Diagnostic Ultrasound - Abdomen and Pelvis

Budd-Chiari Syndrome
TERMINOLOGY
Abbreviations
• Budd-Chiari syndrome (BCS)
Synonyms
• Hepatic venous outflow obstruction
Definitions
• Global or segmental obstruction of hepatic venous outflow
or inferior vena cava (IVC)
○ At level of large hepatic veins or suprahepatic segment
of IVC
IMAGING
General Features
• Best diagnostic clue
○ Narrowing of obliteration of HVs and IVC
○ No flow in HVs/IVC on color Doppler ultrasound
○ Intrahepatic/extrahepatic venous collateralization
• Location
○ Obstruction may be in hepatic veins, IVC, sinusoidal
(parenchymal) veins
Ultrasonographic Findings
• Grayscale ultrasound
○ Acute stage
– HVs visualized, possibly distended
– Partial or complete thrombosis in HVs/IVC
– Involved parenchyma may be hypoechoic due to
edema
○ Chronic stage
– HVs narrowed, nonvisualized, or filled with thrombus
– Compensatory hypertrophy of caudate lobe and
unaffected segments/lobes
– Atrophy of involved segments/lobes
– Regenerative nodules, possibly large
• Color Doppler
○ Acute stage
– Absent or severely restricted flow in HVs/IVC
– Continuous (nonpulsatile) flow in patent portions of
HVs proximal to obstruction
– Intrahepatic collateralization, "bicolored HVs"
□ Opposing flow directions seen in adjacent veins
– HVs may appear tortuous, curvilinear, fragmented,
stenotic, or as fibrous cord with slow, turbulent, or
reversed flow
– Reversed flow in patent portions of IVC
– Reduced velocity, continuous flow in portal vein,
possibly hepatofugal flow
○ Chronic stage
– Stenotic or nonvisualized (occluded) HVs/IVC
– Intrahepatic &/or extrahepatic collateralization
CT Findings
• Acute stage
○ NECT: Narrowed HVs/IVC; hyperdense thrombus;
hypodense affected parenchyma, hepatomegaly, ascites
○ CECT: Classic "flip-flop" pattern
– Early enhancement of caudate lobe and central
portion around IVC, decreased peripheral liver
enhancement
– Later decreased enhancement centrally and increased
enhancement peripherally
• Chronic stage
○ Total obliteration of IVC and HVs
○ Large regenerative nodules: Multiple 1-4 cm hyperdense
and enhancing nodules
○ Atrophy of affected segments, hypertrophied caudate
lobe, collateralization
MR Findings
• Narrowed or absent HVs and IVC, caudate lobe hypertrophy
• Regenerative nodules: High SI on T1WI, iso-/low SI on T2WI,
delayed enhancement without washout
• Parenchymal enhancement pattern analogous to CT
Angiographic Findings
• Classic "spider web" pattern on wedged hepatic
venography
• Thrombus in HVs or IVC, long segmental compression or
stenosis of IVC
• Hepatic arteries: Narrowed and stretched in acute phase,
dilated with arterioportal shunts in chronic phase
Imaging Recommendations
• Best imaging tool
○ Color Doppler sonography for initial diagnosis/exclusion
of BCS
○ CECT or MR for comprehensive assessment
DIFFERENTIAL DIAGNOSIS
Liver Cirrhosis
• Patent HVs and IVC
• Hypertrophy of caudate lobe and lateral segment of left
lobe
• Atrophy of right lobe and medial segment of left lobe
• Portosystemic collaterals, ascites, splenomegaly
• Regenerative nodules usually smaller in size
Portal Vein Thrombosis
• Liver dysfunction, ascites, portosystemic collaterals,
splenomegaly
• Patent HVs/IVC
Acute, Severe Passive Venous Congestion
• Usually in congestive heart failure: Hepatic
congestion/enlargement, ascites
• Dilated but patent HVs/IVC
Acute Hepatitis
• Hepatomegaly, liver dysfunction, ±ascites
• Patent HVs/IVC
PATHOLOGY
General Features
• Etiology
○ Thrombotic occlusion of HVs or IVC
– Cirrhosis-related (immediate cause uncertain)
– Hypercoagulable states dehydration/shock/sepsis
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Diagnoses: Liver
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