Portal hypertension is a syndrome caused by disorders of the liver and its associated vessels and biliary tract. Normal portal pressure is 5-10 mmHg (0.65-1.3 Kpa), which is slightly higher than the inferior vena cava pressure. When the portal venous pressure is higher than the inferior vena cava pressure below 0.65 Kpa (5 mmHg) or when the portal venous pressure is ≥ 2.94 Kpa (30 cmH2O), it suggests the presence of portal hypertension. Interventional techniques involving portal hypertension currently include transjugular route intrahepatic portal-somatic intravenous stent shunt (TIPSS), simple embolization of esophagogastric fundic varices, splenic artery embolization and interventional treatment of Budd-Chiari syndrome.
I. Transjugular route intrahepatic portal vein endoprosthetic shunt
The clinical application of TIPSS in China started in 1992, and then developed rapidly in major and medium-sized cities and regions. after 1995, due to the problems of higher incidence of intermediate and late stenosis after stent implantation, researchers have changed their cautious attitude, and the cumulative number of cases has not increased much.
Indications: (1) cirrhotic portal hypertension, those who have had recent hemorrhage from ruptured esophagogastric fundic varices; (2) patients who have difficulty receiving surgical treatment despite poor medical treatment; (3) those who have received repeatedly ineffective transendoscopic sclerotherapy or rebleeding after surgical treatment; (4) severe fundic varices; (5) those with refractory ascites; (6) patients who have done prophylactic treatment for gastrointestinal bleeding before liver transplantation.
In elective patients, the basic situation can be mastered by referring to the indications for surgical shunt, that is to say: those with Child A and B are listed as indications, which can help the long-term survival of patients after surgery and reduce the occurrence of postoperative complications such as hepatic encephalopathy.
Contraindications include: (1) severe portal stenosis and obstructive lesions; (2) moderate to severe liver function abnormalities and precursors of hepatic encephalopathy; (3) combined hepatocellular carcinoma near the first and second hepatic hilum; (4) uncorrectable coagulation abnormalities; (5) severe renal impairment; (6) organic heart disease with cardiac insufficiency; (7) infection and sepsis, especially biliary infection.
Complications include: complications caused by intraoperative operation of TIPSS and postoperative hepatic encephalopathy due to hemodynamic changes.
Postoperative complications include: (1) hepatic encephalopathy; (2) hypoalbuminism; (3) hepatocellular jaundice; (4) right lobe of the liver atrophy; and (5) spinal cord injury.
Intraoperative complications: the most serious one is abdominal hemorrhage caused by portal vein injury, which should be avoided during the operation.
TIPSS, as a new treatment for portal hypertension in cirrhosis, was applied in China in 1993 and formed a climax of development in the following 2~3 years. By the end of 1995, nearly 1,000 cases were reported in China, and after 1996, this climax gradually declined, and there were even fewer cases.
While TIPSS was “quiet” in China, the basic and clinical applications in Europe and the United States continued to develop steadily. The results of the clinical application of TIPSS in foreign countries show that TIPSS is more effective for acute gastrointestinal hemorrhage caused by portal hypertension, especially hemorrhage caused by fundic varices, and the complete embolization of esophageal and fundic varices is beneficial to the prevention of reissue of blood compared with medical methods. Compared with surgical bypass, TIPSS is less invasive, safer, and relatively simple to perform, and the bypass effect is the same as that of surgical bypass. Therefore, TIPSS should be the preferred option in cases of acute GI bleeding where medical treatment is not effective. It can be concluded that among the available treatments for portal hypertension in cirrhosis, TIPSS is still a valuable and practical technique with all the advantages of medical and surgical approaches. Indeed, the relatively wide grasp of indications for some patients at the early stage of TIPSS application has caused some blindness; the occurrence of stenosis or even occlusion of the internal stent in some patients after surgery, especially the expensive cost has not brought satisfactory long-term results, is also one of the reasons for the current relative stagnation.
The problem of postoperative shunt stenosis and restenosis has not yet made breakthrough progress.
II Embolization of esophagogastric fundic varices
(a) Percutaneous transhepatic gastric coronary vein embolization is an interventional treatment method to treat esophageal variceal bleeding by selectively cannulating the gastric coronary vein through skin and liver puncture to the intrahepatic portal vein branches and occluding the vessels with embolic material is an effective non-surgical hemostasis method to control hemorrhage from esophagogastric fundic varices.
Another method is to use percutaneous transhepatic gastric coronary vein and percutaneous puncture femoral artery cannulation to perform partial splenic artery embolization (referred to as dual interventional therapy).
The indications for percutaneous transhepatogastric coronary vein embolization are: (1) confirmed diagnosis of ruptured esophagogastric variceal bleeding; (2) previous history of bleeding and risk of rebleeding by angiography or endoscopy; (3) ruptured esophageal variceal bleeding from portal hypertension, which has been treated with vasopressin or posterior pituitary hormone and failed conventional medical treatment such as three-chamber balloon compression; (4) bleeding after surgery or after endoscopic sclerotherapy (4) bleeding after surgery or endoscopic sclerotherapy: (5) bleeding patients who cannot tolerate emergency surgical treatment.
Contraindications are: (1) severely impaired liver function; (2) massive ascites; (3) bleeding tendency; (4) sepsis or liver abscess; (5) hepatic hemangioma; (6) stenosis or obstruction of the main trunk of the portal vein, portal vein thrombosis.
Percutaneous transhepatic gastric coronary vein embolization has been shown to have better near-term hemostasis and rebleeding rates than drug and triple-chamber balloon compression hemostasis, and better rebleeding rates and death than endoscopic sclerotherapy. The possibility of offering elective surgery has also been established. However, the long-term efficacy of surgery is questionable and may cause serious complications. The difficulty of surgery, low success rate, and many complications are also its disadvantages.
(ii) Retrograde esophagogastric fundoplication embolization (BALLOON-OCCLUDED RETROGRADE TRANSVENOUS OBLITERATION, B-RTO) via spontaneous splenic-renal or gastric-renal shunt route -B-RTO is indicated for patients with portal hypertension with spontaneous splenic-renal or gastric-renal shunts in the presence of predominantly fundic varices that can be clearly demonstrated on imaging. This procedure is of particular clinical importance in patients with fundic varices who are not indicated for surgical shunts or TIPSS; or who are unable to undergo shunting due to obstructive portal lesions.
The following are indications for this procedure, provided that the imaging data show the presence of a trans-splenic-renal or gastric-renal shunt: (1) a confirmed diagnosis of ruptured esophagogastric fundic variceal bleeding with a predominance of fundic varices; (2) a past history of bleeding with a risk of rebleeding on angiography or endoscopy; (3) esophagus with portal hypertension (3) bleeding from ruptured fundic varices in portal hypertension who have failed conventional medical treatment such as vasopressin or posterior pituitary hormone therapy and three-chamber balloon compression; (4) bleeding after surgery or endoscopic sclerotherapy; (5) bleeding who cannot tolerate emergency surgical treatment; (6) embolization of the gastric coronary vein and short gastric vein after occluding the distal part of the shunt with a balloon during TIPSS, which prevents embolic material from entering the renal vein via spontaneous (6) Embolization of the gastric coronary vein and short gastric vein after balloon occlusion of the distal part of the shunt during TIPSS can avoid misembolism caused by embolic material entering the renal vein through the spontaneous shunt, and can make embolization more complete.
The following conditions are contraindications: (1) severe impairment of liver function; (2) large amount of ascites; (3) bleeding tendency; (4) sepsis or liver abscess.
III. Interventional treatment of hypersplenism
In order to achieve the goal of non-surgical splenectomy, Maddison first reported the application of splenic artery embolization for the treatment of hypersplenism in 1973. In the years that followed, many authors continued to conduct animal studies and clinical applications, confirming the effectiveness of this approach, and gradually investigated the use of partial splenic embolization to address the problem of controlling complications while effectively reducing splenic function. Partial splenic artery embolization is being refined as research on interventional methodology and pathophysiology of treatment outcomes progresses. Currently, this interventional radiological technique has become one of the main methods for the treatment of hypersplenism from all causes.
Splenic embolization therapy can be used as an alternative therapy to splenectomy or to improve platelet function prior to surgery. Depending on the situation, partial or total splenic embolization is chosen to be done.
(a) Indications for interventional therapy: (1) hypersplenism due to portal hypertension in cirrhosis; (2) portal hypertension, variceal bleeding; (3) hypersplenism in children; (4) splenic vein thrombosis after variceal bleeding; (5) Gaucher disease; (6) thalassemia major requiring long-term repeated blood transfusion; (7) chronic thrombocytopenic purpura; (8) Hodgkin’s disease; (9) hepatocellular carcinoma or viral hepatitis, which cannot be performed due to hypersplenism with abnormal blood picture (9) anti-cancer drugs or immunotherapy; (10) splenic hemorrhage after trauma.
(ii) Contraindications to intervention: (1) Systemic infection and sepsis may cause splenic abscess after embolization, which is an absolute contraindication to splenic artery embolization. Both hypoproteinemia and portal to splenic vein reflux caused by portal hypertension at this time are prone to splenic abscess complications. Interventional therapy should be performed electively after improvement of symptoms in internal medicine. (2) Conditions that preclude angiography, such as systemic failure, severe bleeding tendency and iodine allergic reaction, are also contraindications to splenic artery embolization.
(C) Efficacy evaluation The spleen after embolization appears swollen and bruised and lasts for more than 24h. The volume of the spleen gradually decreases over the following months. The specific method of volume measurement is to apply CT area calculation software to calculate the area of each level of the spleen and multiply it by the number of layers and layer thickness. The extent of splenic infarction can be calculated by applying the above method in conjunction with an enhanced CT scan. The results of statistical reports on the recurrence rate and the incidence of serious complications of hypersplenism embolization therapy vary widely, but the reported outcomes since the 1990s have improved significantly from the earlier accounts in the literature. recurrence rates range from 0 to 26% within 1 year, and no fatal complications have been reported. In a group of patients who used the gelatin sponge splenic artery main stem drift embolization method, all presented with embolization volumes ≤50% and all occurred within 1 month of embolization. It is now widely accepted that an embolization volume of 60% to 70% is a safe and effective option when using splenic artery trunk drift embolization. We have applied microsphere embolization of the inferior splenic pole artery with a typical embolic volume of about 30% to 40% with significant efficacy and very few cases of recent recurrence. This may be the result of super-selective cannulation to inject more microspheres for complete embolization of the target artery.
(iv) Complications The main complication of splenic embolization therapy is splenic abscess. There may be multiple factors involved in the development of splenic abscesses. It is hypothesized that in patients with portal hypertension, decreased splenic vein pressure and ischemic constriction of the spleen following splenic artery embolization result in reverse flow of splenic venous blood, causing intestinal bacteria to contaminate the ischemic vascular bed of the spleen. Extensive necrosis of the splenic parenchyma predisposes anaerobic microorganisms to grow in the hypoxic inactivated tissue. In addition, the causes of complications include decreased immune response of the patient and introduction of exogenous bacteria by the catheter or embolic material. Once a splenic abscess occurs, it is difficult to achieve a good outcome with intravenous antibiotic therapy alone. If a ruptured splenic abscess ensues, the condition will be very dangerous. There are reports of successful ultrasound-guided percutaneous percutaneous drainage of splenic abscesses at home and abroad, which is a more ideal treatment method at present.
Clinical practice and experimental research in recent years continue to prompt the emergence of new methods. Our scholars have applied radioactive 131 iodine-iodine oil for splenic artery embolization. 131 iodine-iodine oil is retained in the spleen and continuously irradiates the spleen with у radiation and β radiation to reduce the volume of splenic tissue and achieve partial splenectomy. This method has a low complication rate and is expected to transition to clinical application with successful results in animal trials. The development of microsphere embolic material containing antibiotics is also a promising development direction. This embolic material can slow release antibiotics within the infarct foci and can play a role in inhibiting the formation of splenic abscesses. However, the local drug concentration that can be achieved by this method is yet to be determined. Japanese scholars have reported partial splenic artery embolization with Y-shaped silica pellets, which slowly occludes splenic artery branches over several days using the small spaces between the Y-shaped pellets. This gradual infarction of the splenic tissue resulted in a significant reduction in the pain response after embolization and required only a short period of time with or without the use of pain medication.
Although splenic artery embolization therapy improves symptoms in most patients with hypersplenism, it does not control the primary lesions that cause hypersplenism, such as hematologic, metabolic, and hepatic diseases. Therefore, interventional therapy should be closely combined with other medical treatments in order to obtain a better comprehensive treatment effect.
Interventional treatment of Budd-Chiari syndrome
In recent years, many hospitals in China have carried out the diagnosis and interventional treatment of Budd-Chiari syndrome (BCS) one after another, and achieved promising results. Since there are many debates on the etiology of BCS and its staging, the effect of interventional treatment varies widely among different staging.
The etiology of nearly 70% of BCS is not well understood. Although there are many controversies, it is generally believed to be related to congenital venous malformation or/and hypercoagulable state in the body.
The exact anatomical extent of the hepatic venous outflow tract remains undetermined despite years of controversy. Most scholars believe that the hepatic venous outflow tract should include the small hepatic vein, the large hepatic vein, or/and the inferior vena cava (IVC) that opens into the right atrial segment of the hepatic vein.
In view of the fact that there is no standardized BCS typing, BCS can be divided into two types, A and B, based on the traditional typing such as Okuda: type A, hepatic vein type, of which A1 is pure hepatic vein type, and A2 is hepatic vein lesion with IVC involvement. Type B is the IVC-OL, where B1 is the IVC type and B2 is the IVC predominant lesion with hepatic vein involvement as a side effect. Each of these types can be classified as membranous, segmental or complete, incomplete stenosis or/and occlusion depending on the nature of the lesion.
Regardless of the interventional approach, opening the narrowed or/and occluded hepatic venous outflow tract or/and creating a new effective shunt to normalize the elevated hepatic sinusoidal pressure is the key to treating BCS. Regardless of type A or type B, transcatheter intravenous thrombolytic therapy is the most cost-effective and convenient, yet most important treatment for BCS. Based on hemodynamic principles, it is known that thrombosis is present in both the proximal and distal ends of stenotic or/and occluded veins, and all fresh thrombi are treated with intermittent transcatheter injection of adequate amounts of urokinase or/and other thrombolytic agents as necessary based on reference MRI images. In patients with BCS with hepatic venous outflow tract obstruction caused by fresh thrombus alone, this alone can open all narrowed or/and occluded hepatic venous outflow tracts with satisfactory results. In some patients with BCS caused by fresh thrombus, adequate thrombolytic therapy not only opens some of the narrowed outflow tracts but also creates very favorable conditions for further interventions. However, attention should be paid to prevent thrombus dislodgement while thrombolysis, and balloon catheters or IVC filters can be applied if necessary to avoid embolization of other organs such as heart and lungs.
In patients with mechanical stenosis and/or occlusion of the hepatic venous outflow tract caused by fibrous scarring, mechanical dilatation or/and creation of a new shunt should be performed based on adequate thrombolysis to ensure hepatic venous drainage. The treatment of A1 type BCS should be different depending on the location of the lesion. For A1 type occurring in small, medium or large hepatic veins, TIPSS, simple balloon dilation or second hilarplasty should be performed respectively. It is important to prevent venous stenosis or occlusion and to re-intervene for this purpose. A flexible treatment plan should be adopted for both small and large hepatic veins, and a combination of the three methods mentioned above can be used to reduce portal pressure sufficiently while minimizing liver injury. Treatment of type A2 BCS should focus on various methods to ensure hepatic vein opening while maintaining IVC drainage. The treatment of type B1 BCS is mostly based on balloon dilation or/and internal stenting, but care must be taken to protect the IVC openings of the hepatic veins or/and other veins such as the renal veins from damage to avoid secondary stenosis or/and occlusion of the corresponding veins. In the treatment of type B2 BCS, attention should be paid to the opening of the IVC while ensuring the patency of the drainage of the hepatic vein. For type B BCS with a long stenotic segment that can be passed by a guidewire, stent implantation after balloon dilation is sufficient. For type B BCS with a long occluded segment that cannot be passed by a guidewire, the direction of the puncture needle puncture should follow the center of the strip shadow under imaging guidance. In patients with obstructive lesions caused by diffuse small hepatic venous lesions with IVC in the posterior hepatic segment, TIPSS should be performed so that the ends of the internal stent are directly connected to the portal vein and right atrium to eliminate obstruction caused by IVC and hepatic veins.
Compared with surgical treatment methods, clinical intervention has the advantages of less trauma and definite and certain effect. However, the following points should be noted: (1) the increased portal hypertension consists of three parts: basal physiological pressure, mechanical obstruction pressure and functional vascular pressure, and all kinds of interventions should be based on various necessary and sufficient medical medications including anticoagulation, elimination of functional vascular pressure and symptomatic treatment; (2) it is better to perform liver aspiration biopsy before interventions, so that the degree of liver damage and the patient’s prognosis can be initially determined; (3) all clinical interventions at present have the advantage of being less invasive than surgical treatments. (3) The length of each section of all clinical IVC endoprostheses is mostly 25 mm, and the length of each section should be increased to reduce its intersegmental connection, which has an important role in preventing intimal hyperplasia and stent displacement; (4) A very cautious attitude should be taken towards the implantation of endoprostheses. For intrahepatic veins or/and shunts less than 10 mm in diameter, only transcatheter thrombolysis or/and balloon dilation are generally performed instead of endoprosthesis implantation, because endoprosthesis less than 10 mm in diameter is very prone to stenosis or/and occlusion in the liver, and long-term endoprosthesis implantation not only brings great inconvenience to re-intervention, but also may produce adverse reactions to human body; (5) the method of percutaneous liver puncture is now mostly not used for This method is more traumatic to the liver, and the thrombus formed by the puncture itself can be sufficient to cause severe stenosis or occlusion of normal small and medium-sized hepatic veins.
In conclusion, the etiology of BCS is still unclear, and its definition and clinical staging are controversial. However, regardless of the type of BCS, the use of various imaging examinations to show the location, size, and extent of the lesion is the necessary basis for the correct interventional treatment plan. After comprehensive treatment with catheter thrombolysis, balloon dilation, TIPSS and endoprosthesis implantation, some patients can obtain better treatment results. For some patients with unsatisfactory prognosis, it is hoped that their prognosis can be significantly improved by improving interventional techniques and methods. For patients with severe congestive fibrosis or/and extremely complicated BCS lesions, interventional treatment is difficult to achieve a satisfactory outcome.