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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