WHS guidelines for the treatment of pressure ulcers—2023 update

1 INTRODUCTION

The major populations at risk for developing pressure ulcers are older adults who have multiple risk factors that increase their vulnerability, people who are critically ill and those with spinal cord injury/disease. The reported prevalence of pressure ulcers in the United States is 2.5 million.¹ However, this estimate is derived from acute care facilities and does not include people who are living at home or in nursing facilities. Despite implementation of hospital and facility-based preventive measures, the incidence of pressure ulcers has not decreased in decades. In addition to the burden of pain, infection and death, it is estimated that hospital-acquired pressure ulcers cost the health system $26.8 billion annually with over 50% of the cost attributed to treating Stage 3 and 4 pressure injuries.² Thus, it is critical to examine the literature and develop guidelines that will improve the outcomes of this complex and costly condition.

In 2016 the National Pressure Ulcer Advisory Panel (NPUAP), now National Pressure Injury Advisory Panel (NPIAP), met for a ‘Staging Consensus Conference’. Based on the report of a task force and the consensus obtained at that conference, NPIAP recommended changing terminology from pressure ulcer to pressure injury, attempting to provide a better description of the stages that do not present with an open wound, that is, Stage I and Deep Tissue Injury.³ Even years later, CMS, ICD-10, national and international organisations and the literature in general remain conflicted with some references to injury but most have retained the term ‘ulcer’.⁴ The terminology change is also confusing depending upon the duration of the wound, as clinicians are taught to change to ‘ulcer’ when a wound has been present for more than 30 days and some wounds are always referred to as ulcers, for example, diabetic foot, venous leg and arterial ulcers. This update to the Wound Healing Society guidelines will not, and is not intended to, solve the problems of terminology or staging. For consistency, the authors have agreed to use the ‘pressure ulcer’ terminology in the preamble, stated guideline and principle, yet it will be clear that there is not a consensus in the cited literature.

2 METHODS

There has been a proliferation of clinical guidelines since they were first recommended by the Institute of Medicine in 1990. Although the field has matured since the initial publication of the Wound Healing Society Guidelines in 2006, evidence for treatment of chronic wounds suffers from a lack of unbiased, randomised clinical trials. Thus, large-scale reviews, such as Cochrane, usually state that there is limited evidence to support the questions that are posed. This guideline update is a compendium of the best available evidence for the treatment of Pressure Ulcers published since the last update in 2015.⁵ As such, the current work should be considered supplemental and complimentary to the original and 2015 update. The overall goal of the Wound Healing Society Guideline project is to present clear, concise and commercial free guidelines that clinicians can use to guide care, that researchers can use to develop studies that will improve treatment and that both clinicians and researchers can use to understand the gaps in our knowledge base.

3 RESULTS

4 NUTRITION

Preamble: Successful healing depends on collagen synthesis/deposition and epithelial resurfacing, both processes being highly dependent on adequate nutrient stores and support. Protein, carbohydrates, vitamins, minerals, and trace elements play critical roles in these events. Nutritional status consistently stands out as a significant factor in the prevention and treatment of pressure ulcers. In spite of this very strong association, there are limited definitive studies documenting the efficacy of nutritional therapy for pressure ulcer healing.

Guideline 2.1: Nutritional assessment should be performed on entry to a new healthcare setting and whenever there is a change in an individual's health status that may increase the risk of malnutrition. (Level II – no change).

Principle: Nutritional intake must meet the patient's need for sufficient protein and energy to support the growth of granulation tissue. The patient's weight documented at health care visits or on admission to a clinical setting is a good starting point. Assess body weight regularly and when there is a change in an individual's condition that may increase the risk of undernutrition.

Pressure ulcer patients, even those who are overweight or obese, are often malnourished and protein deficient as evidenced by levels of low nutritional biomarkers and other performance status. Assessment of pre-albumin level (reflecting recent protein consumption) and serum albumin level (reflecting long-term protein consumption) is useful to identify outpatient ambulatory patients who are malnourished. These markers are not very effective in hospitalised or ill patients where levels of serum albumin and pre-albumin are influenced by hydration status, presence of infection, or acute stress and thus may not reflect actual nutritional deficit. No individual clinical parameter accurately and consistently identifies adult malnutrition. The Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition suggest that presence of two or more of the following six parameters are strongly diagnostic of malnutrition: insufficient energy intake, weight loss, loss of muscle mass, loss of subcutaneous fat, localised or generalised fluid accumulation that may mask weight loss, and decreased functional status measured by hand grip. Other laboratory values associated with inflammation such as C-reactive protein, white blood cell count or blood glucose may be helpful in determining if malnutrition is related to starvation, chronic disease or acute disease/injury.

Resting energy expenditure is increased in patients with pressure ulcers while at the same time energy intake may be inadequate. Standard clinical approaches to determine energy requirements may underestimate actual need. Therefore, calculation of intake (kcal/kg/day) to meet true energy demand may require adjustment (increase) to account for this in patients with pressure ulcers. Encourage nutritional support if an individual is undernourished. Under-nutrition is associated with poor clinical outcomes, including increased risk of mortality, so early identification of actual or potential nutritional need allows for timely intervention to mitigate nutritional decline.

Guideline 2.2: Promote nutritional supplementation if an undernourished individual is at risk of developing a pressure ulcer. (Level III – no change).

Principle: Nutrients are basic to cellular integrity and data suggest that a nutritional supplement may have a modest effect in preventing the development of pressure ulcers, largely in stage 1 ulcers. Dietary intake through meals and other supplementation should be monitored to assess intake adequacy.

Guideline 2.3: Ensure adequate dietary intake to prevent under-nutrition to the extent that this is compatible with the individual's wishes. (Level I – increased).

Principle: Adequate nutrition is essential for life and undernutrition is associated with the development of pressure ulcers. Providing nutrition supports pressure ulcer healing or improvement in ulcer status and is associated with preventing pressure ulcers. Nonetheless, the nutritional plan needs to be consistent with the individual's personal goals and medical condition.

Guideline 2.4: If dietary intake continues to be inadequate, impractical or impossible, nutritional support using other routes should be considered with the goal of achieving positive nitrogen balance (~30–35 calories/kg/day and 1.25–1.50 g of protein/kg/day) according to the goals of care. (Level II – increased).

Principle: Anabolism is facilitated with a positive nitrogen balance and when individuals are not able to meet nutritional needs through oral intake, alternative methods should be undertaken to optimise nutritional status.

Guideline 2.5: Give vitamin and mineral supplements if deficiencies are confirmed or suspected. (Level I – increased).

Principle: Supplements of vitamins and minerals that are needed for wound healing should be provided when intake is insufficient or when a deficit is identified. The unique contribution of specific vitamins, minerals or amino acids is uncertain. However, enhanced supplements consisting of various combinations of Vitamins A, C, E, zinc, fatty acids and arginine are associated with pressure ulcer healing and/or prevention of ulcer formation. Amino acid supplements have been effective in the healing some non-pressure related wounds. Emerging evidence suggests that arginine may increase the rate of healing in patients with pressure ulcers.

5 INFECTION

Preamble: Infection results when the microbe: host defence equilibrium is upset in favour of the microbes. Infection plays various roles in aetiology, healing, operative repair, and complications of pressure ulcers. Therefore, guidelines are necessary to address the treatment of infection in each of these circumstances.

Guideline 3.1: Treat distant infections (e.g., urinary tract, cardiac valves, cranial sinuses) with appropriate antibiotics in pressure ulcer-prone patients or patients with established ulcers. (Level II – no change).

Principle: Bacteria entering the bloodstream or lymphatics can lodge in compressed tissue, denervated tissue, oedematous tissue, or established wounds by the compromised tissue acting as a locus minoris resistentiae.

No updated evidence.

Guideline 3.2 (Revised): Remove all necrotic or devitalized tissue by sharp, enzymatic, biological, mechanical, ultrasonic or autolytic debridement. Larval therapy provides both debridement and antibacterial activity. Although there are no recent randomised controlled trials of larval therapy for pressure ulcers, this biologic therapy has been shown to reduce the time to debridement but does not significantly increase the rate of healing in leg ulcers. (Level I – no change).

Principle: Necrotic tissue is laden with bacteria while devitalized tissue impairs the body's ability to fight infection and serves as pabulum for bacterial growth.

Guideline 3.3 (revised): If there is suspected infection in a debrided ulcer, or if contraction and epithelialization from the margin are not progressing within 2 weeks of debridement and relief of pressure, determine the type and level of infection in the debrided ulcer by tissue biopsy or by a validated quantitative swab technique. Punch biopsies are a safe procedure for obtaining tissue for histologic or microbiologic analysis. (Level I – no change).

Principle: The reference standard for the diagnosis of infection of chronic wounds is a tissue biopsy for culture obtained after debridement to remove bacteria that are present as surface colonisation. If quantitative cultures are obtained, microbial loads of >10⁵ of any organism per gram of wound tissue or the presence of any level of beta-haemolytic streptococcus is typically considered an indicator of infection of chronic wounds.

(Level I – no change)

Principle: Classic signs of inflammation (purulent exudate, erythema, heat) may be absent in the presence of a wound infection. These signs are often used to diagnose infection; however, their presence/absence is not specific for infection, particularly in chronic wounds. The term ‘local wound infection’ more accurately describes the stage of infection in which covert (subtle) local clinical signs and symptoms of infection (e.g., pocketing, epithelial bridging and hypergranulation) can be identified by clinicians before the wound exhibits overt (classic) signs and symptoms of infection.

Guideline 3.5: Little evidence exists supporting the use of one type of wound cleansing solution or technique for pressure ulcers. Systemic antibiotics have not been shown to lower bacterial bioburden in wounds. Topical antimicrobials (silver-containing cream, antimicrobial containing foam dressing, cadexomer iodine) have been shown to decrease the bacterial load in an ulcer. Avoid wound cleansing with antiseptic agents as granulation tissue will be destroyed. Furthermore, tap water is also appropriate to use to cleanse wounds. (Level I – no change).

Principle: Pressure ulcers contain an endogenous bacterial load, which should be managed to prevent the progression from colonisation to infection.

Guideline 3.6: Obtain bacterial balance (<10⁵ cfu/g of tissue and no beta-haemolytic streptococci) in the pressure ulcer before attempting surgical closure by skin graft, direct wound approximation, pedicled or free flap. (Level I – no change).

Principle: A wound containing contaminated foci with >10⁵cfu/g of tissue cannot be readily closed, as the incidence of wound site complications including dehiscence and persistent infection is 50%–100%.

Guideline 3.7: Obtain bone biopsy for culture and histology in cases of suspected osteomyelitis associated with a pressure ulcer. (Level I – increased).

Principle: The sensitivity and specificity of noninvasive tests for diagnosing osteomyelitis are not as high as direct bone biopsy and are not as useful in determining treatment.

Guideline 3.8: Once confirmed, osteomyelitis underlying a pressure ulcer should be adequately debrided and treated with culture-guided antibiotics. Flap reconstruction with well-vascularized tissue may facilitate healing of osteomyelitis in appropriately selected patients. (Level I – no change).

Principle: Muscle, myocutaneous, and fasciocutaneous flaps effectively control bacterial levels under acute experimental conditions. However, acute osteomyelitis in pressure ulcers is associated with a high rate of recurrence unless eradicated by a combination of debridement of devitalized bone and antibiotic therapy. Not all patients are appropriate candidates for flap reconstruction. Culture-guided antibiotic therapy for osteomyelitis is recommended for 6 weeks. Eight weeks of antibiotic therapy is recommended for MRSA osteomyelitis.

Guideline 3.9: Heel ulcers do not need debridement if they lack signs of inflammation/infection (oedema, erythema, drainage) and are stable with intact dry eschar. (Level I – increased).

Principle: The determination of whether to debride heel ulcers depends upon the clinical goals. In those patients with dry heel eschar who cannot be revascularized, have multiple comorbidities, and are immobile with no functional goals the heel eschar may be left intact. Heel ulcers with dry eschar should be monitored closely and debrided if they develop signs of infection.

Guideline 3.10: The establishment of bacterial biofilm contributes to the development of chronic non-healing wounds. A biofilm should be suspected with poorly healing chronic wounds, as well as wounds with a high multispecies bacterial burden and can be identified using molecular microbial identification. Sharp debridement significantly reduces the number of microorganisms in a wound bed and is vital in biofilm control. Multiple other approaches and methods, such as laser light therapy, photodynamic therapy, low-frequency ultrasound, larval therapy, and wireless bio-electric dressings, have shown potential in combating biofilm infection. However, further research with randomised controlled trials is warranted to confirm clinical effectiveness of these alternative approaches. (Level I – increased)

Principle: Bacterial biofilm is a significant barrier to wound healing. Biofilms are communities of microorganisms organised into microcolonies that grow within a matrix of secreted extracellular polymeric substance. As a result, they are typically multispecies and metabolically inert. These characteristics make them resistant to most currently used antimicrobial techniques. In animal models, biofilm formation in the wound is associated with continuous inflammation and delayed wound healing.

Guideline 3.11: Minimally invasive methods to monitor the wound bed in real time may provide objective means to evaluate healing and guide therapy. Further research with randomised controlled trials is warranted for standardisation. One example is testing wound fluid for proteolytic activity. High levels of proteases may be indicative of wound infection or may be due to host factors. Concurrent treatment of wound infection with a targeted protease modulator may facilitate wound closure. Wound fluid can be retested as needed until the levels of proteases are normal. Vacuum drainage, extraction from absorbent material or collection beneath occlusive dressings can serve as methods for gathering samples of chronic wound fluid. The choice of collection technique hinges on factors such as the specific wound type and the volume of fluid involved. (Level I – increased).

Principle: The remodelling and deposition of extracellular matrix in the wound bed is affected by proteolytic activity. The total protease activity is a combination of host and bacterial proteases which act synergistically to promote tissue breakdown in infected wounds. Bacterial proteases may upregulate host production of matrix metalloproteinases. The combination of bacterial and host proteases can lead to an imbalance resulting in tissue destruction, cytokine degradation and loss of cellular function. Modulation of protease levels may facilitate healing.

6 WOUND BED PREPARATION

Preamble: Wound bed preparation is defined as the management of the wound to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures. The aim of wound bed preparation is to convert the molecular and cellular environment of a chronic wound to that of an acute healing wound.

Guideline 4.1: Examination of the patient as a whole is important to evaluate and correct causes of tissue damage. It is important to examine the patient's systemic diseases and medications. (Level I – no change).

Principle: When integrating the necessary steps of the wound bed preparation process, it is paramount to first consider other contributing aetiologies that might interfere with wound closure and to evaluate the individuals' other indirect comorbidities. General medical history, including a medication record, will help in identifying and correcting systemic causes of impaired healing. Any major illness, systemic disease or drug therapies that cause alterations in immune functioning, metabolism, nutrition, and tissue perfusion will interfere with wound healing. Systemic disease, such as systemic sepsis, organ failure, (hepatic, renal, respiratory, gut), major trauma/burns, diabetes, autoimmune diseases will delay wound healing.

Guideline 4.2: Examination of the patient as a whole is important to evaluate and correct causes of tissue damage. It is important to examine the patient's nutritional status. (Level II – no change).

Principle: Nutrition must be adequate to provide sufficient protein to support the growth of granulation tissue. Patients' barriers to achieving dietary sustenance should be kept in mind when prescribing supplementation. (See also the nutritional sections of this guideline).

No updated evidence.

Guideline 4.3: Examination of the patient as a whole is important to evaluate and correct causes of tissue damage. It is important to examine the patient's tissue perfusion and oxygenation. (Level I – no change).

Principle: Wounds will heal in an environment that is adequately oxygenated. Oxygen delivery to the wound will be impaired if tissue perfusion is inadequate. Dehydration and factors that increase sympathetic tone such as cold, stress, or pain will all decrease tissue perfusion. Cigarette smoking decreases tissue oxygen by peripheral vasoconstriction. Patients whose wounds are ischemic should be referred to a vascular surgeon before aggressively engaging in moist wound healing and wound debridement.

No updated evidence.

Guideline 4.4: Initial debridement is required to remove the obvious necrotic tissue, excessive bacterial burden, and cellular burden of dead and senescent cells. Please refer to Guideline 3.2 for additional methods of debridement that have been shown to reduce bacterial burden. Maintenance debridement is needed to maintain the appearance and readiness of the wound bed for healing.

The healthcare provider can choose from a number of debridement methods including sharp, mechanical, enzymatic and autolytic. More than one debridement method may be appropriate. (Level I – no change).

Principle: Once tissue perfusion is checked (see Guideline #4.3) and ischemia has been ruled out, initial and maintenance debridement of devitalized tissue in the wound bed should become routine with regards to wound care. Debridement will remove necrotic tissue, senescent cells, decrease bacterial bioburden and disrupt biofilms. The health care provider can choose from a number of debridement methods including sharp, mechanical, enzymatic and autolytic. More than one debridement method may be appropriate. Goals in selecting a debridement method include considerations of pain, acceptability to the patient and caregivers and availability (as not all methods are readily available). Wounds covered with dry eschar that are not infected, but ischemic should not be debrided until patient's arterial flow is re-established and/or unless symptoms of acute infection or wet gangrene ensue.

A. Surgical or sharp debridement: involves use of instruments (scissors, scalpels, forceps) or laser to remove necrotic tissue from the wound. Debridement of large amounts of necrotic tissue should be done in the operating room. Surgical debridement is indicated when the goal is to achieve fast and effective removal of large amounts of necrotic tissue. Surgical debridement is contraindicated if there is lack of expertise in this method, inadequate vascular supply to the wound and absence of systemic antibacterial coverage in systemic sepsis. Relative contraindication is bleeding disorders or anticoagulation therapy.

B. Mechanical debridement: physically removes necrotic tissue with wet-to-dry dressings, wound irrigation, and whirlpool techniques. Wet to dry dressing may induce mechanical separation of eschar but can be painful and if dry, may damage viable newly formed tissue. High or low pressure streams or pulsed lavage may be quite effective in removing loose necrotic tissue, provided the pressure does not cause trauma to the wound bed. Effective ulcer irrigation pressures range from 4 to 15 psi of pressure. A 30 mL syringe filled with saline can be used to flush a wound through an 18 gauge catheter. Irrigation pressures below 4 psi may not be effective to cleanse the wound and pressures greater than 15 psi may cause trauma and drive the bacteria into the tissue. Whirlpool therapy is no longer recommended due to increased risk for bacterial contamination, circulatory compromise and tissue maceration. There are other materials such as monofilament fibre technology that have demonstrated to be effective in removal of slough and biofilms and are atraumatic to wound bed.

C. Enzymatic debridement: is achieved by topical application of exogenous enzymes to the wound surface to remove necrotic tissue.

No updated evidence.

D. Autolytic debridement: is achieved when a moist wound environment is created over time by the use of an occlusive dressing. These dressings allow the natural wound fluid and its endogenous enzymes to soften and liquefy slough and promote granulation. During each dressing change the wound needs to be cleansed to remove devitalized tissue created in the autolytic process. If tissue autolysis is not apparent in 1–2 weeks, another debridement method should be used. Autolytic debridement is not recommended for infected wounds or very deep wounds that require packing.

No updated evidence.

E. Biological debridement: is the application of irradiated maggots delivered from the Lucilia sericata fly to a necrotic wound that both eat and chemically degrade necrotic tissue.

No updated evidence.

Guideline 4.5: Wounds should be cleansed initially and at each dressing change using a pH-balanced, nonirritating, nontoxic solution. Routine wound cleansing should be accomplished with a minimum of chemical and/or mechanical trauma. (Level III – no change).

Principle: Cleansing the wound removes loose impediments that can deter wound healing. Clinical experience has shown that mild soap (non-perfumed, without added anti-bacterial agents and at skin pH: 4.5–5.7) and water for cleansing, used regularly, is effective, safe and cheap. Using tap water from a reliable source does not increase the rate of infection (see Guideline #3.5). A 2008 Cochrane review on wound cleansers specifically for pressure ulcers supports the use of solutions that are least cytotoxic to the wound bed including saline, water, and acetic acid (0.5%–1.0%). However, there is currently no evidence to support the use of any particular wound cleanser over another. Wound antiseptic agents, for example, hydrogen peroxide, hypochlorite solution, acetic acid, chlorhexidine, povidone/iodine, cetrimide, and others have antibacterial properties, but are all toxic to healthy granulation tissue. Solutions with dilute stabilised hypochlorous acid as the active agent have shown efficacy against biofilms. Further studies are necessary to investigate and compare the in vivo efficacy of these products in clinical care.

Guideline 4.6: Infection control should be achieved by reducing wound bacterial burden and achieving wound bacterial balance. (For detailed information on this please refer to Guideline #3 on Infection) (Level I – no change).

Principle: Infection will cause wound healing failure often with progressive deterioration of the wound. Systemically administered antibiotics do not effectively decrease bacterial levels in granulating wounds. Other methods that may be suitable include enhancing host defence mechanisms, debridement, wound cleaning, and topical antimicrobials. For ulcers with 1 × 10⁶ or higher cfu/gram of tissue or any tissue level of beta haemolytic streptococci following adequate debridement, decrease the bacterial level by a topical antimicrobial. Once in bacterial balance, that is, 10⁵ cfu or less/gram of tissue and no beta haemolytic streptococci in the ulcer, discontinue the use of topical antimicrobial to minimise possibility of emergence of resistance. In chronic wounds, the pathogen species maybe more important than number of bacteria. Obtain bone biopsy for culture and histology (gold standard) in case of suspected osteomyelitis. Treat confirmed debrided osteomyelitis with flap containing muscle or fascia and culture-determined antibiotics.

No updated evidence.

Guideline 4.7: For nonischemic wounds, achieve local moisture balance by management of exudate. (Level I – no change).

Principle: Local moisture balance is necessary to facilitate granulation and reepithelization of the ulcer. A moist wound environment accelerates wound healing with more rapid epithelization. Many dressings now combine wound bed preparation, that is, debridement and/or antimicrobial activity, with moisture control. Moist wound dressings should keep the ulcer bed continuously moist and at the same time control the exudate to prevent desiccation of the ulcer bed and maceration of the peri-ulcer skin. The use of haemostatic dressings may be required immediately after sharp debridement, especially in patients taking anticoagulants. Moist dressings should be re-instituted as soon as haemostasis is achieved. Moist dressings may also be used in conjunction with mechanical or enzymatic debridement techniques. (For more details see Guideline #5: Dressings).

Guideline 4.8: Biofilm (new): Early intervention with multiple therapies and effective antibiofilm antiseptics is key to reduce biofilm and inflammation. (Level II).

Principle: Biofilm is prevalent in chronic wounds and a major barrier to wound healing. The immunological response to biofilms causes tissue damage and impairs healing. Wound biofilm makes the chronic wound resistant to topical and systemic antimicrobials unless the biofilm matrix is interrupted by debridement. Biofilms form not only on the surface of the wound but also exist below the surface. Debridement is one of the most important treatment strategies against biofilms, but does not remove all biofilm, and therefore cannot be used alone—this is one of the critical principles of wound bed preparation. Biofilms can reform rapidly; repeated debridement alone is unlikely to prevent biofilm regrowth; however, effective topical antiseptic application within this time-dependent window can suppress biofilm reformation.

Guideline 4.9: There should be an ongoing and consistent documentation of wound history, recurrence and characteristics (location, staging, size, base, exudates, infection condition of surrounding skin and pain). The rate of wound healing should be evaluated to determine if treatment is optimal. (Level III – no change).

Principle: Ongoing evaluations of wound bed preparation are necessary because if the ulcer is not healing at the expected rate, interventions for wound bed preparation need to be reassessed. The longer the duration of the ulcer, the more difficult it is to heal. If an ulcer is recurrent, patient education or issues of prevention and long-term maintenance need to be reassessed.

No updated evidence.

7 DRESSINGS

Preamble: There is a multitude of choices for topical treatment of pressure ulcers. Many dressings combine wound bed preparation, that is, debridement and/or antimicrobial activity, with moisture control and most strive for reducing the frequency of dressing changes to reduce overall treatment cost. These guidelines are intended to assist the clinician in making decisions regarding the value and best use of these advanced wound care products.

Guideline 5.1: Treat all nonischemic wounds using a dressing that will maintain a moist wound environment. (Level I – no change).

Principle: A moist wound environment physiologically favours cell migration and matrix formation while accelerating healing of wounds by promoting autolytic debridement. Moist wound healing also reduces wound pain.

Guideline 5.2 (revised): Use clinical judgement to select a moist wound dressing. (Level I – no change).

Principle: Results from existing studies have not demonstrated any specific moisture retentive topical therapy to be superior in terms of healing rate. Wet-to-dry dressings are not continuously moist and are an inappropriate wound dressing selection. Some dressings can provide both a moist wound environment and decrease bacterial bioburden in the wound (see References #9–17 (below) and also Guideline #4.6).

Guideline 5.3: Select a dressing that will manage the wound exudate and protect the peri-ulcer skin. (Level I – no change).

Principle: Periwound maceration and continuous contact with wound exudate can enlarge the wound and impede healing.

Guideline 5.4: Select a dressing that minimises issues with friction, shearing, skin irritation and additional pressure (Level II – no change).

Principle: Wound location, peri-wound skin quality, incontinence of urine or stool and patient activity can all affect the choice of dressing. Some dressings have been designed to be self-adherent; some are designed to fill a cavity. Additional tissue damage may result if the dressing causes increased pressure on the wound or damages adjacent tissue.

Guideline 5.5: Select a dressing that is cost effective. (Level I – no change).

Principle: Because the initial cost of moist gauze is lower than advanced wound care products, there is a perception that moist gauze is more cost effective. When determining cost efficacy, it is important to take into consideration health care provider time, patient care goals and resources, frequency of dressing changes, ease of use and healing rate, as well as the unit cost of the dressing.

8 SURGICAL TREATMENT

Preamble: Surgical treatment of pressure injury/ulcers is often considered to be a final invasive choice for wounds refractory to less aggressive care or for use when rapid closure is indicated, however, recent literature suggests that surgery can and should be performed safely in properly selected patients. Peri-operative morbidity and greater risk of complications are inherent to surgical options, including anaesthetic risk. Surgical procedures can be divided into those which prepare the patient for successful healing, such as debridement, and those which provide definitive closure. Reports of randomised clinical trials for operative treatment of pressure ulcers are almost non-existent in the literature. A Cochrane review from 2016 found no published or unpublished RCTs addressing surgical treatment of pressure ulcers, nor any registered studies investigating the role of reconstructive surgery in the management of pressure ulcers.¹ A more recent Cochrane review identified a single small RCT but report that the study did not answer the questions posed in terms of the difference in the two techniques on wound healing, reopening or recurrence.²

Guideline 6.1: Irregular wound extensions, forming sinuses or cavities, must be explored and unroofed and treated. (Level III – no change).

Principle: Tissue not exposed to treatment agents or devices cannot be expected to respond to the regimen and proceed to healing. Negative pressure wound therapy with irrigation may facilitate mechanical debridement and cleansing of complex deep wounds.

Guideline 6.2: Necrotic tissue must be debrided. See Guideline #4.4 in Wound Bed Preparation. (Level I – no change).

Principle: Nonviable tissue is detrimental to wound healing. Therefore, it should be debrided to allow the wound to proceed to closure. Debridement should be performed on a regular basis with a systematic approach, as visual inspection is unreliable. Debridement is effective and safe in older adults.

Guideline 6.3: Infected tissue must be treated by topical antimicrobials, systemic antibiotics, or surgical debridement. See Infection Guidelines. (Level I – no change).

Principle (revised): Systemic antibiotics are recommended only when there is clinical evidence of systemic sepsis, spreading cellulitis or underlying osteomyelitis. The NICE guidelines (2014), EPUAP, NPIAP and PPPIA Guidelines for Prevention and Treatment of Pressure Ulcers/Injuries (2019) and the International Wound Infection Institute (IWII, 2022) all recommend using multiple signs and symptoms, observing for indirect indicators of systemic infection (e.g., anorexia, delirium and/or confusion) and only doing a wound culture when infection is suspected. The majority of pressure ulcers will improve with debridement. When possible antibiotic therapy should be held until operative wound and/or bone cultures can be obtained. Infected soft tissue or bone will prevent wound healing, whether it is spontaneous or with the aid of surgical intervention. Only tissue with a low bacterial count (10⁵/g tissue) and with no beta-haemolytic streptococcus will proceed to closure. Bone biopsy remains the gold standard for diagnosing pelvic osteomyelitis associated with pressure ulcers.

Guideline 6.4 (revised): Underlying bony prominences and fibrotic bursa cavities should be removed. (Level II – no change).

Principle: Soft tissue compression between the skeleton and support surfaces leads to pressure necrosis. When performing pressure ulcer surgery, removal of prominences, without excessive excision, alleviates pressure points. Heterotopic ossification associated with pressure ulcers should be removed. Neurogenic heterotopic ossification may require removal to restore joint mobility and remove potential pressure points, however, the rate of recurrence is unpredictable and complications are frequent.

Guideline 6.5: Bone excision must not be excessive. (Level III – no change).

Principle: Extensive bone excision, especially at the ischial location, can expose deeper structures such as the urethra, or cause a shift of weight bearing, resulting in excessive pressure elsewhere.

No updated evidence.

Guideline 6.6 (revised): Patients with sacral and ischial pressure ulcers may benefit from faecal and urinary diversion. However, surgical diversion is not always required to obtain a healed wound and may carry substantial risk. (Level II – no change).

Principle: Unless a fistulous track has developed, surgical diversion of the urinary or faecal stream may not be required to heal peri-anal and perineal pressure ulcers and may carry substantial morbidity and mortality. The risks, benefits and alternative modalities should be evaluated and discussed with the patient and caregivers. Use of a bowel program or catheterization can divert urine and faecal material without the need for additional surgery.

Guideline 6.7: Consider radical procedures such as amputation or hemicorporectomy only in the rare and extreme cases. (Level II – no change).

Principle: Amputation, hemipelvectomy or hemicorporectomy have significant morbidity and mortality, shift pressure points, and rarely address the underlying problem leading to extensive, recurrent pressure ulcers.

Guideline 6.8: A pressure ulcer should be closed surgically if it does not respond to wound care and there is no other contraindication to the surgical procedures. Exceptions may include the elderly or patients with a fatal illness, for whom palliative, local wound care is more appropriate. (Level I – increased).

Principle: Wound closure decreases protein loss, fluid loss, the possibility of wound infection, and the later development of malignancy in the wound. Early complication rates are acceptably low.

Guideline 6.9: Composite tissue closure leads to the best chance of sustained wound closure, although recurrence and recidivism are continuing problems. (Level II – no change).

Principle: The most durable wound closure fills the ulcer with bulk and provides padding over the underlying structures with a tension-free closure. Flap selection for pressure ulcer coverage need not include muscle tissue. It has been demonstrated that there is no statistically significant difference between musculocutaneous, fasciocutaneous, and perforator-based flaps for post-operative complications or recurrence. Therefore, selection of flap material for pressure ulcer coverage can be based on the characteristics of the wound, limitations of the donor and recipient sites and goals of the procedure.

Guideline 6.10: Management to address muscle spasms and fixed contractures must occur preoperatively and continue at least until the wound is completely healed. (Level III – no change).

Principle: Spasm may put traction on a wound to cause dehiscence of the suture line. Spasms and fixed contractures may limit postoperative positioning and leave the patient at risk for new pressure ulcer formation.

Guideline 6.11 (revised): Anchoring the flap with deepithelialized tissue eliminates dead space and may decrease the rate of postoperative dehiscence. (Level III – no change).

Principle: Anchoring the flap to the bone is often difficult. Small case series suggest that inserting a deepithelialized portion of a flap will effectively obliterate undermined areas and reduce shearing forces.

Guideline 6.12 (revised): Address modifiable risk factors prior to proceeding with flap reconstruction in patients with pressure ulcers including optimising glucose control in the peri-operative period. (Level I – no change).

Principle: Numerous factors are associated with flap complications and pressure ulcer recurrence and must be considered when offering flap reconstruction with the goal of optimising the patient's modifiable risk factors prior to surgery. Poorly controlled diabetes leads to significantly greater rates of both dehiscence and pressure ulcer recurrence. Diabetic patients are also more than twice as likely to develop pressure ulcers peri-operatively as nondiabetics and have an increased rate of post-operative infection after flap reconstruction.

Guideline 6.13 (new): Incisional negative pressure wound therapy (iNPWT) may reduce post-operative complications after flap reconstruction for pressure ulcers. (Level III).

Principle: There is a growing body of evidence supporting the use of iNPWT in patients at high risk for surgical complications, specifically surgical site infection and wound dehiscence. Wound dehiscence is the most common complication after flap reconstruction for pressure ulcers. The majority of patients with pressure ulcers fit criteria to be considered at high risk for both wound dehiscence and surgical site infection after flap reconstruction.

Guideline 6.14 (new): A standardised protocol for peri-operative and post-operative management of patients undergoing pressure ulcer reconstruction will lead to reduced complications and reduced recurrence. (Level II).

Principle: Standardised protocols that include wound bed preparation, inclusion of a multi-disciplinary team, flap choice and appropriate off-loading for healing and prevention of recurrence. This is especially important for spinal cord-injured patients who continue to have the greatest risk for recurrence after surgical reconstruction.

9 ADJUVANT THERAPIES

Preamble: Emerging evidence on adjuvant therapies suggests potential benefit for pressure ulcer healing. To date, there are insufficient studies demonstrating superiority over other more traditional wound treatments. Until further evidence of efficacy is established, consider the use of adjuvant therapy after evaluating individual patient and ulcer characteristics and when (1) healing fails to progress using conventional therapy and (2) under circumstances where the economic or physical burden of adjuvant therapy is consistent with patient goals and circumstances.

10 PALLIATIVE WOUND CARE FOR SERIOUSLY ILL PATIENTS WITH PRESSURE ULCERS

Preamble: Palliative wound care refers to the relief of wound symptoms and suffering in the context of a serious illness. In this emerging area of pressure ulcer care for patients with a serious illness, there are varying definitions and inclusion criteria. There are also ethical limitations for clinical trials to include patients who are receiving comfort-focused care in the last few weeks of their life. However, more people are living longer with serious illness, and these patients should be enrolled in studies that will determine how best to optimise their care. The immobility and frailty that accompanies people during a serious illness puts them at high risk of pressure ulcer development. These guidelines refer to patients living with serious illness and reflect the best evidence and current opinion. This is regardless of whether they are in the last few weeks of their life or not. These recommendations should be considered in conjunction with the guidelines for general treatment of pressure ulcers, if appropriate for the patient and their caregivers.

CONFLICT OF INTEREST STATEMENT

None of the authors have reported a conflict of interest relevant to the reported work.