Deep Venous Thrombosis

Deep venous thrombosis (DVT) and acute pulmonary thrombosis (PE) are both integrated into a single disorder, venous thromboembolism (VTE). There are as many as 900,000 hospitalizations per year in the United States due to VTE, and as many as 60,000 to 300,000 deaths.[1]

Deep venous thrombosis (DVT) occurs most often in the lower extremities, but 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 the second-leading preventable cause of hospital mortality. Symptoms of a PE may include dyspnea, chest pain, palpitations, sweating, and hemoptysis.

Risk Factors

Race and ethnicity. A higher risk for VTE may occur in blacks,[2] and a lower risk in Asian-Pacific Islanders and Latinos,[3] compared with whites.

Prior episode(s) of DVT or PE. A previous history is a major indicator of risk.

Age. Risk increases with age, due in part to increased comorbidities.

Recent surgery. Major surgeries (e.g., orthopedic, thoracic, abdominal, and genitourinary) pose the greatest risk, but individualized risk assessments should be done to determine if minor surgeries also require prophylaxis.

Trauma. Examples include fracture of the spine, pelvis, femur, or tibia.

Heritable coagulopathies. Factor V Leiden and prothrombin gene mutations cause about 50% of inherited coagulopathies. Deficiencies of antithrombin and proteins C/S, elevated fibrinogen levels, and other clotting disorders also raise risk. Recurrent fetal loss during the second or third trimester suggests an inherited thrombophilia or antiphospholipid antibody.

Neoplasm and myeloproliferative disorders. Recurrent thrombosis despite therapeutic anticoagulation is more frequent in patients with associated malignancy.

Prolonged immobilization. Venous stasis is common during postoperative convalescence or extended air travel, in nonambulatory patients, and in long-distance truck drivers.

Indwelling central venous catheter.

Pregnancy and exogenous hormones. Fibrinolysis may be impaired during pregnancy and postpartum, and with oral contraceptives and hormone replacement therapy. Patients older than 35 who use oral contraceptives and smoke are at even greater risk.

Gender. DVT more commonly affects men.

Sickle cell disease, heart failure, inflammatory bowel disease, lupus anticoagulant, elevated antiphospholipid antibodies, nephrotic syndrome, obesity, atherosclerosis, winter months, and hyperhomocysteinemia also raise DVT risk.

Diagnosis

Diagnostic procedures must differentiate DVT from other disorders that cause similar symptoms. The initial laboratory evaluation should include a complete blood count and platelet count, coagulation studies (e.g., prothrombin time, activated partial thromboplastin time), renal and liver function tests, and urinalysis. Included in the differential diagnosis are venous valvular insufficiency, muscle strain or rupture, ruptured popliteal (Baker’s) cyst, cellulitis, lymphedema, traumatic injuries and fractures, and idiopathic etiology.

Imaging

Duplex venous ultrasonography is the most common initial diagnostic method for symptomatic DVT. A thrombus can be detected by direct visualization or by inference when the vein fails to collapse when compressed.

Magnetic resonance imaging 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 may detect 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 help identify obstruction in areas typically missed by ultrasound (e.g., inferior vena cava).

Venography works by injecting 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 uncomfortable and time-consuming and requires technical expertise, it is generally reserved for cases in which noninvasive methods yield equivocal or inconsistent findings. For patients with contrast allergy, magnetic resonance venography is an alternative.

Ventilation-perfusion (V/Q) scan is a validated method to identify PE. However, it has relatively poor sensitivity in most clinical situations. Other imaging modalities, such as spiral CT pulmonary angiography and MRA are replacing V/Q scans in many situations. Invasive pulmonary angiography is the most definitive method, but it carries the greatest risks.

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 patient symptoms.

Electrocardiogram (ECG) and chest x-ray (CXR) have limited sensitivity and specificity for PE and are mainly used to exclude other causes of symptoms.

Blood Tests

D-dimer is an end product of the degradation of fibrin clots. A positive result suggests DVT or PE, but the test has poor specificity (about 50%). Sensitivity is up to 98% but is lower in populations at high risk for VTE. A D-dimer level < 500 ng/mL by ELISA in conjunction with a low clinical probability may be useful in excluding DVT. Combination screening with D-dimer and at least one imaging modality may be most effective.[4] ,[5]

Arterial blood gas determination is not sensitive or specific for PE, but severe hypoxemia may indicate massive pulmonary embolism and affect treatment decisions.

Treatment

For reduction in VTE-related mortality, prevention of VTE is far more effective than treatment. Patient education (regarding adequate circulation) and prophylaxis for those at high risk are of paramount importance.

Patients with DVT should be initially treated with d irect oral anticoagulants (available in pill form, including rivaroxaban, dabigatran, and apixaban), intravenous heparin in the hospital, or with subcutaneous low-molecular-weight heparin (LMWH) in an outpatient setting, along with warfarin. Warfarin initially reduces protein C an d S, thus inducing a hypercoagulable state that is countered by the simultaneous use of heparin. Partial thromboplastin time (PTT) should be closely monitored when using IV heparin but not LMWH. Osteoporosis may occur in individuals receiving heparin therapy for more than 6 months, and thrombocytopenia is a possible early heparin-induced side effect. Protamine sulfate reverses heparin’s effects in the case of bleeding or other complications.

Oral anticoagulation with warfarin should be overlapped with heparin until a therapeutic International Normalized Ratio (INR) is reached, and heparin or LMWH can be safely discontinued after 2 or 3 days. Uncomplicated DVT patients are generally treated for 3-6 months. Patients with multiple DVT episodes, high recurrence risk, associated PE, cancer, or coagulopathies may require prolonged or even lifetime warfarin anticoagulation.

Recommended nonpharmaceutical treatments for DVT include elevation of the affected limb and application of warm compresses to the affected area.

If anticoagulation therapy is not viable (e.g., patient has active hemorrhage), external compression devices are a mechanical alternative for DVT prophylaxis and treatment.

Patients are often admitted to the hospital for suspected PE, presence of concomitant illness, morbid obesity, noncompliance with or poor response to oral anticoagulation, or lack of a caretaker.

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 despite adequate anticoagulation, and for prophylaxis in high-risk patients.

Nonsteroidal anti-inflammatory drugs are contraindicated for DVT and PE because they may mask the symptoms of a new thrombus. Aspirin therapy is not adequate for preventing DVT formation or PE.

Nutritional Considerations

DVT is rare in societies in which 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.[6] ,[7] The reasons for this association are unclear. However, dietary intake influences factor VIIc, factor VIIIc, and von Willebrand factor, all of which are, in turn, related to the risk for venous thromboembolism.[8]

In addition, low fiber intake is associated with higher activity of plasminogen activator inhibitor-1 (PAI-1), the body’s main inhibitor of fibrinolysis.[9] Low-fat, high-fiber diets, combined with exercise, improve fibrinolysis[10] ,[11] and may thereby help reduce DVT risk. Some researchers have hypothesized that individuals on low-fiber diets often strain to pass stools, raising intravenous pressures and damaging the valves that facilitate blood return.[6] High-fiber diets help prevent this problem.

The following nutritional factors are associated with reduced risk of DVT:

Low-fat, high-fiber diets. E levated blood cholesterol concentrations are associated with DVT risk.[12] Some evidence suggests that simultaneously elevated cholesterol and triglycerides increase this risk.[13] Greatly reducing dietary cholesterol and saturated fat and increasing dietary fiber have a major effect on blood lipids. Low-fat, vegetarian, and vegan diets are particularly effective for achieving this goal (see Dyslipidemia chapter). Elevated fibrinogen levels, which is another risk factor for DVT,[14] are lower in persons following vegetarian diets.[15] ,[16]

Fruits and vegetable intake. In the Atherosclerosis Risk in Communities Study (ARIC), persons consuming roughly 5 servings of fruits and vegetables each day had about half the risk for venous thromboembolism (DVT or pulmonary embolism) compared with those eating less than 2.5 servings per day.[8]

Fruits and vegetables are also important for patients on anticoagulation therapy.[17] Patients with low intakes of vitamin-K-rich foods have less stable anticoagulation control than those with high intakes, and a double-blind, randomized, placebo-controlled study of 200 patients taking an anticoagulant showed that a daily supplement of 100 μg of vitamin K improved anticoagulation control[18] .

Weight control. Obesity increases the risk for developing DVT.[19] ,[20] The risk may be due to an obesity-related increase in PAI-1[21] or an associated elevation of venous pressure. See Obesity chapter for a discussion of weight-control techniques.

Avoiding red and processed meats. While there does not appear to be a strong relationship between red and processed meat consumption and risk of DVT, high intakes of these foods are linked to increased risk of cancer and cardiovascular disease, both of which increase the risk of developing DVT.[22]

Orders

See Basic Diet Orders and Dyslipidemia chapters.

Individualized exercise prescription to avoid 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.

References

  1. Heit JA: The epidemiology of venous thromboembolism in the community. Arterioscler Thromb Vasc Biol 28:370, 2008  [PMID:18296591]
  2. Tsai AW et al: Cardiovascular risk factors and venous thromboembolism incidence: the longitudinal investigation of thromboembolism etiology. Arch Intern Med 162:1182, 2002  [PMID:12020191]
  3. White RH: The epidemiology of venous thromboembolism. Circulation 107:I4, 2003  [PMID:12814979]
  4. Perrier A et al: Multidetector-row computed tomography in suspected pulmonary embolism. N Engl J Med 352:1760, 2005  [PMID:15858185]
  5. Elias A 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 multicentre clinical outcome study. Thromb Haemost 93:982, 2005  [PMID:15886818]
  6. Burkitt DP, Walker AR, Painter NS: Dietary fiber and disease. JAMA 229:1068, 1974  [PMID:4407955]
  7. Burkitt DP: Varicose veins, deep vein thrombosis, and haemorrhoids: epidemiology and suggested aetiology. Br Med J 2:556, 1972  [PMID:5032782]
  8. Steffen LM et al: Greater fish, fruit, and vegetable intakes are related to lower incidence of venous thromboembolism: the Longitudinal Investigation of Thromboembolism Etiology. Circulation 115:188, 2007  [PMID:17179018]
  9. Boman K et al: Endurance physical activity, diet and fibrinolysis. Atherosclerosis 106:65, 1994  [PMID:8018108]
  10. Lindahl B et al: Improved fibrinolysis by intense lifestyle intervention. A randomized trial in subjects with impaired glucose tolerance. J Intern Med 246:105, 1999  [PMID:10447232]
  11. Marckmann P, Sandström 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 59:935, 1994  [PMID:8147341]
  12. Vayá A et al: Hyperlipidaemia and venous thromboembolism in patients lacking thrombophilic risk factors. Br J Haematol 118:255, 2002  [PMID:12100157]
  13. Kawasaki T et al: Hypercholesterolemia as a risk factor for deep-vein thrombosis. Thromb Res 88:67, 1997  [PMID:9336875]
  14. Vayá A et al: Biological risk factors for deep vein trombosis. Clin Hemorheol Microcirc 26:41, 2002  [PMID:11904470]
  15. Famodu AA et al: The influence of a vegetarian diet on haemostatic risk factors for cardiovascular disease in Africans. Thromb Res 95:31, 1999  [PMID:10403684]
  16. Mezzano D et al: Vegetarians and cardiovascular risk factors: hemostasis, inflammatory markers and plasma homocysteine. Thromb Haemost 81:913, 1999  [PMID:10404767]
  17. Rombouts EK, Rosendaal FR, van der Meer FJ: Influence of dietary vitamin K intake on subtherapeutic oral anticoagulant therapy. Br J Haematol 149:598, 2010  [PMID:20151978]
  18. Rombouts EK, Rosendaal FR, Van Der Meer FJ: Daily vitamin K supplementation improves anticoagulant stability. J Thromb Haemost 5:2043, 2007  [PMID:17666020]
  19. Goldhaber SZ, Tapson VF, DVT FREE Steering Committee: A prospective registry of 5,451 patients with ultrasound-confirmed deep vein thrombosis. Am J Cardiol 93:259, 2004  [PMID:14715365]
  20. Abdollahi M, Cushman M, Rosendaal FR: Obesity: risk of venous thrombosis and the interaction with coagulation factor levels and oral contraceptive use. Thromb Haemost 89:493, 2003  [PMID:12624633]
  21. Skurk T, Hauner H: Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1. Int J Obes Relat Metab Disord 28:1357, 2004  [PMID:15356668]
  22. Lippi G, Cervellin G, Mattiuzzi C: Red meat, processed meat and the risk of venous thromboembolism: friend or foe? Thromb Res 136:208, 2015  [PMID:25962721]

Last updated: January 31, 2018

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TY - ELEC T1 - Deep Venous Thrombosis ID - 1342012 Y1 - 2018/01/31/ PB - Nutrition Guide for Clinicians UR - https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342012/all/Deep_Venous_Thrombosis ER -