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Budd-Chiari Syndrome

  • Author: Praveen K Roy, MD, AGAF; Chief Editor: BS Anand, MD  more...
 
Updated: Dec 16, 2015
 

Practice Essentials

Budd-Chiari syndrome is an uncommon condition induced by thrombotic or nonthrombotic obstruction of the hepatic venous outflow and is characterized by hepatomegaly, ascites, and abdominal pain. See the image below.

Ultrasonogram showing hepatic vein thrombus, with Ultrasonogram showing hepatic vein thrombus, with vessels forming arrow pointing to the thrombus.

The prognosis is poor in patients with Budd-Chiari syndrome who remain untreated, with death resulting from progressive liver failure in 3 months to 3 years from the time of the diagnosis.[1] Following portosystemic shunting, however, the 5-year survival rate for patients with the syndrome is 38-87%. The actuarial 5-year survival rate following liver transplantation is 70%.[2, 3, 4]

Signs and symptoms

Physical examination may reveal the following:

  • Jaundice
  • Ascites
  • Hepatomegaly
  • Splenomegaly
  • Ankle edema
  • Stasis ulcerations
  • Prominence of collateral veins

The clinical variants of Budd-Chiari syndrome have been described as follows[5, 6, 7] :

  • Acute and subacute forms: Characterized by rapid development of abdominal pain, ascites (which can cause abdominal distention), hepatomegaly, jaundice, and renal failure.
  • Chronic form: Most common presentation; patients present with progressive ascites; jaundice is absent; approximately 50% of patients also have renal impairment
  • Fulminant form: Uncommon presentation; fulminant or subfulminant hepatic failure is present, along with ascites, tender hepatomegaly, jaundice, and renal failure.

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

Examination of ascitic fluid provides useful clues to the diagnosis of Budd-Chiari syndrome, including the following:

  • Patients usually have high protein concentrations (>2 g/dL); this may not be present in persons with the acute form of the disease
  • The white blood cell (WBC) count is usually less than 500/µL
  • The serum ascites–albumin gradient is usually less than 1.1 (except in the acute forms of Budd-Chiari syndrome)

Imaging studies

  • Ultrasonography
  • Computed tomography (CT) scanning
  • Magnetic resonance imaging (MRI)
  • Venography

Biopsy

Pathologic findings in liver biopsy are (1) high-grade venous congestion and centrilobular liver cell atrophy, and, possibly, (2) thrombi within the terminal hepatic venules.

See Workup for more detail.

Management

Pharmacologic therapy

  • Anticoagulants
  • Thrombolytics
  • Diuretics

Procedures and surgery

  • Balloon angioplasty
  • Localized thrombolysis
  • Placement of a stent or transjugular intrahepatic portacaval shunt (TIPS)
  • Variceal treatment
  • Paracentesis
  • Portal decompression
  • Percutaneous transhepatic balloon angioplasty (PTBA)
  • Liver transplantation

See Treatment and Medication for more detail.

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Background

Budd-Chiari syndrome is an uncommon condition induced by thrombotic or nonthrombotic obstruction of the hepatic venous outflow and is characterized by hepatomegaly, ascites, and abdominal pain. It most often occurs in patients with underlying thrombotic diathesis, including in those who are pregnant or who have a tumor, a chronic inflammatory disease, a clotting disorder, an infection, or a myeloproliferative disorder, such as polycythemia vera or paroxysmal nocturnal hemoglobinuria. (See Etiology and Clinical Presentation.)

Obstruction of large- or small-caliber veins leads to hepatic congestion as blood flows into, but not out of, the liver. Microvascular ischemia due to congestion causes hepatocellular injury. Portal hypertension and liver insufficiency result.[5, 6] (See Pathophysiology.)

Budd-Chiari syndrome should be considered separate from veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome, which is characterized by toxin-induced, nonthrombotic obstruction of prehepatic veins (see the images below). (See Clinical Presentation and Workup.)

Ultrasonogram showing hepatic vein thrombus, with Ultrasonogram showing hepatic vein thrombus, with vessels forming arrow pointing to the thrombus.
Ultrasonogram showing hepatic vein thrombus. Ultrasonogram showing hepatic vein thrombus.
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Pathophysiology

Occlusion of a single hepatic vein is usually silent. Overt Budd-Chiari syndrome generally requires the occlusion of at least 2 hepatic veins.[8] Venous congestion of the liver causes hepatomegaly, which can stretch the liver capsule and be very painful. Enlargement of the caudate lobe is common because blood is shunted through it directly into the inferior vena cava (IVC).

Hepatic function can be affected to a degree, depending on the amount of stasis and resultant hypoxia. Increased sinusoidal pressure can itself cause hepatocellular necrosis. The literature also suggests that upregulation of specific genes in chronic Budd-Chiari syndrome contributes to liver destruction through the stimulation of extracellular matrix proliferation, which contributes to liver fibrosis.

The most prominent genes involved include matrix metalloproteinase 7 and superior cervical ganglion 10 (SCG10), which are increased in expression, and thrombospondin-1, which is decreased.[9] Overexpression of the proliferating cell nuclear antigen gene, the c -MYC oncogene, and the tumor protein p53 gene may also be etiologic factors for Budd-Chiari syndrome.[10]

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Etiology

Most patients with Budd-Chiari syndrome have an underlying thrombotic diathesis, although in approximately one third of patients, the condition is idiopathic. Causes of Budd-Chiari syndrome include the following:

  • Hematologic disorders
  • Inherited thrombotic diathesis
  • Pregnancy and postpartum[11]
  • Oral contraceptives
  • Chronic infections
  • Chronic inflammatory diseases
  • Tumors
  • Congenital membranous obstruction
  • Hepatic venous stenosis
  • Hypoplasia of the suprahepatic veins
  • Postsurgical obstruction
  • Posttraumatic obstruction
  • Total parenteral nutrition (TPN): Budd-Chiari syndrome has been reported as a complication of TPN via an IVC catheter in a neonate

Hematologic disorders

These include the following:

  • Polycythemia rubra vera
  • Paroxysmal nocturnal hemoglobinuria
  • Unspecified myeloproliferative disorder
  • Antiphospholipid antibody syndrome
  • Essential thrombocytosis

Inherited thrombotic diathesis

Coagulopathies include the following:

  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin III deficiency
  • Factor V Leiden deficiency

Chronic infections

These include the following:

Chronic inflammatory diseases

These include the following:

Tumors

These include the following:

  • Hepatocellular carcinoma (HCC)[12]
  • Renal cell carcinoma
  • Leiomyosarcoma
  • Adrenal carcinoma
  • Right atrial myxoma

Congenital membranous obstructions

These include the following:

  • Type I: Thin membrane is present at the vena cava or atrium
  • Type II: A segment of the vena cava is absent
  • Type III: The inferior vena cava (IVC) cannot be filled, and collaterals have developed

Miscellaneous

Miscellaneous causes of Budd-Chiari syndrome include the following:

  • Alpha1-antitrypsin deficiency
  • Dacarbazine
  • Urethane
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Epidemiology

Budd-Chiari syndrome is extremely rare, and the incidence is not well reported in the literature, although a study by Rajani et al found an incidence of about 1 case per million population per year in Sweden. Congenital membranous forms of Budd-Chiari syndrome are the most common cause of the disease worldwide, particularly in Asia.[13]

A retrospective (2009-2013) nation-wide, population-based study in South Korea found a total of 424 patients with Budd-Chiari syndrome, with an average age- and sex-adjusted prevalence of 5.29 per million population.[14] The female-to-male ratio was 1.8, the median age was 51 years, and the annual case-fatality rate was 2.8%.[14]  

No data suggest that sex affects predisposition to Budd-Chiari syndrome. Nonetheless, in the United States the condition is predominantly seen in women and is associated with hematologic disorders.

Age at presentation is usually in the third or fourth decade of life, although the condition may also occur in children or elderly persons.

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Prognosis

The natural history of Budd-Chiari syndrome is not well known. The following factors, however, have been associated with a good prognosis:

  • Younger age at diagnosis
  • Low Child-Pugh score
  • Absence of ascites or easily controlled ascites
  • Low serum creatinine level

In a systematic review of 79 studies, investigators found that although univariate analysis indicated bilirubin and creatinine levels as well as ascites might be significant prognostic factors, multivariate analyses did not always reveal achievement of statistical significance.[15]

The following formula has been proposed to calculate the prognostic index for Budd-Chiari syndrome; a score of less than 5.4 is associated with a good prognosis:

  • Prognostic index = (ascites score x 0.75) + (Pugh score x 0.28) + (age x 0.037) + (creatinine level x 0.0036)

The 5-year survival rate for patients with the syndrome is 38-87% following portosystemic shunting. The actuarial 5-year survival rate following liver transplantation is 70%.[2, 3, 4] Long-term follow-up in adults has demonstrated 10-year survival rates as high as 55%.

The prognosis is poor, however, in patients with Budd-Chiari syndrome who remain untreated, with death resulting from progressive liver failure in 3 months to 3 years from the time of diagnosis.[1]

In a University of Pennsylvania retrospective study (2008-2013) comprising 47 patients with Budd-Chiari syndrome or hepatic vein thrombosis, there were no significant difference in treatment outcomes among those receiving anticoagulation therapy alone, transjugular intrahepatic portosystemic shunt (TIPS) placement alone, and TIPS in conjunction with anticoagulation.[16] The investigators noted that the significant prognostic predictors for liver transplantation were age, presence of cirrhosis, and presence of chronic kidney disease.

Morbidity and mortality

Morbidity and mortality in Budd-Chiari syndrome are generally related to complications of liver failure and ascites but can also be impacted by the type of concomitant underlying disease, if any. Complications associated with Budd-Chiari syndrome include the following:

  • Hepatic encephalopathy
  • Variceal hemorrhage
  • Hepatorenal syndrome
  • Portal hypertension
  • Complications secondary to hypercoagulable state
  • Complications secondary to hepatic decompensation

Bacterial peritonitis is always of concern in the patient with ascites, especially if paracentesis is undertaken. Complications must also be considered in relation to therapies used (eg, thrombolytics). The mortality rate can be high in patients who develop fulminant hepatic failure.

Budd-Chiari syndrome can also lead to HCC (or oppositely, in some cases, develop secondary to it). In a retrospective study, Liu et al found evidence that HCC in primary Budd-Chiari syndrome is associated with blockage of the inferior vena cava and stricture of the hepatic venous outflow tract. The investigators’ results also indicated that transcatheter arterial chemoembolization (TACE) is an effective treatment for HCC in these patients, with alpha-fetoprotein levels having dropped significantly after TACE treatment. The study included 246 patients with Budd-Chiari syndrome, including 14 with HCC. Ultrasonography, computed tomography (CT) scanning, magnetic resonance imaging (MRI), and angiography were used to determine imaging characteristics in patients with HCC.[17]

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Contributor Information and Disclosures
Author

Praveen K Roy, MD, AGAF Chief of Gastroenterology, Presbyterian Hospital; Medical Director of Endoscopy, Presbyterian Medical Group; Adjunct Associate Research Scientist, Lovelace Respiratory Research Institute

Praveen K Roy, MD, AGAF is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Homayoun Shojamanesh, MD Former Fellow, Digestive Diseases Branch, National Institutes of Health

Homayoun Shojamanesh, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Jack Bragg, DO Associate Professor, Department of Clinical Medicine, University of Missouri School of Medicine

Jack Bragg, DO is a member of the following medical societies: American College of Osteopathic Internists, American Osteopathic Association

Disclosure: Nothing to disclose.

Gautam Dehadrai, MD Department Chair, Section Chief, Department of Interventional Radiology, Norman Regional Hospital

Gautam Dehadrai, MD is a member of the following medical societies: American College of Radiology, Radiological Society of North America, Medical Council of India

Disclosure: Nothing to disclose.

Abhishek Choudhary, MD Resident Physician, Department of Internal Medicine, University Hospital of Missouri-Columbia

Abhishek Choudhary, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Showkat Bashir, MD Assistant Professor, Department of Medicine, Division of Gastroenterology, George Washington University, Washington, DC

Showkat Bashir, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association

Disclosure: Nothing to disclose.

Sarah D Komanapalli, MBBS Resident Physician in Internal Medicine, Marshfield Clinic

Sarah D Komanapalli, MBBS is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Robert Baldassano, MD Director, Center for Pediatric Inflammatory Bowel Disease, Children's Hospital of Philadelphia; Professor, Department of Pediatrics, Division of Gastroenterology and Nutrition, University of Pennsylvania School of Medicine

Robert Baldassano, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Abbott, Inc Consulting fee Consulting

Carmen Cuffari, MD Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Robert J Fingerote, MD, MSc, FRCPC Consultant, Clinical Evaluation Division, Biologic and Gene Therapies, Directorate Health Canada; Consulting Staff, Department of Medicine, Division of Gastroenterology, York Central Hospital, Ontario

Robert J Fingerote, MD, MSc, FRCPC is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, Canadian Medical Association, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Cass R Smith, MD Pediatric Gastroenterologist, Idaho Pediatric Gastroenterology, PA, and St Luke's Boise Regional Medical Center

Cass R Smith, MD is a member of the following medical societies: North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Michael C Stephens, MD, FAAP Assistant Professor of Pediatrics, Section of Pediatric GI and Nutrition, Medical College of Wisconsin; Director of IBD Center, Children's Hospital of Wisconsin

Michael C Stephens, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Ultrasonogram showing hepatic vein thrombus, with vessels forming arrow pointing to the thrombus.
Ultrasonogram showing hepatic vein thrombus.
 
 
 
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