increased mortality[123]. One reason for this discrepancy can be explained by biopsy specimens being not representative of the whole liver due to uneven distribution of the hepatic lesions.

IVC obstruction has a good short term prognosis but there is limited data regarding long term prognosis. In a study from Japan, there was a 25% mortality rate over 15 years in patients with obliterative cavopathy. The main causes of death were liver failure, variceal bleeding and HCC[101,124].

In a series of 237 patients, portal vein thrombosis (PVT) with and without spleno-mesenteric vein thrombosis was identified in 18 (9%) and 15 (7%) patients respectively (total 33 patients, 16%). The five-year survival was 59% in patients with BCS and PVT and 85% in isolated BCS[125].


The diagnosis of BCS requires a high index of suspicion. It should be considered in all patients presenting with ascites, hepatomegaly and RUQ abdominal pain or when intractable ascites occurs in the presence of mildly altered liver function tests. Standard laboratory investigations are rarely helpful in establishing the diagnosis, because abnormal liver function tests are not specific for BCS. Edema of the lower extremities and presence of venous collaterals on the back suggests IVC occlusion. Ascitic fluid analysis adds little specificity to the diagnosis and ascitic fluid albumin content can differ according to the stage of the BCS[126]. Thus, the diagnosis is largely made by imaging studies.

Real-time and Doppler sonography: Real-time or color and pulsed Doppler should be the initial investigation for BCS, with a sensitivity and specificity of nearly 85%[127]. Specific findings for hepatic vein obstruction are abnormal flow in a hepatic vein, large intrahepatic or subcapsular collateral vessels and inability to visualize the junction of major hepatic veins with IVC. Moreover, the presence of intrahepatic venous to venous spider web collaterals is highly suggestive of BCS[128,129] (Figure 4) Acute venous occlusion is identified by enlarged, stenotic, or tortuous hepatic veins, whereas in patients with chronic disease the major hepatic veins may not be readily visualized. Additional findings include: compression of IVC by hypertrophic caudate lobe or obstruction by thrombus, tumor, or membranes[130,131].

Figure 4
Figure 4 Abdominal ultrasonography reveals thick and obliterated middle hepatic veins.

Computed tomography (CT): Failure to visualize the hepatic veins or IVC is suggestive of BCS. Contrast enhancement may be seen more centrally than peripherally resulting in a patchy flea-bitten appearance (Figure 5). CT also allows assessment of the extent of hepatic parenchymal disease, ascites, and splenomegaly[132]. However, the role of CT scan is limited because of false-positive and indeterminate results in almost one-half of the patients[128].

Figure 5
Figure 5 Computed tomography showing central contrast enhancement in the liver.

Magnetic resonance imaging (MRI): In patients with an unremarkable ultrasound examination but in whom the suspicion for BCS is high, MRI with intravenous gadolinium is a reasonable option (Figure 6). It allows excellent visualization of hepatic veins and IVC. Large intrahepatic, comma-shaped collaterals can be seen in patients with chronic obstruction. The major drawback of MRI is that, unlike ultrasonography, it does not provide the direction of hepatic venous blood flow[133,134].

Figure 6
Figure 6 Magnetic resonance imaging of the liver with contrasting agent shows that inferior vena cava is compressed by hypertrophy of caudate lobe and gross lobulation of the liver.

Hepatic venography: Although not considered essential for the diagnosis of BCS, venography provides useful information such as the extent of the thrombosis and caval pressures which help in determining the optimal therapy. Iodinated contrast can be injected into the hepatic veins either by transhepatic puncture or retrograde cannulation through the IVC (Figure 7). Abnormalities specific for BCS include a “spider-web” venous network, a coarse network of collaterals arching outward from the catheter tip, and a patent vein upstream from a stricture. A distorted appearance of hepatic veins that is observed in cirrhosis should not be confused with BCS. Another advantage of venography is that the portal vein can be assessed at the same sitting and if found to be occluded can be dilated with or without stenting in order to decompress the liver. Pressure measurements obtained during venography provide useful information before attempting surgical decompression[135,136]. Also, pressure measurements are useful in the post-surgical follow-up of these patients.

Figure 7
Figure 7 Almost completely obstructed IVC and shows collateral drainage through azygous system.

Liver biopsy: Liver biopsy may demonstrate congestion, hepatocyte necrosis, and fibrosis in the centrilobular area, findings that are similar to those seen in congestive hepatopathy. Venular thrombosis is usually not evident in biopsy specimens. All patients under consideration for surgery should undergo liver biopsy in conjunction with angiography to determine whether the patient will benefit more from a shunt procedure or a liver transplant[135,137].


The goals of treatment are to alleviate venous obstruction, prevent extension of thrombosis in the hepatic veins and preserve hepatic function by decreasing the centrilobular congestion. Diagnostic workup to identify the underlying cause should be considered at the time of the initial diagnosis.

Medical therapy: Medical therapy for BCS consists of efforts to control ascites, to prevent the extension of thrombosis with anticoagulation therapy, to dissolve the clot and relieve the hepatic congestion with thrombolysis and to treat the complications. Additionally, the underlying cause of BCS should be investigated and treated.

Ascites is managed by low-sodium diet, diuretics, and therapeutic paracentesis when needed. The type and duration of optimal anticoagulation therapy has not been established, however most centers give lifelong anticoagulation, initially with heparin followed by warfarin titrated to maintain the INR between 2 and 3[100,126]. During active variceal bleeding, balloon tamponade or endoscopic therapy is preferred to vasoconstrictor agents because the reduction in splanchnic blood flow induced by vasoconstrictors can theoretically precipitate mesenteric and portal vein thrombosis[138].

Medical therapy alone can be a good option for patients in whom there is no ongoing hepatic necrosis, as indicated by the presence of minimal symptoms, relatively normal liver function results, and ascites that is easily controlled[139]. Patients on medical therapy alone should be monitored closely for disease progression and to detect progressive necrosis by serial upper endoscopies and liver biopsies.

Restoration of hepatic blood flow: Relief of venous obstruction can be attempted by thrombolytic therapy, percutaneous angioplasty, transjugular intrahepatic portosystemic shunt (TIPS), or shunt surgery. In patients with an acute presentation, especially when angiography shows presence of a fresh thrombus, thrombolytic therapy can be administered systemically or directly into the thrombosed hepatic vein. The best results are obtained when the thrombolytic agent is administered early directly into the vein, although promising data has been reported with thrombolysis carried out two to three weeks after the onset of symptoms[140,141].

Balloon angioplasty has been used to relieve hepatic outflow obstruction secondary to caval webs or short-segment hepatic vein stenosis[142]. Although short-term results are excellent, the sustained patency rate is only 50% at two years after the procedure[143]. However, the use of intraluminal stents has been shown to increase the long-term patency rates to nearly 90%[144-146]. Once inserted, the stents cannot be removed, and placement of a stent above the intrahepatic IVC may interfere with liver transplantation. Failure of angioplasty or stenting, should prompt consideration for a surgical portosystemic shunt or TIPS[147].

TIPS decompresses the liver by creating an alternative venous outflow tract. It is particularly useful, either alone or as a bridge to liver transplantation, in patients with an acute presentation such as those with variceal bleeding, and patients with fulminant hepatic failure in whom thrombolysis and angioplasty were unsuccessful[148,149]. TIPS may be preferred over surgical shunting because it avoids laparotomy and has less periprocedure mortality and morbidity, its efficacy is not affected by caudate lobe hypertrophy, and it can be done in patients with PVT[150-152]. Although long-term patency rate is only about 50%, patients in whom stent stenosis occurs do not generally worsen, perhaps because the shunt allows time for collateral circulation to develop[153]. The recently introduced, polytetrafluoroethylene-covered stents may improve the patency rates[154]. However, extension of the stent into the suprahepatic IVC may preclude liver transplantation and should be avoided.

Surgical shunts decompress the liver by creating hepatofugal flow through the portal vein. Patients with a non-fulminant presentation and those who have a chronic presentation without significant hepatic fibrosis should be considered for surgical shunting, providing the portal vein is patent[150]. The five-year survival rate after surgical shunting ranges between 57% and 94% and absence of IVC occlusion is associated with better outcomes[155-157].

A pressure difference of at least 10 mmHg between the portal vein and intrahepatic IVC is essential for portocaval and mesocaval shunts to function[123]. Acute hepatic decompensation may occur postoperatively, therefore shunt operations should be performed in centers where rescue liver transplantation can take place.

The type of surgical shunt depends on the anatomy of the obstruction. Side-to-side portacaval shunts have the highest patency rate but may make subsequent liver transplantation more difficult. Side-to-side mesocaval shunts are technically less demanding and do not interfere with liver transplantation but when placed with a synthetic graft, have a higher thrombosis rate than a side-to-side portacaval shunt[147]. Mesoatrial shunt should be considered if there is IVC compression resulting in low portocaval pressure gradient. Mesoatrial shunt has a high rate of thrombosis due to relatively low flow rate in the prosthetic graft[126]. Side-to-side portocaval shunt and cavoatrial shunt have been described for patients with both caval and hepatic venous thrombosis[136,157,158].

In addition to shunts, other surgical procedures can also provide adequate decompression in selected patients. Transatrial membranotomy can be effective in patients with IVC membranes[136,157,159,160]. Dorsocranial resection of the liver is the only feasible procedure if there is both portal and superior mesenteric vein obstruction[161].

Liver transplantation: Patients who have cirrhosis, fulminant hepatic failure or biochemical evidence of advanced liver dysfunction are best managed with liver transplantation[157]. Long term survival rates range from 50% to 95%[155,162-164]. Development of postoperative portal vein or hepatic artery thrombosis occurs in about 12% of patients. Liver transplantation can cure almost all hereditary thrombophilias, however thrombosis can still occur and anticoagulation is necessary[150].


Congestive hepatopathy refers to hepatic manifestations attributable to passive hepatic congestion resulting from right-sided heart failure of any cause including and not limited to constrictive pericarditis (CP), tricuspid regurgitation, cor pulmonale, and cardiomyopathies. Development of hepatic ischemia and infarction secondary to left-sided heart failure which usually coincides with congestive hepatopathy will not be discussed here. However, it should be kept in mind that the clinical picture in congestive hepatopathy varies greatly depending on both the degree and acuity of congestion, and presence or absence of hepatic ischemia and infarction[2].

Clinical Manifestations

Liver dysfunction in congestive hepatopathy is usually mild and asymptomatic and often detected incidentally on routine biochemical testing. Symptomatic patients usually present with mild jaundice which is characteristically absent in patients with CP. In patients with severe heart failure, jaundice may be so deep as to suggest cholestasis[165]. Right upper quadrant discomfort due to stretching of liver capsule and ascites may also be present.

Occasionally, the clinical picture may resemble that of acute viral hepatitis, when jaundice is accompanied by elevated aminotransferase levels due to acute hepatic ischemia[166,167]. Several cases of fulminant hepatic failure resulting in death have been reported due to congestive heart failure. However, most of these patients had characteristics of both hepatic congestion and ischemia[165,168,169].

On physical examination, patients may have tender hepatomegaly, sometimes massive, with a firm and smooth liver edge. Splenomegaly is uncommon, and like ascites is due to transmitted elevated central venous pressure. Jugular venous distention and hepatojugular reflux may be present and are helpful in differentiating congestive hepatopathy from BCS and primary liver diseases. Liver may be pulsatile especially in patients with tricuspid regurgitation. Loss of hepatic pulsatility suggests progression to cardiac cirrhosis.

The most common laboratory finding is elevation of total serum bilirubin level, most of which is unconjugated. Hyperbilirubinemia occurs in up to 70% of patients with congestive hepatopathy[170]. Severe hyperbilirubinemia may develop in patients with severe, usually acute, right-sided heart failure. Serum bilirubin level shows a correlation with right atrial pressure but not with cardiac output[6]. Even in the presence of deep jaundice, serum alkaline phosphatase level is generally only mildly elevated, which helps to distinguish congestive hepatopathy from obstructive jaundice. Serum aminotransferase levels also show a mild elevation unless cardiac output is impaired. In patients with severe acute heart failure, aminotransferase levels may be extremely high secondary to hepatic ischemia and the degree of elevation correlates with the extent of necrosis as seen on liver biopsy specimens. Additionally, the prothrombin time may be mildly abnormal[171], albumin level may be decreased[172], and serum ammonia level may be elevated[173].


Increasing specialization in medicine has caused physicians to overlook diseases that cross the boundaries of two specialties. Congestive hepatopathy may be missed in patients with heart failure and mild hepatic congestion, and in patients with overt hepatic congestion and vague cardiac symptoms[174,175]. Physicians should consider right-sided heart failure in patients with hepatomegaly with or without jaundice. CP is especially difficult to differentiate from primary liver cirrhosis and BCS because of its relatively nonspecific clinical features.

A careful history and a thorough physical examination are crucial in the diagnosis of congestive hepatopathy. Symptoms such as exertional dyspnea, orthopnea, and angina, and physical findings like jugular venous distention, heart murmurs, and rales may help physicians to differentiate congestive hepatopathy from primary liver diseases. In addition to liver biochemical testing, viral hepatitis serology, and abdominal ultrasound with Doppler studies of the liver; EKG and echocardiogram should be performed when congestive hepatopathy is suspected. However, a normal echocardiogram does not always rule out congestive hepatopathy. Upon the finding of dilatation of all three main hepatic veins on abdominal sonogram (Figure 8), physicians should look for a cardiac cause such as constrictive pericarditis more vigorously with cardiac angiogram or other radiological methods.

Figure 8
Figure 8 Ultrasound of the liver shows gross dilatation in the inferior vena cava and hepatic V.

Diagnostic paracentesis in patients with congestive hepatopathy usually reveals a high ascitic fluid protein content and a serum to ascites albumin gradient > 1.1 g/dL reflecting the contribution of “hepatic lymph” and portal hypertension to the ascites[176].

Improvement in liver biochemical tests with treatment of the underlying cardiac disease supports the diagnosis. Liver biopsy may help confirm the diagnosis in equivocal cases.


The characteristic gross appearance of liver in congestive hepatopathy is referred to as the nutmeg liver. This appearance is the result of contrasting areas of red caused by sinusoidal congestion and bleeding in the necrotic regions surrounding the enlarged hepatic veins and yellow due to the normal or fatty liver tissue. Histologically, sinusoidal engorgement and hemorrhagic necrosis is apparent in perivenular areas of hepatic acini. Variable degrees of cholestasis with occasional bile thrombi in the canaliculi may also be apparent. With chronic heart failure, fibrosis develops in perivenular areas, ultimately causing bridging fibrosis between adjacent central veins. This process results in cardiac fibrosis, inappropriately referred as cardiac cirrhosis, which is distinct from primary liver cirrhosis in which fibrous bands tend to link adjacent portal areas. The regeneration of periportal hepatocytes in cardiac fibrosis may result in nodular regenerative hyperplasia. If heart failure is treated successfully, the early histologic changes of congestive hepatopathy may resolve, and even cardiac fibrosis may regress histologically and clinically[2].

Treatment and Prognosis

Treatment of the underlying heart disease is fundamental to the management of congestive hepatopathy and is outside the scope of this review. Jaundice and ascites usually respond significantly to diuresis. However, excessive diuresis may decrease cardiac output and result in hepatic ischemia in patients with severe congestive heart failure.

Most patients with congestive hepatopathy die of cardiac causes and liver disease rarely contributes to the morbidity or mortality in these patients. Unlike patients with liver cirrhosis, those with cardiac fibrosis rarely develop serious complications such as variceal bleeding[177]. Hepatocellular carcinoma may rarely complicate cardiac fibrosis[178]. However, the incidence of hepatocellular carcinoma and liver failure due to congestive hepatopathy is likely to increase as survival is prolonged with advances in the treatment of heart failure.


CP deserves mention because its diagnosis can be easily missed and its clinical manifestations are different from those seen in congestive hepatopathy due to other causes. CP is the result of scarring and loss of elasticity of the pericardial sac which restricts cardiac filling. Tuberculosis, cardiac surgery, radiation therapy, and connective tissue disorders are among common causes, however most of the cases are idiopathic or viral[179-181].

Patients with CP may present with symptoms of fluid overload such as edema and ascites, or symptoms of diminished cardiac output like exertional dyspnea and fatigue. Hepatomegaly, massive ascites, and peripheral edema are common findings. For reasons that are unclear, patients with CP typically do not develop jaundice[5] and very rarely may develop chylous ascites[182-183]. Because its manifestations are protean, it is easy to mistake CP for BCS and liver cirrhosis[184]. Jugular venous distention which was noted in 93% patients in a large series is a critical finding in the diagnosis of CP[180]. Although rarely observed, Kussmaul’s sign, pericardial knock, and pulsus paradoxus may offer additional clues to the diagnosis.

EKG may show a low voltage and nonspecific ST and T wave changes. Chest X-ray may demonstrate pericardial calcification. Echocardiography is essential in the diagnosis of CP, but right and left heart catheterization with hemodynamic evaluation may be required to confirm the diagnosis[185-187].

Cardiac fibrosis develops more frequently and rapidly in CP than in other causes of right-sided heart failure, perhaps due to higher hepatic venous pressures leading to severe zone 3 congestion and necrosis[2]. Pericardiectomy is the standard of treatment and curative if performed early.


The clinical manifestations and liver histology in VOD, BCS, and congestive hepatopathy are similar because of the common underlying mechanism of hepatic injury and adaptation in response to increased sinusoidal pressure. Further animal and in-vitro studies are needed to better understand the pathways involved in sinusoidal injury in response to increased venous pressure. The severity of clinical picture depends mostly on the rapidity and extent of the obstructive process. Physicians should consider congestive hepatopathy and BCS in all patients with tender hepatomegaly and ascites. Presence of jugular venous distention is an invaluable clue to differentiate congestive hepatopathy from BCS and other primary liver diseases. Veno-occlusive disease should be kept in mind in patients who rapidly develop jaundice and ascites with hepatomegaly after HSCT. The advent of interventional radiology and new medical therapies has improved survival in patients with hepatic venous outflow obstruction, although prevention is still mainstay in the management of VOD.


S- Editor Wang J L- Editor Anand BS E- Editor Che YB

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