Deep Vein Thromobsis is exactly as its name suggests: a clot in the veins. They can occur in any vein, although they are much more likely in the veins of the pelvis and legs. If they occur in other locations (e.g. in the arm) they are often indicative of a more sinister underlying cause (e.g. clotting disorder, carcinoma, or an increased clotting risk of unknown cause) and are more likely to require life-long treatment / prevention. On their own, they are not particularly significant, however, they are dangerous because they can embolise, and cause a pulmonary embolism – these can be fatal.


  • Stasis/immobility – e.g. hospital bed, long flight
  • Dehydration
  • Oestrogen (pregnancy, and to a lesser extent, the COC pill)
  • Genetic clotting defect (e.g. lack of protein C)
  • Obesity (atherosclerosis)
  • Age (old)
  • Varicose veins
  • Surgery
  • Previous DVT/embolism
  • Trauma
  • Infection
  • Malignancy
Virchow’s triad of risk factors:
  • Stasis
  • Hypercoagulability
  • Vessel wall injury

Signs & Symptoms

  • Red, swollen leg (particularly calf)
  • Tenderness
  • Pitting oedema
  • Fever


This is often made clinically, using the Well’s score. Treatment can be initiated in cases of high clinical suspicion without further investigation, although in reality often an USS is used for confirmation. Also be aware that there are two separate Well’s scoring systems: one for DVT and one for PE.
  • Score >3 – Treat as DVT – and also perform a compression USS to confirm
  • Score 1-2 – Treat as DVT – and perform compression USS to confirm
  • Score 0 – do a D-dimer test. If negative, then unlikely to be DVT. If positive, Treat as DVT, and perform compression USS.


  • Ruptured Baker’s cyst
  • Cellulitis
  • Lymphadenopathy


A clot develops at a site of damage to a vessel wall (e.g. an atherosclerotic plaque, or perhaps a site of trauma). This can impair venous drainage of the leg. Clots below the knee will rarely embolise, but above the knee, they are far more dangerous. They will often spontaneously resolve over time, however, they are usually treated to reduce the risk of embolism.
  • If they appear in a superficial vein, then they do not embolise, and can be left to resolve, you just have to raise the leg.


  • Venography – this is the gold standard test. A radio-opaque dye is injected into the foot, and then you can see if it is blocked off as it travels up the leg
  • D-dimer – a negative test rules out DVT, but a positive test does not diagnose DVT. D-dimer is a breakdown product of fibrin, and can be released by many things, including MI, malignancy, pregnancy, inflammation, stroke, infarct, trauma, and is often raised post-operatively.
  • Leg measurement – you should measure the diameter of the calf at the same point on each leg, usually 10cm below the tibial tuberosity. If the difference between legs is >3cm this is significant for DVT.
  • USS – has about 90% sensitivity above the knee, but only 50% sensitivity for DVT below the knee. This is the test most often performed as it is cheap and reasonably reliable; and along with clinical factors, is all that is needed for diagnosis.


The aim is to prevent embolism.

LMWH – this is usually started as soon as the diagnosis is made, and is normally continued for a minimum of 5 days. It is usually stopped when the INR is in the target range (2-3)
Warfarin – also started at the same time as heparin, but warfarin actually increases coagulability in the first few days of use; hence the use of heparin initially. Warfarin is continued for:

  • 6 months if it is the first DVT
  • 3 months if it is the first DVT and occurred post operatively
  • Indefinitely if it is a recurrent DVT or if there is a genetic clotting disorder, or if there are other large risk factors.
Thrombolysis may be used if the PE is termed ‘massive’
Paradoxical Embolism
This is basically an embolism that goes through a defect in the heart, and goes on to cause a stroke. The clot passes from a vein to an artery, through some sort of ‘fistula’ – usually a cardiac defect
For example, a DVT could embolise, and travel to the heart. This might in a normal individual, cause a PE. But in the case of a paradoxical embolism it will travel through a defect in the heart from the right side to the left side, and thus miss out the pulmonary circulation. It is then free to travel through the arterial circulation, until it reaches an artery that is so small it cannot travel down it, and thus causes an ischaemic blockage.
  • They will often travel to the brain, and cause a stroke.
These account for about 2% of arterial emboli.


More Information


  • 25-50% of all surgical patients will have a DVT.
  • 65% of all below the knee tumours will be asymptomatic. Below the knee tumours rarely embolise to the lung
  • More common in veins (than arteries) due to the slower flow of blood.
  • They can occur in any vein, but by far the most common places are the legs and pelvis. They can also occur in the arms, although these are less likely to cause direct problems, and are also far less likely to cause PE.

Risk Factors

  • Age
  • Obesity
  • Varicose veins
  • Immobility (generally bed rest >4 days)
  • Pregnancy (oestrogen)
  • Previous DVT / embolism
  • Antithrombin deficiency
  • Protein C deficiency
  • Oestrogen therapy (Pill, HRT) – note only the combined pill, not the progesterone only pill – only a small risk factor.
  • Trauma
  • Surgery – especially pelvic and orthopaedic
  • Recent MI (10% of MI patients will have a DVT)
  • Infection
  • Malignancy
  • Dehydration
  • Congestive heart failure
  • Inherited clotting deficiencies – thrombophilia – factor V lyden.

Virchow’s triad

This is a little way to remember three of the major causatory factors of thrombosis
  • Stasis of blood flow
  • Vessel wall injury
  • Hypercoagulation 



  • Calf – warmth, tenderness, swelling, eythema
  • Mild fever
  • Pitting oedema
  • Horman’s sign – increased resistance/pain on forced foot dorsiflexion – however, you should NOT test for it as it can dislodge the clot! Also this is not diagnostic, as you can get it with other things as well.
  • Well’s score
  • Pain – find out where the pain will be for different clotting sites.


  • Cellulitis – this is normally really bright red, and really warm, and the leg will be tender.
  • Ruptured Baker’s cyst – this is usually a result of pre-existing rheumatoid disease. The cyst is a protrusion of the synovium out of the knee joint, usually out of the back of the joint. It can burst and give you pain down the back of the leg, as the fluid leaks out of the cyst and flows down the back of the calf.
    • Note that both of these can co-exist with a DVT
  • Superficial thrombophlebitis – this is basically thrombus and inflammation of the vein. It is often caused by a blood clot – and when it occurs in deep veins, it will probably be associated with DVT. However, when it occurs superficially, it is virtually never associated with DVT. You may be able to see the distended vein going all the way up the leg. It feels like rubber. it most commonly affects the saphenous vein, and is associated with varicosities. In these cases there may be a superficial clot secondary to the venous wall inflammation. Embolism does not occur from superficial thrombophlebitis. Treatment is generally with analgesics, rest, and elevation of the affected limb. Anticoagulants are not necessary.
  • Injury – causing a muscle haematoma – if you give them heparin, and this will make the haematoma even worse. It can also cause rupture of the plantaris tendon.
Well’s criteria for determining the clinical probability of a DVT
  • Note that this is different to the Well’s score for determining the seriousness of risk factors!
  • These criteria are a clinical assessment of the situation to decide what management plan should be adopted.
Clinical feature
Active cancer – treated within the last 6 months, or undergoing palliative treatment
Paralysis, paresis, plaster immobilisation of leg
Major surgery or recently bedridden (>3 days in last 4 weeks)
Local tenderness along the distribution of the deep venous system
Entire leg swollen
Calf swelling >3cm compared to other leg (measure them both at exactly the same point, usually 10cm below the tibial tuberosity)
Pitting oedema (greater in symptomatic leg)
Collateral superficial veins (non-varicose)
Alternative diagnosis as likely or more likely than that of DVT
  • ≥3 points – very high probability. Treat as DVT and perform compression US to confirm
  • 1-2 points – intermediate risk; treat as DVT and perform compression US to confirm
  • 0 points – perform D-dimer in the hope of a negative result to fully rule out DVT. If test is positive, then treat as suspected DVT and perform compression US. If –negative then DVT can be confidently ruled out.
It would be pretty hard to remember this on the day! So for on the job, you can use the following quick and easy method:
  • Risk factors + alternative diagnosis – low risk
  • Risk factors + no alternative diagnosis – high risk
  • No risk factors + no alternative diagnosis – medium risk
  • Clinical diagnosis alone is highly unreliable however – only 50% accurate! When this is combined with D-dimer, the accuracy is about 80%.
  • Doppler ultrasound is about 90% reliable, but can only really detect clots above the knee. Below the knee, it is only about 70% reliable. Those below the knee will need to be detected with venography.
  • Although venography is the gold standard, it is not used that often. Usually an ultrasound is done first. If this is negative it may be repeated in 1 week, or the patient may go for further tests, or a diagnosis may be made on clinical signs, and the patient put on anticoagulants.


Coagulation investigations

  • Bleeding time – this is the time it takes a small wound to stop bleeding. This can be tested by pricking the finger. The normal value is anywhere between 1-7 minutes.
  • Coagulation time – a pretty inaccurate test, as there are many sources of error. You basically take a blood sample, and test how long it takes for a clot to form. It takes 3-15 minutes in a normal individual
  • Prothrombin time (PT) – this gives an indication of the concentration of prothrombin in the blood. This is dependent on the factors produced in the liver. Heparin is monitored by the APPT, warfarin is monitored by the INR.
  • INR – the internal normalised ratio. This is basically a comparison of the patients clotting ability compared to the ‘average’ of the population. It is a ratio of the patient’s PT to that of the average PT – and as a result, this test only looks at the extrinsic clotting pathway. You can use it to look at liver function, warfarin dose and vitamin K status.
    • This ISI is a different value for different drugs, but is normally between 1.0 and 2.0.
The normal INR value is between 0.9 and 1.3. When someone is on warfarin therapy, the target is usually between 2-4 but may vary for individuals.
  • APPT


This is a test for thrombosis
  • A negative value means there probably isn’t a clot
  • A positive value DOES NOT MEAN there is a clot.
Other causes of a positive result include; infection, inflammation, pregnancy, malignancy, recent bleed, stroke, infarct, trauma, and post-op.
D-dimer is a fibrin degradation product. It will be raised for approximately 3 weeks after a clot.
Measure the leg!
Chose a point, e.g. 3cm below the tibial tuberosity, and measure the circumference on both legs. A difference of >1cm is significant, and >3cm is serious!


This is the gold standard test!
Radio-labelled dye is injected into a vein on the dorsum of the foot, and is then imaged by ‘dynamic x-ray imaging’. Static films are also taken to provide a permanent record.
Venography for DVT’s in the pelvis and IVC can be done by femoral vein catheterisation.


Basically a BP cuff you put round the calf, pump it up to occlude circulation, then let it down, and in a normal patient, blood should flow straight away. You get a graph of blood flow. If the flow is reduced, then there is a likelihood of thrombus.

Doppler USS

Very good for popliteal veins and above (up to the inguinal ligament), but not very good for calf. This is because it is only reliable in large veins.

Fibrinogen testing

Give radiolabeled fibrinogen injection, then look at areas where it collects.


S1-Q3-T3 – commonly comes up in exams, but not often seen in clinical practice.

  • S1 – increased S waves in lead I
  • Q3 – increased Q waves in lead III
  • T3 – inverted T waves in lead III


  • Stop the pill 4 weeks before a planned operation
  • Mobilise early after the operation
  • Heparin – 5000u/12hours may be given pre-operatively, as may enoxaparin (20mg/24hr) or dalteparin – these are LMWH’s, and are likely to cause less bleeding, and do not need monitoring – so in this situation are better than heparin for most patients.


The main aim is to prevent pulmonary embolism.
All patients with thrombus above the knee should receive anticoagulation. Patients with a DVT below the knee will usually receive 6 weeks of LMWH as 30% of the these patients actually have an extension of the clot proximally if nothing is done.
Bed rest is also advised until the patient is fully anti-coagulated.
LMWH’s (e.g. enoxaparin 1.5mg/Kg/24hr) are more effective than unfractioned heparin. Give 5 days worth minimum! Don’t give warfarin on its own!! Remember that it increases coagulation for the first couple of days after administration. Thus typical treatment would be a combination of LWMH and warfarin, started at the same time, and then the LMWH stopped when the INR reaches the target range (usually 2-3). Continue warfarin for:
  • 3 months if DVT was post-op
  • 6 months if there was no cause for the DVT
  • Lifelong if there is recurrent DVT or thrombophilia (genetic clotting defects)
Once the patient is mobilised (i.e. after the period of bed rest), they should wear elasticated stockings! These will reduce the risk of superficial thrombophlebitis as they prevent the pooling of blood in the superficial veins as these become full from their use as collaterals from the primary clot.
The stockings can reduce the incidence of secondary thrombophlebitis by 50%, however the evidence for this is not very solid.
IVC filter – in some rare cases where anti-coagulation fails, then an IVF filter may be implanted to reduce the risk of PE.
Thrombolysis is rarely used, there have been trials, but these have been inconclusive.
Depends on the risk factors – if it is post-op, then probably not very likely, if it is idiopathic, then 5 year risk is about 30%.


This is normally caused by a clot in the legs or pelvis that becomes dislodged, flows via the bloodstream through the right side of the heart and gets lodged in the pulmonary circulation.
It is not always a clot that causes a PE! Fat, air, amniotic fluid. For fat and amniotic fluid, these will normally resolve themselves with supportive care.

Risk factors

Exactly the same as DVT!

Clinical features

These depend on the patient and the size of the embolus. Small emboli may be asymptomatic, whilst large ones are often fatal.
Always make sure you ask about a family history of thrombosis!


  • Pyrexia
  • Cyanosis
  • Tachypnoea
  • Tachycardia
  • Hypotension
  • Raised JVP
  • Pleural rub
  • Pleural effusion
  • Look for signs that could indicate a cause – e.g. DVT, recent surgery, air travel


  • Breathlessness
  • Haemoptysis – as a result of pulmonary infarct
  • Dizziness
  • Syncope (loss of consciousness/fainting)



Will often be normal. The main reason you do a CXR is to exclude other causes.

The CXR may show pulmonary oedema signs such as raised hemidiaphragm. May also show atelectasis – this is little areas of collapsed lung. This occurs because there is loss of blood to some areas of the lung, which results in collapse of these areas – as a conservative mechanism.
Look for atelectasis in both lungs!
If the CXR is normal, but the patient is breathless, this raises the suspicion of PE. If the CXR has bilateral changes, but the patient only has unilateral pain, this also raises the suspicion of PE


Changes here are common but often non-specific (e.g. T wave changes, new onset AF, RBBB right axis deviation). such changes are seen in about 80% of patients. The most common findings are T wave inversion and sinus tachycardia. Larger emboli can cause right heart strain, which will result in the ‘classical’ S1Q3T3 pattern of ECG changes in PE, although this classic sign is actually quite rare (<20% of cases). the S1Q3T3 pattern is:
  • S waves present in lead I
  • Q waves present in lead III
  • T wave inversion in lead III

VQ scan

Only 15-20% of scans will show obvious pulmonary embolic disease
20% will obviously have no PE
The rest (60%) you just cannot tell!
  • Don’t do a VQ scan if there is an abnormal x-ray – it is a waste of time! Because the abnormalities on the x-ray are likely to cause abnormalities on VQ, and as PE doesn’t cause x-ray abnormalities, then x-ray and VQ abnormalities in these patients are likely to be unrelated to PE. Send them straight for CTPA. So VQ is for someone who has been previously well, and not for those with chronic disease


CT-pulmonary angiogram – a CT with contrast. This is a test that use a CT scanner and radioactive dye to look at the pulmonary circulation. Its main use is in the diagnosis of PE. It is much more sensitive and specific than VQ scan.
The emboli have to be quite large to be seen.


  • O2 may often be low
  • CO2 may often be normal or low
The patient will probably be hyperventilating (hence the low CO2)
Metabolic acidosis is commonly seen in those with a massive PE and cardiovascular collapse.


  • Anticoagulate with LMWH – e.g. dalteparin 200u/Kg/24hrs. The max dose is 18,000.
  • At the same time start oral warfarin 10mg
  • Stop the heparin when the INR is >2, and continue warfarin for a minimum of 3 months, aiming for an INR of 2-3.
  • You can place a vena cava filter in patients who continue to develop thrombi despite anticoagulation – but remember that implanting a filter without adequate anticoagulation will increase the risk of thrombus.
  • Thrombolysis may be used if the PE is deemed ‘Massive’ – 50mg alteplase – as long as no contraindications

Continuing Warfarin

  • At the very minimum – 6 weeks
  • Those with an identifiable and reversible risk factor – 3 months
  • Those with idiopathic disease – 6 months
  • There is also evidence that low-intensity warfarin (INR 1.5-2.0) not only reduces the risk of thromboembolism, but also has a low risk of bleeding.


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