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PORTAL VEIN THROMBOSIS 63 yr male with multiple well defined round to oval shaped lesions with variable sizes studding the Rt lobe of the liver ( especially the segment 6 and 7 of the liver ) . The echo pattern of these lesions is heterogeneous – primarily Hyperechoic at places. The largest of all the lesions measures 53mmx 48mmx 56mm in size ( seen in the segment 6/7 of the liver ) . Note is made of prominent main portal vein with intraluminal thrombus in the main portal vein extending to the left and Rt branches also . Periportal collaterals are appreciated on color Doppler. MERCURY IMAGING INSTITUTE SCO 172-173 SEC 9C CHANDIGARH MERCURY IMAGING CENTRE SCO 16-17 SEC 20D CHANDIGARH

Portal vein thrombosis

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Page 1: Portal vein thrombosis

PORTAL VEIN THROMBOSIS

63 yr male with multiple well defined round to oval shaped lesions with variable sizes studding the Rt lobe of the liver ( especially the segment 6 and 7 of the liver ) . The echo pattern of these lesions is heterogeneous – primarily Hyperechoic at places. The largest of all the lesions measures 53mmx 48mmx 56mm in size ( seen in the segment 6/7 of the liver ) . Note is made of prominent main portal vein with intraluminal thrombus in the main portal vein extending to the left and Rt branches also . Periportal collaterals are appreciated on color Doppler.

MERCURY IMAGING INSTITUTE

SCO 172-173 SEC 9C CHANDIGARH

MERCURY IMAGING CENTRE SCO 16-17 SEC 20D

CHANDIGARH

Page 2: Portal vein thrombosis

Dilated main portal vein with intraluminal thrmobus with intermediate to hyperechoic echopattern suggestive of

subacute stage thrombus .

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Serpigenous tracts along the periphery of the intraluminal thrombus – ? Partially patent lumen / recanallization..

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Thrombus extending to the left main branch and more vertically oriented left lobe branches .

Page 5: Portal vein thrombosis

Serpigenous tracts along the periphery of the intraluminal thrombus – ? Partially patent lumen / recanallization..

Page 6: Portal vein thrombosis

PORTAL VEIN THROMBOSIS

ETIOLOGY :• Reduced portal blood flow caused

by hepatic parenchymal disease and abdominal sepsis (ie, infectious or ascending thrombophlebitis) are the major causes.

• Transient PVT is also being recognized with abdominal inflammation such as appendicitis

• Hypercoagulable syndromes can lead to portomesenteric and splenic vein thrombosis.

BRIEF ANATOMY :• Generally, the portal vein enters the

porta hepatis and divides into the right and left main branches. The right main branch divides into anterior and posterior branches that supply the anterior and posterior segments of the right lobe. The left main branch courses horizontally to the left before turning vertically to form the medial and lateral segmental branches.

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Points to remember................• Tumor in the portal vein may

have an appearance identical to that of thrombosis, but this appearance is far less common than others. Tumor in the portal vein is most frequently related to HCC.The thrombus may be partial or complete. It may be mixed with bland thrombus as well.

• Adults who have acute PVT secondary to abdominal sepsis may completely recover, and the vessel may recanalize with successful treatment of the underlying sepsis.

• In children, the portal vein may recanalize with the development of multiple, small, collateral channels. These channels are seen as a partly echogenic band of small vessels extending to the porta hepatis (cavernous transformation). These have a reduced flow velocity of 2-7 cm/s. Nonvisualization of the portal vein is strongly suggestive of occlusion. The portal vein may then be seen as a band of high-level echoes at the porta hepatis.

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RADIOGRAPH

• Hepatosplenomegaly • Enlarged azygos vein.• Para spinal varices .

CONVENTIONAL RADIOGRAPHS CAN HELP TO ASSESS THE FOLLOWING OBSERVATIONS …….

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USG

• On sonograms, echogenic lesions may be present in the portal vein. Clot with variable echogenicity may be depicted. The clot usually has moderate echogenicity, but if it is recently formed, it may be hypoechoic. Patent vessels may have increased intraluminal echogenicity because of erythrocyte rouleaux formation, which makes slow-flowing blood slightly echogenic. Increased or decreased echogenicity may be observed in the lumen of the portal vein. In isolation, this finding is not sufficient to diagnose or exclude PVT.

• PVT eliminates the usual venous flow signal from the lumen of the portal vein during either pulsed or color flow Doppler imaging. Color flow Doppler images can show flow around a thrombus that partially blocks the vein. However, if flow is sluggish, the Doppler signal may not be detected. Color flow may be present in other small collateral vessels.

• Incomplete occlusion may occur. This is common with neoplastic invasion. Alternatively, thrombolytic recanalization may occur. The two cannot be differentiated on sonograms. Cavernous malformation, spontaneous shunts, and splenorenal and portosystemic collaterals may be seen. The underlying cause (eg, hepatocellular carcinoma, metastases, cirrhosis, pancreatic neoplasms) may be evident. The incidence of PVT is reported to be low in portal hypertension.

• The string sign—that is, thickening of the portal vein with narrowing of its lumen—is assumed to be caused by portal phlebitis. This is considered a precursor of PVT in patients with acute pancreatitis. The portal vein thrombus may be calcified. The diameter of the portal vein is larger than 15 mm in 38% of the cases of PVT.

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CT• On contrast-enhanced CT scans, PVT may be

depicted as a low-attenuating center in the portal vein surrounded by peripheral enhancement. Portal vein attenuation is 20-30 HU less than that of the aorta.

• CT angiography (CTA) is an application of helical CT. The rapidity of helical CT allows the maintenance of a higher concentration of intravenous contrast medium, particularly through the arterial enhancement phase, and it has the capability of 3-dimensional (3D) reconstruction. Both peripheral intravenous injections of contrast agent and CT arterial portography have been used as with CTA. CTA has shown great promise in the evaluation of hepatic vessels before liver resection. It provides preoperative surgical information about the segmental location of liver tumors, the segmental venous anatomy, and the presence of significant arterial anomalies. The value of CTA in the evaluation of portal hypertension is unclear, but CTA is likely to be useful because it may delineate the collateral vessels, varices, and other findings in patients with portal hypertension.

• The portal vein supplies 75% of the blood flow to the liver. Therefore, peak liver contrast enhancement occurs during the portal venous phase, about 60 seconds after the start of a bolus injection of contrast material.With helical CT, a liver examination requires about 20 seconds to complete; images can usually be acquired in one breath hold.[18]

• This technique can be extended to acquire a dual-phase contrast-enhanced CT scan in which the liver is imaged twice with a single contrast agent bolus, first during the arterial phase and then through portal venous phase. Dual-phase CT is indicated in some cases involving benign or malignant lesions in which vascular characteristics suggest the correct diagnosis (see the images below).

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MRI• The vascular anatomy of the liver may be

outlined by using spin-echo and gradient-recalled-echo (GRE) techniques, but these techniques cannot demonstrate the direction of portal flow. Time-of-flight MRI with bolus tracking has been successful in the assessment of portal hypertension and its squeal. Phase-contrast sequences can also be used to evaluate the portal vein, and phase-contrast cine MRA can show the direction of portal venous flow and the presence of portal vein thrombus. Magnetic resonance evaluation of the portal venous system accurately demonstrates thrombosis and the collateral circulation. Gadolinium enhancement is useful in this application (see the images below).

• MRCP coupled with dynamic 3D gradient-echo imaging can not only detect portal vein occlusion, cavernous transformation, and gallbladder varices but also depict bile duct abnormalities associated with portal biliopathy.