WOUND HEALING
Phases of wound healingWound healing occurs in 3 phases Inflammatory phase Proliferative phase Remodeling phase
I. Inflammatory phase
Immediate to 2-5 daysHemostasisVasoconstriction – damaged blood vessels constrictPlatelet aggregation – primary hemostasisCoagulation – fibrin – secondary hemostasis (clot – platelets + fibrin)InflammationVasodilationPhagocytosisII. Proliferative phase
2 days to 3 weeks Granulation Fibroblasts lay a bed of collagen to fill the defect Angiogenesis Contraction Wound edges pull together to reduce the defect Epithelialization Epithelial cells migrate across the new tissue to form a barrier between the wound and the environmentIII. Remodeling phase
3 weeks to 2 years New collagen forms which increases the tensile strength of the wound Strength increases and becomes maximum but not as strong as original tissue Scar tissue is only 80% of the strength of the original tissueWound healing
Wound healing is accomplished in one of the following two ways: Healing by first intention (primary union) Healing by second intention (secondary union) Healing of skin wounds is a classical exampleHealing by first intention (primary union)
Occurs in clean, incised wounds with good apposition of the edges – particularly planned surgical incisions(clean wounds – no infections or foreign bodies)The incision causes only focal disruption of epithelial basement membrane continuity and death of a relatively few epithelial and connective tissue cells.As a result, epithelial regeneration predominates over fibrosisHealing by first intention: Sequence of events
ImmediateThe narrow incisional space rapidly fills with fibrin clotted blood Dehydration at the surface produces a scab to cover and protect the healing repair site
Within 24 hrs
Movement and proliferation of epithelial cells across the wound resulting in a thin, but continuous epithelial layer Early inflammation close to the edges (neutrophils)2-3 days
Neutrophils replaced by macrophages Macrophages remove the blood clot Proliferation of epithelial cells Fibroblastic activity10-14 days
Scab loose (aka dry clot) Epithelial covering complete Fibrous union of edges Wound still weak vascularizationBy the end of the first month
Scar comprises of a cellular connective tissue devoid of inflammatory infiltrate, covered by intact epidermis Dermal appendages destroyed in the line of incision are permanently lost Tensile strength of the wound increases and reaches maximum
Healing by second intention (secondary union)
This occurs in open wounds, particularly when there has been significant loss of tissue, necrosis or large wounds with irregular margins Regeneration of parenchymal cells cannot completely reconstitute the original architecture Abundant granulation tissue grows in from the margin to complete the repair Granulation tissues consists of: ECM fibroblasts Macrophages, neutrophils New blood vesselsHealing by second intention (secondary union) sequence of events
EarlyA few days
1 weekEpithelial proliferation
Capillary loops (granulations)
Scab shed
Loose connective Tissue formed by fibroblasts
2 weeks onwards
Months
Full thickness of Epithelium restoredVarying depth of Surface depression
Thick collagenous Scar tissue becoming Less vascular
Secondary union differs from primary union in several respects
inflammatory reaction is more intense larger amounts of granulation tissue formation larger scar ***wound contraction Myofibroblasts: modified fibroblasts with feature of SMC defect significantly decreases in size as wound heals.Wound Strength
Skin wounds 1 week old; 10% of unwounded skin rapid increase in tensile strength as scar tissue accumulates over 2 months Completely healed; 70-80% of unwounded skin Scar tissue is never as strong as the original tissue !!Factors that influence healing
Classified as Systemic and LocalSystemic Factors that Delay/Retard Wound Healing
Nutrition Protein deficiency, Vitamin C deficiency inhibit collagen synthesis Zn deficiency (cofactor in type III collagenase) Metabolic status diabetes mellitus: Susceptibility to infection caused by impaired circulation and increased glucose. Circulatory status inadequate blood supply atherosclerosis, vascular defects Hormones glucocorticoids inhibit collagen synthesis, decrease inflammationLocal Factors that Delay/Retard Wound Healing
Infectionmost important cause of delayed wound healingPersistent injury and inflammationMechanical factorsmotion early in healingForeign material - like suture material and foreign bodiesSize, location & type of woundwounds in ↑ vascularized areas (face) heal faster than in poorly vasc areas (tendon, feet)small wounds heal faster than largerincisions faster than blunt trauma (contusions)
Complications of wound healing
Deficient scar formation ( most important) Excessive formation of repair components Exaggerated contractionDeficient scar formation
Can lead to two types of complications: A. Wound Dehiscence (rupture of wound) most common after abdominal surgery coughing, vomiting, B. Ulceration - defect in the continuityWound Dehiscence
Excessive formation of repair componentsKeloid / hypertrophic scar (excess collagen) Exuberant granulation or proud flesh (excessive granulation tissue that protrudes above the level of the surrounding skin and impairs the growth of epithelium)
Keloid / hypertrophic scar
Raised scars due to accumulation of excess amounts of collagen ( type III – type I)Hypertrophic scars do not grow beyond the boundaries of the original woundKeloids grow beyond the boundaries of the original wound (more serious)Can result from a surgery, an accident, body piercing or can be spontaneousGenetic predispositionMore common in African – AmericansCommonly seen over face, shoulders and chestKeloid
Exuberant granulation (proud flesh)
Excessive granulation tissue Protrudes above surrounding skin Prevents re -epithelialization