7-Wound Healing

Study Notes

Wound healing is a complex process with overlapping phases, initiated by injury. It's categorized by characteristic cellular populations and biochemical activities.
Hemostasis is the first stage, characterized by vasoconstriction, platelet release reaction, and platelet aggregation. It's a reversible process and doesn't require heparin.
Platelet plug formation is the second event, initiated by exposure of subendothelial collagen to platelets. This leads to platelet aggregation, degranulation, and coagulation cascade activation.
Fibrinolysis is the last step of hemostasis, breaking down the clot to restore blood flow.
Inflammation follows hemostasis, involving infiltration of different inflammatory mediators like neutrophils (peak 24-48 hours).
Proliferative phase (Days 4-12) involves fibroblast and endothelial cell invasion, tissue continuity re-establishment.
Maturation and remodeling is the last stage, characterized by scar remodeling and reorganization of collagen.

Neutrophils are the first inflammatory cells to infiltrate the wound, followed by macrophages (48-96 hours).
Macrophages participate in wound debridement and contribute to microbial stasis.
Lymphocytes play a role in modulating the wound environment.

Fibroblasts synthesize the proteins of the matrix and collagen.
Endothelial cells proliferate, promoting angiogenesis (new capillary formation).
Wound contraction reduces the size of the wound.

Collagen deposition and degradation balance for wound strength.
Epithelialization (cell proliferation from the edge) completes re-establishment of skin layers.
Excessive scar formation (hypertrophic or keloid scars) can result and require further treatment.

Local: Mechanical injury, infection, edema, ischemia, radiation exposure, foreign bodies, low oxygen, and nutrition.
Systemic: Trauma, metabolic disease, immunosuppression, connective tissue disorders, and smoking. Age, hypoxia, and anemia/hypoperfusion also play a significant role in impacting the healing process.

Chronic wounds (fail to heal within 4 weeks): Repeated trauma, poor perfusion, excessive inflammation, and secondary infections are factors.
Biofilm formation is a common problem, especially in diabetic ulcers or chronic wounds.
Wound contractures may occur with scars in joints.

Advanced age: Impaired intrinsic physiologic changes, especially among the elderly, delay or impair healing.
Metabolic diseases: Diabetes, and others affect healing.
Nutrition: Impacts healing.
Immunosuppressant drugs and treatments: Delayed healing
Vascular disorders: Affect blood supply, vital for healing, negatively impact healing
Other: Smoking, tissue damage, and infections increase healing time.

Acute: heals within 4 weeks.
Chronic: takes longer than 4 weeks to heal.
Classification by depth: Superficial, partial thickness, full thickness, and extensive injuries.

Goal: Optimal wound environment for healing.
Types of dressings: Absorbent or non absorbent, occlusive or semi-occlusive, and others.
Treatment: Wound debridement (removing all dead tissue), wound care, maintaining a moist wound environment, and addressing secondary complications like infection.

Causes: Vascular compromise, chronic inflammation, infection, and autoimmune diseases.
Types: Ischemic arterial ulcers, venous stasis ulcers, pressure ulcers, and diabetic ulcers.

Etiology: Pressure exceeding blood supply to skin.
Grading: Stage I-IV based on injury depth.
Management: Pressure relief, wound care, and addressing secondary issues (infection, nutrition).

Classification: Neurapraxia (focal demyelination), axonotmesis (interruption of axonal continuity), and neurotmesis (complete transection).
Healing: Survival of axonal cell bodies, regeneration across transected nerve to distal stump, and migration/connection of the regenerating nerve ends.