Congestive splenomegaly is caused by portal hypertension due to liver cirrhosis, inflammation or thrombosis of the portal vein or splenic vein. It often accompanies the manifestations of liver cirrhosis and portal hypertension, such as varices of the lower esophagus or fundus of the stomach, ascites, dyspepsia, etc.; at the same time, it is accompanied by hyperfunction of the spleen, manifested as the phenomenon of 'three lows' with decreased red blood cells, white blood cells, and platelets; at the same time, bone marrow hematopoietic function is vigorous.
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Congestive splenomegaly
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1. What are the causes of the onset of congestive splenomegaly
2. What complications can congestive splenomegaly easily lead to
3. What are the typical symptoms of congestive splenomegaly
4. How to prevent congestive splenomegaly
5. What laboratory tests need to be done for congestive splenomegaly
6. Diet taboos for patients with congestive splenomegaly
7. Conventional methods of Western medicine for the treatment of congestive splenomegaly
1. What are the causes of the onset of congestive splenomegaly
The most common cause of congestive splenomegaly is portal hypertension caused by liver cirrhosis; the second most common cause is inflammation or thrombosis of the portal vein or splenic vein. The etiology of portal hypertension can be divided into three types: pre-hepatic, intra-hepatic, and post-hepatic. Chinese patients mainly have the intra-hepatic type, accounting for about 90%. Pre-hepatic type: There is a problem with the portal vein itself, such as thrombosis of the portal vein, congenital malformation, and external compression, etc., which cause the portal vein blood flow to be unsmooth, and the pressure will naturally increase. These patients have no liver problems, so their liver function is normal or only slightly damaged, and the treatment effect is the best.
2. Enlarged spleen due to congestion can easily lead to what complications
1. Liver and lymph node enlargement:Seen in malignant lymphoma, lymphocytic leukemia, connective tissue disease, benign monocytosis, sarcoidosis, and certain infectious diseases, etc.
2. Liver face, liver palm, and spider veins:Seen in chronic viral hepatitis, liver cirrhosis.
3. Various types of rashes:Commonly seen in various infectious diseases or infectious diseases. Such as typhoid fever, epidemic typhus, brucellosis, sepsis, subacute bacterial endocarditis, etc.
4. Edema and ascites:Seen in chronic right heart failure, constrictive pericarditis, liver cirrhosis portal hypertension inferior vena cava obstruction, and other conditions.
5. Organ enlargement:Seen in chronic heart failure caused by various types of heart disease, and various causes of large amounts of pericardial effusion.
3. What are the typical symptoms of congestive splenomegaly
Congestive splenomegaly often accompanies the manifestations of liver cirrhosis and portal hypertension, such as varices at the lower end of the esophagus or the fundus of the stomach, ascites, dyspepsia, etc.; at the same time, there is hyperfunction of the spleen, manifested as a 'three reductions' phenomenon of reduced red blood cells, white blood cells, and platelets; at the same time, the bone marrow hematopoietic function is vigorous.
4. How to prevent congestive splenomegaly
The key to the disease is the prevention of complications. Splenomegaly is usually associated with liver enlargement, and generally mild splenomegaly is often associated with acute infection, hemolytic anemia, congestive heart failure, leukemia, lymphoma, liver cirrhosis, and rheumatism; severe splenomegaly is related to sexual infection, severe malabsorption, parasitic infection (kala-azar), and other factors. Splenomegaly increases due to mechanisms such as lymphocytic proliferation, cancer cell infiltration, increased macrophages, and blood stasis. Pay attention to preventing the occurrence of the above complications.
5. What laboratory tests are needed for congestive splenomegaly
1. Peripheral blood smear: Due to many hematological lesions being related to congestive splenomegaly, special findings in peripheral blood examination can provide clues for etiological diagnosis (such as lymphocytosis in chronic lymphocytic leukemia, spherocytosis in hereditary spherocytosis), platelets occasionally less than 50,000/μl, with a decrease in mean platelet volume, and in addition to leukemia, the number of white blood cells can be reduced, excessive basophils or nucleated red blood cells or tear-shaped red blood cells appear, suggesting a diagnosis of bone marrow proliferative disease.
2. Bone marrow examination: Single-line (or multi-line) cell proliferation can be seen, but the corresponding peripheral blood cells are reduced; lymphoproliferative diseases show lymphocytic infiltration; myeloproliferative diseases show bone marrow cell proliferation; in acute leukemia, there is an increase in primitive cells; fibrosis is seen in bone marrow fibrosis, myeloid metaplasia; periodic acid-Schiff staining aggregates are seen in amyloidosis; lipid-laden macrophages are seen in Gaucher's disease and related storage diseases.
3. Imaging examination: Colloid spleen scan marked with technetium-99m is a reliable non-invasive examination method. Through examination, it can be determined that the abdominal mass in the upper left quadrant is the spleen, and intrasplenic lesions can also be confirmed. CT scan can determine the size of the spleen and display the abnormal characteristics of various endogenous and exogenous lesions, while magnetic resonance imaging can provide the same information as CT and can also determine blood flow type, especially useful for checking the formation of portal vein and splenic vein thrombosis.
4. Chromium-51 labeled red blood cell and platelet survival and spleen uptake function tests This special examination is beneficial in determining the degree of retention of these cells when considering splenectomy.
5. Blood chemistry tests: Blood chemistry tests are helpful in diagnosing many diseases associated with splenomegaly
(1) Serum electrophoresis showing monoclonal gammopathy or decreased immunoglobulins suggests lymphoproliferative diseases or amyloidosis;
(2) Polyclonal hypergammaglobulinemia may be seen in chronic infections (such as malaria, kala-azar, brucellosis, tuberculosis) or in liver cirrhosis with congestive splenomegaly, sarcoidosis, and collagen vascular diseases; uric acid elevation occurs in myeloproliferative diseases and lymphoproliferative diseases;
(3) Alkaline phosphatase in white blood cells increases in myeloproliferative diseases, but decreases in chronic myeloid leukemia;
(4) Liver function tests may show widespread abnormalities in patients with cirrhotic congestive splenomegaly, with a single increase in serum alkaline phosphatase, similar to that in myeloproliferative diseases, lymphoproliferative diseases, and miliary tuberculosis, indicating liver infiltration. An increase in serum vitamin B12 may be seen in myeloproliferative diseases, especially in chronic myeloid leukemia and polycythemia vera, due to the increased vitamin B12-binding protein released by neutrophils.
6. Dietary taboos for patients with congestive splenomegaly
What to eat for splenomegaly:
Diet should be low in fat, high in protein, high in vitamins, and easy to digest. It is also important to adhere to regular meals, proper portion control, and moderation. Eat more fresh vegetables and fruits, and consume appropriate amounts of carbohydrates, eggs, fish, lean meat, and so on.
7. Conventional methods of Western medicine for treating congestive splenomegaly
Most patients with splenomegaly need to be treated for their primary disease rather than have their spleen removed. Due to the increased susceptibility of patients who have lost their spleen to severe systemic infections caused by capsulated bacteria (such as Haemophilus influenzae, Streptococcus pneumoniae), the indications for splenectomy and radiotherapy must be strictly controlled. Splenic artery embolization has the advantage of preserving the blood storage and immune function of the spleen while solving the problem of splenic hyperfunction. It achieves the therapeutic purpose by embolizing a part of the splenic artery, causing the embolized part of the spleen tissue to necrose due to ischemia.
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