Overview and Risk Factors
Deep venous thrombosis (DVT) leads to approximately 600,000 hospitalizations per year in the United States. Although it most often occurs in the lower extremities, DVT can also develop in the upper extremities, especially in patients with indwelling central venous catheters. DVT most commonly affects the iliac, popliteal, and femoral veins.
Pulmonary embolus (PE), due to embolization of a DVT, is one of the leading preventable causes of morbidity and mortality in hospitals. Symptoms of a PE include dyspnea, chest pain, and hemoptysis.
While DVT is often asymptomatic in the absence of PE, signs and symptoms may include swelling, tenderness, increased warmth and erythema in the affected area of the limb, and a palpable venous cord. Cyanosis of the limb may occur, which indicates deoxygenated hemoglobin trapped in nonfunctioning veins. Rarely, a patient may exhibit a positive Homan's sign (pain along the calf with dorsiflexion of the foot). Mechanisms involved in DVT formation are collectively known as Virchow's triad: venous stasis, hypercoagulability, and intimal injury (damage to the vessel wall).
Prior DVT or PE. A history of previous episodes is the strongest indicator of risk.
Age. Risk increases with age, due in part to the greater likelihood of comorbid illness as one gets older.
Surgery. Major procedures (eg, orthopedic, thoracic, abdominal, and genitourinary) pose the greatest risk and therefore require prophylaxis.
Trauma. Examples include fracture of the spine, pelvis, femur, or tibia.
Coagulopathies. Deficiencies of proteins C and S as well as antithrombin III are well-documented risk factors. Presence of the lupus anticoagulant and activated protein C resistance (also known as factor V Leiden) also poses risk.
Neoplasm. Malignancy may induce a hypercoagulable state.
Prolonged immobilization. Venous stasis occurs in postoperative convalescence, nonambulatory patients, and extended air travel.
Elevated cholesterol. Elevated cholesterol increases risk of microemboli and possible thrombosis, especially when atherosclerosis is present.
Elevated fibrinogen levels.
Pregnancy. Fibrinolysis may be impaired during pregnancy and the postpartum period.
Oral contraceptives and hormone replacement therapy. These hormones may also disrupt fibrinolysis. Patients with the combined factors of age greater than 35 years, use of oral contraceptives, and smoking are at great risk for DVT.
Diagnostic procedures must differentiate DVT from other disorders that cause similar symptoms. Unilateral extremity swelling may be due to hemorrhage, muscle rupture, ruptured popliteal cyst, and lymphedema. Limb pain can result from arthritis, tendonitis, nerve compression, traumatic injuries, and fractures.
Duplex venous ultrasonography is the most common initial diagnostic method for DVT. A thrombus can be detected by direct visualization, or by inference when the vein fails to collapse when compressed.
Magnetic resonance imaging (MRI) offers high sensitivity and specificity for suspected thromboses of the venae cavae or pelvic veins, conditions that other imaging modalities often miss. MRI and magnetic resonance angiography (MRA) also are highly accurate in detecting PE.
Impedance plethysmography measures changes in venous capacity during movement or compression. Venous obstruction alters the venous capacity that occurs following inflation or deflation of the cuff. This test can identify obstruction in areas typically missed by ultrasound (eg, inferior vena cava).
Venography works by injecting a contrast medium into a superficial vein of the foot and moving it to the deep veins by a system of tourniquets. A filling defect or the absence of filling in the deep veins is required to make the diagnosis. Because venography is time consuming and requires technical expertise, it has been replaced almost entirely by noninvasive methods.
Electrocardiogram (ECG) and chest x-ray have limited sensitivity and specificity for PE, and most often are used to exclude other causes of symptoms. However, unusual but useful findings such as ECG signs of right ventricular overload or chest x-ray evidence for pulmonary pruning or infarction, may contribute to diagnosis.
Ventilation-perfusion (V/Q) scan is used to identify PE. Newer and simpler imaging modalities, such as the helical (spiral) CT scan, MRI, and MRA are replacing V/Q scans in many situations. In some cases, CT pulmonary angiography is used after, or instead of, these noninvasive tests.
2D echocardiogram is a rapid and simple procedure for PE diagnosis. Occasionally, the embolus may be seen in transit through the right ventricle or in the proximal pulmonary arteries, and not uncommonly signs of acute right ventricular overload will greatly assist diagnosis and risk stratification. Echocardiography also may identify other etiologies for symptoms in patients with suspected PE.
Arterial blood gas determination is not sensitive or specific for the presence of PE, but severe hypoxemia may indicate massive embolism and affect treatment decisions.
D-dimer test. D-dimer is an end product of the degradation of fibrin clots. A positive result suggests the presence of DVT or PE, but the test has poor specificity (about 50%). Sensitivity is quite high (94% to 98%), so a normal D-dimer level is strong, but not absolute, evidence against the presence of thrombus. Combination screening with D-dimer and at least one imaging modality may be most effective.1,2
Patients with DVT should be initially treated with intravenous heparin in the hospital, or with subcutaneous low-molecular-weight heparin (LMWH) in an outpatient clinic, along with warfarin. Partial thromboplastin time (PTT) should be closely monitored when using IV heparin (this is not done with LMWH). Oral anticoagulation with warfarin should be overlapped with heparin until a therapeutic prothrombin time (PT) or International Normalized Ratio (INR) is reached.
PT and INR are used to monitor the effectiveness of anticoagulant therapy. INR is now the standard warfarin monitoring test, because it includes a mathematical calculation that corrects for the highly variable prothrombin time. Heparin is often administered before warfarin, because warfarin initially reduces protein C and S, thus inducing a hypercoagulable state. Uncomplicated DVT patients are generally treated for 3 to 6 months. Patients with multiple DVT episodes, high recurrence risk, associated PE, cancer, or coagulopathies may require prolonged or even lifetime warfarin anticoagulation.
If anticoagulation therapy is not viable (eg, patient has active hemorrhage), external compression devices are a mechanical alternative for DVT treatment.
Patients are often admitted to the hospital for acute thrombosis above the groin (ie, suspected PE), presence of concomitant illness, morbid obesity, noncompliance with or poor response to oral anticoagulation, or lack of a caretaker.
Recommended treatment for this condition is elevation of the affected limb and application of warm compresses to the affected area.
Nonsteroidal anti-inflammatory drugs are contraindicated for DVT and PE because they may mask the symptoms of a new thrombus.
Surgical procedures for treatment of extensive DVT or PE include balloon or direct thrombectomy and insertion of inferior vena cava filters. Treatment with inferior vena cava filters is also indicated for patients with contraindications or poor response to anticoagulation, and for prophylaxis in high-risk patients.
DVT is rare in societies where diets are primarily based on unrefined plant foods, rather than on animal products or highly refined foods, and, as a result, are lower in fat and higher in dietary fiber.3,4 The reasons for this association are unclear. However, low fiber intake is associated with higher activity of plasminogen activator inhibitor-1 (PAI-1), the body's main inhibitor of fibrinolysis.5 Low-fat, high-fiber diets, combined with exercise, improve fibrinolysis,6,7 and may thereby help reduce DVT risk. Some hypothesize that individuals on low-fiber diets often strain to pass stools, raising intravenous pressures and damaging the valves that facilitate blood return.3 High-fiber diets help prevent this problem.
Two nutritional factors are associated with reduced risk of DVT, without clear evidence of cause and effect.
Low-fat, high-fiber diets. Elevated blood cholesterol concentrations are associated with DVT risk.8 Some evidence suggests that simultaneously elevated cholesterol and triglycerides increase this risk.9 Greatly reducing dietary cholesterol and saturated fat and increasing dietary fiber have a major effect on blood lipids. As explained here, low-fat, vegetarian and vegan diets are particularly effective in achieving this goal. Elevated fibrinogen levels, which is another risk factor for DVT,10 are lower in persons following vegetarian diets.11,12
Weight control. Obesity increases the risk for developing DVT.13,14 The risk may be due to an obesity-related increase in PAI-1,15 or to associated elevation of venous pressure. Click here for a discussion of weight-control techniques.
In addition, constancy of vitamin K intake is important for patients using warfarin anticoagulation. For this population, even small increases in dietary vitamin K appear capable of reducing INR to subtherapeutic levels.16 Conversely, decreased vitamin K may result in prolonged INR and increased bleeding risk. Food sources of vitamin K (mainly green vegetables) need not be eliminated, but vegetable intake should be consistent from day to day to avoid excessively low or high intakes. Patients should not take a vitamin K supplement without physician approval.
Vegetarian diet, low-fat, nondairy
Nutrition consultation to assist patient with diet changes, with outpatient follow up as needed.
Individualized exercise prescription to manage cholesterol levels and decrease extended periods of immobility.
What to Tell the Family
Some evidence suggests that a health-promoting diet, regular exercise, and maintenance of a healthy weight may reduce the risk of DVT. Persons who are on medication to prevent DVT recurrence should follow similar diet and exercise measures, along with maintaining consistency in intake of vitamin K-containing foods. Family members will help adherence and improve their own health by adopting similar diet and exercise routines.
1. Perrier A, Roy PM, Sanchez O, et al. D-dimer, multidetector-row CT may be sufficient to screen for pulmonary embolism. N Engl J Med. 2005;352:1760-1768, 1812-1814.
2. Elias A, Cazanave A, Elias M, et al. Diagnostic management of pulmonary embolism using clinical assessment, plasma D-dimer assay, complete lower limb venous ultrasound, and helical computed tomography of pulmonary arteries. A multicenter clinical outcome study. Thromb Haemost. 2005;93:982-988.
3. Burkitt DP, Walker AR, Painter NS. Dietary fiber and disease..JAMA. 1974;229:1068-1074.
4. Burkitt DP. Varicose veins, deep vein thrombosis, and hemorrhoids: epidemiology and suggested etiology. Br Med J. 1972;2:556-561.
5. Boman K, Hellsten G, Bruce A, Hallmans G, Nilsson TK. Endurance physical activity, diet, and fibrinolysis. Atherosclerosis. 1994;106:65-74.
6. Lindahl B, Nilsson TK, Jansson JH, Asplund K, Hallmans G. Improved fibrinolysis by intense lifestyle intervention. A randomized trial in subjects with impaired glucose tolerance. J Intern Med. 1999;246:105-112.
7. Marckmann P, Sandstrom B, Jespersen J. Low-fat, high-fiber diet favorably affects several independent risk markers of ischemic heart disease: observations on blood lipids, coagulation, and fibrinolysis from a trial of middle-aged Danes. Am J Clin Nutr. 1994;59:935-939.
8. Vaya A, Mira Y, Ferrando F, et al. Hyperlipidemia and venous thromboembolism in patients lacking thrombophilic risk factors. Br J Haematol. 2002;118:255-259.
9. Kawasaki T, Kambayashi J, Ariyoshi H, Sakon M, Suehisa E, Monden M. Hypercholesterolemia as a risk factor for deep-vein thrombosis. Thromb Res 1997;88:67-73.
10. Vaya A, Mira Y, Martinez M, et al. Biological risk factors for deep vein thrombosis. Clin Hemorheol Microcirc. 2002;26:41-53.
12. Mezzano D, Munoz X, Martinez C, et al. Vegetarians and cardiovascular risk factors: hemostasis, inflammatory markers and plasma homocysteine. Thromb Haemost. 1999;81:913-917.
13. Goldhaber SZ, Tapson VF, and the DVT FREE Steering Committee. A prospective registry of 5,451 patients with ultrasound-confirmed deep vein thrombosis. Am J Cardiol. 2004;93:259-262.
14. Abdollahi M, Cushman M, Rosendaal FR. Obesity: risk of venous thrombosis and the interaction with coagulation factor levels and oral contraceptive use. Thromb Haemost. 2003;89:493-498.
15. Skurk T, Hauner H. Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1. Int J Obes Relat Metab Disord. 2004;28:1357-1364.
16. Kurnik D, Loebstein R, Rabinovitz H, Austerweil N, Halkin H, Almog S. Over-the-counter vitamin K1-containing multivitamin supplements disrupt warfarin anticoagulation in vitamin K1-depleted patients. A prospective, controlled trial. Thromb Haemost. 2004;92:1018-1024.