Download - Wound Healing
Wound Healing
Dr. Ateesh Borole Deptt of Plastic Surgery
Overview• Anatomy of Skin and its function• Wound healing in history• Factors influencing wound healing and
breakdown• Nursing management • Plastic / reconstructive surgery
A wound is
A loss of continuity of the skin or mucous membrane, which may involve soft tissues, muscle bone and other anatomical structures Collier 1994
Woundcare in History• Earliest documented evidence 1700 BC
– Smith Papyrus• Honey
• Sasruta ~600BC performed rhinoplasty• Hippocrates - debridement• Celsus AD 37- cardinal signs of infection
Woundcare in history• Pasteur • Lister
• War
Role of Skin•Largest organ of body – 2m2
•1 – 2 mm thick except in specialised areas
•Protective role – first line of defence• Keeps good stuff in
• Keeps bad stuff out
•Principal organ responsible for thermoregulation
•Vitamin D synthesis
•Spatial awareness from tactile stimulation
SkinTwo distinct layers
Epidermis Dermis
Epidermis waterproof
protective barrier of keratinocytes
Dermis strong tensile
base Collagen, GAG
complex
Epidermis
Wound assessment• Site• Environment• Appearance (phase of healing)• Wound aetiology• Clinical manifestation• Health care system
Wound site• Which tissues are involved?• Where is the wound• Does it require any special techniques to treat
Environment• Internal
– Nutritional status– Age– Drug history
• External– Location – Facilities– Mobility
Appearance (Phase of healing)
• What tissue is apparent in the wound• Heamostasis• Inflammation• Granulation• Autolysis- Slough• Epithelium
Wound aetiology• Type of wound
• Acute– Trauma– Burn
• Chronic– Pressure sore– Leg ulcer– Malignancy– Diabetic ulcer
Wound aetiology– Sinus formation– Abcess– Cavity
Clinical manifestations• Slough• Necrosis• Odorous• Infected/colonised• Exudate production
Health Care System• Context• Community or Hospital• Some products only available in hospital
• E.g. Larvae• Growth factor
• Community• Compression bandages
Wound care“The Plastic Surgery ladder”
P rim ary in ten tion
S econ d ary in ten tion
S p lit S k in g ra ft
F u ll th ickn ess G ra ft
Tran sp os it ion flap (R eg ion a l p ed ic le )
D is tan t p ed ic le
F ree F lap
Wound HealingPhases
• Dynamic process• Different phases occur concurrently
granulation epithelisationchemotaxis
Wound Healing Heamostasis
• Haemostasis– Active bleeding stopped, Platelets plug vessels
Wound HealingInflammatory phase
• Inflammatory phase• Neutrophils and Macrophages attracted to wound site• Cytokines initiate repairs• Phagocytosis of dead tissue and contaminants• Growth factors initiate Angiogenesis
Wound HealingProliferative phase
• Proliferation– Fibroblasts from surrounding dermis enter wound– Collagen and GAG is laid down in wound– Keratinocytes from wound margins and deep hair follicles
differentiate to cover wound with epithelium– Myofibroblasts migrate from muscle and encourage wound
Contraction
Wound HealingMaturation Phase
• Maturation– Normally occurs around three weeks – Can last up to 2 years– Remodelling of dermis
– Collagen III to Collagen I – Blood vessels rationalised– Scar shrinks, becomes paler and flatter
Wound HealingImpaired healing
•Infection•Contamination
Wound Care
Formation of the scab and rate of epithelialisation of superficial wounds in the skin of the young
domestic pigWinter (1962) Nature 193: 293-294
Ideal wound dressing• Morison (1992)
– Non adherent– Impermeable to bacteria– Capable of maintaining a high humidity at the wound site while
removing excess exudate– Thermally insulating– Non-toxic and Non-allergenic– Comfortable and conformable– Capable of protecting the wound from further trauma– Requires infrequent dressing changes– Cost effective– Long shelf life– Available in both hospital and community
Wound Care Materials• Grouped according to form or function
• E.g. Hydrocolloids, foams etc• for superficial wounds, high exudate wounds
Wound product treeModern dressings
P ara ffin Tu lle
p la in
M esa ltIn ad in e
B ac tig ras
M ed ica ted
G ran u flexD u od ermcu tin ova
H yd roco llo id s
A llevynM ep ilexL yofoam
F oam
K altos ta tS orb sanA lg os teril
A lg in a tes
In tras iteG ran u g e l
P u rilonN U G e l
H yd rog e ls
Teg ad ermO p s iteep iview
F ilm d ress in g s
C on ven tion a l
V .A .C .
K era tin ocytes
Tissu e C u ltu re
In teg raTran scyte
D erm al m atrices
S k in rep lacem en ts
IG FB ec lap eram in
G rowth F ac tors
N ove l
W ou n d M an ag em en tP rod u c ts
Alginates• Derived from brown seaweed• Dressings contain sodium alginate / Calcium alginate or both• Wound fluid interacts with dressing causing dressing to gel• haemostatic
• Uses– High exudate wounds
• Eg leg ulcers, sinuses
– Easy removal • Good for painful wounds
• Caution• Low exudate wounds• Infected wounds
Hydrocolloids• Carboxymethycellulose, gelatin and pectin• Normally adhesive• Prolonged contact with wound causes dressing to gel• Waterproof barrier on surface makes dressing occlusive and
impermeable
• Uses– Light to moderately exuding wounds
– Grade l-ll presure sores– Minor burns
• Easy removal– But can cause trauma to surrounding tissue
• Commonly Ruck up
Hydrogels• Amorphous hydrophilic gels containing large amounts of
water• Except Nu-Gel
• Donate water into wound to rehydrate devitalised tissue
• Uses– Necrotic and sloughy wounds which require
autolysis– Sinus’s where alternatives are not effective
Foam dressings• Polyurethane foamDifferent compositions give varying characteristics
• Absorb wound fluid therefore reducing maceration• Provide thermal insulation
• Low to high exudate wounds• Cavity dressings available
• Some foams have adhesive backing
Films• Semi permeable allow moisture vapour to
pass from wound• Can be used as secondary dressing• Used prophylactically to prevent shearing
Novel therapies• Large wounds take months to heal• Financial cost is large• Human cost is huge
Vacuum Assisted ClosureV.A.C.
• Developed by Argenta & Morykwas
• First published results 1997
• Intermittent negative pressure of 125mmHg improved granulation by 104% (Banwell 1999)
• Dressings stay in place for up to five days
V.A.C
• Improves local blood flow
• Removes wound fluid and interstitial oedema
• Promotes granulation• Reduces bacterial
count in wound• Reverse tissue
expansion
Indications for V.A.C.• Acute wounds –
– Dehisced wounds– Limb trauma
• Chronic wounds –– Pressure sores– Leg ulcers
• Adjunct to Surgery– Preparation of wound bed, reduction in wound size
• Salvage• Burns
Contraindications• Neopasia• Anti coagulated / Patients with coagulopathy
with caution
Wound treated with V.A.C.
Dehisced Abdominal wound
14 days post application 4 weeks post applicationReady for skin graft
Growth Factors• Predominately produced by macrophages in
wound• Excitement- topical growth factors have
potential to speed up wound healing• In vitro results very encouraging• Clinical trials have proved disappointing• Currently only one preparation licensed
– Beclapermin – ILGF-1
Wound types
Chronic & Acute
Chronic wounds• Decubitus Ulcer (Decube- Latin to lie down)
• Pressure sores
• Leg ulcer• Venous• Arterial• Mixed• Diabetic
• Neoplasm
Pressure sores
• Direct causes• Pressure• Shear• Friction
• 95% Preventable?? (Hibbs 1987)
• Cost to NHS up to £380 million
bed
skin
bone
‘McClemont cone’
Pressure soresCauses
• Pressure– Interface pressure
• Mattress - skin– Skin - sub dermal tissues
» Sub dermal tissue – bone
• Capillary closing pressure» Mean 26mmHg
• Pressure > 26mmHg causes occlusion of vessels > tissue Ischaemia & hypoxia
Pressure increases 3 to 5 times that measured at skin
Pressure soresCauses
– Permanent damage occurs after 1 hour
• Shear Forces– Only occur in conjunction with Pressure– Body moves but skin remains motionless against
surface– Typically occurs when patient slides down bed or in
chair– Blood vessels damaged or broken
Heath 1995
Shear
Pressure SoresCauses
• Friction– Occurs when shearing force overcome– Patient skin slides– Distortion cause tissue damage – Heat dissipates into skin– Abrasive action damages surface– MANUAL HANDLING!!
Pressure Sore assessment• Various grading systems in use• Reasons for use
– Reid & Morison (1994)• To allow clinical staff from other disciplines to record and review
progress of a pressure sore without ambiguity• To audit pressure sores so that comparisons can be made between
different clinical situations and institutions• To allow comparisons to be in clinical trials of wound dressings,
pressure relieving surfaces and beds
UK Consensus Classification
Stage 1
Non Blanching Erythema
Stage 2
Partial Thickness loss
Stage 3
Full thickness loss
Crater / Sinus
Stage 4
Full thickness loss extending to bone
Pressure Sores Prevention / Minimising the Risk
• Prevention better than cure!• Understand the causes
• Extrinisic causes• Nutrition• Physical health
• Assess, re-assess, re-assess• Ensure on right surface
Pressure soresEstimating risk
• Various risk assessment tools available• None replace clinical judgement• Norton and Waterlow in popular use• Norton perceived as too simplistic• Tools based on identifying risk factors• Bed policies often based on outcomes
Waterlow
Beds
• Need depends on risk Mattress replacements
Low air Loss beds
With pulse
High air loss
Air fluidised beds
Leg ulcers• Classified into
• Venous 70%• Arterial 10%• Mixed 15%• Other 5%
• 400,000 patients (Fletcher 1992)
• 1% of patients treated in hospital• Up to 50% of District Nurse time spent treating leg
ulcers
Assessment• History
– Diabetes– DVT– Leg fractures– Intermittent claudication– Duration of this ulcer– Previous ulcers??
• Doppler ultrasound– ABPI (Ankle Brachial Pressure index)
Venous Ulcers• Normally venous system in legs pumps blood back to
heart• Damage to veins or incompetent valves leads to
backlog of blood• Legs become oedematous and discoloured as
Haemoglobin leaks from RBC’s• Ulcers often in gaiter region widespread but flat in
appearance• ABPI >0.8
Venous UlcerManagement
• Aim is to compensate for damage venous ‘pump’• Graduated compression most effective• Patients with ABPI >0.8 compression therapy
• Caution calcification of vessels may give false ABPI
• Four layer or single layer systems available• Surrounding skin often fragile, treat eczema
Arterial ulcers• Arterial insufficiency caused by
– Atherosclerosis– Embolism– PVD
• Poor tissue perfusion leads to ischaemia and ulceration.
Arterial ulcersSigns
• Absent pedal pulses• Poor capillary refill• Cold, shiny, hairless skin• Pain, Intermittent claudication• Usually around foot• Deep punched out appearance• Cliff like edges• Gangrene of distal joints• ABPI <0.5
Arterial Ulcer management
• Symptom relief• Wound dressing• Vascular Surgery
• Angioplasty• Bypass
Diabetic ulcers
• 750,000 IDDM’s – 4% will require Amputation– 6% will require ulcer care (Williams 1994)
• Main Causes– Peripheral neuropathy
– Build up of glucose metabolites in nerve cells (MacIntyre 1994)
– Peripheral vascular disease
Diabetic ulcer management• Identify cause• General control of Diabetes• Wound care
Neoplasm/Malignant ulcersWound management not wound healing
Present as skin cancers- MM,SCC, BCC Or fungating wounds e.g. breast
Wound management problems
• Painful• Freely bleed• Discharge +++• Malodourous
– Due to colonisation by anerobes
Aims
• Reduce pain• Minimise bleeding• Remove excess exudate• Control odour• Restore body symmetry
Grocott P 1992Palliative care
Wounds
Squamous Cell Carcinoma
1 week post graft
1year follow up
Pilonidal sinus
Acute wounds
Acute Wounds• Surgical• Trauma• Burns
Surgical wounds• Normally heal by primary intention• Sutured skin wounds stable at 5 days
Surgical wound dehiscence
• Dehisced wound requires debridement• Treated as cavity wound• Cavity dressing or V.A.C.
Sternotomy wound
Trauma• Bite wounds• Hand injuries• Pre tib lacerations• Projectile injuries• Gun wounds
Trauma
Dog bite to hand
Trauma
Trauma wounds• Puncture wounds should be admitted for
surgical exploration• Copious irrigation• Surgical debridement of devitalised tissue• Antibiotics if indicated
Burn Injury
Burns• 250,000 burn injuries per year• 175,000 seen in A&E• 10,200 admitted to Burn units
• 5600 adults• 4600 children
• 300 deaths per year (NBCR2001)
• 38 Regional burn units
Burn Types• Flame• Electrical• Chemical• Scald• Flash/explosions• Radiation• Cold
• Non Burn injury– Necrotising fasciitis– TENS– Stevens-Johnsons Syndome
Necrotising faciitis
• Skin infection caused by– Strep A– Polymicrobial
• Initially affects fascia only• Require prompt excision• Antibiotics• HBO proved useful with
polymicrobial strain
Skin anatomyepidermis
Skin anatomy
Burn depth
Depth of injury
Jackson 1953
•Three ‘Zones’ of injury
• Coagulation
• Stasis
• Hyperemia
•Zone of Stasis liable to convert conversion and deeper wound
Factors involved in wound conversion
• Local and systemic factors
• Local– Impaired blood
flow– Increased
inflammation– Surface dessication– Exudate buildup– trauma
• Systemic– Sepsis– Hypovolaemia– Malnutrion– Excess Catabolism– Chronic Illness
Superficial
• Bright red ‘angry’• Small blisters, easily
removed• Painful ++ sensitive to
air• Heal 7 – 14 days
• Minimal/ no scarring
Partial Thickness• Involve varying depths
through dermis• Upper ½ to deep
dermal
• Typically red, mottled• Large blisters• Blanches• Painful• 14 – 21 days to heal• Over 21 days prone to
scarring
Deep dermal
•Extends deep into dermis
• few epidermal cells survive
• blisters + / -
•Painful to touch
•6 weeks + to heal
Full thickness
• Involves all layers down to subcutaneous fat
• White/ brown waxy appearance
• Hb staining, coagulated blood vessels
• Normally requires skin graft
How to Treat??
Early surgery Conservative treatment
How to treat
• Frequent dressings
• PT areas heal
• No 2nd wound
• ? More prone to hypertophy
• SSG healed by 2nd week
• Larger area may be debrided
• Two wounds– Graft & donor
• SSG contracts – Will require
reconstruction
Conservatively Early surgery
Conservative treatment
Advantages• Can be treated on out patient basis• PT areas heal allowing ft areas to de-mark• No 2nd woundDisadvantages• Requires frequent dressings• ? More prone to hypertophy• Dressings may be unmanageable at home
Early treatment
Advantages• SSG healed by 2nd week• Shorter treatment timeDisadvantages• Larger area may be debrided• Two wounds
– Graft & donor
• SSG contracts – Will require reconstruction
• Large burns may not have suitable donor areas
Burn Dressings
Simon P Booth
Dressing options• Plain dressings
• Anti bacterial's
• Biological dressings
• Synthetic / engineered dressings
Plain dressings
• Tulle• Non adherents – mepitel, Telfa• Absorbents - Gamgee, Exudry• Hydrocolloids• Films - Opsite
Biological dressingsObtained from either
• donated human cadaver (Allograft)
• animal (Xenograft)
Biological dressings, Allograft• First reported use – Girdner 1881
• Popular use in major burns from 1950» Brook army medical centre
• Described as
• The Gold Standard for covering large Burn wounds
(Herndon 1997)
Biological dressings, Allograft• Obtained in same manner as other donor
organs• Stringent testing for HIV, Hep B• Available in two forms
»Cryopreserved»Glycerolised
• Preservation leaves cells nonviable• Restricted availability
Biological dressings, Xenograft• Readily available
• Pig skin• Available in various presentations, E-Z derm• High immunogenicity• Rejects 2-3 days• Popular in U.S.• ? Should be removed before 3rd day
Synthetic / bio-engineered dressings
• Easily available – no shortage• Ready off the shelf• Provide immediate but temporary wound
closure• ‘skin substitute’ ‘skin replacement’ or ‘skin
equivalent’
Ideal skin substitute
• Inexpensive• Long shelf life• Used off the shelf• Non antigenic• Durable• Flexible• Prevents water loss• Bacterial barrier
• Drapes well• Easy to secure• Grows with child• Applied in one
operation• Does not become
hypertrophic• Does not existSheriden & Tompkins. Burns 25, 1999
Synthetic dressings
S yn th e tic
B iob ran e Tran scyte C E A
B ioen g in eered
D ress in g
Integra
Biobrane• Semi-permeable membrane• Bilayer• Inner layer – nylon mesh
» Allows fibrovascular ingrowth
• Outer layer – silasitic (silicone foam)» Bacterial barrier
• Designed for superficial wounds
Transcyte• Formally known as Dermagraft TC• Temporary bilayer• Outer - silicon• Inner - neonatal fibroblasts seeded on nylon
mesh• Fibroblasts synthesise
» Collagen I III V» Fibronectin» GAG’s» Growth factors
Transcyte• Expensive• Needs to be stored at –20ºC or -70 ºC• Used for partial thickness/deep dermal
wounds
Transcyte
• Neonatal fibroblast seeded on mesh
• Cells synthesise ECM proteins
Transcyte
• Transcyte should be applied to clean wounds
• Viable wound surface
• Silicone layer removed days 12 – 14
Transcyte
Transcyte
Integra
• Bilayered ‘Artificial skin’• Epidermal layer of medical grade silicon• Dermal matrix of cross linked bovine Collagen
and Glycoaminoglycan (obtained from shark cartilage)
• Forms scaffold for infiltrating fibroblasts, macrophages and capillary bundles
Integra
• Fibroblasts degrade matrix laying down human collagen III and producing GAG
• Remodelling phase Collagen III Collagen I
Integra
Burn debrided to viable bed, Integra applied
Fibroblast infiltrate Integra and revascularise wound bed
Integra
Ultra thin SSG applied
Silicone layer removed
Integra
Integra
• Cost +++• Requires close supervision• Strict infection control• Excellent results• Total loss expensive
Cultured epithelial autograft
• Developed by Rheinwald & Green 1975• Large number of cells from small donor (1cm2)• Confluent keratinocytes in 3 weeks• Initial optimism tempered• CEA lacks adhesion molecules (desmosomes)• Fragile – can blister upto 6 months post appplication• Prone to infection• Expensive
Rapid autologous skin culture
• Developed in Perth, Aus• Normal donor site and SSG• SSG 4:1 mesh• Small piece of donor incubated in trypsin (30 mins)
to separate dermis & epidermis• Basal cells scrapped off epidermis and suspendedin
delivery medium• Sub-confluent Keratinocytes, sprayed or dripped on
to wound
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