Stages of Healing

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Exudative or Inflammatory Phase

Immediately after a laceration, fibrin deposits with an influx of platelets, forming a visible clot. The platelets secrete various wound-healing growth factors that activate macrophages and fibroblasts. These growth factors and more then 30 cyto-kines cause an influx of cellular structures. This phase occurs from 0 to 72 hours (Fig. 28-3).

Resorptive Phase

After 24 to 72 hours, the degradation products of fibrin lead to activation of chemotaxis in the resorptive phase. Leukocytes and macrophages migrate into the wound, causing inflammation. The cellular components then begin autolysis and remove injured tissue by a fermentative process. This process creates an effective phagocytosis, a sterilizing defense, and an activation of the immune system.

Proliferative Phase

Between 72 hours and day 7, fibroblasts migrate into the wound, and vascular proliferation occurs. Granulation tissue formation marks the proliferative phase. Epidermal cells begin to grow at the edges of the wound. A delicate balance of cytokine systems leads to new capillary formation to feed and oxygenate the budding granulation tissue. Extracellular matrices form and act as struts to support the new tissue. The primary clots are broken down by naturally developing fibrinolytic compounds (Fig. 28-4).

Regenerative or Remodeling Phase

The remodeling stage is a continuation of the proliferative phase, with ongoing maturation of collagen. The thickening collagen leads to an increased resistance to shearing and tearing forces. The regenerative phase is characterized by epithelialization and scar formation. This last phase may take up to 1 year. Collagen type III is converted into the mature type I collagen (Fig. 28-5). The extracellular matrix and cells within the wound are regulated by cytokines and integrins (transmembrane cell receptors)

Keloids are fibrous elevated scars that extend outside wound margins. Keloids are unlikely to regress, are likely to recur if excised, and are most likely to occur in patients with darker skin (relative risk [RR] 15-20). Keloids are frequently located over the midline chest, cheeks, and ear-lobes, and peak incidence is age 10 to 20 years. Wounds that heal by secondary intention and burn wounds are high risks for developing keloids. Keloids may be painful as well as cosmetically unacceptable (Juckett and Hartman-Adams, 2009) (Fig. 28-7).

INFLAMMATORY PHASE (DAY 3)

Coerper Diabcomp 2009 Wound Healing

Dermis

Fibroblas^TGF-ß1

Fibroblast

Figure 28-3 Cutaneous wound 3 days after injury. The cells and growth factors necessary to facilitate cell migration into the wound are shown. FGF, Fibroblast growth factor; IGF, insulin-like growth factor; KGF, keratinocyte growth factor; PDGF, platelet-derived growth factor; TGF, transforming growth factor; VEGF, vascular endothelial growth factor.

(From Singer AJ, Clark RAF: Mechanisms of disease: cutaneous wound healing. N Engl J Med i999;34i:738; and Ethridge RT, Leong M, Phillips LG. Wound healing. In Townsend CM, Beauchamp RD, Evers BM, Mattox KL [eds]. Sabiston Textbook of Surgery, i8th ed. Saunders-Elsevier, Philadelphia, 2008.)

Dermis

Fibroblas^TGF-ß1

Fibroblast

Figure 28-3 Cutaneous wound 3 days after injury. The cells and growth factors necessary to facilitate cell migration into the wound are shown. FGF, Fibroblast growth factor; IGF, insulin-like growth factor; KGF, keratinocyte growth factor; PDGF, platelet-derived growth factor; TGF, transforming growth factor; VEGF, vascular endothelial growth factor.

(From Singer AJ, Clark RAF: Mechanisms of disease: cutaneous wound healing. N Engl J Med i999;34i:738; and Ethridge RT, Leong M, Phillips LG. Wound healing. In Townsend CM, Beauchamp RD, Evers BM, Mattox KL [eds]. Sabiston Textbook of Surgery, i8th ed. Saunders-Elsevier, Philadelphia, 2008.)

REEPITHELIALIZATION AND NEOVASCULARIZATION (DAY 5)

Burn Wounds Healing

Figure 28-4 Cutaneous wound 5 days after injury. Blood vessels are seen sprouting into the fibrin clot as epidermal cells resurface the wound. Some of the proteinases involved in cell movement at this point are shown. MMP-1, 2, 3, and 13, matrix metalloproteinases 1, 2, 3, and 13 (collagenase 1, gelatinase A, stromelysin 1, and collagenase 3, respectively); t-PA, tissue plasminogen activator; u-PA, urokinase-type plasminogen activator.

(Modified from Singer AJ, Clark RAF. Mechanisms of disease: cutaneous wound healing. N Engl J Med i999;34i:738; and Ethridge RT, Leong M, Phillips LG. Wound healing. in Townsend CM, Beauchamp RD, Evers BM, Mattox KL [eds]. Sabiston Textbook of Surgery, i8th ed. Saunders-Elsevier, Philadelphia, 2008.)

Platelets

• Growth factors, PDGF, TGF-b bFGF, KGF, EGF, IGF

Macrophage

Epithelial cells

Phagocytosis, antimicrobial function

Epithelial cells

• Oxygen radicals H2O2 O2 -OH

Prostaglandins Collagenase

• Oxygen radicals H2O2 O2 -OH

Neutrophils

• Phagocytosis

• Enzymes collagenase, elastase

• Enzymes collagenase, elastase

• Prostaglandins PGE

Growth factors PDGF, TGF-ß, EGF, IGF Cytokines TNF-a, IL-1, IL-6 Fibronectin

T cells

• Phagocytosis

• Antimicrobial function

H2o2 Macrophage

Figure 28-5 Interaction of cellular and humoral factors in wound healing. Note the key role of the macrophage. bFGF, Basic fibroblast growth factor; EGF, epidermal growth factor; GAGs, glycosaminoglycans; H2O2, hydrogen peroxide; iFN-y, interferon gamma; iGF, insulin-like growth factor; iL, interleukin; KGF, kerati-nocyte growth factor; O2- superoxide; PDGF, platelet-derived growth factor; PGE2, prostaglandin E2; TGF, transforming growth factor; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor.

(Modified from Witte MB, Barbul A. General principles of wound healing. Surg Clin North Am i997;77:5i3; and Ethridge RT, Leong M, Phillips LG. Wound Healing. in Townsend CM, Beauchamp RD, Evers BM, Mattox KL [eds]. Sabiston Textbook of Surgery, i8th ed. Saunders-Elsevier, Philadelphia, 2008.)

Figure 28-5 Interaction of cellular and humoral factors in wound healing. Note the key role of the macrophage. bFGF, Basic fibroblast growth factor; EGF, epidermal growth factor; GAGs, glycosaminoglycans; H2O2, hydrogen peroxide; iFN-y, interferon gamma; iGF, insulin-like growth factor; iL, interleukin; KGF, kerati-nocyte growth factor; O2- superoxide; PDGF, platelet-derived growth factor; PGE2, prostaglandin E2; TGF, transforming growth factor; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor.

(Modified from Witte MB, Barbul A. General principles of wound healing. Surg Clin North Am i997;77:5i3; and Ethridge RT, Leong M, Phillips LG. Wound Healing. in Townsend CM, Beauchamp RD, Evers BM, Mattox KL [eds]. Sabiston Textbook of Surgery, i8th ed. Saunders-Elsevier, Philadelphia, 2008.)

t 400 H

9 10 11

Weeks after wounding

Figure 28-6 Rate of wound healing. Based on the rate of maximum collagen strength, limitation of strenuous activity after 6 weeks of wound healing is not indicated.

(From Lawrence WT, Bevin AG, Sheldon GF. Acute wound care. In Emergency Care. Chicago, Scientific American, American College of Surgeons, 1998; and Chavez MC, Maker VK. Office surgery. In Rakel RE. Textbook of Family Medicine, 7th ed. Saunders-Elsevier, Philadelphia, 2007.)

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