Physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues: A scoping review

Abstract

Deep tissue injuries are pressure ulcers which initiate in the subcutaneous tissues and extend through a bottom‐up pathway. Once deep tissue injuries are visual at skin level, serious irreversible tissue damage has already occurred. In pressure ulcer development, inflammation and edema are coupled physiological processes associated with tissue damage arising due to sustained mechanical loading. This study aimed to provide an in‐depth overview of the physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues, in the context of pressure ulceration. A scoping review was performed according to the framework by Arksey and O'Malley. The databases MEDLINE, EMBASE, Web of Science, and Scopus, and the reference lists of included studies were searched for in vivo (animal, human), and in vitro studies matching the study objectives (from inception to 28 May 2018). No restrictions for inclusion were applied for study design, setting, participants, and year of publication. A total of 12 studies were included, varying in study design, sample characteristics, amount and duration of mechanical loads that were applied, follow‐up time, and assessment methods. Neutrophil infiltration and edema occur in the subcutaneous tissues nearly immediately after the application of load on soft tissues. The amount of neutrophils and edema increase in the first days after the mechanical insult and decrease once healing has been initiated and no supplementary mechanical load was applied. One study indicated that edema may extend up to the level of the dermo‐epidermal junction. Further research should focus on how deep tissue inflammation and edema are reflected into unique tissue changes at skin level, and how abnormal inflammatory responses manifest (e.g. when the nervous system is not functioning normally).

The sorptivity and durability of gelling fibre dressings tested in a simulated sacral pressure ulcer system

“…This enables extravasation and infiltration of immune system cells (leukocytes) to the damaged tissue and, consequently, results in exudate leakage from the vasculature surrounding the wound. [4][5][6][7] Exudate is a serum-based fluid with a dynamic composition of neutrophils and proteins, which typically correlate to the healing phase, presence of pathogens, and the overall severity of the specific wound. A mildly moist wound environment is needed for adequate healing 8 as the exudate facilitates transport of essential nutrients, as well as immunological factors, to the wound bed 8,9 ; stimulates fibroblast and endothelial cell proliferation 10 ; and improves epithelisation.…”

Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment

“…However, the mechanism of pressure injury has unique elements that require more specific preventative and therapeutic intervention. Major components of pressure ulcer pathogenesis include ischemia-reperfusion injury, poor lymphatic drainage, cellular deformation, and excess cellular apoptosis and extracellular matrix (ECM) breakdown resulting in a chronic inflammatory state and dysregulated healing [17,18]. Immunocompromised patients, such as those with diabetes or chronically ill patients in the ICU, are particularly prone to the development of chronic pressure ulcers due to immune system dysregulation and impaired wound healing [19].…”

“…Ischemia-reperfusion events within chronic pressure ulcer pathogenesis typically follow a repetitive pattern of insults, rather than a single episode of ischemia followed by reperfusion [20]. Mechanical pressure causes capillary and venous obstruction that results in local tissue ischemia and edema, often starting in deep tissues and extending superficially [17]. The process of ischemia results in reduced ATP generation and impaired mitochondrial oxidative phosphorylation, increased complement and leukocyte activation, and elevated levels of inflammation [20].…”

Novel Functions of the Septin Cytoskeleton

“…1,2 Similarly, the physical properties of affected tissues change due to acute and chronic inflammation-induced development of edema, aberrant tissue remodeling, and fibrosis. 3,4 On a cellular level, inflammatory states result in functional adaptations toward accelerated recognition and elimination of the invaded pathogens, as well as enhanced production of extracellular matrix and tissue turnover. 2,5,6 These alterations of cellular function in inflamed tissues are mediated by reprograming of the fundamental molecular processes, including gene expression, protein synthesis, vesicle trafficking, and cytoskeletal assembly.…”