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

Skin
Two 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
Free Flap Distant pedicle Transposition flap (Regional pedicle) Full thickness Graft Split Skin graft Secondary intention Primary intention

Wound Healing
Phases

chemotaxis

granulation

epithelisation

Dynamic process Different phases occur concurrently

Wound Healing
Heamostasis

Haemostasis
Active bleeding stopped, Platelets plug vessels

Wound Healing
Inflammatory phase

Inflammatory phase

Neutrophils and Macrophages attracted to wound site Cytokines initiate repairs Phagocytosis of dead tissue and contaminants Growth factors initiate Angiogenesis

Wound Healing
Proliferative 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 Healing
Maturation 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 Healing
Impaired healing

Infection Contamination

Wound Care

Formation of the scab and rate of epithelialisation of superficial wounds in the skin of the young domestic pig Winter (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 tree Modern dressings

Wound Management Products Conventional Novel
M dicat d V.A.C. Tissue Culture

Granufl x uoderm cutinova

Allevyn Mepilex Lyofoam

Integra Transcyte Dermal matrices

IGF Beclaperamin

Al inates

Hydrogels

Kaltostat orbsan Al osteril

Intrasite Granugel Purilon NU Gel

Film dressings

Tegaderm Opsite epiview

Hydrocolloids

Paraffi

ll

M alt I adi Bacti ras

oam

lai

Keratinocytes

Skin replacements

Growt Factors

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

Uses
Necrotic and sloughy wounds which require autolysis Sinus s where alternatives are not effective

Donate water into wound to rehydrate devitalised tissue

Foam dressings
Polyurethane foam
Different 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 Closure V.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 application Ready 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
Pressure sores (Decube- Latin to lie down)

Leg ulcer
Venous Arterial Mixed Diabetic

Neoplasm

Pressure sores
bone

Direct causes
Pressure Shear Friction
skin

95% Preventable?? (Hibbs

1987)
bed McClemont cone

Cost to NHS up to 380 million

Pressure sores
Causes Pressure
Interface pressure
Mattress - skin
Skin - sub dermal tissues Sub dermal tissue bone
Pressure increases 3 to 5 times that measured at skin

Capillary closing pressure

Mean 26mmHg

Pressure > 26mmHg causes occlusion of vessels > tissue Ischaemia & hypoxia

Pressure sores
Causes
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

Shear

Heath 1995

Pressure Sores
Causes 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 3 Full thickness loss Crater / Sinus

Stage 2 Partial Thickness loss

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 sores
Estimating 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 Arterial Mixed Other

70% 10% 15% 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 Ulcer
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

Management

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 ulcers
Signs
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 ulcers
Wound 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 1992 Palliative 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 anatomy epidermis

Skin anatomy

Burn depth

Depth of injury

Three Zones of injury Coagulation Stasis Hyperemia

Zone of Stasis liable to convert conversion and deeper wound Jackson 1953

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 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
Conservatively Frequent dressings PT areas heal No 2nd wound ? More prone to hypertophy Early surgery SSG healed by 2nd week Larger area may be debrided Two wounds
Graft & donor

SSG contracts
Will require reconstruction

Conservative treatment
Advantages Can be treated on out patient basis PT areas heal allowing ft areas to de-mark No 2nd wound Disadvantages Requires frequent dressings ? More prone to hypertophy Dressings may be unmanageable at home

Early treatment
Advantages SSG healed by 2nd week Shorter treatment time Disadvantages 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 dressings
Obtained from either donated human cadaver (Allograft) animal (Xenograft)

Biological dressings,
First reported use Girdner 1881 Popular use in major burns from 1950
Brook army medical centre

Allograft

Described as

The Gold Standard for covering large Burn wounds

(Herndon 1997)

Biological dressings,
Allograft other donor Obtained in same manner as
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 exist
Sheriden & Tompkins. Burns 25, 1999

Synthetic dressings
Dressing

Synt etic

Bioengineered

Biobrane

Transcyte

CEA

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 20C or -70 C 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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