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Pulmonary embolism (PE) is a common problem, though its exact incidence is difficult to assess due to its non-specific clinical presentation and frequently suboptimal diagnostic management affecting the quality of reporting. Data collected 3 decades ago in the USA suggested a prevalence of PE of 0.4% among hospitalised patients, while the overall annual incidence was estimated at 600 000 cases. Clinical and postmortem data collected in the Malmo area, a region of Sweden with a particularly high autopsy rate, suggested an incidence of PE of approximately 20/10 000 inhabitants/year.1
Dyspnoea, tachypnoea and chest pain (pleuritic or retrosternal) are the most common symptoms and signs in confirmed PE, but they are just as frequent in patients in whom this diagnosis was suspected but was ultimately ruled out. The same is true for tachycardia, syncope, cough, haemoptysis or low grade fever.2 While most PE episodes occur in the presence of predisposing factors and originate from venous thrombi developing in the lower limbs, deep vein thrombosis is often asymptomatic, and in about 20% of PE cases no provoking factor can be identified.3 Therefore a validated diagnostic strategy aimed at confirming or excluding PE should be implemented in every patient presenting with acute or recurrent cardiorespiratory symptoms and/or signs which cannot be unequivocally explained otherwise.
Mortality of a PE episode is highly related to its haemodynamic consequences. In the minority of cases—those which present with acute right ventricle (RV) failure leading to systemic hypotension—the in-hospital death rate exceeds 15% despite appropriate treatment, and may be as high as >50% in patients with shock.4 However, in the majority of patients with PE survival can be excellent, provided adequate anticoagulation is promptly instituted. Even in mildly symptomatic patients, early diagnosis and treatment of PE is essential to prevent imminent recurrent embolic events, which may be …