Phases of Healing - Stitching It Up
📌 Mnemonic: Heavy Inflammation Produces Remodeling.
- 1. Hemostasis (Immediate):
- Vasoconstriction, platelet aggregation (plug).
- Coagulation cascade activation → Fibrin clot. Key: Thrombin.
- 2. Inflammation (Day 1-6):
- Neutrophils (PMNs, 24-48 hrs): Debris/bacteria clearance.
- Macrophages (Day 2-3+): Crucial; phagocytosis, release GFs (PDGF, TGF-$\beta$).
- 3. Proliferation (Day 4 - Wk 3):
- Fibroblasts: Collagen III synthesis, GFs (FGF).
- Angiogenesis (VEGF), granulation tissue.
- Epithelialization (EGF, KGF).
- Wound contraction (myofibroblasts).
- 4. Remodeling (Wk 3 - 1yr+):
- Collagen III → Collagen I (organized).
- ↑ Tensile strength (max ~80% of original).
- Scar formation & maturation. Apoptosis of cells.

⭐ Absence of macrophages severely impairs wound healing, highlighting their critical role.
Wound Closure Types - Sealing the Deal
- Primary Intention:
- Clean wound, edges apposed (surgical incision).
- Closure: Sutures, staples, adhesives.
- Minimal scar, rapid healing.
- Secondary Intention:
- Wound left open (infected wounds, ulcers).
- Heals by granulation, contraction, epithelialization.
- Larger scar, slower healing.
- Tertiary Intention (Delayed Primary Closure):
- Initially open (contaminated wound); debride, manage infection.
- Surgical closure after 3-5 days.
- Reduced infection risk.

⭐ Tertiary intention (Delayed Primary Closure) is typically performed 3-5 days post-injury, allowing for initial debridement and infection control.
Factors in Healing - Boost or Bust
- Systemic Factors:
- Boost:
- Nutrition: Protein, Vit C, A, Zinc, Copper
- Good oxygenation & perfusion
- Growth factors (PDGF, FGF, EGF)
- Hormones: Insulin, Growth Hormone
- Bust:
- Age (↑), Diabetes Mellitus, Obesity
- Malnutrition (Vit C**↓, Protein↓, Zinc↓**)
- Hypoxia, Ischemia
- Drugs: Corticosteroids, Chemotherapy, NSAIDs
- Smoking, Uremia, Jaundice
- Severe stress (**↑**cortisol)
- Boost:
- Local Factors:
- Boost:
- Moist environment (occlusive dressings)
- Good blood supply
- Absence of infection
- Bust:
- Infection (most common cause of delay)
- Foreign body, Necrotic tissue
- Poor perfusion (e.g., PAD), Edema, Hematoma
- Radiation injury
- Excessive tension/movement
- Desiccation or Maceration
- Boost:
⭐ Infection is the single most common and important cause of delayed wound healing.
Problematic Healing - Scars & Setbacks
- Hypertrophic Scars:
- Raised, red, often pruritic; within wound margins.
- Type III collagen ↑; may regress spontaneously.
- Keloids:
- Extend beyond margins; thick, rubbery, often painful/pruritic.
- Type I & III collagen ↑↑; high recurrence.
- Sites: earlobes, sternum. Darker skin predisposition.

- Atrophic Scars:
- Depressed, thin; loss of collagen/elastin (e.g., acne, striae).
- Other Setbacks:
- Wound Dehiscence: Edges separate. Risks: infection, tension, poor nutrition.
- Contractures: Limit movement, deformity. Common post-burns, over joints.
- Chronic Wounds: Fail to heal > 3 months. E.g., diabetic, venous ulcers.
⭐ Marjolin's Ulcer: SCC in chronic non-healing wounds, old burn scars, or sinus tracts; often aggressive.
High‑Yield Points - ⚡ Biggest Takeaways
- Healing phases: Inflammation (PMNs, Mφ), Proliferation (fibroblasts, new vessels), Remodeling (collagen I).
- Platelets release growth factors (PDGF, TGF-β), initiating the healing cascade.
- Macrophages are critical for debridement and promoting tissue repair.
- Fibroblasts produce collagen type III, later replaced by stronger collagen type I.
- Myofibroblasts cause wound contraction, reducing defect size.
- Final tensile strength is approximately 80% of normal skin.
- Healing impaired by: infection, ischemia, diabetes, malnutrition, corticosteroids.
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