AUTHOR INFORMATION

Section 1 of 12

Authored by Cass Smith, MD, Fellow, Pediatric Gastroenterology, Children's Hospital of Wisconsin

Coauthored by Robert Baldassano, MD, Director, Center for Pediatric Inflammatory Bowel Disease, Associate Professor, Department of Pediatrics, Division of Gastroenterology and Nutrition, 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

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

Edited by Robert Baldassano, MD, Director, Center for Pediatric Inflammatory Bowel Disease, Associate Professor, Department of Pediatrics, Division of Gastroenterology and Nutrition, The Children's Hospital of Philadelphia, University of Pennsylvania; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, The Johns Hopkins University School of Medicine; Steven M Schwarz, MD, FAAP, FACN, Chair, Department of Pediatrics, Long Island College Hospital; Professor of Pediatrics, State University of New York, Downstate Medical Center College of Medicine; and Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, The Johns Hopkins University School of Medicine

Author's Email:	Cass Smith, MD
Editor's Email:	Robert Baldassano, MD

eMedicine Journal, July 25 2006, VOLUME 7, Number 7

INTRODUCTION

Section 2 of 12

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

Pathophysiology: Occlusion of a single hepatic vein is usually silent. Overt BCS generally requires the occlusion of at least two 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 dependent on the amount of stasis and resultant hypoxia. Increased sinusoidal pressure can itself cause hepatocellular necrosis. Recent literature also suggests that upregulation of specific genes in chronic BCS 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 (Paradis, 2005).

Frequency:

• Internationally: BCS is extremely rare, and the incidence is not well reported in the literature; however, membranous (or congenital) forms of BCS are the most common cause of BCS worldwide, particularly in Asia.

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 exist to suggest that sex affects predisposition. However, in the United States, BCS is predominantly seen in women and is associated with hematologic disorders.

Age: BCS is rare in the general population and even more so in children. Peak incidence seems to be in persons aged 40-50.

CLINICAL

Section 3 of 12

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. A variety of other symptoms, which could be related to underlying and predisposing conditions, can accompany the onset of BCS. If the liver has had time to develop collaterals and decompress, patients can be asymptomatic or present with few symptoms. Progression of BCS can lead to liver failure and portal hypertension with corresponding symptoms (eg, encephalopathy, hematemesis).

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 often are mildly elevated. Prolongation of the prothrombin time (PT) is common and can be confusing in the setting of a hypercoagulable state.

Causes: BCS can frequently be idiopathic; however, several main causes of this disorder exist.

• 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 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
  
  
  
  • 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
  
  
  

  DIFFERENTIALS

  Section 4 of 12

  Appendicitis
  Biliary Atresia
  Chronic Granulomatous Disease
  Congenital Hepatic Fibrosis
  Cystic Fibrosis
  Cytomegalovirus Infection
  Intestinal Malrotation
  Intussusception
  Multicystic Renal Dysplasia
  Nephrotic Syndrome
  Pancreatitis and Pancreatic Pseudocyst
  Pericarditis, Constrictive
  Syphilis
  Toxoplasmosis
  

  
  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

  Section 5 of 12

  Lab Studies:
  

  • Evaluate for underlying predisposing conditions, such as malignancy or especially hypercoagulable states, and institute appropriate therapy.
  
  
  

  Imaging Studies:
  

  • BCS 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.
  
  
  
  • Magnetic resonance imaging (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 BCS, as 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).
  
  
  
  • 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 BCS did not have a significant impact on survival (Tang, 2001).

  TREATMENT

  Section 6 of 12

  Medical Care: Aggressively seek specific therapy aimed at correcting or alleviating the obstruction. Also treat underlying conditions aggressively. Symptomatic treatment for BCS 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 TIPS. Recent 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 BCS who have failed medical therapy (Khuroo, 2005).
  
  
  

  Surgical Care:

  • Mesocaval shunt
  
  
  
  • Mesoatrial shunt
  
  
  
  • Portacaval shunt
  
  
  
  • Liver transplantation
  
  
  

  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. Help is often requested of interventional radiologists, hematologists, oncologists, and general surgeons, depending on the situation.

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

  MEDICATION

  Section 7 of 12

  Medications commonly employed in patients with 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.
  

  Drug Category: Diuretic agents -- Diuretics can be useful to reduce the amount of ascites, providing symptomatic relief and reducing the need for paracentesis.

  Drug Name	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.
  Adult Dose	25-200 mg/d PO divided bid/qid; not to exceed 200 mg/d
  Pediatric Dose	1-3.3 mg/kg/d PO divided bid/qid
  Contraindications	Documented hypersensitivity; anuria; renal failure; hyperkalemia
  Interactions	May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone
  Pregnancy	D - Unsafe in pregnancy
  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

  Drug Name	Furosemide (Lasix, Furomide) -- 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.
  Adult Dose	20-80 mg/d PO divided q6-12h; not to exceed 600 mg/d
  Pediatric Dose	Neonates: 0.5-1 mg/kg/dose PO q8-24h; not to exceed 6 mg/kg/dose 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
  Contraindications	Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
  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
  Pregnancy	C - Safety for use during pregnancy has not been established.
  Precautions	Possible ototoxicity, most frequently with rapid IV infusion; possible disturbances in fluid and electrolyte balance

  Drug Name	Chlorothiazide (Diuril, Diurigen) -- Thiazide diuretic. Inhibits sodium-chloride symport, blocking sodium reabsorption in the distal convoluted tubule.
  Adult Dose	250-1000 mg/dose PO qd/qid; not to exceed 2 g/d
  Pediatric Dose	<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
  Contraindications	Documented hypersensitivity; anuria
  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
  Pregnancy	D - Unsafe in pregnancy
  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

  Section 8 of 12

  Further Inpatient Care:
  

  • For patients with 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 BCS. These include older age, male gender, presentation with significant disease, no treatment with TIPS, and an increasing Child–Pugh–Turcotte score (Khuroo, 2005).
  
  
  

  MISCELLANEOUS

  Section 9 of 12

  Medical/Legal Pitfalls:
  

  • BCS 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.
  
  
  

  TEST QUESTIONS

  Section 10 of 12

  CME Question 1: Which of the following is not a cause of Budd-Chiari syndrome (BCS)?

  
  A: Factor V Leiden mutation
  B: Local invasion by tumor
  C: Inflammatory bowel disease
  D: Congestive heart failure
  E: Hypoplasia of the hepatic veins
  
  The correct answer is D: Consider congestive heart failure (CHF) with elevated left-sided pressures and hepatic venous congestion separately from BCS. CHF is in the differential diagnosis of BCS, and its presence should be evaluated early in the workup. Factor V Leiden mutation, local invasion by tumor, inflammatory bowel disease, and hypoplasia of the hepatic veins are all disease processes that can cause BCS.

  CME Question 2: Which of the following therapies could be used in patients with Budd-Chiari syndrome (BCS)?

  
  A: Balloon angioplasty
  B: Anticoagulation
  C: Liver transplantation
  D: Localized thrombolysis
  E: All of the above
  
  The correct answer is E: Any of the above interventions could be appropriate for BCS. Select the most appropriate therapy with regard to the context of the individual clinical picture.

  Pearl Question 1 (T/F): Budd-Chiari syndrome can be considered together with intrahepatic and prehepatic venous obstruction.

  The correct answer is False: Budd-Chiari syndrome and intrahepatic and prehepatic venous obstruction should be considered separately. The therapeutic and prognostic significances of these disorders are very different.

  Pearl Question 2 (T/F): In most cases, only supportive care is required for Budd-Chiari syndrome.

  The correct answer is False: Although supportive care should be provided, aggressively seek to clearly define the obstruction and to alleviate it, if possible, either by removing the obstruction or through diversion.

  Pearl Question 3 (T/F): Worldwide, the most common cause of Budd-Chiari syndrome is congenital (membranous) obstruction.

  The correct answer is True: Membranous (or congenital) forms of Budd-Chiari syndrome are the most common cause worldwide, particularly in Asia.

  Pearl Question 4 (T/F): Workup for coagulopathy should be performed in patients presenting with Budd-Chiari syndrome.

  The correct answer is True: With Budd-Chiari syndrome, evaluate for underlying predisposing conditions, such as malignancy or especially hypercoagulable states.

  PICTURES

  Section 11 of 12

  Caption: Picture 1. Ultrasound showing hepatic vein thrombus with vessels forming arrow pointing to the thrombus.
  	View Full Size Image
  	eMedicine Zoom View (Interactive!)
  Picture Type: Image
  Caption: Picture 2. Ultrasound showing hepatic vein thrombus.
  	View Full Size Image
  	eMedicine Zoom View (Interactive!)
  Picture Type: Image
  Caption: Picture 3. Calcified thrombus in the IVC of a neonate secondary to UVC.
  	View Full Size Image
  	eMedicine Zoom View (Interactive!)
  Picture Type: X-RAY

  BIBLIOGRAPHY

  Section 12 of 12

  • Al-Damegh S: Budd-Chiari syndrome: a short radiological review. J Gastroenterol Hepatol 1999 Nov; 14(11): 1057-61[Medline].
  • Bogin V, Marcos A, Shaw-Stiffel T: Budd-Chiari syndrome: in evolution. Eur J Gastroenterol Hepatol 2005 Jan; 17(1): 33-5[Medline].
  • Colletti RB, Krawitt E: Ascites. In: Wyllie R, Hyams JS, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis, and Management. St. Louis, Mo: Mosby Year Book; 1999: 104-115.
  • El-Youssef M, Freese DK: Budd-Chiari Syndrome. In: Walker WA, et al, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis, and Management. St. Louis, Mo: Mosby Year Book; 2000: 1235-6.
  • Farrell MK, Bucuvalas JC: Systemic Disease and the Liver. In: Suchy FK, ed. Liver disease in Children. St. Louis, Mo: Mosby; 1994: 582-3.
  • Hirshfeld AB, Getachew A, Sessions J: Drug Doses. In: The Harriet Lane Handbook: A Manual for Pediatric House Officers. 15th ed. Philadelphia, Pa: WB Saunders; 2000: 669, 725, 850-1.
  • Ilkgul O, Kilic M, Icoz G, et al: Experience with mesocaval shunt with autologous jugular vein interpositionin patients with Budd-Chiari syndrome. Hepatogastroenterology 2005 May-Jun; 52(63): 662-5[Medline].
  • Jackson EK: Diuretics. In: Goodman & Gillman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, Inc; 1996: 685-713.
  • Janssen HL, Garcia-Pagan JC, Valla DC: The Budd-Chiari syndrome. N Engl J Med 2004 Apr 29; 350(18): 1906-8; author reply 1906-8[Medline].
  • Khuroo MS, Al-Suhabani H, Al-Sebayel M: Budd-Chiari syndrome: long-term effect on outcome with transjugular intrahepaticportosystemic shunt. J Gastroenterol Hepatol 2005 Oct; 20(10): 1494-502[Medline].
  • Mahmoud A, Elias E: New approaches to the Budd-Chiari syndrome. J Gastroenterol Hepatol 1996 Dec; 11(12): 1121-3[Medline].
  • Menon KV, Shah V, Kamath PS: The Budd-Chiari syndrome. N Engl J Med 2004 Feb 5; 350(6): 578-85[Medline].
  • Noone TC, Semelka RC, Siegelman ES: Budd-Chiari syndrome: spectrum of appearances of acute, subacute, and chronicdisease with magnetic resonance imaging. J Magn Reson Imaging 2000 Jan; 11(1): 44-50[Medline].
  • Okuda K, Kage M, Shrestha SM: Proposal of a new nomenclature for Budd-Chiari syndrome: hepatic vein thrombosis versus thrombosis of the inferior vena cava at its hepatic portion. Hepatology 1998 Nov; 28(5): 1191-8[Medline].
  • Olzinski AT, Sanyal AJ: Treating Budd-Chiari Syndrome: making rational choices from a myriad of options. J Clin Gastroenterol 2000 Mar; 30(2): 155-61[Medline].
  • Orloff MJ, Daily PO, Orloff SL: A 27-year experience with surgical treatment of Budd-Chiari syndrome. Ann Surg 2000 Sep; 232(3): 340-52[Medline].
  • Paradis V, Bieche I, Dargere D, et al: Quantitative gene expression in Budd-Chiari syndrome: a molecular approachto the pathogenesis of the disease. Gut 2005 Dec; 54(12): 1776-81[Medline].
  • Rerksuppaphol S, Hardikar W, Smith AL: Successful stenting for Budd-Chiari syndrome after pediatric liver transplantation:a case series and review of the literature. Pediatr Surg Int 2004 Feb; 20(2): 87-90[Medline].
  • Rossle M, Olschewski M, Siegerstetter V, et al: The Budd-Chiari syndrome: outcome after treatment with the transjugular intrahepaticportosystemic shunt. Surgery 2004 Apr; 135(4): 394-403[Medline].
  • Ruh J, Malago M, Busch Y, et al: Management of Budd-Chiari syndrome. Dig Dis Sci 2005 Mar; 50(3): 540-6[Medline].
  • Senzolo M, Cholongitas EC, Patch D: Update on the classification, assessment of prognosis and therapy of Budd-Chiarisyndrome. Nat Clin Pract Gastroenterol Hepatol 2005 Apr; 2(4): 182-90[Medline].
  • Singh V, Sinha SK, Nain CK: Budd-Chiari syndrome: our experience of 71 patients. Journal of Gastroenterology & Hepatology 2000; 15(5): 550-4[Medline].
  • Slakey DP, Klein AS, Venbrux AC: Budd-Chiari syndrome: current management options. Ann Surg 2001 Apr; 233(4): 522-7[Medline].
  • Tang TJ, Batts KP, de Groen PC: The prognostic value of histology in the assessment of patients with Budd-Chiarisyndrome. J Hepatol 2001 Sep; 35(3): 338-43[Medline].
  • Wang ZG, Zhang FJ, Yi MQ: Evolution of management for Budd-Chiari syndrome: a team's view from 2564 patients. ANZ J Surg 2005 Jan-Feb; 75(1-2): 55-63[Medline].
  • Xu PQ, Ma XX, Ye XX: Surgical treatment of 1360 cases of Budd-Chiari syndrome: 20-year experience. Hepatobiliary Pancreat Dis Int 2004 Aug; 3(3): 391-4[Medline].
  • Zeitoun G, Escolano S, Hadengue A: Outcome of Budd-Chiari syndrome: a multivariate analysis of factors related to survival including surgical portosystemic shunting. Hepatology 1999 Jul; 30(1): 84-9[Medline].

  NOTE:

  Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

  eMedicine Journal, July 25 2006, VOLUME 7, Number 7
  © Copyright 2001, eMedicine.com, Inc.

  eMedicine Journals > Pediatrics > Gastroenterology > Budd-Chiari Syndrome

  Please email us with any comments you have on our new chapter format.

  Author Information | Introduction | Clinical | Differentials | Workup | Treatment | Medication | Follow-up | Miscellaneous | Test Questions | Pictures | Bibliography