eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Budd-Chiari Syndrome

Cass R Smith, MD, Pediatric Gastroenterologist, Idaho Pediatric Gastroenterology, PA, and St Luke's Boise Regional Medical Center
Robert Baldassano, MD, Director, Center for Pediatric Inflammatory Bowel Disease, Division of Gastroenterology and Nutrition, Associate Professor, Department of Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania; Michael Stephens, MD, Assistant Professor, Department of Pediatrics, Section of Gastroenterology and Nutrition, Children's Hospital of Wisconsin

Updated: Apr 15, 2009

Introduction

Background

Budd-Chiari syndrome (BCS) refers to the noncardiogenic obstruction of hepatic venous flow at any level above the venule. Obstruction can result from various conditions, particularly prothrombotic states. 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.

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

Ultrasound showing hepatic vein thrombus.

Pathophysiology

Occlusion of a single hepatic vein is usually silent. Overt Budd-Chiari syndrome generally requires the occlusion of at least 2 hepatic veins. 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.¹

Frequency

International

Budd-Chiari syndrome is extremely rare, and the incidence is not well reported in the literature; however, membranous (or congenital) forms of Budd-Chiari syndrome are the most common cause of Budd-Chiari syndrome worldwide, particularly in Asia. One study in Sweden reports an incidence of about 1 case per million population per year.²

Mortality/Morbidity

The mortality rate can be high in patients who develop fulminant hepatic failure. Morbidity and mortality are generally related to complications of liver failure and ascites. The type of concomitant underlying disease, if any, can also impact morbidity and mortality. Long-term observation in adults has demonstrated 10-year survival rates as high as 55%.

Sex

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

Age

Budd-Chiari syndrome is rare in the general population and even more so in children. Peak incidence seems to be in persons aged 40-50 years.

Clinical

History

Patients with acute onset of obstruction typically present with acute right upper quadrant pain. Abdominal distention can also be a significant symptom because ascites develop. Jaundice is rarely observed. Various symptoms that are potentially related to underlying and predisposing conditions can accompany the onset of Budd-Chiari syndrome (BCS). If the liver has had time to develop collaterals and decompress, patients can be asymptomatic or present with few symptoms. Progression of Budd-Chiari syndrome can lead to liver failure and portal hypertension with corresponding symptoms (eg, encephalopathy, hematemesis). The American Association for the Study of Liver Diseases has released guidelines for the management of acute liver failure.³

Physical

Tender hepatomegaly with ascites and splenomegaly are common findings. Engorgement of the vessels of the chest and abdominal wall can also be observed. Bilirubin and transaminases are often mildly elevated. Prolongation of the prothrombin time (PT) is common and can be confusing in the setting of a hypercoagulable state.

Causes

Budd-Chiari syndrome can frequently be idiopathic; however, several main causes of this disorder are noted.

• Mechanical causes
  • Congenital membranous obstruction
    • 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.
  • Hepatic venous stenosis
  • Hypoplasia of the suprahepatic veins
  • Postsurgical obstruction
  • Posttraumatic obstruction
  • Tumor invasion
  • Total parenteral nutrition (TPN): BCS has been reported as a complication of TPN via an IVC catheter in a neonate.
• Causes related to hypercoagulable states
  • Hematologic disorders
    • Polycythemia vera
    • Essential thrombocytosis
    • Paroxysmal nocturnal hemoglobinuria
    • Myeloproliferative disorders, which may account for almost half of cases
  • Coagulopathies
    • Factor V Leiden mutation
    • Protein C deficiency
    • Protein S deficiency
    • Antithrombin II deficiency
  • Antiphospholipid antibody syndrome
  • Other causes of hypercoagulability
    • Collagen vascular diseases
    • Sickle cell disease
    • Inflammatory bowel disease
    • Oral contraceptives
    • Postpartum malignancy
• Causes related to infection
  • Tuberculosis
  • Aspergillosis
  • Filariasis
  • Echinococcus

Differential Diagnoses

Other Problems to Be Considered

Cirrhosis
Neonatal hemochromatosis
Alpha1-antitrypsin deficiency
Infectious hepatitis
Niemann-Pick disease type C
Perforated common bile duct
Meconium peritonitis
Jejunal atresia
Intestinal perforation
Serositis
Eosinophilic enteritis
Henoch-Schönlein purpura
Parvovirus
Central venous hyperalimentation
Obstructive uropathy
Congestive heart failure
Dysrhythmia
Chylous ascites
Neoplasm
Inborn error of metabolism
Pseudoascites - Small intestinal duplication
Celiac disease
Fitz-Hugh Curtis syndrome

Workup

Laboratory Studies

• Evaluate patients with Budd-Chiari syndrome (BCS) for underlying predisposing conditions, such as malignancy or hypercoagulable states, and institute appropriate therapy.

Imaging Studies

• Budd-Chiari syndrome is usually diagnosed initially using Doppler ultrasonography, which has a sensitivity and specificity of 85% or higher.
• Detailed imaging studies are required to determine precisely the level and degree of obstruction. CT scanning can rarely provide such detail, unless a mechanical obstruction, such as a locally invading tumor, is suspected.
• MRI, which has a sensitivity and specificity of 90% or higher, is becoming increasingly useful in providing less-invasive venography, angiography, and cholangiography. MRI may assist in differentiating acute from chronic Budd-Chiari syndrome because it is able to provide a larger image of the vasculature, as well as determine if edema of the parenchyma is present (acute form).

Procedures

• Interventional radiology: Catheterization and venography can clearly delineate the nature and severity of the obstruction. Occasionally, therapeutic interventions can be undertaken at the same time, and they can include balloon angioplasty, placement of a stent, localized thrombolysis, or transjugular intrahepatic portacaval shunt (TIPS).⁴
• Paracentesis: The benefits of therapeutic paracentesis must be carefully weighed against the significant risks that can be associated with this procedure.
• Percutaneous liver biopsy: Liver biopsy can be of prognostic assistance, particularly if liver transplantation is being considered, to establish the degree of hepatocellular damage and the presence and degree of fibrosis.

Histologic Findings

• Histologic findings can range from nearly normal to severe chronic congestion with fibrosis, reversed lobulation, and dilated lymphatic channels.
• The most severe end of this spectrum can include fulminant hepatic failure with massive centrilobular necrosis.
• Adult studies have shown that early pathology related to Budd-Chiari syndrome did not have a significant impact on survival.⁵

Treatment

Medical Care

In patients with Budd-Chiari syndrome (BCS), aggressively seek specific therapy aimed at correcting or alleviating the obstruction. Also treat underlying conditions aggressively. Symptomatic treatment for Budd-Chiari syndrome includes diuretics and therapeutic paracentesis, when necessary (can be associated with catastrophic complications, such as bacterial peritonitis).

• Patients with liver failure and ascites have total body sodium overload, despite typically low serum sodium concentrations. Inducing negative sodium balance can reduce the amount of ascites. Take special care when using diuretics to avoid inducing hepatorenal syndrome or creating electrolyte and fluid disturbances through overly aggressive diuresis. Secondary hyperaldosteronism is a part of this clinical picture, making spironolactone typically the first-line diuretic. Chlorothiazide or furosemide is often added, which can provide synergy and avoid hyperkalemia.
• The benefits of therapeutic paracentesis must be carefully weighed against the significant risks that can be associated with this procedure.
• Anticoagulation is frequently used in hypercoagulable states.
• Systemic thrombolysis can be a high-risk endeavor, and local thrombolysis performed by an interventional radiologist is preferable.
• Other radiologic interventions available include balloon angioplasty, placement of stents, and transjugular intrahepatic portacaval shunt (TIPS). Adult studies suggest that the use of TIPS is safe and increases survival in patients with progressive liver disease and profound involvement of the hepatic vasculature due to Budd-Chiari syndrome who have failed medical therapy.⁶
• A stepwise approach of anticoagulation, vascular intervention, TIPS and transplant can increase survival among patients.⁷

Surgical Care

• Mesocaval shunt
• Mesoatrial shunt
• Portacaval shunt
• Liver transplantation: One study reported that, out of almost 79,000 liver transplantations in the United States from 1987-2006, 510 were for Budd-Chiari syndrome.⁸  Graft survival was as high as 85%.

Consultations

• Consultants should be selected based on the individual clinical situation.
• Early involvement of a hepatologist can help to establish the direction of workup and therapy.
• Consultation with interventional radiologists, hematologists, oncologists, and general surgeons may be required, depending on the situation.

Diet

• Sodium restriction can be an important part of maintaining a negative sodium balance.

Medication

Medications commonly used in patients with Budd-Chiari syndrome (BCS) include diuretics, anticoagulants, and thrombolytics. The therapeutic interventions used (medical or otherwise) must be tailored to each patient's condition. The use of thrombolytics should be reserved for experts familiar with the special circumstances in which they may be appropriate. Use of anticoagulants should be directed towards therapy of an underlying coagulopathy. Typically, the decision to use anticoagulants is made with the assistance and guidance of a pediatric hematologist.

Diuretic agents

Diuretics can be useful to reduce the amount of ascites, providing symptomatic relief and reducing the need for paracentesis.

Spironolactone (Aldactone)

Potassium-sparing diuretic. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.
Spironolactone is often preferred because of its potassium-sparing effects, particularly in a clinical setting that includes secondary hyperaldosteronism.

Dosing

Adult

25-200 mg/d PO divided bid/qid; not to exceed 200 mg/d

Pediatric

1-3.3 mg/kg/d PO divided bid/qid

Interactions

May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone

Contraindications

Documented hypersensitivity; anuria; renal failure; hyperkalemia

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal and hepatic impairment; gynecomastia, impotence, decreased libido, hirsutism, deepening of the voice, menstrual irregularities, diarrhea, gastritis, gastric bleeding, drowsiness, ataxia, confusion, and headache; possible rash and blood dyscrasias

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, results inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Dosing

Adult

20-80 mg/d PO divided q6-12h; not to exceed 600 mg/d

Pediatric

Neonates:
0.5-1 mg/kg/dose PO q8-24h; not to exceed 6 mg/kg/dose PO
2 mg/kg/dose IV qd/bid
Infants and children: 0.5-2 mg/kg/dose PO/IV q6-12h; not to exceed 6 mg/kg/dose

Interactions

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication

Contraindications

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Possible ototoxicity, most frequently with rapid IV infusion; possible disturbances in fluid and electrolyte balance

Chlorothiazide (Diuril, Diurigen)

Thiazide diuretic. Inhibits sodium-chloride symport, blocking sodium reabsorption in the distal convoluted tubule.

Dosing

Adult

250-1000 mg/dose PO qd/qid; not to exceed 2 g/d

Pediatric

<6 months: 20-40 mg/kg/d PO divided q12h; not to exceed 375 mg/d
≥6 months: 20 mg/kg/d PO divided q12h; not to exceed 1 g/d

Interactions

Quinidine (torsades de pointes); possible decreased effects of anticoagulants, uricosuric agents, sulfonylureas, and insulin; possible increased effects of anesthetics, diazoxide, digitalis glycosides, lithium, loop diuretics, and vitamin D; possible reduced thiazide diuretics effectiveness when used with NSAIDs, bile acid sequestrants, and methenamines; increased risk of hypokalemia with coadministration of amphotericin B and corticosteroids

Contraindications

Documented hypersensitivity; anuria

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Fluid and electrolyte disturbances; extracellular volume depletion, hypotension, hypokalemia, hyponatremia, hypochloremia, metabolic acidosis, hypomagnesemia, hyperkalemia, hyperuricemia, and hyperbilirubinemia; possible decreased glucose tolerance

Follow-up

Further Inpatient Care

• For patients with Budd-Chiari syndrome (BCS), hospitalization is generally required for diagnostic evaluation and interventions.
• Patients with lesions that are amenable to balloon dilatation or stents require follow-up catheterizations and frequently repeat dilatations or replacement of stents.

Complications

• Complications are generally related to associated liver failure.
• 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).

Prognosis

• Long-term follow-up in adults has demonstrated 10-year survival rate as high as 55%.
• A few adult studies have identified factors that predicted worse overall survival of patients with Budd-Chiari syndrome. These include older age, male gender, presentation with significant disease, no treatment with transjugular intrahepatic portacaval shunt (TIPS), and an increasing Child–Pugh–Turcotte score.⁶

Miscellaneous

Medicolegal Pitfalls

• Budd-Chiari syndrome is a rare and serious disorder in children.
• Many of the therapeutic interventions available are invasive and require highly specialized expertise.
• Early referral to an appropriate tertiary care center should be considered.

Multimedia

Media file 1: Ultrasound showing hepatic vein thrombus with vessels forming arrow pointing to the thrombus.

Media file 2: Ultrasound showing hepatic vein thrombus.

Media file 3: Calcified thrombus in the inferior vena cava (IVC) of a neonate secondary to an umbilical venous catheter (UVC).

References

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Keywords

Budd-Chiari syndrome, BCS, membranous Budd-Chiari syndrome, membranous BCS, hepatic vein thrombosis, congenital Budd-Chiari syndrome, congenital BCS, veno-occlusive disease, sinusoidal obstruction syndrome, hepatomegaly, liver failure, ascites, jaundice, encephalopathy, hematemesis, congenital membranous obstruction, hepatic venous stenosis, tumor invasion, treatment, diagnosis, polycythemia vera, thrombocytosis, paroxysmal nocturnal hemoglobinuria, myeloproliferative disorder, factor V Leiden mutation, protein C deficiency, protein S deficiency, antithrombin II deficiency, antiphospholipid antibody syndrome, sickle cell disease, inflammatory bowel disease, tuberculosis, aspergillosis, filariasis, echinococcus

Contributor Information and Disclosures

Author

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.

Coauthor(s)

Robert Baldassano, MD, Director, Center for Pediatric Inflammatory Bowel Disease, Division of Gastroenterology and Nutrition, Associate Professor, Department of Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania
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: Nothing to disclose.

Michael Stephens, MD, Assistant Professor, Department of Pediatrics, Section of Gastroenterology and Nutrition, Children's Hospital of Wisconsin
Michael Stephens, MD 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.

Medical Editor

Robert Baldassano, MD, Director, Center for Pediatric Inflammatory Bowel Disease, Division of Gastroenterology and Nutrition, Associate Professor, Department of Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania
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: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor

Chief Editor

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.

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