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DOI:10.2214/AJR.05.0168
AJR 2007; 188:W168-W176
© American Roentgen Ray Society

Pictorial Essay

Budd-Chiari Syndrome: Spectrum of Imaging Findings

Giuseppe Brancatelli1,2,3, Valérie Vilgrain4, Michael P. Federle3, Antoine Hakime4, Roberto Lagalla2, Riccardo Iannaccone5 and Dominique Valla6

1 Sezione di Radiologia, Ospedale Specializzato in Gastroenterologia, Saverio de Bellis, IRCCS, Castellana Grotte, Italy.
2 Istituto di Radiologia, Università di Palermo, Via Villaermosa 29, 90139 Palermo, Italy.
3 Department of Radiology, University of Pittsburgh Medical Center, Pittsburgh, PA, 15213.
4 Service de Radiologie, Hopital Beaujon, Clichy 92118, France.
5 Istituto di Radiologia, Università di Roma La Sapienza, Policlinico Umberto I, Roma 00161, Italy.
6 Service de Hepatologie, Hopital Beaujon, Clichy 92118, France.

Received February 1, 2005; accepted after revision October 6, 2005.

 
Address correspondence to G. Brancatelli (gbranca{at}yahoo.com).

WEB This is a Web exclusive article.


Abstract
Top
 Abstract
Introduction
 Epidemiologic, Etiologic, and...
 Imaging Findings
 Pathologic Aspects
 Treatment
 Summary
 References
 
OBJECTIVE. The objective of our study was to illustrate the imaging findings of Budd-Chiari syndrome, including CT, MRI, sonographic, and angiographic findings.

CONCLUSION. The key imaging findings in Budd-Chiari syndrome are occlusion of the hepatic veins, inferior vena cava, or both; caudate lobe enlargement; inhomogeneous liver enhancement; and the presence of intrahepatic collateral vessels and hypervascular nodules. Awareness of these findings is important for early diagnosis and appropriate treatment.

Keywords: CT • Budd-Chiari syndrome • liver disease • MRI


Introduction
Top
 Abstract
 Introduction
Epidemiologic, Etiologic, and...
 Imaging Findings
 Pathologic Aspects
 Treatment
 Summary
 References
 
The term Budd-Chiari syndrome is applied to the clinical manifestations of hepatic venous outflow obstruction at any level from the small hepatic veins to the junction of the inferior vena cava and the right atrium regardless of the cause of obstruction [1, 2]. Early diagnosis of Budd-Chiari syndrome is important for establishing appropriate treatment. Because of inhomogeneous distribution of disease in the liver, normal biopsy findings do not exclude this entity [1]. Therefore imaging studies combined with clinical information are often essential for reaching a definitive diagnosis. Evaluation of occlusion of the hepatic veins and inferior vena cava, caudate lobe enlargement, inhomogeneous liver enhancement, and presence of intrahepatic collateral vessels and hypervascular nodules is the most important role of imaging examinations of patients with Budd-Chiari syndrome. We illustrate the spectrum of imaging findings in Budd-Chiari syndrome, including CT, MR, sonographic, and angiographic findings.


Epidemiologic, Etiologic, and Pathogenetic Aspects
Top
 Abstract
 Introduction
 Epidemiologic, Etiologic, and...
Imaging Findings
 Pathologic Aspects
 Treatment
 Summary
 References
 
Budd-Chiari syndrome can occur at any age, and it is more common in women. Presentation varies from fulminant signs and symptoms to an asymptomatic condition recognized fortuitously, depending on the temporal nature of the disease (acute, subacute, or chronic). With regard to cause, Budd-Chiari syndrome can be classified into primary or secondary. The primary type is caused by hepatic venous outflow obstruction originating from an endoluminal venous lesion, such as thrombus (Fig. 1A, 1B) or a membrane [1]. Budd-Chiari syndrome is considered secondary when the obstruction of hepatic venous outflow results from the presence in the lumen of material not originating from the venous system (Fig. 2) or from extrinsic compression [1] (Fig. 3). Regardless of cause, blockage of hepatic venous outflow prevents normal drainage of blood. Therefore portal hypertension and intrahepatic and extrahepatic collateral vessels typically develop in patients with Budd-Chiari syndrome.


Figure 1
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  		Fig. 1A —49-year-old woman with Budd-Chiari syndrome. Unenhanced transverse CT scan shows dysmorphic liver with enlarged left lobe and caudate which has normal attenuation compared with other, low-density portions of liver. Ascites (a) is evident.

 

Figure 2
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  		Fig. 1B —49-year-old woman with Budd-Chiari syndrome. Contrast-enhanced transverse CT scan obtained during portal phase shows intense enhancement of caudate lobe and relatively low enhancement of peripheral portions of liver. Inferior vena cava (IVC) is compressed by enlarged caudate lobe. Thrombosis of left hepatic vein (arrow) is evident.

 

Figure 3
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  		Fig. 2 —61-year-old man with hepatocellular carcinoma causing Budd-Chiari syndrome. Contrast-enhanced transverse CT scan obtained during portal phase shows hepatocellular carcinoma invading and expanding inferior vena cava (vertical arrow). Note hepatocellular carcinoma satellite lesion (arrowhead) and metastatic lesion (horizontal arrow) involving right chest wall.

 

Figure 4
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  		Fig. 3 —40-year-old man with iatrogenic variant of Budd-Chiari syndrome 30 days after receiving liver transplant from live donor. Contrast-enhanced transverse CT scan obtained during portal phase shows occlusion of branch of middle hepatic vein (arrow) with congestion, edema, and ischemia of anterior part of right lobe of liver. Sharp demarcation (arrowheads) is evident between normal and abnormally drained liver.

 

Imaging Findings
Top
 Abstract
 Introduction
 Epidemiologic, Etiologic, and...
 Imaging Findings
Pathologic Aspects
 Treatment
 Summary
 References
 
The imaging findings of Budd-Chiari syndrome are variable and depend on the stage of the disease (i.e., acute or chronic).

Sonographic Findings
Conventional gray-scale sonography can show enlargement of the caudate lobe; ascites; splenomegaly; and narrowing, lack of visualization, and thrombosis of the hepatic veins. Color Doppler studies show absent or flat flow in the hepatic veins; reversed flow in the hepatic veins, inferior vena cava, or both; and intrahepatic collateral pathways [3] (Fig. 4). At the level of the portal vein, color Doppler sonography shows slow hepatofugal flow (< 11 cm/s). Bargallo et al. [4] found that visualization of a caudate vein ≥ 3 mm in diameter on gray-scale sonography strongly suggests the diagnosis of Budd-Chiari syndrome in the appropriate clinical setting.


Figure 5
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  		Fig. 4 —44-year-old man with Budd-Chiari syndrome and intrahepatic collateral vessels. Transverse color Doppler sonogram obtained at level of caudate lobe shows lack of color flow in distal portion of middle hepatic vein. Intrahepatic venovenous collateral vessel (arrowheads) is alternative pathway for venous return from proximal patent middle hepatic vein (arrow) to inferior vena cava (IVC).

 
CT Findings
In acute Budd-Chiari syndrome, the morphologic features of the liver usually are normal, and occlusion of the hepatic veins with severe ascites is the typical finding. The liver exhibits patchy, decreased peripheral enhancement caused by portal and sinusoidal stasis and stronger enhancement of the central portion of the liver parenchyma [5, 6] (Fig. 1A, 1B). The thrombosed hepatic veins are hypoattenuating, and the inferior vena cava is compressed by the enlarged caudate lobe. Ascites and splenomegaly are usually present [5, 6].

In subacute or chronic Budd-Chiari syndrome, the morphologic changes in the liver are the result of the type of venous involvement, and portosystemic and intrahepatic collateral vessels are often found. Contrast-enhanced CT is useful for depicting regions of hypoperfused liver parenchyma (Fig. 5). The diameter of the hepatic artery is usually enlarged compared with that of the splenic artery. Chronic thrombosis of the inferior vena cava can evolve into calcification (Fig. 6A, 6B, 6C). Moreover, portal vein thrombosis can develop as the result of underlying thrombophilia and stagnation of portal flow caused by outflow block [2] (Fig. 7A, 7B, 7C). Sometimes the only clue to the diagnosis of Budd-Chiari syndrome is large (comma-shaped) intrahepatic collateral vessels with no ascites or major morphologic changes [1, 2] (Fig. 8A, 8B).


Figure 6
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  		Fig. 5 —43-year-old woman with systemic lupus erythematosus and Budd-Chiari syndrome with impaired circulation in caudate lobe. Contrast-enhanced transverse CT scan obtained during portal phase shows enlarged left lobe and caudate lobe, normal enhancement of ventral portion of caudate lobe, and lack of enhancement of dorsal portion. Straight line (arrowheads) separates normally from abnormally perfused zones.

 

Figure 7
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  		Fig. 6A —71-year-old woman with chronic Budd-Chiari syndrome, inferior vena caval calcification, and portal vein occlusion. Contrast-enhanced transverse CT scan obtained during arterial phase shows increased peripheral enhancement of liver in relation to portal vein occlusion (not shown). Liver exhibits peripheral atrophy with compensatory caudate hypertrophy.

 

Figure 8
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  		Fig. 6B —71-year-old woman with chronic Budd-Chiari syndrome, inferior vena caval calcification, and portal vein occlusion. Contrast-enhanced transverse CT scan obtained during portal phase shows homogeneous enhancement of liver.

 

Figure 9
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  		Fig. 6C —71-year-old woman with chronic Budd-Chiari syndrome, inferior vena caval calcification, and portal vein occlusion. Contrast-enhanced transverse CT scan cephalic in relation to B obtained during portal phase shows hepatic venous occlusion and coarse calcification (arrow) within inferior vena cava caused by chronic thrombosis.

 

Figure 10
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  		Fig. 7A —22-year-old woman with chronic Budd-Chiari syndrome and portal vein occlusion. Gadolinium-enhanced T1-weighted MR image (A) and contrast-enhanced transverse CT scan obtained during portal phase (B) show occlusion of vein (arrow, A and B) draining caudate lobe.

 

Figure 11
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  		Fig. 7B —22-year-old woman with chronic Budd-Chiari syndrome and portal vein occlusion. Gadolinium-enhanced T1-weighted MR image (A) and contrast-enhanced transverse CT scan obtained during portal phase (B) show occlusion of vein (arrow, A and B) draining caudate lobe.

 

Figure 12
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  		Fig. 7C —22-year-old woman with chronic Budd-Chiari syndrome and portal vein occlusion. Contrast-enhanced transverse CT scan caudal in relation to B obtained during portal phase shows cavernous transformation of portal vein (arrow) and gallbladder varices (arrowhead). Ascites is evident. This case is unusual in that caudate lobe has impaired venous drainage with resulting heterogeneous enhancement.

 

Figure 13
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  		Fig. 8A —39-year-old woman with Budd-Chiari syndrome. Contrast-enhanced transverse CT scan obtained during portal phase shows development of intrahepatic (black arrow) and extrahepatic (white arrow) subcutaneous collateral vessels after hepatic venous thrombosis. Ascites and dilatation of azygos vein (arrowhead) are evident.

 

Figure 14
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  		Fig. 8B —39-year-old woman with Budd-Chiari syndrome. Contrast-enhanced transverse CT scan caudal in relation to A obtained during portal phase shows multiple hypervascular nodules resembling focal nodular hyperplasia. Largest nodule exhibits central scar (arrow).

 
Chronic Budd-Chiari syndrome is also characterized by the development of multiple regenerative nodules, which can be viewed as a response to a focal loss of portal perfusion and hyperarterialization in areas with preserved hepatic venous outflow [7-11]. These nodules are usually multiple and have a typical diameter of 0.5-4.0 cm. On multiphasic helical CT, regenerative nodules are markedly and homogeneously hyperattenuating on arterial phase images and remain slightly hyperattenuating on portal venous phase images, allowing differential diagnosis from hepatocellular carcinoma. Hepatocellular carcinoma usually exhibits heterogeneous hyperattenuation in relation to the liver on arterial phase images and hypoattenuation on unenhanced and portal venous phase images [11].

Although to our knowledge the role of MDCT in patients with Budd-Chiari syndrome has been evaluated in only one study [12], it is likely that multiplanar reformation from submillimeter isotropic voxels will provide a useful adjunct to the axial plane images in the near future (Fig. 9).


Figure 15
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  		Fig. 9 —25-year-old woman with Budd-Chiari syndrome. Contrast-enhanced coronal maximumintensity-projection CT scan obtained during portal phase shows patent inferior vena cava with extrinsic compression (arrow) of enlarged caudate lobe (C).

 
MRI Findings
In Budd-Chiari syndrome, MR images obtained with T2-weighted sequences usually show heterogeneously increased signal intensity in the peripheral portion of the liver [13] (Fig. 10A, 10B, 10C). Images acquired with T2-weighted sequences do not depict the hepatic veins or inferior vena cava. Acquisition of T2*-weighted gradient-recalled echo sequences is useful for showing absence of flow in the hepatic veins and inferior vena cava.


Figure 16
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  		Fig. 10A —43-year-old woman with Budd-Chiari syndrome. Contrast-enhanced transverse CT scan obtained during portal phase shows caudate lobe hypertrophy and left lobe atrophy. Central portion of liver is enhanced, and liver periphery is hypoperfused. More cephalic section (not shown) showed hepatic veins as areas of hypoattenuation due to thrombosis.

 

Figure 17
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  		Fig. 10B —43-year-old woman with Budd-Chiari syndrome. Gadolinium-enhanced T1-weighted MR image obtained during portal phase shows straight demarcation (arrows) between normally perfused central portion of liver and hypoperfused periphery.

 

Figure 18
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  		Fig. 10C —43-year-old woman with Budd-Chiari syndrome. T2-weighted fat-saturated MR image shows hyperintensity of liver periphery. Ascites and splenomegaly are evident.

 
MR images acquired with T1-weighted sequences after contrast administration clearly show occlusion of the hepatic veins, inferior vena cava, or both. In acute Budd-Chiari syndrome, the caudate lobe exhibits normal or increased enhancement with decreased enhancement in the periphery of the liver [13] (Fig. 10A, 10B, 10C). In chronic Budd-Chiari syndrome, the enhancement is more variable, and such differences may be more subtle [13].

Regenerative nodules are bright on T1-weighted MR images and strongly hypervascular after IV bolus administration of gadolinium contrast material. The nodules are predominantly isointense or hypointense relative to the liver on T2-weighted images [7-11] (Fig. 11A, 11B). Therefore, large regenerative nodules in patients with Budd-Chiari syndrome have features on MRI that distinguish them from hepatocellular carcinoma, which is usually hypointense in relation to the liver on T1-weighted images and hyperintense on T2-weighted images [11].


Figure 19
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  		Fig. 11A —77-year-old man with Budd-Chiari syndrome and typical large regenerative nodules. Gadolinium-enhanced T1-weighted MR image obtained during arterial phase shows numerous homogeneous hyperintense lesions (arrows) in liver parenchyma.

 

Figure 20
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  		Fig. 11B —77-year-old man with Budd-Chiari syndrome and typical large regenerative nodules. T2-weighted fat-saturated MR image shows only one nodule (arrow) of many as hypointense lesion. On gross specimen (not shown) diffuse nutmeg pattern caused by chronic hepatovenous outflow obstruction was evident along with multiple scattered, round, orange-brown, well-demarcated nodules in both lobes. Histopathologic examination of nodules showed different-sized hepatocytes with proliferation of bile ductules, and nodules were called large (multiacinar) regenerative nodules.

 
Multiphase contrast-enhanced 3D MR angiography of patients with Budd-Chiari syndrome has been described [14, 15] as an effective, noninvasive approach to the evaluation of the hepatic artery, portal and hepatic veins, and inferior vena cava, especially for assessment of vessel patency.

Angiographic Findings
Inferior venacavography or hepatic venacavography shows a spiderweb pattern of collateral vessels pathognomonic of Budd-Chiari syndrome [3] (Fig. 12). In addition, angiographic studies usually show the presence of thrombus within the hepatic veins or inferior vena cava. Another typical feature of Budd-Chiari syndrome is long segmental compression of the inferior vena cava caused by caudate lobe hypertrophy (Fig. 9). The hepatic arteries tend to be dilated and associated with arterioportal shunts.


Figure 21
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  		Fig. 12 —42-year-old woman with Budd-Chiari syndrome. Hepatic venogram obtained with selective catheterization of hepatic vein shows spiderweb pattern. Because of hepatic vein obstruction, collateral channels developed within liver.

 

Pathologic Aspects
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 Abstract
 Introduction
 Epidemiologic, Etiologic, and...
 Imaging Findings
 Pathologic Aspects
Treatment
 Summary
 References
 
At gross pathologic examination, liver affected by acute Budd-Chiari syndrome appears enlarged and congested by occlusion of the hepatic veins or inferior vena cava [16]. In the chronic phase, the liver has a nodular, shrunken, sometimes cirrhotic appearance with hypertrophy of the caudate lobe and variable atrophy of the other portions of the liver [16]. The compensatory hypertrophy of the caudate lobe is explained by preservation of its veins draining directly into the inferior vena cava [16] (Fig. 13). Typical microscopic features of Budd-Chiari syndrome include centrilobular congestion, sinusoidal dilatation, fibrosis, necrosis, and cell atrophy [16].


Figure 22
Figure 22
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  		Fig. 13 —17-year-old girl with Budd-Chiari syndrome. A, Gadolinium-enhanced T1-weighted MR image obtained during arterial phase. Hyperintense structures represent portal venules (arrows), which are visible because of postsinusoidal portal hypertension. B, Gadolinium-enhanced T1-weighted MR image caudal in relation to A obtained during portal phase better shows enlarged caudate lobe that has pseudotumor appearance. Enhancement is still patchy in periphery and homogeneous in center of liver. Direct venous drainage (arrow) of caudate lobe into inferior vena cava is evident.

 
Pathologic examination shows nodules composed of fairly normal or hyperplastic hepatocytes, large arteries extending radially from the center of the nodule, and a central scar in larger lesions [9-10] (Figs. 8A, 8B and 14A, 14B, 14C). Such nodules can resemble focal nodular hyperplasia, and in rare cases they can be difficult to differentiate from hepatocellular carcinoma (Fig. 15A, 15B). To our knowledge, there have been no published cases of large regenerative nodules in Budd-Chiari syndrome degenerating into malignancy.


Figure 23
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  		Fig. 14A —35-year-old man with Budd-Chiari syndrome and large regenerative nodules over 3-year period. Contrast-enhanced transverse CT scan obtained during late hepatic artery phase shows multiple hypervascular nodules. Largest nodule has central scar (arrow), resembling focal nodular hyperplasia. Inferior vena caval stent (S) is evident.

 

Figure 24
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  		Fig. 14B —35-year-old man with Budd-Chiari syndrome and large regenerative nodules over 3-year period. Contrast-enhanced transverse CT scan obtained during late hepatic artery phase 3 years after and at same level as A shows much less conspicuous nodules. Retraction of liver capsule (arrow) adjacent to largest nodule is evident. Mesoatrial surgical shunt (S) was inserted 2 years before A.

 

Figure 25
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  		Fig. 14C —35-year-old man with Budd-Chiari syndrome and large regenerative nodules over 3-year period. Photograph of cut section of fresh explant shows two nodules. At histologic examination, nodules exhibited extensive fibrosis, and typical features of large regenerative nodules were not found. Capsular retraction (arrow) is evident adjacent to larger nodule. Relation between decrease in size of hypervascular nodules and mesoatrial shunt placement can be hypothesized.

 

Figure 26
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  		Fig. 15A —24 year-old woman with Budd-Chiari syndrome and large regenerative nodules with atypical features. Contrast-enhanced transverse CT scan obtained during arterial phase shows multiple homogeneous hyperattenuating lesions (arrows). Intrahepatic collateral vessel (arrowhead) is evident.

 

Figure 27
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  		Fig. 15B —24 year-old woman with Budd-Chiari syndrome and large regenerative nodules with atypical features. Contrast-enhanced transverse CT scan obtained during delayed phase shows hypoattenuating nodules (arrows) with hyperattenuating ring. Case is unusual in that lesions are hypoattenuating in relation to surrounding liver parenchyma on delayed phase images. Presence of hyperattenuating capsule is uncommon and would raise concern about hepatocellular carcinoma.

 

Treatment
Top
 Abstract
 Introduction
 Epidemiologic, Etiologic, and...
 Imaging Findings
 Pathologic Aspects
 Treatment
Summary
 References
 
The therapeutic approach to Budd-Chiari syndrome should be adapted to disease severity. If patients with signs of portal hypertension or of liver failure do not respond to anticoagulation or nutritional therapy, careful follow-up [17] is mandatory to determine the suitable time for treatments such as a surgical shunt (usually portacaval, mesocaval, or mesoatrial) (Fig. 14A, 14B, 14C), placement of metallic stents in the inferior vena cava or hepatic vein (Fig. 16A, 16B), transjugular portosystemic shunt, and liver transplantation [1, 2]. In patients with membranous occlusion of the inferior vena cava or hepatic veins, balloon angioplasty, laser treatment, or stent insertion can be performed. An alternative treatment is surgical membranotomy or membranectomy. For patients who have undergone stent placement, imaging follow-up is necessary to determine the long-term success of the procedure [18].


Figure 28
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  		Fig. 16A —40-year-old man with chronic asymptomatic Budd-Chiari syndrome and intrahepatic collateral vessels. Gadolinium-enhanced T1-weighted MR image obtained during portal phase shows liver with lobulated contours and no flow in hepatic veins. Inferior vena caval stent (arrow) is evident.

 

Figure 29
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  		Fig. 16B —40-year-old man with chronic asymptomatic Budd-Chiari syndrome and intrahepatic collateral vessels. Gadolinium-enhanced T1-weighted MR image cephalic in relation to A obtained during portal phase shows subcapsular collateral veins (arrowheads) draining into inferior vena cava, providing route that is alternative to occluded hepatic veins.

 

Summary
Top
 Abstract
 Introduction
 Epidemiologic, Etiologic, and...
 Imaging Findings
 Pathologic Aspects
 Treatment
 Summary
References
 
Budd-Chiari syndrome is a rare clinical entity characterized by hepatic venous outflow obstruction. Awareness of its imaging findings is important for early diagnosis and appropriate treatment.


Acknowledgments
 
We thank Marie-Pierre Vullierme and Dominique Cazals-Hatem for help with radiologic and pathologic interpretation.


References
Top
 Abstract
 Introduction
 Epidemiologic, Etiologic, and...
 Imaging Findings
 Pathologic Aspects
 Treatment
 Summary
 References
 

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  9. Maetani Y, Itoh K, Egawa H, et al. Benign hepatic nodules in Budd-Chiari syndrome: radiologicpathologic correlation with emphasis on the central scar. AJR 2002;178 : 869-875[Abstract/Free Full Text]
  10. Cazals-Hatem D, Vilgrain V, Genin P, et al. Arterial and portal circulation and parenchymal changes in Budd-Chiari syndrome: a study in 17 explanted livers. Hepatology 2003;37 : 510-519[CrossRef][Medline]
  11. Brancatelli G, Federle MP, Grazioli L, Golfieri R, Lencioni R. Benign regenerative nodules in Budd-Chiari syndrome and other vascular disorders of the liver: radiologic-pathologic and clinical correlation. RadioGraphics 2002;22 : 847-862[Abstract/Free Full Text]
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