Thrombosis (from Ancient Greece ????????? thrÃÆ'³mb? sis "freezing") is the formation of blood clots in the blood vessels, blocking blood flow through the circulatory system blood. When blood vessels (arteries or arteries) are injured, the body uses platelets (thrombocytes) and fibrin to form blood clots to prevent blood loss. Even when blood vessels are not injured, blood clots can form inside the body under certain conditions. A lump, or piece of lump, that breaks free and starts to wander around the body is known as the embolus.
Thrombosis can occur in the veins (venous thrombosis) or in the arteries. Venous thrombosis causes congestion of affected parts of the body, while arterial thrombosis (and rarely severe venous thrombosis) affects blood supply and causes damage to tissues provided by the arteries (ischemia and necrosis). A good piece of artery or venous thrombus can rupture as an embolus that can travel through the circulation and propose other places as emboli. This type of embolism is known as thromboembolism . Complications can arise when venous thromboembolism (commonly called VTE) enters the lungs as pulmonary embolism. Artery emboli may travel further down the affected vein where it can propose emboli.
Video Thrombosis
Signs and symptoms
Thrombosis is generally defined by the type of blood vessel affected (artery or vein thrombosis) and the exact location of the blood vessel or organ provided by it.
Venous thrombosis
deep vein thrombosis
Deep vein thrombosis (DVT) is the formation of blood clots in deep blood vessels. This most often affects the leg veins, such as the femoral vein. Three important factors in the formation of blood clots in the blood vessels - this is the rate of blood flow, blood thickness and the quality of blood vessel walls. The classic signs of DVT include swelling, pain and redness of the affected area.
Paget-Schroetter's Disease
Paget-Schroetter disease is upper limb veins obstruction (such as axillary veins or subclavian veins) by thrombus. This condition usually appears after a strong workout and usually appears in younger people, if not healthy. Men are more affected than women.
Budd-Chiari Syndrome
Budd-Chiari syndrome is a blockage of the hepatic vein or from the liver of the inferior vena cava. This form of thrombosis is accompanied by abdominal pain, ascites, and liver enlargement. Treatment varies between therapy and surgical intervention by using shunts.
Portal vein
Portal vein thrombosis affects the hepatic portal vein, which can lead to portal hypertension and reduced blood supply to the liver. Usually occurs in other disease settings such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.
Renal vein thrombosis
Renal venous thrombosis is a renal vein obstruction by thrombus. This tends to lead to reduced drainage of the kidneys.
Cerebral venous sinus thrombosis
Cerebral venous sinus thrombosis (CVST) is a rare form of stroke that occurs due to blockage of the dural venous sinus by thrombus. Symptoms may include headache, abnormal vision, one of the symptoms of a stroke such as facial and limb weakness on one side of the body and seizures. Diagnosis is usually made with a CT scan or MRI. The majority of affected people make full recovery. The mortality rate was 4.3%.
Venous jugular thrombosis
Jugular venous thrombosis is a condition that may occur due to infection, intravenous drug use or malignancy. Jugular venous thrombosis can have a list of various complications, including: systemic sepsis, pulmonary embolism, and papilledema. Although characterized by sharp pain in the venous site, it can prove difficult to diagnose, because it can occur randomly.
Cavernous sinus thrombosis
Cavernous sinus thrombosis is a special form of cerebral venous sinus thrombosis, where there is a basal cavernous dura cavernosa dura skull, due to the spread of infection and deteriorating endothelial damage from the dangers of the facial triangle. The facial veins in this area anastomose with the superior and inferior ophthalmic vein of the orbit, which flows directly into the posterior to the cavernous sinus through superior orbital fissures. Staphylocaloal or Streptococcal infections of the face, eg nasal or upper lip pustules, may spread directly to the cavernous sinus, causing symptoms such as double vision, squinting, and the spread of infection to cause meningitis.
Arterial thrombosis
Arterial thrombosis is the formation of thrombus in the arteries. In most cases, arterial thrombosis follows the rupture of atheroma (a fat rich deposit in the blood vessel wall), and is therefore referred to as atherothrombosis . Artery embolism occurs when the clump then migrates downstream, and can affect any organ.
Alternatively, arterial occlusion occurs as a consequence of embolism of blood clots originating from cardiogenic "embolism" (embolism). The most common cause is atrial fibrillation, which causes blood stasis in the atria with the formation of an easy thrombus, but blood clots can develop in the liver for other reasons as well.
Stroke
A stroke is a rapid decline in brain function due to an interruption in the blood supply to the brain. This can be caused by ischemia, thrombus, embolus (nested particles) or hemorrhage (bleeding). In thrombotic strokes, thrombus (blood clots) usually form around atherosclerotic plaques. Due to clogged arteries gradually, the incidence of thrombotic stroke is symptomatic at a slower pace. Thrombotic stroke can be divided into two categories - large vessel disease and small vessel disease. The first affects blood vessels such as internal carotids, vertebral, and Willis circles. The latter may affect smaller vessels such as the branches of Willis's circle.
Myocardial infarction
Myocardial infarction (MI) or heart attack, caused by ischemia, (restriction of blood supply), often due to coronary artery obstruction by thrombus. This limitation provides an inadequate supply of oxygen to the heart muscle which then causes tissue death, (infarct). The lesion is then formed which is an infarct. MI can quickly become fatal if emergency medical care is not immediately accepted. If diagnosed within 12 hours of the initial episode (attack) then thrombolytic therapy begins.
Limb ischemia
Arterial or embolus thrombus may also form in the limbs, which can cause acute limb ischemia.
Other sites
Hepatic artery thrombosis usually occurs as a devastating complication after liver transplantation.
Maps Thrombosis
Cause
Prevention of thrombosis begins by assessing the risk of progression. Some people have a higher risk of developing thrombosis and their likelihood of developing thromboembolism. Some of these risk factors are associated with inflammation. "Triad Virchow" has been suggested to describe the three factors necessary for thrombosis formation: blood stasis, vascular wall injury, and altered blood clots. Several risk factors predispose to venous thrombosis while others increase the risk of arterial thrombosis.
Mechanism
Pathogenesis
The main cause of thrombosis is given in the Virchow triad containing a list of thrombophilia, endothelial cell injury, and impaired blood flow.
Hypercoagulability
Hypercoagulation or thrombophilia , caused by, for example, genetic deficiency or autoimmune disorders. Recent studies have shown that white blood cells play an important role in deep vein thrombosis, mediating many pro-thrombotic actions.
Endothelial cell injury
Any inflammatory process, such as trauma, surgery or infection, can cause damage to the endothelial lining of the blood vessel wall. The main mechanism is the exposure of tissue factors to the blood clotting system. Stimulation of inflammation and other stimuli (such as hypercholesterolaemia) can cause changes in gene expression in the endothelium resulting in a pro-thrombotic state. When this happens, the endothelial cell lowers the regulation of substances such as thrombomodulin, which is the key modulator of thrombin activity. The end result is ongoing activation of thrombin and reduces the production of protein C and tissue-inhibiting factor, which improves pro-thrombotic conditions.
Endothelial injury is almost always involved in the formation of thrombi in the arteries, because high levels of blood flow usually inhibit clot formation. In addition, arterial and cardiac clots are usually rich in platelets - which are necessary for clot formation in areas under high pressure due to blood flow.
Blood flow is interrupted
Causes of impaired blood flow include stagnation of blood flow past the point of injury, or venous stasis that can occur in heart failure, or after a prolonged period of sedentary behavior, such as sitting on long aircraft. Also, atrial fibrillation, causes stagnant blood in the left atrium (LA), or left atrial freckle (LAA), and may cause thromboembolism. Cancer or malignancies such as leukemia can lead to an increased risk of thrombosis by the possible activation of coagulation systems by cancer cells or procoagulant drug secretion (paraneoplastic syndrome), by external compression of blood vessels when solid tumors are present, or (more rarely) extension to blood vessels ( for example, kidney cancer cells extend into the renal vein). Also, treatments for cancer (radiation, chemotherapy) often lead to additional hypercoagulability. There were scores that correlated different aspects of patient data (comorbidity, vital signs, etc.) to the risk of thrombosis, such as POMPE-C, which classified the risk of dying from pulmonary embolism in patients with cancer, which typically had more levels high. of thrombosis.
Pathophysiology
Natural history
Fibrinolysis is a physiological breakdown of blood clots by enzymes such as plasmin.
Organization: following the event of thrombosis, the remaining vascular thrombus will be reorganized histologically with several possible outcomes. For occlusive thrombus (defined as thrombosis in small vessels leading to complete occlusion), wound healing will reset the occlusive thrombus to collagen scar tissue, where scar tissue will permanently block the vessels, or contract with myofibroblastic activity to unblock. lumen. For a mural thrombus (defined as a thrombus in a large vessel that restricts blood flow but does not close completely), histologic reorganization of thrombus does not occur through the classical wound healing mechanism. Conversely, platelet-derived growth factor degranulation by frozen platelets will attract layers of smooth muscle cells to cover the clot, and this mural smooth muscle layer will be vasculated by blood within the vessel lumen rather than by vasa vasorum.
Ischemia/infarction: if arterial thrombus can not be pulverized by the body and is not condensed, and if the thrombus is large enough to damage or clog the blood flow in the involved arteries, local ischemia or infarction will occur. Venous thrombus may or may not be ischemic, because the vein distributes deoxygenated blood that is less vital for cell metabolism. However, non-ischemic venous thrombosis may still be problematic, because of swelling caused by blockage in venous drainage. In deep venous thrombosis, it manifests as pain, redness, and swelling; in retinal vein occlusion it may cause macular edema and visual acuity disorders, which if severe enough can lead to blindness.
Embolization
Thrombus can be released and enter the circulation as an embolus, eventually piercing and completely blocking the blood vessels, which unless treated very quickly will cause tissue necrosis (infarction) in the region through the occlusion. Venous thrombosis can cause pulmonary embolism when the migrating embolus is caught in the lung. In people with "shunt" (the relationship between pulmonary and systemic circulation), either in the heart or in the lungs, the vein can also end up in the arteries and cause arterial embolism.
Artery embolism can cause obstruction of blood flow through blocked blood vessels, and lack of oxygen and nutrients (ischemia) from downstream tissues. The tissue can become irreversibly damaged, a process known as necrosis. It can affect any organ; for example, brain artery embolism is one of the causes of stroke.
Prevention
Use of heparin after surgery is common if there is no problem with bleeding. Generally, a risk-benefit analysis is required, as all anticoagulants cause an increased risk of bleeding. In people who are hospitalized, thrombosis is a major cause for complications and sometimes death. In the UK, for example, the Parliamentary Elections Committee heard in 2005 that the annual death rate due to thrombosis was 25,000, with at least 50% of it being obtained at the hospital. Therefore thromboprophylaxis (prevention of thrombosis) is increasingly emphasized. In patients treated for surgery, graded compression stockings are widely used, and in severe disease, prolonged immobility and in all orthopedic surgery, professional guidelines recommend the administration of low molecular weight heparin (LMWH), mechanical calf compression or (if all other things are contraindicated and patients recently experienced deep vein thrombosis) insertion of venous cava filters. In patients with medical illness rather than surgery, LMWH is also known to prevent thrombosis, and in the UK the Chief Medical Officer has issued guidelines for the effect that precautions should be used on medical patients, in anticipation of formal guidelines.
Treatment
Treatment for thrombosis depends on whether it is in the arteries or blood vessels, the impact on the person, and the risk of complications from the treatment.
Anticoagulation
Warfarin antagonists and vitamin K are anticoagulants that can be taken orally to reduce the occurrence of thromboembolism. Where a more effective response is needed, heparin may be given (by injection) simultaneously. As a side effect of any anticoagulant, the risk of bleeding increases, so the ratio of internationalized blood normalization is monitored. Self-monitoring and self-management is a safe choice for competent patients, although their practices vary. In Germany, about 20% of patients are self-administered while only 1% of US patients do self-test at home (according to a 2012 study). Other drugs such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used than warfarin.
Thrombolysis
Thrombolysis is the destruction of pharmacological blood clots by the administration of thrombolytic drugs including the activation of plasminogen recombinant tissue, which increases the destruction of blood clots by the body's enzymes. This carries an increased risk of bleeding so it is generally only used for certain situations (such as severe stroke or massive pulmonary embolism).
Surgery
Arterial thrombosis may require surgery if it causes acute limb ischemia.
Endovascular Treatment
Clot-guiding and thrombolysis techniques guided by catheters are used in certain situations.
Antiplatelet Agents
Arterial thrombosis is platelet-rich thrombocytes, and inhibition of platelet aggregation with antiplatelet drugs such as aspirin may reduce the risk of recurrence or progression.
See also
- The National Blood Clot Alliance
- Blood clotting test
- thrombotic microangiopathy
- Thromboxane
References
Bibliography
- Brunner, Lillian (2010). Brunner & amp; Suddarth's textbook on medical-surgical nursing . Philadelphia: Wolters Kluwer Health/Lippincott Williams & amp; Wilkins. ISBN: 9780781785907.
- Copstead, Lee (2013). Pathophysiology . St. Louis, Mo: Elsevier. ISBN: 9781455726509.
- Hoffman, Barbara (2012). Williams gynecology . New York: McGraw-Hill Medical. ISBN: 9780071716727.
- Moliterno, David (2013). Progress of therapy in thrombosis . Chichester, West Sussex: Wiley-Blackwell. ISBN: 9781405196253.
- Abele, H (2014). Atlas gynecological operation . Stuttgart: Thieme. ISBN: 9783136507049; Access is provided by University of Pittsburgh
External links
- Thrombosis in Curlie (based on DMOZ)
Source of the article : Wikipedia
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