I. Brief description of the case: The patient, Song, female, 79 years old, had advanced pancreatic cancer with combined gastrointestinal bleeding and late progressive platelet drop, but no obvious bleeding changes. The main clinical manifestation is progressive thrombocytopenia, which is difficult to be corrected by blood transfusion therapy, PLT 23-12*109/L, intermittent fever. The main clinical manifestation is progressive thrombocytopenia, which is difficult to be corrected by transfusion therapy. The possibility of thrombocytopenia caused by hypersplenism is very high. Hypersplenism: Hypersplenism refers to the clinical syndrome caused by various causes of splenomegaly and excessive consumption of blood cells. Hypersplenism is a syndrome and is not a diagnostic name for an independent disease. Blood cells and platelets are destroyed during filtration in the overly enlarged spleen, resulting in corresponding clinical manifestations such as anemia, granulocytopenia, thrombocytopenia, and active bone marrow hematopoiesis. Pathogenesis: Primary splenomegaly is rare and there is no recognized cause. It often leads to primary granulocytopenia, primary thrombocytopenia, etc. In addition, aneurysms and cavernous hemangiomas in the spleen itself can cause some degree of hyperfunction. The vast majority of hypersplenism is secondary, meaning that it is not the spleen itself that is ill. The main causes of hypersplenism include: 1. bruised splenomegaly due to portal hypertension, which is by far the most common type of hypersplenism in clinical practice. Portal hypertension is also a clinical syndrome secondary to various causes of cirrhosis. Viral hepatitis, alcoholic liver injury, liver fluke or schistosomiasis, autoimmune hepatitis, Buga syndrome, portal vein thrombosis or spongy vascular degeneration are the more common causes. Chronic hemolytic diseases such as hereditary spherocytosis, autoimmune hemolysis and marine anemia, etc.; 3. Splenomegaly accompanied by various infections, acute infections are common in viral hepatitis or infectious mononucleosis, chronic infections are mostly seen in tuberculosis, brucellosis, malaria, schistosomiasis, hepatic schistosomiasis, etc.; 4. Various immune system diseases, inflammatory granulomas, such as systemic lupus erythematosus 5. malignant neoplasms such as lymphoma, leukemia and metastatic splenic tumors; 7. hereditary lipid deposits such as Gaucher’s disease and Niemann-Pick disease; 8. myeloproliferative disorders such as true erythroblastosis, chronic granulocytic leukemia and myelofibrosis. Symptoms and harms The main harms of hypersplenism are in two aspects. Firstly, the dominant effect of splenomegaly can cause a certain degree of discomfort, mainly in the form of abdominal distention and a feeling of fullness after eating. However, this is often tolerated by the patient, and it is possible to see patients with a “giant spleen”, where the entire left side of the abdomen is occupied by the spleen. The physiological effects are mainly related to the function of the spleen, as the blood passes through it, destroying excessive blood cells and causing a decrease in red blood cell, white blood cell and platelet counts, with a series of symptoms. In short, a decrease in granulocytes, which can cause infections, a decrease in red blood cells, or anemia, can result in pallor and weakness, and a decrease in platelets, which can cause bleeding. In hypersplenism, if accompanied by bone marrow suppression, hematopoiesis may be enhanced, and immune and secretory functions may be affected. However, the relative decrease in blood counts is often easily overlooked. Ancillary tests Many hypersplenic conditions are insidious, i.e., the clinical manifestations may not be obvious due to compensatory bone marrow hyperplasia, which compensates to some extent for the depletion of blood cells. The diagnosis of hypersplenism is commonly made by abdominal ultrasound (or CT) combined with routine blood tests suggesting an increase in spleen size along with a decrease in blood cell and/or platelet counts. It is important to note that there are often physical examination results that indicate an “enlarged spleen”, which is a physician’s judgment based on the average for a normal person and does not necessarily indicate hypersplenism, but requires a clinical diagnosis. In addition, ECT, PET-CT, and pathological biopsy are all possible diagnostic options. However, for the diagnosis of hypersplenism, the most important thing is to identify the primary cause of the disease in order to provide targeted treatment. Treatment modalities and indications: For secondary hypersplenism, active treatment of the primary cause is required. For example, if the infection is controlled, the leukemia is in remission, and the portal hypertension is reduced, most hypersplenism can be relieved to some extent. However, in the case of splenomegaly that remains uncontrollable after non-surgical treatment, surgical or interventional treatment is the preferred modality because there are no specific drugs that can contain it once it causes severe anemia, thrombocytopenia leading to severe bleeding, etc. This generally includes splenectomy, partial splenectomy, and interventional treatment (currently, splenic artery embolization is the main treatment), among which splenectomy has the most direct and definite efficacy. Except for primary hypersplenism and splenic diseases such as splenic tumors, splenectomy for hypersplenism requires strict indications. These include the following diseases: 1) congestive splenomegaly due to portal hypertension; 2) splenomegaly due to infectious diseases such as splenic abscess and tuberculosis; 3) hereditary spherocytosis and autoimmune hemolytic anemia; 4) primary thrombocytopenic purpura where medical treatment has failed; 5) chronic aplastic anemia; 6) chronic granulocytic leukemia causing giant spleen; 7) Gaucher disease 8, certain Hodgkin’s diseases. It is important to emphasize that splenectomy or splenic artery embolization can only relieve the spleen from the hematological system and cannot cure the original disease. In particular, in some hematologic diseases such as erythroleukemia, hypersplenism has a remitting effect on the symptoms of the disease itself; in patients with chronic myelofibrosis, hematopoietic function can be transferred to the spleen during myelosclerosis; or in Gaucher disease, liver lesions may be aggravated after removal of the spleen, and removal of the spleen may do more harm than good. For patients who are suitable for spleen removal, the feasibility of their own conditions and whether they have contraindications to surgery also need to be evaluated in a regular hospital specialty. If surgical treatment is not tolerated, interventional therapy through less invasive treatment is not an inappropriate option. Treatment plan: For this patient with advanced tumor, the treatment is based on a combination of Chinese and Western medicine, the principle of “treat the symptoms urgently, treat the root cause slowly, and tonic for deficiency”, with symptomatic platelet transfusion, subcutaneous injection of interleukin 11, and short-term hormone therapy. The Chinese herbal treatment takes into account the deficiency of qi and blood after the loss of blood, the depletion of yin, the lack of yang energy, the inability to promote blood circulation, the damage to the spleen and stomach, and the loss of spleen control over blood, so we gave intravenous Kanglaite injection to help correct and cultivate the root.