WOUND ASSESSMENT PROF. DR. HARIKRISHNA K.R.NAIR S.I.S KMN MD(UKM) - - PowerPoint PPT Presentation

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WOUND ASSESSMENT

• PROF. DR. HARIKRISHNA K.R.NAIR S.I.S KMN

MD(UKM) FRCPI ICW (GERMANY)OSH(NIOSH) OHD(DOSH) CMIA(MAL) FCWCS Post Grad in Wound Healing & Tissue Repair (Cardiff, UK) CHM(USA) ESWT (Austria , Germany) FMSWCP

WOUND CARE UNIT, DEPT OF INTERNAL MEDICINE, KUALA LUMPUR HOSPITAL ADJUNCT PROFESSOR, IMS, BHU, INDIA ADJUNCT RESEARCH ASSOC. PROFESSOR, PERDANA UNIVERSITY

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KUALA LUMPUR HOSPITAL

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Different etiology of wound

Burn Pressure Ulcer Diabetic Foot Ulcer Venous Leg Ulcer Trauma Dehiscence Minor burn

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Haemostasis Chronic Wound Healing Inflammation Proliferation Remodeling

Phases

Minutes Days Weeks Year +

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General assessment: The general assessment is to identify and eliminate any

underlying causes or contributing factors which may impede the wound healing process; the causes include:

• Age (extremes of age )
• Diseases or co morbidities (e.g. diabetes mellitus , renal

impairment )

• Medication (steroids , chemotherapy )
• Obesity
• Nutrition (refer to chapter on nutrition)
• Impaired blood supply (refer to chapter on arterial and

venous ulcers )

• Lifestyle (smoking , alcohol)

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Assessment of patient

Comprehensive Assessment Multidisplinary approach

Complicating condition

• Vascular problem
• Diabetic
• Smoking
• Immunosuppressive

Pain / Comfort Hygiene Stress Psychosocial Health Wound Etiology

• Pressure / trauma
• Shearing / friction

Nutritional status

• Protein
• Vitamins

Medications Age

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Local assessment is an ongoing process and should include:

• A review of the wound history (How, What,

When, Where, Who)

• Assessment of the physical

wound characteristics

• location, size, base/depth
• presence of pain
• condition of the wound bed

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Wound Appearance - THE COLOUR MODEL

• It is necessary to have a method to appraise the types of wound

without having to resort to specialised histologists for each and every wound.

• The colour method is used to identify and prioritise the treatment
• bjectives in wounds and is also used in research.
• In the early 80s, Lars Hellgrens, a Sweden dermatologist, was the first

to claim that wounds could be categorised according to the colour of the wound surface.

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Black - Necrotic Yellow - Slough Red - Granulation Pink - Epitheliazation

Wound Appearance - THE COLOUR MODEL

Triangle of Wound Assessment

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Triangle of Wound Assessment

Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International 2015

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Triangle of Wound Assessment –Wound bed

Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International 2015

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WOUND BED PREPARATION

Debridement Bacterial Balance Exudate Management

• Dr. Gary Sibbald, et al

‘Preparing the wound bed for healing – debridement, bacterial balance & moisture balance’

Ostomy/ wound management 2000, 46(1)

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TIME –THE CLINICAL ASPECTS

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*T.I.M.E. - Principles of Wound Bed

Assessment and Preparation:

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TIME*+ - Principles of Wound Bed Preparation

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Triangle of Wound Assessment –Wound edge

Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International 2015

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Triangle of Wound Assessment – Periwound skin

Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International 2015

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https://incem.rwth-aachen.de/beneficiaries.html

Migration for healthy skin

Option to use these both.. One here, one at the end of slides as closing?

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Triangle of Wound Assessment – Management plan

Dowsett C et al. Triangle of Wound Assessment Made Easy. Wounds International 2015

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Clinical Appearance: Stage 3 pressure ulcer

Black – necrotic tissue Red – granulation tissue Yellow - slough Exudate – moderate (purulent) with odour Pink – Epithelial tissue Edges - undermining Size 12 x 8 x 1 cm Site – sacral region

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Advancing epidermal margin (epithelialisation)

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TIME (T = Reflects Tissue Viability)

• Viable (granulation, epithelialising)
• Non viable (necrotic, slough, eschar)

How does non viable tissue impede healing?

• Prolongs inflammation
• Impedes epithelialisation
• Antibiotics don’t penetrate to the wound environment
• Dressings are unable to effect the wound millieu
• Medium for bacteria growth

Goals in treating tissue in chronic wounds

• Clear away dead or necrotic tissue – debridement
• Always ensure adequate tissue oxygenation for angiogenesis and

granulation process

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Tissue Non Viable: Necrosis,

Eschar,Slough

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Debridement

Debridement is not a single event - an “initial phase” and a “maintenance phase”. Debridement is an ongoing process.

• V. Falanga, 2000

T

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Method of Debridement (Removal)?

Surgical / scalpel? Mechanical? Enzymatic? Autolytic? Biological? Combination?

Surgical debridement is gold standard of care, once ischemia is excluded.

(Wagner 1984, Knowles 1997, Laing 1994, Steed 1996,, Levin 1996). Hydro surgery debridement machine (eg. Versajet)

T

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Selecting a method of debridement

Characteristic Autolytic Surgical Enzymatic Mechanical

Speed 4 1 2 3 Tissue selectivity 3 2 1 4 Painful wound 1 4 2 3 Exudate 3 1 4 2 Infection 4 1 3 2 Cost 1 4 2 3 Debridement method

Table from Sibbald et al. 2000 1 = most appropriate; 4 = least appropriate

T

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Autolytic Debridement

Definition -The process by which the wound bed utilizes phagocytes and proteolytic enzymes to remove non- viable tissue This process can be promoted and enhanced by maintaining a moist wound environment.

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1 2 3

Autolytic debridement

After 2 days After 4 days

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* As a selective type of debridement, autolysis removes

• nly necrotic tissue

Autolytic Debridement – Hydrogel

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MODE OF ACTION –HYDROGEL

Contains:

Cross-linked carboxymethylcellulose 2.3% Propylene Glycol USP 20.0% Purified Water 77.7 %

• Gently rehydrates

dry necrotic tissue

• Provides moist

wound healing environment

• Softens necrotic

tissue

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Surgical Debridement

• Scalpel/Scissors
• Curet
• Laser
• Hydrosurgery (Versajet)
• Recommended for removal of thick,

adherent eschar and devitalized tissue in large wounds

• Not recommended in severely

compromised patients

• Analgesia/anesthesia may required

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Enzymatic Debridement

• The use of topically applied

enzymatic agents to stimulate the breakdown of non-viable tissue

• Faster debridement process

compared to Autolytic

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TIME (I = Inflammation, Infection)

• Persistent inflammation “wounds become stuck”
• The bacterial continuum
• What is infection?
• How does infection differ between the acute and chronic

wound?

• What factors need to be considered?

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Assessing wound infection

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Clinical Presentation of local wound infection

“Classic” signs & Symptoms

• Advancing erythema
• Fever
• Warmth
• Edema / swelling
• Pain
• Purulence

“Secondary” signs & symptoms

• Delayed healing
• Change in color of wound bed
• Absent/ abnormal granulation

tissue

•  or abnormal odor
•  serous drainage
•  pain at wound site

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Infection Every second counts!

E.coli divide every 20min, therefore a single organism divides into 512 daughter cells in 3hrs or 1,000,000 under 8 hrs

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TIME(M = Moisture Imbalance)

• Desiccation / Maceration
• Composition of chronic wound fluid
• Matching exudate volume with product absorbency for
• ptimal moisture balance

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Optimal Moisture Balance

Maceration Desiccation

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Chronic Wound Fluid Edema Bacterial Burden Breakdown of Necrotic tissue Bioburden control Compression Debridement

Exudate Management

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None Low Moderate Heavy

Exudate Management

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Material Conserve/ Donate Fluid Control Light Moderate High Films

√ √

Sheet hydrogel

√ √

Amorphous hydrogel

√ √

Hydrocolloids

√ √

Sheet foams

√ √ √

Cavity foams

√ √

Alginates

√ √

Hydrofiber

√ √

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TIME E = Edge of Wound

• Non advancing wound edge = non

healing wound

• Undermining (critically colonised or

infected)

• Persisting inflammation
• Non responsive cells

REVIEW T/I/M Factors

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What if the epidermis fails to advance?

Reconsider the principles of Wound Bed Preparation and the acronym TIME:

• Has necrotic tissue been debrided?
• Is there a well vascularised wound bed?
• Has infection been put under control?
• What is the status with inflammation?
• To what level has moisture imbalance been corrected?
• What dressings have been applied?

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FACTORS AFFECTING WOUND HEALING

Systemic Factors Local Factors

Metabolic disorders

• DM , Renal failure

Necrosis , Scab Respiratory disorders (COAD ) Infection Circulatory disorders Anaemia , CCF Prolonged inflammation Immune deficiency HIV , RA ,malignancy Exudate Immunosuppressive therapy Cellular dysfunction Nutritional state Dehydration , vitamin deficiency Biochemical imbalance –pH Medications ( steroids , anti coagulants ) Hypoxia

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Psychological factors Lifestyle factors Stress & anxiety Age Depression Employment Motivation & concordance Hobbies/Interests Factitious injury (intentional / unintentional) Cultural / Religious beliefs Sleep deprivation Financial status

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ABERRANT WOUND HEALING

• Exuberant

granulation

• Hypertrophic Scar
• Keloid formation
• Contracture

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Wound Documentation

Aim of Documentation

• Record the history
• Identify etiological factors
• Identify intrinsic and extrinsic factors that may affect wound

healing

• Obtain a baseline for future comparison
• Provide a legal and organizational record
• Use in evaluation and planning of wound management
• Monitor wound progress
• Communication tool

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Principles of Documentation

• Timely, Accurate and objective
• Concise and Comprehensive
• Legible writing, Include signature and printed name
• Use only organizationally approved abbreviations and colloquialisms
• Regular, Systematic, Standardized, Easily interpreted And Time efficient
• Used to inform management decisions

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Clinical Case 1

28/7/01 3/9/01 25/2/02

5/9/02

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Clinical Case 2

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Clinical Case 3

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Clinical Case 4

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Clinical Case 5

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Clinical Case 6

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Surgical debridement is the gold standard of care , once ischaemia is excluded. –Wagner 1984 , Laing 1994 , Steed 1996 , Levin 1996, Knowles 1997

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SILVER

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FOAM DRESSING

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SILVER

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FOAM DRESSING

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EXUDRY – EXUDATE MANAGEMENT

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CASE 7

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THANK YOU FOR YOUR KIND ATTENTION