Budd-Chiari syndrome classification: Difference between revisions

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*Budd-Chiari syndrome may be classified according to etiology into two subtypes/groups
*Budd-Chiari syndrome may be classified according to etiology into two subtypes/groups
**Primary:Hepatic venous outflow obstruction is a result of thrombosis.
**Primary: Hepatic venous outflow obstruction is a result of thrombosis.
**Secondary:Hepatic venous outflow obstruction is a result of invasion or compression by a tumor.
**Secondary: Hepatic venous outflow obstruction is a result of invasion or compression by a tumor.
*Budd-Chiari syndrome may be classified according to disease duration and severity into four sub types:  
*Budd-Chiari syndrome may be classified according to disease duration and severity into four subtypes:  
**Acute: Rapid development of clinical manifestations within weeks with intractable ascites and hepatic necrosis.
**Acute: Rapid development of clinical manifestations within weeks with intractable ascites and hepatic necrosis.
**Subacute:Insidious onset symptoms develop over 3 months.Clinical manifestations of Ascites and hepatic necrosis may be minimal as portal and hepatic venous collaterals help in decompression of sinusoids.
**Subacute: Insidious onset symptoms develop over 3 months.Clinical manifestations of Ascites and hepatic necrosis may be minimal as the portal and hepatic venous collaterals help in decompression of sinusoids.
**Chronic: Associated with complications of cirrhosis.
**Chronic: Associated with complications of cirrhosis.
**Fulminant liver failure: Characterized by acute liver injury with elevated transaminases, jaundice, hepatic encephalopathy, and an elevated prothrombin time/international normalized ratio; hepatic encephalopathy develops within eight weeks after the development of jaundice.
**Fulminant liver failure: Characterized by acute liver injury with elevated transaminases, jaundice, hepatic encephalopathy, and an elevated prothrombin time/international normalized ratio; hepatic encephalopathy develops within eight weeks after the development of jaundice.
*Venous collaterals are not developed in patients with acute liver failure or acute liver disease whereas venous collaterals are seen in patients with subacute and chronic liver disease.
*Venous collaterals are not developed in patients with acute liver failure or acute liver disease whereas venous collaterals are seen in patients with subacute and chronic liver disease.
*Budd-Chiari syndrome may be classified according to anatomical location of obstruction into 3 subtypes: Type I - truncal type, Type II - radicular type, Type III - venooclusive type.
*Budd-Chiari syndrome may be classified according to the anatomical location of obstruction into 3 subtypes:  
**Type I - truncal type: inferior vena cava occlusion with or without the involvement of hepatic veins.
**Type II - radicular type: major hepatic veins occlusion.
**Type III - venooclusive type: small centrilobular veins occlusion.


==References==
==References==

Revision as of 17:05, 2 November 2017

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Overview

Classification

  • Budd-Chiari syndrome may be classified into several subtypes based on:
    • Etiology
    • Disease duration and severity
    • Anatomical location of occlusion
  • An obstruction below 300µm in diameter is not considered as BCS by some authors.
  • Budd-Chiari syndrome may be classified according to etiology into two subtypes/groups
    • Primary: Hepatic venous outflow obstruction is a result of thrombosis.
    • Secondary: Hepatic venous outflow obstruction is a result of invasion or compression by a tumor.
  • Budd-Chiari syndrome may be classified according to disease duration and severity into four subtypes:
    • Acute: Rapid development of clinical manifestations within weeks with intractable ascites and hepatic necrosis.
    • Subacute: Insidious onset symptoms develop over 3 months.Clinical manifestations of Ascites and hepatic necrosis may be minimal as the portal and hepatic venous collaterals help in decompression of sinusoids.
    • Chronic: Associated with complications of cirrhosis.
    • Fulminant liver failure: Characterized by acute liver injury with elevated transaminases, jaundice, hepatic encephalopathy, and an elevated prothrombin time/international normalized ratio; hepatic encephalopathy develops within eight weeks after the development of jaundice.
  • Venous collaterals are not developed in patients with acute liver failure or acute liver disease whereas venous collaterals are seen in patients with subacute and chronic liver disease.
  • Budd-Chiari syndrome may be classified according to the anatomical location of obstruction into 3 subtypes:
    • Type I - truncal type: inferior vena cava occlusion with or without the involvement of hepatic veins.
    • Type II - radicular type: major hepatic veins occlusion.
    • Type III - venooclusive type: small centrilobular veins occlusion.

References

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