Portal Vein Thrombosis (PTV) is often not discovered until gastrointestinal
hemorrhage develops, unless the thrombosis is discovered during
routine surveillance for a known underlying pathologic condition.
The primary diagnostic procedure however remains color-Doppler ultrasonography
which represents the most simple and the cheapest diagnostic investigation
for the study of the portal and suprahepatic vein system (4).
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,
* Blood dyscrasia (4).
* Iatrogenic causes -
* Umbilical vein catheterization.
* Idiopathic causes.
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
* 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
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).
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
* 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.
* 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.