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.

Partial results of this paper were presented as an oral communication during ESHRE virtual 36 th Annual Meeting.

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Background Pressure injuries (PIs), especially in the sacral region are frequent, costly, and increase morbidity and mortality of patients in an intensive care unit (ICU). These injuries can occur as a result of prolonged pressure and/or shear forces. Neuromuscular electrical stimulation (NMES) can increase muscle mass and improve local circulation, potentially reducing the incidence of PI. Methods We performed a randomized controlled trial to assess the efficacy and safety of NMES in preventing PI in critically ill patients. We included patients with a period of less than 48 h in the ICU, aged ≥ 18 years. Participants were randomly selected (1:1 ratio) to receive NMES and usual care (NMES group) or only usual care (control group—CG) until discharge, death, or onset of a PI. To assess the effectiveness of NMES, we calculated the relative risk (RR) and number needed to treat (NNT). We assessed the muscle thickness of the gluteus maximus by ultrasonography. To assess safety, we analyzed the effects of NMES on vital signs and checked for the presence of skin burns in the stimulated areas. Clinical outcomes were assessed by time on mechanical ventilation, ICU mortality rate, and length of stay in the ICU. Results We enrolled 149 participants, 76 in the NMES group. PIs were present in 26 (35.6%) patients in the CG and 4 (5.3%) in the NMES group (p ˂ 0.001). The NMES group had an RR = 0.15 (95% CI 0.05–0.40) to develop a PI, NNT = 3.3 (95% CI 2.3–5.9). Moreover, the NMES group presented a shorter length of stay in the ICU: Δ = − 1.8 ± 1.2 days, p = 0.04. There was no significant difference in gluteus maximus thickness between groups (CG: Δ = − 0.37 ± 1.2 cm vs. NMES group: Δ = 0 ± 0.98 cm, p = 0.33). NMES did not promote deleterious changes in vital signs and we did not detect skin burns. Conclusions NMES is an effective and safe therapy for the prevention of PI in critically ill patients and may reduce length of stay in the ICU. Trial registration RBR-8nt9m4. Registered prospectively on July 20th, 2018, https://ensaiosclinicos.gov.br/rg/RBR-8nt9m4

Introduction: Pressure injury is 1 of the most common pressure related injuries in patients admitted to the intensive care unit. In individuals with darker skin tones, skin assessment protocols appear to be less effective, resulting in early damage from pressure. Bedside assessment measures using ultrasound and infrared thermography (IRT) have been studied to identify pressure injuries. Patient concerns: A 58-year-old dark-skinned male was admitted to the intensive care unit due to an ischemic stroke. Diagnosis: The visual evaluation of the skin took place on the second day after admission to the intensive care unit (before 48 hours). The patient had a whitish erythema on the left heel (LH) and a large bloody blister on the right heel. There were no signs of color change on the sacrum skin. Interventions: We performed 3 skin evaluations of the sacrum and calcaneus using ultrasound and IRT. Outcomes: Changes in the temperature of the target regions (sacrum, right heel and LH) were observed. The right heel showed higher mean temperatures than the LH in all evaluations. In the first evaluation of the sacrum region, the average temperature was lower (-1.3°C) than in the second and third evaluation (1°C). In the calcaneus, the mean temperature range (right heel - LH) showed a difference of (3.5°C) in the first evaluation, a difference of (1.4°C) in the second evaluation, and a difference of (1.7°C) in the third evaluation. Ultrasound images of the selected regions showed abnormal tissue patterns - edema - since the first evaluation. Conclusion: These findings indicate that the regions with deep tissue injury on ultrasound evaluation were compatible with the regions of abnormal temperatures in the IRT. IRT could identify regions of pathological process, which could be confirmed by abnormal ultrasound findings. Well-designed, randomized research with a larger sample could verify if the combination of these assessment techniques could be used as a potential method for early detection and evaluation of pressure injuries.