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Ultrasound of portal hypertension
Sharlene A. Teefey, MD, FACR Professor of Radiology
Mallinckrodt Institute of Radiology
Washington University School of Medicine
Saint Louis, Missouri
Financial disclosures:
Royalties - Elsiever pub. co.
NIH Grants
Portal Hypertension
Common and less common causes:
Cirrhosis
Cavernous transformation
Budd-Chiari Syndrome
Portal hypertension
- Causes classified according to:
- Primary increased resistance
- Prehepatic
- Intrahepatic
- Posthepatic
- Primary increased flow
Primary increased resistance
- Prehepatic
- PV/SV thrombosis, extrinsic compression of PV
- Intrahepatic
- Presinusoidal*
- Schistosomiasis, sarcoidosis, myeloproliferative diseases, PBC/PSC, toxins
Early in course → progress to sinusoidal*
- Sinusoidal/mixed
- Alcoholic cirrhosis, cirrhosis 2°chronic hepatitis B/C, cryptogenic cirrhosis
- Post sinusoidal
- VOD, HV obstruction (Budd-Chiari)
- Post hepatic
- Constrictive pericarditis, IVC web, severe right heart failure, tricuspid regurgitation
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Primary increased flow
- Arterioportal fistula
- Congenital, post-traumatic, erosion of HA aneurysm into portal vein
- Splenomegaly
- Myelofibrosis
Pathogenesis of portal hypertension
(model: alcoholic cirrhosis)
- Architectural derangement
- Fibrosis, regenerative nodules
- Sinusoidal changes
- Hepatocyte enlargement from alcohol-induced protein and fat deposition
- Compression of sinusoids
- Vasoactive factors
- Vasoconstrictors
- Endothelin, Thromboxane 2
- ↑ production in cirrhosis
- Vasodilators
- Nitric oxide
- ↓ production in cirrhosis
- Imbalance contributes to portal hypertension
Duplex/color Doppler - portal vein
- Hepatofugal flow (main, right, or left)
- Slow, bidirectional flow (alternating hepatopetal and hepatofugal)
- Static blood flow
Ralls, Radiology 1990; 155:517-525
Hepatofugal flow Hepatofugal flow - RPV
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Bidirectional flow Static flow
Duplex/color Doppler - hepatic artery
- Enlarged, tortuous
- High peak systolic and diastolic velocities
- Hepatic arterial buffer response
- Advanced cirrhosis with decreased portal flow
Enlarged HA
Duplex/color Doppler - hepatic veins
- Monophasic
- Loose normal phasicity
- ↑ resistance to transmission of right atrial pressures 2° focal hepatic vein stenoses
Lorenz, JUM 1996; 15:313-316
HV stenosis
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HV stenosis Portosystemic collaterals
- Tributary collaterals
- Normally existing vessels
- Coronary (L gastric), short gastrics, SMV, IMV
Normal coronary vein
PV
Sag.
Coronary veins
Coronary veins
Splenic vein thrombosis
sag.
Short gastric veins
stomach
tr.
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Splenic vein thrombosis
Short gastric veins Portosystemic collaterals
- Developed collaterals
- Normally closed channels
- Spleno-retroperitoneal,paraumbilical,spleno-renal
Recanalized paraumb. vein Splenorenal shunt
Splenorenal shunt Splenoretroperitoneal shunt
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Cavernous transformation
- Formation of portoportal collaterals in the setting of acquired, benign PV thrombosis
- Unusual in setting of cirrhosis
- Unusual in presence of neoplasm
- Causes pre-hepatic portal hypertension
- Develops 6-20 days after thrombosis
- Origin of collateral vessels
- Paracholedochal (adjacent) and epicholedochal (intramural) veins
- Pancreatico-duodenal veins originating at pancreatic head
- Vasa vasorum of PV wall
- Recanalized channels in PV
DeGaetano, AJR 1995; 165:1151-1155Walser, Radiology 2011; 258:146-153
Duplex/color Doppler - portal vein
- Non-visualization
- Multiple periportal collateral vessels
- Intrahepatic extension around thrombosed PV branches
- Portal vein-like waveform
DeGaetano, AJR 1995; 165:1151-1155
Cavernous transformation
Cavernous transformation
Paracholedochal veinsDstl CBD stricture
- Two types of venous collaterals
- Portosystemic collaterals
- Left gastric, perisplenic veins
- Portoportal collaterals
- Intrahepatic
- Pericholecystic
- Shunt blood into a patent right portal vein branch
DeGaetano, AJR 1995; 165:1151-1155
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Pericholecystic veins
Cavernous transformationBudd Chiari syndrome
- Intrahepatic HV thrombosis
- Hypercoagulable states
- Myeloproliferative disorder,antiphospholipid syndrome, factor V leiden mutation, PNH, protein S/C deficiencies, BCP
- Causes post-sinusoidal portal hyperstnsion
- IVC thrombosis (hepatic portion)
- Idiopathic (most common)
- Poor standard of living, inf.?
- Diaphragm motion → injury
- Hypercoagulable state
- Secondary
- Extrinsic compression
- Abscess, hydatid cyst
- Invasion by neoplasm
- HCC, RCC, adrenal carcinoma Okuda, Hepatology 1998; 28:1191-1198
- Fulminant/acute- Visible thrombus
- Obstructive or nonobstructive- No collateral vessels
- Subacute- Collateral vessels
- Chronic- Nonvisualization of hepatic veins- Collateral vessels
Noone, J of MR imag. 2000;11: 44-50
Duplex/color Doppler - hepatic veins
- Collateral vessels
- Intrahepatic
- Occluded HV → patent HV
- Occluded HV → right inferior HV
- Occluded HV → collateral
- Tortuous, comma-shaped
- Flow reversal
- Monophasic waveform
- Caudate veins → IVC
- Subcapsular
- L inferior phrenic vein → SVC
- Extrahepatic
- IVC → azygos system
- Left renal vein → hemiazygos
- Left renal vein → L inferior phrenic vein → SVC
- Superficial abdominal wall
- Inferior epigastric vein → subclavian vein → SVC
Cho, AJR 1996; 167:1163-1167
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Budd-Chiari syndrome Budd-Chiari syndrome
Budd-Chiari syndromeUS plays an important role in the evaluation of the patient with portal hypertension
Findings can have a major influence on patient management