Color Doppler US initially: Highly accurate and cost effective
CT or MR: Complete evaluation and to search for cause
TOP DIFFERENTIAL DIAGNOSES
PATHOLOGY
•
Most often associated with hepatic cirrhosis and pancreatitis
•
Primary PV thrombosis may be 1st sign of hypercoagulable (prothrombotic) condition
CLINICAL ISSUES
•
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
•
Treatment: Anticoagulation for acute bland thrombosis or hypercoagulable condition
Add antibiotics for septic thrombophlebitis
DIAGNOSTIC CHECKLIST
•
Tumor thrombus expands lumen, enhances, and is contiguous with parenchymal mass
•
Thrombosis or fibrosis of extrahepatic portal vein may complicate or preclude liver transplantation
TERMINOLOGY
Synonyms
•
Portal vein thrombosis (PVT)
Definitions
•
Acute, chronic, or neoplastic occlusion of portal vein (PV) due to thrombosis or tumor invasion
•
Chronic PV occlusion with numerous periportal collaterals is referred to as “cavernous transformation”
IMAGING
General Features
•
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 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
CT Findings
•
CECT of acute thrombosis
Arterial phase (25-40 seconds post bolus injection)
–
High attenuation within involved hepatic lobe or segment due to arterioportal shunting
Transient hepatic attenuation difference (THAD)
Venous phase (60-70 seconds post bolus injection)
–
Equilibration of hepatic contrast enhancement
–
Visualization of low-density thrombus
Nonocclusive thrombosis: Low-density thrombus partially filling PV lumen
Occlusive thrombosis: Low-density thrombus filling PV lumen
–
Extent variable: May include major intrahepatic branches, splenic vein, superior mesenteric vein (SMV)
–
Congested (nonoccluded) mesenteric veins upstream from thrombus, mesenteric edema, bowel wall thickening from venous congestion
–
Ileus, ascites, and splenomegaly may be seen
•
CECT of chronic PV thrombosis
Chronic occlusion (cavernous transformation) of PV
–
Numerous periportal collateral veins along usual course of PV
–
Peripancreatic and gallbladder wall varices are common
Nonvisualization of PV &/or splenic vein
–
Thrombosed vein becomes fibrotic “cord” not visible on imaging
Well-developed portosystemic collaterals
–
e.g., splenorenal shunt; esophageal, periumbilical varices
Associated findings
–
Atrophy/hypertrophy complex
Usual pattern is hypertrophy of central (deep) segments, atrophy of peripheral segments
May impart lobulated or rounded contour to liver
–
Increased hepatic artery size &/or flow
•
CECT of PV tumor invasion
Lumen of vein may be expanded by thrombus
–
Main PV > 23 mm diameter
Variable degree of contrast enhancement of intraluminal tumor thrombus
–
Linear enhancing “threads and streaks”
Best seen on arterial phase of biphasic CECT
–
Primary tumor usually visible in hepatic parenchyma or pancreas, often in direct contiguity with thrombus
–
Commonly seen in hepatocellular carcinoma
–
Less common in pancreatic carcinoma, cholangiocarcinoma, endocrine tumor of pancreas, metastases
MR Findings
•
T1WI
High-signal filling defect
•
T2WI
High-signal acute or tumor thrombus
•
T2* GRE
PV tumor enhances avidly, especially on GRE sequences
•
T1WI C+ FS
Liver parenchyma supplied by thrombosed veins may enhance avidly in arterial phase due to increased hepatic artery flow
–
Transient hepatic intensity difference (THID)
Subacute thrombus hyperintense on T1 and T2 due to methemoglobin
Get Clinical Tree app for offline access