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Basic principles of wound healing

Authors
David G Armstrong, DPM, MD, PhD
Andrew J Meyr, DPM
Section Editors
Russell S Berman, MD
John F Eidt, MD
Joseph L Mills, Sr, MD
Deputy Editor
Kathryn A Collins, MD, PhD, FACS

INTRODUCTION

A wound is a disruption of the normal structure and function of the skin and underlying soft tissue [1]. Wounds may be caused by a variety of mechanisms, including acute traumatic injury to the skin (abrasion, puncture, crush, burns, gunshot, animal bite, surgery) and other etiologies that cause initially intact skin to break down. Any mechanism that decreases blood flow in the skin for a prolonged period of time has the potential to cause ischemic breakdown of the skin. Skin perfusion may be impaired due to proximal arterial obstruction (eg, peripheral artery disease), vascular compression (eg, hematoma, immobility causing focal pressure), or microvascular occlusion or thrombosis (eg, vasculitis, cholesterol crystals).

Wound classification and the basic principles of wound healing are reviewed here. The factors responsible for impaired wound healing and wound complications, as well as the clinical assessment and management of wounds, are reviewed elsewhere. (See "Risk factors for impaired wound healing and wound complications" and "Clinical assessment of wounds" and "Basic principles of wound management".)

WOUND ETIOLOGY AND CLASSIFICATION

Wounds may arise through traumatic injury (including surgery) or from the breakdown of previously intact skin and are generally classified as acute or chronic.

Acute wounds — Acute wounds usually have an easily identifiable mechanism of injury with skin integrity disrupted, typically due to some form of trauma. Acute traumatic skin disruption can result from blunt or penetrating mechanisms with an array of wound sizes, depths, and locations. Simple or complicated lacerations, burns, or significant tissue defects may result, each requiring individualized management and care. (See "Basic principles of wound management", section on 'Acute wounds'.)

Surgical wounds are a controlled form of acute wound that is created in the operating room environment. Surgical wounds are classified according to the degree of bacterial load or contamination of the surgical wound and are used to predict the risk of surgical wound infection that can impact wound healing. The four categories are clean, clean-contaminated, contaminated, and dirty. The majority of clean and clean-contaminated wounds are closed primarily at the completion of the surgery; contaminated and dirty wounds as well as surgical wounds requiring removal of staples or sutures due to postoperative wound infection are left open and require wound care. The classification of surgical wounds is presented in more detail elsewhere. (See "Risk factors for impaired wound healing and wound complications", section on 'Surgical wound classification'.)

          
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Literature review current through: Sep 2017. | This topic last updated: Jun 26, 2017.
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References
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  1. Orr JW, Taylor PT. Wound healing. In: Complications in gynecological surgery: Prevention, recognition, and management, JB Lippincott, Philadelphia p.167.
  2. Sheehan P, Jones P, Giurini JM, et al. Percent change in wound area of diabetic foot ulcers over a 4-week period is a robust predictor of complete healing in a 12-week prospective trial. Plast Reconstr Surg 2006; 117:239S.
  3. Diegelmann RF, Evans MC. Wound healing: an overview of acute, fibrotic and delayed healing. Front Biosci 2004; 9:283.
  4. Leibovich SJ, Ross R. The role of the macrophage in wound repair. A study with hydrocortisone and antimacrophage serum. Am J Pathol 1975; 78:71.
  5. Mor-Vaknin N, Punturieri A, Sitwala K, Markovitz DM. Vimentin is secreted by activated macrophages. Nat Cell Biol 2003; 5:59.
  6. Odland G, Ross R. Human wound repair. I. Epidermal regeneration. J Cell Biol 1968; 39:135.
  7. Ross R, Everett NB, Tyler R. Wound healing and collagen formation. VI. The origin of the wound fibroblast studied in parabiosis. J Cell Biol 1970; 44:645.
  8. Darby IA, Hewitson TD. Fibroblast differentiation in wound healing and fibrosis. Int Rev Cytol 2007; 257:143.
  9. Attinger CE, Steinberg JS, Meyr AJ. Debridement of the Diabetic Foot Wound. In: Clinical Care of the Diabetic Foot, Second Edition, Armstrong DG, Lavery LA. (Eds), American Diabetes Association, Alexandria 2010. p.49.
  10. Doillon CJ, Dunn MG, Bender E, Silver FH. Collagen fiber formation in repair tissue: development of strength and toughness. Coll Relat Res 1985; 5:481.
  11. Howes EL, Harvey SC. The strength of the healing wound in relation to the holding strength of the catgut suture. N Engl J Med 1929 1929; 200:1285.
  12. Haukipuro K. Synthesis of collagen types I and III in reincised wounds in humans. Br J Surg 1991; 78:708.
  13. Dodson MK, Magann EF, Meeks GR. A randomized comparison of secondary closure and secondary intention in patients with superficial wound dehiscence. Obstet Gynecol 1992; 80:321.
  14. Walters MD, Dombroski RA, Davidson SA, et al. Reclosure of disrupted abdominal incisions. Obstet Gynecol 1990; 76:597.