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Beyond skin deep: Managing pressure injuries

Podd, Daniel, MPAS, PA-C

Journal of the American Academy of PAs: April 2018 - Volume 31 - Issue 4 - p 10–17
doi: 10.1097/01.JAA.0000531043.87845.9e
CME: Wound Care
Free
CME

ABSTRACT Pressure injuries (previously called pressure ulcers) are a common finding among patients in acute, long-term, or home settings. Numerous pathophysiologic and risk mechanisms factor into the development of pressure injuries. The timely recognition of these injuries is imperative. Many treatments exist for pressure injuries but the focus of patient management should be on preventing injury-related complications.

Daniel Podd is an associate professor at St. John's University in Queens, N.Y., and practices with Doctors on Call/Comprehensive Geriatric Care and at Long Island Queens Medical Center. The author has disclosed no potential conflicts of interest, financial or otherwise.

Earn Category I CME Credit by reading both CME articles in this issue, reviewing the post-test, then taking the online test at http://cme.aapa.org. Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of April 2018.

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Box 1

Box 1

Pressure injuries are common in the acute inpatient setting, in chronic long-term care populations, and in patients at home who have risk factors for skin breakdown, such as immobility, advanced age, and history of a pressure injury. The National Pressure Ulcer Advisory Panel (NPUAP) identifies a pressure injury as an area of increased, unremitting pressure most commonly over a bony prominence, resulting in tissue ischemia and necrosis.1 Each year in the United States, an estimated 1 to 3 million people, mostly patients in acute care, develop pressure injuries, according to NPUAP.1 At any given time, about one-third of patients in acute, long-term, or home-care settings have pressure injuries.2 About 60,000 die from pressure-injury complications each year.2

Although pressure injuries can develop on any part of the body, about 70% occur on the hips and buttocks, most commonly the ischial tuberosity, trochanter, and sacrum.3 The remainder of pressure injuries affect the lower extremities, including the malleolus, heel, patella, and pretibial areas. Pressure injuries are less common on the nose, chin, forehead, occiput, chest, upper back, and elbows.3,4

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RISK FACTORS AND PATHOGENESIS

The pathogenesis of pressure injuries is multifaceted. Risk factors include pressure, friction and shear, moisture (such as from incontinence), advanced age, malnutrition, diabetes, dehydration, and vascular disease.

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Pressure

Impaired mobility is the most important risk factor that contributes to pressure injury development. Common causes of immobility are excessive pharmacologic sedation or anesthesia, neurologic sequelae, advanced dementia, use of restraints, or injury. Long periods of low pressure can be as damaging to a patient's skin integrity as short periods of high pressure.

Unrelieved direct pressure or force on an area causes microvascular circulatory occlusion, which in turn impairs cellular nutrition and removal of waste products.5 Cells then use anaerobic metabolism, producing toxic byproducts that cause tissue acidosis, increased cell membrane permeability, edema, and cell death. Additionally, reperfusion and reoxygenation injury promote endothelial and microvascular damage via the production of superoxide anion, hydroxyl, and hydrogen peroxide free radicals.3

Box 2

Box 2

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Friction and shear

The second factor in pressure injury development is friction generated by skin rubbing against clothing or bedding. A patient sitting up in bed can slide down over time. The skin stays in contact with the patient's clothing and bed linens but the muscles and subcutaneous tissues are drawn down by gravity, and the resulting shearing (a type of friction) can cause a sacral pressure ulcer in combination with pressure.

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Moisture

Perspiration, wound drainage, and urinary or fecal incontinence lead to tissue breakdown and maceration that can initiate or worsen pressure injuries.5

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Other risk factors

Patients over age 65 years are at higher risk for pressure injuries because they typically have reduced subcutaneous fat and capillary blood flow, and because of physiologic skin changes related to aging, including decreased cohesion of the dermis and epidermis and reduced sensory function. The very young are at risk because of skin immaturity and decreased dermal-epidermal cohesion. Other risk factors include undernutrition, malnutrition, a negative nitrogen balance, dehydration, weight loss, diabetes, peripheral neuropathy, peripheral arterial disease, and venous insufficiency.5,6

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Assessing risk

The Braden scale (Table 1) and the Norton scale (Table 2) can be used to assess patient risk for pressure injury development. The Braden scale uses six criteria; scores range from 6 to 23 and a score less than 12 is associated with the most serious risk of pressure injury formation. The Norton scale uses five criteria; scores range from 5 to 20 and patients with a score of less than 14 are at highest risk of pressure injuries.5

TABLE 1

TABLE 1

TABLE 2

TABLE 2

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HISTORY AND PHYSICAL EXAMINATION

Patients may have pain or pruritus at any stage of a pressure injury, although they may not be aware of it if they have impaired sensation or cognition. The appearance and description of the pressure injury is the basis of the physical examination and is used to make the diagnosis (Table 3). Tenderness, erythema of surrounding skin, swelling, warmth, exudate, or a foul odor suggest an underlying infection. The presence of fever and supporting laboratory evidence should raise suspicion of cellulitis, bacteremia, or underlying osteomyelitis.5 Other factors that suggest infection or osteomyelitis include a nonhealing wound, tunneling, reduced joint range of motion, and acute mental status changes.

TABLE 3

TABLE 3

Although the diagnosis of pressure injuries is made on visual inspection, several diagnostic tests are valuable in assessing these injuries. A complete blood cell count with differential may reveal leukocytosis, indicating inflammation or infection, and commonly shows anemia in patients with chronic disease. Elevations of inflammatory markers such as the erythrocyte sedimentation rate (ESR) or C-reactive protein also support inflammation. Because excluding concomitant osteomyelitis is critical, laboratory findings suggestive of bony involvement include a leukocytosis greater than 15,000/mcL, an ESR of greater than 120 mm/h, and radioactive uptake on a nuclear bone scan.4

A bone biopsy and culture can confirm osteomyelitis. Order blood cultures for all patients suspected of having bacteremia, osteomyelitis, or sepsis. Also order tests to assess underlying metabolic and nutritional status, including hemoglobin, hematocrit, serum albumin, prealbumin, protein, transferrin levels, and total and absolute CD4+ lymphocyte counts. Deficiencies in these markers both increase the risk of pressure injury development and prolong healing time of existing injuries.4,5

Consider vascular doppler studies in patients with pressure injuries of the extremities, especially if the patient has manifestations of concomitant peripheral vascular disease or if the cause of the injury is uncertain. An ankle-brachial index (ABI) may be performed in the office or at the bedside as a simple, noninvasive screening assessment for peripheral arterial disease. In patients with noncompressible vessels, a toe-brachial index may be used instead. A patient with diabetic neuropathy may have high hemoglobin A1C and plasma glucose levels and positive findings on nerve conduction velocity and electromyography testing, such as reduced or absent sensory nerve action potentials and denervation.

Because pressure injuries often are heavily colonized with bacteria, routine culturing is not recommended.5 Tissue biopsy or directly swabbing the injury offer diagnostic benefit in patients whose injuries fail to heal and can identify bacterial invasion or infection. Only a tissue biopsy can reliably differentiate between wound contamination and invasion.4,5

About 60% of chronic pressure injuries contain bacterial colonies known as biofilms, which induce chronic inflammation and increase resistance to antibiotics and the body's innate immune defenses.6 Suspect a biofilm if the patient's pressure injury fails to show evidence of healing after 2 weeks of appropriate care, or has friable granulation tissue; a notable odor; a change in exudate character; pocketing or tunneling in the wound bed; or increased pain, heat, exudate, or devitalized tissue. Pocketing refers to the formation of smooth, nongranulating areas at the base of a wound surrounded by granulation tissue. Tunneling is characterized by channels that may extend in any direction through soft tissue immediately adjacent to the pressure injury.

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STAGING AND MONITORING

Once a pressure injury is identified, serial measuring, staging, and photography is essential in the ongoing assessment of the injury's progression or healing.5 The NPUAP revised the staging of pressure injuries in April 2016 (Table 3). The NPUAP's Pressure Ulcer Scale for Healing (PUSH) tool should be used to monitor clinical response.7 The tool measures injury dimensions, amount of exudate, and presence of various types of tissue in the wound, and results can be graphed to show wound progress over time (Table 4).7

TABLE 4

TABLE 4

Once a pressure injury is identified and staged, it permanently retains its diagnosed stage despite any healing, and is not downstaged. The description closed is added to the stage designation for healed pressure injuries.

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MANAGEMENT

When selecting a management approach, consider the stage of the pressure injury. Management is interdisciplinary and focuses on reducing pressure, debriding necrotic and devitalized tissue, preventing and treating infection, and providing direct wound care.5

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Reduce pressure

Advise patients to shift their weight every 10 minutes if they are able. Patients unable to move on their own should be repositioned every 2 hours. Keep the head of the bed at 30 degrees or less (unless contraindicated) to reduce pressure and shearing on the sacrum. Minimize sliding and shearing by raising the patient's knees unless contraindicated, using footboards, and placing pillows under the patient's lower legs.6 To prevent heel injuries, elevate the patient's heels or use pressure-reducing heel devices.

Specialized support surfaces for pressure reduction include foam, air, or gel-filled mattress overlays and low-air-loss devices. These may reduce the frequency of repositioning required in some patients and may be applied to beds and wheelchairs. Tissue pressures below 32 mm Hg (capillary filling pressure) are best for adequate tissue perfusion. The Wound, Ostomy and Continence Nurses Society has an online tool (http://algorithm.wocn.org) that can help clinicians identify appropriate support surfaces. The tool is applicable to adults over age 16 years and bariatric patients in care settings where the length of stay is greater than 24 hours.

More intensive offloading devices such as low-air-loss or air-fluidized beds may be needed for patients with multiple large pressure injuries, nonhealing pressure injuries, after flap surgeries for pressure injuries, or when static devices are not effective.8 Standard hospital mattresses are the least effective surfaces compared with static mattress, mattress overlays, or low-air-loss mattresses.9

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Remove necrotic tissue

Debridement methods include sharp, mechanical, autolytic, and biosurgical. Injuries with thick and extensive eschar or necrotic tissue require debridement to expose granulation tissue, reduce infection risk, and facilitate healing.

Sharp debridement with a sterile scalpel or scissors is the most rapid form of debridement.6 Debridement may be performed at the bedside with a sterile, disposable 5-mm curette or scalpel. Extensive debridement under general anesthesia is reserved for the OR and is appropriate for patients with large pressure wounds with pervasive necrosis. Sharp debridement may be indicated if the pressure injury is infected or if the patient has advancing cellulitis; it is the preferred intervention in patients with systemic infection or sepsis.6 Because healing following sharp debridement depends on proper vascularization, when the pressure injury is on an extremity, perform a vascular assessment of the affected extremity before debridement.8,10 Because sharp debridement is nonselective, viable tissue also may be removed. Anticoagulation therapy is a relative contraindication to this type of debridement.6 Surgical debridement is the first-line treatment if large amounts of infected, necrotic tissue or bone must be removed promptly.11

Mechanical debridement methods include hydrotherapy, wound irrigation, and whirlpool baths, which loosen debris and bacteria; increase local circulation; reduce wound pain and fever; help to gently remove dressings; and can speed wound healing.6,12,13 Wet-to-dry dressings (applying wet dressings and removing them when dry, which also removes devitalized tissue) are no longer recommended in clinical practice guidelines because they can remove viable tissue and cause patient pain.

Additional nonsurgical methods of debridement include autolytic, enzymatic, and chemical.

Autolytic debridement involves providing a moist wound environment that lets the body's own enzymes digest necrotic tissue. This method is slow but is more selective than wet-to-dry dressing changes, removing only nonviable tissue. Autolytic debridement is less expensive than other debridement methods, reduces the need for potentially painful and costly surgical debridement, may reduce patient need for antibiotics, and reduces clinician labor costs.14-16 This method can be used for stage 1 or 2 injuries that are not infected; it is not recommended for very deep ulcers with superficial necrosis or injuries that require packing.11

Enzymatic debridement Similar to autolytic debridement, enzymatic debridement uses enzymes such as collagenase to remove necrotic tissue, and works best in moist wounds.11 Also like autolytic debridement, this method may be suitable for patients in long-term care who are not candidates for sharp debridement. As with autolytic debridement, this method takes longer and cannot be used if the patient has an underlying infection.6,17

Biosurgical debridement This approach entails applying noninfectious maggots (Phaenicia sericata) usually at a density of 5 to 8 per cm2 of the injury. Studies have found that maggot therapy has a higher proportion of complete debridement than conventional therapy alone (80% versus 48%, respectively) for pressure injuries. However, this therapy is not accepted by all patients and not available in all areas.6

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Manage infection

Preventing infection depends on adequate, timely, and complete debridement of necrotic tissue followed by appropriate topical therapy such as papain-urea, hydrogel, or collagenase. Systemic antibiotics are indicated for patients with sepsis, osteomyelitis, cellulitis, fever, and leukocytosis, or to prevent bacterial endocarditis in patients who need debridement and who have prosthetic cardiac valves, congenital cyanotic cardiac malformations, or have had previous episodes of bacterial endocarditis. Empiric broad-spectrum agents covering aerobic Gram-negative rods, Gram-positive cocci, and anaerobes are appropriate (pending the results of a tissue culture and sensitivity done at the time of surgical debridement), and include ampicillin-sulbactam, ticarcillin-clavulanate, or clindamycin with a fluoroquinolone or aminoglycoside. For patients with methicillin-resistant Staphylococcus aureus infection, consider parenteral vancomycin and topical cadexomer iodine dressings.6

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Support a moist wound environment

Moisture-retaining dressings promote reepithelialization up to 40% faster than leaving wounds open to air.6 Appropriate dressing selection is based on the wound characteristics and includes transparent films (semiocclusive), hydrocolloids, hydrogels (occlusive or semiocclusive), alginates, and foams.

Transparent films are suitable for stage 1 and 2 pressure injuries with light or no exudate, and may be used with hydrogel or hydrocolloid dressings for stage 3 and 4 pressure injuries and unstageable injuries.

Hydrocolloids function as primary or secondary dressings for stage 2 to 4 pressure injuries, those with slough and necrosis, or those with light to moderate exudate. Hydrocolloids result in reduced wound size compared with gauze dressings.18

Transparent films and hydrocolloids let wound fluid collect underneath the dressing, expediting epithelial migration. These dressings should be changed every 3 to 5 days and should not be used in patients with fragile skin, infected injuries, or excessive exudate. Hydrocolloids are contraindicated in infected injuries.6,8

Hydrogels may be semipermeable or impermeable and are useful in treating stage 2 to 4 injuries, deep injuries, and those with necrosis or slough. Similar to transparent films and hydrocolloids, they enhance autolysis. Other benefits include a cooling and soothing, analgesic quality, and rehydrating effects in the wound bed. These dressings can be used in infected injuries or as packing in deep injuries. They are not recommended for pressure injuries with heavy exudate. Hydrogels dehydrate if not covered, are difficult to secure, and may cause maceration of periwound tissue. To prevent maceration, apply a barrier to the periwound tissue after wound cleaning. This can be a film-forming liquid acrylate spray or wipe, zinc oxide ointment, petroleum jelly, or an occlusive dressing such as a transparent film or hydrocolloid.19,20

Alginate dressings are absorptive, enhance autolysis, and are indicated as primary dressings for stage 3 and 4 pressure injuries and those with moderate to heavy exudate or tunneling. They can be used on infected injuries and with topical medications. These dressings form an insulating gel within the injury, conform to the shape of the injury, and fill any tissue dead space. Because they are highly absorptive and could cause dehydration, alginates should not be used on injuries with light exudate, dry scarring, or superficial injuries. A secondary dressing, such as a transparent film dressing or hydrogel, is needed to hold the alginate in place.

Wound foam, made of synthetic semipermeable material, acts similar to alginate dressings by promoting autolysis, repelling contaminants, and providing insulation and reabsorption of moderate to heavy exudate. Foam can be a primary dressing for patients with fragile skin, or a secondary dressing for stage 2 to 4 injuries with packing and light to heavy exudate. Topical medications may be administered with foam in place. Foam is waterproof, compressible, comfortable, and can be removed without causing trauma to the injury. A secondary dressing may be required to hold foam in place.

Wound fillers, available as beads, flakes, pastes, and powders, obliterate dead space in cavities, pockets, and undermining wounds and help absorb exudate, retain moisture, and promote autolytic debridement. Because they are nonadhesive, a secondary dressing is needed. Undesirable effects may include a burning sensation upon application and an associated odor. Some fillers require wound irrigation to achieve nontraumatic removal.

Nonwoven moistened gauze may be used for stage 3 and 4 pressure injuries and for deep wounds, especially those with tunneling or undermining. These help to remove dead space, retain moisture, and absorb exudate.

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WOUND CLEANING

Wounds should be cleaned initially and at each dressing change, preferably with 0.9% sodium chloride solution. For clean wounds, avoid using cytotoxic antiseptic agents such as 5% mafenide acetate, 0.25% sodium hypochlorite solution, povidone-iodine, 3% hydrogen peroxide, and 0.25% acetic acid, which kill granulation tissue and can impair wound healing.6,8 Sodium hypochlorite is germicidal, is appropriate for infected and malodorous wounds with large amounts of slough, and debrides necrotic tissue.4,21

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NEGATIVE PRESSURE THERAPY

Negative pressure wound therapy (NPWT) continuously or intermittently applies subatmospheric pressure to the surface of an injury, enhancing wound healing by reducing edema, increasing the rate of granulation tissue formation, and stimulating circulation. Several clinical practice guidelines and panels have recommended use of NPWT with large stage 3 and 4 pressure ulcers that have failed to improve with standard care with moist wound healing.6,22-24

Contraindications to NPWT include exposed blood vessels, anastomotic sites, organs, or nerves; malignancy in the wound; untreated osteomyelitis; and eschar or thick slough in the wound bed.25

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NUTRITIONAL SUPPORT

Optimal patient nutrition is key to wound healing. Patients with weight loss or malnourishment should be assessed by a nutritionist for protein and calorie intake, hydration status, and serum albumin and/or prealbumin.26 A positive nitrogen balance and a total caloric intake of at least 30 kcal/kg (including 1.25 to 1.5 g/kg of protein daily) promote healing and can reduce the size of stage 3 and 4 pressure injuries.27

Although vitamins A, C, and E and zinc are frequently supplemented to promote wound healing, data do not support supplementing these nutrients in patients who do not have nutritional deficiencies.24 For patients with nutritional deficiencies, a daily multivitamin and mineral supplement that provides the recommended daily allowance of vitamins and minerals is recommended.6 The anabolic steroid oxandrolone showed no benefit over placebo for improving healing or the percentage of pressure injuries that remained closed after 8 weeks of treatment.28 Some pressure injuries have improved with topical fatty acid creams and cleansers; however, strong evidence to support the use of these treatments is lacking.9 Local wound application of the platelet-derived growth factor becaplermin is a prospective treatment to encourage granulation tissue production in stage 2 through 4 pressure injuries.29 As an adjunctive therapy, electrical stimulation accelerated wound healing compared with placebo but did not result in complete wound closure.18 Furthermore, more adverse reactions were observed in older adults using stimulation therapy compared with younger persons.18

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COMPLICATIONS

Insufficient treatment or complications such as infection can cause pressure injuries to heal poorly. The use of inappropriate therapy for the corresponding stage of ulcer can contribute to delay treatment in a patient with worsening tissue injury.

Patients with pressure injuries in the perineum may need indwelling urinary catheters and/or rectal tubes to avoid wound contamination. Barriers such as zinc oxide cream or petroleum jelly can help protect skin contaminated by urinary or fecal incontinence.

Surgery is an option for stage 3 or 4 injuries unresponsive to optimal care or when the patient's quality of life would be improved with rapid wound closure. Amputation and hemicorporectomy are sometimes required in patients with large infected pressure injuries.

Up to 32% of patients have underlying osteomyelitis; more rarely, patients may have a Marjolin ulcer, a squamous cell carcinoma within a pressure injury. These conditions should be considered in patients with nonhealing pressure injuries.5,8 Also consider superficial or deep sinus tracts, cellulitis, and tissue calcification. Bacteria from a pressure injury can enter the systemic circulation, causing bacteremia, septic shock, meningitis, endocarditis, and death.5

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CONCLUSION

Pressure injuries are a common finding but with interdisciplinary management and application of key preventive and therapeutic approaches, these injuries and their complications can be reduced.

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REFERENCES

1. National Pressure Ulcer Advisory Panel. Pressure ulcers: incidence, economics, risk assessment. Consensus Development Conference Statement. West Dundee, IL: SN Publications; 1989.
2. Dorner B, Posthauer ME, Thomas D. The Role of Nutrition in Pressure Ulcer Prevention and Treatment. National Pressure Ulcer Advisory Panel White Paper. 2009.
3. Leblebici B, Turhan N, Adam M, Akman MN. Clinical and epidemiologic evaluation of pressure ulcers in patients at a university hospital in Turkey. J Wound Ostomy Continence Nurs. 2007;34(4):407–411.
4. Kirman CN. Pressure injuries (pressure ulcers) and wound care. http://emedicine.medscape.com/article/190115-overview#a1. Accessed January 9, 2018.
5. Kroshinsky D, Strazzula L.Pressure ulcers. http://www.merckmanuals.com/professional/dermatologic-disorders/pressure-ulcers/pressure-ulcers. Accessed January 9, 2018.
6. Bates-Jensen BM, Patlan A. Pressure ulcers. In: Halter JB, Ouslander JG, Studenski S, et al., eds. Hazzard's Geriatric Medicine and Gerontology. 7th ed. New York, NY: McGraw-Hill; 2017. http://accessmedicine.mhmedical.com/content.aspx?bookid=1923&sectionid=144522255. Accessed January 9, 2018.
7. National Pressure Ulcer Advisory Panel. PUSH tool 3.0. http://www.npuap.org/resources/educational-and-clinical-resources/push-tool/push-tool. Accessed January 9, 2018.
8. Bluestein D, Javaheri A. Pressure ulcers: prevention, evaluation, and management. Am Fam Physician. 2008;78(10):1186–1194.
9. Qaseem A, Mir TP, Starkey M, Denberg TD. Risk assessment and prevention of pressure ulcers: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2015;162(5):359–369.
10. Registered Nurses' Association of Ontario. Assessment and management of Stage I to IV pressure ulcers. 2007. http://rnao.ca/sites/rnao-ca/files/Assessment__Management_of_Stage_I_to_IV_Pressure_Ulcers.pdf. Accessed January 30, 2018.
11. Boykin JV. Debridement of decubitus ulcers. In: Granick MS, Gamelli RL, eds. Surgical Wound Healing and Management. Informa Healthcare; 2007:106–110.
12. Ovington LG. Hanging wet-to-dry dressings out to dry. Home Healthc Nurse. 2001;19(8):477–483.
13. Tao H, Butler JP, Luttrell T. The role of whirlpool in wound care. J Am Coll Clin Wound Spec. 2013;4(1):7–12.
14. Sherman RA. Maggot versus conservative debridement therapy for the treatment of pressure ulcers. Wound Repair Regen. 2002;10(4):208–214.
15. Schwarck L. Maggot débridement therapy. J Contin Educ Nurs. 2009;40(1):14–15.
16. Choo J, Nixon J, Nelson EA, McGinnis E. Autolytic debridement for pressure ulcers. Cochrane Database Syst Rev. 2014;10:CD011331.
17. Püllen R, Popp R, Volkers P, Füsgen I. Prospective randomized double-blind study of the wound-debriding effects of collagenase and fibrinolysin/deoxyribonuclease in pressure ulcers. Age Ageing. 2002;31(2):126–130.
18. Qaseem A, Humphrey LL, Forciea MA, et al Treatment of pressure ulcers: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2015;162(5):370–379.
19. Sibbald RG, Elliott JA, Ayello EA, Somayaji R. Optimizing the moisture management tightrope with wound bed preparation 2015. Adv Skin Wound Care. 2015;28(10):466–476.
20. Schuren J, Becker A, Sibbald RG. A liquid film-forming acrylate for peri-wound protection: a systematic review and meta-analysis (3M Cavilon no-sting barrier film). Int Wound J. 2005;2(3):230–238.
21. DeMarco S. Geriatric workforce enhancement program. Wound and pressure ulcer management. http://www.hopkinsmedicine.org/gec/series/wound_care.html. Accessed January 30, 2018.
22. Gupta S, Baharestani M, Baranoski S, et al Guidelines for managing pressure ulcers with negative pressure wound therapy. Adv Skin Wound Care. 2004;17(suppl 2):1–16.
23. Mendez-Eastman S. Guidelines for using negative pressure wound therapy. Adv Skin Wound Care. 2001;14(6):314–322.
24. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;289(2):223–226.
25. Malmsjö M, Bergquist O. NPWT in everyday practice made easy. http://www.woundsinternational.com/made-easys/view/npwt-settings-and-dressing-choices-made-easy. Accessed January 30, 2018.
26. Stechmiller JK, Cowan L, Whitney JD, et al Guidelines for the prevention of pressure ulcers. Wound Repair Regen. 2008;16(2):151–168.
27. Bergstrom N, Horn SD, Smout RJ, et al The National Pressure Ulcer Long-Term Care Study: outcomes of pressure ulcer treatments in long-term care. J Am Geriatr Soc. 2005;53(10):1721–1729.
28. Bauman WA, Spungen AM, Collins JF, et al The effect of oxandrolone on the healing of chronic pressure ulcers in persons with spinal cord injury: a randomized trial. Ann Intern Med. 2013;158(10):718–726.
29. Woelfel JA. Topical treatment of chronic wounds. Pharmacist's Letter & Prescriber's Letter. 2006;22(1):1–8.
30. Bergstrom N, Braden B, Laguzza A, Holman A. The Braden Scale for predicting pressure sore risk. Nurs Res. 1987;36(4):205–210.
31. Norton D, Exton-Smith AN, McLaren R. An Investigation of Geriatric Nursing Problems in Hospital. London: National Corporation for the Care of Old People; 1962.
    32. National Pressure Ulcer Advisory Panel. NPUAP pressure injury stages. http://www.npuap.org/resources/educational-and-clinical-resources/npuap-pressure-injury-stages. Accessed February 20, 2018.
      Keywords:

      pressure injury; ulcer; debridement; wound; dressing; multidisciplinary

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