Diagnosis, Management of, and Return to Play Guidance for Venous Thromboembolism in Athletes : Current Sports Medicine Reports

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Diagnosis, Management of, and Return to Play Guidance for Venous Thromboembolism in Athletes


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Current Sports Medicine Reports 21(4):p 129-136, April 2022. | DOI: 10.1249/JSR.0000000000000949
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Venous thromboembolism (VTE) is not rare and is becoming more recognized in our athletic population. This diagnosis can be elusive. A provider must have a high clinical suspicion and use pretest probabilities to order the appropriate studies and accurately diagnose a VTE. Treatment using direct oral anticoagulants for 3 months is recommended in most cases. Gradual return to play can be achieved after treatment is complete. Some athletes, however, may require lifelong anticoagulation. Return to collision sports may be possible using a timed dose strategy if long-term anticoagulation is needed. The management of an athlete with a VTE should include an individualized treatment plan and involve shared decision making with the athlete, team physicians, and hematologic specialists.


Venous thromboembolism (VTE) in athletes is an unexpected but now more recognized condition in this defined population. The incidence of VTE in the general population is estimated to be 1 to 2/1000 with up to 30% of those dying within a month of diagnosis (1). Although the exact incidence of VTE in an athletic population is not yet known, there are several case reports of athletes dying of sudden cardiac death secondary to thrombosis without classic thromboembolic risk factors (2–5). Are athletes at higher risk for VTE than nonathletes? How are athletes treated for VTE and how do they return to sport with or without anticoagulation? When should an athlete be evaluated for a thrombophilia? An approach to VTE diagnosis, management, and return to play strategy will be reviewed in this article.


The estimated annual incidence of VTE is 1 to 2/1000 with up to 30% morbidity within a month of diagnosis and up to 50% have long-term sequelae (1). In the general population lower extremity VTEs are significantly more common that upper extremity thrombosis. Interestingly, the most common vascular condition in athletes is an upper extremity DVT (6). There are unique circumstances intrinsic to athletic participation that may predispose athletes to thrombosis; however, the incidence of VTE in competitive athletes is unknown (7). A patient successfully anticoagulated for 3 months will have a 30% chance of recurrence, but a less than 1/100,000 chance of death (8,9).

Pathophysiology and Risk Factors

Athletes may have distinct risks that predispose them to thrombus formation. However, the basic concepts of “Virchow Triad” (VT) must first be appreciated when discussing the risk of forming venous clots. VT is venous stasis, endothelial/vessel wall damage, and hypercoaguability/hyperviscosity, which increases the risk of thrombosis.

Increased venous stasis occurs with vascular compression from training-induced muscle hypertrophy, training related-reduced blood pressure and heart rate, and when a lower extremity is injured and immobilized in a splint, brace, or cast (7,10). Prolonged intraoperative time and postoperative immobilization contribute to venous stasis (10). Interestingly long duration travel has been found to be a controversial risk factor in the athletic population (10). Increased leg length has been associated with an increased risk of VTE. Basketball players, runners, and high jumpers, therefore, may be at higher risk. The etiology of this increased risk remains unknown (11).

Endothelial injury may occur due to traumatic soft tissue compression, bony injury, or a significant muscle strain. There is a 12-fold increase in VTE of the lower extremity when there is injury to vascular endothelium (12). Athletes who performed repetitive arm movements (rowers, weightlifters, baseball players, swimmers, gymnasts, basketball players) who also have anatomic variations (hypertrophied muscles, cervical ribs, etc.) are at risk for blood vessel compression/endothelial injury causing Paget-Schroetter syndrome; a subclavian vein thrombosis at the costoclavicular junction (10,13,14).

One could presume that training at prolonged high altitude resulting in higher levels of erythropoietin, along with significant dehydration may result in hyperviscosity of blood leading to an increased risk of VTEs. No current evidence exists that either altitude training or dehydration increases the risk of thrombus formation (10). Androgenic anabolic steroid (AAS) use has been a suspected culprit in several case reports of athletes with VTE due to the prothrombogenic environment AAS create (10). Oral contraceptives (OCPs) with higher levels of ethinyl-estradiol increase the risk of hypercoaguability and thrombosis (10). An example of a “perfect storm” high risk athlete would be a women's basketball player (long legs), who sustained a direct compression trauma to the lower-extremity soft tissues (endothelial damage), is on an ethinyl-estradiol OCP (increased coaguability), and who is immobilized in a cast or walking boot for several days to weeks. All the risk factors that define VT come into play in this potential athletic injury scenario.

Clinical Presentation

Athletes may present with a wide spectrum of clinical signs and symptoms. On occasion, a VTE may occur without any clinical warning, which is most disturbing to clinicians caring for athletes.

The following two cases demonstrate the clinical spectrum of presentations:

  • Case 1: A 21-year-old man sustained a grade 1 medial collateral ligament sprain of his knee during training at a state police academy. He was placed in a knee immobilizer and told to follow up with an orthopedist within the week. Unfortunately, there was an unforeseen delay in the follow-up. Three weeks from the date of the knee injury, while standing in line at the academy dining facility, the state police cadet collapsed. He was quickly stabilized by the emergency medical service and brought to the emergency department (ED). The astute ED physician noted the knee immobilizer, some subtle swelling of the cadet's calf, and immediately got a CT angiogram of the chest. This revealed a massive saddle pulmonary embolism. Tissue plasminogen activator was systemically administered, and he was transferred to the intensive care unit. He quickly stabilized and was discharged to home 3 d postadmission with 3 months of oral anticoagulation.
  • Case 2: A 65-year-old world class male triathlete presented to the office complaining of “just a little” swelling in his right ankle. He had no risk factors for a VTE, including no history of cancer. A typical week of training for him consisted of more than 4 miles of swimming, 20 miles of running, and 100 miles of cycling. He denied any pain in his right leg and denied any chest pain or pressure with exertion. With prompting, he did admit to decreased exercise tolerance only when swimming noting some shortness of breath, which was unusual for him. His examination consisted of no calf tenderness and trace edema about his right ankle. He was sent for a vascular ultrasound (US) to rule out a DVT. US revealed an extensive acute on chronic DVT in the femoral venous system. A CT angiogram was done because of his subjective decline in endurance noted with swimming. Extensive “showering” of chronic thrombosis was noted in both lung fields consistent with pulmonary emboli. It is likely that because of his extensive cardiovascular adaptation to endurance training, he was able to train well with minimal symptoms despite his tremendous thrombus burden in his leg and lungs. A subsequent hypercoaguable workup and cancer screening revealed no abnormalities. He was anticoagulated for 3 months. He preferred to forego lifelong anticoagulation. He has had no VTE events since in the past 15 years.


VTE in athletes can present subtly or dramatically as these two cases illustrate. The clinical examination for a DVT is often unreliable with a sensitivity of 11% and a positive predictive value of only 15% to 25%. Specificity of the clinical examination is 76% to 85% (7). A pulmonary embolism may present with chest discomfort, chest pressure, cough, dyspnea with exertion, or something as innocuous as a relative resting tachycardia. Making a timely diagnosis is imperative to avoid devastating consequences.

Because clinical signs of a VTE are unreliable, a validated clinical prediction model/tool to help determine the pretest probability of a VTE is helpful. The Wells Criteria (for DVT) and Modified Wells Criteria (for PE) may be utilized to assess probability for a first time VTE. There is no validated pretest probability tool for recurrent VTEs (7,15).

Using the Wells and/or Modified Wells clinical criteria calculators a probability score is determined. Refer to the online calculators below for specific clinical criteria.

For the Wells calculation a score of 2 or higher indicates the likely probability of a DVT. A score lower than 2 suggests an unlikely probability.

For the Modified Wells calculation, a score of 0 to 1 is low risk; 2 to 6, moderate risk; and higher than 6, high risk.

By using the Wells (for DVT) or modified Wells (for PE) criteria calculation, the clinician may now determine a diagnostic strategy to rule in or rule out a VTE. Table 1 illustrates a recommended diagnostic strategy to rule in or rule out an initial VTE (7,15).

Table 1 - Testing for VTE based on pretest probability.
Low risk for VTE
Low risk may screen with high sensitivity D-dimer (age adjusted if athlete is older than age 50 yr)
– If negative, ruled out in athlete with low pretest probability for DVT and PE.
– If positive D-dimer then need whole leg compressive duplex US, and if concerns of PE, then V/Q scan or CTPA
– Repeat duplex US in a week if clinically concerned
Intermediate risk for VTE
– Whole leg duplex US as initial test
– If negative, then no further testing unless clinically indicated
High risk for VTE
– PE concern: start with CTPA or V/Q scan (alternative)
▪ If negative, confirm with a negative proximal leg US
–DVT concern only: start with whole leg duplex US
▪ D-dimer negative to confirm, confirm negative with repeat US in 1 wk
Concern for recurrent VTE (no validated scoring model available)
– Low or intermediate risk for PE: start with D-dimer
CTPA if positive D-dimer; compare to previous studies if available
– High risk for PE: CTPA initial study
– Low risk for DVT: D-dimer initial test
– If positive, then confirm with proximal duplex US
– Intermediate or high risk for DVT: proximal duplex US initial test
V/Q scan, ventilation-perfusion scan; CTPA, CT scan with pulmonary angiogram.
(Adapted from references 7,15).


Treatment considerations include: outpatient vs. inpatient management, observe/monitor versus medication, best choice of medication, and duration of treatment. The decision to treat the athlete as an outpatient or inpatient may be assisted by using validated scoring criteria for VTE in conjunction with shared clinical decision making. Although most VTE in athletes are treated in the outpatient setting, clinicians may reference the American Society of Hematology guideline/validated scoring criteria to assist in this decision making as this is beyond the scope of this article (18).

Shared decision making with the athlete must include the risk of bleeding, as well as the risk of recurrence if no medications are taken. VTE BLEED is a scoring tool used to risk stratify patients on long-term anticoagulation as low risk or high risk for a future major bleeding episode (19).

Scoring criteria include:

–Age ≥ 60 years (1.5 points)

–Active cancer (2 points)

–Male hypertension ≥140 mm Hg (1 point)

–Anemia male hemoglobin <13 or female hemoglobin <12 (1.5 points)

–History of major bleeding or nonmajor (double check this) (1.5 points)

–Creatinine clearance <60 mL·min−1 (1.5 points)

A score less than 2 is considered low risk. A score of 2 or greater is considered at high risk for bleeding on long-term anticoagulation. Consider consulting a hematologist if the risk of bleeding seems high. The cost of the medication, ease of dosing, renal function, availability of reversal agents if needed, and the ability to assess pharmacokinetics of the drug in a collision sport athlete must all be considered when prescribing an anticoagulant. If long-term treatment is being considered will there be an impact on the athlete’s career, financial security, and/or psychological well-being if the athlete should need anticoagulation?

Superficial Thrombophlebitis

Most often this condition can be managed conservatively with warm compresses, diclofenac gel four times a day, and follow clinically for any signs of thrombus progression (20). If superficial thrombophlebitis of the lower extremity is > = to 5 cm in length, and/or within 3 cm of saphenofemoral junction, bleeding risk is low, and/or high risk of progression, then rivaroxaban 10 mg daily for 45 d is a reasonable treatment option. No need to repeat the US unless there are signs/symptoms of thrombus progression (20). Compression stockings can be used but do not necessarily reduce the incidence of postthrombotic syndrome (PTS); a chronic pain condition in the extremity occurring after a DVT (21).

Distal Lower Extremity DVT

The decision on whether to treat a DVT that is localized below the popliteal fossa must be individualized to the athlete. If the athlete has minimal symptoms (mild swelling), is at low to moderate risk of clot progression, is medically trustworthy, then that athlete may follow-up with weekly US×2. Conservative measures, such as warm compresses and compressive stockings, may be used until symptoms resolve, and it is evident that the clot has not progressed proximally. If there is a high risk for clot progression (for example, continued prolonged nonweight-bearing) or the athlete has moderate to severe symptoms (intense limb pain) then treat the athlete as if he/she has a proximal DVT (21).

Proximal Lower Extremity DVT and PE

If there are no absolute contraindications then a proximal DVT and/or PE provoked by a major transient risk factor should be treated with a minimum of 3 months of anticoagulation. If the DVT/PE was unprovoked, and/or the athlete has persistent risk factors for another clot, then indefinite anticoagulation should be considered and is recommended by the American Society of Hematology; accounting for bleeding risks, future career, and patient preference (10,19). If the athlete declines long-term anticoagulation with a direct oral anticoagulant (DOAC) or warfarin; a vitamin K antagonist, then a full dose aspirin may be given as an alternative, probably less effective, option (21).

Upper Extremity DVT

An upper extremity DVT (effort induced thrombosis/Paget-Schroetter syndrome) should be treated with catheter directed thrombolysis. This reduces postthrombotic pain syndrome often associated with this condition (22). Then, continue to treat the DVT with at least 3 months of continuous anticoagulation.

Medication Options

The DOAC class of medications has become a favorable anticoagulation option for athletes and nonathletes alike. DOACs have been found to be safer and as effective as vitamin K antagonist (warfarin) in the treatment and prevention of VTE (21). DOACs do have a slightly higher incidence of nonfatal GI bleeds compared with vitamin K antagonists, however (21). Any DOAC medication is acceptable. The DOACs do not require frequent blood monitoring like warfarin. It is recommended that an initial complete blood count (CBC), prothrombin time (PT/international normalized ratio [INR]), and a partial thromboplastin time (PTT) be obtained prior to starting any anticoagulation, including a DOAC medication. Due to the effort and hydration demands of athletics, a DOAC that has a shorter half-life and is not heavily dependent on renal clearance may be preferred. Apixaban and rivaroxaban have shorter half-lives and more predictable pharmacodynamics than other DOACs. There also is no requirement to initially “co-anticoagulate” with any form of heparin (10).

A vitamin K antagonist also can be used to treat a DVT or PE. Warfarin requires a period of anticoagulation with heparin and must be regularly monitored for a consistent therapeutic zone. Consistent dose timing also is critical. This can be challenging with the demands of sports travel as well as varying degrees of dietary consistency at all levels of sports. Warfarin/INR levels can be monitored at home. This may be useful for an athlete with a busy schedule. The medication itself is considerably less expensive than the newer DOAC class of medications. However, the overall cost of usage (medication, laboratory test costs, potential time and fuel utilization to and from the laboratory tests, etc.) arguably makes the difference between warfarin use and DOAC use negligible.

A VTE provoked by the hypercoaguability associated with cancer can be treated effectively with low molecular weight heparin or a DOAC (21).

Duration of Treatment

If the VTE was provoked by a transient major risk factor then 3 months of continuous anticoagulation is required (21). If the cause of the VTE was not identified or provoked or if there are persistent risk factors for a recurrence, then consideration must be given to continue anticoagulation indefinitely. For those athletes who do not want the potential medical challenges of robust anticoagulation a full-dose aspirin could be considered (21). The efficacy of long-term aspirin use compared with a DOAC or a vitamin K antagonist for the prevention of a future VTE is not known. For those athletes found to have a lifelong hypercoaguable risk, indefinite treatment is recommended. Apixaban 2.5 mg twice a day (least renal clearance) or rivaroxaban 10 mg daily are regimens found to be effective (10). If the athlete is going to require lifelong anticoagulation or has decided not to anticoagulate despite the high risk of recurrence then consider getting a baseline US of the affected limb once the 3 months of anticoagulation for the acute DVT has finished (15).

Intermittent Dosing Strategy for High Risk (Collision or Contact) Sports Participation

The decision to return an athlete to a sport that involves a high likelihood of contact or collision can be clinically challenging when the athlete requires lifelong anticoagulation. Is it safe to return an anticoagulated athlete to a contact or collision sport? Is there a strategy or protocol that may be safely used to prevent another VTE while also preventing a major bleed? After 3 months of continuous treatment for an acute unprovoked VTE temporary cessation of anticoagulation is safe with an incidence of a fatal VTE being less than 1 in 100,000 per day (10). For some athletes an individualized drug pharmacokinetic assessment may be helpful to determine optimal timing for administration of a DOAC. Moll et al. (23) recommend using an intermediate dose of rivaroxaban (10 mg daily) or apixaban (2.5 mg twice a day) for those involved in sports at high risk for major bleeding. Pharmacokinetic studies for the individual athlete can be performed to determine the time after drug administration when the drug level is at a therapeutic trough of less than 30 ng·mL−1. Nazha et al. (24) suggest measuring calibrated anti-Xa or anti-IIa levels to determine a potential low therapeutic trough for boxers and wrestlers using one of the above DOACs. Lower levels of anti-Xa or anti-IIa activity correlated with lower concentrations/trough levels of the DOAC. Unfortunately, DOAC metabolism can be affected by exercise intensity, hydration, renal function, and muscle breakdown. As such, the safe threshold drug levels or activity below which bleeding risk is minimal has not been determined with consistency (10). Pharmacokinetic evaluations to determine optimal timing of medication administration are time intensive and costly. These barriers may limit this option to high-level college and professional athletes. I also would recommend that this strategy be done under comanagement and consultation with an experienced hematologist. Finally, there are no clear data on when to restart the DOAC once the practice or competition is complete. It is suggested that with a no- or low-impact sport an athlete may resume the DOAC within 1 to 2 h of completion. Contact sports where significant collision has occurred restart the DOAC approximately 24 h after the competition (23).

Hypercoaguable Evaluation

When an athlete develops a VTE, whether provoked or unprovoked, the clinician must decide when/if the athlete should be evaluated for an acquired or inherited thrombophilia. It is advisable to know the standards of care in the medical community, in particular when to refer to a hematologist. However, much of the preliminary evaluation can be performed by a primary care provider. Table 2 illustrates scenarios necessitating further evaluation and recommending testing. It is recommended that the testing be done more than 2 wk after discontinuation of the anticoagulation therapy. If the athlete is being considered for lifelong anticoagulation, then it is prudent to consult a hematologist. An athlete may be taken off the anticoagulation therapy for 2 wk, laboratory tests drawn, then restarted on the appropriate anticoagulant.

Table 2 - Recommended evaluation after VTE (25).
Conditions/Risks Recommended Evaluation
First unprovoked VTE (consider evaluation) History, physical examination, CBC, Chem 20, UA, chest X-ray, rectal examination with occult blood eval, pelvic examination PAP, sed rate, age-appropriate routine cancer screening, PT, PTT
Under age 45 yr with first VTE Eval for five inherited disorders
– Protein S, C, and anti-thrombin 3 deficiencies
– Factor 5 Leiden (activated protein C resistance)
– Prothrombin gene mutation
– History, physical examination, CBC, Chem 20, UA, PT, PTT
– Antiphosphoplipid syndrome
Has first-degree relative who had a VTE before age 45 yr Eval for 5 inherited disorders
–Protein S, C, and antithrombin 3 deficiencies
–Factor 5 Leiden (activated protein C resistance)
–Prothrombin gene mutation
–History, physical examination, CBC, Chem 20, UA, PT, PTT
Upper extremity VTE (consider evaluation) Eval for 5 inherited disorders
–Protein S, C, and antithrombin 3 deficiencies
–Factor 5 Leiden (activated protein C resistance)
–Prothrombin gene mutation
–History, physical examination, CBC, Chem 20, UA, PT, PTT
–And, Antiphosphoplipid syndrome
Recurrent thrombosis Eval for 5 inherited disorders
–Protein S, C, and anti-thrombin 3 deficiencies
–Factor 5 Leiden (activated protein C resistance)
–Prothrombin gene mutation
–History, physical examination, CBC, Chem 20, UA, chest X-ray, rectal examination with occult blood eval, pelvic examination PAP, SED rate, age-appropriate routine cancer screening, PT, PTT
–Antiphosphoplipid syndrome
Thrombosis in unusual vascular bed (portal or hepatic vein, mesenteric or cerebral vein) Eval for 5 inherited disorders
–Protein S, C, and antithrombin 3 deficiencies
–Factor 5 Leiden (activated protein C resistance)
–Prothrombin gene mutation
–History, physical examination, CBC, Chem 20, UA, chest X-ray, rectal examination with occult blood evaluation, pelvic examination PAP, sed rate, age-appropriate routine cancer screening, PT, PTT
–Antiphosphoplipid syndrome
Arterial thrombosis Eval include:
– History, physical examination, CBC, Chem 20, UA, PT, PTT
– Antiphospholipid syndrome

– First provoked VTE (with known transient risk)
– Known active malignancy
– Known inflammatory bowel disease
– Myeloproliferative disorder
– Heparin-induced low platelets with thrombus
– Retinal vein thrombosis
No further evaluation needed

Management of Bleeding While on an Anticoagulant

An anticoagulated athlete is always at an increased risk of bleeding when compared with an athlete who is not anticoagulated. Those risks are weighed against the benefits gained in an effort to prevent future/recurrent VTE. When choosing an anticoagulant; DOAC, warfarin, or heparin, the clinician must consider costs, availability of a reversal agent, drug half-life, and potential effects of exercise on the metabolism of the drug. The athlete is asked to continuously self-monitor for easy bruising, spontaneous bleeding, excessive menstrual blood loss, and blood or dark/black stools. Heavier menstrual bleeding, dose-related, is a common consequence of DOAC therapy in women (26) (Table 3).

Table 3 - Management of major hemorrhage while anticoagulated (10).
Anticoagulant Recommended Reversal Agent Product Size Average Wholesale Price (AWP)a,b
Kcentra (Four Factor Prothrombin Complex Concentrate) 1 × 500 unit vial $1657.92
Andexxa (Andexanet alpha) 4 × 200 mg vials $26400.00
Dabigatran Praxbind (Idarucizumab) 2 × 2.5 g·50 mL· vials $5135.11
ahttps://abcorderhs.amerisourcebergen.com/. Accessed September 21, 2021.
bRedBook System. Retrieved September 21, 2021, from http://micromedexsolutions.com.

Consider wearing protective equipment over vulnerable areas such as kidneys, ribs, and thighs. A medical alert bracelet with the anticoagulant used, dose taken, and treating physician's phone number also is recommended for all anticoagulated athletes.

Serious or life-threatening bleeds may be mitigated by the use of available reversal agents.

Return to Play Considerations

After a DVT is diagnosed and the athlete is anticoagulated when can that athlete safely begin to exercise again? An athlete with adequate cardiopulmonary reserve and no symptoms of a PE can begin light activities of daily living (ADLs), including slow walking, once anticoagulated. Those on warfarin should have achieved a goal INR between 2 and 3. Once the initial inflammation and edema have improved, walking may reduce the risk of clot progression, improve resolution time, and reduce PTS (7) (Table 4).

Table 4 - Return to training recommendations in weeks after initiation of anticoagulation.
Weeks 1–3 Gradual Return to ADLs
Week 4 Start nonweight-bearing exercise (e.g., swimming)
Week 5 Start nonimpact-loading exercise (e.g., stationary bike/cycling)
Week 6+ Start impact-loading exercise (begin gradual return-to-running program)
Adapted from Roberts' article (27).

A clot does not adhere well to a vessel wall for its initial 3 wk and therefore return to training is not recommended for at least 3 wk. In animal models clot lysis and recanalization occurs during weeks 4 to 6 and therefore swimming can begin at week 4. Cycling can begin at week 5, and progressive running can begin at week 6. Contact and collision activities are not recommended for at least 3 months allowing time for clot resorption (27,28).

The European Society of Cardiology working group recommends repeating an US of the lower extremities after 3 months of VTE treatment for DVT to confirm resolution (29). However, no consensus in the literature exists on whether repeat imaging is needed to confirm clot resolution, in the lungs or extremities, before initiating exercise, return to play, or after the prescribed anticoagulation treatment course.

Guidelines for return to exercise after a PE are not well defined. ADLs are recommended for the first 3 wk. Walking, easy swimming, and cycling may be reasonable beginning at 4 wk postinitiation of anticoagulation. Vigorous sport-specific training is not advised until the completion of 3 months of anticoagulation therapy (10).

An athlete with an upper extremity DVT should be imaged for any structurally impinging lesions. Light upper-extremity ADLs can begin after initiation of anticoagulation. Vigorous training or competition is not advised until after 3 months of anticoagulation has been completed (7).

If an athlete requires lifelong anticoagulation then return to play decisions should consider the following:

  • - Risk of major bleeding versus chance of a recurrent VTE
  • - Type of sport and level of participation (high school vs college vs professional)
  • - Medication choice with consideration for ease of dosing, cost, availability of reversing agent, half-life, and potential effect of exercise on drug metabolism/levels
  • - While anticoagulated, monitor for GI bleeding, excessive bruising, recurrence of symptoms


There are active measures that athletes and sports medicine clinicians can initiate that may decrease the risk of developing a VTE (Table 5). On long trips (>4 h), air or land, stay hydrated, and mobilize leg muscles by either briefly walking or simply contracting all muscle groups in the lower extremities each hour of the journey. Avoid prolonged sitting time with legs crossed, avoid constrictive clothing, and eat low fat foods (30). Athletes with a prior history of VTE, a strong family history of VTE, or a known thrombophilia; a single dose of prophylactic low molecular weight heparin (LMWH) or a DOAC should be considered as this has been shown to inhibit activation of coagulation in hypobaric modes of travel (flight) (10). Graduated compression stockings, for athletes traveling over 4 h in duration, may help reduce venous stasis, a risk factor for clot formation (10). If an athlete is injured and expected to be immobilized for greater than 3 d then consider early anticoagulation with aspirin, LMWH, or a DOAC, and compression stockings, until the athlete is ambulatory once again (31). An athlete who has had arthroscopic lower extremity surgery lasting more than 90 min, and has a personal or family history of VTE, or has a known thrombophilia should have VTE prophylaxis for 14 d postsurgery (10). Finally, in those athletes considered high risk (>2 VTE risk factors) consider delaying prolonged travel for 24 h to avoid the hypercoaguable state believed to be associated with intense exercise (10).

Table 5 - Practical points for prevention of VTE in athletes.
1. Avoid/minimize dehydration
2. Consider personal and family history of thrombosis prior to taking hormonal preparations and performance enhancing drugs
3. Long-haul flights/long distance journeys
–Keep well hydrated
–Take frequent short walks when possible
–Perform leg exercises while seated (e.g., calf pumps and quadriceps contractions)
–Avoid cramped seating positions and baggage at your feet
–Avoid flying immediately after intense exertion (delay travel by 24 h, if able)
–Consider compression garments with prolonged travel/sitting
–Postlower extremity injury followed by expected long travel duration thromboprophylaxis may be considered
4. Postoperative timeframe
–Consider adequate thromboprophylaxis for appropriate duration per guidelines
–Avoid performance enhancing drugs in the immediate postoperative period
Adapted from: Kupchak BR. Exercise and Air-Travel-Induced Alterations in Blood Hemostasis. Semin Thromb Hemost. 2018;44 (8):756–64.


VTE can occur in athletes following strenuous exercise, after a period of lower extremity injury with subsequent immobilization, and after prolonged automobile or air travel. It is unknown whether athletes are at a higher risk for VTE than the general nonathletic population. Athletes may have training-induced physiologic changes that allow the hallmark signs and symptoms of VTE to be less pronounced, thus making it more challenging to detect the athlete afflicted with a potentially life threatening VTE. Athletes diagnosed with a VTE should be anticoagulated. The DOAC anticoagulants are now considered first-line treatment. If a hypercoaguable workup is being considered, testing should be done before initiating anticoagulation, or at a minimum of 2 wk after completion of the acute treatment of the VTE. Guidelines for return to activity include gradual increase in intensity and duration as outlined. Practical management of VTE in athletes should be individualized (Figure). Shared informed decision making with the athlete, team physicians, and hematologic consultants is suggested for safe return to sport.

Management of VTE in athletes (10). Adapted considering the intermittent dosing strategies proposed by Moll et al. and Nazha et al. (23,24).

The author declares no conflict of interest and does not have any financial disclosures.


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