Editor’s note: Lawrence Charles Parish, MD, MD (Hon), FACP, FAAD, was one of the original members of the Editorial Board of Decubitus when it launched its volume 1, number 1 issue, in February 1988. This issue marks volume 25, issue 2, of the journal. Here, Dr Parish’s reflections, along with Clinical Editor R. Gary Sibbald, BSc, MD, MEd, FRCPC(Med Derm), MACP, FAAD, MAPWCA, may help clinicians prepare us for the next 25 years.
What have we learned during this past quarter of a century? Wound care practitioners and investigators are studying wounds, but does the patient suffering with the skin defect have a better outcome?
Discussion over terminology remains: bedsore, pressure ulcer (PrU), or pressure sore? Is the name pressure sore even accurate for the current nomenclature? There is the extreme of torsion stress to downplay the poor connotation of a skin defect. With the pathophysiology of the PrU far from clear, the name is only for reference.
The etiology must include the role of moisture and friction as paramount for superficial ulcers often classified as Stage I or II. These ulcers seldom transition into Stage III or IV ulcers with an etiology more related to pressure and shear as explored in ‘‘Pressure Ulcer Staging Revisited: Superficial Skin Changes and Deep Pressure Ulcer Framework,’’ December 2011 issue of Advances in Skin &Wound Care. Investigating the nomenclature even further, a so-called Stage I PrU is an area of fixed erythema.
The skin can only react in so many ways, and the etiology of this type of skin change is enormous. A lack of sensitivity and specificity exists when PrU prevalence and incidence studies include Stage I lesions that can represent anything dermatological from a suspected deep tissue injury (see ‘‘Deep Tissue Injury: 25 Years of Learning,’’ page 59) to the nonblanchable erythema of pressure-related damage to a fixed drug reaction, urticarial vasculitis, or a plethora of other dermatological diagnoses.
The dermatological definition of an ulcer is loss of skin with a dermal or deeper base, and yet a Stage I lesion has no loss of skin. A Stage II ulcer has loss of skin with an epidermal base (partial loss of epidermis morphologically is an erosion and not an ulcer) or dermal base, but not to subcutaneous fat (the only true ulcer in the Stage I and II classification system). Should all Stage I and II lesions be referred to as PrUs when the main component is probably unwanted skin surface moisture and friction?
A PrU is an ulceration that can extend from the stratum corneum through the dermis and subcutaneous tissue down to bone. It can still be destructive and deceiving, such as the undermining or tunneling that can occur.
Perhaps, not every ‘‘bedsore’’ is a PrU. If the ulcer occurs on the foot, it could be a diabetic foot ulcer. Should the defect be on the leg, then it may be a venous or arterial ulcer. When it develops on the sacrum, it could be even other diagnoses. Could the PrU really be a diagnosis of exclusion?
The wound bed preparation model, which was updated in the journal’s September 2011 issue, explores the diagnosis and treatment of wounds with a ‘‘wholistic’’ approach. To treat the whole patient, we must first look beyond the hole to the treatment of the cause and patient-centered concerns (eg, pain and activities of daily living). The treatment of the causes and other factors, such as incontinence of stool and urine, nutritional deficiencies, friction and shear, and patient/client mobility, is important.
It is also important to note that not all PrUs are preventable. A patient dying of cancer in negative protein balance may develop a PrU as the vital organs fail and the cutaneous blood supply is compromised. And, coexisting medications and diseases may make the PrU unavoidable. We need mechanisms to acknowledge this reality and not penalize healthcare professionals or institutions for poorquality care in these circumstances.
Staging has certain merit, but it may have created more confusion. What may appear to be a Stage I in the left quadrant of the defect could be called a Stage II in the right quadrant. Thus, we may be more correct to use simple descriptors, such as blanchable erythema, nonblanchable erythema, superficial ulcer, deep ulcer, and eschar/gangrene, without implying an etiology before completely assessing and investigating the patient.
Treatment and Prevention
Treatment and prevention are not the same actions and are often confused. Treating the cause of a wound or PrU includes pressure assessment and treatment of all surfaces, such as the bed, chair, commode, car seat, and so on; nutrition includes more than just albumin, but there must be adequate protein intake to produce granulation tissue necessary for the healing process to fill the dermal or deeper defect; friction and shear that are problems with transfers or just sitting up in bed; moisture and the need to avoid the damaging effects from incontinence of stool and urine along with damage from perspiration; and mobility and level of consciousness issues for the bedbound or spinal cord injury population.
Many PrUs can be prevented in the right scenario: a team of healthcare professionals working with patients under an institutional policy with resources to deliver best clinical practices. Is the person with the PrU better off today? The answer is they could be. These improved outcomes require the integrated and specialized interprofessional team approach, facilitated by advances in knowledge and institutional financial and resource support outlined by the knowledge translation into a practice paradigm.