Budd-Chiari syndrome overview

Jump to navigation Jump to search

Budd-Chiari syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Budd-Chiari syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Budd-Chiari syndrome overview On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Budd-Chiari syndrome overview

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Budd-Chiari syndrome overview

CDC on Budd-Chiari syndrome overview

Budd-Chiari syndrome overview in the news

Blogs on Budd-Chiari syndrome overview

Directions to Hospitals Treating Type page name here

Risk calculators and risk factors for Budd-Chiari syndrome overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The Budd-Chiari syndrome is the clinical picture caused by occlusion of the hepatic vein or inferior vena cava. Its presents with the classical triad of abdominal pain, ascites and hepatomegaly. Examples of occlusion include thrombosis of hepatic veins and membranous webs in the inferior vena cava. The syndrome can be fulminant, acute, chronic, or asymptomatic.

Historical Perspective

It is named for George Budd[1][2] and Hans Chiari.[3]

Pathophysiology

Any obstruction of the venous vasculature of the liver is referred to as Budd-Chiari syndrome, from the venules to the right atrium. This leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates. The increased portal pressure causes: 1) increased filtration of vascular fluid with the formation of protein-rich ascites in the abdomen; and 2) collateral venous flow through alternative veins leading to gastric varices and hemorrhoids. Obstruction also causes hepatic necrosis and eventual centrilobular fibrosis due to ischemia. Renal failure may occur, perhaps due to the body sensing an "underfill" state and subsequent activation of the renin-angiotensin pathways and excess sodium retention.

References

  1. Template:WhoNamedIt
  2. G. Budd. On diseases of the liver. London, J. Churchill, 1845. Page 135.
  3. H. Chiari. Erfahrungen über Infarktbildungen in der Leber des Menschen. Zeitschrift für Heilkunde, Prague, 1898, 19: 475-512.