Risk factors for HASPI formation include prolonged periods of immobility, decreased sensory perception, decreased mobility, increased moisture, and poor nutrition, many of which are typically present in hospitalized COVID-19 patients ( 9). Given the significant risk of HASPIs in hospitalized patients, most hospitals have developed protocols involving monitoring for early pressure-induced changes and routine off-loading measures in attempts to prevent them. The most common cause of sacral ulcers in hospitalized patients are hospital- acquired sacral pressure injuries (HASPIs), which occur secondary to unremitting pressure on the sacral and/or buttocks region ( 9, 10). Sacral ulcers are a leading cause of cutaneous-related patient morbidity in hospitalized patients ( 7, 8). These manifestations may cause minor adverse symptoms and exacerbate patient morbidity, but significant skin damage is rare. The skin is among the organs affected by COVID-19, with manifestations including various localized or diffuse exanthems and retiform or acral purpura associated with thrombotic vasculopathy ( 2– 6). Patients with coronavirus disease 2019 (COVID-19) develop multi-organ manifestations and tissue damage secondary to both intrinsic properties of the SARS-CoV-2 virus and the resultant host immune response ( 1). Overall, our results suggest that immunologic dysregulation secondary to SARS-CoV-2 infection, including neutrophil dysfunction and abnormal thrombosis, may play a pathogenic role in development of HASPIs in patients with severe COVID-19. SARS-CoV-2 viral transcripts were detected in skin tissue of COVID-19(+) patients with severe disease. Transcriptional signatures of COVID-19(+) samples were enriched for innate immune responses, thrombosis, and neutrophil activation genes. HASPI skin histology from COVID-19(+) patients predominantly showed thrombotic vasculopathy, with the number of thrombosed vessels being significantly greater than HASPIs from COVID-19(-) patients. Furthermore, COVID-19(+) patients with HASPIs had 2.2x odds of a more severe hospitalization course compared to COVID-19(+) patients without HASPIs. COVID-19(+) patients had a 63% increased HASPI incidence rate, HASPIs of more severe ulcer stage (OR 2.0, p<0.001), and HASPIs more likely to require debridement (OR 3.1, p=0.04) compared to COVID-19(-) patients. We determined the incidence, disease course, and short-term morbidity of HASPIs in COVID-19(+) patients, and characterized the skin histopathology and tissue gene signatures associated with HASPIs in COVID-19 disease. Patient demographics, hospitalization information, ulcer characteristics, and 30-day-related morbidity were collected for all patients with HASPIs, and intact skin was collected from HASPI borders in a patient subset. To explore the role of SARS-CoV-2 infection in HASPI development, we conducted a single institution, multi-hospital, retrospective study of all patients hospitalized for ≥5 days from Mato December 31, 2020. However, it is unknown whether SARS-CoV-2 infection affects HASPI development. Hospitalized patients have an increased risk of developing hospital-acquired sacral pressure injury (HASPI).
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