Deep venous thrombosis (DVT) and acute pulmonary embolism (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]

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.

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, tachycardia, sweating, 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, which indicates deoxygenated hemoglobin trapped in nonfunctioning veins, may occur.

Risk Factors

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

Prior episode(s) of DVT or PE. A previous history of a thromboembolic event 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, extended air travel, non-ambulatory patients, and 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.

Sex. DVT more commonly affects men.

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

Diagnosis

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 treated with direct oral anticoagulants (DOACS) which are available in pill form, including rivaroxaban, dabigatran, edoxaban, and apixaban; intravenous heparin in the hospital; or subcutaneous low-molecular-weight heparin (LMWH) plus warfarin in the outpatient setting. DOACS require no routine therapeutic monitoring. Warfarin initially reduces proteins C and 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 2-3 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-based 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 and may thereby help reduce DVT risk.[10][11] 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. Elevated 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, are lower in persons following vegetarian diets.[14][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] Vitamin K intake has no significant effect on DOAC efficacy.

Weight control. Obesity increases the risk for developing DVT.[19][20] The risk may be due to an obesity-related increase in PAI-1, an associated elevation of venous pressure,[21] or a result of hormonal (estrogenic) or thrombin-mediated effects. 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 and maintain consistent intake of vitamin K-containing foods. Family members will help adherence and improve their own health by adopting similar diet and exercise routines.

References