Guidelines to aid healing of acute wounds by decreasing impediments of healing

Abstract

Achieving uniformity in the care rendered to patients with wounds has been a major desire of clinicians, government regulators, and third-party payers.1 One of the goals of the founders of the Wound Healing Society (WHS) in 1991 was to establish guidelines for wound treatment. One of the first tasks of the WHS Board of Directors following the first annual meeting in Galveston, TX, was to appoint a committee to develop treatment guidelines.1 This committee, under the direction of Gerald S. Lazarus, MD, realized that uniform care guidelines could not be developed because there was no uniformity in the definitions of wounds, wound healing, or wound attributes. The committee developed the necessary definitions and after several public hearings, the article "Definitions and guidelines for assessment of wounds and evaluation of healing" was published in 1994.2 That publication defined an acute wound as one that proceeds through an orderly and timely reparative process to establish sustained anatomic and functional integrity, and defined a chronic wound as one that has failed to proceed through an orderly and timely reparative process to produce anatomic and functional integrity or has proceeded through the repair process without establishing a sustained anatomic and functional result.2 Simply stated, wounds may be classified as those that can repair themselves or can be repaired in an orderly and timely process (acute wounds) and those that cannot (chronic wounds). In 2006, the WHS published "Guidelines for the best care of chronic wounds."1 The chronic wounds chosen for treatment guideline development were venous, diabetic, arterial, and pressure ulcers. Because chronic wounds have impaired healing, evidence-based guidelines were developed to maximize healing trajectories and accelerate healing where possible. However, acute wounds are much more numerous than chronic wounds. There are 50,000,000 elective surgical incisions made each year in the United States, and another 50,000,000 traumatic wounds.3 Add to this 1 million burn injuries and the scope of the problem becomes clear. As opposed to the chronic wound, healing in the acute wound is taken for granted.4 It is assumed that if one debrides a wound of nonviable tissue and repairs it in a physiologic manner, the normal phases of wound healing—reaction, regeneration, remodeling—should proceed without difficulty.3,4,5 Acute wounds are expected to heal with a "normal" wound healing trajectory3; hence, accelerating healing has not been the goal in their treatment. Rather, the goal has been to remove detriments or deterrents to normal healing and eliminate the complications that may prevent an orderly and timely reparative process that could convert the acute wound into a chronic wound. A panel was appointed to develop guidelines to "aid healing of acute wounds by decreasing impediments to healing." The panel consisted of general, vascular, plastic, trauma, burn, and cancer surgeons, nurse clinicians, and researchers drawn from academic, governmental, private practice, and industrial settings. These panel members represented most scientific, medical, and nursing societies/associations that have wound care as a major scope of interest. The panel limited the scope of acute wound healing to integument and soft tissue, and did not address bone, cartilage, neural tissue, or internal organs. Robson MC, Barbul A. Guidelines for the best care of chronic wounds. Wound Rep Regen 2006; 14: 647–8. Lazarus GS, Cooper DM, Knighton DR, Margolis DJ, Pecoraro RE, Rodeheaver G, Robson MC. Definitions and guidelines for the assessment of wounds and evaluation of healing. Arch Dermatol 1997; 130: 489–93. Franz MG, Steed DL, Robson MC. Optimizing healing of the acute wound by minimizing complications. Curr Prob Surg 2007; 44: 679–766. Robson MC. Wound infection: a failure of wound healing caused by an imbalance of bacteria. Surg Clin North Am 1997; 77: 637–50. Robson MC. Disturbances in wound healing. Ann Emerg Med 1988; 17: 1274–8. Previous guidelines, meta-analyses, PubMed, MEDLINE, EMBASE, The Cochrane Database of Systematic Reviews, recent review articles of management of acute wounds and their complications were all searched and reviewed for evidence. Guidelines were formulated, the underlying principle(s) enumerated, and evidence references listed and coded. The code abbreviations for the evidence citations are as follows: The approach used for evidence citations was the same as for the chronic wound guidelines. Major differences exist between this approach to evidence citations compared with past approaches to evidence-based guidelines. Most past approaches relied only on publications regarding clinical human studies. Laboratory or animal studies were not cited. The approach used here and in the previously published guidelines for treatment of chronic wounds used well-controlled animal studies that present proof of principle, especially when a clinical series corroborated the laboratory results. Because of these variations, a different system was used to grade the evidence weight supporting a given guideline. The level strength of evidence supporting a guideline is listed as Level I, Level II, or Level III. The guideline criteria for the levels are: Level I: Meta-analysis of multiple RCTs or at least two RCTs support the intervention of the guideline. Another route would be multiple laboratory or animal experiments with at least two clinical series supporting the laboratory results. Level II: Less than Level I, but at least one RCT and at least two significant clinical series or expert opinion papers with literature analysis, RCT, or multiple clinical series. Level III: Suggestive data of proof of principle, but lacking sufficient data such as meta-analysis, RCT, or multiple clinical series. NB: The suggestion in the guideline can be positive or negative at the proposed level (e.g., meta-analysis and two RCTs stating intervention is not an aid for decreasing impediments to healing). Guidelines have been formulated in 11 categories of impediments to acute wound healing reported to lead to significant complications to normal tissue repair. The categories have been separated into five impediments that are local to the wound environment and six that are systemic conditions affecting the healing of acute wounds. These categories are: Local: Wound perfusion Tissue viability Hematoma and/or seroma Infection Mechanical factors Systemic: Immunology Oncology Miscellaneous systemic conditions Thermal injuries External agents Excessive scarring Each of the guidelines underwent a DELPHI consensus among the panel members. Each set was critically evaluated by all panel members. There was a consensus of at least 10 of 11 panel members on each individual guideline. The majority of the guidelines had unanimous concurrence. The resultant draft, "Guidelines to aid healing of acute wounds by decreasing impediments to healing," was then reviewed by the WHS Board of Directors and posted on its website for public review and comment. All comments received by these two review processes were evaluated and modifications were made in the final document. The final document is presented as follows: #1: Guidelines to decrease the impediment to acute wound healing caused by inadequate wound perfusion #2: Guidelines to decrease the impediment to acute wound healing caused by nonviable tissue #3: Guidelines to decrease the impediment to acute wound healing caused by wound hematoma or seroma #4: Guidelines to decrease the impediment to acute wound healing caused by infection or an increased tissue bioburden #5: Guidelines to decrease the impediment to acute wound healing caused by mechanical factors during wound repair #6: Guidelines to decrease the impediment to acute wound healing caused by systemic immune deficiencies #7: Guidelines to decrease the impediment to acute wound healing caused by cancer and its treatment #8: Guidelines to decrease the impediment to acute wound healing caused by systemic conditions such as diabetes mellitus, obesity, malnutrition, etc #9: Guidelines to decrease the impediment to acute wound healing caused by burn injuries #10: Guidelines to decrease the impediment to acute wound healing caused by external agents such as tobacco, drugs, etc. #11: Guidelines to decrease the impediment to acute wound healing caused by excessive scar formation Preamble: Adequate blood supply is a sine qua non to normal wound healing and tissue repair. Inadequate wound perfusion can occur from systemic causes, regional causes, and local causes. Guideline #1.1: Clinically significant arterial disease should be ruled out, preferably before wounding. In the lower extremity, this can be done by establishing that pedal pulses are clearly palpable or that the ankle–brachial index (ABI) is >0.9. An ABI>1.3 suggests noncompressible arteries. In elderly patients or patients with an ABI>1.2, a normal Doppler-derived wave form, a toe–brachial index of >0.7 or a transcutaneous oxygen pressure of >40 mmHg may help to suggest adequate arterial flow. Color duplex ultrasound scanning provides anatomic and physiologic data confirming an ischemic etiology for the leg wound. Level of evidence: I Principle: Ischemia hinders healing and increases the risk of infection. Although clinical history and physical examination can be very suggestive of ischemia, a definitive diagnosis must be established before undertaking a course of treatment. Successful healing requires that arterial insufficiency be addressed. Evidence: Hirsch A, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, Hiratzka LF, Murphy WRC, Olin JW, Puschett JB, Rosenfield KA, Sacks D, Stanley JC, Taylor LM, White CJ, White J, White RA, Antman EM, Smith SC, Adams CD, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B. ACC/AHA Guidelines for the Management of Patients with Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic): A Collaborative Report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society for Vascular Medicine and Biology, and the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease). American College of Cardiology Web Site. Available at: http://www.acc.org/clinical/guidelines/pad/index.pdf. (STAT) Sahli D, Eliasson B, Svensson M, Blohmé G, Eliasson M, Samuelsson P, Ojbrandt K, Eriksson JW. Assessment of toe blood pressure is an effective screening method to identify diabetes patients with lower extremity arterial disease. Angiology 2004; 55: 641–51. (CLIN S) Teodorescu V, Chen C, Morrissey N, Faries PL, Marin ML, Hollier LH. Detailed protocol of ischemia and the use of noninvasive vascular laboratory testing in diabetic foot ulcers. Am J Surg 2004; 187: 75S–80S. (LIT REV) Hirsch A, Criqui M, Treat-Jacobson D, Regensteiner JG, Creager MA, Olin JW, Krook SH, Hunninghake DB, Comerota AJ, Walsh ME, McDermott MM, Hiatt WR. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA 2001; 286: 1317–24. (CLIN S) Ascher E, Hingorani A, Markevich N, Yorkovich W, Schutzer R, Hou A, Jacob T, Nahata S, Kallakuri S. Role of duplex arteriography as the sole preoperative imaging modality prior to lower extremity revascularization surgery in diabetic and renal patients. Ann Vasc Surg 2004; 8: 433–9. (CLIN S) Padberg FT, Back TL, Thompson PN, Hobson RW. Transcutaneous oxygen (TcPO2) estimates probability of healing in the ischemic extremity. J Surg Res 1996; 60: 365–9. (CLIN S) Butler CM, Ham RO, Lafferty K, Cotton LT, Roberts VC. The effect of adjuvant oxygen therapy on transcutaneous pO2 and healing in the below-knee amputee. Prosthet Orthot Int 1987; 11: 10–6. (RCT) Bercelli SA, Chan AK, Pomposelli FB Jr, Gibbons GW, Campbell DR, Akbari CM, Brophy DT, LoGerfo FW. Efficacy of dorsal pedal artery bypass in limb salvage for ischemic heel ulcer. J Vasc Surg 1999; 30: 499–508. (RETRO S) Lopantalo M, Biancari F, Tukiainen E. Never amputate without consultation of a vascular surgeon. Diabetes Metab Res Rev 2000; 16 (Suppl. l): S27–32. (LIT REV) Attinger CE, Ducic I, Neville RF, Abbruzzese MR, Gomes M, Sidawy AN. The relative roles of aggressive wound care versus revascularization in salvage of the threatened lower extremity in the renal failure diabetic patient. Plast Reconstr Surg 2002; 109: 1281–90. (CLIN S) Moosa HH, Makaroun MS, Peitzman AB, Steed DL, Webster MW. TcPO2 values in limb ischemia: effects of blood flow and arterial oxygen tension. J Surg Res 1986; 40: 482–7. (EXP) Guideline #1.2: Hypotension and skin hypoperfusion should be corrected as soon as possible to improve cutaneous wound healing. Level of evidence: I Principle: Skin blood flow is reduced in multiple medical conditions, including shock and hypotension, hypovolemia, cold, connective tissue disease, arterial and venous impairment, advanced age, pain, smoking, diabetes mellitus, and cold. Conversely, warming can increase perfusion. Evidence: Kumar S, Wong PF, Melling AC, Leaper DJ. Effects of perioperative hypothermia and warming in surgical practice. Int Wound J 2005; 2: 193–204. (STAT) Worthley LI. Shock: a review of pathophysiology and management. Part I. Crit Care Resusc 2000; 2: 55–65. (LIT REV) Saucy F, Dischl B, Delachaux A, Feihl F, Liaudet L, Waeber B, Corpataux JM. Foot skin blood flow following infrainguinal revascularization for critical lower limb ischemia. Eur J Vasc Endovasc Surg 2006; 31: 401–6. (CLIN S) Kamler M, Goedeke J, Pizanis N, Milekhin V, Schade FU, Jakob H. In vivo effects of hypothermia on the microcirculation during extracorporeal circulation. Eur J Cardiothorac Surg 2005; 28: 259–65. (EXP) Kanetaka T, Komiyama T, Onozuka A, Miyata T, Shigematsu H. Laser Doppler skin perfusion pressure in the assessment of Raynaud's phenomenon. Eur J Vasc Endovasc Surg 2004; 27: 414–6. (RCT) Kenney WI, Munce TA. Invited review: aging and human temperature regulation. J Appl Physiol 2003; 95: 2598–603. (LIT REV) Weiss M, Milman B, Rosen B, Eisenstein Z, Zimlichman R. Analysis of the diminished skin perfusion in elderly people by laser Doppler flowmetry. Age Ageing 1992; 21: 237–41. (EXP) Black CE, Huang N, Neligan PC, Levine RH, Lipa JE, Lintlop S, Forrest CR, Pang CY. Effect of nicotine on vasoconstrictor and vasodilator responses in human skin vasculature. Am J Physiol Regul Integr Comp Physiol 2001; 281: R1097–104. (EXP) Williams DT, Price P, Harding KG. The influence of diabetes and lower limb arterial disease on cutaneous foot perfusion. J Vasc Surg 2006; 44: 770–5. (RCT) Ngo BT, Hayes KD, DiMiao DJ, Srinivasan SK, Huerter CJ, Rendell MS. Manifestations of cutaneous diabetic microangiopathy. Am J Clin Dermatol 2005; 6: 225–37. (LIT REV) Rendell M, Bamisedun O. Diabetic cutaneous microangiopathy. Am J Med 1992; 93: 611–8. (CLIN S) Schubert V. Hypotension as a risk factor for the development of pressure sores in elderly subjects. Age Ageing 1991; 20: 255–61. (CLIN S) LoGerfo FW, Coffman S. Vascular and microvascular disease in the foot in diabetes: implications for foot care. N Engl J Med 1984; 311: 1615–9. (LIT REV) Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. N Engl J Med 1996; 334: 1209–15. (RCT) Melling AC, Baqar A, Scott EM, Leaper DJ. Effects of preoperative warming on the incidence of wound infection after clean surgery. Lancet 2001; 358: 876–80. (RCT) Guideline #1.3: There are not enough clinical data to recommend hyperbaric oxygen for improving healing of acute wounds. Level of evidence: II Principle: Although increased oxygen delivered at increased pressures could theoretically augment healing, there are insufficient data to support its use in acute wound healing. Evidence: Friedman HI, Fitzmaurice M, Lefaivre JF, Vecchiolla T, Clarke D. An evidence-based appraisal of the use of hyperbaric oxygen on flaps and grafts. Plast Reconstr Surg 2006; 117 (Suppl.): 175S–92S. (STAT) Kaelin CM, Im MJ, Myers RA, Manson PN, Hoopes JE. The effects of hyperbaric oxygen on free flaps in rats. Arch Surg 1990; 125: 607–9. (EXP) Tai YJ, Birely BC, Im MJ, Hoopes JE, Manson PN. The use of hyperbaric oxygen for preservation of free flaps. Ann Plast Surg 1992; 28: 284–7. (EXP) Garcia-Covarrubias L, McSwain NE, Van Meter K, Bell RM. Adjuvant hyperbaric oxygen therapy in the management of crush injury and traumatic ischemia: an evidence-based approach. Am Surg 2005; 71: 144–51. (STAT) Reedy MB, Capen CV, Baker DP, Petersen WG, Kuehl TJ. Hyperbaric oxygen therapy following radical vulvectomy: an adjunctive therapy to improve wound healing. Gynecol Oncol 1994; 53: 13–6. (CLIN S) Sheffield P. Tissue oxygen measurements with respect to soft tissue wound healing with normobaric and hyperbaric oxygen. HBO Rev 1985; 6: 18–46. (LIT REV) Bouachour G, Cronier P, Gouello JP, Toulemonde JL, Talha A, Alquier P. Hyperbaric oxygen therapy in the management of crush injuries: a randomized double-blind placebo-controlled trial. J Trauma 1996; 41: 333–9. (RCT) Preamble: None of the processes of wound healing can occur unless the tissues within the wound are viable. Attempting to close a wound by edge coaptation, with a skin graft, with a pedicled flap, or even allowing it to heal spontaneously, will be unsuccessful when nonviable tissue is present. Removing nonviable tissue is paramount to successful tissue repair. Guideline #2.1: Debridement is required to remove necrotic tissue and excessive bacterial burden. The health care provider can choose from a number of debridement methods, including surgical, enzymatic, mechanical, biological, or autolytic. More than one debridement method may be appropriate. (Sharp surgical debridement is preferred.) If an alternative form of debridement is unsuccessful in removing the nonviable tissue, surgical debridement is mandated. Level of evidence: I Principle: Necrotic tissue, excessive bacterial burden, and foreign debris can all inhibit wound healing. The method of debridement chosen may depend on the of the wound, the of the health care the of the and Evidence: Steed DL, D, Webster Effect of debridement on the healing of diabetic foot ulcers. J Am Surg 1996; (RCT) V. Debridement index and its with of diabetic foot ulcers. Wound Rep Regen 2002; (RCT) versus for Wound 41: (RCT) A, L, J, Black A of and for pressure 2002; 14: (RCT) Steed Am J Surg 2004; (Suppl.): (LIT REV) JE. the burden. Skin Wound Care 2004; 17: (LIT REV) and Wound Care 1997; (LIT REV) D, Campbell K, D, D, D. the wound bacterial and Wound 2000; (LIT REV) J, DR, of of debridement a Wound Care 1999; M, N, The debridement of chronic a 1999; (STAT) The effect of on and in wounds. J Surg Res (EXP) V. Wound and the of a for multiple of the 2002; 14: (LIT REV) DB, in the treatment of and ulcers. J Am (CLIN S) The and of two wound J 2003; 77: (RETRO S) A, E, F, M, F, C, R. surgical approach versus management for diabetic foot a randomized trial. Diabetic Med (RCT) JL, J, B. Diabetic foot a randomized of two wound healing Wound and Wound Care 11 (Suppl. (RCT) ML, Robson MC, bacterial of wound Ann Surg (EXP) MS, M, R, of wound and in bacterial of of a clinical Wound 2007; 53: (RCT) M, Thompson K, A, and pressure in wounds with Int J Surg 2000; 2: (EXP) wound a of 2006; 20: (EXP) of in wound care. Am J Clin Dermatol 2001; 2: (LIT REV) Preamble: Acute wound most are the of or Acute wound or can and acute wound healing. Acute wound can a wound, wound ischemia to pressure be a for wound or increased Wound are to the increased use of and and therapy in surgical patients. Wound are to the increased use of foreign soft tissue such as used in repair. Guideline should be should and for following a surgical such as or should be and before elective as with can be and with to prevent venous are but will increase the risk of and complications. agents may be during surgical Level of evidence: I Principle: including hematoma are increased when a primary or The most for is impaired or reduced factors and impaired or reduced Patients at risk for a such as ischemia, or may be with a that can be during the an is in but will increase the incidence of hematoma and complications. There is no evidence that or therapy increases the risk of acute wound Evidence: CW, Anderson Jr, of venous 2001; (Suppl.): (STAT) D, B, of the of with or weight J Surg 1996; (RCT) P, MS, and mechanical for in surgery. Cochrane Cochrane Database Rev 2007; (STAT) M, K, WG, JG, preoperative risk factors and in from the of J Am Surg 2002; (STAT) DL, K, Abdominal risk factors for infection and J Surg Res 2003; (STAT) R. A of surgical wounds. Arch Surg (STAT) S, of hematoma with after Plast Reconstr Surg 2001; (CLIN S) A, S, S, JP, weight and in after major surgical of J Surg 1997; (STAT) JF, B. risk of in surgery. (LIT REV) JF, B. The risk of in the of in surgery. (RCT) J, Effects of on and vascular complications following a intervention Res 2005; (RCT) J, and for of following treatment. Cochrane Peripheral Vascular Cochrane Database Rev 2007; (STAT) Collaborative of of in venous and by among surgical and medical patients. 1994; (STAT) E, M, B, of cutaneous surgery in patients under treatment. Plast Surg 2002; (RCT) and J 2002; (LIT REV) Brophy D. therapy in a J 1997; (CLIN S) MS, Baker JW, of perioperative by of during Ann Surg 1987; 44: (RCT) Guideline surgical by or the incidence of wound hematoma formation and wound healing. Level of evidence: I Principle: hematoma in a wound should be and with an is an for wound as are anatomic of an in most wound healing, and an anatomic hematoma formation is and is the risk of the hematoma as a Evidence: ML, S. following for the influence of of Am Surg 1994; 60: (CLIN S) versus incisions for surgery. Cochrane Cochrane Database Rev 2007; (STAT) R, S, A, T, M, Effect of on wound healing in Am J Surg 1990; (CLIN S) R. The of wound infection: a of wounds. Surg Clin North Am 60: (STAT) CD, Wound infection after with or J Surg 1990; 77: (RCT) EM, S, clinical of versus in elective J Surg 2001; (RCT) RF, DB, M, Effects of on wound infection. Am J Surg 1991; (CLIN S) The use of and in surgery. J Surg (LIT REV) Rodeheaver Kenney JG, Am J Surg 1984; (LIT REV) G, used to incisions not increase wound infection Am J Surg 1994; (CLIN S) JC, J, tissue in to wound after in Gynecol (RCT) Franz Acute wound the of acute wound Surg Clin North Am 2003; (LIT REV) Guideline wounds with