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Page 2 of 13 Yang et al. Hepatoma Res 2020;6:37 I http://dx.doi.org/10.20517/2394-5079.2020.09

RISK FACTORS
Hemodynamic changes
Hemodynamic changes are considered to be the most important risk factor in the pathogenesis of PVT. The
formation of pseudolobules in the liver can reduce portal blood flow velocity markedly, causing obstructed
[8]
portal blood flow, increased portal pressure, and decreased blood flow velocity . It can be said that the
hemodynamic changes caused by the primary disease lays the foundation for the development of PVT.

Splenic vein diameter (SVD) is thought to be the most influential risk factor. A retrospective trail conducted
[9]
in China found that 8 factors including the SVD are associated with postoperative PVT formation . SVD
greater than 10 mm has been a cut-off for predictors of PVT development and those greater than 14 mm has
[10]
been a cut-off for predictors of PVT which develops from splenic vein . Some authors even suggest that
[11]
preoperative SVD greater than 8 mm is an independent risk factor for predicting PVT . SVD is inversely
related to the rate of change in portal blood flow, and its sensitivity, specificity and efficiency vary with the
[6]
study’s setting . In addition, spleen weight, discussed below, shows a significant correlation with SVD, where
removal of an enlarged spleen may cause a sudden decrease in splenic vein flow, forming and pushing the
thrombus to migrate to the portal vein. But compared with the weight of the spleen, SVD plays a greater
role in predicting PVT. Some researchers recommend the measurement of SVD preoperatively, and a close
[12]
follow-up of patients with SVD greater than 8 mm .
Generally, for patients with decompensated cirrhosis, PVD is proportional to the degree of portal hypertension,
and once it is determined that PVD is greater than 13 mm, portal hypertension is considered to exist,
[9]
and PVD is the independent risk factor of PVT . Multivariate analysis in some studies certify the significant
relationship between pathogenesis of PVT and a series factors, including wider preoperative PVD, of which
[13]
the cut-off width was determined to be 13 mm . Similarly, in another study, the incidence of PVT in
[14]
patients with a PVD > 13 mm was 35 times that of others with PVD < 13 mm . When PVD becomes larger,
blood flow velocity decreases, and the formation of blood clot is easier.

But some researchers believe that portal blood flow velocity is the only independent risk factor for
[15]
PVT formation, and when velocity is lower than 15 cm/s, the risk of PVT increases significantly . By
dividing cirrhotic patients into two groups according to portal vein flow velocity (≤ 15 cm/s or > 15 cm/s),
the incidence of PVT within one year after surgery for the two groups turns out to be 47.8% and 2.0%,
[14]
respectively . In a study examining the risk factors of PVT after the Hassab procedure, the cut-off points
[16]
for portal vein flow, SVD and PVD were 1822.32 mL/min, 1.37 cm, and 1.56 cm, respectively . Besides,
varicose veins of the esophagus and stomach caused by portal hypertension are also independently associated
[17]
with the development of PVT , and the wider portal collaterals can shunt more blood from the portal
[14]
vein, slowing portal vein blood flow, and may increase the risk of PVT . Slow blood flow not only causes
[18]
the procoagulant substances in the blood to be slowly concentrated locally , but also causes an increase
in pressure on the blood vessel wall according to Bernoulli’s principle, which will damage the endothelial
cells and initiate the coagulation mechanism [3,19] . Therefore, it can be concluded that the wider PVD and
SVD, the slower the blood flow of the portal vein system after operation and the greater the possibility of
[20]
thrombosis .

Splenomegaly
Splenomegaly is common in patients with liver cirrhosis, and patients with splenomegaly are at high
risk of PVT; splenomegaly was previously thought to be related to passive congestion caused by portal
[21]
hypertension . However, there is no necessary correlation between portal vein pressure and spleen size,
because the grown spleen does not retract, and hypersplenism is not relieved after transjugular intrahepatic
[22]
portal body shunt (TIPS) or splenorenal shunt . During years of follow-up of liver transplant recipients,
[22]
portal pressure remained normal, but spleen enlargement persisted . Despite that passive congestion may