wound healing dr bill revell why wounds happen? how wounds heal? when is a wound considered chronic?...
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Wound HealingDr Bill Revell
Why wounds happen?
How wounds heal?
When is a wound
considered chronic?
Nature of good wound
care
Wound healing
Restoration of the normal anatomic
continuity to a disrupted area of tissue
Wounds:
Clean
Contaminated
Infected (>105 bacteria per gram of tissue)
Why do wounds happen? Basic underlying causes must be identified and controlled before healing is begun
Trauma (initial, repetitive)
Scolds/burns (physical and chemical)
Animal bites/insect stings
Pressure
Vascular compromise
Immunodeficiency
Connective tissue disorders
Metabolic disease (including diabetes)
Nutritional deficiencies
Psychosocial disorders
Adverse effects of medications
Often multifactorial Ulcer
Lower leg oedema
Drains copious amount
of fluid irritates skin
Incapacitated sits all day
worsens oedema
Pressure ulcer surrounded by erythema
Spinal cord injured
patient
Chronic pressure ulcer
Erythema
Infection?
Irritation of wound fluid?
Incontinence?
Continual pressure?
How do wounds heal? Haemostasis
Inflammation These two phases often combined as
“inflammatory phase”
Proliferation
Remodelling or maturation
PMN –
Poly
Morpho
Nucleocytes
Neutrophils
Basophils
Eosinophils
1. Haemostasis
Platelets – key role in
forming stable clot
Also constriction of blood
vessels
spasm ultimately relaxes
ADP leaks from damaged
tissues
platelets aggregate and
adhere to exposed collagen
secrete cytokines
(eg PDGF)………
………. blood clotting Intrinsic clotting cascade
Production of thrombin
Initiates production of fibrin (from prothrombin)
Fibrin mesh strengthens platelet aggregate into stable
haemostatic plug
Platelets also secrete cytokines (eg PDGF) factors involved in initiating cascade
Haemostasis usually within minutes
2. Inflammation Local vasodilatation; Fluid leakage in extra
vascular space; Blockage of lymphatic drainage Rubor (redness)
Tumour swelling)
Calor (heat)
Dolor (pain) – produced by distension of tissue spaces
from swelling, and by chemical irritation of
nociceptors) Swelling and pain loss of function
Rubor et tumour cum calore et dolore
Inflammation (up to 4 days)
“Clean up the debris”
Leaky blood vessel plasma
and neutrophils to
surrounding tissue
Neutrophils phagocytose
debris and microorganisms aided by local mast cells
as fibrin breaks down,
degradation products attract
the next cell involvederythema
Macrophage direction……… Macrophages also phagocytose undesirable elements
Also…………
Secrete variety of chemotactic (eg fibronectin) and growth
factors (including angiogenic factors)
Fibroblast growth factor (FGF)
Epidermal growth factor (EGF)
Transforming growth factor beta (TGF)
Interleukin-1 (IL-1)
Which direct the next stage……………
3. Proliferative phase (proliferation, granulation, wound contraction)
4 – approx 21 days
Pebbled red tissue in
wound base
Replacement of dermal
tissues (sometimes
subdermal)
Wound contraction
Proliferation phase (rebuild structure)
Fibroblasts Collagen framework on which further dermal
regeneration occurs
Angiogenesis Pericytes outer lining of blood vessels
Endothelial cells inner vessel layer
Keratinocytes Re-epithelialisation
some differentiate to form protective outer layer
(stratum corneum) – final stage contracture
Re-epithelialisation: concurrent with formation of granulation tissue
Reformation of epithelial (epidermal) sheet
Basal keratocytes switch to migratory phenotype
Secrete connective tissue degrading enzymes;
facilitate movement across newly deposited or
exposed extracellular matrix
Granulation tissue rapidly covered
Reformed epidermis source of growth factors eg IL-1,
TGF-1
Scar following wound healing Red, immature; mature, normal
skin colour
May develop fibrous bands,
nonpliable
May be painful, itchy
Contracture may develop as
scar heals (myofibroblasts)
Scar from larger, deeper
wounds may become raised
above skin level (collagen +++)
hypertrophic scar
Greater response in dark skin
Keloid scars
Hypertrophic
scars larger than
original wound
Most common in
dark skin
4. Remodelling Remodelling dermal tissues to produce greater tensile
strength
Deposition of matrix materials Fibronectin, hyaluronic acid, proteoglycans and collagen serve as
scaffold for cellular migration and tissue support
….and subsequent changes over time
Up to 2 years after wounding Collagen: max level 2-4 weeks post injury
Tensile strength 40% pre-injury strength 1 month post-injury;
increased up to a year
Never >80%
Apparently healed wounds can break down dramatically if
attention not paid to initial causative factors
Wound Healing as House Repair
Phase Post injury days Cells House Building
Haemostasis immediate platelets Capping off gas, water etc
Inflammation 1 - 4 neutrophils Unskilled labourers to clean up the site
Proliferation 4 - 21 macrophages Site supervisor
Granulation
Contracture
Lymphocytes
Angiocytes
Neurocytes
Fibroblasts
keratinocytes
Specialist labourers
Plumber
Electrician
Carpenter/framer
Roofers
Remodelling 21 days to 2 years Fibrocytes Interior finishing
When is a wound considered chronic?
Healthy individuals - acute wound should heal within 3/52…
remodelling for next year or so
Wound may become stuck in one of the stages….. wound
becomes chronic
Definition: “wounds which have failed to proceed through an
orderly and timely process to produce anatomic and functional
integrity, or proceeded through the repair process without
establishing a sustained anatomic and functional result”
Lazarus G et al (1994). Arch. Derm 130: 489-493
Kloth LC and McCullock (2002). Wound healing; alternatives in management
Kloth LC and McCullock (2002). Wound healing; alternatives in management
Principles of Good Chronic Wound Care
Identify and control the underlying
causes
Support patient centred concerns
Optimise local wound care
Occlusive, moist dressings………
Decreased dehydration
and cell death
Increased angiogenesis
Enhanced autolytic
debridement
Increased re-
epithelialisation
Bacterial barrier and
decreased infection rates
Decreased pain
Decreased costs
Occlusive moist dressings and wound healing
Decreased dehydration and cell death
Activity of neutrophils, macrophages, fibrocytes, pericytes etc. Cannot function in
a dry environment
Increased angiogenesis
Cells need moist environment; also, occurs in regions of low PO2. Occlusive
dressings may act as stimulus
Enhanced autolytic debridement
Neutrophil cell life is prolonged, and proteolytic enzymes carried to wound bed
painless debridement. Fibrin degradation products are a factor in stimulating
macrophages to release growth factors into wound bed
Occlusive moist dressings and wound healing:
Increased re-epithelialisation
epidermal cells must spread over wound surface from edges; need blood and
nutrients. Dry, crusted wounds reduce supply and provide a barrier to migration
Bacterial barrier and decreased infection rates
Occlusive dressings can provide a barrier to microorganism migration wound.
Decreased pain
Moist bed insulates and protects nerve endings. Occlusive dressings often
requires less changes
……………….but how moist is moist?
Wound Healing: Summary