PE

• Pulmonary embolism (PE) is the luminal obstruction of one or more pulmonary arteries by an embolised venous thrombus, but can also be due to an embolised solid, liquid, or gas.
• Most PEs originate as thrombi due to deep vein thrombosis, most frequently in the calf veins.

  Other causes include:

  • Fat embolism
  • Air embolism
  • Amniotic fluid embolism
  • Septic emboli
  • De novo thrombosis (rare)
• Pathophysiology:

  • Embolus detaches from its origin and embolises to the pulmonary arteries through the systemic venous system and the right heart
  • Ventilation/perfusion mismatch = impaired gaseous exchange = hypoxaemia (T1RF) and tachypnoea
  • Pulmonary arterial hypertension (due to increased pulmonary vasculature resistance) = right ventricular overload +/- dysfunction
  • Pleural and lung inflammation and infarction = pleuritic chest pain +/- haemoptysis
• Symptoms:

  • Most common = dyspnoea
  • Tachypnoea
  • Pleuritic chest pain
  • Features of concurrent DVT
  • Haemoptysis
  • Others - retrosternal chest pain (due to right ventricular ischaemia), cough
• Clinical findings:

  • Tachycardia
  • Tachypnoea
  • Hypoxia
  • Low-grade fever
  • Pleural rub
  • Gallop rhythm (third heart sound due to rapid ventricular filling in diastole)
  • Wide split second heart sound
  • Tricuspid regurgitation murmur
• Features of a massive PE:

  • Haemodynamic instability: hypotension and cardiogenic shock
  • Presyncope/syncope
  • Elevated jugular venous pressure (JVP)
• Possible ECG findings include:

  • Sinus tachycardia: the most common finding
  • Right ventricular strain pattern: T wave inversion in anterior leads (V1-V4) +/- inferior leads (II, III, aVF)
  • Right bundle branch block (RBBB)
  • Right axis deviation (RAD)
  • The classic ‘S1Q3T3’ ECG change is only seen in <20% patients – large S wave in lead I, large Q wave in lead III, and inverted T wave in lead III
• D-dimer test has a high sensitivity but low specificity for VTE. Many conditions can result in an elevated D-dimer in the absence of VTE:

  • Pregnancy
  • Malignancy
  • Liver disease
  • Severe infection or inflammatory disease
  • Disseminated intravascular coagulation (DIC)
  • Recent trauma/surgery/hospitalised patients
• CXR should be used to exclude differential diagnoses, most patients with PE have a normal CXR but possible findings include:

  • Wedge-shaped pulmonary infarction
  • Atelectasis
  • Pleural effusion
  • Raised hemidiaphragm
• Diagnosis:

  • CTPA
• Echocardiogram:

  • Investigation of choice in haemodynamically unstable patients who are unsuitable for CTPA
  • May show signs of right ventricular dysfunction
  • Patients who have signs of right heart strain will have a follow up echo in 6 weeks to ensure resolution
• Pulmonary embolism rule-out criteria (PERC) - if all the following criteria are absent, probability of PE <2%:

  • Age 50 or above
  • HR 100 or more
  • SpO2 <95% on air
  • Unilateral leg swelling
  • Haemoptysis
  • General anaesthesia within last 4 weeks
  • Previous VTE
  • Hormone use
• PE with haemodynamic instability management:

  • Offer continuous UFH and consider thrombolytic therapy:
  • IV tissue plasminogen activator (e.g. alteplase) is often used
  • Catheter-directed thrombolysis
  • Open pulmonary embolectomy
• Risk assessment for outpatient vs inpatient:

  • Outpatient treatment for low-risk PE can be considered
  • Pulmonary Embolism Severity Index (PESI) score
  • Key requirement for outpatient treatment is being haemodynamically stable
• In haemodynamically stable PE, management involves anticoagulation therapy:

  • First line: apixaban or rivaroxaban, both direct oral anticoagulants (DOACs)
  • Second line: low molecular weight heparin (LMWH) followed by dabigatran/edoxaban OR LMWH followed by warfarin
• The choice of anticoagulants varies in specific patient populations:

  • Pregnant: LMWH only (DOACs and warfarin contraindicated)
  • Active cancer: DOAC preferred over LMWH
  • Severe renal impairment (eGFR < 15 mL/min/1.73m2): UFH or dose-adjusted LMWH
  • Antiphospholipid syndrome (triple positive): initial LMWH and warfarin followed by warfarin monotherapy
• Short-term complications of PE include:

  • Sudden cardiac arrest or death can result from ventricular collapse due to massive embolism and occlusion of the pulmonary vasculature
  • Pulmonary infarction due to obstruction of arterial blood supply, more common when distal arteries are occluded
  • Right ventricular infarction, often secondary to pulmonary hypertension and haemodynamic overload
  • Atelectasis
  • Exudative pleural effusion
• Long-term complications of PE include:

  • Increased risk of recurrence, history of previous VTE is a significant risk factor for future VTEs
  • Chronic thromboembolic pulmonary hypertension (CTEPH) occurs where fibrotic tissue replaces residual emboli causing chronic obstruction of the pulmonary vasculature, and hence pulmonary hypertension - should be excluded in patients with persistent dyspnoea 3-6 months after PE