Analysis of Related Influencing Factors of Portal Vein Thrombosis After Hepatectomy

Introduction

Hepatectomy is still the standard treatment for benign and malignant primary liver disease and metastatic diseases such as colorectal cancer.^1,2 Portal vein thrombosis (PVT) refers to thrombosis occurring in the main portal vein and/or its left and right branches, with or without mesenteric vein and splenic vein thrombosis. ³ PVT (posthepatectomy portal vein thrombosis) after hepatectomy has many risk factors, concealed onset, but no specific clinical manifestations in the early stage, some patients do not have any symptoms and signs, and early diagnosis is difficult. At present, there is a lack of clear guidelines in treatment, and the fatality rate is high.^4,5

Additionally, there are few studies on PVT after hepatectomy, so the prevention and treatment of PVT after hepatectomy is particularly important.^6,7 This study included 1029 patients who underwent hepatectomy in our hospital from March 2018 to March 2023. The related factors of PVT after hepatectomy were analyzed, and the treatment experience was summarized to promote the prognosis of patients after hepatectomy.

Materials and Methods

Results

Discussion

PVT after hepatectomy is a serious complication. If not treated in time, PVT will spread along the portal vein system, resulting in serious complications such as portal hypertension, liver failure, intestinal congestion and necrosis, abdominal bleeding and even death.^6,8 Therefore, it is of great significance to study the related factors of PVT after hepatectomy. The results of this study showed that the incidence of PVT was 2.33%, which was relatively low compared with domestic and foreign studies. The incidence of PVT was less reported in domestic literatures, ranging from 0.21% to 24.72%,^9,10 and that of foreign countries, ranging from 2.1% to 20.0%.^11,12 It may be related to preoperative management evaluation, operation mode, intraoperative operation, postoperative management, and the time span of the study.

The results of this study found that in the PVT group, preoperative hepatitis B, cirrhosis, ascites, intraoperative blood transfusion, postoperative use of hemostatic drugs, preoperative prothrombin time, intraoperative portal blockade time, and operation time, The international standardized ratio of prothrombin time on the first day after surgery, D-dimer on the first day after surgery, fibrin degradation products on the first day after surgery, and postoperative hospital stay were higher than those in the control group (P < .05). Preoperative platelet and albumin in PVT group were lower than those in control group (P < .05). Intraoperative blood transfusion, liver cirrhosis, ascites, international normalized ratio of postoperative prothrombin time, postoperative fibrin degradation products, portal blockade time and albumin were independent risk factors for PVT.

Analysis of the causes can be seen as follows: (1) severe preoperative cirrhosis leads to portal hypertension, slow blood flow, and secondary blood stasis.^13,14 (2) Since antithrombin, protein C, and protein S are synthesized by liver cells, cirrhosis reduces the levels of these inhibitors,^15,16 resulting in a relative imbalance between anticoagulant and procoagulant.^17,18 (3) Ascites and low preoperative albumin are the manifestations of severe cirrhosis (4). If the number or time of the first portal occlusion is long during the operation, the injury of portal vein endothelium will be aggravated and thrombosis will be more likely to occur.^19,20 (5). The International standardized ratio of postoperative prothrombin time and postoperative fibrin degradation products indicate that postoperative hypercoagulability is one of the factors leading to thrombosis.^21,22 (6). Intraoperative blood transfusion suggests surgical trauma, vascular endothelial injury, and poor intraoperative coagulation, leading to thrombosis. ²³

Therefore, to reduce the formation of PVT after hepatectomy, careful evaluation should be conducted before surgery, surgical indications should be understood, surgical plan should be designed well, surgical operation should be carefully performed, and imaging examinations such as upper abdominal color Doppler ultrasound and upper abdominal computed tomography enhancement should be conducted in time when necessary to detect coagulation function after surgery. In addition, anticoagulation therapy should be performed as soon as possible for patients who are at high risk of PVT after hepatectomy and have no anticoagulation contraindications for prevention.^24–26

There are some limitations in this study. First, this is a single-center retrospective study. Due to the small sample size of the experimental group and the relatively simple information of follow-up patients, there are certain errors, which need to be further verified by multicenter prospective research. Second, due to the small sample size, there was no statistical analysis of portal vein reconstruction, splenectomy, postoperative bile leakage, and other factors.

In conclusion, PVT after hepatectomy is not uncommon and is a potentially life-threatening complication that requires a high degree of vigilance. In this study, the independent risk factors for PVT after hepatectomy were lower preoperative albumin, more severe cirrhosis, combined with ascites, longer portal blockade, intraoperative blood transfusion, increased international normalized ratio of postoperative prothrombin time, and increased postoperative fibrin degradation products. Preoperative index monitoring, surgical plan design, intraoperative operation, early postoperative diagnosis, and timely intervention can effectively improve the prognosis of PVT patients.