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[Case Report]

Pulmonary Embolism: Sifting the Risk Factors

Kimberly G. Harmon, MD; Matthew B. Roush, MD

American Medical Society for Sports Medicine
Case Report Series Editor: Kimberly G. Harmon, MD


In Brief: A 20-year-old female college cross-country runner developed chest pain and dyspnea that increased with running. A chest radiograph revealed a right-side pleural effusion, and a ventilation-perfusion scan indicated a probable pulmonary embolism. The diagnosis was left-side pulmonary emboli. Testing for genetic risk factors was negative, leaving oral contraceptive use as the likely cause of the condition. The patient was treated with anticoagulant drugs and discontinuation of oral contraceptives, and was allowed to resume running gradually. Discussion covers genetic and other risk factors, anticoagulation therapy, and return to play.

Chest pain in a fit, normally healthy patient is usually not serious, but clinicians need to be alert to all the possible causes. The following case report describes the diagnosis and treatment of an elite female athlete whose chest pain turned out to be the result of pulmonary emboli. We discuss the appropriate workup of patients at low risk for deep-vein thrombosis (DVT) or pulmonary embolus (PE), giving particular attention to the role of genetic risk factors.

Case Report

History. A 20-year-old female Division 1 cross-country runner began having right upper anterior chest pain at the end of each practice. Because of shortness of breath with exercise, she cut her weekly mileage from 80 to 30 miles. At the end of 2 weeks, she noticed a sharp, stabbing, right-side pain with deep inspiration. She was referred to a sports medicine physician.

Before the appointment, her symptoms abruptly resolved, a change that coincided with her week of taking inert oral contraceptives (OCs). She no longer had the pleuritic pain and was able to complete a 12-mile practice with her teammates. Consequently, she canceled the appointment.

A week later she again developed pleuritic chest pain. Though she was not dyspneic at rest, she was only able to run slowly for 3 to 4 miles. She developed a nonproductive cough, and her appointment was rescheduled.

The patient had been healthy, and her family history was unremarkable. Three months before this episode, she had started taking OCs containing the progestin desogestrel.

Physical findings. At the initial physical exam, her vital signs were normal. A thorough cardiovascular exam was within normal limits, but her pulse of 88 per minute was a relative tachycardia, given that she was a highly conditioned runner. On auscultation of her lungs, she had decreased breath sounds in the right lower lung field along with dullness to percussion. The abdominal exam was normal. Examination of her lower extremities revealed no tenderness, edema, or erythema. Homans' sign—pain with passive dorsiflexion of the foot, signifying thrombosis of the deep calf veins—was absent.

Differential diagnosis. On the basis of the history and physical exam, the differential diagnosis included PE, pneumonia, and viral pleuritis. Cardiac causes such as myocardial ischemia, pericarditis, and congenital heart disease were also included.

Lab and imaging studies. Blood analyses for pH, pressures of CO2 and O2, and bicarbonate level were normal. A chest radiograph obtained at this visit revealed a right-side pleural effusion (figure 1: not shown). In view of this finding, the patient was sent to the hospital for a ventilation-perfusion scan. The scan showed minor decreased ventilation in the right lung base and several nonperfused segments in the base, upper lobe, and lingula of the left lung. The scan was interpreted as indicating a high probability of pulmonary emboli (figure 2: not shown). Venous Doppler ultrasonography of the lower extremities was negative.

Diagnosis. The patient was diagnosed as having left-side pulmonary emboli. If the patient's emboli were caused by a genetic defect, the duration of anticoagulant therapy would be affected, and for that reason a workup for hereditary defects predisposing to venous thromboembolism was performed. The results were entirely normal. The patient's only apparent risk factor was the use of OCs.

Treatment. Over the next 5 days, the patient was hospitalized and treated with the intravenous anticoagulants heparin sodium and coumadin. Her OCs were discontinued. She was asymptomatic at the time of discharge.


The role of oral contraceptives. In active patients who have PE, the usual cause is a hypercoagulable state, which can be the result of a heritable defect, a disease, or an acquired risk factor. The most common acquired cause for a hypercoagulable state is the use of OCs (1). It is estimated that women who use OCs have a risk of DVT that is three to four times greater than that of nonusers (1-3).

Some progestins impart a higher risk of associated thromboembolism. Pills containing third-generation progestins (desogestrel, gestodene) double the risk for thromboembolism relative to low-estrogen-dose pills containing other progestins (4,5). This increase raises the yearly incidence of venous thromboembolic disease to 30 cases per 100,000 women (3). Because of the increased risk of DVT and PE with third-generation progestins, OCs containing other progestins should be primarily prescribed.

Genetic risk factors. Prior to 1993, only 15% of people with unexplained DVT had an identifiable genetic risk factor. In the last 5 years, remarkable advances have occurred in the use of DNA-based technology to identify genetic mutations that are risk factors for thromboembolic events. The most common of these, factor V Leiden (resistance to activated protein C), is present in 3% to 7% of whites (1). The risk for venous thrombosis is increased 8 to 35 times in women with this defect who take OCs (6-8).

Men and women who have unexplained DVT or PE should undergo a laboratory workup. Further, women who have DVT or PE and have no known risk factor other than OC use should undergo a workup. The hematologic analysis should include testing for factor V Leiden as well as prothrombin time (PT), partial thromboplastin time, protein C, protein S, antithrombin III, antiphospholipid and anticardiolipin antibodies, methylenetetrahydrofolate reductase lability, and homocysteine level. In addition, white women who have a family history of thrombosis should at least be tested for factor V Leiden before starting OCs (8).

Duration of therapy. Typically, anticoagulation therapy should be continued for 3 months for a patient who has a first DVT or PE, a thorough negative workup for hereditary thrombophilias, and no other associated risk factors, such as continued OC use, underlying disease, or inactivity. The recurrence rate after 3 months of such therapy for a first episode of venous thromboembolism is 4% to 7% (9). If a coagulation defect is identified, recommendations for anticoagulation vary according to the specific defect.

Return to play. Because DVT and PE are rare in active patients, there are no evidence-based guidelines for return to play. Obviously, any athlete who is taking anticoagulation medications should not return to contact sports. Athletes in noncontact sports should be allowed to return at a gradual pace with close attention to possible complications. Runners in particular need to be monitored for the development of anemia related to unidentified bleeding.

Monitoring can be accomplished by a complete blood count at least once a month or when the index of suspicion for occult bleeding is high. PTs need to be monitored once a week initially and less often when the international normalized ratio (INR) is stabilized in the therapeutic range between 2.0 and 3.0. (The INR is the PT divided by the laboratory's mean PT value and raised to the power of the international sensitivity index of the laboratory's thromboplastin. This calculation adjusts for thromboplastin's varying sensitivity to vitamin-K-dependent factors.)

Case Outcome

Our patient remained at a therapeutically anticoagulated level with an INR between 2.0 and 3.0 after discharge. Monitoring was done twice a week for 2 weeks, weekly for 1 month, and twice monthly for 2 months.

The patient received anticoagulation medication for 3 months but was allowed to begin minimal activity after 1 month of therapy. Initially she began running 1 mile a day; after 1 week she was allowed to increase her mileage by 1 mile per day as long as she remained asymptomatic. Three months after discharge, she was running 30 to 40 miles per week. She was advised not to use OCs. On a return visit at 6 months after the end of treatment, she reported no further problems and has remained symptom free.

Summing Up

Although rare, PE or DVT is possible in a young athlete who has chest pain and dyspnea, especially if the patient is a female who takes OCs. Genetic factors may predispose individuals to PE or DVT, and they multiply the risk if the person also uses OCs. A workup for familial thrombophilia is necessary in these cases, since patients who are genetically predisposed may require long-term anticoagulation. Patients who are taking anticoagulants may return to noncontact sports only gradually and with close monitoring.


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  8. Vandenbroucke JP, Helmerhorst FM, Bloemenkamp KM, et al: Third-generation oral contraceptive and deep venous thrombosis: from epidemiologic controversy to new insight in coagulation. Am J Obstet Gynecol 1997;177(4):887-891
  9. Hull RD, Pineo GF: Current concepts of anticoagulation therapy. Clin Chest Med 1995;16(2):269-280

The American Medical Society for Sports Medicine is a forum for primary care sports medicine physicians. Dr Harmon is a primary care sports medicine physician at the University of Washington and a clinical instructor in the department of family practice at the University of Washington Medical School, both in Seattle. She holds a certificate of added qualifications (CAQ) in sports medicine and is a member of the editorial board of The Physician and Sportsmedicine. Dr Roush is codirector of the sports medicine fellowship program at Ball Memorial Hospital in Muncie, Indiana. He holds a CAQ in sports medicine. Address correspondence to Kimberly G. Harmon, MD, Hall Health Primary Care Center, University of Washington, Box 35440, Seattle, WA 2021195; address e-mail to [email protected].



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