Hilar cholangiocarcinoma (HCCA) is a malignant tumor that involves the opening of the cystic duct and one third of the extrahepatic bile ducts, and often extends to the confluence of the hepatic and biliary ducts, and one or both hepatic ducts, and is also known as central type cholangiocarcinoma or Klatskin tumor. It accounts for 58%～75% of extrahepatic cholangiocarcinomas, and the detection rate and incidence rate have been on the rise in recent years. Due to its special anatomical relationship and biological characteristics, early diagnosis of HCCA has been difficult for a long time, with high misdiagnosis rate, low surgical resection rate and poor prognosis. With the in-depth understanding of its biological characteristics, the emergence of advanced clinical imaging technologies such as magnetic resonance cholangiography (MRC) and spiral CT, and the continuous progress of surgical techniques, the diagnosis rate of cholangiocarcinoma and the number of patients who can be operated on have increased, and the treatment concepts and methods have been continuously updated. At present, the factors affecting the long-term efficacy of surgery are mainly residual cancer cells and lymph node metastasis. Postoperative survival of margin-negative patients is significantly longer than that of margin-positive patients. Radical resection is still the only treatment for cholangiocarcinoma, and several surgical procedures have been applied in the clinic, among which hemihepatic enlarged resection is considered as the standard procedure for cholangiocarcinoma. In recent years, there is a tendency for the operation area to be enlarged gradually, but the risk of operation rises when the resection area is large.Gerhards reported 12 cases of hepatic enlarged resection and vascular resection, the perioperative mortality rate reached 50% (6/12), and all of them died of postoperative hepatic and renal failures. Major hepatic resection often removes greater than 70% of the liver parenchyma and results in a sudden increase in portal pressure. These shocks increase the incidence of postoperative complications and may ultimately lead to the development of fatal hepatic failure. Therefore, surgical management of hilar cholangiocarcinoma continues to be directed toward making the patient safely tolerate the alterations in body function associated with the expanded surgical scope. Preoperative portal vein embolization (PVE) is a kind of interventional therapy. In 1986, Japanese scholars Kinoshita et al. first reported the application of portal vein embolization (PVE) and observed atrophy of the hepatic lobe on the embolized side and hypertrophy of the hepatic lobe on the unembolized side. These hyperplastic future residual liver lobes (Future liver remnant, FLR) could provide sufficient hepatic reserve for most of the hepatic resection. Subsequently, Matsuoka further studied PVE and embolization materials, and in 1989, he guided the four main purposes of PVE: 1) to expand the surgical indications; 2) to prevent tumor dissemination along the portal vein; 3) to prevent portal vein thrombosis; and 4) to cooperate with arterial perfusion to cause complete necrosis of the tumor; 4) to prevent the tumor from spreading; 5) to prevent the tumor from spreading; 6) to prevent the tumor from spreading; and 7) to prevent the tumor from spreading. In recent years, because of its ability to effectively induce the future remnant liver (FRL) to increase in size and function, PVE has been widely used in the preoperative hepatic resection of surgical liver tumors in order to expand the surgical indications and reduce the incidence of postoperative hepatic failure, infection, and hemorrhage.As a preoperative adjuvant therapy, PVE can increase the safety of surgical resection of hepatocellular carcinoma, metastatic hepatocellular carcinoma, and hepatocellular carcinoma. In this chapter, we introduce the current research status of PVE in the treatment of hepatoportal cholangiocarcinoma in recent years, and elucidate its mechanism of action on the diseased liver as well as its role and efficacy in surgical treatment. I. Anatomy of the portal venous system Fig. 1 Abdominal portal venous system The liver is a substantial organ with a complex internal structure, and abundant blood circulation has long hindered the development of hepatic surgery. The portal vein is the main source of blood in the liver (about 70%), originating from the capillaries of the abdominal digestive organs (alimentary canal and pancreas), spleen, etc., and finally forming the portal vein through the step-by-step convergence (as shown in Figure 1). Before performing PVE, it is essential for every surgeon to have an accurate understanding of the anatomical structure of the portal vein and the common branching variations. The main branches of the portal vein are: (a) the superior mesenteric vein, which is located to the right of the homonymous artery and runs alongside it, collecting blood from the distribution of the gastroduodenal artery in addition to that of the homonymous artery. (ii) The splenic vein, composed of several veins of the spleen, runs behind the pancreas and, in addition to collecting blood from the distribution of the artery of the same name, receives the confluence of the inferior mesenteric vein. (c) The inferior mesenteric vein, which receives blood from the distribution of the artery of the same name, lies to the left of the artery of the same name, and behind the pancreas it joins the splenic vein, and in some instances the superior mesenteric vein, or directly into the portal vein (at the angle where the splenic vein and the superior mesenteric vein converge). (d) The left gastric vein, the coronary vein of the stomach, which accompanies the homonymous artery and collects blood from the distribution area of the homonymous artery, travels left along the gastric curvature and then turns to the right before converging on the portal vein trunk. At the cardia, the esophageal venous plexus has a small branch into the left gastric vein, and its main branch, the esophageal vein, into the singular vein or semi-singular vein, thus connecting the portal vein system with the superior vena cava. (e) The right gastric vein, which accompanies the eponymous artery, joins the portal trunk. The right gastric vein often receives the confluence of the anterior pyloric vein, which is commonly used as a marker to identify the pylorus during surgery. (vi) The vein of the gallbladder, which collects blood from the wall of the gallbladder, and joins the portal vein trunk or its right branch. (vii) The accessory umbilical veins, which are several small veins that originate in the periumbilical venous network, travel along the round ligament of the liver, and join the portal vein or its left branch. At the free edge of the hepato-duodenal ligament, there is generally no accessory branch of the portal vein. Posterior to the first duodenum, there are veins from the gastric and pancreatic duodenum that feed directly into the portal vein. At the location of the first porta hepatis, the portal vein divides into a thick, short right trunk and a thin, long left trunk, with the left and right trunks of the portal vein emanating from 1-3 small veins to the caudate lobe to the right and left segments, respectively, and, in some patients, the right anterior lobe portal vein also emanates either directly from the main trunk of the portal vein or from the transverse portion of the left trunk of the portal vein. The portal vein is posterior to the neck of the pancreas at about the height of the second lumbar vertebrae and anterior to the inferior vena cava, where it is joined at a right angle by the superior mesenteric vein and the splenic vein. The inferior mesenteric vein joins the splenic vein in 52.02% of cases; the inferior mesenteric vein joins the superior mesenteric vein in 24.60% of cases; or the splenic vein, the superior and inferior mesenteric veins together join to form the portal vein in 13.29% of cases. Common variations of the portal vein: Although variations of the portal vein are uncommon (10% – 15%), familiarity with portal vein variations is particularly important for preoperative PVE and successful surgical resection. Eleven percent of portal veins are 3-forked, and the portal vein can also be 4-forked. Only 1% of portal veins are not bifurcated, with more variability in the type of intrahepatic branch of the right portal vein. Three common variants are shown in Figure 2. Figure 2 Three variants of the right branch of the portal vein The portal vein branches repeatedly within the liver, eventually forming the interlobular vein (shown in Figure 3), which together with small branches of the hepatic artery enters the hepatic blood sinusoids within the hepatic lobules, joins the sublobular vein via the central vein, and finally enters the inferior vena cava via the hepatic vein. Before entering the hepatic sinusoids, the interlobular veins have traffic branches with the small branches of the hepatic artery. These branches do not open under normal conditions, but do so when the sinusoidal space narrows in cirrhosis, and the high pressure hepatic arterial blood flow flows back into the low pressure portal vein, thereby increasing the pressure in the portal vein. Failure to familiarize oneself with these structures and wrong choice of branch embolization can lead to liver failure or even death. Figure 3 Intrahepatic branching of the portal vein II. Indications for the use of portal vein embolization As a preoperative adjunctive intervention, it is indicated for patients in whom it is estimated that the future residual liver will be insufficient to satisfy the hepatic function after major hepatic resection. By determining the volume of the future residual liver before surgery, the use of embolization technology can make the unembolized area increase compensatory, which can fully meet the requirements of postoperative liver function reserve. On the other hand, for certain patients who are no longer eligible for surgery, PVE combined with TCAE can reduce the tumor volume or even kill the tumor by blocking the pathway of tumor blood supply. There is no international standard for the indications of PVE treatment. However, many scholars and experts agree that PVE treatment should be based on liver function and future residual liver volume.Kubota et al. pointed out the criterion for determining PVE by the volume of the liver to be resected, which was obtained by calculating the values of CT and ICG R15. In patients with normal liver function, if ICG R15 is less than 10%, PVE can be performed when the future residual liver volume is less than 40%, and in patients with jaundice or ICG R15 greater than 10%, PVE can be performed when the future residual liver volume is less than 50%.Tadatoshi Takayama proposed the following criteria for PVE in patients who need to undergo hepatic resection: Patients with normal liver function requiring more than 60% hepatectomy; patients with values 10 to 20% off normal, or with a history of obstructive jaundice requiring 40-60% hepatectomy; patients requiring pancreatic head resection. According to the Oriental Hepatobiliary Hospital of the Second Military Medical University, the criteria for selection of preoperative PVE for hilar cholangiocarcinoma are: absence of cirrhosis and jaundice/biliary dilatation up to the time of PVE.