Guidelines to aid healing of acute wounds by decreasing impediments of healing
2008; Wiley; Volume: 16; Issue: 6 Linguagem: Inglês
10.1111/j.1524-475x.2008.00427.x
ISSN1524-475X
AutoresMichael Franz, Martin C. Robson, David L. Steed, Adrian Barbul, Harold Brem, Diane M. Cooper, David Leaper, Stephen M. Milner, Wyatt G. Payne, Thomas L. Wachtel, Laurel Wiersema‐Bryant,
Tópico(s)Reconstructive Surgery and Microvascular Techniques
ResumoAchieving 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 status of the wound, the capability of the health care provider, the overall condition of the patient, and professional licensing restrictions. Evidence: Steed DL, Donohoe D, Webster MW, Lindsley L. Effect of extensive debridement on the healing of diabetic foot ulcers. J Am Coll Surg 1996; 183: 61–4. (RCT) Saap LJ, Falanga V. Debridement performance index and its correlation with complete closure of diabetic foot ulcers. Wound Rep Regen 2002; 10: 354–9. (RCT) Mulder GD. Cost-effective managed care: gel versus wet-to-dry for debridement. Ostomy Wound Manage 1995; 41: 68–70. (RCT) Alvarez OM, Fernandez-Obregon A, Rogers RS, Bergamo L, Masso J, Black M. A prospective, randomized, comparative study of collagenase and papain-urea for pressure ulcer debridement. Wounds 2002; 14: 293–301. (RCT) Steed DL. Debridement. Am J Surg 2004; 187 (Suppl.): 71S–4S. (LIT REV) Ayello EA, Cuddigan JE. Debridement: controlling the necrotic/cellular burden. Adv Skin Wound Care 2004; 17: 66–75. (LIT REV) Sieggreen MY, Maklebust J. Debridement: choices and challenges. Adv Wound Care 1997; 10: 32–7. (LIT REV) Sibbald RG, Williamson D, Orsted HL, Campbell K, Keast D, Krasner D, Sibbald D. Preparing the wound bed—debridement, bacterial balance, and moisture balance. Ostomy Wound Manage 2000; 46: 14–35. (LIT REV) Mosher BA, Cuddigan J, Thomas DR, Boudreau DM. Outcomes of 4 methods of debridement using a decision analysis methodology. Adv Wound Care 1999; 12: 81–8. (TECH) Bradley M, Cullum N, Sheldon T. The debridement of chronic wounds: a systematic review. Health Technol Assess 1999; 3 (Part 1): (STAT) Alvarez OM, Mertz PM, Eaglstein WH. The effect of occlusive dressings on collagen synthesis and re-epithelialization in superficial wounds. J Surg Res 1983; 35: 142–8. (EXP) 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) Rao DB, Sane PG, Georgiev EL. Collagenase in the treatment of dermal and decubitus ulcers. J Am Geriatr Soc 1975; 23: 22–30. (CLIN S) Capasso VA, Munro BH. The cost and efficacy of two wound treatments. AORN J 2003; 77: 984–1004. (RETRO S) Piaggesi A, Schipani E, Campi F, Romanelli M, Baccetti F, Arvia C, Navalesi R. Conservative surgical approach versus non-surgical management for diabetic neurotrophic foot ulcers: a randomized trial. Diabetic Med 1998; 15: 412–7. (RCT) Jensen JL, Seeley J, Gillin B. Diabetic foot ulcerations. a controlled, randomized comparison of two moist wound healing protocols: Carrasyn Hydrogel Wound dressing and wet-to-moist saline gauze. Adv Wound Care 1998; 11 (Suppl. 7): 1–4. (RCT) Hamer ML, Robson MC, Krizek TJ, Southwick WO. Quantitative bacterial analysis of comparative wound irrigations. Ann Surg 1975; 181: 819–22. (EXP) Granick MS, Tenenhaus M, Knox R, Ulm JP. Comparison of wound irrigation and tangential hydrodissection in bacterial clearance of contaminated wounds: results of a randomized, controlled clinical study. Ostomy Wound Manage 2007; 53: 64–66, 68–70, 72. (RCT) Bhandari M, Thompson K, Adili A, Schaughnessy SG. High and low pressure irrigation in contaminated wounds with exposed bone. Int J Surg Investig 2000; 2: 179–82. (EXP) Draeger RW, Dahners LE. Traumatic wound debridement: a comparison of irrigation Methods 2006; 20: 83–8. (EXP) Mumcuoglu KY. Clinical application of maggots in wound care. Am J Clin Dermatol 2001; 2: 219–27. (LIT REV) Preamble: Acute wound fluid collections most often are the result of bleeding (hematomas), inflammation (seromas), or lymph fluid. Acute wound hematomas or seromas can impair and delay acute wound healing. Acute wound fluid collections can mechanically disrupt a wound, cause wound ischemia due to pressure exceeding capillary perfusion, be a nutrient nidus for wound infection, or cause increased dead space. Wound hematomas are increasingly common due to the increased use of prophylactic and therapeutic anticoagulation and antiplatelet therapy in surgical patients. Wound seromas are increasingly common due to the increased use of foreign material soft tissue implants, such as meshes used in hernia repair. Guideline #3.1: Coagulation should preferentially be normalized preoperatively; correction should continue intraoperatively and for 24 hours following a surgical procedure. Primary coagulopathies such as vitamin K deficiency or hemophilia should be diagnosed and treated before elective operations. Therapeutic anticoagulation, as with warfarin, can be temporarily discontinued and "bridged" with shorter-acting anticoagulants. Prophylactic heparins to prevent venous thromboembolism (VTE) are indicated, but will increase the risk of hematomas and other bleeding complications. Antiplatelet agents may be continued during general surgical procedures. Level of evidence: I Principle: Bleeding complications, including hematoma formation, are significantly increased when a primary or pharmacological coagulopathy exists. The most common mechanism for coagulopathy is impaired or reduced protein-clotting factors and impaired or reduced platelets. Patients at high risk for a hypercoagulable complication such as stroke, myocardial ischemia, or VTE may be "bridged" with a heparin formulation that can be held during the 24-hour period surrounding an operation. Heparin prophylaxis against VTE is indicated in general surgery, but will increase the incidence of hematoma and bleeding complications. There is no evidence that prophylactic or therapeutic antiplatelet therapy increases the risk of acute wound hematomas. Evidence: Geerts WH, Heit JA, Clagett GP, Pineo GF, Colwell CW, Anderson FA Jr, Wheeler HB. Prevention of venous thromboembolism. Chest 2001; 119 (Suppl.): 132S–75S. (STAT) Bergqvist D, Lindgren B, Matzsch T. Comparison of the cost of preventing postoperative deep vein thrombosis with either unfractionated or low molecular weight heparin. Br J Surg 1996; 83: 1548–52. (RCT) Wille-Jorgensen P, Rasmussen MS, Andersen BR, Borly L. Heparins and mechanical methods for thromboprophylaxis in colorectal surgery. Cochrane Colorectal Cancer Group. Cochrane Database Syst Rev 2007; 4. (STAT) Best WR, Khuri SF, Phelan M, Hur K, Henderson WG, Demakis JG, Daley J. Identifying patient preoperative risk factors and postoperative adverse events in administrative databases: results from the Department of Veterans Affairs National Surgical Quality Improvement Program. J Am Coll Surg 2002; 194: 257–66. (STAT) Dunne JR, Malone DL, Tracy K, Napolitano LM. Abdominal wall hernias: risk factors for infection and resource utilization. J Surg Res 2003; 111: 78–84. (STAT) Cruse PJ, Foord R. A five-year prospective study of 23,649 surgical wounds. Arch Surg 1973; 107: 206–10. (STAT) Sharma S, Chang DW, Koutz C. Incidence of hematoma associated with ketorolac after TRAM flap breast reconstruction. Plast Reconstr Surg 2001; 107: 353–5. (CLIN S) Koch A, Bouges S, Ziegler S, Dinkel H, Daures JP, Victor N. Low molecular weight heparin and unfractionated heparin in thrombosis prophylaxis after major surgical intervention: update of previous meta-analyses. Br J Surg 1997; 84: 750–9. (STAT) Ammann JF, Aebi B. Hemorrhage risk of thromboembolism prophylaxis in general surgery. Helv Chir Acta 1983; 50: 7–8. (LIT REV) Ammann JF, Aebi B. The risk of hemorrhaging in the prevention of thromboembolism in general surgery. Chirurg 1983; 54: 29–32. (RCT) Chlan LL, Sabo J, Savik K. Effects of three groin compression methods on patient discomfort, distress, and vascular complications following a percutaneous coronary intervention procedure. Nurs Res 2005; 54: 391–8. (RCT) Dorffler-Melly J, Koopman MMW, Prins MH, Buller HR. Antiplatelet and anticoagulant drugs for prevention of restenosis/reocclusion following peripheral endovascular treatment. Cochrane Peripheral Vascular Diseases Group. Cochrane Database Syst Rev 2007; 4. (STAT) Antiplatelet Trialists' Collaboration. Collaborative overview of randomised trials of antiplatelet therapy-III: reduction in venous thrombosis and pulmonary embolism by antiplatelet prophylaxis among surgical and medical patients. BMJ 1994; 308: 235–46. (STAT) Kargi E, Babuccu O, Hosnuter M, Babuccu B, Altinyazar C. Complications of minor cutaneous surgery in patients under anticoagulant treatment. Aesthetic Plast Surg 2002; 26: 483–5. (RCT) Warkentin TE, Crowther MA. Reversing anticoagulants both old and new. Can J Anaesth 2002; 49: S11–5. (LIT REV) Brophy MT, Flore LD, Deykin D. Low-dose vitamin K therapy in excessively anticoagulated patients: a dose-finding study. J Thromb Thrombolysis 1997; 4: 289–92. (CLIN S) Spotnitz WD, Dalton MS, Baker JW, Nolan SP. Reduction of perioperative hemorrhage by anterior mediastinal spray application of fibrin glue during cardiac operations. Ann Thorac Surg 1987; 44: 529–31. (RCT) Guideline #3.2: Meticulous surgical hemostasis by ligature or electrocautery reduces the incidence of wound hematoma formation and improves wound healing. Level of evidence: I Principle: Surgical hemostasis prevents hematoma formation. Larger bleeding vessels in a wound should be clamped and tied with an absorbable suture. Electrocautery is an option for wound hemostasis, as are topical chemical hemostatic agents. Primary layered anatomic closure of an incision results in most efficient hemostasis, wound healing, and an optimized anatomic result. By achieving complete hemostasis, hematoma formation is minimized and "dead space" is eliminated, reducing the added risk of localized bacteria utilizing the hematoma as a nutrient media. Evidence: Patterson ML, Nathanson SD, Havstad S. Hematomas following excisional breast biopsies for invasive breast carcinoma: the influence of deep suture approximation of breast parenchyma. Am Surg 1994; 60: 845–8. (CLIN S) Brown SR, Goodfellow PB. Transverse versus midline incisions for abdominal surgery. Cochrane Colorectal Cancer Group. Cochrane Database Syst Rev 2007; 4. (STAT) Rappaport WD, Hunter GC, Allen R, Lick S, Halldorsson A, Chvapil T, Holcomb M, Chvapil M. Effect of electrocautery on wound healing in midline laparotomy incisions. Am J Surg 1990; 160: 618–20. (CLIN S) Cruse PJ, Foord R. The epidemiology of wound infection: a 10-year prospective study of 62,939 wounds. Surg Clin North Am 1980; 60: 27–40. (STAT) Johnson CD, Serpell J. Wound infection after abdominal incision with scalpel or diathermy. Br J Surg 1990; 77: 626–7. (RCT) Kearns SR, Connolly EM, McNally S, McNamara DA, Deasy J. Randomized clinical trial of diathermy versus scalpel incision in elective midline laparotomy. Br J Surg 2001; 88: 41–4. (RCT) Kumagai SG, Rosales RF, Hunter GC, Rappaport WD, Witzke DB, Chvapil TA, Chvapil M, Sutherland JC. Effects of electrocautery on midline laparotomy wound infection. Am J Surg 1991; 162: 620–3. (CLIN S) Lawrenson KB, Stephens FO. The use of electro-cutting and electro-coagulation in surgery. Austral NZ J Surg 1970; 39: 417–21. (LIT REV) Keenan KM, Rodeheaver GT, Kenney JG, Edlich RF. Surgical cautery revisited. Am J Surg 1984; 147: 818–21. (LIT REV) Groot G, Chappell EW. Electrocautery used to create incisions does not increase wound infection rates. Am J Surg 1994; 167: 601–3. (CLIN S) Naumann RW, Hauth JC, Owen J, Hodgkins PM, Lincoln T. Subcutaneous tissue approximation in relation to wound disruption after cesarean delivery in obese women. Obstet Gynecol 1995; 85: 412–6. (RCT) Dubay DA, Franz MG. Acute wound healing: the biology of acute wound failure. Surg Clin North Am 2003; 83: 463–81. (LIT REV) Guideline #3.3: Primarily closed, large surface area wounds with sk
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