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Health care providers face the challenge of providing effective care for increasing numbers of patients with chronic wounds. Pressure ulcers, one type of chronic wound, are estimated to affect 1.3–3 million individuals in the United States.1 Prevalence varies among specific clinical populations, with higher percentages reported for the elderly, the acutely ill, and those who have sustained spinal cord injuries.2,3,4 The first comprehensive clinical practice guidelines for the treatment of patients with pressure ulcers were published by the Agency for Healthcare Research and Quality (AHRQ) in 1994. Since that time, a number of professional groups have also developed and published guidelines.

The acceptance and adoption of guideline recommendations in practice is variable and influenced by several factors, including (1) guideline currency with the most recent and comprehensive evidence, (2) recognition and acceptance of guideline validity, (3) breadth of interprofessional representation in guideline development, and (4) guideline presentation and format.5 These issues pertain to guidelines in general, but are also applicable to those specific to chronic wounds. Despite many recent advances in wound care, the challenge of managing chronic wounds remains compounded by the current lack of consensus on clearly defined, comprehensive wound care principles and uniformly accepted analytical methods to evaluate outcomes. With these concerns in mind, the following guidelines were developed to facilitate use by multiple groups in the wound care community of clinicians, researchers, industry, governing agencies, and third-party payers.

The guidelines provide recommendations for treatment of pressure ulcers supported by current evidence. However, treatment decisions also depend on specific patient characteristics, pressure ulcer characteristics/stage, patient circumstances, and overall goals. The development of a treatment plan of care begins with the determination of the goals of therapy. In most cases, the goal of therapy is to produce complete healing with restoration of functional skin integrity to the highest extent possible. However, in certain cases, the goal of therapy may not be complete healing of the wound. For example, in patients who are terminally ill, the goal of therapy may be palliative and focused on reducing discomfort or deterioration of the pressure ulcer, rather than complete healing of the wound. In other cases, the treatment may produce added discomfort or increased risk to the patient. Individual evaluation of each case is necessary within the context of the optimum outcome for that patient.

The specific objectives of this project were to:

  • 1
    Develop comprehensive, evidence- and consensus-based guidelines for pressure ulcer treatment.
  • 2
    Present these guidelines in a clear, simple format designed to enable health care providers to make informed, evidence-supported treatment decisions to manage pressure ulcers appropriately.

METHODS

  1. Top of page
  2. METHODS
  3. RESULTS
  4. Acknowledgment

A search of health care databases for current published evidence-based guidelines addressing the treatment of pressure ulcers was conducted between July 2004 and January 2006 using electronic and online resources. In addition to published guidelines, PubMed, EMBASE, and the Cochrane Database of Systematic Reviews were reviewed for evidence on pressure ulcer treatment. The following guidelines were located and reviewed by the panel and used in the development of the categories of treatment and individual guidelines.

  • 1
    American Family Physician Pressure Ulcer Guideline Panel. Pressure Ulcer Treatment. Am Fam Phys 1995; 51: 1207–23.
  • 2
    American Medical Directors Association (AMDA). Pressure Ulcers, Clinical Practice Guideline. 1996. Columbia, MD: American Medical Directors Association.
  • 3
    AMDA Pressure Ulcer Therapy Companion, Clinical Practice Guideline. 1999. Columbia, MD: American Medical Directors Association.
  • 4
    Bergstrom N, Allman RM, Alvarez OM, Bennett MA, Carlson CE, Frantz RA, Garber SL, Jackson BS, Kaminski Jr MV, Kemp MG, Krouskop TA, Lewis Jr VL, Maklebust J, Margolis DJ, Marvel EM, Reger SI, Rodeheaver GT, Salcido R, Xakellis GC, Yarkony GM. Treatment of pressure ulcers. Clinical Practice Guideline, No. 15. 1994. AHCPR Publication No. 95-0652. Rockville, MD: U.S. Department of Health and Human Services. Public Health service, Agency for Health Care Policy and Research.
  • 5
    Brem H, Lyder C. Protocol for the successful treatment of pressure ulcers. Am J Surg 2004 (Suppl. to July 2004); 188: 9S–17S.
  • 6
    Consortium for Spinal Cord Medicine. Pressure Ulcer Prevention and Treatment following Spinal Cord Injury: A Clinical Practice Guideline for Health-Care Professionals. 2001. Washington, DC: Paralyzed Veterans of America.
  • 7
    European Guidelines for Pressure Ulcer Treatment (2004). http://www.epuap.org/
  • 8
    Folkedahl BA, Frantz R, Goode C. Evidence-Based Protocol Treatment of Pressure Ulcers. 2002. Iowa City: The University of Iowa Gerontological Nursing Interventions Research Center Research Dissemination Core (RDC).
  • 9
    Panel for the Prediction and Prevention of Pressure Ulcers in Adults. Pressure ulcers in adults: prediction and prevention. Clinical Practice Guideline, No. 3 1992. AHCPR Publication No. 92-0047. 1992. Rockville, MD: U.S. Department of Health and Human Services. Public Health service, Agency for Health Care Policy and Research.
  • 10
    Royal College of Nursing. Pressure ulcer risk assessment and prevention. 2001. http://www.nelh.nhs.uk/guidelinesdb/html/PrUlcer-fthtm. Accessed 7/5/04.
  • 11
    Schols JMGA, Jager-v.d.Ende MA. Nutritional Intervention in Pressure Ulcer Guidelines: An inventory. Nutrition 2004; 20: 548–53.
  • 12
    Wound Ostomy Continence Nurses Society. Guideline for Prevention and Management of Pressure Ulcers. 2003. WOCN: Glenview, IL.

The panel used a consensus process to determine the treatment categories. Subgroups of the panel (two to three individuals) were responsible for the development of specific guidelines and review of evidence within treatment categories. The first complete document was reviewed by the full panel and revised. The guidelines were presented for public comment in a forum hosted on the National Institutes of Health (NIH) campus (October 2005). Guidelines were further revised based on verbal and written comments received during the public forum review process. This revision was submitted to full panel review and additional modification before adoption. Additional revisions are based on review and critique provided by the board members of the Wound Healing Society and Wound Healing Foundation.

Evidence and Scientific Basis for Guidelines

The panel identified six categories of pressure ulcer treatment: positioning and support surfaces, nutrition, infection, wound bed preparation, dressings, and surgery and adjuvant therapies. Specific guidelines and the underlying principle(s) were developed in each category. Evidence references for each standard are listed and coded. The code abbreviations for the evidence citations were as follows:

STATStatistical analysis, meta-analysis, consensus statement by commissioned panel of experts
RCTRandomized clinical trial
CLIN SClinical series
COMPComparative study
LIT REVLiterature review
RETROSRetrospective series review
SURVSurvey
EXPLaboratory or animal study
TECHTechnique or methodology description
COST ANALCost analysis
PATH SPathological series review

Classification of Evidence

Our approach differed from the previous approaches used in evidence-based guidelines. In most published guidelines, evidence was based on clinical human studies. Laboratory or animal studies were not cited. Our approach was not limited to human clinical studies or to a specific study design (e.g., RCT). We have used well-controlled animal studies that present proof of principle, especially when a clinical series corroborated the laboratory results. It was also clear that principles that have been validated for other chronic wound types often are applicable to pressure ulcers. Therefore, evidence is included for some guidelines that were not specific for pressure ulcers. Because of these variations, a different system was necessary to grade the evidence weight supporting a given guideline. The strength of evidence supporting a guideline is listed as Level I, Level II, or Level III using the following definitions:

  • Level I: Meta-analysis of multiple RCTs or at least two RCTs supporting the intervention in the guideline or multiple laboratory or animal experiments with at least two clinical series supporting the laboratory results.
  • Level II: Less evidence than Level I, but at least one RCT and at least two significant clinical series or expert opinion papers with literature reviews supporting the intervention. Experimental evidence that is quite convincing but without support by adequate human experience is included.
  • Level III: Suggestive data of proof of principle, but lacking sufficient data such as meta-analysis, RCT, or multiple clinical series.

References:

  • 1
    Lyder CH. Pressure ulcer prevention and management. JAMA 2003; 289: 223–6.
  • 2
    Barrois B, Allaert FA, Colin D. A survey of pressure sore prevalence in hospitals in the greater Paris region. J Wound Care 1995; 4: 234–6.
  • 3
    Allman RM, Paprade CA, Noel LB, et al. Pressure sores among hospitalized patients. Ann Intern Med 1986; 105: 337–42.
  • 4
    Walter JS, Sacks J, Othman R, et al. A database of self-reported secondary medical problems among VA spinal cord injury patients: its role in clinical care and management. J Rehab Res Dev 2002; 39: 53–61.
  • 5
    Shiffman RN, Dixon J, Brandt C, Essahihi A, Hsiao A, Michel G, O'Connell R. The GuideLine implementability appraisal (GLIA): Development and validation of an instrument to identify obstacles to guideline implementation. BMC Med Inform Dec Making 2005; 5: 1–23.

RESULTS

  1. Top of page
  2. METHODS
  3. RESULTS
  4. Acknowledgment

1. POSITIONING AND SUPPORT SURFACES

Preamble: Pressure and compression to soft tissue play a role in the etiology of pressure ulcers. Patient positioning and methods to reduce pressure-related tissue damage are recognized as important treatment components. While there are limited definitive studies, the best current evidence and expert opinion suggest the following guidelines.

Guideline #1.1: Establish a repositioning schedule and avoid positioning patients on a pressure ulcer. (Level II)

Principle: Pressure ulcers are thought to result from compression of soft tissues against a bony prominence. It is reasonable to assume that pressure on an ulcer can result in delayed healing. Patients should be repositioned to relieve pressure over bony prominences. The exact turning interval is not known and is derived empirically. Reductions in pressure incidence have been achieved, but positioning is not universally effective.

Evidence:

  • 1
    Clark M. Repositioning to prevent pressure sores—what is the evidence? Nurs Standard 1998; 13: 56–64. [LIT REV]
  • 2
    Defloor T. Less frequent turning intervals and yet less pressure ulcers. Tijdschrift voor Gerontologie en Geriatrie 2001; 32: 174–7. [RCT]
  • 3
    Knox DM, Anderson TM, Anderson PS. Effects of different turn intervals on skin of healthy older adults. Adv Wound Care 1994; 7: 48–56. [COMP]
  • 4
    Thomas DR. Are all pressure ulcers avoidable? J Am Med Directors Assoc 2001; 2: 297–301. [LIT REV]

Guideline #1.2: Maintain the head of the bed at the lowest degree of elevation consistent with medical conditions and other restrictions. Limit the amount of time the head of the bed is elevated and elevate only when there is a compelling medical indication (e.g., 1–2 hours after tube feeding or with severe respiratory or cardiac compromise). (Level III)

Principle: Elevation of the head of the bed produces shear and friction forces between the skin and the bed surface. Friction and shear may predispose to the development of pressure ulcers.

Evidence:

  • 1
    Thomas DR. Management of pressure ulcers. J Am Med Directors Assoc 2006; 7(1): 46–59. [LIT REV]

Guideline #1.3: Assess all patients for risk of developing a pressure ulcer. Use a pressure-reducing surface in those patients at risk. A pressure-reducing surface is superior to a standard hospital mattress in reducing the incidence of pressure ulcers. (Level I)

Principle: When compared with a standard hospital mattress, a variety of pressure-reducing devices can lower the incidence of pressure ulcers by about 60 percent.

Evidence:

  • 1
    Cullum N, McInnes E, Bell-Syer SEM, Legood R. Support surfaces for pressure ulcer prevention. The Cochrane Database of Systematic Reviews 2004; 3. [STAT]
  • 2
    Thomas DR. Issues and Dilemmas in Managing Pressure Ulcers. J Gerontol: Med Sci 2001; 56: M238–340. [LIT REV]

Guideline #1.4: A static support surface may be appropriate for patients with a pressure ulcer who can assume a variety of positions without placing pressure on the ulcer or “bottoming out.” No difference in pressure ulcers outcomes is documented among different types of static devices. (Level I)

Principle: Static pressure-reducing devices are superior to standard hospital mattresses. However, if the patient “bottoms out” (if there is less than one inch of material between the bed and the pressure ulcer when feeling under the support surface with the palm of your hand), the device may be ineffective.

Evidence:

  • 1
    Cullum N, McInnes E, Bell–Syer SEM, Legood R. Support surfaces for pressure ulcer prevention. The Cochrane Database of Systematic Reviews 2004; 3. [STAT]

Guideline #1.5: A dynamic support surface may be appropriate for patients with a pressure ulcer who cannot assume a variety of positions in bed, or who “bottom out” on a static surface, or whose ulcer is failing to progress toward healing. (Level I)

Principle: Although some patients improve on a static support surface, there is evidence that other patients have an improved outcome on a dynamic support surface. No difference among studied types of dynamic devices has been shown.

Evidence:

  • 1
    Cullum N, McInnes E, Bell-Syer SEM, Legood R. Support surfaces for pressure ulcer prevention. The Cochrane Database of Systematic Reviews 2004; 3. [STAT]

Guideline #1.6: In patients who have a large stage 3 or stage 4 pressure ulcer, or multiple pressure ulcers involving several turning surfaces, a low-air-loss or air-fluidized bed may be indicated. (Level I)

Principle: Several studies have shown improved outcomes for pressure ulcers in patients treated with a low-air-loss or air-fluidized bed. However, these beds have some limitations, including difficulty for patients in self-positioning or for patients with pulmonary compromise.

Evidence:

  • 1
    Allman RM, Walker JM, Hart MK, et al. Air-fluidized beds or conventional therapy for pressure sores: a randomized trial. Ann Intern Med 1987; 107: 641–8. [RCT]
  • 2
    Cullum N, McInnes E, Bell-Syer SEM, Legood R. Support surfaces for pressure ulcer prevention. The Cochrane Database of Systematic Reviews 2004; 3. [STAT]
  • 3
    Economides NG, Skoutakis VA, Carter CA. Evaluation of the effectiveness of two support surfaces following myocutaneous flap surgery. Adv Wound Care 1995; 8: 49–53. [RCT]
  • 4
    Munro BH, Brown L, Heitman BB. Pressure ulcers: one bed or another? Geriatric Nurs 1989; 10: 190–2. [LIT REV]

Guideline #1.7: A patient at risk for a pressure ulcer should avoid prolonged sitting. Postural alignment, distribution of weight, balance, stability, and pressure reduction should be considered in seated individuals. (Level III)

Principle: Tissue compression between the sitting surface and bony prominence should be relieved in at-risk patients. In patients with a pressure ulcer, sitting on the pressure ulcer should be avoided. Reposition the sitting individual to relieve pressure at least every hour. If this schedule cannot be maintained, return the patient to bed. Individuals should be instructed to shift their weight every 15 minutes.

Guideline #1.8: Use a seat cushion based on the needs of the individual who requires pressure reduction in the sitting position. Avoid using doughnut-type devices. (Level III)

Principle: Several seat cushions reduce pressure in sitting individuals. Examine seating cushions and devices for “bottoming out.” There is insufficient evidence on the value of seat cushions in the prevention of pressure ulcers. Ring cushions (doughnut) devices increase venous congestion and edema.

2. NUTRITION

Preamble: Protein, carbohydrates, vitamins, minerals, and trace elements are required for wound healing. Nutrition is valued and considered in practice as a significant factor in the prevention and treatment of pressure ulcers. However, there are limited definitive studies documenting the efficacy of nutritional treatments for pressure ulcer healing. The following guidelines reflect the best current evidence and expert opinion.

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 condition that may increase the risk of undernutrition. (Level II)

Principle: Nutrition must be adequate to provide sufficient protein to support the growth of granulation tissue. The patient's weight on entry to the healthcare system is a good starting point. Assess body weight whenever there is a change in an individual's condition that may increase the risk of undernutrition. Achieving a weight as close to the ideal body weight as possible is the goal. Assessment of pre-albumin level (reflecting recent protein consumption) and serum albumin level (reflecting long-term protein consumption) is useful to identify patients who are outside the norm. Encourage nutritional support if an individual is undernourished. Undernutrition 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. No studies were identified that specifically address the issue of obesity and pressure ulcer development.

Evidence:

  • 1
    Allman RM, Laprade CA, Noel LB. Pressure sores among hospitalized patients. Ann Intern Med 1986; 105(3): 337–42. [STAT]
  • 2
    Baker JP, Detsky AS, Withwell J, Langer B, Jeejeebhoy KN. A comparison of the predictive value of nutritional assessment techniques. Hum Nutr Clin Nutr 1982; 36C: 233–41. [CLIN S]
  • 3
    Bourdel Marchasson I, Barateau M, Rondeau V, DequaeMerchadou L, SallesMontaudon N, Emeriau JP, Manciet G, Dartigues JF. A multicenter trial of the effects of oral nutritional supplementation in critically ill older inpatients. GAGE Group. Groupe Aquitain Gériatrique d'Evaluation. Nutrition 2000; 16: 15. [RCT]
  • 4
    Hartgrink HH, Wille J, Konig P, Hermans J, Breslau PJ. Pressure sores and tube feeding in patients with a fracture of the hip. Clin Nutr 1998; 17: 287–92. [RCT]
  • 5
    Houwing R, Rozendaal M, WoutersWesseling W, Beulens JWJ, Buskens E, Haalboom J. A randomized, double-blind assessment of the effect of nutritional supplementation on the prevention of pressure ulcers in hip fracture patients. Clin Nutr 2003; 22(4): 401–5. [RCT]
  • 6
    Murden RA, Ainslie NK. Recent weight loss is related to short-term mortality in nursing homes. J Gen Intern Med 1994; 9: 648–50. [CLIN S]
  • 7
    Rudman D, Feller AG, Nagraj HS, Jackson DL, Rudman IW, Mattson DE. Relation of serum albumin concentration to death rate in nursing home men. J Parenter Ent Nutr 1987; 11: 360. [CLIN S]
  • 8
    Rypkema G, Adang E, Dicke H, Naber T, de Swart B, Disselhorst L, Goluke-Willemse G, Olde Rikkert M. Cost-effectiveness of an interdisciplinary intervention in geriatric inpatients to prevent malnutrition. J Nutr Health Aging. 2004; 8(2): 122–7. [CLIN S]
  • 9
    Salzberg CA, Byrne DW, Cayten CG, et al. A new pressure ulcer risk assessment scale for individuals with spinal cord injury. Am J Phys Med Rehabil 1996 Mar–Apr; 75(2): 96–104. [CLIN S]
  • 10
    Schue RM, Langemo DK. Prevalence, incidence, and prediction of pressure ulcers on a rehabilitation unit. J Wound Ostomy Continence Nurs 1999 May; 26(3): 121–9. [RETRO S]
  • 11
    Scivoletto G, Fuoco U, Morganti B. Pressure sores and blood and serum dysmetabolism in spinal cord injury patients. Spinal Cord 2004 Aug; 42(8): 473–6. [RCT]
  • 12
    Sullivan DH, Johnson LE, Bopp MM, Roberson PK. Prognostic significance of monthly weight fluctuations among older nursing home residents. J Gerontol Ser A: Biol Sci Med Sci 2004; 59: M633–M639. [RCT]
  • 13
    Thomas DR, Verdery RB, Gardner L, Kant AK, Lindsay J. A prospective study of outcome from protein-energy malnutrition in nursing home residents. J Parenteral Enteral Nutr 1991; 15: 400–04. [CLIN S]
  • 14
    Volkert D, Kruse W, Oster P, Schlierf G. Malnutrition in geriatric patients: diagnostic and prognostic significance of nutritional parameters. Ann Nutr Metab 1992; 36: 97–112. [CLIN S]

Guideline #2.2: Encourage dietary intake or supplementation if an individual who is undernourished is at risk of developing a pressure ulcer. (Level III)

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.

Evidence:

  • 1
    Bourdel-Marchasson I, Barateau M, Rondeau V, Dequae-Merchadou L, Salles-Montaudon N, Emeriau JP, Manciet G, Dartigues JF. A multi-center trial of the effects of oral nutritional supplementation in critically ill older inpatients. GAGE Group. Groupe Aquitain Gériatrique d'Evaluation. Nutrition 2000; 16: 1–5. [RCT]
  • 2
    Delmi M, Rapin CH, Bengoa JM, Delmas PD, Vasey H, Bonjour JP. Dietary supplementation in elderly patients with fractured neck of the femur. Lancet 1990; 335(8696): 1013–6. [RCT]
  • 3
    Hartgrink HH, Wille J, Konig P, Hermans J, Breslau PJ. Pressure sores and tube feeding in patients with a fracture of the hip: a randomized clinical trial. Clin Nutr 1998; 17: 287–92. [RCT]
  • 4
    Houwing R, Rozendaal M, Wouters-Wesseling W, Beulens JWJ, Buskens E, Haalboom J. A randomized, double-blind assessment of the effect of nutritional supplementation on the prevention of pressure ulcers in hip-fracture patients. Clin Nutr 2003; 22(4): 401–5. [RCT]
  • 5
    Langer G, Schloemer G, Knerr A, Kuss O, Behrens J. Nutritional interventions for preventing and treating pressure ulcers. The Cochrane Database of Systematic Reviews 2003, Issue 4, Art. No: CD003216. DOI:10.1002/14651858. CD003216. [STAT]

Guideline #2.3: Ensure adequate dietary intake to prevent undernutrition to the extent that this is compatible with the individual's wishes. (Level III)

Principle: Adequate nutrition is essential for life and undernutrition is associated with the development of pressure ulcers. Nonetheless, the nutritional plan needs to be consistent with the individual's personal goals.

Evidence:

  • 1
    Bergstrom N, Braden B. A prospective study of pressure sore risk among institutionalized elderly. J Am Geriatr Soc 1992; 40: 747–58. [CLIN S]
  • 2
    Berlowitz DR, Wilking SVB. Risk factors for pressure sores: A comparison of cross-sectional and cohort-derived data. J Am Geriatr Soc 1989; 37: 1043–50. [CLIN S]
  • 3
    Finucane TE. Malnutrition, tube feeding and pressure sores: data are incomplete. J Am Geriatr Soc 1995; 43: 447–51. [LIT REV]
  • 4
    Thomas DR. Specific nutritional factors in wound healing. Adv Wound Care 1997; 10: 40–3. [LIT REV]
  • 5
    Thomas DR. The role of nutrition in prevention and healing of pressure ulcers. Geriatr Clin North Am 1997: 13: 497–512. [LIT REV]
  • 6
    Thomas DR, Ashmen W, Morley JE, Evans JE. Nutritional management in long-term care: development of a clinical guideline. J Gerontol: Med Sci 2000; 55: 725–34. [STAT]
  • 7
    Thomas DR, Goode PS, Tarquine PH, Allman R. Hospital-acquired pressure ulcers and risk of death. J Am Geriatr Soc 1996; 44: 1435–40. [CLIN S]

Guideline #2.4: If dietary intake continues to be inadequate, impractical, or impossible, nutritional support (usually tube feeding) should be used to place the patient into positive nitrogen balance (approximately 30–35 calories/kg/day and 1.25–1.50 g of protein/kg/day) according to the goals of care. (Level III)

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 optimize nutritional status.

Evidence:

  • 1
    Chernoff RS, Milton KY, Lipschitz DA. The effect of a very high-protein liquid formula on decubitus ulcers healing in long-term tube-fed institutionalized patients. J Am Diet Assoc 1990; 90: A-130. [CLIN S]
  • 2
    Henderson CT, Trumbore LS, Mobarhan S, Benya R, Miles TP. Prolonged tube feeding in long-term care: Nutritional status and clinical outcomes. J Am Coll Clin Nutr 1992; 11: 309. [CLIN S]
  • 3
    Long CL, Nelson KM, Akin JM Jr, Geiger JW, Merrick HW, Blakemore WZ. A physiologic basis for the provision of fuel mixtures in normal and stressed patients. J Trauma 1990; 30: 1077–86. [CLIN S]
  • 4
    Mathus-Vliegen EM. Old age, malnutrition, and pressure sores: an ill-fated alliance. J Gerontol Ser A, Biol Sci Med Sci 2004 Apr; 59(4): 355–60. [LIT REV]
  • 5
    Mitchell SL, Kiely DK, Lipsitz LA. The risk factors and impact on survival of feeding tube placement in nursing home residents with severe cognitive impairment. Arch Intern Med 1997; 157: 327–32. [CLIN S]
  • 6
    Thomas DR. Improving the outcome of pressure ulcers with nutritional intervention: a review of the evidence. Nutrition 2001; 17: 121–25. [LIT REV]

Guideline #2.5: Give vitamin and mineral supplements if deficiencies are confirmed or suspected. (Level III)

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. No acceleration in healing has been reported with supplemental Vitamin A, Vitamin C, or zinc. Amino acids supplements have been effective in the healing of some non-pressure-related wounds. Arginine has not been found to accelerate healing in patients with pressure ulcers.

Evidence:

  • 1
    Ehrlich HP, Hunt TK. Effects of cortisone and vitamin A on wound healing. Ann Surg 1968; 167: 324. [EXP]
  • 2
    Goode P, Allman R. The prevention and management of pressure ulcers. Med Clin North Am 1989; 73: 1511–1424. [LIT REV]
  • 3
    Gregger JL. Potential for trace mineral deficiencies and toxicities in the elderly. In: Bales CW, editor. Mineral Homeostasis in the Elderly. New York: Marcel Dekker, 1989: 171–200. [LIT REV]
  • 4
    Hallbook T, Lanner E. Serum zinc and healing of leg ulcers. Lancet 1972; 2: 780. [RCT]
  • 5
    Houwing R, Rozendaal M, Wouters-Wesseling W, Beulens JWJ, Buskens E, Haalboom JR. A randomized, double-blind assessment of the effect of nutritional supplementation on the prevention of pressure ulcers in hip-fracture patients. Clin Nutr 2003; 22(4): 401–5. [RCT]
  • 6
    Hunt TK. Vitamin A and wound healing. J Am Acad Dermatol 1986; 15: 817–21. [LIT REV]
  • 7
    Langer G, Schloemer G, Knerr A, Kuss O, Behrens J. Nutritional interventions for preventing and treating pressure ulcers. The Cochrane Database of Systematic Reviews 2003, Issue 4, Art. No: CD003216. DOI:10.1002/14651858. CD003216. [STAT]
  • 8
    Langkamp-Henken B, Herrlinger-Garcia KA, Stechmiller JK, Nickerson-Troy JA, Lewis B, Moffatt L. Arginine supplementation is well tolerated but does not enhance mitogen-induced lymphocyte proliferation in elderly nursing home residents with pressure ulcers. JPEN 2000; 24: 280–7. [RCT]
  • 9
    Norris JR, Reynolds RE. The effect of oral zinc sulfate therapy on decubitus ulcers. J Am Geriatr Soc 1971; 19: 793. [CLIN S]
  • 10
    Prasad AS. Discovery of human zinc deficiency and studies in an experimental human model. Am J Clin Nutr 1991; 53: 403–12. [RETRO S]
  • 11
    Rackett SC, Rothe MJ, Grant-Kels JM. Diet and dermatology. The role of dietary manipulation in the prevention and treatment of cutaneous disorders. J Am Acad Dermatol 1993; 29: 447–61. [CLIN S]
  • 12
    Sandstead SH, Henrikson LK, Greger JL, et al. Zinc nutrition in the elderly in relation to taste acuity, immune response, and wound healing. Am J Clin Nutr 1982; 36(Suppl.): 1046. [CLIN S]
  • 13
    Ter Riet G, Kessels AG, Knipschild PG. Randomized clinical trial of ascorbic acid in the treatment of pressure ulcers. J Clin Epidemiol 1995; 48: 1453–60. [RCT]
  • 14
    Vilter RW. Nutritional aspects of ascorbic acid: uses and abuses. West J Med 1980; 133: 485. [LIT REV]
  • 15
    Waldorf H, Fewkes J. Wound healing. Adv Dermatol 1995; 10: 77–96. [LIT REV]

3. INFECTION

Preamble: Infection results when the bacteria:host defense equilibrium is upset in favor of the bacteria. Infection plays various roles in the etiology, healing, operative repair, and complications of pressure ulcers. Therefore, guidelines are necessary to address the treatment of infection under 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)

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

Evidence:

  • 1
    Alison WE, Phillips LG, Linares HA, et al. The effect of denervation on soft tissue infection pathophysiology. Plast Reconstr Surg 1992; 90: 1031–35. [EXP]
  • 2
    Groth KE. Clinical observations and experimental studies of the pathogens of decubitus ulcers. Acta Chir Scand 1942; 87 (Suppl. 76): 198–207. [EXP]
  • 3
    Hussain T. An experimental study of some pressure effects on tissues with reference to the bedsore problem. J Pathol Bacteriol 1953; 66: 347–58. [EXP]
  • 4
    Krizek TJ, Davis JH. Endogenous wound infection. J Trauma 1967; 6: 239–48. [EXP]
  • 5
    Richardson D. Diagnosis and management of systemic infections and fever in neurological patients. Semin Neurol 2000; 20: 387–91. [LIT REV]
  • 6
    Ricketts LR, Squire JR, Topley E, et al. Human skin lipids with particular reference to the self-sterilizing power of the skin. Clin Sci Mol Med 1951; 10: 89. [EXP]
  • 7
    Robson MC, Krizek TJ. The role of infection in chronic pressure ulcerations. In: Fredericks, S, Brody, GS. editors. Symposium on Neurologic Aspects of Plastic Surgery. St. Louis: CV Mosby Co, 1978. [EXP]
  • 8
    Wall BM, Mangold T, Huch KM, et al. Bacteremia in the chronic spinal cord injury population: risk factors for mortality. J Spinal Cord Med 2003; 26: 248–53. [CLIN S]

Guideline #3.2: Remove all necrotic or devitalized tissue by sharp, enzymatic, biological, mechanical, or autolytic debridement. (See detailed discussion of debridement in Wound Bed Preparation section of these guidelines.) (Level I)

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

Evidence:

  • 1
    Bradley M, Cullum N, Sheldon T. The debridement of chronic wounds: a systematic review. Health Technol Assess 1999; 3: 1–78. [STAT]
  • 2
    Edlich RF, Rodeheaver GT, Thacker JG, et al. Technical factors in wound management. In: Dunphy, JE, Hunt, TK, editors. Fundamentals Wound Manage Surg. South Plainfield, NJ: Chirurgecom, 1977. [EXP]
  • 3
    Falanga V. Wound bed preparation and the role for enzymes: a case for multiple actions of therapeutic agents. Wounds 2002; 14: 47–57. [LIT REV]
  • 4
    Hamer MI, Robson MC, Krizek TJ, et al. Quantitative bacterial analyses of comparative wound irrigations. Ann Surg 1975; 181: 819–22. [EXP]
  • 5
    Steed D, Donohue D, Webster M, et al. Effect of extensive debridement and rhPDGF-BB (Becaplermin) on the healing of diabetic foot ulcers. J Am Coll Surg 1996; 183: 61–4. [RCT]
  • 6
    Witkowski, JA, Parrish, LC. Debridement of cutaneous ulcers: Medical and surgical aspects. Clin Dermatol 1992; 9: 585–91. [LIT REV]

Guideline #3.3: If there is suspected infection in a debrided ulcer, or if contraction and epithelialization from the margin are not progressing within two 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. (Level II)

Principle: High levels of bacteria ≥1 × 106 CFU/gram of soft tissue or any tissue level of beta hemolytic streptococci impede the various wound-healing processes and have been demonstrated to impede spontaneous healing and surgical closure of pressure ulcers. Cultures should be performed to isolate both aerobic and anaerobic bacteria.

Evidence:

  • 1
    Bendy RH, Nuccio PA, Wolfe E, et al. Relationship of quantitative wound bacterial counts to healing of decubiti. Effect of gentamicin. Antimicrob Agent Chemo Ther 1964; 4: 147–55. [RCT]
  • 2
    Heggers JP. Variations on a theme. In: Heggers, JP, Robson, MC, editors. Quantitative Bacteriology: Its Role in the Armamentarium of the Surgeon. Boca Raton: CRC Press, 1991.
  • 3
    Levine NS, Lindberg RB, Mason AD, et al. The quantitative swab culture and smear: a quick method for determining the number of viable aerobic bacteria in open wounds. J Trauma 1976; 16: 84–94. [TECH]
  • 4
    Nystrom PO. The microbiological swab sampler—a quantitative experimental investigation. Acta Pathol Microbiol Scand 1978; 86B: 361–7. [TECH]
  • 5
    Robson MC, Stenberg BD, Heggers JP. Wound healing alterations caused by infection. Clin Plast Surg 1990; 17: 485–92. [LIT REV]
  • 6
    Robson MC. Wound infection: a failure of wound healing caused by an imbalance of bacteria. Surg Clin North Am 1997; 77: 637–50. [LIT REV]
  • 7
    Sapico FL, Ginnas VJ, Thornhill-Joynes M, et al. Quantitative microbiology of pressure sores in different stages of healing. Diagn Microbiol Infect Dis 1986; 5: 31–8. [TECH]
  • 8
    Tobin GR. Closure of contaminated wounds: biologic and technical considerations. Surg Clin North Am 1984; 64: 639–52. [LIT REV]
  • 9
    Stephens P, Wall JB, Wilson MJ, et al. Anaerobic cocci populating the deep tissues of chronic wounds impair cellular wound healing responses in vitro. Br J Dermatol 2003; 148: 456–66. [CLIN S]
  • 10
    Volenec FJ, Clark GM, Manni MM, et al. Burn wound biopsy bacterial quantification: a statistical analysis. Am J Surg 1979; 138: 695–7. [STAT]

Guideline #3.4: For ulcers with ≥1 × 106 CFU/gram of tissue or any tissue level of beta hemolytic streptococci following adequate debridement, decrease the bacterial level with a topical antimicrobial. Once in bacterial balance, discontinue the use of topical antimicrobial to minimize any possible cytotoxic effects due to the antimicrobial agent or bacterial resistance to the agent. (Level I)

Principle: Systemically administered antibiotics do not effectively decrease bacterial levels in granulating wounds. However, topically applied antimicrobials can be effective.

Evidence:

  • 1
    Kucan JO, Robson MC, Heggers JP, et al. Comparison of silver sulfadiazine, povidone-iodine, and physiologic saline in the treatment of chronic pressure ulcers. J Am Geriatr Soc 1981; 24: 232–5. [RCT]
  • 2
    Robson MC, Mannari RJ, Smith PD, et al. Maintenance of wound bacterial balance. Am J Surg 1999; 178: 399–402. [RCT]
  • 3
    Robson MC, Heggers JP. Surgical infection: II. The β-hemolytic streptococcus. J Surg Res 1969; 14: 289–92. [EXP]
  • 4
    Robson MC, Edstrom LE, Krizek TJ, et al. The efficacy of systemic antibiotics in the treatment of granulating wounds. J Surg Res. 1974; 16: 299–306. [EXP]
  • 5
    Robson MC. Wound infection: A failure of wound healing caused by an imbalance of bacteria. Surg Clin North Am 1997; 77: 637–50. [LIT REV]
  • 6
    Stotts NA, Hunt TK. Managing bacterial colonization and infection. Clin Ger Med 1997; 13: 565–73. [LIT REV]

Guideline #3.5: Obtain bacterial balance (<105 CFU/gram of tissue and no beta hemolytic streptococci) in the pressure ulcer before attempting surgical closure by skin graft, direct wound approximation, pedicled, or free flap. (Level I)

Principle: “A wound containing contaminated foci with >105 organisms per gram of tissue cannot be readily closed, as the incidence of wound infection that follows is 50–100%.”

Evidence:

  • 1
    Edlich RF, Rodeheaver GT, Thacker JG, Winn HA, Edgerton MT. Management of soft tissue injury. Clin Plast Surg 1977; 4: 191–8. [LIT REV]
  • 2
    Krizek TJ, Robson MC, Ko E. Bacterial growth and skin graft survival. Surg Forum 1967; 18: 518–9. [RCT]
  • 3
    Liedburg NC, Reiss E, Artz CP. The effect of bacteria on the take of split thickness skin grafts in rabbits. Ann Surg 1955; 142: 92–6. [EXP]
  • 4
    Murphy RC, Robson MC, Heggers JP, et al. The effect of microbial contamination on musculocutaneous and random flaps. J Surg Res 1986; 41: 75–80. [EXP]
  • 5
    Robson MC, Lea CE, Dalton JB, et al. Quantitative bacteriology and delayed wound closure. Surg Forum 1968; 19: 501–2. [RCT]
  • 6
    Robson MC, Krizek TJ, Heggars JP. Biology of surgical infection. Curr Prob Surg 1972; 10: 1–62. [LIT REV].
  • 7
    Tobin GR: Closure of contaminated wounds: biologic and technical considerations. Surg Clin North Am 1984; 64: 639–52. [LIT REV]

Guideline #3.6: Obtain bone biopsy for culture and histology in cases of suspected osteomyelitis associated with a pressure ulcer. (Level II)

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.

Evidence:

  • 1
    Lewis VL, Bailey MH, Pulawski G, et al. The diagnosis of osteomyelitis in patients with pressure sores. Plast Reconstr Surg 1988; 81: 229–32. [RCT]
  • 2
    Han H, Lewis VL, Wiedrich TA, et al. The value of Jamshidi core needle bone biopsy in predicting postoperative osteomyelitis in grade IV pressure ulcer patients. Plast Reconstr Surg 2002; 110: 118–22. [RETRO S]
  • 3
    Huang AB, Schweitzer ME, Hume E, et al. Osteomyelitis of the pelvis/hips in paralyzed patients: accuracy and clinical utility of MRI. J Comput Assist Tomogr 1998; 22: 437–43. [CLIN S]
  • 4
    Sugarman B. Pressure sores and underlying bone infection. Arch Int Med 1987; 147: 553–5. [CLIN S]
  • 5
    Turk EE, Tsokos M, Delling G. Autopsy-based assessment of extent and type of osteomyelitis in advanced-grade sacral decubitus ulcers: a histopathologic study. Arch Pathol Lab Med 2003; 127: 1599–602. [PATH S]

Guideline #3.7: Once confirmed, osteomyelitis underlying a pressure ulcer should be adequately debrided and covered with a flap containing muscle or fascia. (Antibiotic choice, guided by culture results, should be used for three weeks.) (Level I)

Principle: Muscle, musculocutaneous, and fasciocutaneous flaps effectively control bacterial levels and antibiotics have been demonstrated by meta-analysis not to show additional efficacy beyond three weeks.

Evidence:

  • 1
    Calderon W, Chang N, Mathes SJ. Comparison of the effect of bacterial inoculation in musculocutaneous and fasciocutaneous flaps. Plast Reconstr Surg 1986; 77: 785–94. [EXP]
  • 2
    Chang N, Mathes SJ. Comparison of the effect of bacterial inoculation in musculocutaneous and random flaps. Plast Reconstr Surg 1982; 70: 1–10. [EXP]
  • 3
    Ger R. Muscle transposition for treatment and prevention of chronic post-traumatic osteomyelitis of the tibia. J Bone Joint Surg 1977; 59A: 784. [CLIN S]
  • 4
    Gosain A, Chang N, Mathes S, et al. A study of the relationship between blood flow and bacterial inoculation in musculocutaneous and fasciocutaneous flaps. Plast Reconstr Surg 1990; 86: 1152–62. [EXP]
  • 5
    Lazzarini L, Lipsky BA, Mader JT. Antibiotic treatment of osteomyelitis: what have we learned from 30 years of clinical trials? Int J Infect Dis 2005; 9: 127–38.
  • 6
    Mathes SJ, Feng LJ, Hunt TK: Coverage of infected wounds. Ann Surg 1983; 198: 420–9. [CLIN S]
  • 7
    Stengel D, Bauwens K, Sehoul J, et al. Systematic review and meta-analysis of antibiotic therapy for bone and joint infections. Lancet Infect Dis 2001; 1: 175–88. [STAT]
  • 8
    Thornhill-Joynes, M, Gonzales F, Stewart CA, et al. Osteomyelitis associated with pressure ulcers. Arch Phys Med Rehabil 1986; 67: 314–8. [RETRO S]

4. 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 the causes of tissue damage. It is important to examine the patient's systemic diseases and medications. (Level I)

Principle: 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, and drug therapies such as immunosuppressive drugs and systemic steroids, will delay wound healing. Autoimmune diseases such as rheumatoid arthritis, systemic lupus, uncontrolled vasculitis, or pyoderma gangrenosum can impair healing and may require systemic steroids or immunosuppressive agents for adequate control before local wound healing can occur. Patients undergoing major surgery have diminished wound-healing capacity. Smoking is associated with impaired wound healing and increased risk of infection.

Evidence:

  • 1
    William DT, Harding K. Healing responses of skin and muscle in critical illness. Crit Care Med 2003 Aug 31 (8 Suppl.): S547–57. [LIT REV]
  • 2
    Beer HD, Fassler R, Werner S. Glucocorticoid-regulated gene expression during cutaneous wound repair.Vitam Horm 2000; 59: 217–39. [EXP]
  • 3
    Vaseliso M, Guaitero E. A comparative study of some anti-inflammatory drugs in wound healing of the rat. Experientia 1973 Oct 15; 29(10): 1250–1. [EXP]
  • 4
    Jorgensen LN, Kallehave F, Karlsmark T, Gottrup F. Reduced collagen accumulation after major surgery. Br J Surg 1996 Nov; 83(11): 1591–4. [CLINICAL S]
  • 5
    Sorensen LT, Nielsen HB, Kharazmi A, Gottrup F. Effect of smoking and abstention on oxidative burst and reactivity of neutrophils and monocytes. Surgery 2004 Nov; 136(5): 1047–53. [RCT]
  • 6
    Sorensen LT, Karlsmark T, Gottrup F. Abstinence from smoking reduces incisional wound infection: a randomized controlled trial. Ann Surg 2003; 238: 1–5. [RCT]
  • 7
    Lazarus GS, Cooper DM, Knighton DR, et al. Definitions and guidelines for assessment of wounds and evaluations of healing. Arch Dermatol 1994; 130: 489–93. [STAT]
  • 8
    Mustoe T. Understanding chronic wounds. A unifying hypothesis on their pathogenesis and implications for therapy. Am J Surg; 187 (5A): 65s–70s. [LIT REV]

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)

Principle: Nutrition must be adequate to provide sufficient protein to support the growth of granulation tissue. Encourage nutritional support if an individual is undernourished. (Detailed discussion of nutrition is in Nutritional Guidelines.)

Evidence:

  • 1
    Allman RM, Laprade CA, Noel LB. Pressure sores among hospitalized patients. Ann Intern Med 1986 Sep; 105(3): 337–42. [STAT]
  • 2
    Bourdel Marchasson I, Barateau M, Rondeau V, DequaeMerchadou L, SallesMontaudon N, Emeriau JP, Manciet G, Dartigues JF. A multicenter trial of the effects of oral nutritional supplementation in critically ill older inpatients. GAGE Group. Groupe Aquitain Gériatrique d'Evaluation. Nutrition 2000; 16: 15. (RCT-multicenter study)
  • 3
    Hartgrink HH, Wille J, Konig P, Hermans J, Breslau PJ. Pressure sores and tube feeding in patients with a fracture of the hip. Clin Nutr 1998; 17: 287–92. [RCT]
  • 4
    Houwing R, Rozendaal M, WoutersWesseling W, Beulens JWJ, Buskens E, Haalboom J. A randomized, double-blind assessment of the effect of nutritional supplementation on the prevention of pressure ulcers in hip fracture patients. Clin Nutr 2003; 22(4): 401–5. [RCT]
  • 5
    Salzberg CA, Byrne DW, Cayten CG, et al. A new pressure ulcer risk assessment scale for individuals with spinal cord injury. Am J Phys Med Rehabil 1996 Mar–Apr; 75(2): 96–104. [CLIN S]
  • 6
    Schue RM, Langemo DK. Prevalence, incidence, and prediction of pressure ulcers on a rehabilitation unit. J Wound Ostomy Continence Nurs 1999 May; 26(3): 121–9. [RETRO S]
  • 7
    Scivoletto G, Fuoco U, Morganti B. Pressure sores and blood and serum dysmetabolism in spinal cord injury patients. Spinal Cord 2004 Aug; 42(8): 473–6. [RCT]

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)

Principle: Adequate tissue perfusion and oxygenation: 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 decrease tissue perfusion. Cigarette smoking decreases tissue oxygen by peripheral vasoconstriction.

Evidence:

  • 1
    Chang N, Goodson WH 111, Gottrup F, Hunt TK. Direct measurement of wound and tissue oxygen tension in postoperative patients. Ann Surg 1983 Apr; 197(4): 470–8. [CLIN S]
  • 2
    Gottrup F. Oxygen in wound healing and infection. World J Surg 2004 Mar; 28(3): 312–5. Epub 2004 Feb 17. [LIT REV]
  • 3
    Gottrup F. Prevention of surgical—wound infections (editorial). N Engl J Med 2000; 342: 202–4. [LIT REV]
  • 4
    Greif R, Akca O, Horn EP, Kurz A, Sessler DI. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. Outcomes research group. N Engl J Med 2000; 342 (3): 161–7. [RCT]
  • 5
    Hunt TK, Aslam RS. Oxygen 2002: Wounds. Undersea Hyperb Med 2004; Spring; 31(1): 147–53. [LIT REV]
  • 6
    Hopf H, Hunt TK, West JM, et al Wound tissue oxygen tension predicts the risk of wound infection in surgical patients. Arch Surg 1997; 132(9): 997–1004. [CLIN S]
  • 7
    Hunt TK, Hopf HW. Wound healing and wound infection. What surgeons and anesthesiologists can do. Surg Clin North Am 1997 Jun; 77(3): 587–606. [LIT REV]
  • 8
    Jensen JA, Goodson WH, Hopf HW, Hunt TK. Cigarette smoking decreases tissue oxygen. Arch Surg 1991 Sep; 126(9): 1131–4. [RCT]
  • 9
    Jonsson K, Jensen JA, Goodson WH 3rd, Scheuenstuhl H, West J, Hopf HW, Hunt TK. Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients. Ann Surg 1991; 214(5): 605–13. [RCT]
  • 10
    Knighton DR, Halliday B, Hunt TK. Oxygen as an antibiotic. A comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg 1986 Feb; 121(2): 191–5. [EXP]

Guideline #4.4: Initial debridement is required to remove the obvious necrotic tissue, excessive bacterial burden, and cellular burden of dead and senescent cells. Maintenance debridement is needed to maintain the appearance and readiness of the wound bed for healing. 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. (Level I)

Principle: Necrotic tissue, excessive bacterial burden, senescent cells, and cellular debris can all inhibit wound healing. The method of debridement chosen may depend on the status of the wound, the capability of the health provider, the overall condition of the patient, and professional licensing restrictions.

  • 1
    Ayello EA, Cuddigan J. Debridement: controlling the necrotic/cellular burden. Adv Skin Wound Care 2004 March; 17(2): 66–75. [LIT REV]
  • 2
    Gottrup, F. Wound debridement. In: The Oxford European Wound Healing Course Handbook. Positif Press, Oxford, 2002: 116–120. [SURV]
  • 3
    Mosher BA, Cuddigan J, Thomas DR, Boudreau DM. Outcomes of 4 methods of debridement using a decision analysis methodology. Adv Wound Care 1999 Mar; 12(2): 81–8. [TECH]
  • 4
    Saap LJ, Falanga V. Debridement performance index and its correlation with complete closure of diabetic foot ulcers. Wound Rep Regen 2002 Nov–Dec; 10(6): 354–9. [RCT]
  • 5
    Sibbald RG, Williamson D, et al. Preparing the wound bed—debridement, bacterial balance, and moisture balance. Ostomy/Wound Manage 2000; 46(11): 14–35. [LIT REV]
  • 6
    Sieggreen MY, Maklebust J. Debridement: choices and challenges. Adv Wound Care 1997 Mar–Apr; 10(2): 32–7. [LIT REV]
  • 7
    Steed DL. Debridement. Am J Surg 2004 May; 187(5A): 71S–74S. [LIT REV]

Surgical/Sharp Debridement: involves the use of instruments (scissors, scalpels, forceps) or laser to remove necrotic tissue from the wound. Debridement of large amounts of necrotic tissue should be performed 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.

Evidence:

  • 1
    Sorensen JL, Jorgensen B, Gottrup F. Surgical treatment of pressure ulcers. Am J Surg 2004 Jul; 188(1A Suppl.): 42–51. [LIT REV]
  • 2
    Steed DL, Donohue D, Webster MW, Lindsley L. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. Diabetic Ulcer Study Group. J Am Coll Surg 1996 Jul; 183(1): 61–4. [RCT]

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. Whirlpools may be used initially to loosen and remove debris, bacteria, exudates, and necrotic tissue. Prolonged use and periods of wetness may macerate the tissue or may be associated with bacterial contamination.

Evidence:

  • 1
    Capasso VA, Munroe BH. The cost and efficacy of two wound treatments. AORN J 2003 May; 77(5): 984–92, 995–7, 1000–4. [RETRO S]
  • 2
    Hamer MI, Robson MC, Krizek TJ, et al. Quantitative bacterial analysis of comparative wound irrigations. Ann Surg 1975; 181: 819–22. [EXP]
  • 3
    Mulder GD. Cost-effective managed care: gel versus wet-to-dry for debridement. Ostomy Wound Manage. 1995 Mar; 41(2): 68–70, 72, 74 passim. [RCT]
  • 4
    Palmier S, Trial C. Use of high-pressure waterjets in wound debridement. In: Teot L, Banwell PE, Ziegler UE, editors. Surgery in Wounds. Berlin: Springer 2004: 72–6. [SURV]
  • 5
    Xakellis GC, Chrischilles EA. Hydrocolloid versus saline-gauze dressings in treating pressure ulcers: a cost-effectiveness analysis. Arch Phys Med Rehabil 1992 May; 73(5): 463–9. [RCT]

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

Evidence:

  • 1
    Alvarez OM, Fernandez-Obregon A, Rogers RS, et al. A prospective, randomized, comparative study of collagenase and papain-urea for pressure ulcer debridement. Wounds 2002; 14: 293–30. [RCT]
  • 2
    Boxer AM, Gottesman N, Bernstein H, Mandl I. Debridement of dermal ulcers and decubiti with collagenase. Geriatrics 1969 Jul; 24(7): 75–86. [RCT]
  • 3
    Falanga V. Wound bed preparation and the role of enzymes: a case for multiple actions of the therapeutic agents. Wounds 2002; 14: 47–57. [LIT REV]
  • 4
    Rao DB, Sane PG, Georgiev EL. Collagenase in the treatment of dermal and decubitus ulcers. J Am Geriatr Soc 1975 Jan; 23(1): 22–30. [RCT]
  • 5
    König M, Vanscheidt W, Augustin M, Kapp H. Enzymatic versus autolytic debridement of chronic leg ulcers: a prospective randomised trial. J Wound Care 2005; 14(7): 320–3. [RCT]
  • 6
    Wright JB, Shi L. Accuzyme papain-urea debriding ointment: a historical review. Wounds 2003; 15 (Suppl.): 2S–12. [LIT REV]

Autolytic Debridement: is accomplished by moist interactive dressings. These dressings allow the natural wound fluid and its endogenous enzymes to soften and liquefy slough and promote granulation. The wound needs to be cleansed after debridement to remove the necrotic debris.

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.

Evidence:

  • 1
    Alvarez OM, Mertz PM, Eaglstein WH. The effect of occlusive dressings on collagen synthesis and reepithelialization in superficial wounds. J Surg Res 1983; 35(2): 142–8. [EXP]
  • 2
    Barnett SE, Varley SJ. The effects of calcium alginate on wound healing. Ann R Coll Surg Engl 1987; 69: 153–5. [EXPT]
  • 3
    Barr JE, Day AL, Weaver VA, Taylor GM, Dombranski S, et al. Assessing clinical efficacy of a hydrocolloid/alginate dressing on full-thickness pressure ulcers. Ostomy Wound Manage 1995 Apr; 41(3): 28–30, 32, 34–6 passim. [CLIN S]
  • 4
    Kim YC, Shin JC, et al. Efficacy of hydrocolloid occlusive dressing technique in decubitus ulcer treatment: a comparative study. Yonsei Med J 1996 Jun; 37(3): 181–5. [RCT]

Guideline #4.5: Wounds should be cleansed initially and at each dressing change using a neutral, nonirritating, nontoxic solution. Routine wound cleansing should be accomplished with a minimum of chemical and/or mechanical trauma. (Level III)

Principle: Cleansing the wound removes loose impediments to wound healing. Clinical experience has shown that mild soap (non-perfumed, without added antibacterials, and at skin pH: 4.5–5.7) and water for cleansing, used regularly, is effective, safe, and cheap. Sterile saline or water is recommended. Tap water should only be used if the water source is reliably clean. Wound antiseptic agents, e.g., hydrogen peroxide, hypochlorite solution, acetic acid, chlorhexamide, providone/iodine, cetrimide, and others have antibacterial properties but are all toxic to healthy granulation tissue.

Evidence:

  • 1
    Rodeheaver GT. Pressure ulcer debridement and cleansing: a review of current literature. Ostomy Wound Manage 1999 Jan; 45 (1A Suppl.): 80S–85S; quiz86S–87S. [LIT REV]
  • 2
    Rodeheaver GT. Wound cleansing, wound irrigation, wound disinfection. In: Krasner D, Kane D, editors. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, 2nd ed. Wayne, PA: Health Management Publications, Inc.; 1997: 97–108. [LIT REV]
  • 3
    Rodeheaver GT, Kurtz L, Kircher BJ, et al. Pluronic F-68: a promising new skin wound cleanser. Ann Emerg Med 1980; 9: 572–6. [EXP]

Guideline #4.6: Infection control should be achieved by reducing wound bacterial burden and achieving wound bacterial balance. (For detailed guidelines, see Infection.) (Level I)

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 defense mechanisms, debridement, wound cleaning, and topical antimicrobials. For ulcers with 1 × 106 or higher CFU/gram of tissue or any tissue-level beta hemolytic streptococci following adequate debridement, decrease the bacterial level by a topical antimicrobial. Once in bacterial balance, i.e., 105 CFU or less/gram of tissue, and no beta hemolytic streptococci in the ulcer, discontinue the use of topical antimicrobial to minimize the possibility of emergence of resistance. In chronic wounds, the pathogen species may be more important than the 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.

Evidence:

  • 1
    Bendy RH, Nuccio PA, Wolfe E, et al. Relationship of quantitative wound bacterial counts to healing of decubiti. Effect of gentamicin. Antimicrob Agent Chemo Ther 1964; 4: 147–55. [RCT]
  • 2
    Bowler PG, Duerden BL, Armstrong DG. Wound microbiology and associated approaches to wound management. Clin Microbiol Rev 2001; 14: 244–69. [LIT REV]
  • 3
    Kucan JO, Robson MC, Heggers JP, et al. Comparison of silver sulfa-diazine, povidone-iodine, and physiologic saline in the treatment of chronic pressure ulcers. J Am Geriatr Soc 1981; 24: 232–5. [RCT]
  • 4
    Nystrom PO. The microbiological swab sampler—a quantitative experimental investigation. Acta Pathol Microbiol Scand 1978; 86B: 361–7. [TECH]
  • 5
    Robson MC. Wound infection: a failure of wound healing caused by an imbalance of bacteria. Surg Clin North Am 1997; 77: 637–50. [LIT REV]
  • 6
    Robson MC, Edstrom LE, Krizek TJ, et al. The efficacy of systemic antibiotics in the treatment of granulating wounds. J Surg Res 1974; 16: 299–306. [EXP]
  • 7
    Robson MC, Mannari RJ, Smith PD, et al. Maintenance of wound bacterial balance. Am J Surg 1999; 178: 399–402. [RCT]
  • 8
    Robson MC, Stenberg BD, Heggers, JP. Wound healing alterations caused by infection. Clin Plast Surg 1990; 17: 485–92. [LIT REV]
  • 9
    Sapico FL, Ginnas VJ, Thornhill-Joynes M, et al. Quantitative microbiology of pressure sores in different stages of healing. Diagn Microbiol Infect Dis 1986; 5: 31–8. [CLIN S]
  • 10
    Stengel D, Bauwens K, Sehoul J, et al. Systematic review and meta-analysis of antibiotic therapy for bone and joint infections. Lancet Infect Dis 2001; 1: 175–88. [STAT]
  • 11
    Stotts NA, Hunt TK. Pressure ulcers. Managing bacterial colonization and infection. Clin Geriatr Med 1997 Aug; 13(3): 565–73. [LIT REV]
  • 12
    Thornhill-Joynes M, Gonzales F, Stewart CA, et al. Osteomyelitis associated with pressure ulcers. Arch Phys Med Rehabil 1986; 67: 314–18. [RETRO S]
  • 13
    Volenec FJ, Clark GM, Manni MM, et al. Burn wound biopsy bacterial quantification: a statistical analysis. Am J Surg 1979; 138: 695–7. [STAT]

Guideline #4.8: Achieve local moisture balance by management of exudate. (Level I)

Principle: Local moisture balance is necessary to facilitate granulation and reepithelialization of the ulcer. A moist wound environment accelerates wound healing with more rapid epithelialization. Many dressings now combine wound bed preparation, i.e., 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. Use clean, dry dressings for 8–24 hours after sharp debridement associated with bleeding; then reinstitute moist dressings. Clean dressings may also be used in conjunction with mechanical or enzymatic debridement techniques.

(For detailed guidelines, see Dressings.)

Evidence:

  • 1
    Alm A, Hornmark AM, Fall PA, et al. Care of pressure sores: a controlled study of the use of a hydrocolloid dressing compared with wet saline gauze compresses. Acta Derm Venereol (Stockholm) 1989; 149 (Suppl.): 1–10. [RCT]
  • 2
    Agren MS, Karlsmark T, Hansen JB, Rygaard J. Occlusion versus air exposure on full-thickness biopsy wounds. J Wound Care 2001; 10(8): 301–4. [RCT]
  • 3
    Breuing K, Eriksson E, Liu P, Miller DR. Healing of partial thickness porcine skin wounds in a liquid environment. J Surg Res 1992; 52: 50–8. [EXP]
  • 4
    Colwell JC, Foreman MD, Trotter JP. A comparison of the efficacy and cost-effectiveness of two methods of managing pressure ulcers. Decubitus 1993; 6: 28–36. [RCT]
  • 5
    Gorse GJ, Messner RL. Improved pressure sore healing with hydrocolloid dressings. Arch Dermatol 1987; 123: 766–71. [RCT]
  • 6
    Mulder G, Altman M, Seeley J, et al. Prospective randomized study of the efficacy of hydrogel, hydrocolloid, and saline moistened dressings on the management of pressure ulcers. Wound Rep Reg 1993; 1: 213–8. [RCT]
  • 7
    Svensjo T, Pomahac B, Yao F, Slama J, Eriksson E. Accelerated healing of full-thickness skin wounds in a wet environment. Plast Reconstr Surg 2000; 106: 602–12. [EXP]
  • 8
    Vranckx JJ, Slama J, Preuss S, et al. Wet wound healing. Plast Reconstr Surg 2002; 110: 1680–7. [CLIN S]
  • 9
    Winter GD, Scales, JT. Effect of air drying and dressings on the surface of a wound. Nature 1963; 197: 91. [EXP]
  • 10
    Neill K, Conforti C, Kedas A, et al. Pressure sore response to a new hydrocolloid. Wounds 1989; 1(3): 173–85. [RCT]

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 whether treatment is optimal. (Level III)

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.

Evidence:

  • 1
    Brown GS. Reporting outcomes for stage IV pressure ulcer healing: a proposal. Adv Skin Wound Care 2000 Nov–Dec; 13(6): 277–83. [RETRO S]
  • 2
    Lazarus GS, Cooper DM, Knighton DR, Margolis DJ, Pecoraro RE, Rodeheaver G, Robson MC. Definitions and guidelines for assessment of wounds and evaluation of healing. Arch Dermatol 1994 Apr; 130(4): 489–93. [STAT]
  • 3
    Krasner D. Wound Healing Scale, version 1.0: a proposal. Adv Wound Care 1997 Sep; 10(5): 82–5. [LIT REV]
  • 4
    Saap LJ, Falanga V. Debridement performance index and its correlation with complete closure of diabetic foot ulcers. Wound Rep Reg 2002 Nov–Dec; 10(6): 354–9. [RCT]

5. DRESSINGS

Preamble: There is a plethora of choices for topical treatment of pressure ulcers. Many dressings now combine wound bed preparation, i.e., debridement and/or antimicrobial activity, with moisture control. Guidelines assist the clinician in making decisions regarding the value and best use of these advanced wound care products.

Guideline #5.1: Use a dressing that will maintain a moist wound-healing environment. (Level I)

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

Evidence:

  • 1
    Breuing K, Eriksson E, Liu P, Miller DR. Healing of partial thickness porcine skin wounds in a liquid environment. J Surg Res 1992; 52: 50–8. [EXP]
  • 2
    Gorse GJ, Messner RL. Improved pressure sore healing with hydrocolloid dressings. Arch Dermatol 1987; 123: 766–71. [RCT]
  • 3
    Svensjo T, Pomahac B, Yao F, Slama J, Eriksson E. Accelerated healing of full-thickness skin wounds in a wet environment. Plast Reconstr Surg 2000; 106: 602–12. [EXP]
  • 4
    Thomas DR, Goode PS, LaMaster K, Tennyson T. Acemannan hydrogel dressing versus saline dressing for pressure ulcers. A randomized, controlled trial. Adv Wound Care 1998 Oct; 11(6): 273–6. [RCT]
  • 5
    Vranckx JJ, Slama J, Preuss S, et al. Wet wound healing. Plast Reconstr Surg 2002; 110: 1680–7. [CLIN S]
  • 6
    Winter GD, Scales, JT. Effect of air drying and dressings on the surface of a wound. Nature 1963; 197: 91. [EXP]
  • 7
    Ovington, LG. Hanging wet-to-dry dressings out to dry. Home Healthcare Nurse 2001; 19: 477–84. [LIT REV]
  • 8
    Kerstein, MD, Gemmen, E, van Rijswijk, L, Lyder, CH, Golden, K, Harrington, C. Cost and cost effectiveness of venous and pressure ulcer protocols of care. Dis Manage Health Outcomes 2001; 9: 651–6. [COST ANAL]

Guideline #5.2: Use clinical judgment to select a moist wound dressing. (Level I)

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.

Evidence:

  • 1
    Alm A, Hornmark AM, Fall PA, et al. Care of pressure sores: a controlled study of the use of a hydrocolloid dressing compared with wet saline gauze compresses. Acta Derm Venereol (Stockholm) 1989; 149 (Suppl.): 1–10. [RCT]
  • 2
    Blair SD, Jarvis P, Salmon M, McCollum C. Clinical trial of calcium alginate haemostatic swabs. Br J Surg 1990; 77: 568–70. [RCT]
  • 3
    Bouza C, Saz Z, Munoz A, Amate JM. Efficacy of advanced dressings in the treatment of pressure ulcers: a systematic review 2005; 14: 193–9. [STAT]
  • 4
    Bradley M, Cullum N, Nelson EA, et al. Systematic reviews of wound care management: (2) dressings and topical agents used in the healing of chronic wounds. Health Technol Assess 1999; 3: 1–35. [STAT]
  • 5
    Colwell JC, Foreman MD, Trotter JP. A comparison of the efficacy and cost-effectiveness of two methods of managing pressure ulcers. Decubitus 1993; 6: 28–36. [RCT]
  • 6
    Geronemus RG, Robins P. The effect of two new dressings on epidermal wound healing. J Derm Surg Oncol 1982; 8: 850–2. [EXP]
  • 7
    Graumlich JF, Blough LS, McLaughlin RG, Milbrandt JC, Calderon CL, Agha SA, Scheibel LW. Healing pressure ulcers with collagen or hydrocolloid: a randomized, controlled trial. J Am Geriatr Soc 2003 Feb; 51(2): 147–54. [RCT]
  • 8
    Kim YC, Shin JC, Park CI, et al. Efficacy of hydrocolloid occlusive dressing technique in decubitus ulcer treatment: a comparative study. Yonsei Med J 1996; 37: 181–5. [RCT]
  • 9
    Mulder G, Altman M, Seeley J, et al. Prospective randomized study of the efficacy of hydrogel, hydrocolloid, and saline moistened dressings on the management of pressure ulcers. Wound Rep Reg 1993; 1: 213–8. [RCT]
  • 10
    Neill K, Conforti C, Kedas A, et al. Pressure sore response to a new hydrocolloid. Wounds 1989; 1(3): 173–85. [RCT]
  • 11
    Sayag J, Meaume S, Bohbot S. Healing properties of calcium alginate dressings. J Wound Care 1996; 5: 357–62. [RCT]
  • 12
    Thomas DR, Goode PS, LaMaster K, Tennyson T. Acemannan hydrogel dressing versus saline dressing for pressure ulcers. A randomized, controlled trial. Adv Wound Care 1998; 11: 273–6. [RCT]
  • 13
    Xakellis GC, Chrischilles EA. Hydrocolloid versus saline-gauze dressings in treating pressure ulcers: a cost-effectiveness analysis. Arch Phys Med Rehabil 1992; 73: 463–9. [RCT]

Guideline #5.3: Select a dressing that will manage the wound exudate and protect the peri-ulcer skin. (Level I)

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

Evidence:

  • 1
    Bucalo B, Eaglstein WH, Falanga V. Inhibition of cell proliferation by chronic wound fluid. Wound Rep Reg 1993; 1: 181–6. [EXP]
  • 2
    Chapuis A, Dollfus P. The use of a calcium alginate dressing in the management of decubitus ulcers in patients with spinal cord lesions. Paraplegia 1990; 28: 269–71. [CLIN S]
  • 3
    Ladwig GP, Robson MC, Liu R, Kuhn MA, Muir DF, Schultz GS. Ratios of activated matrix metalloproteinase-9 to tissue inhibitor of matrix metalloproteinase-1 in wound fluids are inversely correlated with healing of pressure ulcers. Wound Rep Reg 2002; 10: 26–37. [CLIN S]
  • 4
    Maume S, Van De Looverbosch D, Heyman H, Romanelli M, Ciangherotti A, Charpin S. A study to compare a new self-adherent soft silicone dressing with a self-adherent polymer dressing in stage II pressure ulcers. Ostomy Wound Manage 2003; 49: 44–51. [RCT]
  • 5
    Sayag J, Meaume S, Bohbot S. Healing properties of calcium alginate dressings. J Wound Care 1996; 5: 357–62. [RCT]
  • 6
    Trengrove NJ, Stacey MC, MacAuley S, Bennett N, Gibson J, Burslem F, Murphy G, Schultz G. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Rep Reg 1999; 7: 442–52. [EXP]
  • 7
    Xakellis GC, Chrischilles EA. Hydrocolloid versus saline gauze dressings in treating pressure ulcers: a cost-effectiveness analysis. Arch Phys Med Rehabil 1992; 73: 463–9. [RCT]
  • 8
    Yager DR, Zhang LY, Liang HX, Diegelmann RF, Cohen IK. Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J Invest Derm 1996; 107(5): 743–8. [EXP]

Guideline #5.4: Select a dressing that remains in place and minimizes shear, friction, skin irritation, and additional pressure. (Level II)

Principles: 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.

Evidence:

  • 1
    Day A, Dombranski S, Farkas C, et al. Managing sacral pressure ulcers with hydrocolloid dressings: results of a controlled clinical study. Ostomy Wound Manage 1995; 41: 52–65. [RCT]
  • 2
    Dobrzanski S, Kelly CM, Gray JI, et al. Granuflex dressings in treatment of full thickness pressure sores. Prof Nurse 1990; 5: 594–9. [RCT]
  • 3
    Sasseville D, Tennstedt D, Lachapelle JM. Allergic contact dermatitis from hydrocolloid dressings. Am J Contact Dermat 1997; 8: 236–8. [CLIN S]
  • 4
    Gallenkemper G, Rabe E, Bauer R. Contact sensitization in chronic venous insufficiency: modern wound dressings. Contac Dermatitis 1998; 38: 274–8. [CLIN S]

Guideline #5.5: Select a dressing that is cost effective. (Level I)

Principles: 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, ease of use and healing rate, as well as the unit cost of the dressing.

Evidence:

  • 1
    Bolton LL, van Rijswijk L, Shaffer FA. Quality wound care equals cost-effective wound care: a clinical model. Adv Wound Care 1997; 10: 33–8. [LIT REV]
  • 2
    Chang KW, Alsagoff S, Ong KT, SIm PH. Pressure ulcers randomized controlled trial comparing hydrocolloid and saline gauze dressings. Med J Malaysia 1998; 53: 428–31. [RCT]
  • 3
    Kim YC, Shin JC, Park CI, et al. Efficacy of hydrocolloid occlusive dressing technique in decubitus ulcer treatment: a comparative study. Yonsei Med J 1996; 37: 181–5. [RCT]
  • 4
    Severn MD. Pressure ulcer management in home health care: efficacy and cost-effectiveness of moisture vapor permeable dressing. Arch Phys Med Rehabil 1986; 67: 726–9. [RCT]
  • 5
    Xakellis GC, Chrischilles EA. Hydrocolloid versus saline gauze dressings in treating pressure ulcers: a cost-effectiveness analysis. Arch Phys med Rehabil 1992; 73: 463–9. [RCT]
  • 6
    Ovington LG. Hanging wet-to-dry dressings out to dry. Home Healthcare Nurse 2001; 19: 477–84. [LIT REV]
  • 7
    Kerstein MD, Gemmen E, van Rijswijk L, Lyder CH, Golden K, Harrington C. Cost and cost effectiveness of venous and pressure ulcer protocols of care. Dis Manage Health Outcomes 2001; 9: 631–6. [COST ANAL]

6. SURGERY

Preamble: Surgical treatment of pressure sores is a final invasive choice for wounds refractory to less aggressive care or for use when rapid closure is indicated. Peri-operative morbidity and greater risk of complications are inherent to the use of surgical options. Surgical procedures can be divided into those that prepare the patient for successful healing, and those that provide definitive closure. Reports of randomized clinical trials for operative treatment of pressure ulcers are almost nonexistent in the literature. However, given the magnitude of these treatment options, guidelines are mandatory to address their appropriate use.

Guideline #6.1: Irregular wound extensions, forming sinuses or cavities, must be explored and unroofed and treated. (Level III)

Principle: Tissue not exposed to treatment agents or devices cannot be expected to respond to the regimen and proceed to healing.

Evidence:

  • 1
    Jones, NF, Wexler, MR. Delineation of the pressure sore burns using methylene blue and hydrogen peroxide. Plast Reconstr Surg 1981; 68: 798–9. [TECH]

Guideline #6.2: Necrotic tissue must be debrided. (Level I) See Guideline #4.4 in Wound Bed Preparation.

Principle: Nonviable tissue is detrimental to wound healing. Therefore, it should be debrided to allow the wound to proceed to closure. (See Wound Bed Preparation.)

Evidence:

  • 1
    Bradley M, Cullum N, Sheldon T. The debridement of chronic wounds: a systematic review. Health Technol Assess 1999; 3: 1–78. [STAT]

Guideline #6.3: Infected tissue must be treated by topical antimicrobials, systemic antibiotics, or surgical debridement. (Level I)

(See Guidelines #3.2 and #3.4 in Infection.)

Principle: 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/gm tissue) and with no β-hemolytic streptococcus will proceed to closure.

Evidence: See Guidelines #3.2, #3.3, #3.4, #3.5, #3.6, and #3.7 in Infection.

Guideline #6.4: Underlying bony prominence and fibrotic bursa cavities should be removed. (Level II)

Principle: Soft tissue compression between the skeleton and support surfaces leads to pressure necrosis. Removal of prominences, without excessive excision, alleviates pressure points.

Evidence:

  • 1
    Blocksma R, Kostrubala JG, Greeley PW. The surgical repair of decubitus ulcers. Plast Reconstr Surg 1947; 2: 403. [CLIN S]
  • 2
    Blocksma R, Kostrubala JG, Greeley PW. The surgical repair of decubitis ulcers in paraplegics: further observations. Plast Reconstr Surg 1949; 4: 123. [CLIN S]
  • 3
    Phillips LG, Robson MC. Pathobiology and treatment of pressure ulcerations. In: Jurkiewicz MJ, editor. Plastic Surgery Principles and Practice. St. Louis: Mosby, 1990; 1223. [LIT REV]
  • 4
    Vasconez LO, Schenider WJ, Jurkiewicz MJ. Pressure sores. Curr Probl Surg 1977; 14: 1–62. [LIT REV]
  • 5
    Consortium for Spinal Cord Medicine. Pressure Ulcer Prevention and Treatment Guideline for Healthcare Professionals. Paralyzed Veterans of America, 2000. [STAT]

Guideline #6.5: Bone excision must not be excessive. (Level III)

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.

Evidence:

  • 1
    Arregui J, Cannon B, Murray JE, et al. Long-term evaluation of ischiectomy in the treatment of pressure ulcers. 1965; 36: 583–90. [RETRO S]
  • 2
    Blocksma R, Kostrubala JG, Greeley PW. The surgical repair of decubitus ulcers. Plast Reconstr Surg 1947; 2: 403. [CLIN S]
  • 3
    Blocksma R, Kostrubala JG, Greeley PW. The surgical repair of decubitis ulcers in paraplegics: further observations. Plast Reconstr Surg 1949; 4: 123. [CLIN S]
  • 4
    Phillips LG, Robson MC. Pathobiology and treatment of pressure ulcerations. In: Jurkiewicz, MJ, editor. Plastic Surgery Principles and Practice. St. Louis: Mosby, 1990; 1223. [LIT REV]
  • 5
    Vasconez LO, Schenider WJ, Jurkiewicz MJ. Pressure sores. Curr Probl Surg 1977; 14: 1–62. [LIT REV]
  • 6
    Hackler RH, Zampari, TA. Urethral complications following ischiectomy in spinal cord injury patients: a urethral pressure study. J Urol 1987; 137: 253–5. [CLIN S]

Guideline #6.6: Fecal and urinary diversions are rarely needed to obtain a healed wound. (Level II)

Principle: Unless a fistulous track has developed, urinary or fecal contamination commonly occurs on the surface. Use of a bowel program or catheterization can divert urine and fecal material without the need for additional surgery.

Evidence:

  • 1
    Controller, Department of Medicine and Surgery: Mortality report in spinal cord injury; Reports and Statistics Service, Veterans Administration, Nov. 13, 1958. [STAT]
  • 2
    Conway H, Griffith BH. Plastic surgery for closure of decubitus ulcers in patients with paraplegia; based on experience with 1,000 cases. Am J Surg 1956; 91: 946–75. [CLIN S]
  • 3
    Conway H, et al. The plastic surgical closure of decubitus ulcers in patients with paraplegia. Surg Gynecol Obstet 1947; 85: 321. [CLIN S]
  • 4
    Phillips LG, Robson MC. Pathobiology and treatment of pressure ulcerations. In: Jurkiewicz, MJ, editor. Plastic Surgery Principles and Practice. St. Louis: Mosby, 1990; 1223. [LIT REV]
  • 5
    Vasconez LO, Schenider WJ, Jurkiewicz MJ. Pressure sores. Curr Probl Surg 1977; 14: 1 62. [LIT REV]

Guideline #6.7: Consider radical procedures such as amputation or hemicorporectomy only in the rare and extreme cases. (Level II)

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

Evidence:

  • 1
    Phillips LG, Robson MC. Pathobiology and treatment of pressure ulcerations. In: Jurkiewicz, MJ, editor. Plastic Surgery Principles and Practice. St. Louis: Mosby, 1990; 1223. [LIT REV]
  • 2
    Royer J, Pickrell K, Georgiade N, et al. Total thigh flaps for extensive decubitus ulcers. A 16 year review of 41 total thigh flaps. Plast Reconstr Surg 1969; 54: 109–18. [RETRO S]
  • 3
    Vasconez LO, Schneider WJ, Jurkiewicz MJ. Pressure sores. Curr Prob Surg 1977; 14: 1 62. [LIT REV]
  • 4
    Chan JW, Virgo KS, Johnson FE. Hemipelvectomy for severe decubitus ulcers in patients with previous spinal cord injury. Am J Surg 2003; 185: 69–73. [STAT]

Guideline #6.8: A pressure sore 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 II)

Principle: Wound closure decreases protein loss, fluid loss, the possibility of wound infection, and the later development of malignancy in the wound.

Evidence:

  • 1
    Dumurgier C, Pujol G, Chevalley J, et al. Pressure sore carcinoma: a late but fulminant complication of pressure sores in spinal cord injury patients: case reports. Paraplegia 1991; 29: 390–5. [CLIN S]
  • 2
    Evans GR, Lewis VL, Jr, Manson PN, et al. Hip joint communication with pressure sore: the refractory wound and the role of Girdlestone arthroplasty. Plast Reconstr Surg 1993; 91: 288–94. [CLIN S]
  • 3
    Grotting JC, Bunkis J, Vasconez LO. Pressure sore carcinoma. Ann Plast Surg 1987; 18: 527–32. [CLIN S]
  • 4
    Turba RM, Lewis VL, Green D. Pressure sore anemia: response to erythropoietin. Arch Phys Med Rehabil 1992; 73: 498–500. [CLIN S]
  • 5
    Consortium for Spinal Cord Medicine. Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury: A Clinical Practice Guideline for Healthcare Professionals. Paralyzed Veterans of America, 2000. [STAT]
  • 6
    Bergstrom N, Bennett MA, Carlson CE, et al. Treatment of Pressure Ulcers. Clinical Practice Guideline # 15. Rockville, MD: U.S. Dept. Health and Human Services, Agency for Healthcare Policy and Research, 1994. [STAT]

Guideline #6.9: Composite tissue closure leads to the best chance of sustained wound closure, although recurrence and recidivism are continuing problems. (Level II)

Principle: The most durable wound closure fills the ulcer with bulk and provides padding over the underlying structures with a tension-free closure.

Evidence:

  • 1
    Bruck JC, Buttemeyer R, Grabosch A, et al. More arguments in favor of myocutaneous flaps for the treatment of pelvic pressure sores. Ann Plast Surg 1991; 26: 85–8. [CLIN S]
  • 2
    Conway H, Griffith BH. Plastic surgery for closure of decubitus ulcers in patients with paraplegia; based on experience with 1,000 cases. Am J Surg 1956; 91: 946–75. [RETRO S]
  • 3
    Conway H, et al. The plastic surgical closure of decubitus ulcers in patients with paraplegia. Surg Gynecol Obstet 1947; 85: 321. [CLIN S]
  • 4
    Daniel RK, Faibisoff B. Muscle coverage of pressure points—the roll of myocutaneous flaps. Ann Plast Surg 1982; 8: 446–52. [CLIN S]
  • 5
    Disa JJ, Carlton JM, Goldberg NH. Efficacy of operative cure in pressure sore patients. Plast Reconstr Surg 1992; 89: 272–8. [CLIN S]
  • 6
    Evans GR, Dufresne CR, Manson PN. Surgical correction of pressure ulcers in an urban center: is it efficacious? Adv Wound Care 1994; 7: 40–6. [CLIN S]
  • 7
    Foster RD, Anthony JP, Mathes SJ, et al. Ischial pressure sore coverage: a rationale for flap selection. Br J Plast Surg 1997; 50: 374–9. [CLIN S]
  • 8
    Foster, RD, Anthony, JP, Mathes, SJ, et al. Flap selection as a determinant of success in pressure sore coverage. Arch Surg 1997; 132: 868–73. [CLIN S]
  • 9
    Rogers J, Wilson LF. Preventing recurrent tissue breakdowns after “pressure sore” closures. Plast Reconstr Surg 1975; 56: 419–22. [CLIN S]
  • 10
    Yamamoto Y, Ohura T, Shintomi Y, et al. Superiority of the fasciocutaneous flap in reconstruction of sacral pressure sores. Ann Plast Surg 1993; 30: 116–21. [CLIN S]
  • 11
    Consortium for Spinal Cord Medicine. Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury: A Clinical Practice Guideline for Healthcare Professionals. Paralyzed Veterans of America 2000. [STAT]
  • 12
    Bergstrom N, Bennett MA, Carlson CE, et al. Treatment of Pressure Ulcers. Clinical Practice Guideline #15. Rockville, MD: US Department of Health and Human Services, Agency for Healthcare Policy and Research, 1994. [STAT]

Guideline #6.10: Management to address muscle spasm and fixed contractures must occur preoperatively and continue at least until the wound is completely healed. (Level III)

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 sore formation.

Evidence:

  • 1
    Stal S, Serure A, Donovan W, et al. The perioperative management of the patient with pressure sores. Ann Plast Surg 1983; 11: 347–56. [CLIN S]
  • 2
    Daniel RK, Hall EJ, MacLeod MK. Pressure sores—a reappraisal. Ann Plast Surg 1979; 3: 53–63. [RETRO S]
  • 3
    Conway H, Griffith BH. Plastic surgery for closure of decubitus ulcers in patients with paraplegia; based on experience with 1,000 cases. Am J Surg 1956; 91: 946–75. [RETRO S]
  • 4
    Conway H, et al. The plastic surgical closure of decubitus ulcers in patients with paraplegia. Surg Gynecol Obstet 1947; 85: 321. [CLIN S]
  • 5
    Vasconez LO, Schenider WJ, Jurkiewicz MJ. Pressure sores. Curr Probl Surg 1977; 14: 1–62. [LIT REV]
  • 6
    Haher JN, Haher TR, Devlin VJ, et al. The release of flexion contractures as a prerequisite for the treatment of pressure sores in multiple sclerosis: a report of ten cases. Ann Plast Surg 1983; 11: 246–9. [CLIN S]
  • 7
    Davis, R. Spasticity following spinal cord injury. Clin Orthop Related Res 1975; 112: 66–75. [LIT REV]

7. ADJUVANT AGENTS (TOPICAL, DEVICE, SYSTEMIC)

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.

Topical Agents

Guideline # 7a.1: Consider the use of growth factor therapy for pressure ulcers that are not responsive to initial comprehensive therapy and/or before surgical repair. (Level II)

Principles: Growth factors are required for normal healing, and chronic wounds have shown growth factor deficiencies and imbalances. Achievement of some degree of ulcer closure, even if not complete, increases the ease of surgical closure. However, to date, no growth factor has received approval for pressure ulcer treatment.

Evidence:

  • 1
    Hirshberg J, Coleman J, Marchant B, Rees RS. TGF-beta3 in the treatment of pressure ulcers: a preliminary report. Adv Skin Wound Care 2001; 14(2): 91–5. [RCT]
  • 2
    Robson MC, Maggi SP, Smith PD, Wassermann RJ, Mosiello GC, Hill DP, Cooper DM. Ease of wound closure as an endpoint of treatment efficacy. Wound Rep Reg 1999; 7: 90–6. [RCT]
  • 3
    Kawai K, Suzuki S, Tabata Y, Nishimura Y. Accelerated wound healing through the incorporation of basic fibroblast growth factor-impregnated gelatin microspheres into artificial dermis using a pressure-induced decubitus ulcer model in genetically diabetic mice. Br J Plast Surg 2005 June 9; 58:1115–23. [EXP]
  • 4
    Kallianinen LK, Hirshberg J, Marchant B, Rees RS. Role of platelet-derived growth factor as an adjunct to surgery in the management of pressure ulcers. Plast Reconstr Surg 2000; 106: 1243–8. [RCT]
  • 5
    Ladwig GP, Robson MC, Liu R, Kuhn MA, Muir DF, Schultz GS. Ratios of activated matrix metalloproteinase-9 to tissue inhibitor of matrix metalloproteinase-1 in wound fluids are inversely correlated with healing of pressure ulcers. Wound Rep Reg 2002; 10: 26–37. [CLIN S]
  • 6
    Landi F, Aloe L, Russo A, Cesari M, Onder G, Bonini S, Carbonin PU, Bernabei R. Topical treatment of pressure ulcers with nerve growth factor: a randomized clinical trial. Ann Intern Med 2003 Oct 21; 139(8): 635–41. [RCT]
  • 7
    Mustoe TA, Cutler NR, Allman RM, Goode PS, Deuel TF, Prause JA, Bear M, Serdar CM, Pierce GF. A phase II study to evaluate recombinant platelet-derived growth factor-BB in the treatment of stage 3 and 4 pressure ulcers. Arch Surg 1994; 129: 213–9. [RCT]
  • 8
    Payne WG, Ochs DE, Meltzer DD, Hill DP, Mannari RJ, Robson LE, Robson MC. Long-term outcome study of growth factor-treated pressure ulcers. Am J Surg 2001 Jan; 181(1): 81–6. [RCT]
  • 9
    Pierce GF, Tarpley JE, Allman RM, Goode PS, Serdar CM, Morris B, Mustoe TA, Vande Berg J. Tissue repair processes in healing of chronic pressure ulcers treated with recombinant platelet-derived growth factor BB. Am J Pathol 1994; 145: 1399–410. [RCT]
  • 10
    Rees RS, Robson MC, Smiell JM, Perry BH. Becaplermin gel in the treatment of pressure ulcers: a phase II randomized, double-blind, placebo-controlled study. Wound Rep Reg 1999 May–Jun; 7(3): 141–7. [RCT]
  • 11
    Robson MC, Hill DP, Smith PD, Wang X, Meyer-Siegler K, Ko F, VandeBerg JS, Payne WG, Ochs D, Robson LE. Sequential cytokine therapy for pressure ulcers: clinical and mechanistic response. Ann Surg 2000 Apr; 231(4): 600–11. [RCT]
  • 12
    Brem H, Lyder C. Protocol for the successful treatment of pressure ulcers. Am J Surg 2004 (Suppl. to July 2004); 188: 9S–17S.
Devices

Guideline #7b.1: Consider using negative pressure wound therapy (NPWT) for stage III or IV pressure ulcers that fail to progress in healing with conventional therapy. (Level I)

Principle: NPWT applies negative pressure to the wound removing wound exudates and debris. Current evidence indicates that NPWT may support pressure ulcer healing by increasing wound perfusion and formation of granulation tissue and by reducing bacterial load.

Evidence:

  • 1
    Evans D, Land L. Topical negative pressure for treating chronic wounds. The Cochrane Database of Systematic Reviews 2001, Issue 1. Art. No.: CD001898. DOI: 10.1002/14651858.CD001898. [STAT]
  • 2
    Ford CN, Reinhard ER, Yeh D, Syrek D, De Las Morenas A, Bergman SB, Williams S, Hamori CA. Interim analysis of a prospective, randomized trial of vacuum-assisted closure versus the healthpoint system in the management of pressure ulcers. Ann Plast Surg 2002; 49: 55–61. [RCT]
  • 3
    Joseph E, Hamori CA, Bergman S, Roaf E, Swann NF, Anastasi GW. A prospective, randomized trial of vacuum-assisted closure versus standard therapy of chronic nonhealing wounds. Wounds 2000; 12: 60–7. [RCT]
  • 4
    Morykwas MJ, Argenta LC, Shelton-Brown EI, McGuirt W. Vacuum-assisted closure: a new method for wound control and treatment: animal studies and basic foundation. Ann Plast Surg 1997; 38: 553–62. [EXP]
  • 5
    Wanner MB, Schwarzl F, Strum B, Zaech GA, Pierer G. Vacuum-assisted wound closure for cheaper and more comfortable healing of pressure sores: a prospective study. Scand J Plast Reconst Surg 2003; 37: 28–33. [RCT]

Guideline #7b.2: Electrical stimulation may be useful in the treatment of pressure ulcers that have not healed with conventional therapy. (Level I)

Principle: Improvement in the healing of chronic wounds is reported in response to electrical stimulation. The most effective type of electrical stimulation treatment and specific types of chronic wounds that are most likely to respond to this therapy have not been determined.

Evidence:

  • 1
    Gardner SE, Frantz RA, Schmidt FL. Effect of electrical stimulation on chronic wound healing: a meta-analysis. Wound Rep Reg 1999; 7: 495–503. [STAT]
  • 2
    Kloth LC, Feedar JA. Acceleration of wound healing with high voltage, monophasic, pulsed current. Phys Ther 1988; 68: 503–8. [RCT]
  • 3
    Reger SI, Hyodo A, Negami S, Kambic HE, Sahgal V. Experimental wound healing with electrical stimulation. Artif Organs 1999; 23: 460–2. [EXP]
  • 4
    Wood JM, Evans PE III, Schallreuter KU, Jacobson WE, Sufit R, Newman J, White C, Jacobson M. A multicenter study on the use of pulsed low-intensity direct current for healing chronic stage II and stage III decubitus ulcers. Arch Dermatol 1993; 129: 999–1009. [RCT]
Systemic

Guideline # 7c.1: Hyperbaric oxygen therapy has not been shown to have a statistically significant effect on pressure ulcer healing. Further studies are needed to evaluate the efficacy of hyperbaric oxygen in pressure ulcers. (Level I)

Evidence:

  • 1
    Kranke P, Bennett M, Roeckl-Wiedmann I, Debus S. Hyperbaric oxygen therapy for chronic wounds. The Cochrane Database of Systematic Reviews 2004, Issue 1. Art. No.:CD004123.pub2. DOI:10.1002/14651858.CD004123.pub2. [STAT]
  • 2
    Roeckl-Wiedmann I, Bennett M, Kranke P. Systematic review of hyperbaric oxygen in the management of chronic wounds. Br J Surg 2005; 92: 24–32. [STAT]

Acknowledgment

  1. Top of page
  2. METHODS
  3. RESULTS
  4. Acknowledgment

This work was supported by the Wound Healing Foundation through a grant to the Wound Healing Society.