Rapid Recap is distributed each month using suggested topics or topics on trend (seasonal/disease trends). NWAS-wide clinicians, irrespective of grade, are invited to contribute towards writing content in future issues in a supportive process. Please get in touch with rapid.recap@nwas.nhs.uk.
This month's Rapid Recap looks at Pulmonary Embolism.
A plain-text version can be found at the bottom of this page.
Pulmonary embolism (PE) is an obstruction of the pulmonary blood vessels. PE is commonly precipitated by a deep vein thrombosis (DVT), with the two conditions often referred to as venous thromboembolism (VTE) - other forms of PE are rarer, but can include air, fat, and amniotic fluid.
In the context of VTE, a PE is part of a thrombus that travels in the circulation to the lung vasculature; it is composed of red cells, platelets and fibrin. Virchow’s triad describes the three overarching factors contributing to VTE development.
Hypercoagulability – (e.g. cancer, pregnancy)
Venous stasis (e.g. immobility, polycythaemia)
Endothelial injury (e.g. smoking, surgery)
Signs and symptoms will differ depending upon the size and location of PE (i.e. multiple small PEs, segmental emboli with pulmonary infarction, major PE with large branch obstruction, and massive pulmonary emboli).
Symptoms are typically sudden in onset and may include dyspnoea, pleuritic pain, substernal pain, apprehension, cough, haemoptysis, syncope, and cardiac arrest (7-11% of cases, see JRCALC).
Signs may include:
Respiratory rate >20 breaths per minute
Pulse rate >100 BPM (most common presentation)
<92% on room air
Signs of deep vein thrombosis (DVT)
Haemodynamic problems occur when >30-50% of the pulmonary arterial bed is occluded, resulting in reduced blood flow through the lungs and decreased preload to the left side of the heart. This can result in hypotension, syncope or collapse, and in some cases, cyanosis (because of a mismatch between ventilation and pulmonary perfusion leading to hypoxaemia).
Cyanosis typically presents as a bluish discoloration of the lips, tongue, nail beds, and mucous membranes, and is indicative of systemic hypoxaemia. However, in individuals from ethnic backgrounds, with pigmented skin, signs of cyanosis and pallor can be more difficult to detect, potentially delaying diagnosis and treatment.
Pallor in individuals with darker skin tones may appear as ashen, grey, or dull, rather than pale. In medium-brown skin, it may appear slightly yellowish or muted in hue. Alternative sites for assessing pallor include the palmar surfaces, mucous membranes (such as the oral mucosa), and the conjunctivae, where colour changes may be more evident.
Additionally, signs such as skin flushing due to increased perfusion or fever may not be visually apparent in richly pigmented skin. Palpation of the skin for localised warmth or coolness can be a useful adjunct to visual assessment.
Clinicians should adopt an inclusive and multimodal approach to clinical assessment to ensure timely recognition of PE.
Risk factors can be identified through thorough history taking. Clinical assessments should adopt an ABCDE approach to maintain structure, remembering to apply and monitor pulse oximetry. Patients may present with unilateral swelling of the lower limbs; they may also be warm and red.
ECG Monitor and record 12-lead ECG – be aware that the classic S1 Q3 T3 12-lead ECG presentation is often NOT present, even during massive PE. Other patterns, such as RBBB, and right heart strain patterns may be identified. However, the most common finding in PE is tachycardia.
Did you know: The Wells criteria may be used to estimate the pre-test probability of a patient having PE; however, any patient where PE is suspected requires further investigation, including D-dimer test (measure of blood-clot related protein).
See JRCALC, for more detail about the management of PE.