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Vascular Disease
Vascular Disease

Pulmonary Embolus



Pulmonary embolism is the complete or partial obstruction of the pulmonary arterial system due to an embolus, most commonly as a complication of lower limb deep venous thrombosis.


Pulmonary emboli almost always originate from venous thrombi, most commonly in the deep veins of the leg. Proximal lower limb DVTs are significantly more likely to embolise than distal (below knee) DVTs. Less commonly, thrombi may form in the iliac veins, veins of the upper limb or within the right heart.
  • Risk Factors

  • Genetic Predisposition

  • Inherited hypercoagulability - protein C or S deficiency, factor V Leiden, prothrombin gene mutation, sickle cell disease, hyperhomocysteinaemia, antithrombin III deficiency
  • Family history of VTE
  • Patient  Factors

  • Advanced age
  • Past history of VTE
  • Acquired hypercoagulability - antiphospholipid syndrome, hyperviscosity, PNH, TTP, HITS
  • May-Thurner syndrome (anatomical variant where the right common iliac artery overlies and compresses the left common iliac vein)
  • Malignancy
  • Hormonal therapy - oestrogen-containing oral contraceptives, hormone replacement, SERMs
  • Venous pathology - varicose veins, superficial vein thrombosis
  • Environmental Triggers

  • Trauma
  • Surgery - particularly hip / knee surgery or major surgery
  • Pregnancy / peripartum period
  • Continuous immobilisation >72 hours - bedrest, neurologic pathology, cast
  • Hospital or nursing home admission
  • Long-distance travel (air, land or sea)


  • History

  • Symptoms of PE - pleuritic chest pain, shortness of breath, haemoptysis
  • Symptoms of DVT - painful, swollen upper or lower limb
  • Recent travel - long flights, car rides, bus rides or train rides
  • Long periods of immobilisation
  • Recent trauma, surgery
  • Pregnancy or recent delivery
  • Past medical history - past VTE, clotting disorder, malignancy, varicose veins
  • Medications - hormonal therapy
  • Family history - VTE, clotting disorder
  • Examination

  • Signs of PE - tachycardia, tachypnoea, hypoxia
  • Signs of right ventricular failure (massive PE) - tricuspid regurgitation, hypotension
  • Signs of DVT - upper or lower limb erythema / pitting oedema / tenderness
  • Investigations

  • D-dimer (if Well's score <2)
  • ECG - sinus tachycardia, RBBB, right axis deviation, S1Q3T3
  • Arterial blood gas
  • Chest x-ray
  • Imaging - CT pulmonary angiogram vs. V/Q scan
  • Renal function (to guide choice of anticoagulant)
  • Consider

  • Venous duplex ultrasound - to assess for DVT
  • Echocardiogram - to assess for RV dilatation / strain
  • Pulmonary angiography (gold standard; rarely used)
The D-dimer has high sensitivity (97-100%) and is very likely to be positive in the presence of PE. However, the test has poor specificity and positive predictive value as many other conditions can cause a positive result. The d-dimer is useful only in patients with a low pre-test likelihood of PE (as assessed using a tool such as the Well's Criteria) - a negative test in low risk patients makes a diagnosis of PE very unlikely. Ordering this test in non-low risk patients is likely to cloud the clinical picture as a positive result is difficult to interpret.
An ECG should be performed in all patients suspected of pulmonary embolus, mainly to exclude cardiac ischaemia. The most common ECG finding in the case of PE is sinus tachycardia, though right bundle branch block and/or right axis deviation may be present. The classic S1Q3T3 sign (deep S wave in I, pathologic Q wave in 3 and T wave inversion in 3) is both uncommon and non-specific.
An arterial blood gas may reveal a reduced PaO₂, though in small pulmonary emboli the patient may not be hypoxic. PaCO₂ may be normal or reduced due to hyperventilation.
The chest x-ray in PE is generally normal, and is useful for excluding other differential diagnoses such as pneumonia, pulmonary oedema, pneumothorax or pleural effusion. Pulmonary arterial enlargement may be visible in massive PE.
  • Imaging

  • Pulmonary embolism may be confirmed using one of four imaging modalities. CTPA and ventilation/perfusion (V/Q) scans are the most commonly used in clinical practice; MRI is rarely used due to access and difficulty of obtaining adeqaute images; and pulmonary angiography (the gold standard) is rarely performed.
CT pulmonary angiography (CTPA) involves injection of IV contrast followed by imaging of the pulmonary vasculature. If a PE is present, a filling defect may be seen in the main, lobar or segmental arteries; subsegmental PEs are often difficult to visualise. CTPAs are also useful for visualising differential diagnoses for PE such as pneumonia, pulmonary oedema, pneumothorax and pleural effusions. The main drawback of CTPA is that it is relatively contraindicated in patients with renal dysfunction (generally CrCl <30), and a renal physician should be consulted prior to injecting contrast media in these patients. Additionally, CTPA should be avoided in pregnant patients due to the risks of radiation exposure.
The ventilation/perfusion (V/Q) scan is a nuclear imaging modality used to assess for mismatch between ventilation and perfusion using technitium-99 labelled particles; there is almost always a V/Q defect with PE and therefore a negative scan has a high negative predictive value for PE. Other conditions causing a perfusion defect (such as atelectasis, consolidation, ILD, COPD or tumours) will also result in a positive test, and therefore V/Q scans should be avoided in these patients. It is important to note that as an indirect means of assessing for PE, V/Q scans only provide a probability of PE (low, intermediate or high) and cannot confirm the diagnosis in every case.
  • Pearls: CTPA vs V/Q Scan

  • CTPA - superior to V/Q scans, though (relatively) contraindicated in renal dysfunction and pregnancy
  • V/Q - can be used in renal failure and pregnancy, though less likely to be diagnostic and may be confounded by other causes of perfusion defect (atelectasis, consolidation, ILD, COPD, tumours)
If PE is confirmed, a venous duplex ultrasound should be performed to assess for a DVT. A DVT is found in 30-50% of cases of pulmonary embolism.
In patients with a massive pulmonary embolus, an echocardiogram may be useful to assess for right ventricular dilatation, strain and ventricular wall hypokinesis. Thrombi are rarely seen on transthoracic echo.

Risk Stratification

The Well's Criteria are used to stratify risk of PE based on risk factors, and estimate pre-test probability of PE. 


Prevention of pulmonary embolism is as per deep venous thrombosis, with chemoprophylaxis and/or mechanical prophylaxis. See the deep venous thrombosis page for more information.
  • IVC Filters

  • In patients with deep venous thrombosis who cannot be anticoagulated, an IVC filter may be appropriate to prevent embolism into the pulmonary vasculature. IVC filters are a temporary measure to be used until the patient becomes eligible for anticoagulation.


It is important to consult local guidelines (or a haematologist) regarding the management of pulmonary embolism.
  • Thrombolysis

  • Patients with acute massive pulmonary embolism may be thrombolysed with tissue plasminogen activator (tPA) if they are haemodynamically unstable. There is emerging evidence that haemodynamically stable patients with evidence of right heart dysfunction may be thrombolysed, though this remains controversial.
  • Anticoagulation

  • The mainstay of treatment for pulmonary embolism is anticoagulation. There are many different options for anticoagulation, as outlined below. Duration of anticoagulation depends on many factors including whether the PE is thought to be provoked, recurrent and/or in the context of thrombophilia.
  • Pearls: Choice of Anticoagulant

  • Heparin infusion - short-term, for bridging or in the perioperative period. APTT must be monitored regularly as per local protocol.
  • Low molecular weight heparin (e.g. enoxaparin) - first line for patients with active malignancy; also used for bridging. Contraindicated if CrCl <30.
  • Warfarin - must be bridged. INR must be monitored. Can be used in renal failure. Inferior to enoxaparin in active malignancy.
  • Dabigatran - contraindicated if CrCl <30.
  • Rivaroxaban - contraindicated if CrCl <30, severe liver disease, on protease inhibitors / azoles, pregnancy / breastfeeding. Potential role in active malignancy.
  • Apixaban - contraindicated if CrCl <25, severe liver disease, on protease inhibitors / azoles, pregnancy / breastfeeding.
  • Contraindications to Anticoagulation

  • Absolute - active bleeding, major trauma, platelets <50, bleeding diathesis, perioperative
  • Relative - past incompressible bleed, intracranial or spinal tumour, platelets <100, large AAA, high falls risk
  • Duration of Anticoagulation

  • Provoked VTE (transient risk factors) - 3 months then reassess based on risk of recurrence and bleeding
  • First unprovoked VTE - 3 months then continue depending on risk of recurrence and bleeding
  • Recurrent unprovoked VTE - long-term anticoagulation
  • Thrombophilia - consider long-term anticoagulation
In patients undergoing surgical procedures, consult either local guidelines or the team performing the procedure regarding when to withhold the anticoagulant and whether bridging therapy is needed.
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