Wound & Healing

By Assistant Professor Dr Hiwa Omer Ahmed 1/10/2005

Classification of Wounds

Incised wound


Abrasion, scratch


•Tidy wound


•Untidy wound

Surgical classification


•Clean contamina ted

•contamin ated


Wound healing
• • • Primary intension Secondary intension Tertiary intension tsg psg ssg


1.Coa gu lat io n
• Coagula tio n Injury causes hemorrhage from damaged vessels and lymphatics (Fig. 85). Vasoconstriction occurs almost immediately as a result of release of catecholamines. Various other vasoactive compounds, such as bradykinin, serotonin, and histamine, are released from tissue mast cells


Healing Continue
The inflammatory phase is characterized by the sequential migration of leukocytes into the wound (Fig. 8-6). Within 24 h the wound is predominated by polymorphonuclear leukocytes, and then by macrophages. Although it is well known that inflammatory cells regulate connective tissue matrix repair, the specific messengers of regulation are now defined. These are the various cytokines that in the past were termed“ growth factors.”





Fib ropla sia After 5 to 7days
• It is during the phase of fibroplasia that the healing events most important to the surgeon occur. In particular, the fibrous protein collagen is synthesized. It is not only the synthesis but also the cross-linking and deposition of collagen and other matrix proteins that provide the healed wound with strength and integrity (Fig. 8-7). Within 10 h after injury, there is evidence of increased wound collagen synthesis. After 5 to 7days,


matrix deposition

• Connective tissue is the process whereby fibroblasts are recruited to the site of injury and produce a new connective tissue matrix. This process is of major importance in primary wound closure, be it of skin, tendon, or intestine at an anastomosis.

Rem od eli ng
• Remo delin g The wound is an “up-regulated” process until “remodeling.” At that point, acute and chronic inflammatory cells diminish gradually, angiogenesis ceases, and fibroplasia ends. The equilibrium between collagen synthesis and collagen degradation is gradually restored


• Cytokines are really “wound hormones” (Fig. 8-10). They may beendocrine, like somatomedin or insulinlike growth factor (IGF-1), whenthey are secreted by one cell and then circulate in the bloodstream to reach a distant target cell. Others are paracrine, produced by one cell andaffecting an adjacent target cell; examples include transforming growthfactor beta (TGF- b) and platelet-derived growth factor (PDGF). Autocrinefactors are secreted by a cell and then act on receptors on the same cell.

Other factors
• Basic FGF (bFGF) is a potent angiogenic factor, causes increased epithelial cell migration, and hastens wound contraction.

Epithelial growth factor (EGF) stimulates epithelial migration and mitosis.

Contractio n

• Contraction is the mechanism whereby there is spontaneous closure of full-thickness skin wounds or constriction of tubular organs such as the common bile duct or esophagus after injury

Contaction continue
• Epithelialization All surfaces exposed to the external environment are covered by epithelial cells. Skin is an example of epithelialization, but mechanisms of epithelial repair are similar throughout the body. The outer layer of skin, the epidermis, is composed of a stratified squamous epithelium that protects the body from fluid loss, bacterial invasion, electromagnetic radiation, and general trauma. Normally the epidermal thickness is maintained at a constant level. Cells in the basal layer of the epidermis divide and migrate superficially and mature in the process.


Conclusion of healing

• Nutrition • The precise caloric requirements for optimal wound healing have not been defined. Large injuries such as burns greatly increase metabolic rate, whereas smaller injuries such as isolated fractures do not increase nutritional requirements. Protein depletion impairs wound healing if recent weight loss exceeds 15% to 25% of body weight. The risk of wound dehiscence is increased in hypoalbuminemic patients

• Vitamin C (ascorbic acid) deficiency causes scurvy. In patients with this deficiency, wound healing is arrested during fibroplasia.

• Vitamin A (retinoic acid) requirements increase during injury. Severely injured patients require supplemental vitamin A to maintain normal serum levels. Vitamin A also partially reverses the impaired healing in chronically steroid-treated patients.

• Vitamin B 6 (pyridoxine) deficiency impairs collagen cross-linking. Vitamin B 1 (thiamine) and vitamin B 2 (riboflavin) deficiencies cause syndromes associated with poor wound repair.

• Deficiencies of trace metals such as zinc and copper have been implicated in poor wound repair, since these divalent cations are cofactors in many important enzymatic reactions. Zinc deficiency is associated with poor epithelialization and chronic, nonhealing wounds.

• Oxygen, Anemia, and Perfusion • Wounds require adequate oxygen delivery to heal well. Oxygen is required for successful inflammation, angiogenesis, epithelialization, and matrix deposition. Ischemic wounds heal poorly and have a much greater risk of infection

Diabetes Mellitus and Obesity
• Wound healing is impaired in diabetic patients by unknown mechanisms. Healing is enhanced if glucose levels are well controlled. The high incidence of chronic cutaneous wounds in these patients often relates to the combination of neuropathy, vasculopathy, impaired host defense against infection, and metabolic disorders. Obesity interferes with repair independently of diabetes. Obese patients with diabetes have impaired wound healing regardless of the degree of glucose control and insulin therapy. Poor wound perfusion and necrotic adipose debris probably impair healing in both diabetic and nondiabetic obese patients.

Corticosteroids, Chemotherapy, and Radiation Therapy
• • •

Corticosteroids, Chemotherapy, and Radiation Therapy Use of pharmacologic steroids impairs healing, especially when given in the first 3 days after wounding. Steroids reduce wound inflammation, epithelialization, and collagen synthesis. Both radiation and chemotherapeutic agents have their greatest effects on dividing cells. The division of endothelial cells, fibroblasts, and keratinocytes is impaired in irradiated tissue, which slows wound healing. Irradiated tissue usually has some degree of residual endothelial cell injury and endarteritis, which causes atrophy, fibrosis, and poor tissue repair. Chemotherapeutic agents are not administered until at least 5 to 7 days postoperatively to prevent impairment of the initial healing events.


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