Pressure injuries have been identified as one of the main health hazards among bedridden elderly people. Bedridden elderly people often stay in the same position for a long time, because they cannot switch positions; thus, the blood flow in the part of the body that is being compressed between the bed and their own weight is continuously blocked. As a result, redness and ulcers occur due to lacking oxygen and nutrients in the skin tissues, and these sites are often infected with microorganisms and, thus, become suppurative wounds, a condition commonly determined as pressure injuries. If left untreated, the pressure injury will recur with microbial infections, often resulting in cellulitis, osteomyelitis, and sepsis. The skin microbiome, in which many types of bacteria coexist, is formed on the skin surface. However, it remains unclear what characteristic of the skin microbiome among the bedridden elderly constitutes the development and severity of pressure injuries and the development of post-pressure injury infections.
The most common site of a pressure injury is the area that is in direct contact with the bed and is continuously compressed, i.e., back of head, ear, shoulder, elbow, hip area, sacrum, heel, and ankle . External factors (pressure acting perpendicular to the tissue and stress against tension and shear caused by friction between the tissue and the supporting surface) and internal factors (aging, undernutrition, paralysis, various skin abnormalities, etc.) have been determined to be the causative factors of pressure ulcers . Especially in the case of undernutrition, the risk of developing a pressure injury remains high . In addition, the symptoms of pressure injuries only become severe if left untreated.
One indicator of pressure injury progression is the National Pressure Ulcer Advisory Panel (NPUAP) classification , which categorizes pressure injuries into the following: suspected Stage 1 pressure injury, Stage 2 pressure injury, Stage 3 pressure injury, Stage 4 pressure injury, Unstageable pressure injury, and Deep tissue pressure injury. Stage 1 pressure injury indicates intact skin with a localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. The presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration. Stage 2 pressure injury indicates a partial-thickness loss of skin with exposed dermis. The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose is not visible, and deeper tissue is not visible. Granulation tissue, slough and eschar, are not present. These injuries commonly result from adverse microclimates and shear in the skin over the pelvis and shear in the heel. Stage 3 pressure injuries indicate full-thickness skin losses, in which adipose is visible in the ulcer and granulation tissue, and epibole (rolled wound edges) is often present. Slough and/or eschar may be visible. The depth of the tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage, or bone is not exposed. If slough or eschar obscures the extent of tissue loss, this is an unstageable pressure injury. Stage 4 pressure injuries indicate that full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining, and/or tunneling often occur. The depths vary by anatomical location. If slough or eschar obscures the extent of the tissue loss, this is an unstageable pressure injury. Unstageable pressure injuries indicate full-thickness skin and tissue loss, in which the extent of tissue damage within the ulcer cannot be confirmed, because it is obscured by slough or eschar. If slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar (dry, adherent, and intact, without erythema or fluctuance) on an ischemic limb or heels should not be softened or removed. Deep tissue pressure injuries indicate intact or nonintact skin with localized areas of persistent non-blanchable deep red, maroon, purple discoloration, or epidermal separation revealing a dark wound bed or blood-filled blister. Pain and temperature changes often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone–muscle interface. The wound may evolve rapidly to reveal the actual extent of the tissue injury or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscles, or other underlying structures are visible, this indicates a full-thickness pressure injury .
Basically, as the pressure injury progresses, the category in the NPUAP classification shifts from a Stage 1 pressure injury to a Stage 4 pressure injury, and the range of the injury progresses from the epidermis to the dermis and further to the subcutaneous tissue and bone. It should be noted that the lesions are usually infected with pathogenic microorganisms, which are mainly bacteria, and the infection often contributes to the onset, progression, and recurrence of the pressure injury. Further, the infection on the pressure injury lesions often results in cellulitis, osteomyelitis, and sepsis, which, in turn, can lead to death . It is thought that the majority of pressure injury infections are caused by the dermis getting exposed due to damage to the epidermis and with the exposed area getting infected with pathogenic microorganisms .
What kind of bacteria exist in the prelesion of a pressure injury, and which bacteria contribute to the onset, progression, and recurrence of pressure injuries? Although various investigators have examined and reported on the above questions, there remains no clear answer.
2. The Skin and the Skin Residential Microbiome among Bedridden Elderly and Their Association with the Risk of Pressure Injury
2.1. Skin Structure, Skin Physiology, and Skin Residential Microbiome in Elderly People
2.2. Characteristics of Residential Microbiome of the Dorsal Sacral Skin in Bedridden Elderly People Compared with Ambulatory Elderly People and Healthy Young People
2.3. Association of Skin Microbiome with the Onset of Pressure Injury and Post-Pressure Injury Infections in Bedridden Elderly
- 1. Chew, H.-S.J.; Thiara, E.; Lopez, V.; Shorey, S. Turning frequency in adult bedridden patients to prevent hospital-acquired pressure ulcer: A scoping review. Int. Wound J. 2017, 15, 225–236.
- 2. Krapfl, L.A.; Gray, M. Does Regular Repositioning Prevent Pressure Ulcers? J. Wound Ostomy Cont. Nurs. 2008, 35, 571–577.
- 3. Black, J.M.; Edsberg, L.E.; Baharestani, M.M.; Langemo, D.; Goldberg, M.; McNichol, L.; Cuddigan, J.; National Pressure Ulcer Adisory Panel. Pressure ulcers: Avoidable or unavoidable? Results of the National Pressure Ulcer Advisory Panel Consensus Conference. Ostomy Wound Manag. 2011, 57, 24–37.
- 4. Low, L.L.; Vasanwala, F.F.; Tay, A.C. Pressure Ulcer Risk Assessment and Prevention for the Family Physician. Proc. Singap. Healthc. 2014, 23, 142–148.
- 5. Hagisawa, S.; Ferguson-Pell, M. Evidence supporting the use of two-hourly turning for pressure ulcer prevention. J. Tissue Viability 2008, 17, 76–81.
- 6. Cooper, K.L. Evidence-Based Prevention of Pressure Ulcers in the Intensive Care Unit. Crit. Care Nurse 2013, 33, 57–66.
- 7. Moore, Z.; Cowman, S.; Conroy, R.M. A randomised controlled clinical trial of repositioning, using the 30 tilt, for the prevention of pressure ulcers. J. Clin. Nurs. 2011, 20, 2633–2644.
- 8. Rich, S.E.; Margolis, D.; Shardell, M.; Hawkes, W.G.; Miller, R.R.; Amr, S.; Baumgarten, M. Frequent manual repositioning and incidence of pressure ulcers among bed-bound elderly hip fracture patients. Wound Repair Regen. 2010, 19, 10–18.
- 9. Shea, J.D. Pressure sores: Classification and management. Clin. Orthop. Relat. Res. 1975, 112, 89–100.
- 10. International Association of Enterostomal Therapists. Dermal wound: Pressure sores. Philosophy of the IAET. J. Enteros. Ther. 1988, 15, 4–17.
- 11. Zeller, J.L.; Lynm, C.; Glass, R.M. JAMA patient page. Pressure ulcers. JAMA 2006, 296, 1020.
- 12. Medical Advisory Secretariat. Management of Chronic Pressure Ulcers. Ont. Health Technol. Assess. Ser. 2009, 9, 1–203.
- 13. Edsberg, L.E.; Blacj, J.M.; Goldberg, M.; McNichol, L.; Moore, L.; Sieggreen, M. Revised national pressure ulcer advisory panel pressure injury staging system: Revised pressure injury staging system. J. Wound Ostomy Cont. Nurs. 2016, 43, 585–597.
- 14. Norman, G.; Dumville, J.C.; Moore, Z.E.H.; Tanner, J.; Christie, J.; Goto, S.; Cochrane Wounds Group. Antibiotics and anti-septics for pressure ulcers. Cochrane Database Syst. Rev. 2016, 4, CD011586.
- 15. Bowler, P.G.; Duerden, B.I.; Armstrong, D.G. Wound Microbiology and Associated Approaches to Wound Management. Clin. Microbiol. Rev. 2001, 14, 244–269.
- 16. Centers for Disease Control and Prevention (CDC); Horan, T.C.; Andrus, M.; Dudeck, M.A. CDC/NHSN surveillance defini-tion of health care–associated infection and criteria for specific types of infections in the acute care setting. Am. J. Infect. Cont. 2008, 36, 309–332.
- 17. Bowler, P.G. The 10(5) bacterial growth guideline: Reassessing its clinical relevance in wound healing. Ostomy Wound Manag. 2003, 49, 4–53.
- 18. Davies, C.E.; Hill, K.E.; Newcombe, R.G.; Stephens, P.; Wilson, M.J.; Harding, K.G.; Thomas, D.W. A prospective study of the microbiology of chronic venous leg ulcers to reevaluate the clinical predictive value of tissue biopsies and swabs. Wound Repair Regen. 2007, 15, 17–22.
- 19. Madsen, S.M.; Westh, H.; Danielsen, L.; Rosdahl, V.T. Bacterial colonisation and healing of venous leg ulcers. APMIS 1996, 104, 895–899.
- 20. Trengove, N.J.; Stacey, M.C.; McGechie, D.F.; Stingemore, N.F.; Mata, S. Qualitative bacteriology and leg ulcer healing. J. Wound Care 1996, 5, 277–280.
- 21. Percival, S.L.; Bowler, P.G. Biofilms and their potential role in wound healing. Wounds 2004, 16, 234–240.
- 22. Wolcott, R.D.; Rhoads, D.D.; Dowd, S.E. Biofilms and chronic wound inflammation. J. Wound Care 2008, 17, 333–341.
- 23. Nagase, S.; Ogai, K.; Urai, T.; Shibata, K.; Matsubara, E.; Mukai, K.; Matsue, M.; Mori, Y.; Aoki, M.; Arisandi, D.; et al. Distinct Skin Microbiome and Skin Physiological Functions Between Bedridden Older Patients and Healthy Peo-ple: A Single-Center Study in Japan. Front. Med. 2020, 7, 101.
- 24. Schommer, N.N.; Gallo, R.L. Structure and function of the human skin microbiome. Trends Microbiol. 2013, 21, 660–668.
- 25. Ying, S.; Zeng, D.N.; Chi, L.; Tan, Y.; Galzote, C.; Cardona, C.; Lax, S.; Gilbert, J.; Quan, Z.-X. The influence of age and gen-der on skin-associated microbial communities in urban and rural human populations. PLoS ONE 2015, 10, e0141842.
- 26. Roghmann, M.C.; Lydecker, A.D.; Hittle, L.; DeBoy, R.T.; Nowak, R.G.; Johnson, J.K.; Mongodin, E. Comparison of the mi-crobiota of older adults living in nursing homes and the community. mSphere 2017, 2, e00210-17.
- 27. Christensen, G.J.M.; Brüggemann, H. Bacterial skin commensals and their role as host guardians. Benef. Microbes 2014, 5, 201–215.
- 28. Lambers, H.; Piessens, S.; Bloem, A.; Pronk, H.; Finkel, P. Natural skin surface pH is on average below 5, which is beneficial for its resident flora. Int. J. Cosmet. Sci. 2006, 28, 359–370.
- 29. Mugita, Y.; Minematsu, T.; Huang, L.; Nakagami, G.; Kishi, C.; Ichikawa, Y.; Nagase, T.; Oe, M.; Noguchi, H.; Mori, T.; et al. Histopathology of Incontinence-Associated Skin Lesions: Inner Tissue Damage Due to Invasion of Proteolytic Enzymes and Bacteria in Macerated Rat Skin. PLoS ONE 2015, 10, e0138117.
- 30. Rippke, F.; Berardesca, E.; Weber, T.M. pH and Microbial Infections. Curr. Probl. Dermatol. 2018, 54, 87–94.
- 31. Shibata, K.; Ogai, K.; Ogura, K.; Urai, T.; Aoki, M.; Arisandi, D.; Takahashi, N.; Okamoto, S.; Sanada, H.; Sugama, J. Skin Physiology and its Microbiome as Factors Associated with the Recurrence of Pressure Injuries. Biol. Res. Nurs. 2021, 23, 75–81.