Wound Facts & Prevention

The cost of wound care is high. In the United States alone, spending on wound care and management exceeded approximately $3.3 billion in 1995 and is expected to grow with the increase in the elderly population.2

Unlike acute wounds that typically heal in a matter of days to weeks, the Wound Healing Society has defined chronic wounds as those that "fail to progress through a normal, orderly and timely sequence of repair or wounds that pass through the repair process without restoring anatomic and functional results."2,3 Chronic wounds, such as venous ulcers, are often associated with an underlying condition or complication such as vascular insufficiencies, infection, or malnutrition, and are most commonly seen in elderly individuals.

Figure 1

Wound Classification

Wounds are broadly defined as partial-thickness, full-thickness, or complex, depending on the depth of injury (Fig 1). In partial-thickness wounds, all or a portion of the dermis remains intact. In full-thickness wounds, however, the entire dermis, including sweat glands and hair follicles, is severed or lost. Finally, full-thickness wounds are considered complex when the underlying subcutaneous fat tissue is also damaged or destroyed.

Normal Wound Healing

Wound healing is a complex, multifaceted, and dynamic process.4,5-7 In healthy, uncompromised individuals, most wounds undergo a normal healing process without complication to achieve complete wound closure.2

At both the clinical and cellular levels, wound healing has been traditionally described as having distinct, but chronologically overlapping, components (phases) [Fig 2].5,7
  • Coagulation/hemostasis6,8,9
    • Ruptured vessels induce platelet aggregation, degranulation, and release of cytokines and growth factors from granules, initiating the healing cascade.
  • The inflammatory component (phase)2,5
    • Recruitment of platelets, neutrophils, lymphocytes, macrophages, and epithelial cells to the wound site.
    • Fibrin clot formation.
    • Release of potent chemical mediators (cytokines, growth factors) that ultimately stimulate epithelization, connective tissue contraction, and angiogenesis

Figure 2. The normal healing process: overlapping components of healing (simplified). Following injury, coagulation and the recruitment of complement factors at the wound site stimulate inflammation, cell migration, and proliferation, leading to matrix synthesis/deposition, angiogenesis, and remodeling.9,12

The Normal Healing Process

  • The proliferative component (phase)2,5,7,9,10
    • Formation of granulation tissue (composed of macrophages, fibroblasts, and new vasculature in a loose connective tissue matrix)
    • Fibroblast migration, proliferation, and collagen synthesis (new dermal matrix)
    • Epithelization in which epithelial cells proliferate at the wound edges and are stimulated to migrate over the granulating wound bed
    • Wound contraction by myofibroblasts aids in epithelization
  • The remodeling component (phase)2,5,7
    • Lasts up to 2 years postinjury
    • Wound shrinkage and strengthening are achieved through a delicate balance of collagen deposition and degradation
    • Tensile strength of the scar increases from 30% of the skin’s original strength at 3 weeks to approximately 80% by 6 months

References:
1. Data on file, Organogenesis Inc.
2. Kane DP, Krasner D. Wound healing and wound management. In: Krasner D, Kane D, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 2nd ed. Wayne, Pa: Health Management Publications Inc; 1997:1-4.
3. Lazarus GS, Cooper DM, Knighton DR, et al. Definitions and guidelines for assessment of wounds and evaluation of healing. Wound Rep Reg. 1994;2:165-170.
4. Sabolinski MLAlvarez OAuletta Met al. Cultured skin as a "smart material"for healing wounds: experience in venous ulcers. Biomaterials. 199623. Knighton DRFiegel VD. Growth factors and comprehensive surgical care of diabetic wounds. Curr Opin Gen Surg. 1993:32-39.
5. Waldorf H, Fewkes J. Wound healing. Adv Dermatol. 1995;10:77-96.
6. Martin P. Wound healingÑaiming for perfect skin regeneration. Science. 1997;276:75-81.
7. Clark RAF. Mechanisms of cutaneous wound repair. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine. 4th ed. New York, NY: McGraw-Hill Inc; 1993:473-482.
8. Kerstein MD. The scientific basis of healing. Adv Wound Care. 1997;10:30-36.
9. Witte MB, Barbul A. General principles of wound healing. Surg Clin North Am. 1997;77:509-528.
10. Hunt TK, Zabel DD. Critical care of wounds and wounded patients. In: Ayres SM, Grenvik A, Holbrook PR, et al, eds. Textbook of Critical Care. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1995:1475-1486.