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- 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
-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- and PDGF from plateletsTNF- and -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, osteomyelitisMarjolins ulcer
Tetanus Pressure ulcers
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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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Differences between acute andchronic wound healing
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-IL-1bIL-2IL-9
MMP
TIMPAnti-
inflammatorycytokines
IL-4IL-10TGF
Differences between acute andchronic wound healing
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 Marjolins 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 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
Determine the potential for healing
Blood supply
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Determine the potential for healing
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:
Treat the wound
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
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, di
