R E V I E W COPD and PE: A clinical dilemma Teng Moua1 Kenneth Wood2 1Department of Internal Medicine, 2Section of Pulmonary and Critical Care Medicine, University of Wisconsin Hospitals and Clinics, Madison, WI, USA Correspondence: Kenneth E Wood University of Wisconsin Hospitals and Clinics, Section of Pulmonary and Critical Care Medicine, 600 Highland Ave, Madison,WI 53792–9988, USA Tel + 1 608 261 1299 Fax +1 608 263 3104 Email kew@medicine.wisc.edu Abstract: Dyspnea in patients with known chronic obstructive pulmonary disease (COPD) can be a clinical challenge due to the nonspeciﬁc nature of atypical presentations. Typical features of fever, productive cough, and wheezing on presentation support COPD exacerbation, while absence of such ﬁndings may warrant further evaluation for underlying etiologies, including pulmonary embolism (PE). It is suspected that one in four patients with atypical COPD exacerba- tion may have PE as an underlying or concomitant cause of acute dyspnea. This review discusses the clinical presentation of COPD and PE, and presents an overview of the rationale for pursuing work-up for thromboembolic disease in the setting of known obstructive lung diseases. Keywords: pulmonary embolism, chronic obstructive pulmonary disease, COPD, dyspnea Introduction The chronic obstructive pulmonary disease (COPD) patient presenting with acute dys- pnea can be a diagnostic challenge in both the outpatient and inpatient arenas. Many cardiopulmonary diseases, including acute pulmonary embolism (PE), are worsened or masked by the presence of COPD. While diagnostic tests such as B-type natriuretic peptide have led to differentiating dyspnea in heart failure from COPD exacerbation, there are no proven clinical criteria to help delineate acute pulmonary embolism from COPD. This is attributable to the overlap and nonspeciﬁcity of clinical features com- mon to both diseases. Guidelines presented by the World Health Organization (WHO) and Global Initiative for Chronic Obstructive Lung Disease (GOLD) for the diagnosis of COPD stress the chronicity of dyspnea with exposure to relevant risk factors (GOLD et al 2005). Further diagnostic evaluation includes pulmonary function testing that reveals obstruction and supportive ﬁndings on chest X-ray (CXR). Acute exacerbation is diagnosed by clinical means and presents with a worsening of dyspnea with or without sputum change, a decline in exercise tolerance, and exam ﬁndings of air trapping and poor lung aeration. The progression usually takes a few days and does not present acutely although the patient may be in respiratory distress at the time of evaluation. The presentation of pulmonary embolism is similarly subtle with nonspeciﬁc clinical features such as acute dyspnea, tachycardia, and pleuritic chest pain. While COPD remains a clinical diagnosis, PE requires objective conﬁrmation of clot by an imaging study to warrant appropriate anticoagulation therapy. When recognizing that the mortality of untreated PE may be as high as 25%, it is crucial to incorporate PE into the differential diagnosis of a COPD exacerbation, and instructive to review the incidence of PE in COPD patients in the reported literature. Prevalence and risk of PE with COPD Thromboembolism represents a spectrum of disease, ranging from deep venous thrombosis (DVT) to PE and infarct. The incidence of DVT is 160 per 100,000 per- sons, with 44% developing either symptomatic or asymptomatic PE (Kummer 1998). International Journal of COPD 2008:3(2) 277–284 © 2008 Dove Medical Press Limited. All rights reserved 277