Pulmonary Embolism (also known as pulmonary embolus) is most commonly a complication of venous thromboembolism (VTE) from another source – e.g. a clot in the legs or pelvis (a DVT) 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 pulmonary embolism. Fat, air, amniotic fluid can all also be causes. For fat and amniotic fluid, these will normally resolve themselves with supportive care. Air is often an iatrogenic cause (e.g. accidentally injected intravenously).
- <5% if no haemodynamic instability
- 30% if shock present
- 70% with cardiac arrest (in hospital)
For VTE pulmonary embolism:
- Family History
- Bed rest >24 hours
- Immobility >48 hours
- POP – plaster of Paris over limb
- Pregnancy (oestrogen) – risk is highest in the 4 weeks after birth
- Previous DVT / embolism
- Oestrogen therapy (Pill, HRT) – note only the combined pill, not the progesterone only pill
- Surgery – especially pelvic and orthopaedic
- Recent MI (10% of MI patients will have a DVT)
- Congestive heart failure
- Antithrombin deficiency
- Protein C deficiency
- Inherited clotting deficiencies – thrombophilia – factor V Leiden
- Varicose veins
- Tachypnoea – 90% of patients have RR >16
- Tachycardia – 45% of patients
- Hypotension – 25% of patients
- Raised JVP
- Pleural rub
- Pleural effusion
- Look for signs that could indicate a cause – e.g. DVT, recent surgery, air travel – only 33% of patients have clinical evidence of DVT
- Atrial fibrillation (rare)
- Pleuritic chest pain (pain worse on inspiration) – 75% of patients
- Breathlessness – 85% of patients
- Cough – 50% of patients
- Haemoptysis – as a result of pulmonary infarct – 30% of patients
- Dizziness / pre-syncope – 15% of patients
- Syncope (loss of consciousness/fainting) – 15% of patients
- Non-pleuritic chest pain – 15% of patients
Shortness of breath typically occurs within seconds to minutes of onset, and pain develops later.
Beware of patients with unexplained syncope. In one study, 25% of patients admitted to hospital with unexplained syncope had PE.
Probably the most important question is should I investigate?
Defining risk of the probability of PE is important. There are two tools to help with this:
PERC stands for Pulmonary Embolism Rule-out Criteria.The PERC score is useful to rule out PE in low risk patients. If the patient’s score = 0, then there is a <2% chance of PE, and in the absence of convincing clinical signs, you can usually safely exclude PE as a differential.
Each factor below gives a score of 1. All factors must be negative for a negative PERC score. Any positive factor results in the need for further work up (move onto the Well’s Score)
- Age >50
- HR >100
- SaO2 on room air <95%
- Unilateral leg swelling
- Recent surgery or trauma
- Previous PE or DVT
- Exogenous Oestrogen – oral contraceptives, hormone resplacement or other oestrogen hormones
Well’s score for PE
This can stratify patients as low or high risk. In high risk patients, you should proceed straight to imaging. In low risk patient, you should consider a D-dimer test.
|Clinically suspected DVT||3|
|PE is most likely diagnosis||3|
|Immobilisation >3 days OR surgery – in previous 4 weeks||1.5|
|History of DVT or PE in past||1.5|
Interpretation of Well’s Score
- Score >6.0 — High (probability 59%)
- Score 2.0 to 6.0 — Moderate (probability 29%)
- Score <2.0 — Low (probability 15%)
- Score > 4 — PE likely. Consider diagnostic imaging.
- Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.
D-Dimer is a fibrin degradation product – and as such, levels are raised by the presence of a blood clot in the circulation. A D-Dimer blood test can be useful to rule out PE or DVT as a differential. A negative D-Dimer PLUS a low Well’s score means that PE or DVT is extremely unlikely. Conversely, many factors can cause a positive D-Dimer – so having a raised D-Dimer does not necessarily mean there is a clot.
- D-Dimer should only be used as a ‘rule-out’ test in low probably cases – based on the Well’s score
- A positive D-Dimer in a low probably case indicates the need for further investigation (e.g. CTPA or VTE)
- In high probably cases, you should skip the D-Dimer and go straight to imaging
In reality it can be a tricky test to use. Even just a recent common cold can result in a raised D-Dimer! Almost any factor that causes inflammation will also result in a raised D-Dimer. Do be selective when requesting a D-DImer for your patients. Even if your patient has a low risk Well’s score, doing a D-Dimer might not always be the best option – for example if they have recently had cellulitis or some other infection.
“Should I do a D-Dimer?” is often a difficult questions which should involve consultation with your senior clinicians. Common pitfalls include:
- Delaying of imaging in cases with a high probably – D-Dimer not necessary
- Clinical confusion in cases which could have been ruled out clinically (e.g. PERC rule), which subsequently report a positive D-Dimer (most likely caused by another factor unrealted to any potential VTE). In these cases patient’s often undergo unnecessary imaging to “exclude” a PE.
D-Dimer also rises with age. Some centres now report an age specific reference range for D-Dimer.
- Traditional reference range for D-Dimer – normal <0.50
- Example of age adjusted:
- Age <50 – normal <0.50
- Age >50 – normal range is <0.50 PLUS 0.1 for every decade of life over the age of 50, e.g.:
- Age 60 – normal <0.60
- Age 70 – normal <0.70
Other factors that caused an increased D-Dimer include liver disease, high rheumatoid factor, malignancy, trauma, pregnancy and recent surgery.
Will often be normal. The main reason CXR is performed is to exclude other causes.
- S waves present in lead I
- Q waves present in lead III
- T wave inversion in lead III
- VQ scans should not be performed in patients with CXR abnormalities – the abnormalities on the x-ray are likely to cause abnormalities on VQ, irrespective of the presence of PE. VQ is only suitable for patients who have been previously well, and not for those with chronic disease.
- O2 may often be low
- CO2 may often be normal or low
Troponin is raised in 20-40% of patients with PE as a result of the extras stress and stretch placed on the right ventricle in PE patients (due to increased pulmonary arterial pressure).
Higher troponin has been associated with a worse prognosis.
Is used to look for right ventricle strain and dilatation in patients with suspected massive PE. The degree of RV dysfunction can be used as a predictor of death.
PE with signs of right heart strain in the haemodynamically unstable patient (raised troponin, heart motion abnormalities on echo – often done at the bedside in ED) should be considered for thrombolysis – e.g. 50mg alteplase (be wary of a long list of contraindications!).
This type of PE is sometimes termed “massive PE”. This scenario is typically caused by a “saddle” PE – sitting at the major bifrucation of the pulmonary veins.
Typically this is a decision made by the treating consulting in hospital (usually ED physician) perhaps in conjunction with respiratory and or haematology specialists. These patient will also require ongoing anticoagulation as below.
The vast majority of patients do not require thrombolysis and do not have massive or saddle PE.
The other main treatment is anticoagulation. This can be done either with warfarin, or a NOAC – such as rivaroxaban. In most circumstances a NOAC is favorable as it does not required monitoring, and it does not require the use of a heparin at the start of the treatment period.
Example of warfarin treatment
- 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.
In patients with recurrent thrombus despite anticoagulation a vena cava filter may be considered – but remember that implanting a filter without adequate anticoagulation will increase the risk of thrombus.
Continuation of anticoagulant therapy
This decision made be made in conjunction with a haematologist.
- At the very minimum – 6 weeks. Usually in cases of obvious ‘provoked’ PE (e.g. after surgery)
- Those with an identifiable and reversible risk factor – 3 months
- Those with idiopathic disease – 6 months
- Those with recurrent clots – often longer than 6 months – sometimes lifelong
- There is also evidence that low-intensity warfarin (INR 1.5-2.0) not only reduces the risk of thromboembolism, but also has a lower risk of bleeding.
- They will often travel to the brain, and cause a stroke.
Like any chest pain presentation, differentiating PE can be difficult. Typically, larger PE’s (and sicker patients) are easier to differentiate. Using the Chest Pain Differentializer might be useful.
- Acute Coronary Syndrome
- Pleuritic chest pain
- Pneumonia (viral or bacterial)
- Musculoskeletal back pain
- Embolus of other cause (fat, amniotic fluid, air)
- Dissecting Aortic Aneurysm
- Syncope of another cause
- Exacerbation of COPD
- Age Adjusted D-Dimer Testing
- Clinical presentation, evaluation, and diagnosis of the non-pregnant adult with suspected acute pulmonary embolism – UpToDate