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Deep vein thrombosis in athletes: risks of racing and resting.

Deep vein thrombosis (DVT) is defined as the formation of a blood clot or thrombus in a deep vein. In severe cases, the thrombus can dislodge and travel to the lungs, causing a pulmonary embolism (PE). Most pulmonary emboli originate from DVT of the proximal lower extremity veins, such as the femoral, popliteal, and iliac veins (1). The mechanisms underlying DVT, known as Virchow's triad, are venous stasis, endothelial cell injury, and hypercoagulability. Classic symptoms of DVT involve swelling, pain, and discoloration in the affected extremity. Physical examination may reveal the palpable cord of a thrombosed vein as well as edema, tenderness, and warmth in the affected extremity. Symptoms of PE include unexplained shortness of breath, tachycardia, chest pain or palpitations, anxiety and/or sweating, and emergence of a cough that results in production of blood (2).

Deep Vein Thrombosis and Pulmonary Embolism in Endurance Athletes

Interestingly, endurance athletes are exposed to many of the physical factors contributing to DVT, experiencing repetitive microtrauma, endothelial damage, and dehydration/hemoconcentration during competition, followed by periods of inactivity, immobility, and stasis while traveling to and from and/or recovering from the athletic event. There are several published case studies regarding athletes who have experienced DVT and PE following competition or physical activity. Tao and Davenport reported a female triathlete who was diagnosed with DVT and PE after competing in a Half Ironman triathlon (3). The patient competed in the triathlon and traveled five hours by car the following morning, after which she experienced symptoms of left lower extremity swelling and pain, accompanied thereafter by dyspnea and lightheadedness upon exertion. She was not properly diagnosed and treated until she visited the emergency department three weeks after the triathlon. There are also several published cases of DVT and PE occurring after running or jogging (4-6). For example, Mackie and Webster described two male marathon runners who developed DVT and PE approximately one week after running a marathon; in both cases, DVT was misdiagnosed initially (either as a muscle strain or Baker's cyst) (5). It should be noted that these reports of lower extremity DVT in endurance athletes are distinct from the belter understood effort thrombosis of the upper extremity occasionally observed in young athletes (known as Paget-Schroetter syndrome), where repetitive upper arm movements induce microtrauma of the venous intima and thrombus formation in the axillary-subclavian vein (7), (8).

Less rigorous evidence (i.e., web-based self-reports and articles) detail multiple cases of lower extremity DVT in healthy athletes who participate in either recreational or competitive physical activity. These include the self-reported case of Kikkan Randall, an Olympic cross-country skier, who noted lingering soreness in her hips and left thigh three weeks after the Canadian Nation Championships. Physical therapy to treat what she thought was post-competition muscle pain was unsuccessful, and she was eventually admitted to the emergency department with DVT that required multiple hospitalizations to resolve the clot (9). Other published web reports include those of Steve Lehman, a triathlete who was diagnosed with DVT and bilateral PE after competing in the U.S. National Track (bicycle racing) Championships and driving nine hours home the following day (10), and Tom Isbell, a recreational bicyclist who was diagnosed with DVT after struggling with left calf cramps for a month (11).

Common Misdiagnosis of DVT and PE in Athletes

Deep vein thrombosis is a relatively common diagnosis in the emergency room; the estimated annual incidence of venous thromboembolism is 117 cases per 100,000 persons (12). However, a similar paradigm in most case studies and anecdotal reports in athletes is that DVT in these individuals was misdiagnosed, resulting in a delay in treatment even when symptoms were relatively severe (3,5). The difficulty in making a prompt diagnosis may be caused in part by the relative unfamiliarity of physicians with the potential for DVT risk and incidence in healthy, athletic, and/or younger individuals. Approximately half of all cases of DVT occur in hospitalized patients or nursing home residents (13), and the incidence of DVT has been estimated to be up to nine-fold higher in individuals greater than 85 years old relative to younger adults (12). Moreover, the most commonly used test to confirm suspected DVT in patients, Doppler ultrasonography of the venous vasculature in the affected limb, is relatively expensive to administer and requires specialized equipment and trained technicians and vascular specialists. Physicians may be hesitant to order this evaluation in athletic individuals whose symptoms mimic typical post-exercise musculoskeletal pain and who may not exhibit tachycardia with PE due to baseline bradycardia (3).

Effects of Exercise on Coagulation and Fibrinolysis

Blood clots are constantly formed via the coagulation cascade and resorbed to maintain hemostatic balance. In healthy humans, clot formation is a transient response to perturbations such as endothelial injury or hypercoagulability. Activation of thrombin and ultimately fibrin--either through the intrinsic or extrinsic coagulatory pathway--result in clot formation, whereas activation of plasmin, driven by tissue-type plasminogen activator (t-PA) bound to the clot itself, results in clot breakdown or fibrinolysis. It has been established that endurance exercise activates the coagulatory system, with upregulation of procoagulatory factors such as thrombin-antithrombin complex and prothrombin fragment 1 and 2 (14-16). However, the fibrinolytic system (e.g., t-PA antigen and t-PA activity) appears activated in coordination with the coagulatory system following exercise (14), (17), (18), such that changes in coagulation are generally paralleled by an activation of fibrinolysis to preserve hemostatic balance. Sumann et al. studied 13 athletes who were competing in the Tyrolean Speed Marathon, a marathon with a downhill net vertical loss of 800 meters. Authors reasoned that changes in coagulation and fibrinolysis associated with intense endurance exercise would be pronounced during eccentric (downhill) exercise in which microtrauma of skeletal muscle and the microvasculature would be substantial. Indeed, blood coagulatory factors were increased immediately after the marathon. Authors, however, also observed a hyperactivation of fibrinolytic factors immediately after the marathon such that there was no apparent disruption in hemostasis associated with the marathon (17). Therefore, although endurance sport activity may expose an athlete to several factors known to increase the risk of clot formation, studies involving direct measurements of coagulatory and fibrinolytic factors do not indicate that physical activity and competition disrupt the balance between clot formation and degradation in most athletes.

Factors that May Disrupt the Balance of Hemostasis Following Physical Activity

So what factors, then, may account for the case studies and self-reported incidence of DVT and/or PE after extended physical activity or endurance competition in otherwise healthy athletic individuals? There are many additional risk factors for DVT which include use of estrogenic medications (e.g., oral contraceptives) and thrombophilias (i.e., clotting disorders such as Factor V Leiden mutation, activated protein C resistance, deficiencies of protein S, C, and antithrombin III, hyperhomocysteinemia, and anticoagulant protein deficiency) (19). Certainly these additional risk factors may predispose an individual to DVT following endurance exercise. The triathlete described in the case study by Tao and Davenport reported use of oral contraceptives (3), and Kikkan Randall, the cross-country skier, were both on oral contraceptives and had May-Thurner syndrome, a syndrome that occurs in young, healthy women in which compression of the left iliac vein by the artery causes narrowing of the vein (9). Cases of deep vein thrombosis have also been reported in athletes with protein C deficiency (protein C degrades Factor V in the clotting cascade, thereby preventing activation of thrombin and clot formation) (20). Other factors hypothesized to increase DVT risk, specific to athletes, include slower blood flow associated with the chronic bradycardia observed in trained athletes, higher venous compliance, and compression of the venous structure by muscle hypertrophy, all of which may result in increased venous stasis (3).

In addition, several of the known cases of DVT in athletes have occurred after athletes traveled home from events or long periods of physical activity. It has been well-documented that car, bus, train or air travel activate the coagulatory system (21,22). Therefore, it is possible that superimposing travel upon an athlete who has recently engaged in endurance exercise may shift the hemostatic balance in athletes post-competition, thereby increasing DVT risk in certain individuals. Interestingly, Siegel et al. noted that 24 hours after the Boston Marathon fibrinolytic activity returned to baseline levels where as markers of coagulation remained elevated in healthy runners (16). This period 24 hours after activity--when an individual is most likely to travel--may represent a particularly susceptible period to clot formation, although it should be noted that the investigation of downhill marathon running did not find evidence of a hemostatic imbalance 24 hours after the event (17). Regardless, there is substantial anecdotal and case report evidence detailing athletic individuals who have experienced DVT after the combination of competition and travel (9), (10), (23) and an online registry,, details numerous cases of athletes who have experienced DVT after air flight. To date, no rigorous data exist to support the premise that DVT risk may be augmented in athletes traveling to and from competitions.

A hypothesis integrating these potential mechanisms underlying DVT risk in endurance athletes may be as shown in Figure 1. Following endurance exercise, both coagulatory and fibrinolytic activation occurs, increasing both clot formation and degradation (Figure la). In the majority of athletes, hemostatic balance is maintained, as supported by the quantitative data regarding coagulatory and fibinolytic markers after exhaustive endurance exercise. In certain individuals, however, the balance between coagulation and fibrinolysis is disrupted due to the imposition of additional coagulatory stressors such as prolonged stasis, air flight, genetic predisposition, and use of estrogenic medications. Consequently, clot formation outweighs degradation and DVT results (Figure 1b).


Future Directions

The majority of endurance athletes are able to compete and participate in physical activity uneventfully over the course of the lifetime, with no incidence of DVT or PE. However, case reports and a large body of anecdotal evidence indicate that in at least a small fraction of otherwise healthy, avid exercisers, there may be an augmented risk of DVT following endurance exercise. Clearly, more rigorous studies are needed to quantify the risk of DVT and PE in this healthy population. Studies to date have not generally included athletes stratified by risk factors for DVT, nor have they followed substantial numbers of athletes post-competition to determine whether certain conditions such as travel augment coagulatory activation and/or result in thrombotic events.

In addition, a common feature of published case reports and anecdotal reports is the lag time between onset of symptoms and accurate diagnosis. Tao et al. hypothesized that this might be attributable to both patient attitude--athletes expect post-exercise musculoskeletal pain--as well as physician unfamiliarity with DVT in healthy and/or relatively young athletic individuals. Moreover, there may also be a lag time between the events precipitating DVT and the onset of symptoms, further delaying diagnosis. For example, the Polish Olympian Kamila Skolimowska collapsed and died of PE at a training camp in Portugal, having arrived from Poland approximately 10 to 14 days earlier (23). Therefore, educating medical practitioners, sports participants, and coaches about the potential risk for DVT in certain athletic individuals, as well as recognition of symptoms and contributing factors, may be important, especially once more quantitative data on the topic are assembled.

Finally, preventing DVT following athletic participation and/or competition remains the ultimate goal. Again, there are not data to specifically address prevention of DVT in athletes, but existing recommendations will most likely apply. These include avoiding prolonged periods of venous stasis (i.e., using active recovery following an intense endurance event rather than immobility) as well as counteracting the effects of air travel by performing hourly leg exercises, avoiding crossed legs, and remaining adequately hydrated during post-exercise flights (23), (24). Individuals with known thrombophilic disease may take more substantial precautions, such as abstaining from estrogenic medication use, taking aspirin or low molecular weight heparin prior to travel, and avoiding exercise during very cold conditions, when DVT risk is augmented (23), (25). The combination of more rigorous research, education of medical and sports professionals and participants, and development of guide-fines for prevention should ultimately mitigate thrombotic events in otherwise healthy athletic individuals for whom exercise confers myriad benefits.

Ed. Note: At the 39th Annual AMAA Sports Medicine Symposium in April, Dr. Beth Parker will be speaking on "Post-Competition Deep Vein Thrombosis in Endurance Athletes." Her lecture will cover risk factors and critically review existing case studies and research reports on athletes and DVT. See for the program agenda.


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Beth Parker, PhD (1); Paul D. Thompson, MD (1); Peter Kriz, MD (2); and Pierre d'Hemecourt, MD(2)

1. Henry Low Heart Center, Division of Cardiology, Hartford Hospital, Hartford, CT

2. Children's Hospital, Boston, MA

Corresponding Author:

Beth Parker, PhD

Henry Low Heart Center

Hartford Hospital

Hartford, CT 06102

Tel: 860-545-1508

Fax: 860-545-2882
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Author:Parker, Beth; Thompson, Paul D.; Kriz, Peter; d'Hemecourt, Pierre
Publication:AMAA Journal
Article Type:Clinical report
Geographic Code:1USA
Date:Jan 1, 2010
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