Thrombus falls off

Introduction A blood clot is a process in which the blood is coagulated in the living body, blood is coagulated, or some of the blood is formed and agglomerated to form a solid mass, called thrombosis. The solid mass formed is called a thrombus. Unlike blood clots, blood clots form in the state of blood flow. Thrombosis is a process of multifactorial changes involving many genetic and environmental factors that interact with each other. In patients with clinically common thrombogenic qualities, the most important features are family history, recurrent episodes, severity of seizure symptoms, and unusual thrombosis sites. Thrombosis 9embolism is said to stick to a place where the thrombus falls off and moves to another place, blocking blood vessels, such as the cerebral blood vessels, causing a stroke.

Cause

The thrombus forms in the blood vessels and generally does not move if there is no external force. However, if you accidentally apply an external force, such as a massage, the thrombus will fall off. At this time, the blood clot will move along the blood line. The most dangerous place is the pulmonary artery and vein, the coronary vein, which is prone to death. The cause of the formation should be related to the slowing of blood flow, arteriosclerosis, and abnormal blood coagulation.

an examination

Related inspection

Angiography

CT or ultrasound diagnosis. The thrombus forms in the blood vessels and generally does not move if there is no external force. However, if you accidentally apply an external force, such as a massage, the thrombus will fall off. At this time, the blood clot will move along the blood line. The most dangerous places are pulmonary arteries and veins, coronary veins, prone to death, blood clotting, angiography, and MRI.

Differential diagnosis

Thrombosis should be differentiated from the following symptoms

Microthrombosis: In the presence of procoagulant factors and the involvement of triggering cofactors, it can cause fibrin deposition and platelet aggregation, twisting into a mass 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.

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.

Portal venous stasis: Thrombosis is often secondary to: 1 cirrhosis or extrahepatic compression causes portal vein congestion and portal venous stasis; 2 intra-abdominal suppurative infections, such as gangrenous appendicitis, ulcerative colitis, strangulation Sexual paralysis, etc.; 3 certain blood abnormalities, such as polycythemia vera, hypercoagulable state caused by oral contraceptives; 4 trauma caused by trauma or surgery, such as mesenteric hematoma, splenectomy, right colon resection and so on. About 1/4 of patients have no obvious cause, called primary mesenteric venous thrombosis. After venous thrombosis, it can continue to spread to the proximal and distal ends. When the venous return of the affected bowel is completely blocked, the intestine is congested and edematous, and the subserosal bleeds first, then spreads into pieces. The intestinal wall and mesentery are thickened and edematous. In addition, hemorrhagic infarction occurred in the intestines, which was dark purple. A large amount of bloody fluid oozes from the intestinal wall and mesentery to the intestinal and abdominal cavities. Acute venous occlusion can also reflect the process of stenosis and thrombosis of visceral arteries and accelerate intestinal necrosis. Finally, it also leads to hypovolemia and toxic shock in infection.

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