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PROPRIETARY & CONFIDENTIAL

© 2018 ConvaTec Inc. TM indicates a trade mark of ConvaTec Inc

Wound

Management

An Update in Best

Practice

Margaret Armitage

Senior Medical Affairs

Specialist

ConvaTec UKI

Session content: Case study approach

Basic wound assessment and wound tissue type

classification

Overview of local wound factors that delay healing;

exudate, infection & biofilm

A practical approach on dressing selection

Wound Assessment

Acute….wounds expected to heal within a

predictable time span.

Eg: surgical wound, trauma wound

Chronic….a more long term wound. Slow or fails

to heal.

Eg: leg ulcer, pressure ulcer

Images used with permission from their respective owners.

Wound Assessment

Wound Depth

Superficial wounds….only the epidermis involved

Partial thickness wounds…..penetrate the

epidermis and dermis, expose nerve endings, &

can be painful & moist.

Full thickness wound….involves total loss of

epidermis and dermis, extending into

subcutaneous tissues, and sometimes down to

muscle, ligaments and bone.

Key point:

Wound healing is multifactorial and application of

any wound dressing is of little value unless all the

factors that may delay wound healing have been

assessed and addressed…

General factors that could delay wound healing…

Wound Assessment

One of the keys to successful wound management is careful and accurate assessment of the wound…

Knowledge

Your Nose…

Your Ears…

Your Mouth…

Your Eyes…

http://eslprograms.vcc.ca/ESLWEB/Mouth.gif

Wound Challenge… “Olive”


Local factors that could delay wound healing...

Excess Exudate

Infection

Biofilm

Oedema

Ischemia

Low oxygen levels

Elevated proteases

Neuropathy

Venous insufficiency

Slough / necrotic tissue


What is exudate?

Slow escape of liquid containing proteins and white

blood cells from blood vessels as a result of

inflammation. It is a normal part of the body’s

defence mechanism1.

Effects of exudate production on wound healing

Exudate assists healing2:

Prevents wound bed from drying

out.

Aids migration of tissue-

repairing cells.

Provides essential nutrients for

cell metabolism.

Assists separation of dead or

damaged tissue (autolysis).

Excess exudate may2:

Cause maceration of surrounding tissue.

Delay or prevent wound healing.

Cause subsequent breakdown and further deterioration of the wound bed.

Cause physical and psychosocial morbidity/increased demand on healthcare resources.


Optimise the wound bed…

Too wet

Remove moisture

Absorption / Retention /

Sequestration

Debridement

Treat infection

Too dry

Add moisture

Moisture balance

Maintain

I.e. Hydrogels

Hydrocolloids

Films

I.e. Hydrofiber®

Alginates

Foams

Super Absorbents

Poor Exudate Management

Note the maceration to the surrounding skin


Potential complications of poor exudate management…

Delayed healing and or wound deterioration

Increased risk of systemic or local infection

Increased nursing/podiatry time & dressing costs

Damage to wound surface

Damage to surrounding skin

Failure of odour control

Detrimental effect on quality of life

Bulky dressings

Frequent dressing changes

Pain


Wound infection

Wound infection occurs when the balance between

the patient’s resistance and the microorganisms

present in the wound is disrupted and organisms

overwhelm the immune defences3.

The cost of infection

Infected wounds negatively affect patient quality of life:

Pain, malodour, frequent dressing changes, loss of appetite.

Can lead to serious health complications:

Lower limb amputation, sepsis, even death.

Are a burden on Healthcare Organisations4,5

Delay wound healing.

Require specialist intervention.

Associated with hospital admission/delayed discharge.

How infection affects wound healing?

Prolongs the inflammatory phase

Decreased tissue perfusion (minimal oxygen and nutrition)

Inhibition of granulation/epithelialisation and collagen

synthesis.

Toxins/enzymes that damage the tissue locally

If the patient is systemically unwell (septic),

energy that would normally be used to heal the

wound is diverted to maintaining the patients

physiological status.


Local barriers to wound healing...

What is biofilm?

There are many definitions of biofilm.6-12

Simply put it can be described as:

Bacteria

attached to a

surface

embedded in a

protective slime.

Communities of microbes attached to a surface (e.g. catheter, wound),

embedded within a self-produced slime that provides protection against

antimicrobial agents and host defences.

How do Biofilms form?

Stage 1 – Reversible surface attachment

Bacteria begin to attach to the host surface

Stage 2 – Permanent surface attachment

Bacteria multiple and become firmly attached

Gene patterns change to enhance survival (Quorum sensing)

Stage 3 – Production of EPS

The bacteria secrete a protective matrix – ‘slime’

Biofilm is common

Biofilm is common, and

has been found in:

Alpine streams

Shower head

Biofilm is very common in

healthcare:13

Dental plaque on teeth14

Cystic Fibrosis infections15

Urinary tract infections16

Biofilm accounts for over

80% of all infections in

healthcare12

Dental plaque

biofilm

(stained)

Biofilm is present in

the majority of

chronic wounds17

and is a major

contributing factor

to delayed wound

healing.6,18,19

Why is biofilm a problem?

Biofilm exists in at least 78.8% of chronic wounds.17

Biofilm can be difficult to remove completely and reforms

quickly.20

Biofilm keeps the wound in a low-grade inflammatory state

and is a physical barrier to healing.18,19

Delays granulation and re-epithelialisation.

Biofilm tolerates antiseptics,21 antibiotics22 and host

defences.19

Planktonic bacteria vs. biofilm bacteria

Planktonic: free-living / swimming; isolated; susceptible

Biofilm: surface-attached; communities; protected; tolerant

Signs a Biofilm may be present

History of antibiotic failure or persistent infection despite

choice of antibiotic treatment

Local or systemic signs of infection that resolve with

antimicrobial therapy, but recur when therapy has ceased

Wet highly exuding wound

Dark unhealthy granulation tissue

Culture-negative result despite a high suspicion of clinical

infection:

Because biofilm bacteria are often non-culturable in microbiology labs

Swabbing and culturing only picks up a fraction of the bioburden


How can we manage them?

Evidence to date suggests that physical removal, i.e.

vigorous debridement or physical cleansing are the best

methods for reducing biofilm burden23

A biofilm can start reforming within hours. A mature biofilm

is present within 24 hours23

However there is debate as to whether wound biofilm can

be difficult to visualise!23

Key point…

Management of the three barriers to healing:

Excess Exudate

Infection

Biofilm

....are fundamental to successful wound healing!

Hence, we should consider a dressing regime that manages

all symptoms at the wound bed…

Dressing selection…?

Key point:

One of the keys to successful wound management is careful and accurate assessment of the wound bed.

How do I choose a dressing…???

Ask ‘what do I want the dressing to do…?’

Rehydrate...add moisture?

Absorb exudate? RETAIN exudate.

Deslough?

Reduce bacterial contamination?

Promote granulation?

Promote a moist wound bed?

Wound Progression…

Wound Challenge… back to “Olive”

How would you assess this

wound?

What do you consider to be the

key challenges?

How would you manage this

wound?


Key points:

There are many dressing and treatment choices available to

clinicians

Treatment choice should be based on wound assessment

findings together with a clear understanding of the benefits

and limitations of each option

Consider your local wound care formulary before making

your dressing selection.

The clinician must be clear what desired outcomes are

required

Thank-you for your attention…

References:

1. Oxford Medical Dictionary 2010

2. World Union of Wound Healing Societies (WUWHS). Principles of best practice: Wound exudate and the role of

dressings. A consensus document. London: MEP Ltd; 2007. http://www.woundsinternational.com/clinical-

guidelines/wound-exudate-and-the-role-of-dressings-a-consensus-document/page-1. Accessed November 2013.

3. European Wound Management Association(2006). Position Document: Identifying criteria for wound infection. MEP,

London

4. Drew P, Posnett J, Rusling L. The cost of wound care for a local population in England. Int. Wound J. 2007;4:149-155.

5. Harding K, Posnett J, Vowden K. A new methodology for costing wound care. Int Wound J. 2012; doi: 10.1111/iwj.

12006

6. Leaper DJ, Schultz G, Carville K, et al. Extending the TIME concept: what have we learned n the past 10 years. Int.

Wound J. 2012;9(Suppl. 2):1-9.

7. Costerton JW, Stewart SS, Greenberg EP. Bacterial Biofilms: A Common Cause of Persistent Infections. Science.

1999;284:1318-1322

8. Scali C, Kunimoto B. An Update on Chronic Wounds and the Role of Biofilms. Journal of Cutaneous Medicine and

Surgery. 2013;17(6):371-376.

9. Hoiby N, Ciofu O, Johansen HK et al. The clinical impact of bacterial biofilms. Int. J. Oral Sci. 2011;3:55-65.

10. Kimberly A, Mancle BS, Robert S, et al. Wound biofilms: Lessons learned from oral biofilms. Wound Rep. Reg.

2013;21(3):352-62.

11. Burmolle M, Thomsen TT, Fazli M, et al. Biofilms in chronic infections – a matter of opportunity – monospecies biofilms

in multispecies infections. FEMS Immunol. Med. Microbiol. 2010;59:324-336.

12. Sanchez Jr CJ, Mende K, Beckius ML, et al. Biofilm formation by clinical isolates and the implications in chronic

infections. BMC Infectious Diseases. 2013;13:47-12.

http://www.woundsinternational.com/clinical-guidelines/wound-exudate-and-the-role-of-dressings-a-consensus-document/page-1

References:

13. NIH (2002). Research on microbial biofilms. http://grants.nih.gov/grants/guide/pa-files/PA-03-047.html. Accessed

November 2013.

14. Marsh PD, Bradshaw DJ. Dental plaque as a biofilm. J. Industr. Microbiol. 1995;15:169-175.

15. Costerton JW. Cystic fibrosis pathogenesis and the role of biofilms in persistent infection. Trends Microbiol. 2001; 9:50-

52.

16. Trautner BW, Darouiche RO. Role of biofilm in catheter-associated urinary tract infection. Am. J. Infect. Control.

2004;32(3):177-183.

17. Malone, M,. Bjarnsholt, T., McBain, AJ., et al. The prevalence of biofilms in chronic wounds: a systematic review and

meta-analysis of published data J Wound Care 2017; 26 (1)

18. Metcalf DG, Bowler PG . Biofilm delays wound healing: a review of the evidence. J. Burns Trauma. 2013;1:5-12.

19. Gurjala AN, Geringer MR, Seth AK, et al. Development of a novel, highly quantitative in vivo model for the study of

biofilm-impaired cutaneous wound healing. Wound Rep. Regen. 2011;19:400-10.

20. Hurlow J, Bowler PG. Clinical experience with wound biofilm and management. A case series. Ostomy Wound

Management. 2009;55:38-49.

21. Percival SL, Hill KE, Malic S, et al. Antimicrobial tolerance and the significance of persister cells in recalcitrant chronic

wound biofilms. Wound Rep. Regen. 2011;19:1-9.

22. Stewart PS, Costerton JW. Antibiotic resistance of bacterial in biofilms. The Lancet. 2001;358:135-138

23. Wounds International. Biofilms made easy:Vol1/Issue3/May2010

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