Venous thromboembolism in cancer and thromboprophylaxis

• Active cancer is one of the strongest acquired risk factors for venous thromboembolism, raising the risk roughly four- to seven-fold compared with people without cancer, and VTE is the second leading cause of death in people with cancer after progression of the cancer itself. ^[1][4]
• The clot can be a deep vein thrombosis, a pulmonary embolism, or a thrombus on a central venous catheter, and it is often found incidentally on imaging done for cancer staging.
• Risk is not uniform: it depends on cancer type and stage, treatment, mobility, and patient factors, which is why risk scores such as the Khorana score are used to select who should receive primary prophylaxis.
• Treatment of confirmed VTE in cancer favours anticoagulation for 3 to 6 months initially, with LMWH or a direct oral anticoagulant (apixaban, rivaroxaban or edoxaban) as first-line choices; warfarin is no longer the default. ^[1][3]
• Prevention is offered to hospitalised patients with cancer and reduced mobility, to most patients having major cancer surgery (with 4 weeks of LMWH after major abdominal or pelvic surgery), and to selected high-risk outpatients (Khorana score 2 or more) on systemic anticancer therapy with a low bleeding risk. ^[1]

By the end of this page you should be able to:

1. Explain why active cancer promotes thrombosis, using Virchow's triad and tumour-specific factors.
2. Identify which cancers and treatments carry the highest VTE risk and state representative incidence rates.
3. Calculate the Khorana risk score, name its five components and the risk levels they define, and contrast it with the Vienna CATS, PROTECHT, CONKO and COMPASS-CAT models.
4. Diagnose VTE in a patient with cancer using the standard DVT and PE pathway, and recognise when VTE is incidental.
5. Prescribe initial and maintenance anticoagulation for cancer-associated VTE, including drug, dose, route and minimum duration, and manage recurrence on treatment.
6. Apply VTE prophylaxis in hospital, after cancer surgery and in ambulatory patients, and know when prophylaxis should not be given.
7. Tailor treatment and prophylaxis to renal function, drug interactions, bleeding risk, thrombocytopenia risk factors and low-resource settings.
8. Communicate the prognosis, bleeding risks and the balance of benefit and harm in shared decision making.

"Cancer-associated VTE" and "malignancy-associated thrombosis" are used interchangeably in the literature. VTE is the umbrella term covering DVT and PE, and the subject here is how cancer changes risk, diagnosis, prevention and treatment compared with VTE in patients without cancer.

Cancer-associated VTE is common and serious. It is the second leading cause of death in people with cancer after progression of the malignancy itself, and survivors have high rates of recurrent VTE and anticoagulant-related bleeding. The risk of VTE is increased four- to seven-fold in people with cancer compared with people without cancer. The prevalence is rising because patients live longer, receive more thrombogenic treatments, have incidental VTE detected on surveillance imaging, and use more central venous catheters. ^[1][4]

Incidence varies widely by tumour. In a large cohort of over 6500 patients with active cancer and a first VTE, lung, stomach, ovarian, pancreatic and brain cancers were associated with incidence rates of 10.1 to 14.6 events per 100 person-years, while bladder, breast, prostate, haematological, colon and uterine cancers were associated with 2.7 to 7.0 events per 100 person-years. The risk is driven by grade and stage as much as by site: in the Vienna Cancer and Thrombosis Study, regionally advanced and distant cancers carried hazard ratios of 3.7 and 5.4 for VTE compared with localised cancers, and high-grade tumours (G3 or G4) carried twice the risk of low-grade tumours. A meta-analysis of common cancers reported first VTE rates of 68 per 1000 person-years in high-risk patients (high-grade or metastatic disease, or high-risk treatment) versus 13 per 1000 person-years in lower-risk patients. ^{[4] [1]}

Cancer surgery adds a further surge. In a meta-analysis of about 1.5 million patients who had oncologic surgery, the overall postoperative VTE incidence was 2.3%, with the highest rates in bone and soft tissue cancer (10.6%) and lung cancer (8.1%). VTE risk after any cancer surgery also rises with prolonged immobility and delayed postoperative mobilisation. ^[4]

The three elements of Virchow's triad explain most cancer VTE.

• Endothelial injury. Tumour invasion of vessels, surgery, radiation, central venous catheters and the cytotoxic effects of chemotherapy damage the endothelium and expose subendothelial tissue factor.
• Stasis. Hospitalisation, surgery, bed rest, reduced mobility and compression of veins by tumour slow venous return.
• Hypercoagulability. Cancer cells and their inflammatory environment release tissue factor and pro-inflammatory cytokines; platelet and leucocyte counts rise; natural anticoagulants may be consumed.

These influences are not independent. A patient with metastatic pancreatic cancer receiving gemcitabine through a central line and lying in bed after surgery has several operating at once, which is why risk rises multiplicatively rather than additively. ^[4]

Metastatic and poorly differentiated tumours generate more tissue factor and mucins than localised, well-differentiated disease. Pancreatic, gastric, lung, ovarian, brain and high-grade haematological cancers are the highest-risk types in most series, and advanced stage increases risk several-fold. VTE risk is concentrated in the period after diagnosis and during active treatment, varying by cancer type. ^[4]

• Chemotherapy raises VTE risk substantially (one population study estimated an odds ratio of 6.5 with chemotherapy versus 4.1 in patients with cancer not receiving chemotherapy).
• Hormonal therapy, especially tamoxifen combined with chemotherapy, is thrombogenic, predominantly in the first 2 years.
• Anti-angiogenic and immunomodulatory agents (thalidomide, lenalidomide, pomalidomide with steroids) are strongly thrombogenic in myeloma.
• Erythropoiesis-stimulating agents increase VTE (relative risk 1.75) and are a component of the Khorana score. ^[4]
• Cancer surgery, particularly major abdominal and pelvic surgery, confers a high but time-limited risk.
• Central venous catheters create catheter-related thrombosis, most often in the subclavian or brachiocephalic veins.
• Hospitalisation and acute medical illness act on top of the cancer.

Older age, prior VTE, family history, hereditary thrombophilia (factor V Leiden, protein C, protein S or antithrombin deficiency, prothrombin gene mutation), obesity (body mass index 35 kg per m2 or more), underweight, varicose veins, comorbidities (heart, lung, renal disease), smoking and prolonged immobility each add risk. ^[4]

Raised white cell and platelet counts, low haemoglobin, raised D-dimer, soluble P-selectin and factor VIII are all associated with higher VTE risk in cancer and form the basis of several risk scores. ^[4]

Cancer tissue factor activates factor VII and drives thrombin generation directly. Inflammatory cytokines upregulate endothelial adhesion molecules, so leucocytes and platelets aggregate on damaged endothelium. Turnover of mucin-secreting tumours can activate P-selectin and generate platelet-rich microthrombi, explaining why pancreatic and gastric cancers are particularly thrombogenic. Chemotherapy causes endothelial damage and transient falls in natural anticoagulants. The result is a venous thrombus that forms in the valve pockets of the deep veins, grows by platelet and fibrin accretion, and can fragment to produce pulmonary embolism. A thrombus on a central venous catheter forms where the catheter injures the vessel wall and alters flow. ^[1][4]

The Khorana score is the best-known and most widely validated model for selecting ambulatory patients with cancer for primary prophylaxis. Five parameters are scored, each as 1 point except site of cancer, which counts as 2 for very high-risk tumours and 1 for high-risk tumours.

Maximum score is 6. A score of 0 indicates low VTE risk (symptomatic VTE risk 0.3 to 1.5%), 1 to 2 indicates intermediate risk (1.8 to 4.8%), and 3 or more indicates high risk (6.7 to 12.9%). ^[4]

The score is calculated once, before starting chemotherapy, and it was validated in patients starting systemic treatment. Although the original validation defined high risk as 3 or more, the CASSINI and AVERT prophylaxis trials used a cut-off of 2 or more because the 6-month cumulative incidence of VTE in patients with a score of 2 was nearly 10%, which is high enough to justify prophylaxis. Current American Society of Clinical Oncology (ASCO) guidance and the ITAC guidelines therefore use a Khorana score of 2 or more to identify ambulatory patients at intermediate-to-high VTE risk. ^[1][4]

The Khorana score is a baseline screen. On its own it misses some high-risk patients and labels some low-risk ones incorrectly, so several refined models exist.

• Vienna CATS score: adds D-dimer (above 1.44 microg per L) and soluble P-selectin (above 53.1 ng per L) to Khorana variables, improving discrimination but needing assay availability. ^[4]
• PROTECHT score: replaces body mass index with platinum-based and gemcitabine chemotherapy.
• CONKO score: replaces body mass index with World Health Organisation performance status of 2 or more.
• COMPASS-CAT score: for ambulatory patients with common solid tumours; low or intermediate risk is 0 to 6 and high risk is 7 or more, using cancer type, stage, time since diagnosis, central venous catheter, cardiovascular risk factors, recent hospitalisation, prior VTE and platelet count. ^[4]

A simplified D-dimer and tumour-site model has also been proposed for solid tumours, using a 6-month prediction window. In practice, the Khorana score is still the most widely recommended because every component is routinely available before chemotherapy. ^[4]

The clinical picture of cancer-associated VTE is the picture of VTE, complicated by cancer.

• Deep vein thrombosis presents as a swollen, painful, warm, tender leg, often unilateral. Many DVTs in patients with cancer are clinically silent.
• Pulmonary embolism presents with breathlessness, pleuritic chest pain, tachypnoea, hypoxia or haemoptysis; massive PE presents with syncope, hypotension and cardiac arrest.
• Catheter-related thrombosis presents with arm, neck or facial swelling, discomfort and visible collateral veins on the affected side, often with an indwelling catheter.

Three situations are especially common in cancer and are worth recognising.

1. Incidental VTE. A thrombus found on a staging CT, PET-CT or ultrasound that was done for cancer rather than for symptoms. Incidental VTE has the same outcome as symptomatic VTE and is managed the same way. ^[1]
2. Recurrent thrombosis on anticoagulation. Often the first sign of progression of the underlying tumour or of poor adherence.

For general DVT diagnosis and anticoagulation (Wells score, D-dimer, compression duplex ultrasound, DOAC dosing, post-thrombotic syndrome), see the cardiology deep vein thrombosis topic. The same diagnostic pathway applies to patients with cancer; the differences are in risk factors, treatment choice and duration. ^[1][3]

The approach is the same as for any suspected VTE, with attention to features that are more common in cancer:

• Clinical assessment of symptoms, risk factors and differential diagnoses (cellulitis, superficial thrombophlebitis, muscle injury, Baker's cyst, lymphoedema). See the cardiology deep vein thrombosis topic for a full differential diagnosis table.
• Wells score for DVT or PE, in which active cancer counts as a major item. ^[3]
• D-dimer as an exclusion test in low-probability patients; it is less specific in cancer because malignancy, chemotherapy and infection raise it.
• Compression duplex ultrasound of the proximal leg veins to confirm or exclude DVT; distal (calf) vein studies where available.
• CT pulmonary angiography (or ventilation-perfusion scanning where appropriate) for suspected PE.
• Incidental VTE should be confirmed and characterised: its site, whether it is proximal or distal, symptomatic or not.
• Baseline blood tests, including full blood count, renal and hepatic function and coagulation profile, before starting therapeutic anticoagulation. ^[3]

There is no separate staging system for cancer VTE. Three judgments decide management:

1. Provoked or unprovoked, by cancer. In cancer-associated VTE the cancer is the persistent provoking factor; this is what drives a longer initial treatment course and extended anticoagulation in many patients. ^[3]
2. Risk of recurrence against risk of bleeding. The ITAC and NICE guidelines use cancer type, activity of disease, renal function, drug interactions, thrombocytopenia and bleeding history.
3. Modified Ottawa score of 1 or more identifies patients with cancer and VTE at high risk of recurrence, based on data from trials such as CASTA-DIVA; these patients were the target of high-intensity or alternative-regimen studies. ^[1]

Patients with unprovoked VTE and no known cancer should not have extensive cancer screening; history, examination and baseline tests are appropriate, and further investigation is reserved for relevant symptoms or signs. ^[3]

When VTE is confirmed in a patient with cancer, start therapeutic anticoagulation promptly unless there is a contraindication. Add leg elevation, analgesia and graduated compression for symptom relief, and mobilise as pain allows.

Specific emergencies:

• Haemodynamically unstable PE: continuous unfractionated heparin infusion and consider systemic thrombolysis. ^[3]
• Limb-threatening (phlegmasia) iliofemoral DVT: thrombolysis or thrombectomy may be needed on top of anticoagulation; escalation is a specialist decision.
• Contraindication to anticoagulation (active major bleeding, recent neurosurgery, brain metastases with haemorrhage): consider an inferior vena cava filter, with a plan to start anticoagulation as soon as it is safe. ^[1]

Warfarin was the historical standard after an initial heparin, but LMWH monotherapy replaced it because of better efficacy without more bleeding. Since 2016, direct oral anticoagulants have become first-line options for many patients with cancer. ^[1]

Key treatment statements, with their strength where given:

• Initial treatment: LMWH is recommended for the first up to 10 days when creatinine clearance is 30 mL per min or more (grade 1A). Rivaroxaban or apixaban for the first 10 days, or edoxaban after at least 5 days of parenteral anticoagulation, can also be used when there is no high risk of gastrointestinal or genitourinary bleeding (grade 1A). Unfractionated heparin (grade 2C) and fondaparinux (grade 2D) are alternatives. ^[1]
• Maintenance: LMWH or a direct oral anticoagulant for a minimum of 6 months (grade 1A). Direct oral agents are recommended in the absence of strong drug-drug interactions, impaired gastrointestinal absorption or high bleeding risk (grade 1A). Use caution, and expect more gastrointestinal bleeding, with edoxaban or rivaroxaban in upper gastrointestinal tract malignancies. ^[1]
• Maximum conventional course studied: new trial and cohort data have supported LMWH or direct oral anticoagulant treatment for up to 12 months for cancer VTE. ^[1]
• After 6 months: continue, stop or change anticoagulation based on an individual assessment of benefit and risk, tolerability, drug availability, patient preference and cancer activity, because no data settle the question. ^[1]
• Active cancer, confirmed proximal DVT or PE (NICE): anticoagulation for 3 to 6 months, reviewed at 3 to 6 months; consider a direct oral anticoagulant, and if one is unsuitable use LMWH alone or with a vitamin K antagonist. ^[3]
• Recurrent VTE on treatment: three options can be considered: (1) increase LMWH by 20 to 25%, or switch to a direct oral anticoagulant; (2) when on a direct oral anticoagulant, switch to LMWH; (3) when on a vitamin K antagonist, switch to LMWH or a direct oral anticoagulant. The decision is individual and effect is monitored by symptom improvement. ^[1]
• Thrombolysis: only case by case, with expert advice and careful attention to bleeding risk such as brain metastasis. ^[1]
• IVC filters: might be considered when anticoagulation is contraindicated, or in PE recurring despite optimal anticoagulation (grade supported by very-low-quality evidence), with periodic reassessment and resumption of anticoagulation when safe. ^[1]

Catheter-related thrombosis has its own rules: anticoagulate for a minimum of 3 months and for as long as the catheter remains. The catheter can stay in place if it is functional, well positioned and not infected, with symptom resolution on close surveillance. There is no standard approach to duration beyond this. ^[1]

Patients with cancer on cancer-modifying treatment (radiotherapy, chemotherapy, immunotherapy) who are mobile should not receive routine prophylaxis unless another VTE risk factor is present, because the bleeding risk then outweighs the benefit. ^[2]

The patients who should receive prophylaxis when hospitalised are:

• Patients with cancer and reduced mobility admitted to hospital: prophylaxis with LMWH or fondaparinux if creatinine clearance is 30 mL per min or more, or unfractionated heparin otherwise (grade 1B in the ITAC guideline). Direct oral anticoagulants are not recommended routinely in this setting. ^[1][2]
• Myeloma treated with thalidomide, pomalidomide or lenalidomide plus steroids: consider aspirin (75 mg or 150 mg daily) or LMWH. ^[2]
• Pancreatic cancer receiving chemotherapy: consider LMWH. ^[2]
• If prophylaxis is started, continue it for as long as chemotherapy continues. ^[2]

General hospital measures apply to every patient: risk assessment with a validated national tool, reassessment when the clinical condition changes, mobilisation as soon as possible, adequate hydration, and re-assessing at every consultant review. Hospital prophylaxis should start as soon as possible and within 14 hours of a decision to admit. ^[2]

Surgery is the clearest indication for prophylaxis in cancer. The 2022 ITAC recommendations (unchanged since 2019) are:

• LMWH once daily (if creatinine clearance is 30 mL per min or more) or low-dose unfractionated heparin three times daily to prevent postoperative VTE (grade 1A). There is no evidence that one LMWH is superior to another. ^[1]
• Start pharmacological prophylaxis 2 to 12 hours before operation and continue for at least 7 to 10 days. ^[1]
• Use the highest prophylactic dose of LMWH (grade 1A). ^[1]
• There is insufficient evidence for fondaparinux (grade 2C) or direct oral anticoagulants (grade 2B) in place of LMWH for postoperative cancer prophylaxis. Apixaban 2.5 mg twice daily has been compared with enoxaparin 40 mg daily for 28 days in a small randomised trial, with similar VTE and bleeding rates. ^[1]
• Extended prophylaxis for 4 weeks with LMWH after major abdominal or pelvic surgery (laparotomy or laparoscopy) in patients with cancer who do not have a high risk of bleeding (grade 1A). A meta-analysis of 18 studies (7495 patients) showed a reduced risk of symptomatic VTE (1.0% versus 2.0%) without increased clinically relevant non-major bleeding. NICE describes the same approach as 28 days postoperatively after major cancer surgery in the abdomen. ^{[1] [2]}
• Preoperative prophylaxis reduces postoperative VTE (odds ratio 0.59 in a meta-analysis of gynaecological and gynaecological cancer surgery) without increased bleeding. ^[1]
• Mechanical methods (intermittent pneumatic compression, graduated compression stockings) are not recommended as monotherapy except when pharmacological prophylaxis is contraindicated. Combining intermittent pneumatic compression with LMWH may be best for VTE prevention in major abdominopelvic surgery. ^[1]
• Inferior vena cava filters are not recommended for routine prophylaxis. ^[1][2]

Routine primary prophylaxis for all ambulatory patients with cancer is not recommended, because unselected populations have low absolute VTE rates and an uncertain benefit-risk balance. ^[1][4]

Prophylaxis is offered to selected high-risk ambulatory patients:

• Locally advanced or metastatic pancreatic cancer on systemic anticancer therapy with a low bleeding risk: LMWH (grade 1A) or a direct oral anticoagulant, rivaroxaban or apixaban (grade 1B). In a meta-analysis of five trials, thromboprophylaxis cut the VTE rate by 69% (relative risk 0.31, 95% confidence interval 0.19 to 0.51) without excess bleeding. ^[1]
• Any ambulatory patient on systemic anticancer therapy who is at intermediate-to-high VTE risk identified by a validated risk assessment model, meaning a Khorana score of 2 or more, and who is not actively bleeding and not at high bleeding risk: a direct oral anticoagulant, rivaroxaban or apixaban (grade 1B). ^[1]
• Multiple myeloma on immunomodulatory drugs (thalidomide, lenalidomide, pomalidomide) with steroids or other systemic therapy: consider aspirin 100 mg daily, prophylactic LMWH, or a vitamin K antagonist or apixaban at prophylactic doses; these have shown similar effectiveness for VTE prevention. ^[1]
• Low-risk (by Khorana score) patients with lung cancer: LMWH prophylaxis is not recommended outside a clinical trial, because the benefit is offset by bleeding risk. ^[1]

The evidence base is two phase 3 trials. CASSINI randomised 841 patients with a Khorana score of 2 or more to rivaroxaban 10 mg once daily or placebo for up to 6 months; VTE or VTE-related death occurred in 6.0% versus 8.8% (hazard ratio 0.66, p = 0.10) in the intention-to-treat analysis, but 2.6% versus 6.4% in the on-treatment analysis. AVERT randomised 574 patients with a Khorana score of 2 or more to apixaban 2.5 mg twice daily or placebo; VTE occurred in 4.2% versus 10.2% (hazard ratio 0.41, p less than 0.001). Major bleeding rates were low in both trials. ^[4]

A pooled meta-analysis of six trials (4626 patients) found that primary thromboprophylaxis reduced VTE by 55% in patients with a Khorana score of 3 or more and by 42% in those with a score of 2 or more, without increased major bleeding. Earlier LMWH studies in mixed cancer populations also showed about a 50% relative reduction in VTE. ^[1][4]

Routine anticoagulation to prevent catheter-related thrombosis is not recommended. Good catheter practice is the prophylaxis: insert on the right side in the jugular vein, with the catheter tip at the junction of the superior vena cava and right atrium (grade 1B), and prefer implanted ports over peripherally inserted central catheter lines. ^[1]

• Recurrent thrombosis, often the first sign of cancer progression.
• Bleeding on anticoagulation. In the CARAVAGGIO trial, major bleeding was similar at 6 months on apixaban (3.8%) and dalteparin (4.0%), but one meta-analysis of gastrointestinal cancers showed a higher risk of major bleeding on direct oral anticoagulants than on LMWH (relative risk 2.3). LMWH versus direct oral anticoagulant meta-analyses overall showed no increase in major bleeding (relative risk 1.31, 95% confidence interval 0.83 to 2.08) with a significant increase in clinically relevant non-major bleeding. ^[1]
• Post-thrombotic syndrome after DVT, a chronic painful swollen leg with possible ulceration. Graduated compression stockings do not prevent it; symptomatic use is acceptable. ^[3]
• Chronic thromboembolic pulmonary hypertension after PE.
• Treatment failure (recurrence despite anticoagulation): check adherence, address other sources of hypercoagulability, then increase the dose or change drug class. ^[1][3]

Overall, cancer-associated VTE is a marker of a more aggressive disease: the malignancy itself remains the main determinant of survival.

• Renal impairment. ITAC recommends LMWH and direct oral anticoagulants when creatinine clearance is 30 mL per min or more; unfractionated heparin or dose-adjusted regimens are used below this. NICE allows apixaban or rivaroxaban with creatinine clearance 15 to 50 mL per min, with dose adjustment, and LMWH or unfractionated heparin with creatinine clearance under 15 mL per min. ^[1][3]
• Extremes of body weight (under 50 kg or over 120 kg): use therapeutic-level monitoring to ensure adequate anticoagulation. ^[3]
• Drug interactions. Check every direct oral anticoagulant against the cancer regimen; strong interactions with CYP3A4 or P-glycoprotein inducers or inhibitors (for example many kinase inhibitors, anticonvulsants, antifungals) can make a direct oral agent unsuitable, in which case LMWH is preferred. ^[1][3]
• Upper gastrointestinal cancers. Expect higher gastrointestinal bleeding risk with rivaroxaban and edoxaban; choose LMWH or apixaban, or address prophylaxis without these agents. ^[1]
• Thrombocytopenia. Severe thrombocytopenia is common in haematological malignancies and during chemotherapy; hold or reduce anticoagulation and seek haematology advice when platelets are very low. Specific thresholds are not stated in the guidelines cited here. ^[1]
• Pregnancy and breastfeeding. Use LMWH or unfractionated heparin; direct oral anticoagulants and warfarin are contraindicated. Treatment duration is decided with haematology and obstetrics on an individual basis. ^[3]
• Older adults. Higher VTE and bleeding risks with age; frailty and falls matter more than the thrombosis risk score alone.

• Risk assessment and D-dimer, plus compression duplex ultrasound of the proximal veins where available, make the diagnosis. Where ultrasound is unavailable and probability is high, weigh the harm of missing VTE against treatment risk.
• Unfractionated heparin by infusion or a monitored subcutaneous regimen is cheap and reversible, and is a legitimate alternative to LMWH or direct oral agents. Warfarin is inexpensive and effective where INR testing and patient education are available. ^[1][2]
• Khorana score and clinical judgement remain the simplest way to identify outpatients who may benefit from prophylaxis.
• Catheter care: right internal jugular placement and careful attention to asepsis prevent more thromboses than drugs do.
• Basic measures available everywhere are mobilisation, hydration, leg elevation, analgesia and avoidance of central lines when peripheral access suffices.

• Active cancer raises VTE risk four- to seven-fold, via endothelial injury, stasis and cancer-driven hypercoagulability. ^[4]
• High-risk tumours are pancreatic, gastric, lung, ovarian, brain and high-grade haematological cancers, especially when advanced or metastatic.
• Incidence ranges from 2.7 to 7.0 per 100 person-years in lower-risk cancers to 10.1 to 14.6 in lung, stomach, ovarian, pancreatic and brain cancers. ^[4]
• Khorana score of 0 is low risk, 1 to 2 intermediate and 3 or more high risk; guidelines use 2 or more for prophylaxis decisions in outpatients on systemic therapy. ^[1][4]
• Incidental VTE is managed like symptomatic VTE. ^[1]
• Initial treatment: therapeutic anticoagulation with LMWH or a direct oral anticoagulant (apixaban, rivaroxaban or edoxaban); LMWH 1 mg per kg twice daily (enoxaparin) if a twice-daily regimen is required; apixaban 10 mg twice daily for 7 days then 5 mg twice daily; rivaroxaban 15 mg twice daily for 21 days then 20 mg once daily; edoxaban after at least 5 days of parenteral therapy. ^[1]
• Minimum treatment duration is 6 months; extend based on cancer activity, bleeding risk, tolerability and patient preference. ^[1][3]
• Hospitalised patients with cancer and reduced mobility receive LMWH or fondaparinux if creatinine clearance is 30 mL per min or more, or unfractionated heparin; mobile patients on cancer treatment generally do not. ^[1][2]
• After major cancer surgery in the abdomen or pelvis, give 4 weeks (28 days) of LMWH to patients without a high bleeding risk. ^[1][2]
• Ambulatory patients with a Khorana score of 2 or more on systemic anticancer therapy, and patients with pancreatic cancer with a low bleeding risk, are candidates for prophylaxis with LMWH or a direct oral anticoagulant. ^[1]
• Myeloma on immunomodulatory drugs plus steroids is prophylaxed with aspirin, LMWH or a vitamin K antagonist or prophylactic apixaban. ^[1][2]
• Catheter-related thrombosis is treated for at least 3 months and routine prophylaxis is not recommended; good insertion technique is the prevention. ^[1]

• Cardiology: deep vein thrombosis and pulmonary embolism - for general diagnosis, Wells scoring, imaging and anticoagulation duration.
• Cardiology: anticoagulant and antithrombotic drugs - for dosing, renal adjustment, reversal and monitoring details.
• Haematology-oncology topics on individual malignancies - for tumour-specific VTE risk and chemotherapy regimens.
• Surgery and perioperative care - for thromboprophylaxis after cancer surgery and mechanical methods.