Types of Wound Healing:Â
-
Primary:
- Direct approximation of wound edges w\in hours of wound creation
- Example: sutures, stables, skin grafts
- Contraindications: bites, infections, crush injuries, > 6-8 hrs since injury, retained foreign body
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Secondary:
- Wound left open to heal spontaneously: epithelialization, contraction, granulation
- Requires dressing changes
- Inferior cosmetic result
-
Delayed primary:
- When the wound is left open (debridement, packing, antibiotics) to control infection and form granulation tissue for a few days, then the wound can be closed (suturing, graft, flap)
Classification of Wound Healing:Â
 | Definition | Example | Risk of infection |
Clean | Operative, non-traumatic, no inflammation, no break in technique, no entering of resp\GI\GU | Thyroidectomy, hip replacement | <2% |
Clean-contaminated | Operative, non-traumatic, entering resp\GI\GU w\out significant spillage | Tonsillectomy, cholecystectomy | 5-10% |
Contaminated | Operative w\ major break in technique, traumatic, entering resp\GI\GU w\ gross spillage, evidence of inflammation | Large bowel resection, biliary or GU surgeries w\ infected bile or urine | 15% |
Dirty | Operative, traumatic, fecal contamination, foreign body, necrosis, pus, perforation | Empyema, abscess I&D, wound debridement | 40% |
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Stages of Wound Healing:Â
-
Inflammatory (1-6 days): limits damage and prevents further injury:
- Hemostasis: vasoconstriction + platelet plug (within minutes)
- Vasodilation and increased permeability:
- Cell migration: margination, diapedesis, chemotaxis
-
Proliferative (day 4 – week 3):
- Matrix formation:
- Fibroblast migration (7 day)
- Collagen synthesis (D5-wk3); mainly type III here -> tensile strength begins to inc at D4-5
- Glycosaminoglycan production
- Angiogenesis: VEGF\NO
- Epithelialization: begins 24-48 h
- Matrix formation:
-
Remodeling (week 3 – 1 year):
- Collagen: increased collagen synthesis and organization (type I replaces type III, until normal 4:1 ratio is achieved)
- Contraction: due to myofibroblasts
- Scar formation and remodeling: begins at D21
Factors Affecting Wound Healing:
Local |
Systemic |
–  Blood\oxygen supply (atherosclerosis, Raynaud’s, scleroderma, PVD)
–Â Â Retained foreign body –Â Â Infection (inc risk due to hematoma\seroma) –Â Â Temperature –Â Â Radiation |
–Â Â Age
–Â Â Hereditary conditions: collagen vascular diseases (EDS, progeria, Werner syndrome) –Â Â Nutritional (proteins, vit C) –Â Â Smoking –Â Â Chronic ds (DM, Ca, CVD) –Â Â Immunodeficiency (steroids, chemo, radio) |
Abnormal Wound Healing:
Hypertrophic scar |
Keloid |
–Â Â Elevated, but remains w\in borders of original scar
–Â Â Type III collagen oriented parallel to epidermal surface + abundant myofibroblasts and collagen –Â Â Associated w\ poor technique during suturing –Â Â Site: flexor surfaces –Â Â More common than keloids, less likely to recur after therapy |
–Â Â Scar growing outside original wound borders
–Â Â Disorganized type I & III collagen, hypocellular collagen bundles –Â Â Related to genetic and endocrine influences (inc in preg and puberty) –Â Â Site: sternum, shoulder, face, earlobes –Â Â More resistant to therapy |
Random notes:
Download the PDF version: here
References:
- Salah Aldekhayel’s lecture
- Essentials of plastic surgery
- Toronto notes