Wound Care & Scar Management

The inflammatory phase begins within minutes of tissue injury and lasts 24–48 hours. Hemostasis is the immediate priority: platelet aggregation and fibrin deposition form the initial wound matrix, which serves as a scaffold for subsequent cell migration. Platelets are the first responders, releasing chemotactic factors (PDGF, TGF-β) that recruit inflammatory cells and producing fibrin and fibronectin that form the provisional clot matrix. Neutrophils are the first immune cells to arrive at the wound site, peaking at 24–48 hours. They perform tissue debridement through proteolytic enzyme release and clear bacteria through phagocytosis and reactive oxygen species. Macrophages arrive next and are the critical orchestrators of wound healing. They phagocytose debris and bacteria, secrete growth factors (PDGF, FGF, VEGF, TGF-β) that stimulate fibroblast proliferation and extracellular matrix production, and mediate the transition from the inflammatory to the proliferative phase. Macrophage depletion experiments demonstrate that wounds cannot progress beyond the inflammatory phase without macrophage signaling.

The proliferative phase begins around day 5 and lasts approximately one month. Three concurrent processes characterize this phase: re-epithelialization, fibroplasia with granulation tissue formation, and wound angiogenesis. Re-epithelialization begins within hours of injury as keratinocytes at the wound edge lose their desmosomal attachments and begin migrating across the wound surface in a ‘leapfrog’ pattern, guided by matrix metalloproteinases (MMPs). This process is accelerated in moist wound environments and retarded by desiccation and eschar formation. Fibroplasia involves fibroblast migration into the wound along the provisional fibronectin matrix. Fibroblasts deposit Type III collagen, forming granulation tissue. Some fibroblasts differentiate into myofibroblasts expressing α-smooth muscle actin, which generate contractile forces that reduce wound size by up to 40–80% (wound contraction). Concurrent angiogenesis, driven by VEGF and FGF, establishes new blood vessel networks within the granulation tissue.

The remodeling phase begins around 3–4 weeks after injury and continues for 12–15 months. During this extended phase, the wound transitions from metabolically active granulation tissue to a relatively acellular, collagen-dense scar. The hallmark event is the replacement of Type III collagen with Type I collagen, which is stronger and more organized. Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) regulate this turnover. Collagen fibers progressively organize along lines of mechanical tension, increasing wound tensile strength. Wound tensile strength follows a predictable trajectory: approximately 3–5% of normal skin strength at 1 week, 20% at 3 weeks, 50–60% by 3 months, and a maximum of 70–80% of original skin strength. Wounded skin never regains 100% of its original tensile strength.

Multiple local and systemic factors can impair wound healing by disrupting one or more phases of the repair cascade.

A chronic wound is defined as one that has not healed by 12 weeks or fails to reduce in size by 50% within 4 weeks. Chronic wounds are arrested in the inflammatory or proliferative phase. Pathologic features include elevated MMP levels that degrade new matrix as quickly as it is deposited, defective fibroblast infiltration, persistent biofilm-associated infection, and perivascular fibrin cuffs that impair oxygen delivery. Management focuses on addressing the underlying cause (vascular insufficiency, pressure, infection), debridement of nonviable tissue, moisture balance through appropriate dressings, and topical antimicrobial therapy when clinically infected.

Immediately after wound closure, a pressure dressing is applied to minimize dead space, reduce the risk of hematoma formation, and immobilize the repair. Components of a standard pressure dressing: • Non-adherent contact layer (petrolatum gauze or Adaptic) directly over the wound • Absorbent gauze layer to wick exudate • Conforming wrap or tape providing gentle compression The pressure dressing is typically left in place for 24–48 hours. The patient is instructed to keep the dressing clean and dry, avoid strenuous activity, and sleep with the head elevated (for facial wounds) to reduce edema. For flap repairs, bolster dressings provide additional immobilization during the critical first 48–72 hours. For skin grafts, the bolster remains for 5–7 days.

After pressure dressing removal, the wound transitions to a moist healing protocol. Evidence consistently demonstrates that moist wound environments accelerate re-epithelialization by 30–50% compared to dry healing, reduce pain, and produce superior cosmetic outcomes. Standard moist wound care protocol: 1. Gentle cleansing: wash the wound with mild soap and water or dilute hydrogen peroxide (1:1 with water) once or twice daily. Avoid aggressive scrubbing. 2. Apply a thin layer of plain white petrolatum (Vaseline) or antibiotic ointment to the wound surface. Petrolatum is preferred. It provides equivalent moisture retention without the risk of contact dermatitis associated with topical antibiotics (especially neomycin and bacitracin). 3. Cover with a non-adherent dressing or adhesive bandage. 4. Repeat the clean-apply-cover cycle once or twice daily until suture removal or full re-epithelialization.

The choice of wound dressing depends on the wound type, location, exudate level, and whether the wound is healing by primary intention (sutured) or secondary intention (open).

The optimal time for suture removal depends on the anatomic location (blood supply and mechanical stress), the type of closure, and whether deep (buried) sutures were placed to support the wound.

Postoperative activity restrictions are designed to prevent wound complications during the critical early healing phase. • First 24–48 hours: Strict rest. No bending, lifting, or straining. Head elevation for facial wounds. No alcohol (increases bleeding risk). • Days 2–7: Light activities of daily living permitted. No exercise, heavy lifting (>10 lbs), or activities that increase blood pressure or heart rate. • Days 7–14: Gradually resume light exercise (walking). Avoid swimming, contact sports, and activities that place direct stress on the wound. • After suture removal: Progressive return to full activity. Continue sun protection of the scar for 6–12 months.

Scar prevention strategies should be initiated immediately after suture removal and continued for a minimum of 3–6 months:

Hypertrophic scars and keloids represent excessive fibroproliferative responses to wound healing. Understanding the distinction is critical for treatment selection and prognosis.

Treatment of hypertrophic scars and keloids follows a stepwise approach, escalating from conservative measures to procedural interventions: