Dr Yap Gaik Chin 
Wound Care Team 
Surgical Department
 Management of non healing wound is a 
complex process and requires a 
multidisciplinary approach 
 Starts from the first assessment upon 
inspection of patient by making a general 
assessment and further local assessment of the 
wound
 Assessment ( General & local ) 
 TIME – wound bed preparation 
 Wound cleansing 
 Types of debridement 
 Types of dressing
 Age 
 Psychosocial health 
 Complicating conditions 
 vascular problem, diabetic, smoking, 
immunosuppressive 
 Nutritional status 
 Pain/Comfort 
 Hygiene
 Wound etiology 
 Pressure, trauma, shearing, friction 
 Size 
 Wound edges 
 Wound Bed 
 necrotic, granulation tissue, odour, exudate 
 Surrounding skin ( colour, moisture)
 In early 1980s, Lars Hellgrens, a Sweeden 
dermatologist was the first to claim that 
wounds could be categorised according to the 
colour of the wound surface 
 Red-Granulation 
 Yellow-Slough 
 Pink-Epithelialization 
 Black-Necrotic
 Mnemonic for Principles of Wound Bed 
Preparation 
 What is wound bed preparation? 
 Management of wound to accelerate 
endogenous healing or facilitate the 
effectiveness of other therapeutic measures
 T : Tissue Viability 
 I : Inflammation, Infection 
 M : Moisture Imbalance 
 E : Epidermal Margin/ Edge of Wound
 Viable ( Granulation, Epithelialising) 
 Non viable ( Necrotic, Sloughly, Eschar) 
 How does non viable tissue impede healing? 
 Prolongs inflammation 
 Impedes epitheliazation 
 Medium for bacteria growth
 Clear away dead or necrotic tissue 
 Debridement 
 Always ensure adequate tissue oxygenation 
for angiogenesis and granulation process
 The bacterial continuum 
 What is infection? 
 End spectrum of bacterial continuum , more 
infected than critically colonized wound 
 Assessing of wound infection 
1. Contamination 
2. Colonized 
3. Critically colonized 
4. Infection ( Local, Systemic)
 Classic Presentation of infection of local wound 
1. Advancing erythema 
2. Fever 
3. Warmth 
4. Oedema/ Swelling 
5. Pain 
6. Purulence
 Secondary clinical presentation of local wound 
1. Delayed healing 
2. Change in colour of wound bed 
3. Absent/abnormal granulation tissue 
4. ↑ or abnormal odour 
5. ↑ drainage/exudate 
6. ↑ pain @ wound site
 Too much moisture –impede wound healing 
 Cause Dessication / Maceration of skin 
 Need to match exudate volume with product 
absorbency for optimal moisture balance
 Non advancing wound edge 
 Also known as non healing wound 
 Undermining of edge is either critically 
colonised or infected
 Reconsider the principles of wound bed 
preparation and the acronym TIME, 
1. Has necrotic tissue been debrided? 
2. Is there a well vascularised wound bed? 
3. Has infection been adequately controlled? 
4. What is the status of inflammation or 
infection in this patient? 
5. How well is moisture balance optimized? 
6. What dressings have been applied before?
 Removing foreign debris & necrotic tissue 
 The process of removing inflammatory 
contaminants from the wound surface since 
necrotic tissue, excess exudate and foreign 
objects impede healing & ↑ the risk of infection 
 Routine cleansing ( Fluid irrigation, mild scrub) 
 Debridement
 Antibiotic should be used to reduce bacterial 
level within the wound 
 Selection of antibiotic is based upon proven 
efficiency against microorganisms obtained 
from culture.
 Saline 
 Octanisept 
 Superoxide solution 
 Water for irrigation 
 PHMB with Betaine
 Antiseptics should not be used to clean 
wounds 
 Topical antiseptics: 
1. Betadine 
2. Povidone-Iodine 
3. Dakin’s Solution ( Eusol) 
4. Acetic Acid-> effective against Pseudomonas 
A organisms 
5. Hydrogen Peroxide
 A method of high pressure irrigation which is a 
gentle mechanical action to loosen debris and 
necrotic tissue
 Wound healing is impaired due to prolong 
inflammation 
 Necrotic tissue –culture medium for bacteria 
 Amtibiotics do not reach the wound milieu 
 Dressings especially antimicrobial or silver do 
not reach wound bed 
 For staging of undetermined stage pressure 
ulcer
 Surgical 
 Mechanical 
 Autolytic 
 Enzymatic 
 Biological 
 Maggot Debridement Therapy( MDT)
 Wound bed utilizes phagocytes and proteolytic 
enzymes to remove non viable tissueining a 
moist environment 
 This process can be promoted and enhanced by 
maintaining a moist environment
 Recommended for removal of thick, adherent 
eschar and devitalized tissue in large wounds 
 Not recommended in severely compromised 
patients 
 Analgesia / anaesthesia may be required
 The use of topically applied enzymatic agents 
to stimulate the breakdown of non viable tissue 
 Faster debridement process compared to 
autolytic 
 Eg: Honey, Prolase dressing
 Used for decades where dressings are allowed 
to proceed from moist to dry 
 Manually removing the dressing causes a form 
of non selective debridement 
 Works best on wounds with moderate 
amounts of necrotic debris
 Small maggots are introduced to a wound to 
consume necrotic tissue 
 Able to debride a wound within 1-2/7 
 The maggots derive nutrients through a 
process called ` extracorporeal digestion’
 Protect wound from trauma or microbial 
contamination 
 Absorb drainage and debride wound 
 Control & prevent haemorrhage ( pressure 
dressing) 
 Reduce pain 
 Maintain temperature and moisture of wound 
 Provide psychological comfort
 Traditional 
 Conventional 
 Leaves, herbs, Honey, Gauze 
 Advanced/ environmental dressings 
I. more expensive 
II. Can be left in situ for several days 
III. Films, Alginates, Silver, Hydrogels, Foams, 
Hydrocolloids, Charcoals
 Safe and easy to use 
 Remove excess exudate 
 Provide thermal insulation 
 Trauma protection 
 Provide barrier to pathogens 
 Allow gaseous exchange 
 Water proof 
 Non adherent 
 Maintain moist wound healing environment
 The Compendium of Wound Care Dressings in 
Malaysia, Volume 2 , Harikrishna K.R Nair
Wound management

Wound management

  • 1.
    Dr Yap GaikChin Wound Care Team Surgical Department
  • 2.
     Management ofnon healing wound is a complex process and requires a multidisciplinary approach  Starts from the first assessment upon inspection of patient by making a general assessment and further local assessment of the wound
  • 3.
     Assessment (General & local )  TIME – wound bed preparation  Wound cleansing  Types of debridement  Types of dressing
  • 4.
     Age Psychosocial health  Complicating conditions  vascular problem, diabetic, smoking, immunosuppressive  Nutritional status  Pain/Comfort  Hygiene
  • 5.
     Wound etiology  Pressure, trauma, shearing, friction  Size  Wound edges  Wound Bed  necrotic, granulation tissue, odour, exudate  Surrounding skin ( colour, moisture)
  • 6.
     In early1980s, Lars Hellgrens, a Sweeden dermatologist was the first to claim that wounds could be categorised according to the colour of the wound surface  Red-Granulation  Yellow-Slough  Pink-Epithelialization  Black-Necrotic
  • 7.
     Mnemonic forPrinciples of Wound Bed Preparation  What is wound bed preparation?  Management of wound to accelerate endogenous healing or facilitate the effectiveness of other therapeutic measures
  • 8.
     T :Tissue Viability  I : Inflammation, Infection  M : Moisture Imbalance  E : Epidermal Margin/ Edge of Wound
  • 9.
     Viable (Granulation, Epithelialising)  Non viable ( Necrotic, Sloughly, Eschar)  How does non viable tissue impede healing?  Prolongs inflammation  Impedes epitheliazation  Medium for bacteria growth
  • 10.
     Clear awaydead or necrotic tissue  Debridement  Always ensure adequate tissue oxygenation for angiogenesis and granulation process
  • 11.
     The bacterialcontinuum  What is infection?  End spectrum of bacterial continuum , more infected than critically colonized wound  Assessing of wound infection 1. Contamination 2. Colonized 3. Critically colonized 4. Infection ( Local, Systemic)
  • 12.
     Classic Presentationof infection of local wound 1. Advancing erythema 2. Fever 3. Warmth 4. Oedema/ Swelling 5. Pain 6. Purulence
  • 13.
     Secondary clinicalpresentation of local wound 1. Delayed healing 2. Change in colour of wound bed 3. Absent/abnormal granulation tissue 4. ↑ or abnormal odour 5. ↑ drainage/exudate 6. ↑ pain @ wound site
  • 14.
     Too muchmoisture –impede wound healing  Cause Dessication / Maceration of skin  Need to match exudate volume with product absorbency for optimal moisture balance
  • 15.
     Non advancingwound edge  Also known as non healing wound  Undermining of edge is either critically colonised or infected
  • 16.
     Reconsider theprinciples of wound bed preparation and the acronym TIME, 1. Has necrotic tissue been debrided? 2. Is there a well vascularised wound bed? 3. Has infection been adequately controlled? 4. What is the status of inflammation or infection in this patient? 5. How well is moisture balance optimized? 6. What dressings have been applied before?
  • 17.
     Removing foreigndebris & necrotic tissue  The process of removing inflammatory contaminants from the wound surface since necrotic tissue, excess exudate and foreign objects impede healing & ↑ the risk of infection  Routine cleansing ( Fluid irrigation, mild scrub)  Debridement
  • 18.
     Antibiotic shouldbe used to reduce bacterial level within the wound  Selection of antibiotic is based upon proven efficiency against microorganisms obtained from culture.
  • 19.
     Saline Octanisept  Superoxide solution  Water for irrigation  PHMB with Betaine
  • 20.
     Antiseptics shouldnot be used to clean wounds  Topical antiseptics: 1. Betadine 2. Povidone-Iodine 3. Dakin’s Solution ( Eusol) 4. Acetic Acid-> effective against Pseudomonas A organisms 5. Hydrogen Peroxide
  • 21.
     A methodof high pressure irrigation which is a gentle mechanical action to loosen debris and necrotic tissue
  • 22.
     Wound healingis impaired due to prolong inflammation  Necrotic tissue –culture medium for bacteria  Amtibiotics do not reach the wound milieu  Dressings especially antimicrobial or silver do not reach wound bed  For staging of undetermined stage pressure ulcer
  • 23.
     Surgical Mechanical  Autolytic  Enzymatic  Biological  Maggot Debridement Therapy( MDT)
  • 24.
     Wound bedutilizes phagocytes and proteolytic enzymes to remove non viable tissueining a moist environment  This process can be promoted and enhanced by maintaining a moist environment
  • 25.
     Recommended forremoval of thick, adherent eschar and devitalized tissue in large wounds  Not recommended in severely compromised patients  Analgesia / anaesthesia may be required
  • 26.
     The useof topically applied enzymatic agents to stimulate the breakdown of non viable tissue  Faster debridement process compared to autolytic  Eg: Honey, Prolase dressing
  • 27.
     Used fordecades where dressings are allowed to proceed from moist to dry  Manually removing the dressing causes a form of non selective debridement  Works best on wounds with moderate amounts of necrotic debris
  • 28.
     Small maggotsare introduced to a wound to consume necrotic tissue  Able to debride a wound within 1-2/7  The maggots derive nutrients through a process called ` extracorporeal digestion’
  • 29.
     Protect woundfrom trauma or microbial contamination  Absorb drainage and debride wound  Control & prevent haemorrhage ( pressure dressing)  Reduce pain  Maintain temperature and moisture of wound  Provide psychological comfort
  • 30.
     Traditional Conventional  Leaves, herbs, Honey, Gauze  Advanced/ environmental dressings I. more expensive II. Can be left in situ for several days III. Films, Alginates, Silver, Hydrogels, Foams, Hydrocolloids, Charcoals
  • 31.
     Safe andeasy to use  Remove excess exudate  Provide thermal insulation  Trauma protection  Provide barrier to pathogens  Allow gaseous exchange  Water proof  Non adherent  Maintain moist wound healing environment
  • 32.
     The Compendiumof Wound Care Dressings in Malaysia, Volume 2 , Harikrishna K.R Nair

Editor's Notes