Wound Healing

PLASTIC AND RECONSTRUCTIVE SURGERY PRESENTATION

ANATOMY OF THE SKIN, WOUND HEALING

Dr Bashiru Aminu

outline

• Case presentation• Introduction• Definition• classification• Basic anatomy and physiology• Stages of wound healing• Factors affecting wound healing• Complications of wound healing

Case presentation

• I. M. 26yr student, Auna,kontagora 3/52 • 3/7 GSW ® hand, accidental• Haemodynamically stable findings in hand • Initial resuscitation, debridment• Wound care, physiotherapy• Awaiting skin cover for residual wound

Case one

Case presentation

• H. S. 24yr student, yalwa, jigawa 3/12, 3/52• Post flame burn wounds on (L)leg,thigh ff RTA• Mss- 15% full thickness burn whole (L) leg,

posterior aspect of the thigh with purulent discharge and extensive slough

• Had resuscitation, debridment• subsequent skin cover• Residual wound with exuberant ganulation

requiring shave down but is financially inept

Case two

Introduction

Definitions- Replacement of damaged tissue by living tissue

Wound healing and the care giver- Hallmark of surgical practice

- Therapeutic applications- Still not fully understood- various commercial products

anatomy

• General Characteristics– Largest organ (sensory) of the body• Protects against :

– pathogens and irritants and loss of fluid

• Provides temperature control- thermoregulation

– Normally dry, supple, acidic-antifungal• Acid mantle (pH of 4.5 to 5.5)• Elastic and well hydrated

Layers of the skinEpidermisoutermost layerprimarily dead cells-

epithelial cellsNo blood vessels.06 to 6 mm thick

DermisInner layerProvides strength and

endurancehas collagen, elastin, blood

vessels, epidermal appendages

Key cells: fibroblasts and macrophages

Anatomy Cont’d

• Subcu Tissue(not a true skin layer)– Provides padding

(adipose) and even pressure

– Needed for prevention of skin breakdown

– Fascia

• Muscle layer– highest metabolic

rate– rich blood flow– uses O2 at most

rapid rate– first tissue to get in

“trouble” with prolonged pressure

Phases of wound healing

1. Inflammatory phase: 1-3 days

2. Destructive/Demolition phase: 3-4 days= Lag/preparatory phase

3. Proliferative phase: 4-21 days

4. Maturation/Remodeling phase: 21 days – 1 year

• All the events occur simultaneously, they overlap, interact and influence each other

1. Inflammatory phase: 1-3 days

Aim: - Attainment of haemostasis - Reduction of bio-burden

- Initial vasoconstriction- Activation of the clothing cascade- extrinsic & intrinsic- Platelet de-granulation :- release of growth factors

- Activation of complement system - Release of vaso-active amines - vasodilatation

- Fibrin is converted to fibrin (scaffold for cellular migration)- Ground substance depolymerizes & becomes metachromatic

-sulphated & non-sulphated

2. Destructive/Demolition phase: 3-4 days

Aim: - Remove devitalized tissue - Prevent invasive bacterial infection

- Neutrophils infiltrate – phagocytosis - collagenases

* Absence does not affect overall wound healing* Persistence is associated with chronicity (non-healing)

- Monocytes/macrophages- - phagocytose debris & bacteria- produce growth factors

- Lymphoctes – role not clear- usher in the next phase (proliferative)

- Mast cells – role not clear

3. Proliferative phase: 4-21 days

Aim: To provide a balance b/w scar formation & regeneration

-Re-epithelialization (esp when wound edges are close together)* Keratinocytes - desmosomal regression* Keratinocytes - develop actin in their cytoplasm* Keratinocytes - migrate into the wound by amoiboid movts

- progress under eschar-Granulation tissue formation (replacing fibrin matrix)- New migratn platform

- Fibroblasts- workhorses- Macrophages- GF which stimulate fibroblasts & endoth cells- Endothelial cells – angiogenesis/vasculogenesis – pink granulation

- Collagen type III is formed and replaces fibrin matrix- hydroxylation of proline & Lysine residues- Glycosylation of hydroxyproline & hydroxylysine- Formation of protocollagen- Secretion of protocollagen- Formation of collagen

* Wound contraction – myoepithelial cells (intracellular actin)

4. Maturation/Remodeling phase: 21 days – 1 year

Aim: To maximize the strength & structural integrity of the wound

- The processes of granulation tissue formation are “turned off”- Fibroblasts rapidly disappear- Newly formed vessels regress- pale granulation tissue

*Mechanism – Apoptosis- programmed cellular self destruction - Endarteritis obliterans

*Dysregulation of granulation (no “turn off”) - Fibroplasia - Replacement of type III collagen by type I collagen

- Degredation of type III collagen by metalloproteinases(secreted by fibroblasts, macrophages & endoth cells)

- Increases tensile strength (20% - max 70%)

- Cross-linkage & re-arrangement of type I collagen

- Scar contracture: - joints, hollow structures

Abnormal wound healing* Classification based on balance b/w scar formation & regeneration

1. Inadequate regeneration: corneal ulcers, bone on-union, CNSRx – Implanted neural stem/progenitor cells

- Use of developmental morphogens- Reducing scar formation- steroids, pressure, irradiation, etc

2. Inadequate scar formation: unstable scars(burns, diabetic ulcers, pr ulcers)Rx – Stimulate scar tissue formation- GFs, Vit C

3. Excessive regeneration: periph N (neuromas), hyperkeratosis(psoriasis), adenomatous polyps

Rx – Irritant injections (alcohol)

4. Excessive scar tissue formation (fibroplasia) – H.S, keloidsRx – steroids, pressure, irradiation, etc

-Stimulating regeneration (fetal wound healing research)

Factors affecting wound healing

1. Local factors 1. Oxygen supply(oedema, tissue damage, tight sutures)-Oxid burst, coll synth2. Blood supply- Head & neck3. Infection: prol infl, free ox radicals, micro-thrombosis, competitive exhaustion. 4. Immobilization – repetitive trauma, frequent dressings5. Foreign bodies- eg sutures6. Surgical technique- wound edge apart, rough T handling, excess tension 7. Irradiation

2. Systemic factors1. Age- Elderly, fetus2. Systemic diseases- CLD, renal dx, CCF, D/M, malignant dx3. Nutritional-Vit C, proteins, trace elements (Zc – children in Middle E)4. Cytotoxics- dose-dependent

Complications of wound healing

1. Infection

2. Scarring- H.S., keloids, unstable s., dyschromias, cicatrization

3. Implantation cysts

4. Stitch granulomas/sinuses

5. Wound failure/dehisence – partial(superf, deep), complete(burst abd)

6. Neoplasia (Marjolinulcer):- SCC, BCC, BSC, M. M., soft T sarcomas

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