In 1973, Madisom first reported a clinical trial of splenic artery embolization for the treatment of portal hypertension with hypersplenism, which resulted in spleen shrinkage and rapid improvement in peripheral blood cells. 1980, Spigos et al. applied partial splenic embolization PSE, which significantly reduced the complications associated with total splenic embolization. In 1985, Jonasson et al. reported that partial splenic embolization of the splenic artery with gelatin sponge pellets for the treatment of hypersplenism was safe and effective with few serious complications at long-term (1-8 years) follow-up.
Partial splenic artery embolization has been widely used in the treatment of hypersplenism in China and abroad as an alternative treatment to surgical splenectomy with low complication rate and mortality. The Department of Radiology of Donghu Hospital, in cooperation with clinical departments, has successfully carried out interventional techniques in three cases of cirrhosis combined with hypersplenism, and achieved quite satisfactory clinical results. In order to improve the understanding of interventional treatment of hypersplenism, we intend to further discuss the clinically relevant issues in the light of the literature.
I. Causes of hypersplenism in cirrhosis, the anatomical basis and mechanism of PSE for hypersplenism
1. Causes of hypersplenism in cirrhosis.
Stagnant splenic blood return and increased splenic artery blood flow are the main causes of splenomegaly and hypersplenism in portal hypertension in cirrhosis. Portal hypertension is the initiating factor for the occurrence of hypersplenism, which can lead to increased resistance to splenic venous blood flow, resulting in passive spleen stasis and enlargement. Increased blood flow in the splenic artery due to transmitter secretion leads to active congestion of the splenic artery, which maintains and develops splenic stasis and enlargement. The result is massive blood stagnation in the enlarged spleen and massive destruction of blood cells by the functionally active macrophage system. Hypersplenism in cirrhosis can cause a series of clinical consequences. Patients are often prone to infections, bleeding and even liver failure due to immune deficiency and coagulation dysfunction, while the increased blood return from the splenic vein leads to further increase in portal vein pressure, increasing the possibility of ruptured esophageal varices and bleeding.
2. Anatomical basis of PSE for hypersplenism.
The segmental distribution characteristics of splenic artery provide the anatomical basis for PSE procedure. After the splenic artery emanates from the abdominal arterial trunk, it divides into first-level terminal branches near the splenic hilum, namely the splenic lobe artery (mostly 2 branches), and each splenic lobe artery then divides into one to three splenic segmental arteries (secondary branches), which can also divide into subsegmental arteries (tertiary branches, 9-21, average 16). In some cases, the splenic lobar artery divides into the splenic pole artery before the splenic lobar artery divides, forming a pole segmental branch. Each splenic lobe, segment, and subsegment has very few vascular anastomoses, which are treated as hypovascular areas. The above features provide an anatomical basis for PSE procedures, i.e., when a ligation or embolization of a lobe or segmental branch is performed, ischemic infarction of the splenic tissue in the corresponding region occurs.
However, in recent years, it is generally accepted that intrapleural artery anastomosis is not uncommon despite the clearer lobulation and segmentation of the splenic artery. The literature reports 6.6% to 15.3% of splenic artery branches in extrasplenic anastomoses (interlobular anastomoses) and 15.3% to 43.3% in intrasplenic anastomoses (intrasplenic interlobular and intersegmental anastomoses). The occurrence of lobar or intersegmental anastomoses has also been reported in 52% of cases.
Whether the presence of splenic artery anastomoses affects the efficacy of PSE depends on the choice of embolization material and the segment of the splenic artery to be embolized. The pathological changes after PSE are multifocal wedge-shaped ischemic areas in the spleen in the early stage, followed by coagulation necrosis and punctate hemorrhage after one week, and granulation in the necrotic area after 2-3 weeks. After two to three weeks, granulation tissue formed in the necrotic area, followed by fibrosis, spleen volume reduction, and peripheral fibrous scar like armor to limit spleen tissue regeneration.
3. Mechanism of PSE for hypersplenism.
PSE is performed by blocking some of the splenic artery blood flow, reducing the blood flow in the spleen, causing infarction of the splenic parenchyma, and reducing the sites of blood cell destruction to achieve the purpose of treatment. Many studies have also demonstrated the immune mechanism of platelet elevation after PSE, with a significant reduction in platelet antibody secretion and prolonged platelet survival after surgery. When the degree of embolization exceeds 60%, it also effectively reduces portal vein pressure, thereby reducing the initiating factor of hypersplenism recurrence and the risk of esophageal rupture and bleeding. PSE has been widely used in the treatment of hypersplenism in cirrhosis because it is less invasive, has fewer complications, and has a wider range of indications than surgical splenectomy, while preserving the immune function of the spleen.
Indications and contraindications for hypersplenism embolization (including the treatment of hypersplenism outside of cirrhosis)
1, Indications.
Interventional treatment is suitable for all causes of splenomegaly combined with hypersplenism with surgical indications.
(1) hypersplenism caused by portal hypertension or other causes.
(2) Portal hypertension combined with ruptured esophageal vein bleeding.
(3) Autoimmune thrombocytopenic purpura, which does not improve significantly by medical treatment.
(4) Thalassemia, hereditary spherical or oval erythropoiesis.
(5) Splenic aneurysms and vascular malformations.
(6) ruptured hemorrhage from splenic trauma or subperitoneal hematoma
(7) Gaucher’s disease causing hepatosplenomegaly.
(8) leukopenia prior to renal transplantation and during intervention for hepatocellular carcinoma
(9) myelodysplasia with thrombocytopenia.
(10) Splenic, portal vein thrombosis or cavernous lesions complicated by hypersplenism and splenomegaly.
2. Contraindications.
(1) Extreme systemic failure, severe infection, and fever should be considered as absolute contraindications.
(2) Obvious bleeding tendency and coagulation dysfunction should be considered as relative contraindications.
(3) Failure of selective cannulation of the splenic artery and inability to inject embolic agents into the abdominal arterial trunk.
(4) Those who are not suitable for arteriography are also not suitable for splenic embolization.
3.Modality and degree of splenic artery embolization
1.The modes of splenic artery embolization are as follows.
(1) Splenic artery trunk embolization: 1~3 large stainless steel spring coils or detachable balloons are commonly used and placed in the splenic artery trunk, which is equivalent to splenic artery ligation.
(2) Total splenic embolization: the amount of splenic tissue infarction reaches 90% or more. Because of the severe reaction of the patient after embolization and the high incidence of splenic abscess, and because it does not meet the purpose of preserving part of the splenic function, this method is generally not commonly used, but can be used for the treatment of splenic malignancy.
(3) Partial splenic embolization (PSE): The infarction rate of splenic tissue is below 90%. Two methods are often used for embolus injection.
Low-pressure flow control method: The embolic agent is injected into the main trunk of the splenic artery, and the embolus randomly and uniformly obstructs the corresponding caliber splenic artery branches along the blood flow. For the size of splenic embolization, the lack of precise calculation methods makes it a clinical challenge to correctly determine the extent of embolization intraoperatively.
Super-selective inferior splenic pole artery embolization method: This method was first attempted by domestic scholars to avoid complications such as left-sided chest pain and restricted respiration resulting in left lower pneumonia and atelectasis after embolization of the superior splenic pole artery, and the embolization volume is easier to control. re-enlargement is not known.
2. Selection of PSE embolization volume
The amount of embolization is generally considered to be 40%-70%, too little can not achieve the therapeutic effect, too much will increase the complications, such as giant spleen patients, embolization 50%-60% can be serious postoperative reactions and complications, so a small number of embolization methods should be adopted, the first embolization 20%-40%, 2-3 months after surgery again embolization 20%-30%, and if necessary, a third embolization; for patients with portal vein For hypersplenic patients with portal hypertension, the embolization volume should be small if the purpose is to increase red blood cells and platelets, and large if the purpose is to reduce splenic vein return flow and relieve portal hypertension. In general, the size of embolization volume should be flexible according to the patient’s specific situation.