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Approximately 25% of Hospitalizations for COPD Exacerbations May Involve Pulmonary Embolism or Thrombosis

Andrew C. Faust, Pharm.D. Candidate, The University of Texas at Austin
Reviewed by Henry I. Bussey, Pharm.D., FCCP, FAHA
April, 2009

Nearly 30% of acute exacerbations of COPD stem from unknown causes. However, a recent review article fills in the current knowledge gap and implicates pulmonary emboli in up to 25% of all COPD exacerbations requiring hospitalization.1 Additionally, this article, along with several others, suggests the thromboembolic events found in patients with COPD may, in fact, be due to pulmonary thrombosis (rather than embolism).

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of mortality worldwide, accounting for over 3 million deaths annually. While the disease is a chronic condition, the vast majority of COPD-related deaths occur during acute exacerbations. Earlier studies indicate 50-70% of exacerbations are attributable to infectious processes, and 10% are due to environmental irritants, however, a large portion (up to 30%) of acute exacerbations are of unknown origin. Additionally, a study by Sidney and colleagues published in 2005 suggests the risk of thromboembolic disorders in patients with COPD is almost double that of patients without COPD. These findings, along with the improvements in diagnosing pulmonary embolisms (PE), form the background of an analysis performed by Rizkallah and colleagues to ascertain the prevalence of PE in patients with COPD who required hospitalization for an acute exacerbation.

Rizkallah and colleagues assessed five prospective studies for a total of 550 patients included in the review. These studies were performed in various European countries (France, Switzerland, and the Netherlands) and the United States and the data were derived from a variety of practice settings (emergency department, inpatient, and outpatient). Based on the analysis of the five included studies, the investigators found the overall prevalence of PE was 19.9% (95% CI, 6.7-33%). In the four studies that assessed inpatient hospitalized patients, the prevalence of PE was higher at 24.7% (95% CI, 17.9-31.4%). On the other hand, the one study that looked at emergency department COPD patients, the prevalence of PE was 3.3%. However, patients in that particular study were less likely to possess venous thromboembolic (VTE) risk factors than patients in the studies that included hospitalized patients. In general, the overall rate of deep vein thrombosis (DVT) was lower than that of PE (12.4% vs. 19.9%).

The results of this article highlight a deficit in the current approach to the treatment of acute COPD exacerbations. As previously stated, approximately 30% of COPD exacerbations that require hospitalization are of unknown etiology. Taken with the findings of this analysis, it is reasonable to conclude that a portion of these cases may be due to a PE. Although this article concluded the overall prevalence of PE in COPD exacerbation was 19.9%, there are limitations intrinsic to the process of performing a meta-analysis that reduce the generalizability to all practice settings, especially when a heterogeneous group of studies comprise the make-up of the meta-analysis. Thus, while PE may be a large contributor to COPD exacerbations, the true prevalence cannot be accurately derived from this meta-analysis. However, the findings of this study do suggest that PEs play a role in COPD exacerbations and, therefore, further studies should be conducted in this area. Physicians should be aware of the impact of PEs in the setting of acute exacerbations of COPD and, in the face of such findings, it may be prudent to evaluate patients with an acute exacerbation of COPD without a clear etiology for PE.

This article also draws attention to the unexpected differences between prevalence of PE and DVT. As stated above, the overall prevalence of DVT was 12.4%. This finding is somewhat surprising given the higher prevalence of PE in the same population. Previous studies have demonstrated a high number of in situ thrombi in the setting of COPD. Additionally, imaging techniques cannot reliably differentiate between in situ thrombosis and embolism. Therefore, the divergence between the number of patients with DVT and patients with PE may be explained by the two clinical events being caused by two completely separate processes. If this is indeed the case and COPD patients are at risk for the development of pulmonary thrombosis, there may be some requirement for anticoagulation. However, since there is a scarcity of data in this area, further studies should be conducted to evaluate the risk of developing pulmonary thrombosis, which patients, if any, would benefit from anticoagulation, and how to anticoagulate these patients.


  1. Rizkallah J, Man SF, Sin DD. Prevalence of pulmonary embolism in acute exacerbations of COPD: a systematic review and metaanalysis. Chest. 2009 Mar;135(3):786-93.

  2. Sidney S, Sorel M, Queensberry CP Jr., et al. COPD and incident cardiovascular disease hospitalizations and mortality: Kaiser Permanente Medical Care Program. Chest. 2005; 128: 2068-75.

  3. Russo A, De Luca M, Vigna C, et al. Central pulmonary artery lesions in chronic obstructive pulmonary disease: a transesophageal echocardiography study. Circulation. 1999; 100: 1808-15.
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