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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
THANK YOU