Introduction

Pulmonary Embolism (also known as pulmonary embolusis most commonly a complication of venous thromboembolism 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.

Some studies suggest that ‘silent’ pulmonary emobile occurs in up to 40% of DVT patients.
Mortality
  • <5% if no haemodynamic instability
  • 30% if shock present
  • 70% with cardiac arrest (in hospital)

Risk factors

Exactly the same as DVT!
  • Age
  • Obesity
  • Varicose veins
  • Immobility
    • Bed rest >24 hours
    • Immobility >48 hours
    • POP – plaster of Paris over limb
  • Pregnancy (oestrogen) – risk is highest in the 4 week after birth
  • 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
  • Smoking
  • Congestive heart failure
  • Inherited clotting deficiencies – thrombophilia – factor V Leiden

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!

Signs

  • Pyrexia
  • Cyanosis
  • 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 patient have clinical evidence of DVT

Symptoms

  • 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 / syncope – 15% of patients
  • Syncope (loss of consciousness/fainting) – 15% of patients
  • Non-pleuritic chest pain – 15% of patients

Diagnosis

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 Score

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
  • Haemoptysis
  • 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.

FactorScore
Clinically suspected DVT3
PE is most likely diagnosis3
Tachycardia >100bpm1.5
Immobilisation >3 days OR surgery – in previous 4 weeks1.5
History of DVT or PE in past1.5
Haemoptysis1
Malignancy1

Interpretation of Well’s Score

Traditional interpretation

  • Score >6.0 — High (probability 59%)
  • Score 2.0 to 6.0 — Moderate (probability 29%)
  • Score <2.0 — Low (probability 15%)

Alternative interpretation

  • Score > 4 — PE likely. Consider diagnostic imaging.
  • Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.

D-Dimer

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 means that PE or DVT is extremely unlikely. However, many factors can cause a positive D-Dimer – so having a raised D-Dimer does not necessarily mean there is a clot.

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. Even if your patient has a low risk Well’s score, doing a D-Dimer might not always be practical – for example if they have recently had cellulitis or some other infection.

D-Dimer also rises with age. Other factors that caused an increased D-Dimer include liver disease, high rheumatoid factor, malignancy, trauma, pregnancy and recent surgery.

Investigations

CXR

Will often be normal. The main reason CXR is performed 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 a pulmonary embolism. If the CXR has bilateral changes, but the patient only has unilateral pain, this also raises the suspicion of pulmonary embolism. 

ECG

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

VQ scans use much less radiation than a CTPA. As such, VQ scans are used to assess for PE in patients who are at risk from higher radiation doses – such as pregnant women, and younger female patients.
However, VQ scans are also much less accurate at diagnosing PE. They need to be interpreted by a specialist. A negative VQ scan has a very high negative predictive value, but positive scans are less useful.
The result of a VQ scan is usually given as a risk probability – high risk, intermediate risk or low risk.
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

CTPA

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.

ABG

  • 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.
You cannot exclude a PE with an arterial blood gas.

Troponin

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.

Echocardiography

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. 

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.
  • 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.
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