Introduction

Thrombosis is a single concept with enormous clinical reach. The same biological process drives deep vein thrombosis after a long-haul flight, the heart attack that follows a ruptured atherosclerotic plaque, and the stroke that suddenly changes a life. This guide walks through the causes, types, diagnosis, and treatment of thrombosis. We start with how clotting normally works, then look at what goes wrong.

Normal Blood Clotting Process (Hemostasis)

Hemostasis is the balanced system that stops bleeding without producing unwanted clots. It has four steps:

1. Vasoconstriction. The damaged vessel narrows to slow blood flow.
2. Primary hemostasis. Platelets stick to the injury and to each other, forming a soft plug.
3. Secondary hemostasis (coagulation cascade). Clotting factors activate in sequence, producing fibrin, a tough protein mesh that reinforces the plug.
4. Fibrinolysis. Once the vessel heals, the enzyme plasmin dissolves the clot and restores normal flow.

When this balance tips toward excessive clotting, thrombosis results. When it tips the other way, bleeding disorders appear.

Why Thrombosis Happens: Virchow's Triad

The 19th-century pathologist Rudolf Virchow identified three conditions that promote venous clot formation. Every risk factor we discuss below fits under one of these three headings:

• Endothelial injury. Damage to the inner vessel lining exposes tissue factor and activates platelets. Surgery, central venous catheters, trauma, and inflammation all do this.
• Stasis. Slow blood flow lets clotting factors accumulate locally. Bed rest, long flights, casts, paralysis, and pregnancy reduce flow.
• Hypercoagulability. The blood itself becomes more clot-prone. This can be inherited (thrombophilia) or acquired (cancer, hormone therapy, COVID-19).

Most real-world thrombosis happens when two or three of these elements combine. A hospitalized patient with cancer who has just had surgery hits all three at once.

Inherited Causes (Thrombophilia)

Inherited thrombophilias are genetic mutations that raise clotting risk. Most carriers are asymptomatic until a trigger (surgery, pregnancy, immobility) tips the balance.

Factor V Leiden

A mutation in the F5 gene produces a Factor V protein that resists inactivation by activated protein C. The clot-forming signal stays on longer than it should. Factor V Leiden is the most common inherited thrombophilia, affecting about 5% of people of European descent. Heterozygotes have a roughly 4- to 8-fold increased risk of venous thromboembolism (VTE); homozygotes face an even higher risk [4].

Prothrombin G20210A Mutation

A point mutation at position 20210 of the prothrombin gene raises prothrombin levels, leading to more thrombin generation and a higher tendency to clot. The risk profile resembles heterozygous Factor V Leiden.

Antithrombin, Protein C, and Protein S Deficiencies

These three proteins are the body's natural brakes on clotting. Inherited deficiencies are rarer than Factor V Leiden but carry a higher per-person risk. They are more likely to cause thrombosis in young adulthood and may run strongly in families.

Hyperhomocysteinemia

Elevated blood homocysteine (above 15 µmol/L) is linked to higher VTE risk. Causes include rare genetic defects and, more commonly, deficiencies of vitamins B6, B12, or folate. Treatment focuses on vitamin replacement.

Other Inherited Factors

Dysfibrinogenemia (abnormal fibrinogen) and rare deficiencies of regulatory proteins such as thrombomodulin can also predispose to clots.

Acquired Causes

Acquired causes account for the majority of thrombosis cases and rarely act alone. The risk multiplies when factors combine. To better conceptualize how these factors interact, clinical risks can be categorized by their severity:

Surgery and Immobility

Surgery damages vessels and triggers inflammation. Bed rest, long flights, and casts produce stasis. Together they account for a large fraction of hospital-acquired VTE [4].

Cancer

Cancer cells release tissue factor and other procoagulant substances. Some chemotherapy agents further raise the risk. Cancer-associated thrombosis is sometimes the first sign of an undiagnosed malignancy.

Pregnancy and the Postpartum Period

Pregnancy raises levels of several clotting factors and reduces protein S. The pressure of the uterus on pelvic veins adds stasis. Risk is highest in the first six weeks after delivery.

Hormonal Therapy

Estrogen-containing contraceptives and hormone replacement therapy increase clotting factor production and reduce natural anticoagulants. The absolute risk for a healthy young woman on the combined pill is small, but it climbs sharply when combined with smoking, obesity, or an inherited thrombophilia.

Antiphospholipid Syndrome (APS)

APS is the most clinically important acquired thrombophilia. Antibodies against phospholipid-binding proteins promote both venous and arterial clots, and in pregnancy cause recurrent miscarriage. Diagnosis requires persistent positive testing for lupus anticoagulant, anti-cardiolipin, or anti-β2-glycoprotein I antibodies on two occasions at least 12 weeks apart. Patients with confirmed APS, particularly those who are "triple-positive" for all three autoantibodies, are treated with warfarin rather than a DOAC. Trials such as the TRAPS study demonstrated unacceptably high rates of recurrent arterial thrombosis (such as ischemic strokes) when DOACs like rivaroxaban were used in these high-risk patients [12].

Heparin-Induced Thrombocytopenia (HIT)

HIT is a paradoxical reaction in which heparin triggers antibodies against platelet factor 4. Despite a falling platelet count, patients develop new clots, often severe. Suspect HIT when platelets drop by 50% or more between days 5 and 14 of heparin exposure. Treatment is to stop all heparin immediately and switch to a non-heparin anticoagulant such as argatroban or fondaparinux [8].

Inflammatory Conditions

Inflammatory bowel disease, lupus, and systemic infection all raise clotting risk through chronic endothelial activation.

COVID-19

COVID-19 reshaped thinking about infection-related thrombosis. Hospitalized patients during the pandemic had VTE rates around 25%, rising to 35% or higher in intensive care, even on prophylactic anticoagulation [10]. The mechanism involves direct viral injury to vessel linings, intense inflammation, and immobility. However, with widespread immunity and the evolution of the Omicron lineage, baseline VTE rates have dropped significantly, aligning closer to standard viral respiratory infections [13]. For treatment, clinical trials such as ACTIV-4a introduced nuanced approaches, utilizing therapeutic-dose heparin for non-critically ill hospitalized patients to improve outcomes rather than relying solely on standard prophylactic doses [14].

Other Acquired Factors

Obesity, smoking, varicose veins, central venous catheters, and certain medications (including some chemotherapy agents) all contribute. Most patients with thrombosis have more than one of these.

Arterial vs. Venous Thrombosis

Arterial and venous thrombosis share the word "clot" but differ in nearly everything else.

The composition difference matters clinically. Arterial clots form under fast flow, so platelets dominate, which is why antiplatelet agents (aspirin, clopidogrel) are central to arterial disease. Venous clots form under slow flow, so fibrin and trapped red cells dominate, which is why anticoagulants (which target the coagulation cascade) are the mainstay.

Types of Venous Thrombotic Events

Deep Vein Thrombosis (DVT)

DVT usually forms in the deep veins of the calf or thigh. Symptoms include leg pain, swelling, redness, and warmth, though many cases are silent. Doppler ultrasound is the first-line imaging test [3].

Pulmonary Embolism (PE)

PE happens when a fragment of a DVT breaks off and lodges in a pulmonary artery. Symptoms include sudden shortness of breath, chest pain that worsens with breathing, rapid heart rate, and sometimes coughing up blood. CT pulmonary angiography is the standard diagnostic test [3]. Untreated PE can be fatal within hours.

Superficial Thrombophlebitis

A clot in a vein just under the skin causes a tender, red, cord-like swelling. Most cases are managed with compression and anti-inflammatory drugs, though extension into deeper veins requires anticoagulation.

Cerebral Venous Thrombosis (CVT)

CVT is a clot in the brain's draining veins or dural sinuses. It causes severe headache, seizures, vision changes, or focal neurological deficits. MR or CT venography confirms the diagnosis. Anticoagulation is the cornerstone of treatment, even when small areas of brain hemorrhage are present.

Splanchnic Vein Thrombosis

Clots in the portal, mesenteric, splenic, or hepatic veins are uncommon but can be devastating. Mesenteric venous thrombosis presents with severe abdominal pain out of proportion to physical findings and demands urgent imaging. Note that this is different from acute arterial mesenteric ischemia, which is usually embolic from the heart.

Renal Vein Thrombosis

Renal vein thrombosis is most often seen in patients with nephrotic syndrome, where heavy urinary protein loss disrupts the anticoagulant balance.

Diagnosis of Thrombosis

Modern diagnosis of thrombosis follows a structured pathway, not just a hunch.

Step 1: Clinical Pretest Probability (Wells Score)

The Wells score for DVT assigns points for features such as active cancer, recent immobility, calf swelling, and a likely alternative diagnosis [5]. The Wells score for PE includes similar items plus signs of DVT, hemoptysis, and heart rate over 100 beats per minute. The score sorts patients into low, intermediate, or high probability and guides what comes next.

Step 2: D-Dimer Blood Test

D-dimer is a fragment released when clots break down. A negative D-dimer in a low- or intermediate-probability patient reliably rules out thrombosis without imaging. A positive result is non-specific and requires imaging. For patients over 50, an age-adjusted cutoff (age × 10 ng/mL) improves specificity without missing clots [6].

Clinical practice has also advanced to incorporate clinical probability into D-dimer thresholds using tools like the YEARS algorithm. If a patient lacks all three YEARS criteria (clinical signs of DVT, hemoptysis, and PE as the most likely diagnosis), a higher D-dimer threshold of 1,000 ng/mL safely rules out PE, drastically reducing unnecessary CT scans without compromising patient safety [15].

Step 3: Imaging

• Doppler ultrasound for suspected DVT.
• CT pulmonary angiography for suspected PE.
• MR or CT venography for cerebral venous thrombosis.
• V/Q scan as an alternative for PE when contrast or radiation must be avoided (for example, in pregnancy).

Other Useful Tests

A complete blood count, basic coagulation panel, and renal function tests help guide anticoagulation choice. Thrombophilia testing is reserved for unprovoked thrombosis in younger patients or those with strong family history, and even then is rarely done in the acute setting because heparin and DOACs interfere with several assays.

Why Early Diagnosis Matters

Early treatment limits clot extension, prevents embolization, and reduces long-term complications such as post-thrombotic syndrome and chronic thromboembolic pulmonary hypertension.

Treatment of Thrombosis

Treatment has two goals: deal with the existing clot, and prevent the next one.

Anticoagulation: The Foundation

Anticoagulants do not actively dissolve clots. They prevent new clot formation and growth, while the body's own fibrinolytic system removes what is already there.

• DOACs (direct oral anticoagulants). Apixaban, rivaroxaban, edoxaban, and dabigatran are now first-line for most non-cancer VTE. They use fixed doses, do not require routine monitoring, and have fewer drug and food interactions than warfarin [1,2]. Furthermore, updated International Society on Thrombosis and Haemostasis (ISTH) guidelines now endorse standard DOAC dosing even in patients with extreme obesity (BMI > 40 or weight > 120 kg), removing prior clinical hesitations regarding their efficacy in this population [16].
• Low molecular weight heparin (LMWH). Examples include enoxaparin and dalteparin. Used for initial treatment when a DOAC requires a heparin lead-in (dabigatran, edoxaban), in pregnancy, and historically in cancer-associated thrombosis.
• Warfarin. Still preferred for patients with mechanical heart valves and confirmed antiphospholipid syndrome [1]. Requires INR monitoring (target 2.0–3.0 for most indications).
• Cancer-associated thrombosis. Recent trials (Caravaggio, Hokusai-VTE Cancer) showed apixaban and edoxaban are non-inferior to LMWH for many cancer patients [11]. Current guidelines accept either LMWH or an oral factor Xa inhibitor as first-line. However, a critical clinical exception exists: for patients with luminal gastrointestinal (GI) or genitourinary (GU) malignancies (especially with intact primary tumors), DOACs carry a significantly higher risk of mucosal bleeding. In these specific cancers, LMWH often remains the preferred agent [17].

Standard treatment duration is at least three months for most VTE [1]. Extended (often indefinite) anticoagulation is used for unprovoked clots, recurrent events, or strong persistent risk factors. To assist in the complex decision of whether to extend therapy, clinicians increasingly utilize validated clinical prediction rules, such as the HERDOO2 rule or the DASH score, to identify patients with an unprovoked VTE who have a low enough recurrence risk to safely discontinue anticoagulants after the initial 3 to 6 months [18].

Reversal Agents

When bleeding or urgent surgery requires rapid reversal:

• Idarucizumab reverses dabigatran.
• Andexanet alfa reverses apixaban and rivaroxaban.
• Vitamin K and prothrombin complex concentrate reverse warfarin.

The Horizon: Factor XI Inhibitors 

The next generation of anticoagulants, including Factor XI and XIa inhibitors (e.g., milvexian, asundexian, abelacimab), are currently in advanced clinical trials. These drugs aim to theoretically "decouple" thrombosis from hemostasis, preventing pathological clot formation while presenting a near-zero risk of major bleeding [19].

Thrombolysis

Tissue plasminogen activator (alteplase) actively dissolves clots and is reserved for life-threatening situations: massive PE with hemodynamic instability, extensive iliofemoral DVT in young patients, and acute ischemic stroke within the time window. Bleeding risk is high.

Catheter-Directed and Surgical Approaches

Catheter-directed thrombolysis or mechanical thrombectomy can be used for large central clots in selected patients. Inferior vena cava filters are reserved for patients who cannot receive anticoagulation, not as a routine add-on [1].

What About Compression Stockings?

Compression stockings remain useful for symptom relief in DVT and for prevention in high-risk settings. However, updated guidance no longer recommends them routinely for preventing post-thrombotic syndrome after acute DVT, based on the SOX trial which showed no benefit [9].

Addressing Risk Factors

Long-term prevention means treating what put the clot there in the first place. Weight management, smoking cessation, control of blood pressure and diabetes, and reviewing hormonal therapy all reduce recurrence risk.

Post-Thrombotic Syndrome (PTS)

Up to half of patients with proximal DVT develop PTS within two years [4]. Symptoms include chronic leg pain, swelling, skin discoloration, and in severe cases venous ulcers. Risk factors include extensive DVT, recurrent ipsilateral DVT, obesity, and poor early anticoagulation. PTS is a major reason why thrombosis is not just an acute illness but a chronic condition for many survivors.

Frequently Asked Questions (FAQs)

What is thrombosis in simple terms?

Thrombosis is the formation of a blood clot inside a blood vessel. The clot, called a thrombus, can partly or fully block blood flow. When it happens in a deep leg vein it is called deep vein thrombosis (DVT); when a piece breaks off and lodges in the lungs it becomes a pulmonary embolism (PE). Thrombosis can also affect arteries, contributing to heart attacks and strokes.

Is thrombosis the same as a stroke or heart attack?

No, but they are related. Heart attacks and most strokes are caused by thrombosis when a clot forms inside an artery feeding the heart or brain. Thrombosis is the underlying clot; the heart attack or stroke is the tissue damage that results.

How is thrombosis diagnosed?

Doctors combine three things: a clinical scoring tool (most commonly the Wells score), a blood test called D-dimer, and imaging. For suspected DVT, a Doppler ultrasound of the leg is the usual test. For suspected PE, a CT pulmonary angiogram is the standard. A low Wells score plus a normal D-dimer can often rule out a clot without imaging.

What is the difference between DOACs and warfarin?

Both prevent clotting, but they work differently. Warfarin blocks vitamin K, which the liver needs to make several clotting factors; it requires regular blood-test monitoring (INR) and interacts with many foods and drugs. DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) block one specific clotting factor directly, use fixed doses, and do not need routine monitoring. Current guidelines favor DOACs for most non-cancer thrombosis.

Can thrombosis be prevented?

Often, yes. Move around regularly on long flights or after surgery, stay hydrated, maintain a healthy weight, avoid smoking, and discuss risk with your doctor before starting estrogen-containing medications. Hospitalized patients are usually given preventive blood thinners or compression devices. People with a strong family or personal history of clots may need lifelong measures.

Does COVID-19 increase the risk of blood clots?

Yes. Hospitalized COVID-19 patients had VTE rates around 25% during the pandemic, rising to 35% or higher in intensive care. The risk comes from inflammation, immobility, and direct effects on blood vessel linings. Routine clot prevention is now standard for hospitalized COVID-19 patients, and clinicians remain alert for thrombosis in severely ill survivors.

Glossary of Related Medical Terms

• Anticoagulant — A medication that slows blood clotting. Common types include warfarin, heparin, and direct oral anticoagulants (DOACs).
• Coagulation cascade — A step-by-step chain reaction of clotting proteins (factors) in the blood that produces fibrin to stabilize a clot.
• D-dimer — A protein fragment released when a clot breaks down. A blood test for it helps rule out (but not confirm) thrombosis.
• DOAC (direct oral anticoagulant) — A newer class of blood thinners that block specific clotting factors (thrombin or factor Xa) directly. Examples: apixaban, rivaroxaban, dabigatran, edoxaban.
• Embolus — A clot (or other material) that has broken loose and travels through the bloodstream.
• Endothelium — The thin inner lining of blood vessels. Damage to it triggers clotting.
• Fibrin — A protein that forms the mesh of a stable blood clot.
• Fibrinolysis — The body's process of breaking down clots once healing is complete.
• Hemostasis — The balanced system that stops bleeding without causing unwanted clots.
• Hypercoagulability — A state in which blood clots more easily than normal.
• Pulmonary embolism (PE) — A life-threatening blockage of a lung artery, usually by a clot that traveled from a deep vein.
• Post-thrombotic syndrome (PTS) — Long-term leg pain, swelling, and skin changes that follow DVT.
• Thrombophilia — Any inherited or acquired condition that increases clotting risk.
• Thrombus — A blood clot that has formed inside a blood vessel and remained there.
• Thrombolytic — A "clot-busting" drug that actively dissolves an existing clot (e.g., alteplase).
• Virchow's triad — The three conditions that promote thrombosis: endothelial injury, blood stasis, and hypercoagulability.

Disclaimer: This article is intended for educational and informational purposes only. It is not intended to be a substitute for informed professional medical advice, diagnosis, or treatment. While the information presented here is derived from credible medical sources and is believed to be accurate and up-to-date, it is not guaranteed to be complete or error-free. See additional information.

References

1. Stevens, S. M., Woller, S. C., Baumann Kreuziger, L., Bounameaux, H., Doerschug, K., Geersing, G. J., Huisman, M. V., Kearon, C., King, C. S., Knighton, A. J., Lake, E., Murin, S., Vintch, J. R. E., Wells, P. S., & Moores, L. K. (2021). Executive Summary: Antithrombotic Therapy for VTE Disease: Second Update of the CHEST Guideline and Expert Panel Report. Chest, 160(6), 2247–2259. https://doi.org/10.1016/j.chest.2021.07.056
2. Ortel, T. L., Neumann, I., Ageno, W., Beyth, R., Clark, N. P., Cuker, A., Hutten, B. A., Jaff, M. R., Manja, V., Schulman, S., Thurston, C., Vedantham, S., Verhamme, P., Witt, D. M., D Florez, I., Izcovich, A., Nieuwlaat, R., Ross, S., J Schünemann, H., Wiercioch, W., … Zhang, Y. (2020). American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism. Blood advances, 4(19), 4693–4738. https://doi.org/10.1182/bloodadvances.2020001830
3. Lim, W., Le Gal, G., Bates, S. M., Righini, M., Haramati, L. B., Lang, E., Kline, J. A., Chasteen, S., Snyder, M., Patel, P., Bhatt, M., Patel, P., Braun, C., Begum, H., Wiercioch, W., Schünemann, H. J., & Mustafa, R. A. (2018). American Society of Hematology 2018 guidelines for management of venous thromboembolism: diagnosis of venous thromboembolism. Blood advances, 2(22), 3226–3256. https://doi.org/10.1182/bloodadvances.2018024828
4. Khan, F., Tritschler, T., Kahn, S. R., & Rodger, M. A. (2021). Venous thromboembolism. Lancet (London, England), 398(10294), 64–77. https://doi.org/10.1016/S0140-6736(20)32658-1
5. Wells, P. S., Anderson, D. R., Rodger, M., Forgie, M., Kearon, C., Dreyer, J., Kovacs, G., Mitchell, M., Lewandowski, B., & Kovacs, M. J. (2003). Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis. The New England journal of medicine, 349(13), 1227–1235. https://doi.org/10.1056/NEJMoa023153
6. Righini, M., Van Es, J., Den Exter, P. L., Roy, P. M., Verschuren, F., Ghuysen, A., Rutschmann, O. T., Sanchez, O., Jaffrelot, M., Trinh-Duc, A., Le Gall, C., Moustafa, F., Principe, A., Van Houten, A. A., Ten Wolde, M., Douma, R. A., Hazelaar, G., Erkens, P. M., Van Kralingen, K. W., Grootenboers, M. J., … Le Gal, G. (2014). Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA, 311(11), 1117–1124. https://doi.org/10.1001/jama.2014.2135
7. Garcia, D., & Erkan, D. (2018). Diagnosis and Management of the Antiphospholipid Syndrome. The New England journal of medicine, 378(21), 2010–2021. https://doi.org/10.1056/NEJMra1705454
8. Greinacher A. (2015). Heparin-Induced Thrombocytopenia. The New England journal of medicine, 373(19), 1883–1884. https://doi.org/10.1056/NEJMc1510993
9. Kahn, S. R., Shapiro, S., Wells, P. S., Rodger, M. A., Kovacs, M. J., Anderson, D. R., Tagalakis, V., Houweling, A. H., Ducruet, T., Holcroft, C., Johri, M., Solymoss, S., Miron, M. J., Yeo, E., Smith, R., Schulman, S., Kassis, J., Kearon, C., Chagnon, I., Wong, T., … SOX trial investigators (2014). Compression stockings to prevent post-thrombotic syndrome: a randomised placebo-controlled trial. Lancet (London, England), 383(9920), 880–888. https://doi.org/10.1016/S0140-6736(13)61902-9
10. Klok, F. A., Kruip, M. J. H. A., van der Meer, N. J. M., Arbous, M. S., Gommers, D. A. M. P. J., Kant, K. M., Kaptein, F. H. J., van Paassen, J., Stals, M. A. M., Huisman, M. V., & Endeman, H. (2020). Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thrombosis research, 191, 145–147. https://doi.org/10.1016/j.thromres.2020.04.013
11. Agnelli, G., Becattini, C., Meyer, G., Muñoz, A., Huisman, M. V., Connors, J. M., Cohen, A., Bauersachs, R., Brenner, B., Torbicki, A., Sueiro, M. R., Lambert, C., Gussoni, G., Campanini, M., Fontanella, A., Vescovo, G., Verso, M., & Caravaggio Investigators (2020). Apixaban for the Treatment of Venous Thromboembolism Associated with Cancer. The New England journal of medicine, 382(17), 1599–1607. https://doi.org/10.1056/NEJMoa1915103
12. Pengo, V., Denas, G., Zoppellaro, G., Jose, S. P., Hoxha, A., Ruffatti, A., Andreoli, L., Tincani, A., Cenci, C., Prisco, D., Fierro, T., Gresele, P., Cafolla, A., De Micheli, V., Ghirarduzzi, A., Tosetto, A., Falanga, A., Martinelli, I., Testa, S., Barcellona, D., … Banzato, A. (2018). Rivaroxaban vs warfarin in high-risk patients with antiphospholipid syndrome. Blood, 132(13), 1365–1371. https://doi.org/10.1182/blood-2018-04-848333
13. O'Carroll, A., Richard, S. A., Byrne, C., Rusiecki, J., Wier, B., Berjohn, C. M., Fries, A. C., Lalani, T., Smith, A. G., Mody, R. M., Ganesan, A., Huprikar, N., Colombo, R. E., Schofield, C., Lindholm, D. A., Mende, K., Jones, M. U., Flanagan, R., Larson, D. T., Ewers, E. C., … Pollett, S. D. (2024). Estimating the Effect of Coronavirus Disease 2019 (COVID-19) Vaccination and Infection Variant on Post-COVID-19 Venous Thrombosis or Embolism Risk. Open forum infectious diseases, 11(11), ofae557. https://doi.org/10.1093/ofid/ofae557
14. ATTACC Investigators, ACTIV-4a Investigators, REMAP-CAP Investigators, Lawler, P. R., Goligher, E. C., Berger, J. S., Neal, M. D., McVerry, B. J., Nicolau, J. C., Gong, M. N., Carrier, M., Rosenson, R. S., Reynolds, H. R., Turgeon, A. F., Escobedo, J., Huang, D. T., Bradbury, C. A., Houston, B. L., Kornblith, L. Z., Kumar, A., … Zarychanski, R. (2021). Therapeutic Anticoagulation with Heparin in Noncritically Ill Patients with Covid-19. The New England journal of medicine, 385(9), 790–802. https://doi.org/10.1056/NEJMoa2105911
15. van der Hulle, T., Cheung, W. Y., Kooij, S., Beenen, L. F. M., van Bemmel, T., van Es, J., Faber, L. M., Hazelaar, G. M., Heringhaus, C., Hofstee, H., Hovens, M. M. C., Kaasjager, K. A. H., van Klink, R. C. J., Kruip, M. J. H. A., Loeffen, R. F., Mairuhu, A. T. A., Middeldorp, S., Nijkeuter, M., van der Pol, L. M., Schol-Gelok, S., … YEARS study group (2017). Simplified diagnostic management of suspected pulmonary embolism (the YEARS study): a prospective, multicentre, cohort study. Lancet (London, England), 390(10091), 289–297. https://doi.org/10.1016/S0140-6736(17)30885-1
16. Martin, K., Beyer-Westendorf, J., Davidson, B. L., Huisman, M. V., Sandset, P. M., & Moll, S. (2016). Use of the direct oral anticoagulants in obese patients: guidance from the SSC of the ISTH. Journal of thrombosis and haemostasis : JTH, 14(6), 1308–1313. https://doi.org/10.1111/jth.13323
17. Lyman, G. H., Bohlke, K., Khorana, A. A., Kuderer, N. M., Lee, A. Y., Arcelus, J. I., Balaban, E. P., Clarke, J. M., Flowers, C. R., Francis, C. W., Gates, L. E., Kakkar, A. K., Key, N. S., Levine, M. N., Liebman, H. A., Tempero, M. A., Wong, S. L., Somerfield, M. R., Falanga, A., & American Society of Clinical Oncology (2015). Venous thromboembolism prophylaxis and treatment in patients with cancer: american society of clinical oncology clinical practice guideline update 2014. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 33(6), 654–656. https://doi.org/10.1200/JCO.2014.59.7351
18. Rodger, M. A., Le Gal, G., Anderson, D. R., Schmidt, J., Pernod, G., Kahn, S. R., Righini, M., Mismetti, P., Kearon, C., Meyer, G., Elias, A., Ramsay, T., Ortel, T. L., Huisman, M. V., Kovacs, M. J., & REVERSE II Study Investigators (2017). Validating the HERDOO2 rule to guide treatment duration for women with unprovoked venous thrombosis: multinational prospective cohort management study. BMJ (Clinical research ed.), 356, j1065. https://doi.org/10.1136/bmj.j1065
19. Fredenburgh, J. C., & Weitz, J. I. (2021). Factor XI as a Target for New Anticoagulants. Hamostaseologie, 41(2), 104–110. https://doi.org/10.1055/a-1384-3715