Budd-Chiari syndrome classification: Difference between revisions
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{{Budd-Chiari syndrome}} | {{Budd-Chiari syndrome}} | ||
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==Overview== | ==Overview== | ||
Budd-Chiari syndrome may be classified into several subtypes based on etiology, disease duration, severity and anatomical location of the 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 | Budd-Chiari syndrome (BCS) may be classified into several subtypes based on [[etiology]], [[disease]] duration, severity and [[anatomical]] location of the [[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 primary and [[secondary]] sub-types. Budd-Chiari syndrome may be classified according to [[disease]] duration and severity into [[acute]], [[subacute]], [[chronic]], [[fulminant liver failure]]. Budd-Chiari syndrome may be classified according to the [[Anatomical|anatomical location]] of [[obstruction]] into type I (truncal), type II -(radicular) and type III (venooclusive) disease. | ||
==Classification== | ==Classification== | ||
Budd-Chiari syndrome may be classified into several subtypes based on:<ref name="pmid2940846">{{cite journal |vauthors=Murphy FB, Steinberg HV, Shires GT, Martin LG, Bernardino ME |title=The Budd-Chiari syndrome: a review |journal=AJR Am J Roentgenol |volume=147 |issue=1 |pages=9–15 |year=1986 |pmid=2940846 |doi=10.2214/ajr.147.1.9 |url=}}</ref><ref name="pmid12971957">{{cite journal |vauthors=Langlet P, Escolano S, Valla D, Coste-Zeitoun D, Denie C, Mallet A, Levy VG, Franco D, Vinel JP, Belghiti J, Lebrec D, Hay JM, Zeitoun G |title=Clinicopathological forms and prognostic index in Budd-Chiari syndrome |journal=J. Hepatol. |volume=39 |issue=4 |pages=496–501 |year=2003 |pmid=12971957 |doi= |url=}}</ref><ref name="pmid17569137">{{cite journal |vauthors=Aydinli M, Bayraktar Y |title=Budd-Chiari syndrome: etiology, pathogenesis and diagnosis |journal=World J. Gastroenterol. |volume=13 |issue=19 |pages=2693–6 |year=2007 |pmid=17569137 |pmc=4147117 |doi= |url=}}</ref> | |||
* | *[[Etiology]] | ||
* | *[[Disease]] duration and severity | ||
* | *[[Anatomical]] location of [[occlusion]] | ||
*An [[obstruction]] below 300µm in [[diameter]] is not considered as BCS by some authors | |||
=== Classification based on etiology === | |||
Budd-Chiari syndrome may be classified according to [[etiology]] into two subtypes/groups | |||
*Primary: [[Hepatic venous obstruction|Hepatic venous outflow obstruction]] is a result of [[thrombosis]]. | |||
*Secondary: [[Hepatic venous obstruction|Hepatic venous outflow obstruction]] is a result of [[invasion]] or compression by a [[tumor]]. | |||
* | === Classification based on disease duration and severity === | ||
Budd-Chiari syndrome may be classified according to [[disease]] duration and severity into four subtypes: | |||
*[[Acute]]: Rapid [[development]] of [[Clinical|clinical manifestations]] within weeks with intractable [[ascites]] and [[Necrosis|hepatic necrosis]]. | |||
*[[Subacute]]: Insidious onset [[symptoms]] develop over 3 months. [[Clinical|Clinical manifestations]] of [[ascites]] and [[Necrosis|hepatic necrosis]] may be minimal as the [[portal]] and [[Collaterals|hepatic venous collaterals]] help in [[decompression]] of [[sinusoids]]. | |||
*[[Chronic]]: Associated with [[complications]] of [[cirrhosis]]. | |||
*[[Fulminant liver failure]]: Characterized by [[Acute liver failure|acute liver injury]] with [[elevated transaminases]], [[jaundice]], [[hepatic encephalopathy]], and an elevated [[Prothrombin time (PT)|prothrombin time]]/[[international normalized ratio]]; [[hepatic encephalopathy]] develops within eight weeks after the [[development]] of [[jaundice]]. | |||
* | *[[Collaterals|Venous collaterals]] are not developed in [[patients]] with [[acute liver failure]] or [[Acute liver failure|acute liver]] disease whereas [[Collaterals|venous collaterals]] are seen in patients with [[subacute]] and [[chronic liver disease]]. | ||
=== Classification based on anatomical location === | |||
Budd-Chiari syndrome may be classified according to the [[Anatomical|anatomical location]] of [[obstruction]] into 3 subtypes: | |||
*Type I (truncal): [[inferior vena cava]] [[occlusion]] with or without the involvement of [[hepatic veins]]. | |||
*Type II (radicular): major [[Hepatic vein obstruction|hepatic veins occlusion]]. | |||
*Type III (veno-occlusive): small centrilobular [[Veins|veins occlusion]]. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Latest revision as of 19:25, 29 November 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]
Overview
Budd-Chiari syndrome (BCS) may be classified into several subtypes based on etiology, disease duration, severity and anatomical location of the 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 primary and secondary sub-types. Budd-Chiari syndrome may be classified according to disease duration and severity into acute, subacute, chronic, fulminant liver failure. Budd-Chiari syndrome may be classified according to the anatomical location of obstruction into type I (truncal), type II -(radicular) and type III (venooclusive) disease.
Classification
Budd-Chiari syndrome may be classified into several subtypes based on:[1][2][3]
- Etiology
- Disease duration and severity
- Anatomical location of occlusion
- An obstruction below 300µm in diameter is not considered as BCS by some authors
Classification based on etiology
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.
Classification based on disease duration and severity
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.
Classification based on anatomical location
Budd-Chiari syndrome may be classified according to the anatomical location of obstruction into 3 subtypes:
- Type I (truncal): inferior vena cava occlusion with or without the involvement of hepatic veins.
- Type II (radicular): major hepatic veins occlusion.
- Type III (veno-occlusive): small centrilobular veins occlusion.
References
- ↑ Murphy FB, Steinberg HV, Shires GT, Martin LG, Bernardino ME (1986). "The Budd-Chiari syndrome: a review". AJR Am J Roentgenol. 147 (1): 9–15. doi:10.2214/ajr.147.1.9. PMID 2940846.
- ↑ Langlet P, Escolano S, Valla D, Coste-Zeitoun D, Denie C, Mallet A, Levy VG, Franco D, Vinel JP, Belghiti J, Lebrec D, Hay JM, Zeitoun G (2003). "Clinicopathological forms and prognostic index in Budd-Chiari syndrome". J. Hepatol. 39 (4): 496–501. PMID 12971957.
- ↑ Aydinli M, Bayraktar Y (2007). "Budd-Chiari syndrome: etiology, pathogenesis and diagnosis". World J. Gastroenterol. 13 (19): 2693–6. PMC 4147117. PMID 17569137.