Pulmonary embolism (PE) is a condition where a blood clot (thrombus) forms in the pulmonary arteries. This is usually the result of a deep vein thrombosis (DVT) that developed in the legs and travelled (embolised) through the venous system and the right side of the heart to the pulmonary arteries in the lungs. Once they are in the pulmonary arteries they block the blood flow to the lung tissue and create strain on the right side of the heart. DVTs and PEs are collectively known as venous thromboembolism (VTE).
There are a number of factors for developing a DVT or PE. In many of these situations we give patients prophylactic treatment with low molecular weight heparin to reduce the risk.
- Recent surgery
- Long haul flights
- Hormone therapy with oestrogen
- Systemic lupus erythematosus
TOM TIP: In your exams when a patient is presenting with possible features of a DVT or PE, ask about risk factors such as periods of immobility, surgery and long haul flights to score extra points from your examiners.
Every patient admitted to hospital should be assessed for their risk of venous thromboembolism (VTE). If they at increased risk of VTE they should receive prophylaxis with a low molecular weight heparin such as enoxaparin unless contraindicated. Contraindications include active bleeding or existing anticoagulation with warfarin or a NOAC. Anti-embolic compression stockings are also used unless contraindicated. The main contraindication for compression stockings is significant peripheral arterial disease.
Pulmonary embolism can present with subtle signs and symptoms. In patients with potential features of a PE, risk factors for PE and no other explanation for their symptoms have a low threshold for suspecting a PE. Presenting features include:
- Shortness of breath
- Cough with or without blood (haemoptysis)
- Pleuritic chest pain
- Raised respiratory rate
- Low grade fever
- Haemodynamic instability causing hypotension
There may also be signs and symptoms of a deep vein thrombosis such as unilateral leg swelling and tenderness.
The Wells score predicts the risk of a patient presenting with symptoms actually having a DVT or pulmonary embolism. It takes in to account risk factors such as recent surgery and clinical findings such as tachycardia (heart rate >100) and haemoptysis.
NICE recommend assessing for alternative causes with a:
- Chest xray
Perform a Wells score and proceed based on the outcome:
- Likely: perform a CT pulmonary angiogram
- Unlikely: perform a d-dimer and if positive perform a CTPA
There are two main options for establishing a definitive diagnosis: CT pulmonary angiogram or ventilation–perfusion (VQ) scan.
CT pulmonary angiogram (CTPA) involves a chest CT scan with an intravenous contrast that highlights the pulmonary arteries to demonstrate any blood clots. This is usually the first choice for investigating a pulmonary embolism as it tends to be more readily available, provides a more definitive assessment and gives information about alternative diagnoses such as pneumonia or malignancy.
Ventilation-perfusion (VQ) scan involves using radioactive isotopes and a gamma camera to compare the ventilation with the perfusion of the lungs. They are used in patients with renal impairment, contrast allergy or at risk from radiation where a CTPA is unsuitable. First, the isotopes are inhaled to fill the lungs and a picture is taken to demonstrate ventilation. Next a contrast containing isotopes is injected and a picture is taken to demonstrate perfusion. The two pictures are then compared. With a pulmonary embolism there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue. This area of lung tissue will be ventilated but not perfused.
TOM TIP: Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed. This is because the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic. It is one of the few causes of a respiratory alkalosis, the other main cause being hyperventilation syndrome. Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2.
- Admission to hospital
- Oxygen as required
- Analgesia if required
- Adequate monitoring for any deterioration
Initial Management (LMWH)
The initial management is with treatment dose low molecular weight heparin (LMWH). It should be started immediately before confirming the diagnosis in patients where DVT or PE is suspected and there is a delay in getting the scan. Examples are enoxaparin and dalteparin.
Switching to long term anticoagulation:
The options for long term anticoagulation in VTE are warfarin, a NOAC or LMWH.
The target INR for warfarin is 2-3. When switching to warfarin continue LMWH for 5 days or the INR is 2-3 for 24 hours on warfarin (whichever is longer).
NOACs or DOACs are essentially oral anticoagulants that are not warfarin. They are an alternative option for anticoagulation that does not require monitoring. Originally they were called “novel oral anticoagulants” but this has been changed to “non-vitamin K oral anticoagulants” because they are no longer novel. This is changing to DOACs, standing for “direct-acting oral anticoagulants”. The main three options are apixaban, dabigatran and rivaroxaban.
LMWH long term is first line treatment in pregnancy or cancer.
Continue anticoagulation for:
- 3 months if there is an obvious reversible cause (then review)
- Beyond 3 months if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause such as thrombophilia. This is often 6 months in practice.
- 6 months in active cancer (then review)
Where there is a massive PE with haemodynamic compromise there is a treatment option called thrombolysis. Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. It is only used in patients with a massive PE where the benefits outweigh the risks. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.
There are two ways thrombolysis can be performed:
- Intravenously using a peripheral cannula.
- Directly into the pulmonary arteries using a central catheter. This is called catheter-directed thrombolysis.
In catheter directed thrombolysis a catheter is inserted into the venous system, through the right side of the heart and in to the pulmonary arteries. The operator can then administer the thrombolytic agent directly into the location of the thrombus. Special equipment can also be used to physically break down the thrombus and aspirate it. There is a risk of damaging the pulmonary arteries doing this.
Last updated April 2019