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Page 4 of 13 Yang et al. Hepatoma Res 2020;6:37 I http://dx.doi.org/10.20517/2394-5079.2020.09

study revealed that PVT occurred in 12 (55%) patients of the LS group, but in only 4 (19%) of the open
splenectomy group, and that LS leads to a higher incidence rate of PVT than does open splenectomy [39,40] .
Due to hypercapnia caused by CO , blood viscosity increases; in addition, blood flow velocity decreases with
2
the positive pressure caused by pneumoperitoneum during the laparoscopic operation [13,41] . Consequently,
[42]
from a certain perspective, open surgery has a relative preventive effect on PVT itself compared with LS .

Coagulation and anticoagulation disorder
In the coagulation system of patients with liver cirrhosis, procoagulant factors and anticoagulant factors
[43]
are in a dangerous equilibrium ; they are too complex and delicate to strike a balance: bleeding or
[45]
[44]
thrombosis , which may be disrupted by splenectomy, infection, acute renal failure, etc. . Patients with
cirrhosis are not sensitive or even resistant to thrombomodulin, and the blood coagulation state is higher
[46]
in patients with Child-Pugh C than in patients with A or B . It has been reported that a decrease in the
levels of anticoagulant protein C and protein S can promote the pathogenesis of thrombosis, and in cirrhosis,
the synthesis of protein C and S is impaired, so as cirrhosis worsens, factor VIII (procoagulant) increases,
[46]
while protein C, one of the anticoagulants decreases ; increased levels of factor VIII and decreased levels
[47]
of protein C may be the major factors for PVT . However, protein C and protein S in PVT might not be
associated with PVT in liver cirrhosis, especially when the impact of liver function is excluded [48,49] .

Preoperative antithrombin III (AT-III) is an important risk factor for PVT, where the synthesis of it is
reduced because of cirrhosis, and it is further reduced after splenectomy, leading to overconsumption
of anticoagulants [50,51] . Some authors have demonstrated that prophylaxis with AT-III concentrates and
[51]
danaparoid sodium after splenectomy can dramatically reduce the incidence of PVT .
Prolonged prothrombin time (PT) is thought to be an independent factor in the occurrence of postoperative
[29]
PVT , but other researchers hold a different opinion that the formation of PVT has nothing to do with
[52]
PT , which may be so because traditional coagulation indicators do not reflect the true coagulation status
[53]
of patients with liver cirrhosis .
[54]
Fibrinogen can participate in the development of thrombosis , and increased fibrinogen indicates a
[55]
decrease in fibrinolytic activity and increases the incidence of thrombus .
Liver cirrhosis
[56]
Different causes of liver cirrhosis lead to different PVT risks . As decreased liver synthesis results in
hypoproteinemia, extravasation of plasma water, and hypercoagulable blood concentration, it is easy to
[57]
form thrombus in the portal vein system . Because of the special pathophysiology of patients with liver
[58]
cirrhosis, the incidence of PVT after splenectomy is higher . A study showed that the incidence of PVT
[59]
in patients with and without cirrhosis was 32.0% and 9.5% . Liver dysfunction can affect the formation of
[51]
PVT by affecting the synthesis of coagulation factors, thrombin, albumin, etc. . Studies show that Child-
[60]
Pugh scores are significantly higher in patients with postoperative PVT than in patients without PVT .
[15]
Meanwhile, incidence of PVT increases when MELD score is ≥ 13 points . Studies have shown the portal
[41]
vein system rapidly forms a thrombus long before the improvement of liver function after splenectomy ,
and some authors believe that traditional serological indicators (ALT, AST, etc.) have no relationship with
[52]
PVT formation , but ascites may be an important predictor of PVT, and albumin and hemoglobin decrease
in cirrhotic patients significantly, which have potential value for the prediction [18,61] .
[17]
The occurrence and development of PVT has been shown to be related to the degree of esophageal varices ,
which is caused by portal hypertension. Another study showed that the portal venous blood flow velocity in
the severe gastroesophageal varices group was (12.13 ± 2.59) cm/s, while in the non-severe gastroesophageal
[62]
varices group, velocity was (15.26 ± 5.06) cm/s . As is known to all, cirrhosis is an irreversible disease that