Pulmonary embolism

Introduction

Pulmonary embolus (PE) is the third most common cardiovascular disease, more often seen in the elderly with co-morbidity (cancer, trauma, immobility, surgery or severe medical disease). Historically, when diagnosed clinically and untreated, it has a high mortality. Treating PE with anticoagulation reduces in-hospital mortality to between 4% and 12%.

The diagnosis and management of PE is often difficult. It requires careful clinical assessment, documented risk stratification (preferably a validated score such a Wells, PERC, etc.) and appropriate selection of diagnostics, none of which are truly definitive. Possible alternative serious conditions should always be considered. All PE diagnostic tests (including D-dimer) need risk assessment to ensure safe and appropriate usage (see risk assessment, further on). Generally, with PE risk below 5% (most low-risk emergency patients), an alternative diagnosis should be sought, with PE investigation pursued if no definitive alternative is found. Overly aggressive radiological investigation in 5% risk populations potentially finds more false-positive venous thromboembolism (VTE) than real PE/deep venous thrombosis (DVT). The diagnostic threshold is 70% to 80% PE probability, where treatment benefits clearly outweigh treatment risks. Most diagnostic guidelines use Wells, and/or PERC (if low-risk Wells) and/or D-dimer (if low-risk Wells and positive PERC) for most emergency department (ED) patients, followed by computed tomographic pulmonary angiography (CTPA) or occasionally nuclear ventilation/perfusion scan (V/Q) for definitive diagnosis. Venous ultrasound (US or CT venography) may assist after indeterminate imaging. Echocardiography, if available, is useful for PE risk stratification and particularly for managing unstable cases ( Fig. 5.5.1 ).

Almost all cases of diagnosed PE will be anticoagulated, the majority on direct oral anticoagulants (DOACs) or novel oral anticoagulants (NOACs), some with heparin/warfarin. Thrombolysis or embolectomy (when thrombolysis is contraindicated or fails) is indicated in shocked patients (massive PE, blood pressure [BP] <90 mm Hg for >15 minutes or if patient is requiring inotropic support due to PE); thrombolysis is not routinely administered for submassive PE. Disposition decisions (e.g. home therapy, intensive monitoring) are assisted by prognostic decision making based on validated scores (e.g. the Simplified Pulmonary Embolism Severity Index [SPESI]) or PE severity markers (e.g. biomarkers such as brain natriuretic peptide [BNP], troponin, etc.) or echocardiography.

Aetiology, pathogenesis and pathology

Up to 30% of PEs, particularly ED presentations, are idiopathic. Most risk factors act via more than one item in Virchow’s triad (e.g. vessel wall injury, venous stasis or hypercoagulable states). The major risk factors associated with secondary (provoked) PE are as follows:

• Surgery or trauma; particularly pelvis/ lower abdomen, lower limb or central nervous system (CNS) (provokes 15% to 30% of PE)

• Cancers (15% to 25%)

• Systemic disease with immobilization (>24 hours bed rest), particularly heart disease/strokes (15% to 25%)

• A history of DVT/PE (particularly unprovoked, 5% to 15%).

PE incidence rises exponentially with age, with those above 85 years of age having 60 times the incidence of 18- to 25-year-olds, mainly driven by co-morbidity. Hypercoagulable states (e.g. antithrombin III deficiency, factor V Leiden, antiphospholipid syndrome, protein C/S deficiencies etc.), indwelling venous devices, hormone contraception or therapy, obesity, later pregnancy/post-partum, many vasculitic/autoimmune diseases, smoking, use of non-steroidal anti-inflammatory drugs and long-haul air travel increase the risk of PE.

Prevention

The greatest preventable cause of DVT/PE is surgery. Stasis from illness-related bed rest—particularly cancer, stroke and cardiopulmonary disease—are also common. Low-dose preventive low-molecular-weight heparin (LMWH) or NOACs/DOACs make surgery safer and more effective and improve outcomes for high-risk hospitalized medical patients. Thrombo-prophylaxis risk assessment should be performed and started as early as possible.

Clinical Features

Examination

Physical signs confirming PE (e.g. persistent unexplained tachycardia [>100] at rest) are rare but can significantly increase PE diagnostic probability; this is incorporated into most prediction rules. Leg (or arm) DVT signs (e.g. a swollen, oedematous leg with pain in the venous distribution or significant thrombophlebitis) increase PE risk and mandate imaging. Other features include tachypnoea (50% to 80%), cough (10% to 20%), mild fever (<38.5°C), wheeze and pleural effusion/rub; but these are not discriminatory for PE. Occasionally elevated jugular venous pressure (JVP), a loud cardiac S(P)2 heart sound or a pulmonary systolic murmur may suggest right ventricular strain.

Electrocardiography

At least 21 potential ECG features have been postulated for PE, but they are insensitive and most lack specificity. The most significant are tachycardias (particularly atrial), right bundle branch block (often incomplete/transient), right axis deviation (particularly S1-S3), T-wave inversion (especially deep V1-V3) and the S1-Q3-T3 pattern. The more features present, the more suggestive for right ventricular (RV) strain. These changes have been associated with poorer PE outcomes, particularly the rare S1-Q3-T3 pattern.