Pulmonary embolism

Pulmonary embolism is a condition where a blood clot (thrombus) forms a blockage in a lung artery or arteries, usually caused by a clot in another part of the body, often the leg or the arm, which travels through the bloodstream and becomes lodged in the blood vessels of the lung (Righini et al, 2017). This can cause chest pain, difficulty in breathing, haemoptysis, tachycardia, and cardiac arrest dependent upon the size of the clot though may also present with little or no symptoms. The incidence of venous thromboembolism (VTE is the collective term for deep vein thrombosis and pulmonary embolism) is around 1 in 1000 annually (Lee and Levine, 2003) with additional risk factors both transient and ongoing. It is the third most common cause of death from cardiovascular disease after heart attack and stroke (Nicholson et al, 2020). 

A pulmonary embolus (PE) is a blockage of an artery or arteries in the lungs from a clot (thrombus) that has travelled through the bloodstream into the lungs. It can occur rapidly and be difficult to diagnose as symptoms and presentation will be similar to other conditions including pneumonia, acute myocardial infarction, or angina (Tapson, 2009). It can vary in severity with either few or no symptoms to a life-threatening emergency with severe hypoxia and haemodynamic collapse.

The common signs and symptoms of a PE include:

• dyspnoea – may be of sudden onset
• pleuritic chest pain
• haemoptysis
• syncope and/or dizziness
• signs of DVT
• tachycardia
• tachypnoea
• hypotension (Stein et al, 2007)

PE however can be asymptomatic and may be discovered incidentally when assessment for another condition is made (Dentali et al, 2010).

The three factors that are primarily involved in the aetiology of PE include:

• alteration in the blood-clotting mechanism
• alteration in the anatomical structure of the lining of a blood vessel
• alteration in blood flow (Mehta et al, 2020)

Anything that prevents or reduces blood from flowing or clotting properly will increase the risk of thrombosis and an untreated deep vein thrombosis will increase risk of PE if the clot travels (embolises) through the bloodstream into the lungs.

Active cancer is responsible for around 20% of all VTE events with the thrombosis risk associated with cancer being fourfold higher than the general population (Heit, 2015)

Hospital admission is known to increase the risk of thrombosis, in particular surgical intervention (Lester et al, 2013) though appropriate risk assessment and prophylaxis administration will reduce the incidence seen (Sweetland et al, 2009; Khanna et al, 2014).

Medications such as hormone replacement therapy or the

A physical examination and review of general medical history is the first step to exclude other causes. If clinical suspicion is low, then consider using the pulmonary embolism rule out criteria (PERC) to help determine if any further investigations are needed (Freund et al, 2015).

If PE is suspected the 2 level Wells score is used to estimate the clinical probability of PE which scores as either PE likely or PE unlikely. If PE likely is the result, then radiological investigation being one of computed tomography pulmonary angiogram, ventilation/perfusion single photon emission computed tomography (V/Q SPECT) or V/Q planner scan is carried out. If there is likely to be a delay in obtaining imaging then therapeutic anticoagulation, following guidance in the treatment section, should be initiated until a scan has been performed. If PE diagnosed, then either continue anticoagulation or start treatment using options covered in treatment section. Where no

Treatment for a newly diagnosed PE is with therapeutic anticoagulation and has three phases being initial, long term and extended treatment. The goal of treatment is to reduce mortality and recurrence of thrombosis. For high-risk PE further initial treatment may be needed detailed in the next section which would impact on which treatment is commenced.

Anticoagulation suppresses blood clot formation and propagation and should be taken for a minimum of three months at which point a review should be carried out looking at the need for long term treatment dependent upon what provoking factors contributed to the PE formation (Kearon and Akl, 2014).

Simple analgesia may be required, paracetamol or codeine, but it is best to avoid non-steroidal anti-inflammatory medication as this may increase risk of bleeding.

Treatment options should be discussed as part of a shared decision process considering patient blood results.

Identification of massive or non-massive PE and whether the patient is haemodynamically stable will identify what treatment is needed and whether thrombolysis or catheter directed thrombolysis is indicated (Sekhri et al, 2012). This will also influence on whether the patient can be treated as an outpatient or inpatient and whether a higher level of care in a high dependency or critical care unit is needed.

Classification of severity of PE is on the basis of estimated early death risk with presence of right ventricular dysfunction being a major risk factor here along with shock, persistent arterial hypotension where prompt reperfusion treatment is needed (Bryce et al, 2019). Most PE diagnoses appear to be haemodynamically stable at presentation and not considered high risk (Konstantinides et al, 2016).

Therapeutic anticoagulation, assuming no other treatment are being used, treatment will offer a choice of a direct oral anticoagulant (DOAC), low molecular weight heparin

References

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Bryce YC, Perez-Johnston R, Bryce EB et al. Pathophysiology of right ventricular failure in acute pulmonary embolism and chronic thromboembolic pulmonary hypertension: a pictorial essay for the interventional radiologist. Insights Imaging. 2019;10(1):18. http://doi.org/10.1186/s13244-019-0695-9.

Hotoleanu C. Genetic Risk Factors in Venous Thromboembolism. Adv Exp Med Biol. 2017;906:253-272. http://doi.org/10.1007/5584_2016_120

Chopra N, Doddamreddy P, Grewal H, Kumar PC. An elevated D-dimer value: a burden on our patients and hospitals. Int J Gen Med. 2012;5:87-92. http://doi.org/10.2147/IJGM.S25027.

Dentali F, Ageno W, Becattini C et al. Prevalence and clinical history of incidental, asymptomatic pulmonary embolism: a meta-analysis. Thromb Res. 2010;125(6):518-22. http://doi.org/10.1016/j.thromres.2010.03.016

Devis P, Knuttinen MG. Deep venous thrombosis in pregnancy: incidence, pathogenesis and endovascular management. Cardiovasc Diagn Ther. 2017 Dec;7(Suppl 3):S309-S319. http://doi.org/10.21037/cdt.2017.10.08

Douma RA, le Gal G, Söhne M, Righini M, Kamphuisen