Venous Thromboembolism: Deep Vein Thrombosis and Pulmonary Embolism

Venous thromboembolism includes deep vein thrombosis and pulmonary embolism. A clot usually forms in a deep vein and can travel to the lungs, where it may obstruct blood flow and strain the heart. Symptoms alone cannot confirm or exclude VTE, so clinical probability tools and objective testing guide safe diagnosis.

What venous thromboembolism means Venous thromboembolism, usually shortened to VTE, is the collective term for deep vein thrombosis and pulmonary embolism. A deep vein thrombosis, or DVT, is a blood clot within a deep vein, most often in a leg or pelvis. A pulmonary embolism, or PE, occurs when clot material travels through the right side of the heart and lodges within a pulmonary artery. These are different parts of the same disease process. A person can have DVT without recognised PE, PE without obvious leg symptoms, or both at the same time. VTE can be fatal when missed, but unnecessary imaging and anticoagulation also cause harm. Safe care combines clinical probability assessment with objective testing rather than relying on symptoms alone. How blood normally remains fluid Blood must remain fluid while circulating but clot rapidly after vessel injury. The vessel lining, platelets, clotting proteins and natural anticoagulant systems continuously balance these opposing needs. Venous clots are rich in fibrin and trapped red cells. They often develop where blood flow is slow and the coagulation system is activated. A clot is not simply thick blood. It is an organised biological response occurring in a particular vessel and clinical setting. Virchow's triad Virchow's triad is the classic framework explaining why venous clots form. The three components are venous stasis, injury or activation of the vessel lining, and hypercoagulability. A person may have one dominant factor, but several usually interact. Major surgery can cause immobility, tissue injury and a temporary increase in coagulation activity at the same time. The framework helps clinicians recognise risk without implying that every exposed person will develop a clot. Venous stasis Venous stasis means that blood is moving more slowly than usual through a vein. Walking and calf muscle contraction normally help return leg blood towards the heart. Bed rest, paralysis, a plaster cast, prolonged sitting and severe illness reduce this pumping effect. Slow flow allows activated clotting factors to accumulate and gives blood cells more opportunity to interact with the vein wall. Stasis alone may not be enough, but it becomes important when combined with inflammation, cancer, pregnancy or another prothrombotic state. Endothelial injury or activation The endothelium is the inner lining of blood vessels. Healthy endothelium discourages inappropriate clotting. Surgery, trauma, central venous catheters and inflammation can injure or activate this lining. Activated endothelial cells express signals that recruit platelets, white cells and clotting proteins. Venous thrombosis often involves biochemical activation rather than a visible tear in the vein. Hypercoagulability Hypercoagulability means that the balance of haemostasis is shifted towards clot formation. Cancer, pregnancy, oestrogen exposure, inflammation and some inherited conditions can increase procoagulant activity or reduce natural anticoagulant pathways. Antiphospholipid syndrome is an acquired autoimmune thrombophilia that can cause venous and arterial thrombosis. Hypercoagulability raises risk but does not confirm that a current symptom is caused by VTE. Where DVT develops DVT commonly develops in the deep veins of the calf, thigh or pelvis. A proximal DVT involves the popliteal vein or a more central vein above it. Proximal clots have a greater risk of embolising than isolated distal calf clots. Pelvic and iliac vein thrombosis can cause swelling of most of the leg and may be difficult to visualise on a standard proximal ultrasound. Upper limb DVT can occur, particularly around central venous catheters, pacemaker leads or thoracic outlet compression. How a pulmonary embolus forms Part of a venous clot can detach and travel through larger veins into the right atrium and right ventricle. It then enters the pulmonary arteries, where the vessel becomes too narrow for it to pass. The obstruction reduces blood flow through part of the lung and can increase pressure suddenly within the pulmonary circulation. A large burden can overwhelm the right ventricle, reduce left heart filling and cause shock or cardiac arrest. Risk is cumulative VTE risk rises as risk factors accumulate. An older person with cancer who has major pelvic surgery and then remains immobile has several elements of Virchow's triad. A younger person with no persistent risk may still develop VTE after a strong temporary exposure such as major trauma or pregnancy. Risk assessment considers the complete situation rather than counting one factor in isolation. Previous VTE A previous DVT or PE is one of the strongest predictors of another event. Risk is influenced by whether the first event was provoked by a temporary factor, was unprovoked or occurred with a persistent condition such as active cancer. Previous recurrence, residual risk factors and the bleeding risk of long term anticoagulation affect prevention planning. New symptoms still require objective assessment because post thrombotic symptoms can mimic recurrence. Immobility and hospital admission Acute illness and reduced mobility are major VTE risks. Hospital admission often combines bed rest, infection, dehydration, inflammation, invasive devices and surgery. NICE recommends formal assessment of VTE and bleeding risk for hospital patients and reassessment when the clinical condition changes. Prophylaxis is offered when the expected reduction in thrombosis outweighs the bleeding risk. Surgery and trauma Major surgery activates coagulation and commonly reduces mobility. Orthopaedic, abdominal, pelvic and cancer surgery can create particularly important risk. Trauma, fractures and lower limb immobilisation add tissue injury and stasis. The procedure type, anaesthetic duration, mobility, cancer status and bleeding risk determine the prophylaxis plan and duration. Cancer Cancer can activate coagulation directly through tumour and inflammatory pathways. Surgery, chemotherapy, hormonal treatment, central lines and reduced mobility can add further risk. Some cancers, including pancreatic, gastric, lung, brain, ovarian and haematological malignancies, are especially thrombogenic, although any active cancer can be relevant. Anticoagulant choice considers tumour site, gastrointestinal or genitourinary bleeding risk, kidney function and medicine interactions. Pregnancy and the postnatal period Pregnancy increases clotting tendency, slows venous return from the legs and can compress pelvic veins. Risk rises further with previous VTE, thrombophilia, obesity, immobility, severe infection, caesarean birth and major obstetric complications. The risk remains increased after birth, especially during the first six weeks. Pregnancy specific assessment and treatment are required because symptoms, tests, imaging choices and anticoagulant safety differ from non pregnant care. Oestrogen containing medicines Combined hormonal contraception and oral oestrogen containing hormone replacement therapy increase VTE risk. The absolute risk for an individual depends on age, body weight, smoking, family history, previous VTE and other conditions. Progestogen only contraception usually has a different and generally lower thrombosis profile than combined oestrogen methods. A person with suspected VTE should tell clinicians about contraception, HRT, fertility treatment and gender affirming hormones without stopping essential treatment before receiving advice unless emergency clinicians direct otherwise. Long distance travel Prolonged travel can reduce leg movement and contribute to venous stasis. Risk is greater during journeys lasting several hours when another factor such as previous VTE, recent surgery, pregnancy, cancer or marked immobility is present. Regular movement, calf exercises, comfortable clothing and normal hydration are sensible measures. Aspirin is not a substitute for appropriate anticoagulant prophylaxis. High risk travellers should obtain individual advice about stockings or anticoagulation. Body weight and lifestyle factors Obesity is associated with higher VTE risk through inflammation, venous stasis and accompanying illness. Smoking may add vascular and inflammatory risk and often coexists with cancer, heart or lung disease. Weight or smoking status must not be used to dismiss symptoms or assign blame. Risk reduction focuses on feasible activity, smoking support and management of the full clinical context. Inherited thrombophilia Inherited thrombophilias include factor V Leiden, the prothrombin gene variant and deficiencies of antithrombin, protein C or protein S. Their effects vary substantially. Some are common with modest risk, while antithrombin deficiency can carry greater familial risk. A positive test does not prove that current symptoms are VTE and does not automatically mean lifelong anticoagulation. Testing is selective because anticoagulants, pregnancy and acute thrombosis can distort results and because many results do not change management. Antiphospholipid syndrome Antiphospholipid syndrome, or APS, is an acquired autoimmune thrombophilia associated with thrombosis and selected pregnancy complications. Diagnosis requires an appropriate clinical event and persistent laboratory antibodies on repeat testing at the required interval. Triple positive APS means that lupus anticoagulant, anticardiolipin and anti beta 2 glycoprotein I tests are all positive. Warfarin is generally preferred after thrombosis in high risk APS because DOACs have been associated with more recurrent events in this group. Typical DVT symptoms DVT can cause unilateral leg swelling, pain, tenderness, warmth and colour change. The calf or thigh may feel tight or heavy, and superficial veins can become more visible. Symptoms can develop gradually or over several hours. A pelvic clot may cause swelling of the entire leg. Some DVTs cause few or no symptoms, and many painful swollen legs have another cause. DVT is not diagnosed from appearance alone Cellulitis, a ruptured Baker's cyst, muscle injury, superficial thrombophlebitis, lymphoedema and chronic venous disease can resemble DVT. Heart, kidney or liver disease can cause bilateral swelling. Clinical examination estimates probability and identifies alternative diagnoses, but it cannot safely confirm or exclude DVT. Objective testing prevents both missed thrombosis and unnecessary anticoagulation. The two level DVT Wells score NICE recommends the two level DVT Wells score when DVT is suspected. The score combines findings such as active cancer, recent immobility or surgery, deep vein tenderness, unilateral swelling and previous DVT. It subtracts points when another diagnosis is at least as likely. A score of 2 or more means DVT is likely. A score of 1 or less means DVT is unlikely. The score does not diagnose DVT and should be used only within the validated pathway. D dimer D dimer is a fragment produced when cross linked fibrin is broken down. A sensitive negative D dimer can help exclude VTE when the pre test clinical probability is low or unlikely. A positive result does not rule VTE in. D dimer rises with age, pregnancy, infection, inflammation, cancer, surgery, trauma and many other conditions. Its value comes from combining high sensitivity with an appropriate probability assessment, not from treating the number as a clot measurement. Age adjusted D dimer D dimer levels rise with age, making false positive results more common in older adults. NICE advises considering an age adjusted threshold in people over 50. The laboratory method and local pathway determine the exact interpretation. Age adjustment should not be used to dismiss a high probability presentation or replace imaging when the pathway requires it. Compression ultrasound Proximal leg vein ultrasound assesses whether deep veins compress normally under gentle probe pressure. A vein containing acute thrombus may not collapse. Doppler techniques also assess flow where needed. For likely DVT, NICE recommends proximal ultrasound with the result available within four hours if possible. If imaging is delayed, interim therapeutic anticoagulation may be given after clinical assessment while ultrasound is arranged within 24 hours. Why a repeat ultrasound may be needed A first proximal ultrasound can be negative when a clot is confined to the calf or is too early to detect proximally. When the ultrasound is negative but D dimer is positive in the NICE likely DVT pathway, a repeat proximal scan is offered six to eight days later. The repeat looks for extension into the proximal veins. New or worsening symptoms before the planned scan require earlier reassessment. Distal DVT An isolated distal DVT is confined to calf veins below the popliteal vein. Some distal clots resolve without extension, while others propagate and can embolise. Management varies according to symptoms, clot extent, provoking factors, cancer, previous VTE and bleeding risk. A specialist or local protocol decides between anticoagulation and structured ultrasound surveillance where this distinction has been established. Iliofemoral DVT Iliofemoral DVT affects the iliac or common femoral venous pathway and can obstruct a large proportion of leg drainage. It may cause severe whole leg swelling, pain and cyanotic colour change. Selected people with recent symptoms, good functional status, reasonable life expectancy and low bleeding risk may be considered for catheter directed thrombolysis. Most people still require anticoagulation, and invasive treatment is not routine for every proximal DVT. Phlegmasia Phlegmasia is an uncommon extreme form of extensive venous obstruction. The leg becomes massively swollen and painful and may appear blue or pale. Arterial inflow can become compromised. This threatens the limb and can cause shock or venous gangrene. Immediate vascular and thrombosis specialist assessment is required rather than waiting for an ordinary outpatient ultrasound pathway. Typical pulmonary embolism symptoms PE can cause sudden or progressive breathlessness, pleuritic chest pain, coughing blood and a rapid heart rate. Pleuritic pain is sharp and worsens with a deep breath or cough. Other presentations include faintness, collapse, unexplained low oxygen, new atrial arrhythmia or worsening heart failure. A small PE may cause mild symptoms, while a large PE can present with cardiac arrest. PE symptoms are not specific Pneumonia, pneumothorax, acute coronary syndrome, aortic dissection, pericarditis, asthma and musculoskeletal pain can resemble PE. Anxiety and panic can cause breathlessness and tachycardia, but they should not be assumed until dangerous causes have been considered. A normal chest examination, normal oxygen saturation or absence of leg symptoms does not exclude PE. Equally, breathlessness and a positive D dimer do not confirm PE without imaging or another objective diagnosis. The PERC rule When overall clinical suspicion is genuinely low and other diagnoses are feasible, NICE advises considering the pulmonary embolism rule out criteria, known as PERC. PERC uses eight features to identify a very low risk group in whom further PE testing may be unnecessary. It should not be applied after deciding that PE is likely, and it is not a self assessment checklist. Using it outside a low risk clinical setting can miss VTE. The two level PE Wells score When PE is suspected, NICE recommends the two level PE Wells score. It includes clinical DVT signs, whether an alternative diagnosis is less likely, tachycardia, recent surgery or immobilisation, previous VTE, haemoptysis and malignancy. A score above 4 means PE is likely. A score of 4 or less means PE is unlikely. The score guides the next test and does not measure PE severity after the diagnosis is confirmed. The PE diagnostic pathway A person with likely PE usually proceeds directly to computed tomography pulmonary angiography, known as CTPA. If imaging cannot be performed immediately, interim therapeutic anticoagulation is offered when safe. A person with unlikely PE usually has a D dimer first. A negative result can exclude PE within the pathway, while a positive result leads to imaging. Skipping probability assessment leads to avoidable scans, incidental findings and false positive diagnoses. Computed tomography pulmonary angiography CTPA uses intravenous iodine based contrast and timed CT imaging to show pulmonary arteries. It can identify filling defects caused by emboli and assess alternative chest diagnoses. The scan involves radiation and contrast exposure and can detect small emboli of uncertain clinical importance. Image quality can be limited by movement, poor contrast timing or severe illness, so an indeterminate result requires further clinical planning rather than automatic reassurance. Ventilation perfusion scanning A ventilation perfusion scan compares air entry with blood flow within the lungs. A perfusion defect in a normally ventilated region can support PE. NICE recommends considering V/Q SPECT, or a planar V/Q scan when SPECT is unavailable, for contrast allergy, severe renal impairment or high radiation concern. Pre existing lung disease and an abnormal chest X ray can make results less definitive. Imaging during pregnancy Suspected VTE during pregnancy requires prompt objective testing and specialist maternity involvement. Compression ultrasound is used for suspected DVT. For suspected PE, chest X ray helps choose between CTPA and V/Q imaging according to the local pregnancy pathway. Both approaches involve a small radiation exposure with different maternal and fetal distributions. The risk of missing PE is much greater than the diagnostic radiation risk when imaging is clinically indicated. LMWH is usually started while testing proceeds unless strongly contraindicated. ECG, chest X ray and blood gases An ECG can show sinus tachycardia, right heart strain or another cardiac diagnosis, but a normal ECG does not exclude PE. Chest X ray often appears normal or non specific and mainly helps identify alternatives and guide V/Q suitability. Arterial blood gas can show low oxygen and respiratory alkalosis, but normal gases do not rule out PE. These tests support the assessment and cannot replace the probability and imaging pathway. Cardiac biomarkers Troponin and natriuretic peptides can rise when PE strains the right ventricle. They help assess prognosis after PE has been diagnosed or is strongly suspected. An elevated troponin does not prove that PE caused the chest symptoms because acute coronary syndrome, sepsis and kidney disease can also raise it. Normal biomarkers can support lower risk classification but do not exclude a small PE. Echocardiography Echocardiography can show right ventricular enlargement, reduced function and raised pulmonary pressure. In a haemodynamically unstable person who cannot be moved safely for CTPA, major right heart strain can support immediate emergency PE treatment after other causes are considered. A normal echocardiogram does not exclude PE in a stable person. The test is also used for risk stratification and assessment of persistent breathlessness after treatment. PE severity is not defined by clot size alone The physiological effect of PE depends on embolic burden, previous heart and lung reserve and the response of the right ventricle. A clot described as large on CT may be tolerated by one person, while a smaller burden can destabilise someone with severe cardiopulmonary disease. Severity assessment uses blood pressure, perfusion, oxygenation, right heart function, biomarkers and clinical risk tools. Anatomical wording on the scan should not be interpreted without this context. High risk or massive PE High risk PE is the modern term for PE causing haemodynamic instability. The older term massive PE is still widely used. Features include cardiac arrest, obstructive shock or persistent hypotension not explained by another cause. The right ventricle cannot pump effectively against the sudden pulmonary obstruction, so circulation to the body collapses. This is a medical emergency requiring immediate resuscitation, specialist reperfusion assessment and anticoagulation when appropriate. Intermediate risk or submassive PE Intermediate risk PE describes a person who is not hypotensive but has evidence that the right heart is under strain. The historical term submassive PE is sometimes used. Modern approaches divide intermediate risk further using clinical score, right ventricular imaging and cardiac biomarkers. These patients require close observation because deterioration can occur. Routine systemic thrombolysis is not recommended while haemodynamic stability is maintained because major bleeding risk can outweigh benefit. Low risk PE Some people with confirmed PE have stable observations, no important right heart strain and a low predicted short term complication risk. NICE supports outpatient treatment for carefully selected low risk patients using a validated risk tool and a structured follow up pathway. Suitability also depends on bleeding risk, pain control, oxygen needs, comorbidities, home circumstances, medicine access and ability to seek urgent help. A low risk label does not mean that anticoagulation or follow up is optional. Anticoagulation is the primary treatment Anticoagulants reduce the formation and extension of fibrin clot. They do not instantly dissolve the existing thrombus. The body's own fibrinolytic and healing systems gradually organise or remove it. Treatment lowers the risk of extension, embolisation, recurrence and death. The medicine, dose and duration depend on the clot, kidney and liver function, pregnancy, cancer, APS, body weight, bleeding risk and preference. Interim therapeutic anticoagulation When the diagnostic scan or D dimer result cannot be obtained within the recommended time, NICE advises interim therapeutic anticoagulation in relevant pathways. Baseline full blood count, kidney and liver function, PT and APTT are taken, but treatment is not delayed while waiting for results when immediate anticoagulation is indicated. Results are reviewed within 24 hours and the regimen is adjusted if needed. Interim treatment is stopped if objective testing excludes VTE unless the person has another reason for anticoagulation. Direct acting oral anticoagulants Direct acting oral anticoagulants, shortened to DOACs, inhibit a specific clotting factor. Apixaban and rivaroxaban inhibit factor Xa and can be started without an initial heparin course for most confirmed proximal DVT or PE. NICE offers apixaban or rivaroxaban first for most adults when neither is unsuitable. Dabigatran and edoxaban are alternatives after at least five days of LMWH. DOAC practical safety DOACs have predictable dosing and do not require routine INR monitoring. Their effect falls relatively quickly when doses are missed, so adherence is essential. Kidney function, liver disease, body weight, age and medicine interactions affect choice and dose. People should carry an anticoagulant alert card and tell clinicians, dentists and pharmacists before procedures or new prescriptions. Low molecular weight heparin Low molecular weight heparin, or LMWH, is given by subcutaneous injection. It acts rapidly and is central to treatment during pregnancy and in selected cancer, renal, procedural and inpatient situations. Dose is usually based on body weight and adjusted or monitored in selected extremes of weight, kidney impairment and pregnancy. Bleeding, heparin induced thrombocytopenia and injection site bruising are important safety considerations. Unfractionated heparin Unfractionated heparin is commonly given by continuous intravenous infusion and adjusted using laboratory monitoring. Its short half life and reversibility can be useful in haemodynamic instability, severe renal failure, high bleeding risk or when an urgent procedure is possible. NICE recommends continuous UFH for confirmed PE with haemodynamic instability while thrombolysis is considered. It requires close monitoring and carries a higher heparin induced thrombocytopenia risk than LMWH. Warfarin Warfarin reduces production of vitamin K dependent clotting factors. Its effect develops slowly, so treatment for acute VTE begins with LMWH or UFH overlap for at least five days and until the INR is therapeutic on consecutive readings. Dose is adjusted using the international normalised ratio, or INR. Diet, alcohol, illness and many medicines can alter its effect. Warfarin remains important in triple positive APS, established renal failure and other situations where a DOAC is unsuitable. Anticoagulation in pregnancy LMWH is the standard treatment for acute VTE during pregnancy because it does not cross the placenta. DOACs are avoided because pregnancy safety and efficacy are not established. Warfarin crosses the placenta and can harm the fetus, although it has specialist roles in exceptional circumstances such as some mechanical heart valves. Treatment usually continues through pregnancy and for at least six weeks after birth, with at least three months of treatment in total under the specialist pathway. Timing around labour, regional anaesthesia and delivery requires a written maternity and haematology plan. Anticoagulation during breastfeeding LMWH and warfarin can generally be used during breastfeeding. DOACs are usually avoided because evidence about transfer into breast milk and infant safety is limited or unfavourable for routine use. The postnatal plan considers bleeding, birth complications, kidney function and the intended duration of treatment. A person should not stop anticoagulation to breastfeed without specialist advice. Severe renal impairment Kidneys clear different anticoagulants to different degrees. NICE provides several options when creatinine clearance is between 15 and 50 millilitres per minute, with product specific adjustment and specialist monitoring. In established renal failure below 15 millilitres per minute, LMWH, UFH or heparin followed by warfarin are used according to local expertise. An automatically reported eGFR is not always the value used for anticoagulant dosing. Creatinine clearance and the medicine's prescribing information matter. Antiphospholipid syndrome treatment NICE recommends heparin overlap followed by a vitamin K antagonist for confirmed VTE in triple positive APS. MHRA safety guidance advises that DOACs are not recommended in APS, particularly in high risk triple positive disease, because recurrent thrombosis can be more frequent. Testing can be distorted by acute thrombosis and anticoagulants, so specialist interpretation is needed. Do not change from a DOAC to warfarin or stop treatment independently while awaiting an APS review. Active cancer and anticoagulation People with active cancer and confirmed proximal DVT or PE receive anticoagulation for three to six months initially, followed by review. A DOAC may be suitable, but gastrointestinal or genitourinary tumours, mucosal lesions and medicine interactions can increase bleeding concerns. LMWH remains appropriate for selected people, including those with vomiting, absorption problems, interactions or a high bleeding risk from a particular tumour. Treatment often continues while cancer remains active if recurrence risk outweighs bleeding risk. How long treatment continues NICE recommends at least three months of anticoagulation for confirmed proximal DVT or PE. At three months, the clinician reviews whether the event was provoked or unprovoked, whether risk factors persist and how much bleeding risk treatment creates. The decision is not simply three months for every person or lifelong treatment for every unprovoked event. Preferences, recurrence risk, bleeding history and treatment burden are discussed explicitly. Provoked VTE A provoked VTE occurs after a recent major temporary risk factor such as surgery, trauma, substantial immobility, pregnancy or the puerperium. The recurrence risk is generally lower when the factor has resolved than after an unprovoked event. NICE advises considering stopping anticoagulation after three months when a provoking factor is no longer present and the course has been uncomplicated. Some persistent or minor factors require more individual interpretation than a clearly major transient exposure. Unprovoked VTE An unprovoked VTE has no recent major temporary trigger and is not explained by ongoing hormonal therapy in the NICE definition. Recurrence risk is higher after treatment stops. NICE advises considering anticoagulation beyond three months and explaining that continued treatment is likely to offer net benefit when bleeding risk is low. The decision is reviewed periodically because age, kidney function, falls, cancer, medicines and personal priorities can change. Recurrent VTE A second unprovoked VTE often leads to a recommendation for extended or indefinite anticoagulation when bleeding risk permits. A clot occurring during anticoagulation prompts confirmation of the diagnosis, assessment of adherence, dose, interactions, absorption and underlying hypercoagulability. The specialist may increase the dose or change to an anticoagulant with a different mechanism. Treatment failure should not be assumed from symptoms alone because post thrombotic pain and breathlessness can mimic recurrence. Thrombolysis Thrombolytic medicines activate fibrin breakdown and can dissolve clot more rapidly than anticoagulation alone. Their major limitation is serious bleeding, including intracranial haemorrhage. NICE advises considering systemic thrombolysis for PE with haemodynamic instability. It is not routinely offered for haemodynamically stable PE, even when right ventricular dysfunction is present, unless rescue treatment becomes necessary after deterioration. Catheter and surgical reperfusion Catheter directed therapy delivers thrombolytic medicine or mechanical treatment near the pulmonary clot. Surgical embolectomy removes clot through an operation. These approaches may be considered for life threatening PE when systemic thrombolysis is contraindicated, has failed or is unlikely to be sufficient. Availability and evidence vary, so decisions are made by experienced multidisciplinary teams. Resuscitation and anticoagulation planning continue while reperfusion is arranged. Inferior vena cava filters An inferior vena cava filter is a device placed in the large abdominal vein to catch embolising clot. It does not treat the existing DVT and can itself cause thrombosis or long term device complications. NICE does not recommend routine filters. They are considered when anticoagulation is contraindicated or after confirmed PE during treatment despite addressing anticoagulation failure. A retrieval plan must be documented and the filter removed as soon as safely possible. Bleeding is the main anticoagulant hazard Anticoagulants reduce harmful clotting but also reduce the ability to stop bleeding. Minor bruising or slightly prolonged bleeding can occur, but major bleeding can involve the brain, gastrointestinal tract, urinary tract or internal tissues. Risk rises with previous bleeding, older age, kidney or liver disease, uncontrolled hypertension, alcohol excess, cancer and interacting medicines. Benefit and harm are reassessed rather than assuming that one risk permanently outweighs the other. Medicine interactions and avoidable bleeding NSAIDs such as ibuprofen and naproxen increase gastrointestinal and other bleeding risk with anticoagulants. Aspirin and antiplatelet medicines also increase bleeding and should be combined only for a clear indication. Some antibiotics, antifungals, anti seizure medicines, HIV treatments and herbal products alter anticoagulant levels. Ask a pharmacist or prescriber before starting an over the counter medicine, supplement or new prescription. Reversal of anticoagulation Life threatening bleeding may require stopping the anticoagulant, resuscitation, source control and a reversal strategy. Vitamin K and prothrombin complex concentrate can reverse warfarin in major bleeding. Specific reversal agents exist for dabigatran and selected factor Xa inhibitors, while prothrombin complex concentrate may be used in some pathways. The choice depends on the drug, last dose, kidney function, bleeding site and urgency. A person should not skip doses after minor bruising without advice because stopping treatment can expose them to recurrent PE. Post thrombotic syndrome A DVT can damage venous valves and leave persistent obstruction. Post thrombotic syndrome can cause chronic leg aching, heaviness, swelling, itching, skin discolouration and, in severe cases, venous ulcers. Symptoms can worsen with prolonged standing and improve with elevation or movement. New sudden swelling still requires reassessment because recurrence, cellulitis and other conditions can resemble post thrombotic syndrome. Compression stockings after DVT NICE does not recommend elastic compression stockings routinely to prevent post thrombotic syndrome or VTE recurrence. They may be offered to manage persistent leg swelling or discomfort after DVT when arterial circulation and skin condition permit. Correct measurement, application and replacement are important. Stockings do not replace anticoagulation during acute treatment and should not delay assessment of new symptoms. Chronic thromboembolic pulmonary hypertension A small proportion of people develop persistent organised clot and scarring within pulmonary arteries after PE. This can create chronic thromboembolic pulmonary hypertension, shortened to CTEPH. Symptoms include persistent or progressive exertional breathlessness, reduced stamina, chest discomfort, faintness and signs of right heart failure. It is important because pulmonary endarterectomy, balloon pulmonary angioplasty and specialist medicines can substantially improve selected patients. Persistent symptoms after PE Breathlessness and fatigue can continue for weeks or months after PE because of deconditioning, anxiety, residual vascular obstruction or another heart or lung condition. Persistent symptoms should not be dismissed automatically as expected recovery. Clinical review may include echocardiography, lung imaging, exercise assessment and referral to a pulmonary hypertension centre when CTEPH is suspected. Sudden worsening requires urgent reassessment for recurrent PE or another acute diagnosis. Preventing hospital acquired VTE NICE recommends assessing VTE and bleeding risk promptly after hospital admission and repeating the assessment when the condition changes. Early mobilisation, adequate ordinary hydration and avoiding unnecessary immobilisation are basic measures. Pharmacological prophylaxis commonly uses LMWH when thrombosis risk outweighs bleeding risk. Mechanical prophylaxis uses intermittent pneumatic compression or anti embolism stockings in selected patients and procedures. Mechanical prophylaxis Intermittent pneumatic compression sleeves inflate around the legs and promote venous flow. Anti embolism stockings apply graduated pressure but require correct sizing and regular skin and circulation checks. Mechanical methods are useful when bleeding risk delays anticoagulant prophylaxis or when procedure specific guidance recommends them. They can cause skin damage or be unsuitable with severe peripheral arterial disease, leg wounds or unusual limb anatomy. Pharmacological prophylaxis Prophylactic anticoagulant doses are lower than treatment doses used for confirmed VTE. NICE recommends LMWH first line for many acutely ill medical and surgical patients whose VTE risk exceeds bleeding risk. Fondaparinux or UFH may be used in selected situations. The dose, timing and duration depend on surgery, renal function, body weight, anaesthesia and current bleeding. Pregnancy prevention planning Pregnancy and postnatal VTE prevention uses a structured risk assessment covering previous VTE, thrombophilia, age, body weight, immobility, multiple pregnancy, caesarean birth and complications. LMWH may be recommended during pregnancy, after birth or both. Timing around labour and epidural or spinal anaesthesia must be planned because recent LMWH increases spinal haematoma risk. A pregnant person with a previous VTE should seek preconception or early antenatal specialist review rather than waiting for symptoms. Preventing travel associated VTE During long journeys, move the ankles and legs regularly and walk when safe. Avoid becoming significantly dehydrated, although excessive fluid does not provide extra protection. People at high risk may be advised to wear properly fitted below knee compression stockings or receive anticoagulant prophylaxis. Routine aspirin or anticoagulants are not recommended for low risk travellers because bleeding harm can exceed benefit. Cancer investigation after unprovoked VTE Unprovoked VTE can occasionally be the first sign of cancer. NICE recommends medical history, physical examination and review of baseline blood tests for people without known cancer. Further cancer testing is guided by relevant symptoms or signs rather than routine extensive CT scanning of every person. Age appropriate screening and investigation of concerning features continue through ordinary pathways. When thrombophilia testing helps NICE does not recommend hereditary thrombophilia testing after a provoked VTE or while long term anticoagulation will continue. Antiphospholipid antibody testing can be considered after an unprovoked event if stopping anticoagulation is planned. Hereditary testing can be considered when an unprovoked event and a first degree family history may change the decision to stop treatment. Testing healthy relatives routinely is not recommended because results can create anxiety without improving care. Recovery and activity Once anticoagulation has started and the person is stable, ordinary walking is usually encouraged rather than prolonged bed rest. Activity is increased according to pain, breathlessness and medical advice. Contact sports and activities with high trauma risk require discussion while anticoagulated. Return to work, driving and flying depends on symptoms, treatment stability, the type of work and current regulatory or travel guidance. Follow up Follow up confirms medicine adherence, renal and liver safety, bleeding risk and the intended treatment duration. The clinician reviews whether the event was provoked, whether cancer or APS concerns remain and whether oestrogen containing medicines should change. Persistent leg symptoms, breathlessness or reduced exercise tolerance are assessed for post thrombotic syndrome, CTEPH or another diagnosis. Before anticoagulation stops, the person receives recurrence symptoms and a clear plan for future surgery, pregnancy, immobilisation and travel. The main safety message A painful swollen leg or unexplained chest symptoms can be VTE, but neither can be diagnosed accurately from symptoms alone. Probability tools determine whether D dimer or imaging is the correct next test. D dimer helps rule out VTE in low probability pathways but does not rule it in. Anticoagulation is effective for most confirmed VTE, while haemodynamic instability from PE can require immediate thrombolysis or another reperfusion treatment. Collapse, severe hypoxia, hypotension and major anticoagulant bleeding require emergency care.

VTE develops when venous stasis, vessel wall activation and hypercoagulability combine. Safe diagnosis uses clinical probability plus D dimer or imaging, while treatment balances rapid prevention of clot extension against bleeding risk and the need to address the provoking cause.