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Different degrees of ischaemic injury in the right and left ventricle in cases of severe, nonfatal, pulmonary embolism

Fracasso, T. ; Schrag, B. ; Sabatasso, S. ; Lobrinus, J.A. ; Schmeling, A. ; Mangin, P.

In: International Journal of Legal Medicine, 2015, vol. 129, no. 3, p. 525-529

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    Titre
    • Different degrees of ischaemic injury in the right and left ventricle in cases of severe, nonfatal, pulmonary embolism
    Auteur
    • Fracasso, T.. University Center of Legal Medicine, Lausanne—Geneva, Geneva University Hospitals, Geneva, Switzerland
    • Schrag, B.. Service of Legal Medicine, Valais Hospital, Sion, Switzerland
    • Sabatasso, S.. University Center of Legal Medicine, Lausanne—Geneva, Geneva University Hospitals, Geneva, Switzerland
    • Lobrinus, J.A.. Clinical Pathology Service, Geneva University Hospitals, Geneva, Switzerland
    • Schmeling, A.. Institute of Legal Medicine, Münster University Hospital, Münster, Germany
    • Mangin, P.. University Center of Legal Medicine, Lausanne—Geneva, Geneva University Hospitals, Geneva, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • International Journal of Legal Medicine, 2015, vol. 129, no. 3, p. 525-529. Springer Berlin Heidelberg
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:332810
    Summary
    Pulmonary fat embolism (PFE) is a common complication of blunt force traumas with bone fractures. Severe forms cause impedance to right ventricular (RV) ejection, with eventual right heart ischaemia and failure. In a prospective study, we have investigated 220 consecutive autopsy cases (73 females, 147 males, mean age 52.1years, min 14years, max 91years). PFE was detected in 52 cases that were divided into three groups according to the degree of PFE (1-3). A fourth group of cases of violent death without PFE was used for comparison. In each case, histology (H&E, Masson) and immunohistochemistry (fibronectin and C5b-9) were performed on six cardiac samples (anterior, lateral and posterior wall of both ventricles). The degree of cardiac damage was registered in each sample and the mean degree of damage was calculated in each case at the RV and left ventricle (LV). Moreover, a parameter ∆ that is the difference between the mean damage at the RV and the LV was calculated in each case. The results were compared within each group and between the groups. In the present study, we could not detect prevalent RV damage in cases of high degree PFE as we did in our previous investigation. In the group PFE3 the difference of the degree of damage between the RV and LV was higher than the one observed in the groups PFE0-2 with the antibody anti-fibronectin. Prevalent right ventricular stress in cases of severe PFE may explain this observation.