Calcified myocardial necrosis in pediatric patients after cardiopulmonary resuscitation
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CASE REPORT
Calcified myocardial necrosis in pediatric patients after cardiopulmonary resuscitation Claas T. Buschmann • Werner Stenzel Hubert Martin • Frank L. Heppner • Saskia S. Guddat • Michael Tsokos
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Accepted: 8 December 2012 Ó Springer Science+Business Media New York 2012
Abstract We report three autopsy cases of wide-spread myocardial necrosis with calcification in pediatric patients after temporary generalized hypoxia and initially successful cardiopulmonary resuscitation, but subsequent in-hospital death. Autopsy and histological workup in all three cases showed multiple circumscribed calcified and necrotic areas in progressive stages of organization within the myocardium. We conclude that these macro- and microscopic autopsy features appear to be related to reperfusion injuries in children as a consequence of hypoxic-ischemic changes occurring in the peri- and postresuscitation period. Keywords Pediatrics Cardiopulmonary resuscitation Hypoxia Myocardial calcification Autopsy
Introduction An imbalance in oxygen supply and demand, e.g., during cardiac arrest, and generalized hypoxia before cardiopulmonary resuscitation (CPR) attempts, results in tissue hypoxia, microvascular dysfunction, and finally tissue necrosis with organ failure and cell death. Its extent depends on various factors, e.g., the affected cell/tissue type, the duration of ischemia, the patient’s age and pre-existing
C. T. Buschmann (&) S. S. Guddat M. Tsokos Institute of Legal Medicine and Forensic Sciences, Charite´, Universita¨tsmedizin Berlin, Turmstr. 21, Building N, 10559 Berlin, Germany e-mail: [email protected] URL: http://remed.charite.de W. Stenzel H. Martin F. L. Heppner Department of Neuropathology, Charite´, Universita¨tsmedizin Berlin, Charite´platz 1, 10117 Berlin, Germany
diseases. After a prolonged period of ischemia, sufficient reperfusion may lead to an initial satisfactory performance of the impaired tissue or organ, but also might cause reperfusion injuries related to oxidative stress by peroxidation of the membrane phospholipids and resulting in changes in the permeability of the cell membrane and cell death [1]. Such hypoxic conditions with subsequent reperfusion-related tissue injury contribute to morbidity and mortality in a considerable range of pathologies. They are also a major challenge during cardiothoracic, vascular and general surgery and solid organ transplantation [2]. Generally, cardiac oxidative stress severely compromises the cardiac antioxidant cellular system, causes cardiac antioxidant cellular system injuries and may result in oxidative damage such as depletion of nonenzymatic antioxidants such as glutathione [3]. In particular myocardial reperfusion injuries after cardiac arrest and generalized hypoxia with subsequent successful CPR have been widely described and evaluated concerning occurrence, pathophysiology and therapeutic options, particularly in adult patients [2, 4–8]. When compared to adults, children present a different pattern of physiological response to
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