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The Scientific World Journal
Volume 2012, Article ID 657316, 6 pages
http://dx.doi.org/10.1100/2012/657316
Research Article

Diffuse Alveolar Damage of the Lungs in Forensic Autopsies: Assessment of Histopathological Stages and Causes of Death

1Department of Pathology, Yedikule Teaching Hospital for Chest Diseases and Thoracic Surgery, 34020 Istanbul, Turkey
2Department of Forensic Pathology, Istanbul University, Institute of Forensic Medicine, 34452 Istanbul, Turkey
3Department of Pathology, Istanbul Medical Faculty, Istanbul University, 34452 Istanbul, Turkey

Received 23 July 2012; Accepted 2 September 2012

Academic Editors: J. M. Nesland, G. Pasquinelli, and K. Szuhai

Copyright © 2012 Halide Nur Urer et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Introduction. Diffuse alveolar damage (DAD) is a morphological prototype of acute interstitial pneumonia. Hospital autopsies or open-lung biopsies are used to monitor common alveolar damage and hyaline membrane (HM) development histopathologically. The aim of this study was to detect histopathological profiles and frequency of DAD and HM in adult forensic autopsies. Materials and Methods. In total, 6813 reports with histopathological samples in 12,504 cases on which an autopsy was performed between 2006 and 2008 were investigated. Sixty-six individuals >18 years of age who were diagnosed with DAD were included. Hematoxylin- and eosin-stained lung preparations were reexamined in line with the 2002 American Thoracic Society/European Respiratory Society idiopathic interstitial pneumonia consensus criteria. Results. Histopathological examination revealed that 50 cases (75.7%) were in the exudative phase and 16 (24.2%) were in the proliferative phase. Only the rate of alveolar exudate/oedema in exudative phase cases ( 𝑃 = 0 . 0 0 3 ); those of alveolar histiocytic desquamation ( 𝑃 = 0 . 0 3 7 ), alveolar fibrosis ( 𝑃 = 0 . 0 1 7 ), chronic inflammation ( 𝑃 = 0 . 0 2 ), and alveolar fibrin ( 𝑃 = 0 . 0 0 1 ) in proliferative cases were significantly higher. The presence of alveolar fibrin was the only independent variable in favour of proliferative cases ( 𝑃 = 0 . 0 1 6 ). Conclusion. The detection of all DAD morphological criteria with the same intensity is not always possible in each case. Forensic autopsies may provide a favourable means for expanding our knowledge about acute lung damage, DAD, and interstitial lung disease.