Other presentations
The classic triad of symptoms is abdominal pain (61%), ascites (83%), and hepatomegaly (67%).[1]Northup PG, Garcia-Pagan JC, Garcia-Tsao G, et al. Vascular liver disorders, portal vein thrombosis, and procedural bleeding in patients with liver disease: 2020 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021 Jan;73(1):366-413.
https://journals.lww.com/hep/fulltext/2021/01000/vascular_liver_disorders,_portal_vein_thrombosis,.26.aspx
http://www.ncbi.nlm.nih.gov/pubmed/33219529?tool=bestpractice.com
[6]Mitchell MC, Boitnott JK, Kaufman S, et al. Budd-Chiari syndrome: etiology, diagnosis and management. Medicine (Baltimore). 1982;61:199-218.
http://www.ncbi.nlm.nih.gov/pubmed/7045569?tool=bestpractice.com
[7]Hemming AW, Langer B, Greig P, et al. Treatment of Budd-Chiari syndrome with portosystemic shunt or liver transplantation. Am J Surg. 1996;171:176-180.
http://www.ncbi.nlm.nih.gov/pubmed/8554136?tool=bestpractice.com
Acute Budd-Chiari syndrome (BCS) is observed in 20% of patients.[8]Hadengue A, Poliquin M, Vilgrain V, et al. The changing scene of hepatic vein thrombosis: recognition of asymptomatic cases. Gastroenterology. 1994;106:1042-1047.
http://www.ncbi.nlm.nih.gov/pubmed/8143970?tool=bestpractice.com
These patients develop severe right upper quadrant abdominal pain, hepatomegaly, jaundice, and intractable ascites within a few weeks. Between 5% and 20% of cases are detected following investigation of slightly abnormal results in liver function tests, but have no symptoms.[8]Hadengue A, Poliquin M, Vilgrain V, et al. The changing scene of hepatic vein thrombosis: recognition of asymptomatic cases. Gastroenterology. 1994;106:1042-1047.
http://www.ncbi.nlm.nih.gov/pubmed/8143970?tool=bestpractice.com
[9]Murad SD, Valla DC, de Groen PC, et al. Determinants of survival and the effect of portosystemic shunting in patients with Budd-Chiari syndrome. Hepatology. 2004;39:500-508.
http://www.ncbi.nlm.nih.gov/pubmed/14768004?tool=bestpractice.com
The fulminant form of BCS is uncommon. Patients rapidly develop hepatic encephalopathy, renal failure, and coagulopathy. The liver is enlarged and tender.[10]Valla DC. Hepatic vein thrombosis (Budd-Chiari syndrome). Semin Liver Dis. 2002;22:5-14.
http://www.ncbi.nlm.nih.gov/pubmed/11928075?tool=bestpractice.com
Patients with inferior vena cava compression or thrombosis present with leg edema or venous collaterals over the trunk in addition to hepatomegaly, ascites, and abdominal pain. The symptoms are less severe than in hepatic vein thrombosis.[11]Kage M, Arakawa M, Kojioro M, et al. Histopathology of membranous obstruction of the inferior vena cava in the Budd-Chiari syndrome. Gastroenterology. 1992;102:2081-2090.
http://www.ncbi.nlm.nih.gov/pubmed/1587428?tool=bestpractice.com
[12]Shrestha SM, Okuda K, Uchida T, et al. Endemicity and clinical picture of liver disease due to obstruction of the hepatic portion of the inferior vena cava in Nepal. J Gastroenterol Hepatol. 1996;11:170-179.
http://www.ncbi.nlm.nih.gov/pubmed/8672764?tool=bestpractice.com