EPIDEMIOLOGY OF VENOUS THROMBOEMBOLIC DISEASE

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AGE

Age is now a well accepted risk factor for VTE, confirmed by results reported by the World Health Organization and several other countries.26 The mean age is approximately 60 years of age, based on several studies.27, 61, 63, 75 In a study of 16 French hospital centers, more than one half of the patients with either DVT or PE were between the ages of 65 and 85 years, and less than 5% were under the age of 24.27 Stein et al reported a linear increase in the incidence of PE with increasing age up

SURGERY

Surgery has been established as a risk factor for VTE by multiple studies. It is thought that trauma to major vessels during surgery, prolonged immobilization, and anesthetic agents contributes to this risk. Firm data from the literature state that the highest risk for DVT is in patients with major trauma, orthopedic surgery, and abdominal surgery.7 From pooled data presented in the fifth American College of Chest Physicians' Consensus Conference on Antithrombotic Therapy, the total prevalence

RECURRENT THROMBOEMBOLISM

Prior history of DVT or PE remains a strong risk factor for new venous thromboembolic disease. Multiple studies have found the percentage of patients with VTE confirmed by imaging had a history of DVT or PE in the range of 21% to 26%.27, 61, 63 Prandoni et al's study revealed that 78 of 355 patients (22.0%) treated with 3 months of oral anticoagulants developed recurrent thromboses following cessation of anticoagulation.66 Forty-five percent of these were in the same leg, 35.9% were in the

PREGNANCY AND POSTPARTUM

Many studies have found that younger women have a higher incidence of DVTs or pulmonary emboli compared with men of the same age. For example, Coon et al found a 10-fold higher frequency of DVT in women than in men under the age of 40 years.12 In younger women, 50% of these were due to pregnancy, and many are from oral contraceptive use.

Pregnancy causes alterations in several clotting factors; there are relative increases in procoagulants like fibrinogen, factor VII, factor X, and factor VIII,

ORAL CONTRACEPTIVES

The thrombogenicity of oral contraceptives has been known for many years. Some of the first oral contraceptives used high doses of estrogen, which has been blamed as the chief mediator of thrombophilia. The amount of estrogen has been decreased to lower the risk of thrombosis for oral contraceptive users. In the 1960s, several studies reported a relative risk of about four to eight for idiopathic DVT for women taking oral contraceptives compared to placebo. Since the reduction of estrogen

HORMONE REPLACEMENT THERAPY

The association between hormone replacement therapy and venous thrombosis also has been established. Douketis et al examined nine studies on the role hormone replacement therapy in VTE.19 The pooled data from five case-control studies reveals a relative risk of 2.4.19 None of these studies contained level one data (evidence from randomized, controlled trials or meta-analyses). The HERS study released in 1998 examined 2,763 women with known coronary heart disease and on hormone replacement

TRAVEL

Travel has been associated historically with DVT. It is thought that venous stasis is increased by the high pressures from the edge of a person's seat on the back of the calves with prolonged sitting, which decreases venous blood flow and gradually increases the hematocrit with a concomitant rise in plasma protein concentration. A classic history for pulmonary embolism is shortness of breath after arising from a seated position after a long trip. Ferrari et al found that the most common

MALIGNANCY

Multiple epidemiologic studies have found cancer as a risk factor for VTE in a significant percentage of patients, ranging anywhere from 16.5% to 32%.2, 27, 61 It is thought that neoplastic cells produce certain procoagulants very early in the course of the disease, even before overt malignancy is diagnosed.33 Several studies that followed patients prospectively with idiopathic DVT report a high incidence of malignancy diagnosed shortly after the diagnosis of the VTE. An Italian study by

INHERITED HYPERCOAGUABLE STATES

Inherited hypercoaguable states are rare causes of VTE but do pose significant risk if present. Many patients inherited disorders, such as protein C deficiency, protein S deficiency, and antithrombin III deficiency, present with VTE disease at an early age; approximately one half of the episodes occur when there is increased risk from additional risk factors, such as the use of oral contraceptives, surgery, or pregnancy.1 Fifty percent of patients with a single DVT with protein C deficiency,

MEDICAL ILLNESSES

Several nonmalignant medical illnesses increase the risk of VTE. Among them are myocardial infarction, stroke, spinal cord injury, nephrotic syndrome, and congestive heart failure. Smoking and obesity are modifiable risk factors that have also been associated with venous thrombosis.

Patients with an acute myocardial infarction have a moderate risk of VTE. In the absence of aspirin or anticoagulation, the incidence of DVT and clinical PE is 24% and 2.6% to 6.1%, respectively.7, 9 The risk

VENA CAVAL FILTERS

The placement of vena caval filters in patients who cannot receive anticoagulation can be a lifesaving procedure; however, their long-term safety has been called into question by recent studies that have shown a small but noticeable number of patients who experience recurrent thromboembolism. In 1984, Greenfield published a paper that emphasized that anticoagulation after vena caval filter placement does not influence the long-term patency of the filter and even suggested that PE occurs

SUMMARY

From the information presented in this article, it can be concluded that clinical suspicion of VTE should be increased in patients with a history of VTE, recent surgery, spinal cord injury, trauma, or malignancy. A variety of medical illnesses also increase the risk of venous thrombosis, including congestive heart failure, myocardial infarction, stroke with paresis, nephrotic syndrome, cigarette smoking, and obesity. Hypercoagulable states, such as antithrombin III deficiency, protein C

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    Address reprint requests to Victor Kim, MD, Department of Internal Medicine, Jefferson Medical College, 1025 Walnut Street, 800 College Building, Philadelphia, PA 19107

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