Does COVID-19 infection increase the risk of pressure injury in critically ill patients? A narrative review

Patients 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. Abbreviations: ACE2 = angiotensin-converting enzyme 2, AP = alternative complement pathway, ARDS = acute respiratory distress syndrome, C4d = complement component 4d, C5b-9 = complement membrane attack complex, CoVs = coronaviruses, ECM = extracellular matrix, eNOS = endothelial nitric oxide sintetase, ICU = intensive care unit, IL-1 = interleukin-1, IL-10 = interleukin-10, IL-1alpha = interleukin-1alpha, IL-1beta = interleukin-1beta, IL-6 = interleukin-6, LP = lectin complement pathway, MASP-2 = mannose-binding protein-associated serine protease 2, MBL = mannose-binding lectin, NOX2 = NADPH oxidase 2, PAI-1 = plasminogen activator inhibitor 1, PI = pressure injury, PubMed = Public Medline, RAAS = renin-angiotensin-aldosterone system, SARS-CoV = severe acute respiratory syndrome-related coronavirus, SciELO = Scientific Electronic Library Online, TNF-alpha = alpha tumor necrosis factor.