Microthrombosis

Introduction Under the influence of the procoagulant factor and the triggering cofactor, it can cause fibrin deposition and platelet aggregation, twisting into a group to form microthrombus and block microvessels. Condensed platelets release procoagulant substances, activate thrombin, further promote fibrin formation and deposition, leading to disseminated intravascular coagulation. If fibrin is deposited on the surface of red blood cells, it can wrap and stick to each other during the circulation to form a large clot, extending from the capillaries to the venules, causing local blood flow obstruction. When the wrapped red blood cells gradually degenerate and decompose, the released hemoglobin and thromboplastin can promote blood coagulation.

Cause

Thromboembolic diseases are more common in the clinic and involve a wide range of causes. In recent years, with the development of basic medicine, the deeper research on platelet biochemistry, vascular endothelial cell function, chemical structure of clotting factors and ultrastructure has gained more understanding of the thrombosis process. Thrombosis is currently thought to be caused by a combination of factors, including vascular wall, platelet, blood flow velocity, blood viscosity and coagulation activity. Recently, studies on blood protease inhibitors have found that some patients with congenital thrombotic substances or congenital thrombosis have further understanding of the etiology and pathogenesis of thromboembolic diseases. The common causes are as follows:

Thrombotic quality

(1) Deficiency of anticoagulant substances: antithrombin III deficiency, abnormal antithrombin III disease, protein C deficiency, protein S deficiency, and heparin cofactor II deficiency.

(2) abnormal fibrinolytic: plasminogen deficiency, lack of fibrinolysis activator, increased fibrinolysis inhibitor, abnormal fibrinogenemia.

2. Venous thrombosis

(1) blood stasis: pregnancy, obesity, trauma, surgery, congestive heart failure, bedriding for too long.

(2) Coagulation: malignant tumors, myeloproliferative diseases.

(3) Others: oral contraceptives, hemolytic crisis.

3. Arterial thrombosis

(1) abnormal blood vessel wall: atherosclerosis, hyperlipidemia, diabetes.

(2) Increased blood viscosity: polycythemia vera, plasma cell disease, burns.

(3) abnormal platelet function: essential thrombocytosis.

4. Microcirculation thrombosis

(1) Embolization: more common in arterial thrombosis.

(2) Increased blood coagulation activity: bacterial endotoxin, virus, hemolysis, necrotic tissue, tumor cells, thrombotic thrombocytopenic purpura, serum disease, disseminated intravascular coagulation.

an examination

Related inspection

Angiographic angioscope

1. Red thrombus: When fibrin is attached to the surface of red blood cells, several or dozens of red blood cells are stuck together to form a mass or a bad shape, which often adheres to the pathological vessel wall or blocks microcirculation. This type of thrombus is loose and can be re-discreted after being impacted by blood flow. Because it is easy to occur in the slow blood flow, it is more common in the venous system.

2, white thrombus: When the platelets condense in the damaged blood vessel wall, immediately deform or rupture, stimulate the coagulation system, so that fibrin adheres to it, becomes the core of the thrombus and gradually increases. This type of thrombus is more common in the arterial system with rapid blood flow. If red blood cells are involved, a mixed thrombus is formed. In the arterial system, if red blood cells are involved, a mixed thrombus is formed.

3. Fibrin thrombosis: This thrombus occurs in the capillaries of organs such as the lungs, brain, spleen and kidneys. It can block the microcirculation and cause microscopic necrosis of the tissue. It is more common in various types of shock, heterogeneous blood transfusion, dead fetus, cancer spread and leukemia. Although fibrin thrombus is common in systemic hypercoagulable state, in the disseminated intravascular coagulation, due to the consumption of fibrinogen, factor V, factor four, secondary fibrinolysis, increased fibrin degradation products and anticoagulation The action of blood enzymes and the formation of stimuli can increase the permeability of blood vessels and produce a tendency to hemorrhage.

Differential diagnosis

Need to be distinguished from related symptoms:

Migratory superficial vein thrombosis: venous thrombosis can occur in the pathogenesis of superficial venous thrombosis, often involving the great saphenous vein or small saphenous vein or its branches, mostly on the basis of varicose veins. The main feature is the pain in the thrombus formation. The superficial vein has a red, low-heat cord, tenderness, and redness around it. The embolus is not easy to fall off and generally does not cause pulmonary embolism. In addition, migratory superficial vein thrombosis is often a suggestive symptom of cancer.

Inferior vena cava thrombosis: deep vein thrombosis is a common clinical disease, and inferior vena cava thrombosis is a serious type, with many complications and poor prognosis. In recent years, the incidence rate is on the rise, especially in the advanced stage of the tumor. The increase of inferior vena cava thrombosis after tumor radiotherapy and chemotherapy and inferior vena cava filter implantation has attracted the attention of doctors.

Thrombosis: The post-thrombotic syndrome of senile venous thrombosis is characterized by large veins forming thrombus in the lower extremities. It is difficult to dissolve and recanal naturally, causing thrombosis and venous occlusion, and the venous valve often occurs even if it is dredged again. Incomplete function.

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