wound healing and wound care. notes/1/2/om...learning outcome by the end of this presentation, you...

Wound healing andWound care.

Odunayo M. Oluwatosin, FMCS (Nig)Department of Surgery

Learning outcomeby the end of this presentation, you should be able to:

• Describe the process of wound healing.

• Discuss complications of wounds healing.

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Learning outcomeby the end of this presentation, you should be able to:

• Discuss the total care of a patient whopresents with a wound / ulcer

• Compare the present mode of wound carewith the past

• Contrast the present mode of wound carewith the past

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A wound is an area of thebody whose normal integrity

has been compromised

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Wound can be found in:• Skin,• Mucosa,• Bone,• Brain

Can be:• Acute• Chronic

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Acute wound• Trauma• Surgery• Infection• Inflammation

Chronic wound• Poorly treated trauma• Vascular disease• Haematological disease• Pressure• Infection• Endocrine• Malignancy

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Aetiology

Traumatic wounds on the face

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Phases of wound healing

• haemostasis• inflammation• proliferation• maturation

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Haemostasis• microvascular injury leads to extravasation of

blood,• activation of coagulation cascade,• constriction of injured vessels,• clot formation,• platelet aggregation.• Fibrin, fibronectin, vW (von Willibrandt) factor,

and thrombospondin, provide initial matrix forcellular migration

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Inflammation

• Initial inflammatory exudate contains mainlypolymorphs that later gets replaced bymonocytes and lymphocytes.

• Monocytes must be present to trigger offfibroblast invasion of the wound as well asproliferation

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Proliferation

• Fibroplasia• Epithelialisation• Angiogenesis

• commences 3 days into wound healing• lasts weeks depending on the size of wound, and type

of tissue involved.• replacement of provisional fibrin/fibronectin matrix by

a more definitive framework comprises

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Fibroplasia

• commences 2-4 days after wounding.• fibroblasts are attracted to site by PDGF and

TGF-β• they proliferate and construct new

extracellular matrix (ECM) which initiallycomprises fibronectin and hyaluronan butlater, collagen and proteoglycan.

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Fibroplasia

• During the first three weeks, all wounds gainstrength at the same rate

• thereafter the gain in strength becomesvariable depending on the tissue.

• for the skin, peak tensile strength is achieved60 days after injury.

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Epithelialisation

• Epithelial mobilisation, migration, division,and differentiation are stimulated by anapparent loss of contact inhibition.

• EGF stimulates mitogenesis and chemotaxis

• β-FGF and keratinocyte growth factor (KGF)stimulate epithelial proliferation.

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Epithelialisation

• Advancing cells bridge the wound

• Cellular differentiation from the base to thesurface occurs.

• The rate of epithelialisation increases if:the wound does not require debridement,the basal lamina is intactthe wound is kept moist.

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Angiogenesis• Stimulated by:

TGF-β and PDGF from plateletsTNF-α and β-FGF from macrophages.

• The capillary sprouts invade fibrin to formgranulation tissue network

• With time, blood vessel density reduces andscar tissue develops.

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Maturation orremodelling

• Balance develops between collagenformation and degradation

• This reaches a steady state at 21 days afterwounding.

• The eventual tensile strength achieved is only80% of normal.

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Maturation• Collagen degradation is by matrix

metalloproteinases (MMPs)

• Produced by: fibroblasts, granulocytes,macrophages.

• Tissue inhibitors of MMP (TIMP) deactivateMMPs.

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MMP TIMP

• While early collagen deposition isdisorganised, local forces cause the laiddown collagen to orientate in an organisedfashion.

• Subsequently, activity of MMPs decreases

• Tissue inhibitors of MMP (TIMP) activityincrease.

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Maturation

• macrophage, and fibroblast density becomesreduced by apoptosis

• capillary outgrowth stops

• acellular and avascular scar results

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Maturation

Complications of wound healing

• Wound infection• Systemic infections• Chronic wounds and ulcers

Scars and contractureskeloidsLymphoedemaBone complications: osteitis, osteomyelitis

Marjolin’s ulcer• Tetanus• Pressure ulcers

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24

R. Gary Sibbald, Kevin Woo, ElizabethA. Ayello. Increased Bacterial Burdenand Infection: The Story of NERDS andSTONES. ADV SKIN WOUND CARE2006;19:447-61

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Acutewound

Chronicwound

Repetitive traumaLocal tissue ischaemia

Necrotic tissueHeavy bacterial burden

Tissue breakdown

Differences between acute andchronic wound healing

• In a chronic wound, the timely and orderlymanner of acute wound healing enumeratedpreviously is disrupted.

• This disruption occurs in most cases in theinflammatory and the proliferative phases

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The disruption manifests in:• alterations in protease activity,• alteration in cytokine profile and

inflammatory response,• changes in cellular profile and activity,• changes in the composition of extracellular

matrix and environment,

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Pro-inflammatory

cytokines

TNF-αIL-1bIL-2IL-9

MMP

TIMPAnti-

inflammatorycytokines

IL-4IL-10TGF


The disruption manifests in:• presence of free radicals and role of nitric

oxide,• accumulation of necrotic tissue and slough,• presence of micro organisms,• disease specific pathological change.

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Keloid

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Bone complications

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Lymphoedema

Total care of a patient who presentswith a wound / ulcer

• Identify and treat the cause

• Address patient-centeredconcerns

• Provide local wound care

• Denis Okan, Kevin Woo, Elizabeth A. Ayello, R. Gary Sibbald. The Role of Moisture Balance inWound Healing. Adv Skin Wound Care 2007; 20: 39-53 35

Identify and treat the cause

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• Venous leg ulcers• Arterial ulcers• Pressure ulcers• Diabetic foot ulcers• Malignant ulcers and Marjolin’s ulcer

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Identify and treat the cause

Address patient-centered concerns

• Provide emotional support• Assess and consider financial situation• Provide patient and family education• Assess and provide/facilitate optimum

health care

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Otherpatient

concerns

Frequentdressings/

odour/discharge

Anxiety/distress/

depression

Socialisolation

Polypharmacy

Work andwalking

concerns

Decreasein physical

activity

Fear ofamputation/

lifeadjustment Change of

bodyimage/

deformity

Pain

Woundinformation

Is tetanus-prone Is not tetanusprone

Time since injury >6 hours <6 hoursDepth of injury > 1 cm < 1 cmMechanism ofinjury

Crush, burn,gunshot,frostbite,penetrationthrough clothing

Sharp cut

Dead tissuepresent

Yes No

Foreign material(grass, dirt, etc.)contamination

Yes No

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Pain management

• Injury pain (immediate, severe, regressive),background pain which is prolonged untilwounds are healed

• Procedural pain (dressing changes,physiotherapy, post operative) which issevere and repetitive.

• WHO pain ladder• Appropriate timing

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Total care of a patient who presentswith a wound / ulcer

• Identify and treat the cause

• Address patient-centeredconcerns

• Provide local wound care

• Denis Okan, Kevin Woo, Elizabeth A. Ayello, R. Gary Sibbald. The Role of Moisture Balance inWound Healing. Adv Skin Wound Care 2007; 20: 39-53 42

Provide local wound care

Determine the potential for healing

Assess the wounda) Obtain the wound historyb) Assess and monitor the physical characteristics of

the woundc) Assess and manage wound pain

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Local Wound Carea) Tissue concernsb) Infection/Inflammation concernsc) Moisture concernsd) Edge concerns


Blood supply

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Risk factors and co-morbidities that mayaffect wound healing:a) Drugs i.e. immunosuppressive agents and systemic

steroidsb) Periwound edema in a chronic woundc) Serum albumin: <30g/L delays healing, <20g/L very

hard to heal or non-healing woundsd) Hemoglobin: <100g/L delayed healing, < 70-80g/L very

hard to heal or non-healing woundse) Diseases or treatments that impair immunity such as

rheumatoid arthritis and collagen vascular diseases (lupus,scleroderma, dermatomyositis), chemotherapy and radiationtherapy

f) Chronic diseases such as uncontrolled diabetes,hepatic/renal/lung disease and vascular disease

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Treat the wound


Assess the wounda) Obtain the wound historyb) Assess and monitor the physical characteristics of

the woundc) Assess and manage wound pain

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Local Wound Carea) Tissue concernsb) Infection/Inflammation concernsc) Moisture concernsd) Edge concerns

Local Wound CareWound Bed Preparation:

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To accelerate endogenous healing

To facilitate the effectiveness ofother therapeutic measures

TIME principles of Wound BedPreparation

TIME

TISSUE

INFECTIONINFLAMMATION MOISTURE

EDGEOF

WOUND

Wound cleansing(from page 12 of UK policy doc.)

• Normal saline• High quality pure water• Chlorhexidine gluconate 0.015 - 0.05% w/v

• Povidone-iodine 10%

• Cetrimide 0.15%

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The effects of water compared withother solutions for wound cleansing

• Water is frequently used for cleaning wounds toprevent infection. This can be tap water, distilledwater, cooled boiled water or saline.

• Using tap water to cleanse acute wounds inadults does not increase the infection rate,however, there is no strong evidence

• That cleansing per se is better than not cleansing.The reviewers concluded that where tap water ishigh quality (drinkable), it may be as good asother methods such as sterile water or saline (andmore cost-effective),

• But more research is needed.

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24/03/03 Reconstructive surgery 51

Wound cleansing

Swab Irrigate

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TISSUE

For clean wounds, no raw surface:Gauze dressing

For raw surface like skin graft donorsite, partial thickness burn, abrasion:Non-adherent dressingsOpsite, Tulle gras, Jelonet, Sofratulle,Vaseline gauze, Bactigras, Melolin,Mepitel,

Temporary biosynthetic skin


TISSUE

NECROTIC TISSUE

Dehydrates, shrinks,inhibits autolysis andseparation becomesdelayed indefinitely

SLOUGH

Mixture of fibrin,deoxyribonucleo-protein, serous

exudates, leukocytesand bacteria

Non viable

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Methods ofdebridement ofnon-viable tissue:

•surgical•mechanical•autolytic•chemical•biological•enzymatic

TISSUE


TISSUE

Sharp debridement and wound excision must be thorough


Beware of the closed degloving wound

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TISSUE

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TISSUE

Hydrocolloids, Hydrogels,Films, Honey:

• Absorb fluid andprogressively movebacteria and cellulardebris away from thesurface of the wound

• Facilitate tissue digestionand separation of theslough

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TISSUE

Hypochlorite solutionAserbine

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TISSUE

Larvae of Luciliasericata (greenbottlefly) digest necrotictissue and pathogens

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TISSUE

VaridaseIruxol

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INFECTIONINFLAMMATION

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Topical antibiotics and antiseptics:

• Honey• Silver sulphadiazine• Impregnated gauze – sofratulle, bactigras,• Inadene• Iodine based polysaccharide bead

dressings e.g. Iodosorb, Iodoflex• Metronidazole gel,• Mupirocin (Bactroban), fusidic acid

(Fucidin)• Nanocrystalline silver

“A moist wound healingenvironment enhances re-epithelialization in open wounds,but excessive wound fluid can slowdown wound healing and causemaceration”

(Bishop et al 2003)65

MOISTURE

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MOISTURE

Absorbent dressings:

FoamHydrofibreCalcium alginateCrystalline salineHydropolymer foamAcrylic dressing

Proper moisture balance produces:

• Decreased healing time• Decreased rate of infection• Reduced wound trauma• Fewer dressing changes• Reduced pain• Increased cost effectiveness

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MOISTURE

Dressing Water Absorbed (grams)Gauze 6” x 9” 4-ply 28.0

ABD Pad 5” x 9” 111.9EXU-DRY 6” x 9” 214.8

Absorbency

Low Moderate High

Films

Replicare / hydrocolloids

AlgiSite* M / alginates

Allevyn and other Foams

EXU-DRY

Gauze

RELATIVE MOISTURE MANAGEMENT

• 20 to 40% reduction in two and fourweeks is likely to be a reliablepredictor of healing

• Non-healing edge is cliff like; healingedge is sloppy and bluish tinged

• Consider removal of hyper-keratoticand fibrotic rim

• Use growth factors

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EDGEOF

WOUND

WOUND MANAGEMENT PRODUCTSFOR TYPES OF WOUNDS

(page 8 of UK policy paper)

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• Healing is a matter of time, but it is sometimes also amatter of opportunity.Read more:http://www.brainyquote.com/quotes/authors/h/hippocrates.html#ixzz1kM4R2jiv

• Make a habit of two things: to help; or at least to do noharm.Read more:http://www.brainyquote.com/quotes/authors/h/hippocrates.html#ixzz1kM4fNvM0

• Science is the father of knowledge, but opinion breedsignorance.Read more:http://www.brainyquote.com/quotes/authors/h/hippocrates.html#ixzz1kM4xMqEj

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