Is my patient with varicose veins at higher risk of venous thromboembolism?

Although varicose veins are common and usually not associated with serious health complications, increasing scientific evidence suggests that they are associated with increased risk of subsequent incident deep venous thrombosis (DVT) and pulmonary embolism (PE). 1-3

A 2018 retrospective cohort study involving patients with the diagnosis of varicose veins and controls (>200,000 subjects each) based on claims data from Taiwan found a higher incidence rate of DVT among cases (hazard ratio [HR] 5.3, 95%C.I. 5.1-5.6). Increased risk of DVT with varicose veins was reported in all age groups but decreased with increasing age.  The HR was higher within the first year of the diagnosis of varicose veins. 1

In the same study, the incidence of PE was higher among participants with varicose veins (HR 1.7 95% C.I. 1.5-1.9).  Again, the association did not significantly differ by age.1  Other smaller studies have found similar association between DVT and varicose veins. 2,3

Although these studies at best demonstrate an association (not necessarily a cause and effect relationship) between varicose veins and venous thromboembolism, several possible explanations have been posited. Animal studies have demonstrated higher concentrations of macrophages, monocytes, neutrophils, lymphocytes, and matrix metalloproteinases in venous valves exposed to high pressure for prolonged periods.  The resultant inflammatory state in patients with varicose veins may in turn promote a prothrombotic state contributing to venous thromboembolism. 1,4

Bonus Pearl: Did you know that nearly 1 of 4  adults in the United States have been reported to have varicose veins?

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References

  1. Chang SL, Huang YL, Lee MC, et al. Association of varicose veins with incident venous thromboembolism and peripheral artery disease. JAMA 208;319:807-817. https://jamanetwork.com/journals/jama/fullarticle/2673551
  2. Muller-Buhl U, Leutgeb R, et al. Varicose veins are a risk factor for deep venous thrombosis in general practice patients. Vasa 2012;41:360-65. https://pubmed.ncbi.nlm.nih.gov/22915533/
  3. Engbers MJ, Karasu A, Blom JW, et al. Clinical features of venous insufficiency and the risk of venous thrombosis in older people. Br J Haematol 2015;171:417-23. https://pubmed.ncbi.nlm.nih.gov/26221838/
  4. Riva N, Donadini MP, Ageno W. Epidemiology and pathophysiology of venous thromboembolism: similarities with atherothrombosis and the role of inflammation. Thromb Haemost 2015;113:1176-1183. https://pubmed.ncbi.nlm.nih.gov/25472800/

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is my patient with varicose veins at higher risk of venous thromboembolism?

My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

Not likely! There is no evidence that TKA causes Baker’s cyst (also known as popliteal cyst). Instead, the finding of Baker’s cyst following TKA may be best explained by its well-known association with osteoarthritis, one of the main indications for TKA.1,6,7

In a study of 2025 patients who underwent primary TKA, 0.6% were diagnosed with Baker’s cysts within 6 weeks to 2 years postoperatively (75% symptomatic), but whether the cysts were present prior to TKA was unclear. There was no reported association between surgical technique or perioperative course and Baker’s cyst diagnosis.9

Actually, there might be a correlation between TKA and Baker’s cyst resolution.2,3 Among patients with known cysts preoperatively, 15% and 67% of patients may experience resolution of the cyst at 1 year and 4-6 years following surgery, respectively. 2,3

A Baker’s cyst is a fluid-filled pocket in the posterior aspect of the knee, typically seen in adults with degenerative changes in the patellofemoral joint, as may occur with meniscal tears and arthritis. When symptomatic, it can be treated non-operatively with ultrasound-guided aspiration and corticosteroid injection or operatively with surgical excision or attempted repair of the underlying defect. 4,8

 

Bonus Pearl: Did you know that the ‘crescent sign’ (bruising below the medial malleolus associated with fluid from ruptured cyst moving inferiorly toward the ankle) was first described in 1976 and may help distinguish calf pain due to Baker’s cyst from that of deep venous thrombophlebitis? 5

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 Contributed by Anamika Veeramani, Medical Student, Harvard Medical School

 

References

  1. Guermazi A., Hayashi D., Roemer F, et al. Cyst-like lesions of the knee joint and their relation to incident knee pain and development of radiographic osteoarthritis: The MOST study. Osteoarthritis and Cartilage 2010; 18:1386-1392. doi:10.1016/j.joca.2010.08.015. https://pubmed.ncbi.nlm.nih.gov/20816978/
  2. Hommel H., Becker R., Fennema P., et al. (2020). The fate of Baker’s cysts at mid-term follow-up after total knee arthroplasty. The Bone & Joint Journal, 2020;102-B(1):132-136. doi:10.1302/0301-620x.102b1.bjj-2019-0273.r2. https://pubmed.ncbi.nlm.nih.gov/31888367/
  3. Hommel, H., Perka, C., Kopf, S. The fate of Baker’s cyst after total knee arthroplasty. The Bone & Joint Journal 2016;98-B(9):1185-1188. doi:10.1302/0301-620x.98b9.37748. https://pubmed.ncbi.nlm.nih.gov/27587518/
  4. Leib AD, Roshan A, Foris LA, et al. Baker’s Cyst. [Updated 2020 Mar 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430774/
  5. Mizumoto, J. The crescent sign of ruptured baker’s cyst. Journal of General Family Medicine, 2019;20(5): 215-216. doi: 10.1002/jgf2.261. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6732489/
  6. Rupp, S., Seil, R., Jochum, P., & Kohn, D. Popliteal Cysts in Adults. The American Journal of Sports Medicine 2002; 30(1): 112-115. doi:10.1177/03635465020300010401. https://pubmed.ncbi.nlm.nih.gov/11799006/
  7. Sansone, V., Ponti, A. D., Paluello, G. M., & Maschio, A. D. Popliteal cysts and associated disorders of the knee. International Orthopaedics 1995;19(5): 275-279. doi:10.1007/bf00181107. https://pubmed.ncbi.nlm.nih.gov/8567131/
  8. Smith, M., Lesniak, B., Baraga, M., Kaplan, L., Jose, J. Treatment of Popliteal (Baker) Cysts with Ultrasound-Guided Aspiration, Fenestration and Injection: Long-term Follow-up. Sports Health 2015; 7(5): 409-414. doi: 10.1177/1941738115585520. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547114/
  9. Tofte, J. N., Holte, A. J., & Noiseaux, N. Popliteal (Baker’s) Cysts in the Setting of Primary Knee Arthroplasty. The Iowa Orthopedic Journal 2017;37:177-180. https://pubmed.ncbi.nlm.nih.gov/28852354/

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

Is intermittent pneumatic compression effective in reducing the risk of deep vein thrombosis in non-surgical hospitalized patients at high risk of major bleed?

The weight of the evidence to date suggests that intermittent pneumatic compression (IPC) is effective in reducing the risk of deep venous thrombosis (DVT) in hospitalized patients with stroke. 1,2 Whether IPC is also effective in non-surgical hospitalized patients without stroke at high risk of DVT and major bleed needs further studies.

A 2013 multicenter randomized trial (CLOTS 3) involving over 2,000 immobile hospitalized patients post-stroke found a significantly lower risk of DVT in proximal veins or any symptomatic DVT in the proximal veins within 30 days of randomization (8.5% vs 12.1%; absolute reduction risk 3.6%, 95% C.I. 1.4-5.8). Of note, the rate of concurrent heparin or low molecular weight heparin (LMWH) prophylaxis was similar between the 2 groups (17%). 1

A meta-analysis including the CLOTS 3 study and 2 other smaller trials 2 in patients with stroke found a risk reduction for proximal DVT (O.R. 0.66, 95% C.I 0.52-0.84) with nearly significant reduction in deaths by the end of the treatment period (O.R. 0.81, 95% 0.65-1.01).1

Although IPC may also be effective in non-surgical hospitalized patients without stroke but at high risk of DVT and bleed, proper trials in this patient population is lacking. In fact, the 2012 American College of Chest Physicians guidelines on antithrombotic therapy and prevention of thrombosis classifies use of IPC in preventing DVT’s in non-surgical acutely ill hospitalized patients as category 2C recommendation (weak, low quality evidence). 3

The patient population and methodology of above studies should be distinguished from those of a 2019 published trial involving only critically ill patients—all receiving pharmacologic thromboprophylaxis—which reported no reduction in the incidence of proximal lower-limb DVT with the addition of IPC. 4

 

Bonus Pearl: Did you know that venous thromboembolism has been reported in up to 42% of hospitalized patients who have had a stroke? 1

 

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References

  1. Dennis M, Sandercock P, Reid J, et al. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicenter randomized controlled trial. Lancet 2013;382:516-24. https://www.thelancet.com/cms/10.1016/S0140-6736(13)61050-8/attachment/1a0438d2-86eb-4da1-8bdb-92c0aec18b8d/mmc1.pdf
  2. Naccarato M, Chiodo Grandi F, Dennis M, et al. Physical methods for preventing deep vein thrombosis in stroke. Cochrance Database Syst Rev 2010;8:CD001922. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD001922.pub3/full
  3. Guyatt GH, Akl EA, Crowther M, et al. Executive summary: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. CHEST 2012;141 (suppl):7S-47S. http://www.sphcs.org/workfiles/CardiacVascular/7S-full.pdf
  4. Arabi YM, Al-Hameed F, Burns KEA, et al. Adjunctive intermittent pneumatic compression for venous thromboprophylaxis. N Engl J Med 2019;380:1305-15. https://pubmed.ncbi.nlm.nih.gov/30779530/

 

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is intermittent pneumatic compression effective in reducing the risk of deep vein thrombosis in non-surgical hospitalized patients at high risk of major bleed?

What’s the evidence that patients with Covid-19 are at high risk of blood clots?

Although we often think of it as a respiratory disease, emerging evidence suggests that Covid-19, particularly when severe,  is also associated with high risk of thrombotic events, including pulmonary embolism, venous thrombosis, and arterial thrombotic events.1

A Chinese study found that ICU patients with severe Covid-19 had a venous thromboembolism (VTE) incidence of 25%, with disseminated intravascular coagulopathy (DIC) found in the majority of fatal cases.2

A prospective Dutch study involving critically ill ICU patients with Covid-19 reported VTE in 27% and arterial thrombotic events in another 3.7%, despite standard VTE prophylaxis.3 The authors suggested the use of “high prophylactic doses” of anticoagulants in these patients due to concern over hypercoagulability.

An ICU French study also found high frequency of thrombotic complications in Covid-19 patients with ARDS, with 11.7% of patients having pulmonary embolism vs 2.1% in non-Covid-19 patients with ARDS. As with the Dutch study, thrombotic complications occurred despite standard prophylactic anticoagulation.4

Postmortem studies have also shown marked changes in lung microvasculature with the presence of microthrombi, with some calling it “pulmonary intravascular coagulopathy” to distinguish it from DIC.1

A NEJM letter reported 5 Covid-19 patients less than 50 years of age who presented with large vessel stroke symptoms without an alternative explanation.5 Of interest, 2 of these patients had no other symptoms suggestive of Covid-19.  A pre-print article from China reported an acute stroke incidence of 5% in hospitalized patients with Covid-19.6

The finding of a hypercoagulable state in patients with severe Covid-19 is not surprising given the frequent association of this infection with a high inflammatory state and the well-known capability of SARS-CoV-2 to attack the endothelial surfaces of blood vessels. High inflammatory state can promote activation of blood coagulation through release of inflammatory cytokines (eg, IL-6, IL-8, and TNF-alpha).1

Perhaps even more intriguing is the finding of extremely high levels of factor VIII found in some Covid-19 patients which could make them hypercoagulable.7 This phenomenon should be suspected when a patient appears to be resistant to anticoagulation by heparin based on aPTT but not based on anti-Xa assay.7

 Bonus pearl: Did you know that the overall incidence of VTE is lowest among Asians-Pacific islanders, followed by Hispanics and Caucasians, with highest rate among African-Americans? 1 ,8

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References

  1. Fogarty H, Townsend L, Cheallaigh CN, et al. COVID-19 coagulopathy in Caucasian patients. Br J Haematol 2020, https://onlinelibrary.wiley.com/doi/epdf/10.1111/bjh.16749
  2. Cui S, Chen S, Li X, et al. Huang C, Wang Y, Li X, et al. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J Thromb Haematol 2020, April 9. https://onlinelibrary.wiley.com/doi/epdf/10.1111/jth.14830
  3. Klok FA, Kruip MJHA, van der Meer NJM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020. https://www.sciencedirect.com/science/article/pii/S0049384820301201?via%3Dihub
  4. Helms J, Tacquard C, Severac F, et al. High risk of thrombosis in patients in severe SARS-CoV-2 infection: a multicenter prospective cohort study. Intensive Care Med 2020; https://www.esicm.org/wp-content/uploads/2020/04/863_author_proof.pdf
  5. Oxley TJ, Mocco J, Majidie S, et al. Large-vessel stroke as a presenting feature of Covid-19 in the young. N Engl J Med. 2020, April 28. https://www.nejm.org/doi/full/10.1056/NEJMc2009787?query=featured_home
  6. Li Y, Wang M. Acute cerebrovascular disease following COVID-19: A single center, retrospective, observational study. 2020. https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3550025
  7. Beun R, Kusadasi N, Sikma M, et al. Thromboembolic events and apparent heparin resistance in patients infected with SARS-CoV-2. Int J Lab Hematol 2020, April 20. https://onlinelibrary.wiley.com/doi/abs/10.1111/ijlh.13230
  8. White RH, Keenan CR. Effects of race and ethnicity on the incidence of venous thromboembolism. Thromb Res 2009;123 Suppl 4:S11-S17. doi:10.1016/S0049-3848(09)70136-7

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What’s the evidence that patients with Covid-19 are at high risk of blood clots?

Should my patient with below-knee venous thrombosis receive anticoagulation?

In contrast to proximal lower extremity deep venous thrombosis for which anticoagulation (AC) is standard therapy, whether below-knee deep venous thrombosis (BKDVT) (eg,  involving peroneal, soleus, tibial, or gastrocnemius veins) should routinely receive AC is a matter of debate because of lack of solid supportive evidence. 1-3

The American College of Chest Physicians (ACCP) recommends AC for patients with BKDVT who are severely symptomatic or have risk factors for extension of the thrombus but this recommendation is based on low-quality scientific evidence (grade 2C or “weak”).3 For other patients, surveillance ultrasound is recommended in 2 weeks to exclude clot propagation more proximally, and therefore the need for AC.  Of course, decision regarding AC should be made in the context of the patient’s risk of serious bleeding.

The following facts about BKDVT may help in therapeutic decision making:1

  • Most cases resolve spontaneously without AC
  • The incidence of propagation varies from 3%-32%
  • Embolization is unlikely in the absence of extension into proximal veins

Also remember that clot propagation usually occurs within 2 weeks of initial diagnosis. That’s why surveillance ultrasound is recommended during this period when watchful waiting is preferred.

References 

  1. Fleck D, Albadawi H, Wallace A, etal. Below-knee deep vein thrombosis (DVT): diagnostic and treatment patterns. Cariovasc Diagn Ther 2017;7(Suppl3):S134-39. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5778527/
  2. Olson EJ, Zander AL, Van Gent J-M, et al. Below-knee deep vein thrombosis: An opportunity to prevent pulmonary embolism? J Trauma Acute Care Surg 2014;77:459-63. https://www.ncbi.nlm.nih.gov/pubmed/25159251
  3. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease. Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. CHEST 2012;141 (Suppl):e419S-e494S. https://www.ncbi.nlm.nih.gov/pubmed/22315268

 

Should my patient with below-knee venous thrombosis receive anticoagulation?

My patient with significant dyspnea appears to have an acute exacerbation of his chronic obstructive pulmonary disease (AE-COPD). How often do AE-COPD and pulmonary embolism (PE) coexist?

Simultaneous presence of PE in patients with AE-COPD is not rare, particularly in those with unexplained AE-COPD.

A recent systematic review and meta-analysis reported a pooled PE prevalence of 16.1% (95% C.I. 8.3%-25.8%) in unexplained AE-COPD, with 68% of emboli found in the main pulmonary arteries, lobar arteries or inter-lobar arteries (i.e. not subsegmental); the pooled prevalence of deep venous thrombosis (DVT) was 10.5% (95% C.I. 4.3%-19.0%) 1. Pleuritic chest pain and signs of cardiac failure were associated with AE-COPD, while symptoms suggestive of a respiratory tract infection argued against PE.

It remains unclear, however, if the threshold for evaluation of venous thromboembolism (VTE) should necessarily differ between patients with explained vs unexplained AE-COPD.

In one small study, the prevalence of VTE in “unexplained” AE-COPD was significantly higher (25%) than “explained” AE-COPD (including cases with  tracheobronchitis, pneumonia, cardiac disorders, exposure to irritant inhalants, and lack of compliance with treatment), but the VTE prevalence for the latter group was still 8.4%2.  Serum D-dimer level and Wells criteria may help exclude VTE in this patient population.

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References

  1. Aleva FE, Voets LWLM, Simons SO, et al. Prevalence and localization of pulmonary embolism in unexplained acute exacerbations of COPD: A systematic review and meta-analysis. CHEST (2016), doi: 10.1016/j.chest.2016.07.034.
  2. Gunen H, Gulbas G, In E, Yetkin O, Hacievliyagil SS. Venous thromboemboli and exacerbations of COPD. Eur Respir J 2010;35:1243-1248.

 

Contributed by Jeff Greenwald, MD, Core Educator Faculty, Department of Medicine, Massachusetts General Hospital

My patient with significant dyspnea appears to have an acute exacerbation of his chronic obstructive pulmonary disease (AE-COPD). How often do AE-COPD and pulmonary embolism (PE) coexist?

My bed-bound, debilitated patient is being transferred to a long-term facility (LTF). Should I continue the venous thromboembolism (VTE) prophylaxis she has been receiving in the hospital?

There are no randomized-controlled studies that examine the effectiveness of VTE prophylaxis in debilitated patients following discharge from the hospital, and currently  the literature does not recommend prophylaxis for chronic immobility as a single risk factor for VTE (1). However, given the expected morbidity, potential mortality and hospital readmission associated with VTE,  prophylaxis should be considered in residents of LTFs with the following comorbidities (2):

  • Acute exacerbation of congestive heart failure
  • Acute exacerbation of chronic obstructive pulmonary disease
  • Acute infection (e. g. pneumonia, urosepsis, skin and soft tissue infections, infectious diarrhea)
  • Acute exacerbation of inflammatory/autoimmune diseases
  • Active malignancy
  • Immobility and prior VTE

 

Unless contraindicated, patients should receive prophylactic doses of unfractionated heparin, enoxaparin, or other approved drugs. Mechanical VTE prophylaxis should be used only when the risk of bleeding is considered unacceptably high or when there are drug intolerances or adverse effects.

The need for VTE prophylaxis should be reassessed regularly taking into account patient’s overall health status, mobility, drug tolerance and goals of care.

 

References

  1. Pai M, Douketis JD. Preventing venous thromboembolism in long-term care residents: Cautious advice based on limited data. Cleveland Clin J Med 2010;77: 123-130.  https://www.ncbi.nlm.nih.gov/pubmed/20124270    
  2. Robinson Am. Venous thromboembolism prophylaxis for chronically immobilized long-term care residents. Ann Long-Term Care 2013;10:30. https://www.managedhealthcareconnect.com/article/venous-thromboembolism-prophylaxis-chronically-immobilized-long-term-care-residents
My bed-bound, debilitated patient is being transferred to a long-term facility (LTF). Should I continue the venous thromboembolism (VTE) prophylaxis she has been receiving in the hospital?

What is the role of direct oral anticoagulant (DOAC) agents in preventing venous thromboembolism (VTE) in patients who undergo hip or knee arthroplasties?

DOACs (eg, rivaroxaban, apixaban,and dabigatran) are increasingly considered for use after hip and knee arthroplasties due to their demonstrated efficacy against VTE prophylaxis and an acceptable safety profile. 

In a meta-analysis involving 16 trials in over 38,000 patients, when compared to enoxaparin, the risk of symptomatic VTE appeared to be significantly lower with rivaroxaban (relative risk 0.48, 95% C.I. 0.3-0.75), and similar with dabigatran and apixaban (1).

In the same study, compared to enoxaparin, the relative risk of clinically relevant bleeding was significantly higher with rivaroxaban (1.25, 95% C.I. 1.1-1.5), similar with dabigatran , but lower with apixaban (0.82, 95% C.I. 0.7-0.98) (1). The authors concluded that new anticoagulants did not differ significantly for efficacy and safety.

Of course, the decision to use a DOAC vs enoxaparin should be made on an individual basis taking into account a variety of factors,  such as patient preferences, cost, comorbidities, patient compliance with medications, etc…  

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 Reference

1.  Gomez-Outes, Suarez-Gea L, Vargas-Castrillon E.  Dabigatran, rivaroxaban, or apixaban versus enoxaparin for thromboprophylaxis after total hip or knee replacement: systematic review, meta-analysis, and indirect treatment. BMJ 2012;344:e3675. https://pubmed.ncbi.nlm.nih.gov/22700784/ 

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is the role of direct oral anticoagulant (DOAC) agents in preventing venous thromboembolism (VTE) in patients who undergo hip or knee arthroplasties?