Blue-purple skin changes

Introduction If the red blood in the blood (a hemoglobin that does not carry oxygen) increases, the skin will have a blue-violet change in the skin, medically known as cyanosis, often most prominent in the tongue, lips, auricles, cheeks, and extremities. The skin blue-purple change is more common in platelet purpura, which is a type of blood plate that is less prone to coagulation and blood disease due to less platelets.

Cause

The etiology and pathogenesis of this disease have not been fully elucidated. Acute type occurs mostly after acute viral upper respiratory infection has healed, suggesting that thrombocytopenia is associated with an immune response to the primary infection. About half of chronic patients can detect anti-platelet antibodies in serum.

I. Platelet-related antibodies Anti-platelet antibodies are present in the serum of chronic ITP patients. If the plasma of a chronic ITP patient is delivered to a normal person, the normal person's thrombocytopenia can be reduced; if the normal human platelet is delivered to the ITP patient, the input platelet is destroyed in a short time. It was confirmed that the shortening of platelet life in ITP patients was due to the presence of platelet-destroying antibodies in serum, called platelet-associated antibodies (PAIC3), 95% of which were IgG type, and a small amount of IgM and IgM type. Platelet-associated complement C3 (PAC3) is present in the blood circulation of ITP patients, and its increase is directly proportional to the increase in PAIg.

Second, the platelet destruction mechanism The average life expectancy of platelets is 7 to 11 days, while the lifespan of platelets in ITP patients is only 40 to 230 minutes. Because the spleen contains a large number of macrophages, it can produce high concentrations of anti-platelet antibodies, and the slow blood flow can block the antibody-coated platelets, so the spleen becomes the main site of platelet destruction. The liver and bone marrow are also places where platelets are destroyed. Chronic ITP platelet destruction is caused by the phagocytosis of macrophage cells by binding of anti-platelet antibodies to their associated antigens. Acute ITP platelet destruction is caused by the adsorption of viral antigens on the surface of platelets and binding to the corresponding antiviral antibodies, resulting in destruction of platelets.

Third, megakaryocyte maturation disorder Because platelets and megakaryocytes have a common antigen, anti-platelet antibodies can also inhibit bone marrow megakaryocytes, causing maturity disorders, thereby affecting platelet production.

Fourth, other factors

1, the role of estrogen: chronic type is more common in women of childbearing age, easy to relapse during pregnancy, suggesting that estrogen may play a role in the pathogenesis of this disease, it may be that estrogen can increase the ability of macrophages to phagocytosis and destruction of platelets;

2, the antibody damages the capillary endothelial cells, causing the capillary permeability to increase and aggravate the bleeding.

an examination

Related inspection

Blood routine platelet-associated immunoglobulin (PAIgG, PAIgA, PAIgM) White blood cell count (WBC) Red blood cell test flexion thumb fist test

First, thrombocytopenic purpura symptoms

1, acute type

Most children under the age of 10 have a history of viral infection before the disease. Most of the above respiratory infections, rubella, measles and chickenpox are also available; after vaccination. The incubation period between infection and sable is more than 1-3 weeks.

Mainly for the skin, mucous membrane bleeding, often more serious, skin bleeding is varying in size, uneven distribution, with more limbs. Mucosal bleeding has nasal discharge, bleeding gums, and buccal mucosa. Often there are digestive tract, urinary tract bleeding, ocular bleeding under the membrane, a small number of retinal hemorrhage. Spinal cord or intracranial hemorrhage is common and can cause paralysis of the lower extremities or intracranial hypertension, which can be life-threatening.

2, chronic type

Mostly 20-50 years old, women are 3-4 times male. Insidious onset. Patients may have persistent bleeding or recurrent episodes, and some may have localized bleeding tendency, such as repeated epistaxis or menorrhagia. Defects and ecchymoses can occur in any part of the skin and mucous membranes, but more distal to the extremities. There may be bleeding in the digestive tract and urinary tract. Deep hematoma can also occur after trauma.

Second, the diagnosis of thrombocytopenic purpura

1, blood:

Acute platelets are significantly reduced, mostly below 20 × 109 / L. When the bleeding is severe, it can be accompanied by anemia, and white blood cells can be increased. Occasionally, eosinophilia. Chronic, platelets are mostly in the range of 30-80 × 109 / L, common large deformed platelets.

2, bone marrow:

Acute type, the number of megakaryocytes is normal or increased, mostly naive, with smooth cell edges, no protrusions, few cytoplasm and large particles. Chronic, megakaryocytes generally increase, granular megakaryocytes increase, but the cytoplasm contains less particles, basophilic.

3. Immunological examination:

4. Other:

The bleeding time was prolonged, the beam arm test was positive, the blood clot contraction was poor, platelet adhesion and aggregation function were weakened, and the life of the 51Cr or 111In labeled platelets was shortened.

Differential diagnosis

Differential diagnosis of skin blue-purple changes:

(1) Aplastic anemia: manifested as three major symptoms of fever, anemia, and hemorrhage. The liver, spleen, and lymph nodes are not large. Similar to idiopathic thrombocytopenic purpura with anemia, but the anemia is heavier, the total number of white blood cells is Neutrophils are reduced, and reticulocytes are not high. The bone marrow red, granulocyte system has reduced blood function, and megakaryocytes are reduced or extremely difficult to find.

(2) Acute leukemia: ITP is especially needed to identify leukemia with no increase in white blood cells. It can be confirmed by bloody smear showing various stages of immature white blood cells and bone marrow examination.

(3) allergic purpura: for symmetrical hemorrhagic rash papules, the lower limbs are more common, platelets are many, generally easy to identify.

(4) lupus erythematosus: early manifestations of thrombocytopenic purpura, suspected of anti-nuclear antibodies and lupus cells (LEC) can help identify.

(5) Wiskortt-Aldrich syndrome: In addition to hemorrhage and thrombocytopenia, combined with extensive eczema throughout the body and easy to infect, platelet adhesion decreased, no agglutination reaction to ADP, adrenaline and collagen. It is a recessive hereditary disease, which occurs in male infants and dies within 1 year of age.

(6) Evans syndrome: characterized by simultaneous autoimmune thrombocytopenia and hemolytic anemia, Coomb s test is positive, the condition is more serious, most patients are effective by hormone or splenectomy.

(7) Thrombotic thrombocytopenic purpura, seen at any age, the basic pathological changes are eosinophilic embolization of small arteries, previously thought to be platelet embolism, and confirmed by fibrin embolization by fluorescent antibody test. This vascular damage can occur in various organs. Clinical manifestations of thrombocytopenic hemorrhage and hemolytic anemia, hepatosplenomegaly, hemolysis is more urgent, fever, and abdominal pain, nausea, diarrhea and even coma, convulsions and other neurological symptoms. Reticulocytes increase, and nucleated red blood cells appear in the surrounding blood. Serum anti-human globulin test is generally negative. Can show renal dysfunction, such as hematuria, proteinuria, azotemia, acidosis. The prognosis is severe, and there is only a temporary combination of adrenocortical hormones.

(8) Secondary thrombocytopenic purpura: Both severe bacterial infection and viremia can cause thrombocytopenia. Various splenomegaly diseases, bone marrow-infested diseases, chemical and drug allergies and poisoning (drugs can directly destroy platelets or inhibit their function, or combine with plasma components to form antigen complexes, which in turn produce antibodies, and then allergic to antigenic antibodies Reaction, destruction of platelets. Allergic reactions can be seen at the beginning of chills, fever, headache and vomiting, etc.), hemolytic anemia can be associated with thrombocytopenia, should be carefully examined to find out the cause to identify with idiopathic thrombocytopenic purpura.

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