Deep vein thrombosis (DVT) leading to a blood clot in a deep leg vein of an extremity (usually the upper or lower leg) or in the pelvis. DVT is the leading cause of pulmonary embolism. DVT occurs under conditions that impede venous return, leading to endothelial injury and dysfunction or a hypercoagulable state. DVT can be asymptomatic or cause pain and swelling in a limb; pulmonary embolism is an immediate complication. The diagnosis is made by history and physical examination and confirmed by objective tests, usually with duplex sonography. The d-dimer test is used when a DVT is suspected. A negative result from DVT, while a positive result is non-specific and additional tests required to confirm a DVT. Treatment is with anticoagulants. The prognosis is good upon prompt and appropriate treatment in general. Among the common long-term complications include venous insufficiency with or without post-thrombotic syndrome.
DVT in the lower extremities or the pelvis is most common (deep veins of the legs.). You can develop (4 to 13% of DVT cases) also in the deep veins of the upper extremities.
Deep vein thrombosis (DVT) leading to a blood clot in a deep leg vein of an extremity (usually the upper or lower leg) or in the pelvis. DVT is the leading cause of pulmonary embolism. DVT occurs under conditions that impede venous return, leading to endothelial injury and dysfunction or a hypercoagulable state. DVT can be asymptomatic or cause pain and swelling in a limb; pulmonary embolism is an immediate complication. The diagnosis is made by history and physical examination and confirmed by objective tests, usually with duplex sonography. The d-dimer test is used when a DVT is suspected. A negative result from DVT, while a positive result is non-specific and additional tests required to confirm a DVT. Treatment is with anticoagulants. The prognosis is good upon prompt and appropriate treatment in general. Among the common long-term complications include venous insufficiency with or without post-thrombotic syndrome. DVT in the lower extremities or the pelvis is most common (deep veins of the legs.). You can develop (4 to 13% of DVT cases) also in the deep veins of the upper extremities. Deep veins of the legs. DVT of the lower extremities can cause much more likely to pulmonary embolism (PE), possibly due to the greater amount of blood clots. The femoral – and Poplitealvenen in the thighs and the posterior Tibialvenen and Peronealvenen in the lower legs are most commonly affected. A lower leg vein thrombosis is less likely as a source of large emboli, but can progress into the proximal femur sections from which can then pulmonary embolism occur. About 50% of patients with DVT have occult pulmonary embolism and about 30% of patients with pulmonary embolism have a demonstrable DVT. Tips and risks Approximately 50% of patients with DVT have occult pulmonary embolism. Etiology Many factors can contribute to DVT (see Table: Risk factors for venous thrombosis). Cancer is a risk factor for DVT, especially in elderly patients and in patients with recurrent thrombosis. The association is strongest for mucin secreting endothelial cell tumors such as intestinal or pancreatic cancer. Occult cancers may be present with apparently idiopathic DVT in patients; an extensive evaluation of patients with tumors is not recommended, unless have major risk factors for cancer or symptoms of occult cancer in patients. Risk factors for venous thrombosis age of> 60 years Cancer smoking (including passive smoking) estrogen receptor modulators (eg tamoxifen, raloxifene) heart failure hypercoagulable: antiphospholipid syndrome antithrombin iii deficiency Factor V Leiden (activated protein C resistance) heparin-induced T hrombozytopenie Hereditary hyperhomocysteinemia fibrinolytic defects increase in the factor VIII increase in the factor XI paroxysmal nocturnal hemoglobinuria Protein C deficiency Protein S deficiency prothrombin gene variant G-A immobilization indwelling venous limb trauma Myeloproliferative disease (hyperviscosity) Nephrotic syndrome Obesity Oral contraceptives or estrogen therapy pregnancy and childbirth Earlier venous thromboembolism sickle cell anemia surgery within the last 3 months injury pathophysiology DVT of the lower extremities DVT results from mostly Impaired venous return (eg. B. Endothelial in immobilized patients) injury or dysfunction (z. B. after bone fractures) hypercoagulability TVT of the upper extremities is usually apparent from a endothelial injury due to central venous catheters, pacemakers or pressure injection of drugs DVT of the upper limbs occasionally occurs as part of the Vena cava superior syndrome (SVC), or resulting from a hypercoagulable state or compression of the subclavian vein at the thoracic inlet. The compression may occur due to a normal or an additional first rib or a sliver (thoracic outlet syndrome) or during a stressful arm movement (effort thrombosis or Paget–Schroetter syndrome, the 1 to 4% of cases of TVT the upper extremities omitted). Deep vein thrombosis usually begins in the venous valve leaflets. The thrombi consist of thrombin, fibrin and erythrocytes, with relatively few platelets (red thrombus); without treatment, the thrombus may increase in the proximal direction toward or migrate to the lungs. Complications Common complications of deep vein thrombosis Chronic venous insufficiency post-thrombotic syndrome pulmonary embolism Less common DVT leads to Leukophlegmasie (Phlegmasia alba dolens) or Phlegmasia coerulea dolens (acute massive vein occlusion); both lead if they are not immediately diagnosed and treated adequately, venous gangrene. In the Phlegmasia alba dolens, a rare complication of DVT during pregnancy, the leg is milk-white. The pathophysiology is unclear, but edema may increase soft tissue pressure across the capillary perfusion pressure, resulting in Gewebeischiämie and wet gangrene. When Phlegmasia coerulea dolens a massive venous thrombosis caused an almost complete venous occlusion; the leg becomes ischemic, extremely painful and cyanotic. The pathophysiological Usache can be a complete stasis of venous and arterial blood flow in the lower extremities, as the venous return is misplaced or a massive edema pushes off the arterial blood flow. Venous gangrene may result. Rarely venous blood clotting can infect. A festering thrombophlebitis (Lemierres syndrome), bacterial (usually by anaerobic bacteria) infection of the internal jugular vein and the surrounding soft tissue, can follow a tonsillopharyngitis and is complicated by bacteremia and sepsis. In septic Beckenvenenthrombophlebitis the thrombus develops postpartum pelvic become infected, leading to intermittent fever. A purulent (septic) thrombophlebitis, a bacterial infection of a superficial vein, comprising an infection and blood clot, which usually is caused by the insertion of a venous catheter. Symptoms and complaints DVT can occur in out-patients or as a complication of surgery or extensive medical condition. The hospitalized high-risk patients most deep vein thrombosis occur in the small calf veins are asymptomatic and may never discovered. When present, symptoms (eg. As vague pain, tenderness along the distribution of the veins, edema and erythema) are not specific, vary in frequency and strength, and are similar to those in the legs in the arms. Dilated superficial collateral veins may become visible and palpable, a lower leg pain that is caused by dorsiflexion of the foot at an outstretched knee (Homan mark), sometimes occurs at distal deep TVT of the leg, but is neither sensitive nor specific. Sensitivity and swelling of the entire leg,> 3 cm circumference difference between the lower legs, edema and superficial collateral veins can have the greatest specific accuracy. The TVT can be assumed with a combination ? 3 risk factors and in the absence of other probable diagnosis (see table: Wahrscheinlichkeite deep vein thrombosis based on clinical factors). There may be low fever; DVT may be the cause of a FUO (fever of unknown origin), particularly in post-operative patients. Symptoms of pulmonary embolism occurring may be shortness of breath and pleuritic chest pain. Wahrscheinlichkeite deep vein thrombosis based on clinical factors factors sensitivity along distribution of the veins in calf or thigh swelling of the entire leg swelling of the calf (> 3 cm difference in circumference between the calves, measured 10 cm below the tibial tuberosity) pitting edema Advanced superficial collateral veins Cancer (including the felling, in which the treatment was set within 6 months) immobilization of the lower limb (eg. As a result of paralysis, paresis, Cast, or recent long-distance travel) operation that has led to immobility for> 3 days within the last 4 weeks probability probability corresponds to the number of factors; where 2 are subtracted if another diagnosis is just as likely or more likely than DVT. Ho: ?3 points Moderate Probability: 1-2 points Low Probability: ? 0 Based on the data from Anand SS, Wells PS, Hunt D, et al: Does this patient deep vein thrombosis? Journal of the American Medical Association 279 (14): 1094 to 1099, 1998. Common causes an asymmetrical swelling of the leg that mimic DVT, is a soft tissue trauma, cellulitis, venous or lymphatic obstruction in the pelvic area or popliteal bursitis (Baker -Zyste) that impede venous return. Tumors in the abdominal or pelvic area that impede venous or lymphatic return flow are less common causes. The use of drugs which edema in the depending parts of the body cause (such as dihydropyridines, calcium antagonists, estrogens, high-dose opioids.), Venous pressure (usually due to right heart failure), and a hypoalbuminemia typically cause a symmetric bilateral swelling of the legs; However, the swelling can be asymmetrical, if simultaneously a venous insufficiency is present or is more pronounced in one leg. Common causes of lower leg pain that resemble the acute DVT include venous insufficiency and post-thrombotic syndrome, cellulitis, which can cause the lower leg painful erythema, a ruptured popliteal cyst (Baker’s cyst pseudo-DVT), a lower leg swelling, pain and sometimes can cause a bruise in the region of the medial Malleololi and partial or complete tears of the calf muscles or plantaris one. Diagnostic sonography Sometimes d-dimer test history and physical examination will help the possibility of DVT before further investigations to determine (see table: Wahrscheinlichkeite deep vein thrombosis based on clinical factors). Diagnosis is typically provided by ultrasound with Doppler flow studies (duplex sonography). The need for further tests (eg., D-dimers), their selection and sequence depend on the pretest probability and sometimes on the results of sonography. No single test protocol is best, an approach is described in approach to investigating suspected deep vein thrombosis. Clinical calculator: probability of DVT: Wells score-system approach to the study with suspected deep venous thrombosis Ultrasound Ultrasound has thrombi after by direct visualization of the venous limitation and by detecting a changed compressibility of the vein or in the case of Doppler flow measurements to detecting an altered venous blood flow. The test has a sensitivity of> 90% and a specificity of> 95% for femoral and popliteal vein thrombosis, but is less accurate when iliac or Beckenvenenthrombosen.d dimer d-dimers are a by-product of fibrinolysis; increased levels speak for the existence and the lysis of thrombi. d-dimer measurements vary in sensitivity and specificity, but most are sensitive and not specific. Only the most accurate tests should be used. The enzyme-linked immunosorbent assay (ELISA), for example, is a very sensitive test with a sensitivity of about 95%. If the pretest probability of DVT is low, DVT can be excluded safely in patients with a normal d-dimer levels by a sensitive test. Thus, a negative d-dimer test patients can with a low probability of DVT, where no ultrasound is necessary to identify with. However, a positive test result is non-specific; because the level may be increased by other conditions (eg., liver disease, trauma, pregnancy, positive rheumatoid factor, inflammation, recent surgery, cancer), any further investigations required. When the pretest probability of DVT is moderate or high, a determination of D-dimer at the same time as the duplex sonography can be performed. A positive result of the ultrasound confirms the diagnosis regardless of the D-dimer level. If the ultrasound does not provide evidence of DVT helps a normal d-dimer levels exclude DVT. In patients with an elevated d-dimer levels, ultrasonography should be repeated after a few days or should additional imaging techniques, such as venography, werden.Venographie applied depending on the clinical suspicion of a contrast venography has been the definitive test to diagnose DVT , She was replaced in large part by the ultrasound, which is non-invasive, available more quickly and accurately almost the same for the detection of DVT. A venography is indicated when the results of the ultrasound are normal, but the pre-test suspected DVT is high. The complication rate is 2%, mostly due to a Kontrastmittelallergie.Weitere test procedure Non-invasive alternatives to contrast venography are currently being investigated. They include the MR venography and direct MRI scan of thrombi with the T1-weighted gradient echo sequence, and a water-excitation radio-frequency pulse; theoretically capable latter method, simultaneous images of thrombi in the deep veins of the leg and subsegmental pulmonary delivery (for the diagnosis of pulmonary embolism). If the symptoms and complaints of pulmonary embolism speak, an additional imaging (z. B. ventilation / perfusion [V / Q] -Szintigramm or CT pulmonary angiography) erforderlich.Bestimmung the cause patients with a confirmed DVT and an obvious cause (eg. B. immobilization, surgery, leg injury) do not require further investigation. Studies on the detection of a hypercoagulopathy be controversial; but they are sometimes performed in patients who have idiopathic (unknown cause) DVT or recurrent DVT and in patients who themselves had a thrombosis or have a family history of other thrombosis, and also in young patients with no predisposing risk factors. Some evidence indicates that the presence of hypercoagulopathy the recurrence of DVT less predicts well as the clinical risk factors. The study of patients with DVT in terms of cancer is unproductive. A selective examination by complete medical history and physical examination and basic “routine” -Testungen (complete blood count, chest x-ray, urinalysis, liver enzymes and electrolytes, BUN and creatinine i. S.), focused on the detection of cancer, is probably sufficient. In addition, should any age and gender cancer screenings for patients (eg. As mammography, colonoscopy) that are due to be carried out. Prognosis Without appropriate therapy, there is a risk of 3% for a fatal pulmonary embolism in the DVT of the lower extremity; Deaths of DVT of the upper extremities are very rare. The risk of recurrent DVT is the lowest in patients with temporary risks (z. B. surgical Tauma, transient immobility) and highest in patients with persistent risk factors (eg., Cancer), idiopathic DVT or incomplete lysis of a previous DVT (residual Thrombus). A normal d-dimer levels after discontinuation of warfarin may help in predicting a relatively low risk of re-DVT or pulmonary embolism. The risk of venous insufficiency predict is difficult. Risk factors for post-thrombotic syndrome are a proximal thrombosis, recurrent ipsilateral DVT, and a body mass index (BMI) of ?22 kg / m2. Anticoagulation treatment with an injectable heparin followed by an oral anticoagulant (warfarin or a factor Xa inhibitor or a direct Thrombininhemmer). Treatment is aimed primarily at avoiding a pulmonary embolism, and only secondarily to a relief of symptoms and prevention of recurrent DVT, of chronic venous insufficiency and post-thrombotic syndrome. The treatment of DVT of the upper and lower extremity is usually the same. All patients with DVT are treated with anticoagulants, initially with injectable heparin (unfractionated or low molecular) for a short time, followed by a prolonged treatment with an orally administered substance (eg. As warfarin), with 24-48 h is begun. Selected patients may continue treatment with a low molecular weight heparin, rather than switching to an oral medication. An inadequate anticoagulation in the first 24-48 h increases the risk of recurrence or pulmonary embolism. An acute DVT can be outpatients, unless severe symptoms requiring parenteral analgesia; also when other illnesses preclude a safe outpatient care or other factors (eg. as functional subject, socio-economically) could prevent the patients from also carry out the prescribed treatments. General supportive measures include pain with analgesics which short (3- to 5-day) may include periods of administration of a NSAID. An extended treatment with NSAIDs and aspirin should be avoided because their antiplatelet effect can increase the risk of bleeding complications. In addition, the legs should be elevated (supported by a pillow or other soft surface to avoid venous compression) during rest periods. Patients can be as physically active as they tolerate it; there is no evidence that early activity increases the risk of Thrombusverschleppung or a pulmonary embolism, it can even help to reduce the risk of post-thrombotic syndrome one. Anticoagulants The following anticoagulants (. Anticoagulants and their sites of action) are most commonly used: Low molecular weight heparins (LMWH) Unfractionated heparin (UFH) fondaparinux Marcumar non-warfarin oral anticoagulants: Factor Xa inhibitors (eg rivaroxaban, apixaban.), Direct thrombin inhibitors (dabigatran) LMWHs (eg enoxaparin, dalteparin, tinzaparin-see table. Some options for low molecular weight heparin * for thromboembolic disease) are the initial treatment of choice, as they can be given on an outpatient basis. LMWH are as effective as UFH to reduce a reflection of the occurrence of DVT, a Thrombusvergrößerung and the risk for a fatal outcome due to a pulmonary embolism. As well as UFH LMWH catalyze the effect of antithrombin (containing the proteases of the coagulation inhibited), which leads to an inactivation of the coagulation factor Xa and to a lesser extent of factor IIa. LMWH also have a low antithrombin-mediated anti-inflammatory action that supports the thrombus and promotes the disappearance of symptoms and inflammation. LMWH are typically given subcutaneously in a standardized weight adjusted dose (z. B. enoxaparin 1.5 mg / kg s.c. once daily or 1 mg / kg s.c. every 12 h or 200 I.U./kg dalteparin s.c. once daily). Patients with renal insufficiency may be treated with UFH or reduced doses of LMWH. A monitor is not reliable because LMWH not significantly extend the results of the global tests for blood clotting. In addition, they have a predictable dose response, and there is no clear relationship between the anticoagulant effect of LMWH and bleeding. The treatment is continued until a full anticoagulation with warfarin is reached (typically about 5 days). However, there are indications that LMWH is more effective for long-term treatment of DVT in high-risk patients, such as cancer. So LMWH may be an acceptable alternative to warfarin for some patients; but warfarin is likely to be the treatment of choice for most patients because of its low cost and oral administration. UFH can (10-30 ml / min creatinine clearance) instead of LMWH be used with renal failure in hospitalized patients, since it is not excreted by the kidneys. UFH is as a bolus and infusion (weight-based dosage of heparin.) Administered to achieve complete anticoagulation (z. B. Activated PTT [APTT] 1.5 to 2.5 times ho high as of the reference range) , For outpatients UFH may be given 333 I.U./kg as an initial bolus, then 250 I.U./kg can s.c. every 12 h be replaced by intravenous UFH in order to facilitate the mobility; the dose does not seem to be adapted to the need aPTT. The treatment is continued until a full anticoagulation with warfarin is reached. Complications of heparin include bleeding and thrombocytopenia (rarely with LMWH), urticaria and rarely thrombosis and anaphylaxis. The long term use of UFH causes hypokalemia, liver enzyme elevations and osteopenia. Rarely causes subcutaneously given UFH skin necrosis. Stationary and if possible outpatients should in terms of possible bleeding with serial blood counts and, if appropriate, be monitored with tests for occult blood in the stool. Bleeding due to overdose of heparin can be stopped with protamine sulfate. The dose is 1 mg protamine for each milligram of LMWH that is infused than 1 mg in 20 ml normal saline slowly over 10 to 20 minutes. If a second dose is required, this should be one-half the first dose. However, the exact dose is unknown because protamine partially neutralizes the LMWH-mediated inactivation of factor Xa. While all infusions, patients should be observed in terms of hypotension and anaphylaxieähnliche reactions. Since intravenous UFH has a half-life of 30 to 60, patients receiving UFH, no protamine added (for. Example, when UFH> 60 min was administered before) or it is administered in a dose that on the basis of geschätzen amount of remaining in the plasma heparin, is based is determined on the half-life of UFH. Fondaparinux, a parenteral, selective factor Xa inhibitor can be used as an alternative to UFH or LMWH for the initial treatment of DVT or pulmonary embolism. It is s.c. in a fixed dose of 7.5 mg once / day administered (10 mg for patients> 100 kg 5 mg for patients <50 kg). It has the advantage of solid dosage and caused less likely thrombocytopenia. Parenteral direct thrombin inhibitors (argatroban, bivalirudin, desirudin) are available, but do not play a role in the treatment and prevention of DVT or PE. Argatroban can be useful for the treatment of DVT in patients with heparin-induced thrombocytopenia. Vitamin K antagonists such as warfarin, are the drugs of choice for long-term anticoagulation of patients, with the exception of pregnant women (which should continue treatment with heparin), and patients who develop new or worsening venous thromboembolism occur under phenprocoumon treatment (this may be candidates for a V. cava inferior screen / filter). The intake of 5-10 mg warfarin can be started with heparin at the same time as it takes about 5 days to insert the desired therapeutic effects. Elderly patients and patients with liver disease typically need lower Marcumardosen. The therapeutic goal is an INR of 2.0 to 3.0. The INR is determined weekly during the first one to two months and monthly thereafter, the dosage is increased or decreased to maintain the INR is within this range from 0.5 to 3 mg. Patients taking warfarin should be informed about possible drug interactions, incl. Interactions with food and non-prescription herbal medication. called non-warfarin oral anticoagulants also direct oral anticoagulants (DOACs), are available as alternatives to warfarin as 1st-line therapy for the treatment of DVT and PE available; not all DOACs are currently approved by the FDA for this indication (see table: Oral anticoagulants). Substances factor Xa inhibitors (rivaroxaban, apixaban, Edoxaban) and a direct thrombin inhibitor include (dabigatran). Compared with warfarin has been shown for these substances is that they provide similar protection against recurrent DVT and have a similar (or in the case of apixaban maybe less) risk of severe bleeding. Ihre Vorteile sind, dass sie innerhalb einiger Stunden wirksam sind (daher benötigen sie - mit der Ausnahme von Dabigatran - keine parenterale Überbrückungsbehandlung mit einem Heparin) und sie mit einer festen Dosierung verabreicht werden (daher sind keine durchgehenden Labortests notwendig). Ihre Nachteile sind, dass sie teuer sind und derzeit (außer bei Dabigatran und Edoxaban) keine Gegenmittel verfügbar sind, um ihrer gerinnungshemmenden Wirkung bei Patienten mit lebensbedrohlicher Blutung oder solchen, die eine dringende Operation benötigen, entgegen zu wirken. Idarucizumab ist ein humanisierter monoklonaler Antikörper gegen Dabigatran, was ein wirksames Mittel gegen Dabigatran ist. Gegenmittel für die anderen direkten oralen Antikoagulantien werden derzeit entwickelt. Wenn eine lebensbedrohliche Blutung auftritt, kann mit Prothrombinkomplexkonzentrat (PCC) versucht werden, die gerinnungshemmende Wirkung von Rivaroxaban und Apixaban zu verringern, und aktivierte PCC können für Dabigatran verwendet werden (wenn das Antidot nicht verfügbar ist). In seltenen Fällen kann eine Hämodialyse oder Hämoperfusion dabei helfen, die gerinnungshemmende Wirkung von Dabigatran, die nicht stark proteingebunden ist, zu reduzieren; solc