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Deep Venous Thrombosis (DVT)

By James D. Douketis, MD, Professor, Divisions of General Internal Medicine, Hematology and Thromboembolism, Department of Medicine; Director, Vascular Medicine Research Program, McMaster University; St. Joseph's Healthcare Hamilton

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Deep venous thrombosis (DVT) is clotting of blood in a deep vein of an extremity (usually calf or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. DVT results from conditions that impair venous return, lead to endothelial injury or dysfunction, or cause hypercoagulability. DVT may be asymptomatic or cause pain and swelling in an extremity; pulmonary embolism is an immediate complication. Diagnosis is by history and physical examination and is confirmed by objective testing, typically with duplex ultrasonography. d-Dimer testing is used when DVT is suspected; a negative result helps to exclude DVT, whereas a positive result is nonspecific and requires additional testing to confirm DVT. Treatment is with anticoagulants. Prognosis is generally good with prompt, adequate treatment. Common long-term complications include venous insufficiency with or without the postphlebitic syndrome.

DVT occurs most commonly in the lower extremities or pelvis (see Figure: Deep veins of the legs.). It can also develop in deep veins of the upper extremities (4 to 13% of DVT cases).

Deep veins of the legs.

Lower extremity DVT is much more likely to cause pulmonary embolism (PE), possibly because of the higher clot burden. The superficial femoral and popliteal veins in the thighs and the posterior tibial and peroneal veins in the calves are most commonly affected. Calf vein DVT is less likely to be a source of large emboli but can propagate to the proximal thigh veins and from there cause PE. About 50% of patients with DVT have occult PE, and at least 30% of patients with PE have demonstrable DVT.

Pearls & Pitfalls

  • About 50% of patients with DVT have occult pulmonary emboli.


Many factors can contribute to DVT (see Table: Risk Factors for Venous Thrombosis). Cancer is a risk factor for DVT, particularly in elderly patients and in patients with recurrent thrombosis. The association is strongest for mucin-secreting endothelial cell tumors such as bowel or pancreatic cancers. Occult cancers may be present in patients with apparently idiopathic DVT, but extensive workup of patients for tumors is not recommended unless patients have major risk factors for cancer or symptoms suggestive of an occult cancer.

Risk Factors for Venous Thrombosis

Age > 60 yr


Cigarette smoking (including passive smoking)

Estrogen receptor modulators (eg, tamoxifen, raloxifene)

Heart failure


Indwelling venous catheters

Limb trauma

Myeloproliferative disease (hyperviscosity)

Nephrotic syndrome


Oral contraceptives or estrogen therapy

Pregnancy and postpartum

Prior venous thromboembolism

Sickle cell anemia

Surgery within the past 3 mo



Lower extremity DVT most often results from ,

  • Impaired venous return (eg, in immobilized patients)

  • Endothelial injury or dysfunction (eg, after leg fractures)

  • Hypercoagulability

Upper extremity DVT most often results from

  • Endothelial injury due to central venous catheters, pacemakers, or injection drug use

Upper extremity DVT occasionally occurs as part of superior vena cava (SVC) syndrome or results from a hypercoagulable state or subclavian vein compression at the thoracic outlet. The compression may be due to a normal or an accessory first rib or fibrous band (thoracic outlet syndrome) or occur during strenuous arm activity (effort thrombosis, or Paget-Schroetter syndrome, which accounts for 1 to 4% of upper extremity DVT cases).

Deep venous thrombosis usually begins in venous valve cusps. Thrombi consist of thrombin, fibrin, and RBCs with relatively few platelets (red thrombi); without treatment, thrombi may propagate proximally or travel to the lungs.


Common complications of deep venous thrombosis include

Much less commonly, acute DVT leads to phlegmasia alba dolens or phlegmasia cerulea dolens, both of which, unless promptly diagnosed and treated, can result in venous gangrene.

In phlegmasia alba dolens, a rare complication of DVT during pregnancy, the leg turns milky white. Pathophysiology is unclear, but edema may increase soft-tissue pressure beyond capillary perfusion pressures, resulting in tissue ischemia and wet gangrene.

In phlegmasia cerulea dolens, massive iliofemoral venous thrombosis causes near-total venous occlusion; the leg becomes ischemic, extremely painful, and cyanotic. Pathophysiology may involve complete stasis of venous and arterial blood flow in the lower extremity because venous return is occluded or massive edema cuts off arterial blood flow. Venous gangrene may result.

Rarely, venous clots can become infected. Jugular vein suppurative thrombophlebitis (Lemierre syndrome), a bacterial (usually anaerobic) infection of the internal jugular vein and surrounding soft tissues, may follow tonsillopharyngitis and is often complicated by bacteremia and sepsis. In septic pelvic thrombophlebitis, pelvic thromboses develop postpartum and become infected, causing intermittent fever. Suppurative (septic) thrombophlebitis, a bacterial infection of a superficial peripheral vein, comprises infection and clotting that usually is caused by venous catheterization.

Symptoms and Signs

DVT may occur in ambulatory patients or as a complication of surgery or major medical illness. Among high-risk hospitalized patients, most deep vein thrombi occur in the small calf veins, are asymptomatic, and may not be detected.

When present, symptoms and signs (eg, vague aching pain, tenderness along the distribution of the veins, edema, erythema) are nonspecific, vary in frequency and severity, and are similar in arms and legs. Dilated collateral superficial veins may become visible or palpable. Calf discomfort elicited by ankle dorsiflexion with the knee extended (Homans sign) occasionally occurs with distal leg DVT but is neither sensitive nor specific. Tenderness, swelling of the whole leg, > 3 cm difference in circumference between calves, pitting edema, and collateral superficial veins may be most specific; DVT is likely with a combination of 3 in the absence of another likely diagnosis (see Table: Probability of Deep Venous Thrombosis Based on Clinical Factors).

Low-grade fever may be present; DVT may be the cause of fever without an obvious source, especially in postoperative patients. Symptoms of PE, if it occurs, may include shortness of breath and pleuritic chest pain.

Probability of Deep Venous Thrombosis Based on Clinical Factors


Tenderness along distribution of the veins in calf or thigh

Swelling of entire leg

Calf swelling (> 3 cm difference in circumference between calves, measured 10 cm below tibial tuberosity)

Pitting edema greater in affected leg

Dilated collateral superficial veins

Cancer (including cases in which treatment was stopped within 6 mo)

Immobilization of lower extremity (eg, due to paralysis, paresis, casting, or recent long-distance travel)

Surgery leading to immobility for > 3 days within the past 4 wk


Probability equals the number of factors, subtracting 2 if another diagnosis is as likely as or more likely than DVT.

  • High probability: 3 points

  • Moderate probability: 1–2 points

  • Low probability:       0 points

Based on data from Anand SS, Wells PS, Hunt D, et al: Does this patient have deep vein thrombosis? Journal of the American Medical Association 279 (14):1094–1099, 1998.

Common causes of asymmetric leg swelling that mimic DVT are soft-tissue trauma, cellulitis, pelvic venous or lymphatic obstruction, and popliteal bursitis (Baker cyst) that obstructs venous return. Abdominal or pelvic tumors that obstruct venous or lymphatic return are less common causes. Use of drugs that cause dependent edema (eg, dihydropyridine Ca channel blockers, estrogen, high-dose opioids), venous hypertension (usually due to right heart failure), and hypoalbuminemia typically cause symmetric bilateral leg swelling; however, swelling may be asymmetric if venous insufficiency coexists and is worse in one leg.

Common causes of calf pain that mimic acute DVT include venous insufficiency and postphlebitic syndrome; cellulitis that causes painful erythema of the calf; ruptured popliteal (Baker) cyst (pseudo-DVT), which causes calf swelling, pain, and sometimes bruising in the region of the medial malleolus; and partial or complete tears of the calf muscles or tendons.


  • Ultrasonography

  • Sometimes d-dimer testing

History and physical examination help determine probability of DVT before testing (see Table: Probability of Deep Venous Thrombosis Based on Clinical Factors). Diagnosis is typically by ultrasonography with Doppler flow studies (duplex ultrasonography). The need for additional tests (eg, d-dimer testing) and their choice and sequence depend on pretest probability and sometimes ultrasonography results. No single testing protocol is best; one approach is described in One approach to testing for suspected deep venous thrombosis..

One approach to testing for suspected deep venous thrombosis.


Ultrasonography identifies thrombi by directly visualizing the venous lining and by demonstrating abnormal vein compressibility or, with Doppler flow studies, impaired venous flow. The test is >90% sensitive and > 95% specific for femoral and popliteal vein thrombosis but is less accurate for iliac or calf vein thrombosis.

d -Dimer

d-Dimer is a byproduct of fibrinolysis; elevated levels suggest recent presence and lysis of thrombi. d-Dimer assays vary in sensitivity and specificity; however, most are sensitive and not specific. Only the most accurate tests should be used. For example, a highly sensitive test is enzyme-linked immunosorbent assay (ELISA), which has a sensitivity of about 95%.

If pretest probability of DVT is low, DVT can be safely excluded in patients with a normal d-dimer level on a sensitive test. Thus, a negative d-dimer test can identify patients who have a low probability of DVT and do not require ultrasonography. However, a positive test result is nonspecific; because levels can be elevated by other conditions (eg, liver disease, trauma, pregnancy, positive rheumatoid factor, inflammation, recent surgery, cancer), further testing is necessary.

If pretest probability of DVT is moderate or high,d-dimer testing can be done at the same time as duplex ultrasonography. A positive ultrasound result confirms the diagnosis regardless of the d-dimer level. If ultrasonography does not reveal evidence of DVT, a normal d-dimer level helps exclude DVT. Patients with an elevated d-dimer level should have repeat ultrasonography in a few days or additional imaging, such as venography, depending on clinical suspicion.


Contrast venography was the definitive test for the diagnosis of DVT but has been largely replaced by ultrasonography, which is noninvasive, more readily available, and almost equally accurate for detecting DVT. Venography may be indicated when ultrasonography results are normal but pretest suspicion for DVT is high. The complication rate is 2%, mostly because of contrast dye allergy.

Other testing

Noninvasive alternatives to contrast venography are being studied. They include MRI venography and direct MRI of thrombi using T1-weighted gradient-echo sequencing and a water-excitation radiofrequency pulse; theoretically, the latter test can provide simultaneous views of thrombi in deep veins and subsegmental pulmonary arteries (for diagnosis of PE).

If symptoms and signs suggest PE, additional imaging (eg, ventilation/perfusion [V/Q] scanning or CT pulmonary angiography) is required.

Determination of cause

Patients with confirmed DVT and an obvious cause (eg, immobilization, surgical procedure, leg trauma) need no further testing. Testing to detect hypercoagulability is controversial but is sometimes done in patients who have idiopathic (or unprovoked) DVT or recurrent DVT, in patients who have a personal or family history of other thromboses, and in young patients with no obvious predisposing factors. Some evidence suggests that presence of hypercoagulability does not predict DVT recurrence as well as clinical risk factors.

Screening patients with DVT for cancer has a low yield. Selective testing guided by complete history and physical examination and basic "routine" tests (CBC, chest x-ray, urinalysis, liver enzymes, and serum electrolytes, BUN, creatinine) aimed at detecting cancer is probably adequate. In addition, patients should have any age- and gender-appropriate cancer screening (eg, mammography, colonoscopy) that is due.


Without adequate treatment, lower extremity DVT has a 3% risk of fatal PE; death due to upper extremity DVT is very rare. Risk of recurrent DVT is lowest for patients with transient risk factors (eg, surgery, trauma, temporary immobility) and greatest for patients with persistent risk factors (eg, cancer), idiopathic DVT, or incomplete resolution of past DVT (residual thrombus). A normal d-dimer level obtained after warfarin is stopped may help predict a relatively low risk of DVT or PE recurrence. Risk of venous insufficiency is difficult to predict. Risk factors for postphlebitic syndrome include proximal thrombosis, recurrent ipsilateral DVT, and body mass index (BMI) 22 kg/m2.


  • Anticoagulation with an injectable heparin followed by an oral anticoagulant (warfarin, or a factor Xa or direct thrombin inhibitor)

Treatment is aimed primarily at PE prevention and secondarily at symptom relief and prevention of DVT recurrence, chronic venous insufficiency, and postphlebitic syndrome. Treatment of lower and upper extremity DVT is generally the same.

All patients with DVT are given anticoagulants, initially an injectable heparin (unfractionated or low molecular weight) for a brief period, followed by longer term treatment with an oral drug (eg, warfarin) started within 24 to 48 h. Select patients may continue treatment with a low molecular weight heparin rather than switching to an oral drug. Inadequate anticoagulation in the first 24 to 48 h may increase risk of recurrence or PE. Acute DVT can be treated on an outpatient basis unless severe symptoms require parenteral analgesics, other disorders preclude safe outpatient discharge, or other factors (eg, functional, socioeconomic) might prevent the patient from adhering to prescribed treatments.

General supportive measures include pain control with analgesics, which may include short (3- to 5-day) courses of an NSAID. Extended treatment with NSAIDs and aspirin should be avoided because their antiplatelet effects may increase the risk of bleeding complications. In addition, elevation of legs (supported by a pillow or other soft surface to avoid venous compression) is recommended during periods of inactivity. Patients may be as physically active as they can tolerate; there is no evidence that early activity increases risk of clot dislodgement and PE and may help to reduce the risk of the postphlebitic syndrome.


The anticoagulants (see Figure: Anticoagulants and their sites of action.) most often used are the following:

  • Low molecular weight heparins (LMWHs)

  • Unfractionated heparin (UFH)

  • Fondaparinux

  • Warfarin

  • Non-warfarin oral anticoagulants: factor Xa inhibitors (eg, rivaroxaban, apixaban), direct thrombin inhibitors (dabigatran)

LMWHs (eg, enoxaparin, dalteparin, tinzaparin—see Table: Some Low Molecular Weight Heparin* Options in Thromboembolic Disease) are the initial treatment of choice because they can be given on an outpatient basis. LMWHs are as effective as UFH for reducing DVT recurrence, thrombus extension, and risk of death due to PE. Like UFH, LMWHs catalyze the action of antithrombin (which inhibits coagulation factor proteases), leading to inactivation of coagulation factor Xa and, to a lesser degree, factor IIa. LMWHs also have some antithrombin–mediated anti-inflammatory properties, which facilitate clot organization and resolution of symptoms and inflammation.

LMWHs are typically given sc in a standard weight-based dose (eg, enoxaparin 1.5 mg/kg sc once/day or 1 mg/kg sc q 12 h or dalteparin 200 units/kg sc once/day). Patients with renal insufficiency may be treated with UFH or with reduced doses of LMWH. Monitoring is not reliable because LMWHs do not significantly prolong the results of global tests of coagulation. Furthermore, they have a predictable dose response, and there is no clear relationship between the anticoagulant effect of LMWH and bleeding. Treatment is continued until full anticoagulation is achieved with warfarin (typically about 5 days). However, evidence suggests that LMWH is effective for long-term DVT treatment in high-risk patients, such as those with cancer. Thus, LMWH may become an acceptable alternative to warfarin for some patients, although warfarin is likely to be the treatment of choice for most patients because of its low cost and oral route of administration.

UFH may be used instead of LMWH for hospitalized patients and for patients who have renal insufficiency or failure (creatinine clearance 10 to 30 mL/min) because UFH is not cleared by the kidneys. UFH is given as a bolus and infusion (see Figure: Weight-based heparin dosing.) to achieve full anticoagulation, (eg, activated PTT [aPTT] 1.5 to 2.5 times that of the reference range). For outpatients, UFH 333 units/kg initial bolus, then 250 units/kg sc q 12 h can be substituted for IV UFH to facilitate mobility; the dose does not appear to need adjustment based on aPTT. Treatment is continued until full anticoagulation has been achieved with warfarin.

Complications of heparins include bleeding, thrombocytopenia (less common with LMWHs), urticaria, and, rarely, thrombosis and anaphylaxis. Long-term use of UFH causes hypokalemia, liver enzyme elevations, and osteopenia. Rarely, UFH given sc causes skin necrosis. Inpatients and possibly outpatients should be screened for bleeding with serial CBCs and, where appropriate, testing for occult blood in stool.

Bleeding due to overheparinization can be stopped with protamine sulfate. The dose is 1 mg protamine for each milligram of LMWH given as 1 mg in 20 mL of normal saline infused slowly over 10 to 20 min. If a 2nd dose is required, it should be one half the first dose. However, the precise dose is undefined because protamine only partially neutralizes LMWH inactivation of factor Xa. During all infusions, patients should be observed for hypotension and a reaction similar to an anaphylactic reaction. Because UFH given IV has a half-life of 30 to 60 min, protamine is not given to patients receiving UFH (eg, if UFH was given > 60 min beforehand) or is given at a dose based on the amount of heparin estimated to be remaining in plasma, based on the half-life of UFH.

Fondaparinux, a parenteral selective factor Xa inhibitor, may be used as an alternative to UFH or LMWH for the initial treatment of DVT or PE. It is given in a fixed dose of 7.5 mg sc once/day (10 mg for patients> 100 kg, 5 mg for patients < 50 kg). It has the advantage of fixed dosing and is less likely to cause thrombocytopenia.

Parenteral direct thrombin inhibitors (argatroban, bivalirudin, desirudin) are available but do not have a role in treatment or prevention of DVT or PE. Argatroban may be useful to treat DVT in patients with heparin-induced thrombocytopenia.

Vitamin K antagonists, including warfarin, are the drugs of choice for long-term anticoagulation for all patients except pregnant women (who should continue to take heparin) and patients who have had new or worsening venous thromboembolism during warfarin treatment (who may be candidates for an inferior vena cava filter). Warfarin 5 to 10 mg can be started immediately with heparin because it takes about 5 days to achieve desired therapeutic effect. The elderly and patients with a liver disorder typically require lower warfarin doses. Therapeutic goal is an INR of 2.0 to 3.0. INR is monitored weekly for the first 1 to 2 mo of warfarin treatment and monthly thereafter; the dose is increased or decreased by 0.5 to 3 mg to maintain the INR within this range. Patients taking warfarin should be informed of possible drug interactions, including interactions with foods and nonprescription medicinal herbs.

Non-warfarin oral anticoagulants, also called direct oral anticoagulants (DOACs), are available as alternatives to warfarin as a 1st-line treatment for the treatment of DVT and PE; not all DOACs are currently FDA-approved for this indication (see Table: Oral Anticoagulants). Drugs include factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) and a direct thrombin inhibitor (dabigatran). Compared to warfarin, these drugs have been shown to give similar protection against recurrent DVT and have similar (or with apixaban, perhaps lower) risk of serious bleeding.

Their advantages are that they are effective within several hours (thus, except for dabigatran, do not require parenteral bridging treatment with a heparin), and they are given as a fixed dose (thus do not require ongoing laboratory testing).

Their disadvantages are that they are expensive, and currently (except for dabigatran and edoxaban) there are no available antidotes to reverse their anticoagulant effect in patients with life-threatening bleeding or who need urgent surgery. Idarucizumab is a humanized monoclonal antibody to dabigatran that is an effective antidote to dabigatran. Antidotes for the other direct oral anticoagulants are currently being developed. If life-threatening bleeding occurs, prothrombin complex concentrate (PCC) may be tried to decrease the anticoagulant effect of rivaroxaban and apixaban, and activated PCC may be used for dabigatran (if the antidote is not available). Rarely, hemodialysis or hemoperfusion may help decrease the anticoagulant effect of dabigatran, which is not highly protein bound; such measures are not effective on rivaroxaban and apixaban. Supportive care with intravenous fluids and packed RBC transfusions are sufficient for many bleeding episodes in patients who are receiving a DOAC.

If used, rivaroxiban 15 mg po bid is started immediately upon diagnosis and given for 3 wk followed by 20 mg po once/day for 9 wk. Apixaban 10 mg po bid is started immediately upon diagnosis and given for 7 days followed by 5 mg po bid for 6 mo. Dabigatran 150 mg po bid is given only after an initial 5 to 7 days of treatment with LMWH.

Duration of treatment varies. Patients with transient risk factors for DVT (eg, immobilization, surgery) can usually stop taking warfarin after 3 to 6 mo. Patients with nonmodifiable risk factors (eg, hypercoagulability), idiopathic (or unprovoked) DVT with no known risk factors, or recurrent DVT should take warfarin for at least 6 mo and, in selected patients, probably for life unless complications occur.

Bleeding is the most common complication. Risk factors for severe bleeding (defined as life-threatening hemorrhage or loss of 2 units of blood in 7 days) include

  • Age 65

  • History of prior GI bleeding or stroke

  • Recent MI

  • Coexisting anemia (Hct < 30%), renal insufficiency (serum creatinine > 1.5 mg/dL), or diabetes

In patients who are actively bleeding or may be at increased risk of bleeding, anticoagulation can be reversed with vitamin K; the dose is 1 to 2.5 mg po if INR is 5 to 9, 2.5 to 5 mg po if INR is > 9, and 5 to 10 mg IV (given slowly to avoid anaphylaxis) if hemorrhage occurs. If hemorrhage is severe, a transfusion of coagulation factors, fresh frozen plasma, or prothrombin complex concentrate should also be given. Selected patients with overanticoagulation (INR 5 to 9) who are neither actively bleeding nor at increased risk of bleeding can be managed by omitting 1 or 2 warfarin doses and monitoring INR more frequently, then giving warfarin at a lower dose. Rarely, warfarin causes skin necrosis in patients with protein C or S deficiency or factor V Leiden mutations.

Anticoagulants and their sites of action.

LMWH = low molecular weight heparin; TF = tissue factor; UFH = unfractionated heparin.

Inferior vena cava filter (IVCF)

An IVCF may help prevent PE in patients with lower extremity DVT who have contraindications to anticoagulant therapy or in patients with recurrent DVT (or emboli) despite adequate anticoagulation. An IVCF is placed in the inferior vena cava just below the renal veins via catheterization of an internal jugular or femoral vein. Some IVCFs are removable and can be used temporarily (eg, until contraindications to anticoagulation subside or resolve).

IVCFs reduce risk of acute embolic complications but can have longer-term complications (eg, venous collaterals can develop, providing a pathway for emboli to circumvent the IVCF, and increased risk of recurrent DVT). Also, IVCFs can dislodge or become obstructed by a clot. Thus, patients with recurrent DVT or nonmodifiable risk factors for DVT may still require anticoagulation despite the presence of an IVCF. A clotted filter may cause bilateral lower extremity venous congestion (including acute phlegmasia cerulea dolens), lower body ischemia, and acute kidney injury. Treatment for a dislodged filter is removal, using angiographic or, if necessary, surgical methods. Despite widespread use of IVCFs, efficacy in preventing PE is unstudied and unproved. IVCFs should be removed whenever possible.

Thrombolytic (fibrinolytic) drugs

Streptokinase, urokinase, and alteplase lyse clots and may be more effective to prevent postphlebitic syndrome than heparin alone, but the risk of bleeding is higher than with heparin. Their use is under ongoing study, especially in patients with PE and right ventricular dysfunction and in combination with percutaneous mechanical thrombectomy for extensive proximal DVT.

Thrombolytic therapy alone may be indicated for large proximal thrombi, especially those in the iliofemoral veins, and for phlegmasia alba or cerulea dolens. Local administration of thrombolytic therapy with an indwelling catheter (during percutaneous thrombectomy) may be preferable to IV administration.


Surgery is rarely needed. However, thrombectomy, fasciotomy, or both are mandatory for phlegmasia alba dolens or phlegmasia cerulea dolens unresponsive to thrombolytics to try to prevent limb-threatening gangrene.


It is preferable and safer to prevent DVT than to treat it, particularly in high-risk patients (see Table: Risk of Deep Venous Thrombosis and Pulmonary Embolism in Surgical Patients). The following modalities are used (for a more complete discussion, see DVT Prevention).

  • Prevention of immobility

  • Anticoagulation (eg, LMWH, fondaparinux, adjusted-dose warfarin)

  • Intermittent pneumatic compression

  • IVCF

Key Points

  • Symptoms and signs are nonspecific, so clinicians must be alert, particularly in high-risk patients.

  • Low-risk patients may have d-dimer testing, as a normal result essentially excludes DVT; others should have ultrasonography.

  • Treatment initially is with an injectable heparin (unfractionated or LMWH) followed by oral warfarin or perhaps a LMWH; the role of oral factor Xa and direct thrombin inhibitors is evolving.

  • Duration of treatment is typically 3 or 6 mo depending on the presence and nature of risk factors; certain patients require lifelong treatment.

  • Preventive treatment is required for bedbound patients with major illness and/or those undergoing certain surgical procedures.

  • Early mobilization, leg elevation, and an anticoagulant are the recommended preventive measures; patients who should not receive anticoagulants may benefit from intermittent pneumatic compression devices, elastic stockings, or both.

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