Microangiopathic hemolytic anemia

Introduction to microangiopathic hemolytic anemia Microangiopathic hemolytic anemia is a severe diffuse thrombotic microangiopathy characterized by microvascular hemolytic anemia, reduced consumption of platelet aggregation, and organ damage caused by microthrombus (such as the kidney, central nervous system, etc.) . It is a hemolytic anemia syndrome in which small blood vessel lesions cause red blood cells to break. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: anemia

Causes of microangiopathic hemolytic anemia

(1) Causes of the disease

A disease associated with microangiopathic hemolytic anemia.

(two) pathogenesis

Microvascular damage (25%):

Microvascular injury is the key mechanism for the occurrence of this disease. The damaged microvessels are narrowed by fibrin deposition, thrombosis or other factors. When red blood cells flow through, they are forced to pass through or block the fibrin filament under the pressure of blood circulation. It is crushed, split, and intravascular hemolysis occurs. Some damaged red blood cells are spleen, mononuclear macrophages in tissues such as liver are phagocytized, and extravascular hemolysis occurs. This pathogenesis is caused by various diseases mentioned above. Common to microangiopathic hemolytic anemia, these diseases differ in the specific processes that damage microvasculature, cause fibrin deposition and thrombosis.

Coagulation system damage (15%):

Activation of the coagulation system often plays an important role in the occurrence of this disease. Experiments have shown that injection of endotoxin or thrombin into animals can cause microangiopathic hemolysis. If heparin is given to animals in advance, it can be avoided, and drugs that inhibit fibrinolysis can be avoided. Aggravated, when the blood vessel is completely blocked by a dense thrombus, the red blood cells cannot pass, and no hemolysis occurs. The loose fibrin network has a certain gap, and the red blood cells enter the fibrin network depending on the blood circulation pressure and deformation performance, and are blocked in the On the fine fibrin filament, if the blood circulation pressure is large, the compression of the red blood cells through the fibrin filament can be split, and therefore, the pressure is also a condition for causing destruction of the red blood cells.

Other (8%):

There are also some diseases, diffuse or local microvascular disease, but no coagulation abnormalities like diffuse intravascular coagulation, can be seen in cavernous hemangioma, renal transplant rejection, malignant hypertension, eclampsia, certain blood vessels Inflammation (such as rickettsial infection, nodular arteritis, Wegener granulomatosis) and some widely metastatic cancers, hemolysis can be light and heavy.

Microvascular hemolytic anemia prevention

Actively treat the primary disease and prevent the disease from developing.

Prevention of anemia: As long as daily life and dietary attention are adjusted, anemia can be prevented. To prevent anemia, we must first provide sufficient hematopoietic material for the bone marrow. Iron is the main raw material for making hemoglobin. Infants and young children need more iron to meet the needs of growth and development. Usually consciously give your baby more iron-rich foods, such as lean meat, pork liver, egg yolk and kelp, hair dish, seaweed, fungus, fragrant ru, beans. Pay attention to the reasonable combination of diet, such as eating some fruits after a meal, the fruit is rich in vitamin C and fruit acid, which can promote the absorption of iron. Drinking strong tea after a meal is caused by the combination of iron and tannic acid in the tea to form a precipitate, which affects the absorption of iron. Cooking food in a wok is good for preventing anemia.

Microvascular hemolytic anemia complications Complications anemia

Complications of microangiopathic hemolytic anemia occur in a variety of diseases and pathophysiological processes such as infection, drugs, autoimmune diseases, tumors, and bone marrow transplant pregnancy.

Symptoms of microangiopathic hemolytic anemia Common symptoms Red blood cell life shortens Skin mucosal bleeding Red blood cells Increased jaundice Unexplained fever Hemoglobinuria Hereditary hemorrhagic hair...

Hemolysis occurs more acutely, with more severe hemoglobinuria and anemia, in addition to the performance of the primary disease.

Examination of microangiopathic hemolytic anemia

1. Peripheral blood:

Finding malformed broken red blood cells in the smear is typical of this disease. These broken red blood cells are shaped like helmets, spines, triangles, and smaller red blood cells and spherical cells can be seen. Excessive hemolysis can occur in peripheral blood. There are nucleated red blood cells, reticulocytes increase, white blood cell counts are often mild, moderately elevated, but the morphology is normal, there may be abnormalities of thrombocytopenia and coagulation indicators.

2. Bone marrow:

The erythroid cell line is proliferating and the megakaryocyte cell line can also be increased.

3. Increased free hemoglobin in serum, reduced haptoglobin.

4. Increased bilirubin:

Increased indirect bilirubin.

5. Urine occult blood:

Positive or visible hemoglobinuria, chronic may have hemosiderin urine.

Diagnosis and diagnosis of microangiopathic hemolytic anemia

According to the clinical manifestations and laboratory test results, it can be diagnosed.

1. Domestic diagnostic criteria:

(1) clinical manifestations: 1 with varying degrees of skin, mucosal bleeding; 2 hemolysis can suddenly increase and fever, jaundice and anemia.

(2) Laboratory examination: 1 peripheral blood smears appear more broken red blood cells (3% or more), can be helmet-shaped, triangular, zigzag, etc.; 2 plasma free hemoglobin can often exceed 50mg / L; 3 platelet count is obvious Reduction; 4 severely hemolytic blood may appear nucleated red blood cells and multi-stained red blood cells, bone marrow erythrocyte system hyperplasia is active; 5 reticulocytes often increase; 6 indirect bilirubin increased; 7 haptoglobin decreased; 8 hemoglobinuria; Chronic cases may have hemosiderin urine.

According to the clinical manifestation 2 plus the laboratory test, the first item and any two of the other items can be diagnosed.

2. Foreign diagnostic criteria:

(1) The ruptured red blood cells are between 3% and 5%.

(2) The clinical data meet the following items: 1 anemia, jaundice, hemoglobinuria; 2 reticulocyte increase; 3 shortened red blood cell life; 4 hyperhemoglobinemia; 5 hemosiderin urine.

Anyone who meets item (1) plus any two items in paragraph (2) can be diagnosed.

The key to identification is the diagnosis of the primary disease and the identification of various diseases that may be associated with this disease. This is also the premise of correct and timely treatment of this disease.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.