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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.
Diagnosis is by history, physical examination, and duplex
ultrasonography, with D-dimer or other testing as necessary. Treatment
is with anticoagulants. Prognosis is generally good with
prompt, adequate treatment; common long-term complications include
venous insufficiency with or without postphlebitic syndrome.
DVT occurs most commonly occurs in the lower extremities, or pelvis (see Fig. 1: Peripheral Venous and Lymphatic Disorders: Deep veins of the legs. ). It can also develop in deep veins of the upper extremities (4 to 13% of DVT cases).
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 veins in the calves are most commonly affected. Calf vein DVT is less likely to be a source of large emboli but can cause repeated showers of small emboli or propagate to the proximal thigh veins and from there cause PE. About 50% of patients with DVT have occult PE, and at least 30% with PE have demonstrable DVT.
Etiology
Many factors can contribute to DVT (see Table 1: Peripheral Venous and Lymphatic Disorders: 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. Occult cancers may be present in patients with apparently idiopathic DVT, but extensive workup of patients for tumors is not recommended.
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Table 1
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Risk Factors
for Venous Thrombosis
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Age > 60 yr
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Cancer
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Cigarette smoking (including passive smoking)
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Estrogen receptor modulators (tamoxifen, raloxifene)
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Heart failure
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Hypercoagulability disorders
Antiphospholipid antibody syndrome
Factor V Leiden mutation (activated protein C resistance)
Hereditary fibrinolytic defects
Heparin-induced thrombocytopenia and thrombosis
Increase in von Willebrand's factor
Paroxysmal nocturnal hemoglobinuria
Prothrombin G-A gene variant
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Immobilization
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Indwelling venous catheters
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Limb trauma
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Myeloproliferative disease (hyperviscosity)
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Nephrotic syndrome
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Obesity
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Oral contraceptives or estrogen therapy
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Pregnancy and postpartum
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Prior venous thromboembolism
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Sickle cell anemia
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Surgery within past 3 mo
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Trauma
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Pathophysiology
Lower extremity DVT most often results from impaired venous return (eg, in immobilized patients), endothelial injury or dysfunction (eg, after leg fractures), or 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).
DVT 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.
Complications
Common complications include chronic venous insufficiency and postphlebitic syndrome, as well as PE.
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, is infection and clotting usually caused by venous catheterization.
Symptoms and Signs
DVT may occur in ambulatory patients or as a complication of surgery or major medical illness. In high-risk hospitalized patients, most deep vein thrombi occur in the small calf veins, are asymptomatic, and are never 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 2: Peripheral Venous and Lymphatic Disorders: 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. If PE occurs, symptoms may include shortness of breath and pleuritic chest pain (see Pulmonary Embolism (PE): Symptoms and Signs).
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Table 2
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Probability of
Deep Venous Thrombosis
Based on Clinical Factors
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Factors
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Tenderness along distribution of the veins in calf or thigh
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Swelling of entire leg
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Calf swelling (> 3 cm difference in circumference between calves, measured 10 cm below tibial tuberosity)
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Pitting edema greater in affected leg
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Dilated collateral superficial veins
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Cancer (including cases in which treatment was stopped within 6 mo)
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Immobilization of lower extremity (eg, due to paralysis, paresis, casting, recent long-distance travel)
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Surgery leading to immobility for > 3 days within past 4 wk
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Probability
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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
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Based on data from Anand SS Well, PS, Hunt, D et al: JAMA 279(14):1094–1099,1998.
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Common causes of asymmetric leg swelling that mimic DVT are soft-tissue trauma, cellulitis, pelvic venous or lymphatic obstruction, and popliteal bursitis (Baker's 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 cause symmetric bilateral leg swelling; 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's) 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.
Diagnosis
History and physical examination help determine probability of DVT before testing (see Table 2: Peripheral Venous and Lymphatic Disorders: 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 Fig. 2: Peripheral Venous and Lymphatic Disorders: One approach to testing for suspected deep venous thrombosis..
Ultrasonography
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 possibly immediate venography depending on clinical suspicion. Newer latex qualitative assays are highly specific (up to about 99%) but should not yet be used to confirm DVT without ultrasonography.
Venography
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 magnetic resonance 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 helical CT) 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 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 aimed at detecting cancer is probably adequate.
Prognosis
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, heart failure, malignancy), 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 impossible to predict. Risk factors for postphlebitic syndrome include proximal thrombosis, recurrent ipsilateral DVT, and body mass index (BMI) ≥ 22 kg/m2.
Treatment
Treatment is aimed primarily at PE prevention (see also Pulmonary Embolism (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 mol wt), followed by warfarin started within 24 to 48 h. Inadequate anticoagulation in the first 24 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 other than aspirin and NSAIDs (because of their antiplatelet effects) and, during periods of inactivity, elevation of legs (supported by a pillow or other soft surface to avoid venous compression). Patients may be as physically active as they can tolerate; there is no evidence that early activity increases risk of clot dislodgement and PE.
Anticoagulants
The anticoagulants most often used are the following:
Low mol wt heparins (LMWH; eg, enoxaparin, dalteparin, tinzaparin—see Table 5: Pulmonary Embolism (PE): Some Anticoagulation Options Other Than Heparin in Thromboembolic Disease) are the initial treatment of choice because they can be given on an outpatient basis. LMWHs are as effective as unfractionated heparin (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, 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 LMWH overdose and bleeding. Treatment is continued until full anticoagulation is achieved with warfarin. 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 Fig. 2: Pulmonary Embolism (PE): Weight-based heparin dosing.) to achieve full anticoagulation, (eg, activated PTT [aPTT] 1.5 to 2.5 times that of the reference range). UFH 333 units/kg initial bolus, then 250 units/kg q 12 h sc can be substituted for IV UFH to facilitate mobility in outpatients; the dose does not appear to need adjustment based on aPTT. Treatment is continued until full anticoagulation has been achieved with warfarin.
Complications of heparin include bleeding, thrombocytopenia (less common with LMWHs), urticaria, and, rarely, thrombosis and anaphylaxis. Long-term use of UFH causes hypokalemia, liver enzyme elevations, and osteoporosis. Rarely, UFH given sc causes skin necrosis. Inpatients and possibly outpatients should be screened for bleeding with serial CBCs and tests for occult blood in stool. Bleeding due to overheparinization can be stopped with protamine sulfate. The dose is 1 mg protamine for each mg LMWH given as 1 mg in 20 mL normal saline infused slowly over 10 to 20 min. If a 2nd dose is required, it should be at ½ the first dose. However, the precise dose is undefined because protamine only partially neutralizes LMWH inactivation of factor Xa. With all infusions, the patient 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 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 produce 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. 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 (see Table 4: Pulmonary Embolism (PE): Drug, Herbal Preparation, and Food Interactions With Warfarin).
Patients with transient risk factors for DVT (eg, immobilization, surgery) can stop taking warfarin after 3 to 6 mo. Patients with nonmodifiable risk factors (eg, hypercoagulability), spontaneous DVT with no known risk factors, or recurrent DVT should take warfarin for at least 6 mo and probably for life unless complications occur.
Bleeding is the most common complication. Risk factors for major 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; and coexisting anemia (Hct < 30%), renal insufficiency (serum creatinine > 1.5 mg/dL), or diabetes. Anticoagulation can be reversed with vitamin K; the dose is 1 to 4 mg po if INR is 5 to 9, 5 mg po if INR is > 9, and 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. Overanticoagulation (INR > 3 or 4) without bleeding can be managed by omitting several warfarin doses and more frequent INR monitoring, 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.
Other anticoagulants, such as direct thrombin inhibitors (DTIs, eg, hirudin given sc; lepirudin, bivalirudin, desirudin, argatroban, given parenterally; dabigatran given po) and oral factor Xa inhibitors (eg, rivaroxaban and apixaban) are being evaluated for the treatment of DVT (see Table 5: Pulmonary Embolism (PE): Some Anticoagulation Options Other Than Heparin in Thromboembolic Disease).
Inferior
vena cava filter (IVCF)
An IVCF may help prevent PE in patients with lower extremity DVT and contraindications to anticoagulants or 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 and subacute thrombotic complications but can have longer-term complications (eg, venous collaterals can develop, providing a pathway for emboli to circumvent the IVCF). Also, IVCFs can dislodge or become obstructed by clot. Thus, patients with recurrent DVT or nonmodifiable risk factors for DVT may still require anticoagulation. A clotted filter may cause bilateral lower extremity venous congestion (including acute phlegmasia cerulea dolens), lower body ischemia, and acute renal failure. 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.
Thrombolytic
(fibrinolytic) drugs
Streptokinase, urokinase, and alteplase lyse clots and appear to more effectively prevent postphlebitic syndrome than heparin alone, but risk of bleeding is higher. Their use is under study. Thrombolytics may be indicated for large proximal thrombi, especially those in the iliofemoral veins, and for phlegmasia alba or cerulea dolens. Local perfusion with an indwelling catheter may be preferable to IV administration.
Surgery
Surgery is rarely needed. However, thrombectomy, fasciotomy, or both are mandatory for phlegmasia alba or cerulea dolens unresponsive to thrombolytics to try to prevent limb-threatening gangrene.
Prevention
Patients at low risk of DVT (eg, those who are undergoing minor surgery but have no clinical risk factors for DVT; those who must be temporarily inactive for long periods, as during an airplane flight) should be encouraged to walk or otherwise move their legs periodically; no medical treatment is needed. Dorsiflexion 10 times/h is probably sufficient.
Patients at higher risk of DVT (eg, those undergoing minor surgery if they have clinical risk factors for DVT; those undergoing major surgery, especially orthopedic surgery, even without risk factors; bedbound patients with major medical illnesses) require additional preventive treatment (see Table 3: Peripheral Venous and Lymphatic Disorders: Risk of Deep Venous Thrombosis and Pulmonary Embolism in Surgical Patients). Most of these patients can be identified and should receive thrombosis prophylaxis.
After surgery, elevating the legs and avoiding sitting in chairs (which, by placing the legs in a dependent position, impedes venous return) can help. Additional treatment may involve low-dose UFH, LMWH, warfarin, newer anticoagulants such as fondaparinux, compression devices or stockings, or a combination, depending on patient's risk level, type of surgery (if applicable), projected duration of preventive treatment, contraindications, adverse effects, relative cost, ease of use, and local practice. Low-dose UFH 5000 units sc is given 2 h before surgery and q 8 to 12 h thereafter for 7 to 10 days or until patients are fully ambulatory. Bedbound patients who are not undergoing surgery are given 5000 units sc q 12 h until risk factors are reversed.
LMWHs are more effective than low-dose UFH for preventing DVT and PE, but widespread use is limited by cost. For example, enoxaparin 30 mg sc q 12 h, dalteparin 2500 units once/day, and tinzaparin 3500 units once/day are equally effective. Fondaparinux, 2.5 mg once/day, is equal to or more effective than LMWH depending on the surgical setting (eg, orthopedic surgery).
Warfarin at a target INR of 2.0 to 3.0 is proven to be effective in orthopedic surgery.
Newer anticoagulants (eg, hirudin, lepirudin) are effective for preventing DVT and PE, but their cost-effectiveness and safety compared with heparin and warfarin require further study. Aspirin is better than placebo but worse than all other available drugs for preventing DVT and PE and is not recommended as the sole method of prevention (see Table 5: Pulmonary Embolism (PE): Some Anticoagulation Options Other Than Heparin in Thromboembolic Disease).
Intermittent pneumatic compression (IPC) uses a pump to cyclically inflate and deflate hollow plastic leggings, providing external compression to the lower legs and sometimes thighs. IPC may be used instead of or with anticoagulants before and during surgery. IPC is recommended after knee surgery. IPC is probably more effective for preventing calf than proximal DVT. IPC is usually contraindicated in obese patients and can theoretically trigger PE in immobilized patients who, without preventive treatment, develop occult DVT.
The benefit of graded compression stockings is questionable except for low-risk surgical patients. However, combining stockings with other preventive measures may be more protective than any single approach.
For elective neurosurgery, spinal cord injury, or multiple trauma, low-dose UFH (q 8 h), LMWH, or adjusted-dose warfarin is recommended.For hip and other lower extremity orthopedic surgery, LMWH, fondaparinux, or adjusted-dose warfarin is recommended. For patients undergoing total knee replacement and some other high-risk patients, IPC is also beneficial. For orthopedic surgery, preventive treatment may be started before or after surgery and continued for at least 14 days. Fondaparinux 2.5 mg once/day is more effective than LMWH for orthopedic surgery. For neurosurgery patients, physical measures (IPC, elastic stockings) have been used because intracranial bleeding is a concern; however, LMWH appears to be an acceptable alternative. Limited data support the combination of IPC, elastic stockings, and LMWH in patients with spinal cord injury or multiple trauma.
For patients who are at very high risk of venous thromboembolism and bleeding and are taking anticoagulants, IVCF placement is an option.
Preventive treatment is also indicated for patients who have a major medical illnesses requiring bed rest (eg, MI, ischemic stroke). Low-dose UFH is effective in patients who are not already receiving IV heparin or thrombolytics; IPC, elastic stockings, or both may be used when anticoagulants are contraindicated. After a stroke, low-dose UFH or LMWH can be used; IPC, elastic stockings, or both may be beneficial. Other recommendations include low-dose UFH for patients with heart failure, warfarin (target INR 2.0 to 3.0) for those with metastatic breast cancer, and warfarin 1 mg once/day for those with cancer and an indwelling central venous catheter. Fondaparinux 2.5 mg once/day is also recommended in patients with major medical illnesses.
In patients with symptomatic DVT, primary prevention of venous insufficiency and postphlebitic syndrome is recommended; knee-high compression stockings providing 30 to 40 mm Hg pressure are used.
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Table 3
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Risk of Deep Venous Thrombosis
and
Pulmonary Embolism in Surgical Patients
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Risk Category
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Examples
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Preventive Measures
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Risk of DVT/PE(%)
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Calf
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Proximal
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PE
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Fatal PE
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Low
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Nonmajor surgery* in patients < 40 yr with no clinical riskfactors
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Early and aggressive ambulation
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2
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0.4
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0.2
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0.002
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Moderate
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Nonmajor surgery in patients with risk factors; minor surgery in patients 40–60 yr with no clinical risk factors; major surgery in patients < 40 yr with no other clinical risk factors
Immobilized patients with major medical illnesses
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LDUH q 12 h, LMWH, fondaparinux IPC, with or without elastic stockings
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10-20
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2-4
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1-2
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0.1-0.4
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High
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Nonmajor surgery in patients > 60 yr or 40–60 with risk factors; major surgery in patients > 40 yr or with other clinical risk factors
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LDUH q 8 h, LMWH, fondaparinux, or IPC
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20-40
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4-8
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2-4
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0.4-1.0
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Very high
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Major surgery in patients > 40 yr with previous venous thromboembolic, malignant, or hypercoagulability disorder; in patients of any age, hip or knee arthroplasty or hip fracture surgery; elective neurosurgery; multiple trauma or spinal cord injury
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LMWH, oral anticoagulation, IPC or elastic stockings plus either LDUH q 8 h or LMWH
Fondaparinux for orthopedic, abdominal, or thoracic surgery or for acute, severe illness
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40-80
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10-20
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4-10
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0.2-5
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DVT = Deep venous thrombosis; PE = pulmonary embolism; LDUH = low-dose unfractionated heparin; LMWH = low mol wt heparin; IPC = intermittent pneumatic compression.
* Nonmajor surgery is defined here as an operation that does not involve general anesthesia or respiratory assistance.
Adapted with permission from Geerts WH, Heit JA, Clagett GP, et al: Prevention of venous thromboembolism. Chest 119:132S–175S, 2001.
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Last full review/revision March 2008 by Alexander G.G. Turpie, MD
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