Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients

Characterization of the transcriptional signatures of 771 human genes and 19 coronavirus genes in skin samples collected from the borders of hospital-acquired sacral pressure injuries (HASPIs) that developed in individuals with and without COVID-19. Samples included pressure ulcers from individuals without COVID-19 (10), pressure ulcers from individuals with COVID-19 (5), as well as pressure ulcers with thrombotic vasculopathy histopathology from individuals with COVID-19 (8). Patients with HASPIs were identified as having been hospitalized for greater than 5 days within Cleveland Clinic between March 1 and December 31, 2020, with an ICD-10 diagnosis of sacral ulcer or photographic documentation of sacral ulceration at some point during hospitalization. Histopathologic characteristics of biopsied patients were qualitatively and quantitatively assessed using hematoxylin & eosin (H&E) stained tissue specimens by a board-certified dermatopathologist. For COVID-19(+) patients, 4mm biopsies from (typically) areas of sacral purpura were obtained. For control COVID-19(-) specimens, which were typically submitted to pathology during debridement, a search of Cleveland Clinic pathology archives was performed to find specimens from pressure ulcers. H&E sections of all available specimens were reviewed to identify those appropriate to use as control specimens. Any specimens with histologic features suggestive of secondary infection, extensive epidermal ulceration, or prominent fibrosis (supporting significant chronicity) were excluded. RNA was extracted from Formalin-Fixed and Paraffin Embedded (FFPE) tissue biopsies and analyzed using NanoString Human Autoimmune Profiling Panel and spike in Coronavirus Panel Plus probe sets. Raw data was initially processed using the nSolver Analysis Software (V.4.0).