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July 2009 Case of the Month
Compiled by: SalvadorB. Trinidad, M.D.
History: A 58-year-old male with hepatitis C and rising alpha-fetoprotein
Exam: MRI of the liver was performed. T1, T2, and T2 fat-suppressed sequences were performed in multiple planes with and without Gadolinium. Arrows denote lesions. A CT of the liver post-intravenous contrast, on a different patient was also provided for completeness.
Findings:
On the axial T1 (Fig. 1),“A” denotes a low-signal tubular structure conforming to the portal vein.
On the axial T2 (Fig. 2),“O” denotes an intermediate- to low-signal tubular structure conforming to the portal vein.
On the axial STIR (Fig. 3),“C” denotes a high-signal tubular structure conforming to the portal vein.
On the coronal T1 (Fig. 4), “F” and “G” denotes a intermediate- to low-signal tubular structure conforming to the portal vein.
On the axial post-contrast CT of a different patient (Fig. 5), “H” denotes a low- density tubular structure conforming to the portal vein.
On the coronal post-contrast CT of a different patient (Fig. 6),“J” denotes a low- density tubular structure conforming to the portal vein.
Figure 1
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Figure 2
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Figure 3
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Figure 4
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Figure 5
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Figure 6
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Diagnosis: Acute portal vein trombosis.
Discussion:The portal vein is formed from the confluence of the splenic vein and the superior mesenteric vein. Approximately 75% of the blood supply to the liver is from the portal venous system. The remaining 25% is from the hepatic artery. In portal vein thrombosis, the hepatic artery becomes an important hepatic blood supply.
Portal vein thrombosis has a variety of causes. It may be caused by venous stasis from liver disease, such as cirrhosis or extrinsic compression of the portal vein. Tumors such as hepatocellular, cholangiocarcinoma, and metastasis may directly invade the portal vein. Thrombus from the SMV or splenic vein also may propagate into the portal vein.
Inherited and acquired disorders of the coagulation pathway are also important etiologies of portal vein thrombosis.Protein C and S disorders are inherited. Acquired disorders include antithrombin III deficiency, and malnutrition or any other etiology of an increased thrombogenic state may lead to portal vein thrombosis.
Chronic portal vein thrombosis leads to portal venous hypertension with development of collateral circulation. Variceal bleeding is one of the most serious and life-threatening complications.
Treatment: Supportive care as well as anticoagulation is the primary treatment. Acute thrombosis may be treated with thrombolyitics.
References:
1. Albertyn LE. “Acute portal vein thrombosis.” Clin Radiol, Nov. 1987; 38(6):645-8.
Cohen J, Edelman RR, Chopra S. “Portal vein thrombosis: A review.” Am J Med, Feb. 1992; 92(2):173-82.
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