Тромбоз глубоких вен: симптомы, диагностика и лечение

Formation of a blood clot (thrombus) in a deep vein

Deep vein thrombosis (DVT) is a type of venous thrombosis involving the formation of a blood clot in a deep vein, most commonly in the legs or pelvis. Using blood thinners is the standard treatment. Typical medications include rivaroxaban, apixaban, and warfarin. Beginning warfarin treatment requires an additional non oral anticoagulant, often injections of heparin. though they can develop suddenly or over a matter of weeks. The legs are primarily affected, with 4–10% of DVT occurring in the arms. In those who are able to walk, DVT can reduce one's ability to do so. The pain can be described as throbbing and can worsen with weight bearing, prompting one to bear more weight with the unaffected leg. Additional signs and symptoms include tenderness, pitting edema (see image), dilation of surface veins, warmth, discoloration, a "pulling sensation", and even cyanosis (a blue or purplish discoloration) with fever. Rarely, a clot in the inferior vena cava can cause both legs to swell. Superficial vein thrombosis, also known as superficial thrombophlebitis, is the formation of a blood clot (thrombus) in a vein close to the skin. It can co occur with DVT and can be felt as a "palpable cord".

A pulmonary embolism (PE) occurs when a blood clot from a deep vein (a DVT) detaches from a vein (embolizes), travels through the right side of the heart, and becomes lodged as an embolus in a pulmonary artery that supplies deoxygenated blood to the lungs for oxygenation. and can vary based upon where the embolus is lodged in the lungs. An estimated 30–50% of those with PE have detectable DVT by compression ultrasound. It is life threatening, limb threatening, and carries a risk of venous gangrene. Phlegmasia cerulea dolens can occur in the arm but more commonly affects the leg. If found in the setting of acute compartment syndrome, an urgent fasciotomy is warranted to protect the limb. Superior vena cava syndrome is a rare complication of arm DVT.

In most suspected cases, DVT is ruled out after evaluation. Cellulitis is a frequent mimic of DVT, with its triad of pain, swelling, and redness. superficial vein thrombosis, muscle vein thrombosis, and varicose veins.

DVT and PE are the two manifestations of the cardiovascular disease venous thromboembolism (VTE). DVT is classified as acute when the clots are developing or have recently developed, whereas chronic DVT persists more than 28 days. An episode of VTE after an initial one is classified as recurrent. Bilateral DVT refers to clots in both limbs while unilateral means only a single limb is affected. DVT in a leg above the knee is termed proximal DVT (proximal). DVT in a leg below the knee is termed distal DVT (distal), also called calf DVT when affecting the calf, and has limited clinical significance compared to proximal DVT. Calf DVT makes up about half of DVTs. Iliofemoral DVT is described as involving either the iliac, or common femoral vein; elsewhere, it has been defined as involving at a minimum the common iliac vein, which is near the top of the pelvis. DVT can be classified into provoked and unprovoked categories. The distinction between these categories is not always clear.

Traditionally, the three factors of Virchow's triad—venous stasis, hypercoagulability, and changes in the endothelial blood vessel lining—contribute to VTE and were used to explain its formation. More recently, inflammation has been identified as playing a clear causal role. Other related causes include activation of immune system components, the state of microparticles in the blood, the concentration of oxygen, and possible platelet activation. Previous VTE, particularly unprovoked VTE, is a strong risk factor. Major surgery and trauma increase risk because of tissue factor from outside the vascular system entering the blood. hip fracture, and long bone fractures are also risks. paralysis, sitting, long haul travel, bed rest, hospitalization, catatonia, and in survivors of acute stroke. Conditions that involve compromised blood flow in the veins are May–Thurner syndrome, where a vein of the pelvis is compressed, and venous thoracic outlet syndrome, which includes Paget–Schroetter syndrome, where compression occurs near the base of the neck. Infections, including sepsis, COVID 19, HIV, and active tuberculosis, increase risk. Chronic inflammatory diseases and some autoimmune diseases, such as inflammatory bowel disease, systemic sclerosis, Behçet's syndrome, primary antiphospholipid syndrome, increase risk. SLE itself is frequently associated with secondary antiphospholipid syndrome. Cancer can grow in and around veins, causing venous stasis, and can also stimulate increased levels of tissue factor. Cancers of the blood, lung, pancreas, brain, stomach, and bowel are associated with high VTE risk. Solid tumors such as adenocarcinomas can contribute to both VTE and disseminated intravascular coagulation. In severe cases, this can lead to simultaneous clotting and bleeding. Chemotherapy treatment also increases risk. Obesity increases the potential of blood to clot, as does pregnancy. In the postpartum, placental tearing releases substances that favor clotting. Oral contraceptives and hormonal replacement therapy increase the risk through a variety of mechanisms, including altered blood coagulation protein levels and reduced fibrinolysis. Dozens of genetic risk factors have been identified, mildly increases VTE risk by about three times. Having a non O blood type roughly doubles VTE risk. Individuals without O blood type have higher blood levels of von Willebrand factor and factor VIII than those with O blood type, increasing the likelihood of clotting. The genetic variant prothrombin G20210A, which increases prothrombin levels, hyperhomocysteinemia, paroxysmal nocturnal hemoglobinuria, nephrotic syndrome, chronic kidney disease, polycythemia vera, essential thrombocythemia, intravenous drug use, and smoking. Some risk factors influence the location of DVT within the body. In isolated distal DVT, the profile of risk factors appears distinct from proximal DVT. Transient factors, such as surgery and immobilization, appear to dominate, whereas thrombophilias and age do not seem to increase risk. Common risk factors for having an upper extremity DVT include having an existing foreign body (such as a central venous catheter, a pacemaker, or a triple lumen PICC line), cancer, and recent surgery.

Blood has a natural tendency to clot when blood vessels are damaged (hemostasis) to minimize blood loss. Clotting is activated by the coagulation cascade and the clearing of clots that are no longer needed is accomplished by the process of fibrinolysis. Reductions in fibrinolysis or increases in coagulation can increase the risk of DVT. DVT most frequently affects veins in the leg or pelvis including the popliteal vein (behind the knee), femoral vein (of the thigh), and iliac veins of the pelvis. Extensive lower extremity DVT can even reach into the inferior vena cava (in the abdomen). Upper extremity DVT most commonly affects the subclavian, axillary, and jugular veins. This is the preferred process. Aside from the potentially deadly process of embolization, a clot can resolve through organization, which can damage the valves of veins, cause vein fibrosis, and result in non compliant veins. [[File:2134 Thoracic Upper Limb Veins. jpg|thumb|350px|left|Upper extremity DVTs can occur in the subclavian, axillary, brachial, ulnar, and radial veins (pictured) and the jugular and brachiocephalic veins (not pictured). The cephalic and basilic veins, however, are superficial veins. but clotting in the veins mostly occurs without any such mechanical damage. NETs provide "a scaffold for adhesion" of platelets, red blood cells, and multiple factors that potentiate platelet activation. In addition to the pro coagulant activities of neutrophils, multiple stimuli cause monocytes to release tissue factor. Monocytes are also recruited early in the process. Hospitalized patients often have elevated levels for multiple reasons.

Treatment for DVT is warranted when the clots are either proximal, distal and symptomatic, or upper extremity and symptomatic. Providing anticoagulation, or blood thinning medicine, is the typical treatment after patients are checked to make sure they are not subject to bleeding. However, treatment varies depending upon the location of DVT. For example, in cases of isolated distal DVT, ultrasound surveillance (a second ultrasound after 2 weeks to check for proximal clots), might be used instead of anticoagulation. Although, those with isolated distal DVT at a high risk of VTE recurrence are typically anticoagulated as if they had proximal DVT. Those at a low risk for recurrence might receive a four to six week course of anticoagulation, lower doses, or no anticoagulation at all. together with warfarin is given, which is followed by warfarin only therapy. of 2.0–3.0, with 2.5 as the target. The benefit of taking warfarin declines as the duration of treatment extends, and the risk of bleeding increases with age. Periodic INR monitoring is not necessary when first line direct oral anticoagulants are used. Overall, anticoagulation therapy is complex and many circumstances can affect how these therapies are managed. The duration of anticoagulation therapy (whether it will last 4 to 6 weeks, When proximal DVT is provoked by surgery or trauma a 3 month course of anticoagulation is standard. Those who finish warfarin treatment after idiopathic VTE with an elevated D dimer level show an increased risk of recurrent VTE (about 9% vs about 4% for normal results), and this result might be used in clinical decision making. Thrombophilia test results rarely play a role in the length of treatment. Treatment for acute leg DVT is suggested to continue at home for uncomplicated DVT instead of hospitalization. Factors that favor hospitalization include severe symptoms or additional medical issues. Early walking is suggested over bedrest. Graduated compression stockings—which apply higher pressure at the ankles and a lower pressure around the knees as the potential benefit of using them for this goal "may be uncertain". They are, however, recommended in those with isolated distal DVT. but it is only about 33% as effective as anticoagulation in preventing recurrent VTE.

Acutely ill hospitalized patients are suggested to receive a parenteral anticoagulant, although the potential net benefit is uncertain. efn|Page e197S of Kahn et al. Mechanical prophylaxis is suggested when risks for bleeding and thrombosis are elevated. For the critically ill, either pharmacological or mechanical prophylaxis is suggested depending upon the risk. Heparin can also be used in outpatients with cancer who have solid tumors and additional risk factors for VTE—listed as "previous venous thrombosis, immobilization, hormonal therapy, angiogenesis inhibitors, thalidomide, and lenalidomide"—and a low risk of bleeding. >

The risk of VTE is increased in pregnancy by about four to five times because of a more hypercoagulable state that protects against fatal postpartum hemorrhage. Preventive measures for pregnancy related VTE were suggested by the American Society of Hematology in 2018.

[[File:Serena Williams at 2013 US Open. jpg|thumb|upright=1.2|Serena Williams has spoken at length about a frightening encounter she had with VTE while she was hospitalized in 2017. Head injuries prompting brain bleeds are of particular concern. This has caused NASCAR driver Brian Vickers to forego participation in races. Professional basketball players including NBA players Chris Bosh and hall of famer Hakeem Olajuwon have dealt with recurrent blood clots, and Bosh's career was significantly hampered by DVT and PE. Tennis star Serena Williams was hospitalized in 2011 for PE thought to have originated from DVT. Years later, in 2017, due to her knowledge of DVT and PE, Serena accurately advocated for herself to have a PE diagnosed and treated. During this encounter with VTE, she was hospitalized after a C section surgery and was off of blood thinners. After feeling the sudden onset of a PE symptom, shortness of breath, she told her nurse and requested a CT scan and an IV heparin drip, all while gasping for air. She started to receive an ultrasound to look for DVT in the legs, prompting her to express dissatisfaction to the medical staff that they were not looking for clots where she had symptoms (her lungs), and they were not yet treating her presumed PE. After being diagnosed with PE and not DVT, and after receiving heparin by IV, the coughing from the PE caused her C section surgical site to open and the heparin contributed to bleeding at the site. Serena later received an IVC filter while in the hospital. Other notable people have been affected by DVT. Former United States (US) President Richard Nixon had recurrent DVT, and so has former Secretary of State Hillary Clinton. She was first diagnosed while First Lady in 1998 and again in 2009. Dick Cheney was diagnosed with an episode while Vice President, and TV show host Regis Philbin had DVT after hip replacement surgery. DVT has also contributed to the deaths of famous people. For example, DVT and PE played a role in rapper Heavy D's death at age 44. NBC journalist David Bloom died at age 39 while covering the Iraq War from a PE that was thought to have progressed from a missed DVT, and actor Jimmy Stewart had DVT that progressed to a PE when he was 89.

VTE costs the US healthcare system about $7 to 10 billion dollars annually. In Europe, the costs for an initial VTE hospitalization are significantly less, costing about €2000 to 4000 (2011 estimate). Post thrombotic syndrome is a significant contributor to DVT follow up costs. Outpatient treatment significantly reduces costs, and treatment costs for PE exceed those of DVT.

A 2019 study published in Nature Genetics reported more than doubling the known genetic loci associated with VTE. In their updated 2018 clinical practice guidelines, the American Society of Hematology identified 29 separate research priorities, most of which related to patients who are acutely or critically ill.