Acute pulmonary embolism: a concise review of diagnosis and management

Abstract

An acute pulmonary embolism (aPE) is characterised by occlusion of one or more pulmonary arteries. Physiological disturbance may be minimal, but often cardiac output decreases as the right ventricle attempts to overcome increased afterload. Additionally, ventilation‐perfusion mismatches can develop in affected vascular beds, reducing systemic oxygenation. Incidence is reported at 50–75 per 100 000 in Australia and New Zealand, with 30‐day mortality rates ranging from 0.5% to over 20%. Incidence is likely to increase with the ageing population, increased survival of patients with comorbidities that are considered risk factors and improving sensitivity of imaging techniques. Use of clinical prediction scores, such as the Wells score, has assisted in clinical decision‐making and decreased unnecessary radiological investigations. However, imaging (i.e. computed tomography pulmonary angiography or ventilation‐perfusion scans) is still necessary for objective diagnosis. Anti‐coagulation remains the foundation of PE management. Haemodynamically unstable patients require thrombolysis unless absolutely contraindicated, while stable patients with right ventricular dysfunction or ischaemia should be aggressively anti‐coagulated. Stable patients with no right ventricular dysfunction can be discharged home early with anti‐coagulation and review. However, treatment should be case dependent with full consideration of the patient’s clinical state. Direct oral anti‐coagulants have become an alternative to vitamin K antagonists and are facilitating shorter hospital admissions. Additionally, duration of anti‐coagulation must be decided by considering any provoking factors, bleeding risk and comorbid state. Patients with truly unprovoked or idiopathic PE often require indefinite treatment, while in provoked cases it is typically 3 months with some patients requiring longer periods of 6–12 months.

Warfarin is not the anticoagulant of choice for malignancy‐associated venous thromboembolism

“…In a recent article in the Internal Medical Journal Hepburn‐Brown et al . published a detailed review of the diagnosis and management of acute pulmonary embolism (aPE) . The review focused on the diagnosis, pathophysiology and acute management of aPE, while maintenance treatment was covered in brief.…”

“…The setting of cancer‐associated thrombosis (CAT) represents a special situation. The use of VKA is acknowledged as an option for the management of cancer‐associated thrombosis in available guidelines . The use of VKA is dependent on the clinical stability of the patient as well as consistency of dietary intake and stable gut function (including the absence of nausea, vomiting and altered bowel habit).…”

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Warfarin is not the anticoagulant of choice for malignancy-associated venous thromboembolismIn a recent article in the Internal Medical Journal Hepburn-Brown et al published a detailed review of the diagnosis and management of acute pulmonary embolism (aPE). 1 The review focused on the diagnosis, pathophysiology and acute management of aPE, while maintenance treatment was covered in brief. Direct oral anticoagulants (DOAC), and the vitamin K antagonist (VKA) warfarin are suggested as the 'recommended anticoagulants' for ongoing treatment following aPE in all situations, including in the presence of a provoked irreversible aPE in the setting of malignancy (table 3 in Hepburn-Brown et al 1 ).

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“…1 The review focused on the diagnosis, pathophysiology and acute management of aPE, while maintenance treatment was covered in brief. Direct oral anticoagulants (DOAC), and the vitamin K antagonist (VKA) warfarin are suggested as the 'recommended anticoagulants' for ongoing treatment following aPE in all situations, including in the presence of a provoked irreversible aPE in the setting of malignancy (table 3 in Hepburn-Brown et al 1 ). Lowmolecular-weight heparin (LWMH) was not presented as a recommended option.…”

“…The use of VKA is acknowledged as an option for the management of cancerassociated thrombosis in available guidelines. 1,2 The use of VKA is dependent on the clinical stability of the patient as well as consistency of dietary intake and stable gut function (including the absence of nausea, vomiting and altered bowel habit). These factors may change over short periods of time in patients with active malignancy making the use of VKA in the ambulatory setting complicated, and stretching the available resources of cancer services.…”