Clinics and Research in Hepatology and Gastroenterology
Pictorial reviewCT features of non-malignant portal vein thrombosis: A pictorial review
Introduction
The portal venous system provides three quarters of the blood to the liver, which is composed of the portal vein and its tributes (i.e. superior and inferior mesenteric veins, splenic vein, left and right gastric veins, paraumbilical vein, and cystic veins) [1], [2]. The linchpin of this system is the portal vein that situates in the posterior of the pancreas. The diameter of the portal vein is 10 to 13 mm, and the length is 50 to 90 mm. The portal vein originates from the confluence of the superior mesenteric vein and splenic vein, and often divides into the right and left portal vein branches in the liver hilum, ultimately ending at the hepatic sinusoids.
Portal vein thrombosis (PVT) is characterized by the formation of thrombus within the portal trunk, with or without the extension of thrombus into the intrahepatic portal vein branches, splenic vein or mesenteric veins [3], [4]. It is a rare clinical entity in general population (the annual incidence is estimated at less than 4/1,000,000 [5]), but a relatively frequent entity in liver cirrhosis (the prevalence is 5 to 20% [6], and the incidence of de novo PVT is 8 to 16% per year [7], [8], [9], [10]). Common causes of PVT include a combination of various risk factors, such as inherited or acquired prothrombotic disorders, other thrombophilic factors, and local risk factors [3], [4], [11]. Severe PVT-related complications are potentially lethal, such as ischemic intestinal infarction as acute thrombus extends to the mesenteric venous arch, and massive variceal bleeding as long-standing PVT leads to presinusoidal portal hypertension [3]. On the other hand, occlusive PVT can greatly change the natural history of cirrhotic patients [12], [13], because it can not only increase the incidence of variceal rebleeding [14], but also significantly decrease the cirrhotic patients’ survival [15]. Based on the clinical significance of PVT, early diagnosis is very critical to allow for rapid establishment of appropriate treatment and its resultant improvement of prognosis [16]. In current clinical practice, dynamic contrast-enhanced CT scan has been regarded as an accurate and convenient diagnostic modality of PVT and its associated abnormalities [11], [17].
Given that the pathogenesis, treatment selection, and prognosis are significantly different between malignant and benign patients [18], malignant PVT will not be discussed in the paper. Previous studies have demonstrated four major CT characteristics to distinguish malignant from benign nature of PVT, as follows:
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direct tumor invasion into the portal vein;
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neovascularity of the thrombus in the arterial phase;
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disruption of vessel walls;
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portal vein diameter greater than 23 mm [19], [20]. Thus, the pictorial review aims to illustrate various CT features of non-malignant PVT with special emphasis on the evolution of PVT, CT signs of portal hypertension, and abnormalities of hepatic perfusion and morphology.
Section snippets
Evolution of portal vein thrombosis
The development of PVT is a dynamic process from recent thrombus to cavernous transformation of the portal vein in a few days [21], [22] (Fig. 1), from partial obstruction, to complete obstruction and to fibrotic cord [23] (Fig. 2), and with increased extent of involvement of intrahepatic and extrahepatic portal venous system occlusion. But several sporadic cases have reported spontaneous resolution of the occluded portal vein or superior mesenteric vein in the absence of anticoagulant or
Signs of portal hypertension
The main complication of long-standing PVT is presinusoidal portal hypertension. As portal pressure is severely increased, the spleen is enlarged (Fig. 5) and collateral veins can develop within the walls or at the periphery of the structures adjacent to the obstructed portion of the portal vein [3], such as oesophagus (Fig. 6), gastric fundus (Fig. 7), duodenum (Fig. 7), bile duct (Fig. 8), gallbladder (Fig. 6), and pancreas (Fig. 4). In the absence of underlying hepatic disease, the umbilical
Abnormalities of hepatic perfusion and morphology
The portal vein and hepatic artery account for nearly all of the blood supply to the liver. In the early stages of PVT, portal venous perfusion of the liver is significantly decreased. As a response to a decreased portal vein flow, hepatic arterial bed is immediately dilated in the lobar in which the intrahepatic portal vein branch is occluded [3]. Thus, the irregular intrahepatic distribution of arterial blood can be only detected in the arterial phase of contrast-enhanced CT scans, but not in
Conclusion
In conclusion, dynamic CT scans play several important roles in the diagnosis and assessment of non-malignant PVT, including:
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to promptly establish a diagnosis of PVT;
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to assess whether thrombus was extended to the splenic vein and superior mesenteric vein;
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to evaluate the degree of PVT (partial obstruction, complete obstruction, or fibrotic cord);
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to distinguish the stage of PVT (acute or chronic stage);
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to observe hepatic perfusion and morphology abnormalities;
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to exclude the neoplastic obstruction;
Disclosure of interest
The authors declare that they have no conflict of interest concerning this article.
Acknowledgement
None.
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