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      Acute or chronic pulmonary emphysema? Or both?—A contribution to the diagnosis of death due to violent asphyxiation in cases with pre-existing chronic emphysema

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          Abstract

          The diagnosis of death due to violent asphyxiation may be challenging if external injuries are missing, and a typical acute emphysema (AE) “disappears” in pre-existing chronic emphysema (CE). Eighty-four autopsy cases were systematically investigated to identify a (histo-) morphological or immunohistochemical marker combination that enables the diagnosis of violent asphyxiation in cases with a pre-existing CE (“AE in CE”). The cases comprised four diagnostic groups, namely “AE”, “CE”, “acute and chronic emphysema (AE + CE)”, and “no emphysema (NE)”. Samples from all pulmonary lobes were investigated by conventional histological methods as well as with the immunohistochemical markers Aquaporin 5 (AQP-5) and Surfactant protein A1 (SP-A). Particular attention was paid to alveolar septum ends (“dead-ends”) suspected as rupture spots, which were additionally analyzed by transmission electron microscopy. The findings in the four diagnostic groups were compared using multivariate analysis and 1-way ANOVA analysis. All morphological findings were found in all four groups. Based on histological and macroscopic findings, a multivariate analysis was able to predict the correct diagnosis “AE + CE” with a probability of 50%, and the diagnoses “AE” and “CE” with a probability of 86% each. Three types of “dead-ends” could be differentiated. One type (“fringed ends”) was observed significantly more frequently in AE. The immunohistochemical markers AQP-5 and SP-A did not show significant differences among the examined groups. Though a reliable identification of AE in CE could not be achieved using the examined parameters, our findings suggest that considering many different findings from the macroscopical, histomorphological, and molecular level by multivariate analysis is an approach that should be followed.

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            Chronic obstructive pulmonary disease (COPD) is a major public health problem associated with long-term exposure to toxic gases and particles. We examined the evolution of the pathological effects of airway obstruction in patients with COPD. The small airways were assessed in surgically resected lung tissue from 159 patients--39 with stage 0 (at risk), 39 with stage 1, 22 with stage 2, 16 with stage 3, and 43 with stage 4 (very severe) COPD, according to the classification of the Global Initiative for Chronic Obstructive Lung Disease (GOLD). The progression of COPD was strongly associated with an increase in the volume of tissue in the wall (P<0.001) and the accumulation of inflammatory mucous exudates in the lumen (P<0.001) of the small airways. The percentage of the airways that contained polymorphonuclear neutrophils (P<0.001), macrophages (P<0.001), CD4 cells (P=0.02), CD8 cells (P=0.038), B cells (P<0.001), and lymphoid aggregates containing follicles (P=0.003) and the absolute volume of B cells (P=0.03) and CD8 cells (P=0.02) also increased as COPD progressed. Progression of COPD is associated with the accumulation of inflammatory mucous exudates in the lumen and infiltration of the wall by innate and adaptive inflammatory immune cells that form lymphoid follicles. These changes are coupled to a repair or remodeling process that thickens the walls of these airways. Copyright 2004 Massachusetts Medical Society
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              Physiological changes in respiratory function associated with ageing.

              Physiological ageing of the lung is associated with dilatation of alveoli, enlargement of airspaces, decrease in exchange surface area and loss of supporting tissue for peripheral airways ("senile emphysema"), changes resulting in decreased static elastic recoil of the lung and increased residual volume and functional residual capacity. Compliance of the chest wall diminishes, thereby increasing work of breathing when compared with younger subjects. Respiratory muscle strength also decreases with ageing, and is strongly correlated with nutritional status and cardiac index. Expiratory flow rates decrease with a characteristic alteration in the flow-volume curve suggesting small airway disease. The ventilation-perfusion ratio (V'A/Q') heterogeneity increases, with low V'A/Q' zones appearing as a result of premature closing of dependent airways. Carbon monoxide transfer decreases with age, reflecting mainly a loss of surface area. In spite of these changes, the respiratory system remains capable of maintaining adequate gas exchange at rest and during exertion during the entire lifespan, with only a slight decrease in arterial oxygen tension, and no significant change in arterial carbon dioxide tension. Ageing tends to diminish the reserve of the respiratory system in cases of acute disease. Decreased sensitivity of respiratory centres to hypoxia or hypercapnia results in a diminished ventilatory response in cases of heart failure, infection or aggravated airway obstruction. Furthermore, decreased perception bronchoconstriction and diminished physical activity may result in lesser awareness of the disease and delayed diagnosis.
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                Author and article information

                Contributors
                ninasophia.mahlke@med.uni-duesseldorf.de
                Journal
                Int J Legal Med
                Int J Legal Med
                International Journal of Legal Medicine
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0937-9827
                1437-1596
                28 June 2021
                28 June 2021
                2022
                : 136
                : 1
                : 133-147
                Affiliations
                [1 ]GRID grid.411327.2, ISNI 0000 0001 2176 9917, Institute of Legal Medicine, , Heinrich Heine University Düsseldorf, ; Düsseldorf, Germany
                [2 ]GRID grid.411327.2, ISNI 0000 0001 2176 9917, Institute of Systems Neuroscience, Medical Faculty, , Heinrich Heine University Düsseldorf, ; Düsseldorf, Germany
                [3 ]GRID grid.8385.6, ISNI 0000 0001 2297 375X, Institute of Neuroscience and Medicine, Brain & Behaviour (INM-7), , Research Centre Jülich, ; Jülich, Germany
                [4 ]GRID grid.411327.2, ISNI 0000 0001 2176 9917, Institute for Anatomy I, , Heinrich Heine University Düsseldorf, ; Düsseldorf, Germany
                Author information
                http://orcid.org/0000-0002-2922-5110
                http://orcid.org/0000-0002-9820-8672
                Article
                2619
                10.1007/s00414-021-02619-7
                8813827
                34181078
                51045922-4a19-4c1b-9614-7ece75f70adf
                © The Author(s) 2021

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 28 December 2020
                : 30 April 2021
                Funding
                Funded by: Universitätsklinikum Düsseldorf. Anstalt öffentlichen Rechts (8911)
                Categories
                Original Article
                Custom metadata
                © Springer-Verlag GmbH Germany, part of Springer Nature 2022

                Law
                acute versus chronic pulmonary emphysema,violent asphyxiation,aquaporin 5,surfactant protein a1,transmission electron microscopy

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