Pulmonary embolism

Pulmonary embolism (PE) is a form of venous thromboembolism and is a serious complication of deep vein thrombosis which can lead to death in 30 – 60% of cases, and is more common in case of proximal DVT.

PE is classified into three different types:

• Nonmassive PE
• Submassive PE
• Massive PE

Massive pulmonary embolism refers to PE which causes obstructive shock and haemodynamic instability, usually because of a saddle-thrombus (thrombus at the pulmonary trunk bifurcation). Submassive PE causes RV dysfunction but not haemodynamical instability. Nonmassive PE causes neither.

Risk factors

• Hereditary pro-coagulant mutation (Leiden, AT III def, etc.)
• Immobility
• Post-surgery
• Smoking
• Obesity

Clinical features

Pulmonary embolism has no specific symptoms and can be difficult to recognise clinically. Symptoms occur acutely and are not specific for PE. The most common symptoms include dyspnoea, pleuritic chest pain, dizziness, and cough. Other possible symptoms include tachypnoea, haemoptysis, and jugular vein distension. Symptoms of DVT may be present. Massive PE gives syncope or haemodynamic instability.

Diagnosis and evaluation

When PE is suspected, we calculate the pre-test probability of PE to determine how to proceed, as for DVT. The pre-test probability of PE can be calculated with the Wells score for PE (which is different from the one for DVT), or the revised Geneva score.

• Low or intermediate pre-test probability for PE
  • -> measure D-dimer
    • D-dimer negative: PE excluded
    • D-dimer positive: perform CTPA
• High pre-test probability for PE
  • -> perform CTPA

In patients with low pre-test probability, the pulmonary embolism rule-out criteria (PERC) may be applied. If all these eight criteria are fulfilled, PE is excluded, and D-dimer testing is not necessary.

Clinical findings

Pulmonary embolism causes a sudden increased load on the right ventricle, which may manifest on the ECG. These ECG findings are not specific for PE, but most people with PE have one or more ECG abnormality. Some of the possible signs include:

• Sinus tachycardia
• SIQIIITIII-pattern (S-wave in I, Q-wave in III, and T inversion in III)
• RBBB

Arterial blood gas may show hypocapnia and hypoxaemia. Troponins and NT-proBNP may be positive due to the strain on the heart.

Imaging

The gold standard for PE diagnosis is CT pulmonary angiography (CTPA), a rapid sequence with IV contrast where the CT scanner spirals around the patient in one breath hold. The scan itself takes only seconds, but the whole procedure including administration of contrast and set-up takes up to 10 minutes.

CTPA shows pulmonary emboli as partial or complete filling defects located within the contrast-enhanced lumens of the pulmonary arteries. It's a highly specific and sensitive examination for PE.

An alternative to CTPA is V/Q scan, but this is rarely needed.

Echocardiography is useful in PE, as it allows for ruling out other differential diagnoses (tamponade, myocardial ischaemia, valvular disease, etc.), and in case of massive PE right ventricular strain may be visible.

Chest radiography is not used for evaluation of PE, but in 2% of cases, the Westermark sign may be present. This is only seen in large emboli and is characterised by the distal blood vessels of a lung being collapsed and therefore smaller than normal, called focal peripheral hyperlucency.

Treatment

If the patient is haemodynamically unstable, they must be stabilised first. These patients often require ventilation and fluid resuscitation.

Once the patient is stabilised, definitive treatment must be initiated. Patients with massive PE should be managed with anticoagulation as well as thrombolysis or embolectomy. Thrombolysis involves administration of a tPA like alteplase via a peripheral IV catheter or directly into the pulmonary circulation to dissolve the clot. Embolectomy refers to physical removal of the clot, with a catheter or surgery.

Patients with nonmassive PE should be anticoagulated with LMWH or UFH, or given IVC filter is anticoagulation is contraindicated. Anticoagulation should also be initiated in patients at high suspicion for PE, even if the diagnosis isn’t made yet, as long as there are no contraindications.

After the first 5 – 10 days of intravenous anticoagulation, we may switch to oral anticoagulants, preferably DOACs. After three months, the patient is reassessed as described for DVT.

Complications

• Obstructive shock
• Death

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