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Original Research: CRITICAL CARE MEDICINE |

ARDS: A Clinicopathological Confrontation

Quentin de Hemptinne, MD; Myriam Remmelink, MD, PhD; Serge Brimioulle, MD; Isabelle Salmon, MD, PhD; and; Jean-Louis Vincent, MD, PhD, FCCP
Author and Funding Information

*From the Department of Intensive Care (Drs. de Hemptinne, Brimioulle, and Vincent) and the Department of Pathology (Drs. Remmelink and Salmon), Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium.

Correspondence to: Jean-Louis Vincent, MD, PhD, FCCP, Department of Intensive Care, Erasme Hospital, Route de Lennik, 808, 1070 Brussels, Belgium; e-mail: jlvincen@ulb.ac.be


None of the authors has any conflicts of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2009;135(4):944-949. doi:10.1378/chest.08-1741
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Background:  The heterogeneity of populations meeting criteria for ARDS may explain in part why no specific treatment has yet been shown to decrease mortality. To define the pathologic alterations associated with the syndrome, particularly the typical pattern of diffuse alveolar damage (DAD), and to evaluate whether etiologies or precipitating factors were missed, we evaluated patients who died with a clinical diagnosis of ARDS and who had a postmortem examination.

Methods:  We conducted a 3-year (2002 to 2004) review of all patients with ARDS (using the American-European Consensus Conference criteria) who died in our ICU and had a postmortem examination. Discrepancies between antemortem and postmortem diagnoses were classified as major and minor using the Goldman classification.

Results:  Of 9,184 hospital admissions, 376 patients had a clinical diagnosis of ARDS. Of these, 169 died; 69 had a postmortem examination, and 64 of these had complete data for analysis. The main cause of death was multiple organ failure (27 of 64 patients). Postmortem examination revealed DAD in 32 patients (50%), pneumonia without DAD in 16 patients (25%), and invasive pulmonary aspergillosis in 8 patients (12.5%). Major unexpected findings were found in 15 patients (23%): 7 Goldman class I (including 4 cases of invasive pulmonary aspergillosis and 1 of disseminated tuberculosis) and 8 Goldman class II.

Conclusions:  In this study, ARDS remains a heterogeneous syndrome because only half of patients with ARDS had typical DAD. Open lung biopsy, if performed, might have led to appropriate therapy and potentially better outcome in five of the patients.

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