See also: venous thrombosis - Coumadin
The term trombo [from thrombos = lump] indicates the presence of a blood clot that adheres to the undamaged walls of the vessels, whether they are arterial, venous, capillary or coronary (which provide blood circulation to the heart).
The presence of a thrombus is a potentially serious condition, since if it reaches significant dimensions it can obstruct the lumen of the vessel and block its flow.
If the thrombus affects a vein (venous thrombosis - red thrombus) it leads to a circulatory stasis with the appearance of edema, that is, an accumulation of fluid in the tissue spaces present between one cell and another, causing an abnormal swelling of the organs or regions concerned. Examples are thrombophlebitis, or superficial thrombosis, and deep vein thrombosis . The first condition manifests itself through the five cardinal signs typical of inflammation (low-grade fever, redness, edema, pain and loss of function), with the characteristic formation of a painful cord along the course of the obstructed vein; rarely gives rise to serious complications due to the formation of emboli. Deep vein thrombosis, on the other hand, is more dangerous, above all because, despite being asymptomatic in about 50% of cases, the thrombus can detach, migrate to the right heart and from here to the lungs.
We often tend to confuse the meaning of the terms thrombus and embolus or to use them improperly as synonyms. In reality embolization is a serious complication of thrombosis. In fact, it takes the name of embolus, although in reality the concept is broader, any fragment of thrombus detached from the main thrombotic mass that travels in the circulatory stream, at least until, unfortunately, it reaches a smaller diameter vessel occluding it and causing ischemia ( ie decrease or suppression of blood flow in a given body district). If the embolus detaches from a venous thrombus it can reach the lungs and obstruct a pulmonary artery (which carries venous blood). Both conditions (arterial and venous embolism) are potentially lethal and occur, respectively, with suffering of tissues affected by ischemia, up to the compromise of the organs involved (for example, heart attack or stroke), and with chest pain, tachycardia, dyspnoea and sudden death.
When the embolus detaches from a thrombus that has been invaded by pathogenic microorganisms (suppurative thromboarteritis) it can propagate the infection remotely, causing rapid degeneration and necrosis of the elements of the vessel wall, until they perforate them.
What are the causes of thrombosis?
Blood coagulation is a process of vital importance but it must absolutely remain in balance; if it were poorly effective it would in fact cause excessive bleeding, while an increase in hemostatic activity would lead to thrombus formation.
The coagulation process is, in reality, given by an innumerable cascade of chemical reactions involving, in addition to the "famous" platelets and vitamin K, many enzymes and chemical factors. This means that at the base of the thrombosis there can be many triggers. Among these the most important are represented by the so-called Triad of Virchow :
- ENDOTHELIAL DAMAGE,
- STASI OR TURBULENCE OF THE BLOOD FLOW
- BLOOD HYPERCOAGULABILITY.
In arterial and cardiac thrombosis the damaging factor prevails (endothelial damage due to atherosclerosis) and turbulent, whereas venous thrombus is preferably formed in the presence of blood stasis.
More specifically, venous thromboses are usually the consequence of one or more of the following risk factors: trauma, surgery, prolonged immobility, varicose veins, infections, venous wall lesions, hypercoagulability and venous stasis, infectious diseases, burns, tumors malignant, advanced age, estrogen therapy, obesity, pregnancy and childbirth.
Arterial thromboses generally affect diseased arteries at a lesion secondary to atherosclerosis (disease due to the presence of atheromas - obstructive formations conceptually similar to thrombus, but formed by different elements such as cholesterol, macrophages, lipids and calcium crystals -). When the superficial wall of the atherosclerotic plaque breaks down, a clot is formed, just as it happens when we get a wound. Within the artery the coagulation mechanisms thus give rise to a hard substance (thrombus or clot) that can interrupt the blood flow causing a sudden enlargement of the plaque. Due to the lesion, a piece of atheroma may also come off and, transported to the periphery by the blood, it would occlude smaller vessels (embolism). The main risk factors for the development of arterial thrombosis are therefore of genetic origin (familiarity for the pathology) and individual (age, sex, sedentary life and obesity, smoking, diet rich in cholesterol and saturated fats, stress, bad eating habits and diabetes). Hyperlipidemia, hyperhomocysteinemia and the finding of high levels of antiphospholipid antibodies are associated with an increased risk of thrombosis.
Antithrombotic care and therapy
To be in balance, the coagulation process uses, as mentioned, numerous factors. Some of these favor platelet aggregation and fibrin production, others, which intervene when the damaged vessel has been repaired, inhibit the aforementioned processes by dissolving the clot.
For the treatment and above all for the prevention of thrombosis, numerous anticoagulant drugs are now available which, although acting with different mechanisms of action, are intended to "dilute the blood" and limit platelet aggregation.
