The blood returns from the legs to the heart and is pushed further through the pulmonary arteries to the lungs, where it is saturated with oxygen. On this route, venous clots are dangerous for health. Especially when the clot breaks away from the wall of the deep leg vein and gets into the lungs. Then it threatens our lives.
Reasonable fear of a clot in the leg vein
When the blood becomes excessively sticky and clumps too quickly, we are afraid in the first place of life-threatening deep vein thrombosis, i.e. the so-called venous thrombosis. This applies especially to older people, over 60 years of age, obese people, people suffering from varicose veins and phlebitis, women using hormonal contraception and hormone replacement therapy, people with congenital excessive blood viscosity and diseases or disabilities that force them to stay still for a long time. In a medical language the cause of justified anxiety is thrombotic disease complicated by pulmonary embolism, or shorter - thromboembolic disease of leg veins.
Venous thrombosis
The onset of thromboembolism is thrombosis of deep leg veins. Venous thrombosis is an intense development of a blood clot in the vein, resulting in a blood clot - a plug that adheres to the vein wall and impairs the flow of blood from the leg to the heart. What is this caused? First, the "sticking" of platelets to the walls of the veins (and to each other); usually in the vicinity of venous valves. Secondly, "braiding" glued platelets with fibrin - a strong protein fiber. The fibrin fiber is created in specific circumstances from the previously liquid blood plasma protein fibrinogen.
The mechanism of a venous thrombus
The most important factor initiating thrombus formation is damage to the inner surface of the vessel wall. It may occur as a result of blood stagnation and hypoxia of cells forming the inner lining of the vessel (the so-called endothelium), as well as due to mechanical damage to the venous valves by the stream flowing under increased blood pressure. As a result, platelets are activated that begin to adhere to the damaged endothelium and to each other. Often it is enough to slow the flow of blood in the veins so that the platelets begin to clump together and initiate a blood clot. The slowdown results in a change of the flow of blood from a calm (laminar) to turbulent - imitating damage to the vessel, which is characterized by turbulence in the bloodstream especially around the valves and at the vascular fork. The "deceitful" blood plates release enzymes that transform the liquid protein - fibrinogen into strong fibrin fibers that strengthen the thrombus. In the fibrin net, the erythrocytes and platelets then bind - resulting in an increasingly larger thrombus. The clot is usually placed in the veins of the calf, on the venous valve. It completely or partially clogs the vessel, preventing normal blood flow. The clogging of one of the large veins of the deep leg or thigh makes the blood virtually no place to return to the heart and begins to accumulate rapidly in the vessels below the obstacle, and then gets out of the vessels into the tissues, forming a swelling.
Diseases and immobility promote clots
To slow down blood flow or venous stasis in the lower extremities, he predicts a longer immobilization of the patient in bed, because the muscular pump, which determines proper venous return of the blood, does not work then.This process may intensify co-existing other diseases that impair venous circulation, eg chronic heart failure, chronic venous insufficiency, phlebitis and varicose veins, and external vein compression.
Venous thrombosis initiated by varicose veins
The reason for the thrombosis of these veins is released, and sometimes completely stopped blood flow in irregular distension of the surface veins - the so-called varicose veins. Stagnation in varicose veins leads to chronic inflammation, which initiates the formation of wall clots. A vein in the vein is an ideal breeding ground for bacteria that in many healthy people lie dormant in the tonsils or under-treated teeth, which deepens the inflammation and its extent. However, the clot of the superficial vein, unlike the thrombus in the deep vessel, usually clings tightly to the wall and almost never threatens pulmonary embolism. However, it slows down the flow of blood from the legs, although surface vein tasks can almost completely take over very efficient deep veins. It also causes significant complaints by letting you know about severe pain, redness of the skin and spongy thickening. Inflammation of varicose veins, although sometimes accompanied by turbulent symptoms, is usually easy to treat with antibiotic and anti-inflammatory drugs and a flexible tourniquet to improve venous circulation.
Deep vein thrombosis
When inflammation of the deep veins is added to the varicose veins, venous thrombi is located in the deep veins of the leg and pelvis. Deep vein thrombosis hinders blood flow to the heart, causes skin changes, swelling of the limb, sometimes severe pain. Although thrombosis does not directly threaten life, the detachment of a blood clot from the vein wall can cause pulmonary embolism.
Pulmonary embolism a threat to life!
When the clot breaks off the wall, the veins may flow with the bloodstream to the heart and then clog up the pulmonary arteries. And that means pulmonary infarction and in case of massive obstruction, acute circulatory failure that threatens sudden death.
Thromboembolic disease of leg veins
As you can see, thromboembolism has two conjugate disease processes - deep veins of the lower limbs (DVT) and life-threatening pulmonary embolism (ZTP). Unfortunately, in a civilized world it is quite a common disease. For example, in the US, the inflammation of the deep veins of the lower limbs occurs in about 2 million people, and the pulmonary embolism in about 600,000. In Poland, about 50,000 people suffer from deep vein thrombosis every year, and about 20,000 pulmonary embolism, of which about 30 percent, unfortunately, die.
ed. Edward Ozga Michalski, MA
drug consultation med. Michał Wojtyczka
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