Thrombi and Emboli. An abnormal clot that develops in a blood vessel is called a thrombus. Once a clot has developed, continued flow of blood past the clot is likely to break it away from its attachment and cause the clot to flow with the blood; such freely flowing clots are known as emboli. Also, emboli that originate in large arteries or in the left side of the heart can flow peripherally and plug arteries or arterioles in the brain, kidneys, or elsewhere. Emboli that originate in the venous system or in the right side of the heart generally flow into the lungs to cause pulmonary arterial embolism.

Cause of Thromboembolic Conditions. The causes of thromboembolic conditions in the human being are usually twofold: (1) A roughened endothelial surface of a vessel—as may be caused by arteriosclerosis, infection, or trauma—is likely to initiate the clotting process, and (2) blood often clots when it flows very slowly through blood vessels, where small quantities of thrombin and other procoagulants are always being formed.

Use of t-PA in Treating Intravascular Clots. Genetically engineered tPA is available. When delivered through a catheter to an area with a thrombus, it is effective in activating plasminogen to plasmin, which in turn can dissolve some intravascular clots. For instance, if used within the first hour or so after thrombotic occlusion of a coronary artery, the heart is often spared serious damage.

FEMORAL VENOUS THROMBOSIS AND MASSIVE PULMONARY EMBOLISM

Because clotting almost always occurs when blood flow is blocked for many hours in any vessel of the body, the immobility of patients confined to bed plus the practice of propping the knees with pillows often causes intravascular clotting because of blood stasis in one or more of the leg veins for hours at a time. Then the clot grows, mainly in the direction of the slowly moving venous blood, sometimes growing the entire length of the leg veins and occasionally even up into the common iliac vein and inferior vena cava. Then, about 1 out of every 10 times, a large part of the clot disengages from its attachments to the vessel wall and flows freely with the venous blood through the right side of the heart and into the pulmonary arteries to cause massive blockage of the pulmonary arteries, called massive pulmonary embolism. If the clot is large enough to occlude both pulmonary arteries at the same time, immediate death ensues. If only one pulmonary artery is blocked, death may not occur, or the embolism may lead to death a few hours to several days later because of further growth of the clot within the pulmonary vessels. However, again, tPA therapy can be a lifesaver.

DISSEMINATED INTRAVASCULAR COAGULATION

Occasionally the clotting mechanism becomes activated in widespread areas of the circulation, giving rise to the condition called disseminated intravascular coagulation. This condition often results from the presence of large amounts of traumatized or dying tissue in the body that releases great quantities of tissue factor into the blood.

Frequently, the clots are small but numerous, and they plug a large share of the small peripheral blood vessels. This process occurs especially in patients with widespread septicemia, in which either circulating bacteria or bacterial toxins—especially endotoxins—activate the clotting mechanisms. Plugging of small peripheral vessels greatly diminishes delivery of oxygen and other nutrients to the tissues, a situation that leads to or exacerbates circulatory shock. It is partly for this reason that septicemic shock is lethal in 85 percent or more of patients.

A peculiar effect of disseminated intravascular coagulation is that the patient on occasion begins to bleed. The reason for this bleeding is that so many of the clotting factors are removed by the widespread clotting that too few procoagulants remain to allow normal hemostasis of the remaining blood.

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المزيد

مواضيع ذات صلة

Conditions that Cause Excessive Bleeding in Humans

Absent Intrinsic Factor Secretion and Pernicious Anemia

Subclinical Hyperthyroidism

Thyrotoxic Periodic Paralysis: Clinical Features

Nutritional Causes of Folate Deficiency

Neurologic Dysfunction with Cobalamin Deficiency

Sclerosing Thyroiditis (Riedel’s Thyroiditis) : Clinical Features

Infectious Thyroiditis

Leukopenia

Morphologic Expression of Megaloblastosis

Presentations Associated with Sideroblastic Anemia or Porphyrinuria

Sideroblastic Anemia and Porphyrinuria Caused by Drugs