• Miriam Viviane Baron, Michele Paula Dos Santos, Taís Michele Werle, Gabriela D L G Scherer, Mariana Martins Dantas Santos, Luis Manuel Ley Dominguez, Cristine Brandenburg, Gabriela Feltez, Aline Ronis Sampaio, Marcus Vinicius de Mello Pinto, Sonia Carvalho, Patrícia Froes Meyer, Felice Picariello, Esteban Fortuny Pacheco, Isabel Cristina Reinheimer, Alexandre Gomes Sancho, and Bartira Ercília Pinheiro da Costa.
• Graduate Program in Medicine and Health Sciences of the Pontifical Catholic University of Rio Grande do Sul (PUC/RS), Porto Alegre, Rio Grande do Sul, Brazil,School of Medicine of the Pontifical Catholic University of Rio Grande do Sul (PUC/RS), Porto Alegre, Rio Grande do Sul, Brazil,Universidad Popular Autónoma del Estado de Puebla, Puebla, Puebla, México,Universidade Estadual Vale do Acaraú, Fortaleza, Ceará, Brazil,Federal University of Health Sciences of Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil,Instituto Celulare, Itaipava, Rio de Janeiro, Brazil,Rigshospital, Copenhagen East, København, Denmark,Centro Universitário do Rio Grande do Norte, Natal, Rio Grande do Norte, Brazil,Università degli Studi di Napoli Federico II, Napoli, Campania, Italia,Universidad Finis Terrae, Providencia, Santiago, Chile,Unigranrio, Rio de Janeiro, Rio de Janeiro, Brazil.
• Medicine (Baltimore). 2022 Mar 18; 101 (11).

AbstractPatients with severe COVID-19 may have endothelial dysfunction and a hypercoagulable state that can cause skin damage. In the presence of external pressure on the tissues, the local inflammatory process regulated by inflammatory cytokines can increase and prolong itself, contributing to the formation of pressure injury (PI). PI is defined as localized damage to the skin or underlying tissues. It usually occurs as a result of intense and/or prolonged pressure in combination with shear. The aim of the study is to perform a narrative review on the physiological evidence of increased risk in the development of PI in critically ill patients with COVID-19.In patients with severe COVID-19 a pattern of tissue damage consistent with complement-mediated microvascular injury was found in the lungs and skin of critically ill COVID-19 patients, suggesting sustained systemic activation of complement pathways. Theoretically, the same thrombogenic vascular changes related to COVID-19 that occur in the skin also occur in the underlying tissues, making patients less tolerant to the harmful effects of pressure and shear. Unlike the syndromes typical of acute respiratory illnesses and other pathologies that commonly lead to intensive care unit admission, COVID-19 and systemic viral spread show that local and systemic factors overlap. This fact may be justified by current epidemiological data showing that the prevalence of PI among intensive care unit patients with COVID-19 was 3 times higher than in those without COVID-19. This narrative review presents physiological evidence to suggesting an increased risk of developing PI in critically ill patients with COVID-19.Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.

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