Lesson 4: Wound Healing Physiology Flashcards
Tissue repair - Regeneration
- Lost tissue is replaced with “more of the same”
- Limited to wounds of skin layers only
- For epidermal or partial dermal loss, but structures will not regenerate
- Ie. Superficial scars and burns
Tissue Repair - Scar Formation
- Connective tissue repair
- Replacement of lost tissue with granulation or scar tissue
- For deep dermal loss or wounds to subcutaneous tissue, muscle, or bone
Tissue Repair - Acute
- Usually d/t surgery or trauma with presence of bleeding
- Usually heal d/t growth factors
Tissue Repair - Chronic
- Usually d/t chronic conditions or failure of acute wound healing
- Delated d/t lack of growth factors
Primary Wound Intention
- Wound closed surgically with minimal tissue defects and heals quickly
- Ie. Surgical incisions
Secondary Wound Intention
- Wounds that heal by granulation/epithelialization “from the bottom up”
- Ie. Pressure injuries, dehiscence, and ulcers
Tertiary Wound Intention
- Wounds with delayed closure
- Wound is initially left open to heal via secondary intention then is closed
Acute Partial Thickness Repair
Inflammation
- Crust collection to create scab
Epithelial resurfacing
- Keratinocyte proliferation and lateral migration or cells
- Cells migrate and attach to extracellular matrix
- Growth factors stimulate cell production
- Wound changes from “red and wet” to “pink and dry”
Repair process
- Reestablishing normal skin layers
- Cells switch to vertical migration
- Initiates normal epidermal regeneration with skin thickness and pigment return
Dermal repair
- Separation of epidermal and dermal layers
- Collagen synthesis
- Reestablishing rete ridges and dermal papillae
Wound is superficial, pink/red, and painful
- keep moist and protected
Use AMD to manage bacterial loads
Acute Full Thickness Repair
Inflammatory Phase
- Control bleeding and establish clean wound bed
- Hemostasis and release of growth factors
- Initiated by blood in contact with collagen + vasoconstriction
- Activates clotting pathways
Clean-up phase
- Eliminate necrotic tissue and control bacterial loads
Proliferative “rebuilding” Phase
- Epithelial resurfacing
- Need incisional protection until intact skin barrier is reestablished
- Granulation tissue formation
- Fills defect with new connective tissue
Contraction Phase
- Fibroblasts reorganize and “shrink” ECM to contract wound edges
- Actin fibers attach to wound edges and cause contraction
Maturation Phase
- Scar tissue tensile strength increases
- Goal = strong and mature scar
Chronic Full Thickness Repair
Inflammatory Phase
- Goal = establish clean wound bed
- No bleeding + no growth factors = no wound progress
- Wound will not progress until all dead tissue is done and bacterial loads are managed
- Surgical debridement can convert chronic wound into acute
- Eliminate necrosis, manage bacterial loads, and manage exudate
Proliferative Phase
- Goal = fill wound bed with new connective tissue and cover connective tissue with new skin
- Key processes
— Granulation tissue formation
— Contraction
— Epithelial resurfacing
— Delayed until healthy bed of granulation tissue is formed
- Complication
— Failure to transition from clean non-granulation → granulation
Contraction Phase
- Occurs simultaneously with granulation tissue formation
- Epithelial resurfacing can’t happen unless wound edges are open
- Closed wound edge = epibole
Maturation Phase
- Essentially unchanged from acute wounds
- A plastics flap can help increase tissue strength
Key Cells Regulating Wound Repair
- Macrophages (control bacterial loads, break down necrotic tissue, produce growth factors)
- Fibroblasts (make new collagen and connective tissue proteins0
- Endothelial cells (make new blood vessels)
- Keratinocytes (for resurfacing)
- Growth factors and cytokines (control repair process by directing cell migration and proliferation process)
- Matrix metalloprotease (MMP)
- Tissue inhibitors of MMPs (TIMPs)
