The reference value of platelet count is (100 ~ 300) × 109/L, and it is abnormal to fall below or above this range. When the number of platelets is more than 400× 109/L, it is called thrombocytosis. Primary thrombocytosis is common in myeloproliferative diseases, such as chronic myelogenous leukemia, polycythemia vera and primary thrombocytosis. Reactive thrombocytosis is common in patients with acute and chronic inflammation, iron deficiency anemia and cancer. The platelet count of this thrombocytosis is generally less than 500× 109/L, and it will decrease rapidly after treatment and improvement. Platelets will increase significantly after splenectomy, often higher than 600×109/L/L. If the increase of platelet count is related to some diseases (secondary thrombocytosis), we should treat the primary disease. If the treatment is successful, the platelet count usually returns to normal level. If the cause of the increase in platelet count is not clear (primary thrombocytosis), drugs to reduce platelet production are usually used. When the platelet count exceeds 750,000/μ L or complications such as bleeding and thrombosis occur, treatment is usually started. The drug is used continuously until the platelet count drops below 600,000/μ L. The anticancer drug hydroxyurea is usually used, although the anticoagulant anagrelide is sometimes used. Because hydroxyurea can also reduce the production of red blood cells and white blood cells, its dosage must be adjusted to maintain a sufficient number of red blood cells and white blood cells. Low dose aspirin can reduce platelet adhesion, inhibit thrombosis and delay the use of the above drugs. If drug therapy is not enough to reduce platelet production, patients should be given platelet removal therapy. Removing platelets is to draw blood, remove platelets from it, and then return the platelet-removed blood to the body. This treatment is usually combined with medication. Thrombocytopenia is poor thrombosis and bleeding caused by decreased platelet count (thrombocytopenia) or decreased function (platelet insufficiency). The platelet count is lower than the normal range 140000 ~ 400000/μ L. Thrombocytopenia may be caused by insufficient platelet production, retention of platelets in the spleen, dilution of platelets due to increased destruction or utilization (Table 133-65438+) or scattered ecchymosis at the slightly injured site. Mucosal bleeding (nosebleed, gastrointestinal tract and urogenital tract and vaginal bleeding); And massive postoperative bleeding. Massive gastrointestinal bleeding and central nervous system bleeding can be life-threatening. However, thrombocytopenia is not manifested as intra-tissue bleeding secondary to coagulation diseases (such as deep visceral hematoma or hemophilia). The diagnosis must thoroughly understand the patient's medication history. Exclude drugs that increase platelet damage in sensitive patients. About 5% of patients treated with heparin may have thrombocytopenia (see heparin-induced thrombocytopenia below). In order to keep the arteriovenous catheter unobstructed, even if a very small amount of heparin is used for flushing, it will cause thrombocytopenia. Other drugs rarely induce thrombocytopenia, such as quinidine, quinine, sulfanilamide, oral hypoglycemic agents, gold salts, rifampicin and so on. There are also very important contents in the medical history, which may lead to hints on the basis of immunity. Suggest the signs and symptoms of thrombotic thrombocytopenia (see TTP-HUS)； below); /kloc-blood transfusion within 0/0 days suggests that it may be purpura after blood transfusion, and heavy drinking suggests thrombocytopenia caused by alcohol. 5% of pregnant women may have mild thrombocytopenia during delivery. Because patients infected with human immunodeficiency virus (HIV) are often accompanied by thrombocytopenia, they can be distinguished from idiopathic thrombocytopenic purpura (see ITP). From this, we can get the risk factors and history of other HIV infection symptoms. Physical examination is also very important for diagnosis: (1) Thrombocytopenia is usually secondary to infectious or active systemic lupus erythematosus (SLE) and thrombotic thrombocytopenia (TTP), and sometimes fever occurs. However, idiopathic thrombocytopenic purpura (ITP) and drug-related purpura did not have fever. (2) Spleen of patients with thrombocytopenia is not enlarged due to the increase of platelet destruction (such as idiopathic thrombocytopenic purpura, drug-related immune thrombocytopenia, thrombotic thrombocytopenic purpura). The spleen of patients with thrombocytopenia secondary to retention of platelets in the spleen is mostly palpable, as is the spleen of patients with thrombocytopenia secondary to lymphoma or myeloproliferative diseases. (3) Other signs of chronic liver disease are also significant for diagnosis, such as spider nevus, jaundice and liver palm. (4) Thrombocytopenia often occurs in the third trimester of pregnancy. Peripheral blood cell count is a key examination to determine thrombocytopenia and its severity. At the same time, blood smear examination can provide clues for pathogenic examination (table 133-2). If thrombocytopenia is not accompanied by other diseases (such as liver disease or disseminated intravascular coagulation), the screening test of hemostasis function (see 13 1 section) is normal. If bone marrow examination shows abnormalities other than thrombocytopenia on blood smear, there is an indication for this examination. This examination can provide information on the number and morphology of megakaryocytes and determine whether there are diseases that cause bone marrow failure (such as abnormal proliferation of bone marrow). Anti-platelet antibody examination has little clinical significance. If the patient's medical history or examination provides the risk basis of HIV infection, HIV antibody examination should be carried out. Except ecchymosis, purpura and mucosal bleeding (slight or excessive), the physical examination results were negative. The results of peripheral blood tests were normal except for the decrease of platelet count. Bone marrow examination can usually find that megakaryocytes are normal or increase in number, and others are normal. The treatment of thrombocytopenia varies with its etiology and severity, so it is necessary to find out the cause quickly and correct it if possible (for example, heparin should be stopped for heparin-related thrombocytopenia). Because repeated platelet transfusion will produce allogeneic platelet antibodies, the curative effect will be reduced. Therefore, it should be used intermittently to prevent the production of the above antibodies. If thrombocytopenia is caused by platelet consumption, platelet transfusion should be reserved for the treatment of fatal or central nervous system bleeding. If thrombocytopenia is caused by bone marrow failure, platelet transfusion is reserved for treating acute bleeding or severe thrombocytopenia (such as platelet count < 10000/μ L). Adult treatment usually begins with oral corticosteroids (such as prednisone 1mg/kg/ day). If effective, platelet count will return to normal within 2~6 weeks, and then corticosteroids will be gradually reduced. However, the curative effect of most patients is not satisfactory. Or relapse after reducing the dose of adrenal steroids. Splenectomy can relieve 50%~60% of patients. For patients who are refractory to steroids and splenectomy, the efficacy of other drugs has not been confirmed. Because of the long course of chronic ITP and the low mortality rate of patients with chronic ITP, the advantages and disadvantages of treatment methods still need to be carefully weighed. Use synthetic androgens (danazol), or use azathioprine, vincristine, cyclophosphamide or cyclosporine. For ITP patients with fatal bleeding, intravenous immunoglobulin (IVIg) can be used, which can inhibit mononuclear macrophages from clearing antibody-coated platelets. The dose of IVIg was 1g/kg, 1 day or 2 consecutive days. The platelet count of patients can often increase within 2~4 days. However, it only lasts 2-4 weeks. High dose methylprednisolone1g/(kg d) intravenous drip for 3 days can increase the number of platelets rapidly, and the cost is slightly lower than IVIg. For patients with fatal bleeding, platelets should also be infused. Because glucocorticoid or IVIg may take effect within a few days, ITP patients should not be given prophylactic platelet transfusion. Children are treated in the opposite way to adults. Corticosteroids or IVIg can quickly restore platelet count, but it can't improve the clinical effect. Because most children can recover naturally from severe thrombocytopenia within a few days or weeks, supportive therapy alone is sometimes recommended. Splenectomy should be delayed for at least 6~ 12 months for children with chronic ITP who are ineffective in using corticosteroids or IVIg, because children without spleen will increase the risk of serious infection even if they get sick.

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