What is new in our understanding of pressure injuries: the inextricable association between sustained tissue deformations and pain and the role of the support surface

Abstract

For referencing Gefen A & Soppi E. What is new in our understanding of pressure injuries: the inextricable association between sustained tissue deformations and pain and the role of the support surface.

COVID-19: pressure ulcers, pain and the cytokine storm

“…Indeed, elevated creatinine kinase levels confirm skeletal muscle tissue involvement in COVID-19. 8 Inflammation, which is a key factor in PU development, 1,2 as detailed in the recent International Clinical Practice Guideline, 3 is fundamentally correlated to pain in general 9 and to pain caused by COVID-19 in particular (Fig 1). The pro-inflammatory cytokines IL-6 and TNF-α contribute not only to the onset and maintenance of inflammation following localised mass cell death events, as in a forming PU, but also to the development of pain by stimulating nociceptors.…”

“…10 Specifically, IL-6 and TNF-α, which are associated with forming PUs, [11][12][13] are also known to play important roles in pathological pain. 9,14,15 Irritation of nociceptors by pro-inflammatory cytokines, causing an 'inflammatory pain', is the first of the three possible primary pain contributors to the localised pain sensation associated with exposure to sustained cell and tissue deformations and consequent cell death (Fig 1). 9 The second pain contributor, 'nociceptive pain', is caused by mechanical irritation of nociceptors as the inflammatory oedema builds up and interstitial pressures rise (Fig 1).…”

“…9,14,15 Irritation of nociceptors by pro-inflammatory cytokines, causing an 'inflammatory pain', is the first of the three possible primary pain contributors to the localised pain sensation associated with exposure to sustained cell and tissue deformations and consequent cell death (Fig 1). 9 The second pain contributor, 'nociceptive pain', is caused by mechanical irritation of nociceptors as the inflammatory oedema builds up and interstitial pressures rise (Fig 1). 9,16 If the skin breaks down and an open wound forms, direct mechanical loading on the exposed nerve endings will further intensify the above nociceptive pain.…”

“…9 The second pain contributor, 'nociceptive pain', is caused by mechanical irritation of nociceptors as the inflammatory oedema builds up and interstitial pressures rise (Fig 1). 9,16 If the skin breaks down and an open wound forms, direct mechanical loading on the exposed nerve endings will further intensify the above nociceptive pain. 17 The third pain contributor, 'ischaemic pain', is due to the ischaemic and acidotic biochemical conditions that form in and around a PU site once the inflammatory oedema and associated increased interstitial pressures join the pressure and shear caused by the body weight forces or medical device to compromise the blood perfusion and tissue oxygenation (Fig 1).…”

“…17 The third pain contributor, 'ischaemic pain', is due to the ischaemic and acidotic biochemical conditions that form in and around a PU site once the inflammatory oedema and associated increased interstitial pressures join the pressure and shear caused by the body weight forces or medical device to compromise the blood perfusion and tissue oxygenation (Fig 1). 9 Accumulation of lactic acid in ischaemic tissue regions (as hypoxic cells shift to an anaerobic metabolic pathway) lowers the tissue pH and causes extracellular ATP levels to rise, both of which escalate the ischaemic pain. [18][19][20][21] The multifactorial localised pain, consisting of the above inflammatory, nociceptive and ischaemic pain components (Fig 1), is therefore strongly coupled with the main vicious cycle of PU development, in which inflammatory and ischaemic damages also play a key role.…”