Pulmonary Embolism (PE)

Causes

• Provoked PE - associated with a recent (≤3 months) and transient major risk factor, such as significant immobility, surgery, trauma, pregnancy or puerperium, or use of hormonal therapy (combined contraceptive pill or hormone replacement therapy)
• Unprovoked PE - occurs in the absence of a recent (≤3 months) major clinical risk factor in a person who is not using hormonal therapy.

Clinical

• may be asymptomatic
• SOB, cough +/- haemotypsis
• pleuritic chest pain
• associated leg pain/swelling, signs of DVT
• massive PE - central cyanosis, altered/LOC, collapse or shock

• tachypnoea, tachycardia, hypotension
• elevated JVP, parasternal heave, loud P2
• Fever is common in PE and can occur in ≥25% patients
• clinical categorisation to direct Mx:
  • massive (high risk)- shock, persistent brady or asystole
  • sub-massive (intermediate risk) - evidence of RV dysfunction but no signs of shock
  • low risk - no evidence of RV dysfunction or shock

Investigations

• bloods: FBC, U&E's, clotting, d-Dimer
• ECG - often normal
  • sinus tachycardia
  • signs of R heart strain -SI, QIII, TIII (probably <10%), non-specific ST changes or TWI in anterior leads, right axis deviation, S wave (I and aVL) > 1.5mm, Q in III and aVF, P pulmonale & RBBB
• ABG - hypoxia. Repeat after exercising may enhance diagnostic workup. Resp alkalosis. Metabolic acidosis if shock
• CXR - only to rule out other pathology
• CTPA - may not pick up smaller emboli

Management

• Low molecular weight heparin (LMWH)
• Fondaparinux.
• Unfractionated heparin.
• Oral anticoagulants: Warfarin, apixaban, or rivaroxaban.
• LMWH followed by an oral anticoagulant (dabigatran or edoxaban)
• Thrombolysis - only for massive. Debate continues about their place in sub-massive
  • plasminogen activators - fibrin specific rt-PA or non selective agents - streptokinase, urokinase
• IVC filters and embolectomy