Portal vein thrombosis (PVT)
PVT is a major cause of non-cirrhotic portal hypertension. PVT may be bland or malignant. If extensive acute thrombosis is present, and especially if the superior mesenteric venous system is also involved then presentation is likely to be with acute ischemic bowel, mimicking SMA occlusion. PVT, like thrombosis elsewhere, can occur due to disturbance of any one of Virchow’s triad, and causes can be thought of in these terms: 1-reduced flow or portal hypertension due to cirrhosis most common. 2- hypercoagulable state as inherited prothrombotic conditions (protein S deficiency, protein C deficiency). 3- endothelial disturbance due to local inflammation/infection as in acute pancreatitis or ascending cholangitis. In addition, HCC has a predilection to invade the portal vein, with tumor thrombus occluding the lumen.
Radiographic features: Acutely only the thrombus may be evident, with associated findings related to ischemic bowel (especially if superior mesenteric vein is involvemed as well). In chronic cases, cavernous transformation of portal vein may be seen, with numerous periportal veins replacing the normal single channel of portal vein. US: Acute thrombosis may be difficult to detect with grey-scale as the thrombus may be hypoechoic. With time it becomes more echogenic and easier to detect. Color doppler is able to demonstrate absent flow in portal vein and even detect partial thrombosis.
The SMV, intrahepatic branches of portal vein, and hepatic veins should also be examined, to assess extent of thrombosis (note: 20% of patients with Budd-Chiari syndrome will also have PVT). Colour Doppler helps to evaluate for tumor thrombus, which will show internal color vascularity. Bland thrombus, in comparison, is bland on colour Doppler.
NECT scans are usually incapable of demonstrating the thrombus, except is some acute cases where the thrombus is hyperattenuating. In longstanding cases, low density change in the liver may be evident, related to increased arterial supply, and representing fatty change.
The diagnosis can reliably be made on portal venous phase contrast enhanced CT studies. Findings: complete or partial NON-opacification of part of, or the whole portal vein. Enhancement of the walls of the portal vein thought to represent either dilated vasa vasorum or a thin peripheral lumen remaining patent. If enhancement of thrombus is present then this suggests that the thrombus is not bland but represents tumour thrombus, frequently from HCC. Cavernous transformation appears as multiple small periportal vessels, which represent dilated collateral veins. findings of portal hypertension may be evident.
MRI: 3D contrast enhanced MRA is the most sensitive modality (98% sensitive and 99% specific) for demonstrating portal venous thrombosis. T1: acute thrombus will have high SI. T2: acute thrombus may have high SI. chronic thrombus may be low SI on T2. Tumour thrombus is hyperintense on T2. T1 + Gad: Tumour thrombus enhances.
18F-FDG PET/CT: ability to differentiate between bland thrombus and malignant portal vein thrombosis. bland thrombus = no FDG-avidity, tumour thrombus moderately to highly FDG-avid. possible visualization of further sites of thrombosis.