Portal vein Thrombosis

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Etiology :
Reduced portal blood flow because of hepatic parenchymal disease and abdominal sepsis are the major causes. With decompensated liver cirrhosis spontaneous bacterial peritonitis was diagnosed in 10 % of cases and portal thrombosis in 5 %of cases (2). Portal vein thrombosis can result from multiple causes :
* Causes secondary to a tumor - hepatocellular carcinoma, cholangiocarcinoma, pancreatic carcinoma, gastric carcinoma.
* Inflammation : pancreatitis, prenatal omphalitis, appendicitis, diverticulitis.
* cirrhosis.
* trauma
* Blood dyscrasia (4).
* Iatrogenic causes -
* Umbilical vein catheterization.
* Idiopathic causes.

Sonography :
Portal vein thromboses (PTV) is being recognized with increasing frequency at ultrasonography. Color Doppler can also be employed to detect portal venous flow, with parameters chosen to maximize sensitivity to slow flow by increasing Doppler gain, decreasing scale, and increasing sample volume. Reduced portal blood flow because of hepatic parenchymal disease and abdominal sepsis are the major causes. Transient PVT is also being recognized with increasing frequency, partly because of the great increase in the use of ultrasonography in the evaluation of patients with abdominal inflammation such as appendicitis. Tumor in the portal vein may have an appearance identical to that of thrombosis, but this appearance is far less common than others.
On sonograms, echogenic lesions may be present in the portal vein. Clot exhibits variable echogenicity. It is usually of moderate echogenicity but if recently formed it may be hypoechoic. Patent vessels may show increased intraluminal echogenicity because of erythrocyte rouleaux formation making slow-flowing blood slightly echogenic. Increased or decreased echogenicity within the lumen of portal vein in isolation is not sufficient to either diagnose or exclude portal vein thromboses. PVT eliminates the venous flow signal normally obtained from the lumen of the portal vein during either pulsed or color flow Doppler. Colour flow Doppler can show flow around a thrombus that partially blocks the vein, however if flow is sluggish Doppler signal may not be detected. There may be colour flow in other small vessel collaterals. Incomplete occlusion may occur with neoplasic invasion or thrombolytic recanalization. The two cannot be differentiated on ultrasound. Recanalization of periportal venous collaterals can occur, causing multiple serpiginous channels in the portal region (called "cavernous transformation of the portal vein" or "portal cavernoma"). The underlying cause (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 due to 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.
If the diagnosis of portal venous thrombosis has been made, the hepatic parenchyma should be closely scrutinized to exclude diffuse liver disease, hepatoma, or other focal lesion. The inferior vena cava, hepatic veins, and hepatic artery should also be assessed for patency.
* Portosystemic venous collaterals : the demonstration of portosystemic venous collaterals indicates the of portal hypertension or thrombosis: Sonography of portosystemic venous collaterals :
_ 1. Umbilical vein :Umbilical vein collateral flow is an important feature of portal hypertension or thrombosis.
_ 2. Coronary vein : The diameter of a normal coronary vein is up to 4 mm, whereas a diameter of greater than 7mm is evidence of an abnormal portal-systemic gradient. A coronary vein is seen as a prominent cephalad directed vessel that joins with the portal vein near the termination of the superior mesenteric vein.
_ 3.Splenosystemic collaterals : The demonstration of splenic vein occlusion by ultrasound is straightforward as it is possible in most subjects to trace the splenic vein to the portal vein. With splenic vein occlusion, collaterals may be identified in the pancreatic bed or the gastro-esophageal area.
_ 4. Splenorenal veins : Tortuous inferiorly directed vessels from the splenic hilum to the left kidney, primarily seen on coronal images. The left renal vein may be dilated.
_ 5. Short gastric and gastro-esophageal veins : Tortuous vessels near the tipper pole of the spleen and gastro-esophageal junction are seen primarily on coronal images.
_ 6. Right gastric veins : These vessels are cephalad directed, and seen along the inferior border of the left lobe of the liver on longitudinal scans.
* Cavernous transformation of the portal vein : Cavernous transformation of the portal vein occurs with long-standing portal vein thromboses because of the development of multiple small vessels in and around the recanalizing portal vein. A leash of fine serpiginous vessels is seen in place of the portal vein. The application of colour or pulsed Doppler shows blood flow in these periportal collaterals around the thrombosed portal vein or replacing the vein.

Differential :
Portal vein thrombosis which occurs in the course of cirrhosis, associated or not with hepatocellular carcinoma, can be either cruoric or neoplastic. ultrasound guided biopsy of the portal thrombus provided a definitive diagnosis (7).

Treatment :
The development of PVT can precipitate the need for emergency endoscopy for sclerotherapy of varices, TIPS creation (5), surgical portocaval shunt creation (3), transjugular or transhepatic portomesenteric thrombolysis and thrombectomy, or even resection of ischemic bowel or liver transplantation. However, PVT may complicate sclerotherapy. Fine-needle aspiration biopsy of PVT can be performed with color Doppler sonographic guidance to assess therapeutic effectiveness and to to exclude the presence of a vascular neoplasic extension (7).

Reference :
* 1: Wang MC, Li S, Zhu JY, Leng XS, Du RY. [The reason and treatment of portal vein thrombosis in patients with portal hypertension postoperation] Zhonghua Wai Ke Za Zhi. 2004 Mar 7;42(5):269-71. Chinese.
* 2: Russo G, Giolitto G, Felaco FM, Pasquale G, Galante D, Gaeta GB. [Spontaneous bacterial peritonitis in patients with liver cirrhosis. Differential aspects with portal thrombosis] Infez Med. 1997;5(3):174-7. Italian.
* 3: Audet M, Baiocchi GL, Portolani N, Becmeur F, Caga M, Giulini SM, Cinqualbre J, Jaeck D, Wolf P. A surgical solution to extrahepatic portal thrombosis and portal cavernoma: the splanchnic-intrahepatic portal bypass. Dig Liver Dis. 2003 Dec;35(12):903-6.
* 4: Cavaliere G, Leanza A, Mirabella C, Rapisarda A, Meli S, Noto P, Zingali C, Pepi F, Noto R. Dangerous thrombophilic states and internal pathologies: 3 cases of thrombosis of the abdominal veins. Eur Rev Med Pharmacol Sci. 2001 Sep-Dec;5(5-6):167-72.
* 5: Stein M, Link DP. Symptomatic spleno-mesenteric-portal venous thrombosis: recanalization and reconstruction with endovascular stents. J Vasc Interv Radiol. 1999 Mar;10(3):363-71.
* 6: Valeri A, Venneri F, Presenti L, Nardi F, Grossi A, Borrelli D. Portal thrombosis. A rare complication of laparoscopic splenectomy. Surg Endosc. 1998 Sep;12(9):1173-6.
* 7: Duchmann JC, Joly JP, Biny JP, Sevestre H, Capron JP. [Portal thrombosis and liver cirrhosis. Value of ultrasound-guided puncture-biopsy of the thrombus] Gastroenterol Clin Biol. 1995 Jun-Jul;19(6-7):581-6. French.
* 8: Giordano G, Angelelli G, Margari A, Mustacchio N, Scattarella M, Macarini L, Cannone G, Ialongo P. [Portal thrombosis: the diagnostic and therapeutic aspects and clinical cases] G Chir. 1994 May;15(5):247-54. Italian.