Hypersplenism (referred to as hypersplenism) is a syndrome with clinical manifestations of splenomegaly and a decrease in one or more types of blood cells with a corresponding increase in bone marrow hematopoietic cells; the symptoms are relieved by splenectomy. I. Splenic function The spleen is an integral part of the monocyte-macrophage system, with a large number of macrophages distributed in the red marrow, forming a reticular filter bed. 5%-10% of the splenic blood flow flows slowly through the red marrow, and the cells containing bacteria, foreign bodies, or cells covered with antibodies and complement on the surface will be sufficiently contacted and phagocytosed by macrophages. Splenic blood flow from the small arteries enters the venous sinuses via the microvessels. The endothelial cells of the venous sinus form many 1-3 μm lacunae through which blood passes before returning to the small vein. Red blood cells and white blood cells are about 7-12 μm in diameter and have to be deformed to pass through the clefts of the venous sinus. Senescent, damaged, and poorly deformed cells in the blood stream cannot pass through the fissure and are retained. Filtering blood through phagocytosis and retention mechanism is the main function of the spleen. Secondly, the spleen has the function of blood storage. However, its role in regulating blood volume is limited due to the poor contractility of the splenic envelope. However, most of the circulating neutrophils and about 1/3 of the platelets are stored in the spleen. Second, etiology and pathogenesis Hypersplenism is related to splenomegaly, and the etiology of splenomegaly includes: 1. Infectious diseases Infectious mononucleosis, subacute infective endocarditis, cornual tuberculosis, brucellosis, schistosomiasis, black fever and malaria. 2.Immune diseases Autoimmune hemolytic anemia, rheumatoid arthritis, Felty syndrome, systemic lupus erythematosus and tuberculosis. 3.Siltation diseases Congestive heart failure, constrictive pericarditis, Budd-Chiari syndrome, cirrhosis, portal or splenic vein thrombosis. 4.Diseases of blood system (1) hemolytic anemia: hereditary spherocytosis, thalassemia and sickle cell anemia, etc. (2) Infiltrative splenomegaly: all kinds of acute and chronic leukemia, lymphoma, myeloproliferative diseases and lipid storage disease, malignant histiocytosis and amyloidosis. 5.Diseases of spleen Splenic lymphoma, splenic cyst and splenic hemangioma. 6.Primary splenomegaly Pathogenesis is unknown. When splenomegaly is caused by various reasons, the proportion of blood flow through the red marrow will increase, thus making the spleen hyperfiltration function. When the spleen is enlarged, 90% of the platelets can be retained in the spleen, and normal or abnormal blood cells are retained or destroyed in the spleen. Decreased circulating blood cells may cause compensatory enhancement of bone marrow hematopoiesis. Splenomegaly is often accompanied by increased plasma volume and increased splenic blood flow, which overloads the splenic vein and thus causes increased portal venous pressure. The latter, in turn, can lead to further splenomegaly, increasing splenic blood flow and forming a vicious cycle. Implementation of splenectomy can not only eliminate hypersplenism, but also interrupt the link of disease development. III.CLINICAL PRESENTATIONS Hematocrit may present with anemia, infection and bleeding tendency. Splenomegaly is usually asymptomatic and is often detected on physical examination. Sometimes the symptoms of megasplenism are also mild. Patients may feel abdominal discomfort, reduced appetite or discomfort when sleeping to one side. The presence of pain and rubbing sensation in the left quarter ribs associated with breathing often suggests the possibility of splenic infarction. Various causes of splenomegaly have different degrees of hemopenia due to hypersplenism. Hematopenia is usually more pronounced in stasis splenomegaly. In splenomegaly due to infiltration, such as in chronic leukemia, hypersplenism tends to be less pronounced. The degree of clinical splenomegaly is not necessarily parallel to hypersplenism. Laboratory tests: Blood cells are reduced in hypersplenism, but cell morphology is normal. In the early stage, leukopenia and thrombocytopenia are predominant, and in severe hypersplenism, there may be a marked reduction in the three lineages. Bone marrow examination shows a proliferative picture, and there may be maturation disorder, which is due to the massive destruction of peripheral blood cells, prompting the excessive release of cells. V. Diagnosis 1. If splenomegaly is present and the spleen is not palpable under the ribs, B-mode ultrasonography of the splenic region can be used for clinical reference. 2.Red blood cells, white blood cells or platelets can be reduced singly or simultaneously. 3.Proliferative bone marrow image. 4, Splenectomy can bring the blood cell count close to or back to normal. The first 3 bases for diagnosis are the most important. Treatment The primary disease should be treated. If the primary disease permits, splenectomy can be considered. Indications: 1, splenomegaly causing obvious compression symptoms; 2, severe hemolytic anemia; 3, thrombocytopenia causing hemorrhage; 4, extreme granulocytopenia and history of recurrent infections. Secondary thrombocythemia after splenectomy carries the risk of thrombotic complications in bedridden or elderly patients, removes the protective blood-filtering organs, and predisposes young patients to blood-borne infections. Therefore, special care should be taken in splenectomy in young, elderly and bedridden patients.