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Acute, chronic, or neoplastic occlusion of portal vein (PV) due to thrombosis, thrombophlebitis, or tumor invasion
Chronic PV occlusion with numerous periportal collaterals is referred to as "cavernous transformation"
Color Doppler US initially : Accurate and cost effective
Periportal collaterals may be mistaken for patent PV
Tumor vessels may be evident within PV mass
Multiphasic, multiplanar enhanced CT or MR
Contrast-enhanced CT of acute PV thrombosis
Arterial phase (25-40 seconds post bolus injection)
High attenuation/intensity within involved hepatic lobe or segment due to arterioportal shunting
Transient hepatic attenuation difference
Venous phase (60-70 seconds post bolus injection)
Equilibration of hepatic contrast enhancement
Visualization of low-density thrombus
CECT of chronic PV thrombosis
Numerous periportal collateral veins along usual course of PV
Peripancreatic and gallbladder wall varices are common
Nonvisualization of PV &/or splenic vein
CECT of PV tumor invasion
Lumen of vein may be expanded by thrombus
Variable degree of contrast enhancement of intraluminal tumor thrombus
Contiguity of parenchymal tumor with PV thrombus
Most often associated with hepatic cirrhosis and pancreatitis
Primary PV thrombosis may be 1st sign of hypercoagulable (prothrombotic) condition
PV tumor invasion (usually from hepatocellular carcinoma) is associated with poor clinical outcome
Primary PV thrombosis may mimic cirrhosis
Results in dysmorphic and malfunctioning liver
Often results from prothrombotic condition
Thrombosis or fibrosis of extrahepatic PV may complicate or preclude liver transplantation
Treatment: Anticoagulation for acute bland thrombosis or hypercoagulable condition
Add antibiotics for septic thrombophlebitis
Portal vein (PV) thrombosis
Acute, chronic, or neoplastic occlusion of PV due to thrombosis or tumor invasion
Chronic PV occlusion with numerous periportal collaterals is referred to as cavernous transformation
Best diagnostic clue
Low-attenuation thrombus in PV on CECT
On MR and power Doppler: Absence of blood flow or flow void in PV
May be caused or simulated by slow flow in portal hypertension
Nonvisualization of PV (chronic occlusion)
Cavernous transformation of PV (collateralization in porta hepatis)
Location
May involve any portion of intra- or extrahepatic PV
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