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