WHEN BACTERIA BECOMES A PROBLEM IN A WOUND

1. WHEN BACTERIA BECOMES A PROBLEM IN A WOUND NORDIC SCIENTIFIC SYMPOSIUM 06.10.2005 MARCUS GÜRGEN SENIOR CONSULTANT SURGEON OUTPATIENT WOUND CLINIC/DEPT. OF SURGERY SØRLANDET HOSPITAL FLEKKEFJORD / NORWAY

2. ØVERLI

3. INTRODUCTION • 1 in 4 people with chronic wounds are receiving antibiotics at any one time and 60% have received a systemic antibiotic within the previous 6 months (Tammelin, Hambræus, Lindhom 1998) • There is uncertainty associated with managing infections in a chronic wound • There is an overuse of antibiotics in patients with chronic wounds • Antimicrobial resistance is a common problem

4. BACTERIA IN PRESSURE ULCERSTammelin, Lindhom, Hambræus. Chronic ulcers and antibiotic treatment. J Wound Care 1998;7(9):35-38.

5. BACTERIAL BURDEN ADAPTED FROM BROWNE ET AL. 2001

6. BACTERIAL BALANCE CONTAMINATION BACTERIA IS FOUND IN ALL TYPES OF CHRONIC WOUNDS – NOT MULTIPLYING, NO TISSUE DAMAGE, TRANSIENT PRESENCE INFECTION = NUMBER OF ORGANISMS x VIRULENCE HOST RESISTANCE H E A L I N G COLONIZATION BACTERIA ATTACHED TO TISSUE AND MULTIPLYING – DO NOT INITIATE WOUND INFECTION SYMBIOTIC RELATIONSHIPS TO HOST- ACCELERATES HEALING N O N - H E A L I N G CRITICAL COLONIZATION INCREASED BACTERIAL BURDEN IN THE SUPERFICIAL COMPARTMENT SUBTLE SIGNS OF INFECTION – LOCAL HOST RESPONSE? TRANSITION FROM COLONIZATION TO INFECTION OR TRANSITION TO PERSISTANCE / CHRONIC INFLAMMATION? INFECTION MICROBIAL GROWTH, MULTIPLICATION AND INVASION INTO HOST TISSUE - CELLULAR DAMAGE AND HOST IMMUNOLOGICAL REACTIONS BACTERIAL IMBALANCE ADAPTED FROM SIBBALD 2002, BOWLER 2002, EWMA POSITION DOCUMENT 2005

7. INFECTION ”Host resistance is the single most important determinant of wound infection and must be meticulously assessed in every situation where a chronic wound fails to heal” ADAPTED FROM DOW 1999

8. LOCAL FACTORS Wound size Wound age Wound localization Impaired blod flow / pressure Necrosis Excessive moisture Edema Foreign bodies Inciting event SYSTEMIC FACTORS Metabolic disease Systemic disease Chronic disease Old age Malnutrition Alcohol- / drug abuse Steroids / hormones / vitamine-K-antagonist Use of antibiotics without indication ”HOST RESISTANCE”FACTORS RESPONSIBLE FOR RISK OF INFECTION

9. INFECTION IN CHRONIC WOUNDS

10. ”Infection” is a clinical diagnosis Traditional signs of infection Abscess (swelling) Cellulitis (local redness and warmth) Discharge (serous + inflammation, sero-/ hemopurulent, pus) IDENTIFYING INFECTION

11. OTHER CRITERIA INCREASE IN MOISTURE VOLUME POCKETING NON-HEALING FRIABLE GRANULATION TISSUE WOUND INFECTION INCREASE IN PAIN MALODOUR DISCOLOURATION WOUND ENLARGING FORMATION OF NECROSIS

12. A DELPHI APPROACHCutting KF, White RJ, Mahoney P, Harding KG. Clinical identification of wound infection: a Delphi approach. European Wound Management Association (EWMA). Position Document: Identifying criteria for wound infection. London: MEP Ltd, 2005: 6-9. EG DIABETIC ULCERS EG VENOUS ULCERS KEY • Cellulitis • Lymphangitis • Phlegmon • Purulent exudate • Pus / absess • Cellulitis HIGH mean score 8 or 9 • Delayed healing despite appropriate compression therapy • Increase in local skin temperature • Increase in ulcer pain / change in nature of pain • Newly formed ulcers within inflamed margins of pre-existing ulcers • Wound bed extension within inflamed margins MEDIUM mean score 6 or 7 LOW mean score 4 or 5 • Crepitus in the joint • Erythema • Fluctuation • Increase in exudate volume • Induration • Localised pain in a normally asensate foot • Malodour • Probes to bone • Unexpected pain / tenderness • Discolouration eg dull, dark brick red • Friable granulation tissue • Increase in wound viscosity • Increase in exudate volume • Malodour • Sudden increase in amount of slough • Sudden appearance of necrotic black spots • Ulcer enlargement • Blue-black discolouration and haemorrhage • Bone or tendon exposed • Delayed / arrested wound healing despite • offloading and debridement • Deterioration of the wound • Friable granulation tissue • Local edema • Sinuses developing • Spreading necrosis / gangrene • Colour change to yellow or gray

13. Swabs Clean wound for debris (irrigation) and necrosis Collect material from the center of the wound, best from the border between healthy and infected tissue (not the edges!) Take biopsies in case of exposed / infected bone Choice of antibiotic after testing No need to take swabs from all chronic wounds! Blood tests CRP WBC Blood sedimentation LABORATORY TESTS • Radiologic • In case of osteomyelitis SUPPORT CLINICAL DIAGNOSIS

14. TREATING INFECTION IDENTIFY UNDERLYING HOST FACTORS CORRECT UNDERLYING HOST FACTORS DEBRIDEMENT WOUND CLEANSING MOISTURE CONTROL CONSIDER SPECIFIC ANTIMICROBIAL THERAPY OBSERVE AND ADJUST THERAPY IF NECESSARY

15. LOCAL FACTORS Wound size Wound age Wound localization Impaired blood flow / pressure Necrosis Excessive moisture Edema Foreign bodies Inciting event SYSTEMIC FACTORS Metabolic disease Systemic disease Chronic disease Old age Malnutrition Alcohol- / drug abuse Steroids / hormones / vitamine-K-antagonist Use of antibiotics without indication TREATING INFECTIONUNDERLYING CAUSES

16. TREATING INFECTIONDEBRIDEMENT • Debridement • Reduces bacterial burden • Important: continuity • Method of debridement must meet patient-related criteria

17. TREATING INFECTIONWOUND CLEANSING • Wound cleansing can in most cases be done with water from the spring (irrigation) • Antiseptics are generally cytotoxic • If use of antiseptics is considered one must remember that wounds are most vulnerable for cytotoxic substances in the inflammatory phase of wound healing • Can be used in case of MRSA, stimulation of non-healing wounds, wounds with increased bacterial burden or infected wounds (Schultz, Sibbald, Falanga 2003) • I do not recommend this because we have better tools to treat these types of wounds

18. TREATING INFECTIONMOISTURE CONTROL • Moisture-absorbing products • Compression • Topical negative pressure • Elevation

19. TREATING INFECTIONANTIMICROBIAL THERAPY • Non-healing • Increase in exudate volume • Friable granulation tissue • Discolouration • New areas of slough • Malodour SUPERFICIAL LOCAL THERAPY WITH SILVER OR IODINE DEEP SYSTEMIC THERAPY • Local warmth • Pain • Cellulitis > 2 cm • Exposed bone • Necrosis spreading • Streptococcus gr. A ADAPTED FROM SIBBALD 2003

20. Use of local antibiotics is not recommended because of: Common allergens Breed resistance Lack of therapeutic amount of antibiotic substances No moisture balance properties Lack of autolytic debridement Cadexomer with iodine: Starch molecules provide absorption capacity Slow release of iodine which in other forms would be cytotoxic Autolytic debridement modality Not available in all countries TREATING INFECTIONSUPERFICIAL COMPARTMENT

21. TREATING INFECTIONSUPERFICIAL COMPARTMENT • Silver: • Silver has antimicrobial properties, nanocrystalline silver kills more than 150 different types of bacteria / fungi, and MRSA • Kills microbes at the infection site by blocking transport mechanisms in bacteria, impairing bacterias cell replication and by damaging structural and receptor functions in bacteria • Has antiinflammatory capability • Allergy to silver is rare • No resistance if concentration of silver > 30- 40 ppm • Bonded to several dressing materials fitting different types of wounds in different phases of wound healing • Safe • Up to 7 days wear-time • Cost-effective

22. TREATING INFECTIONSUPERFICIAL COMPARTMENT • Protease-modulating matrix • One product binds harmful MMP to cellulose and thus protects GF • Another product replaces damaged ECM proteins • Promising study results • Expensive products

23. TREATING INFECTIONSUPERFICIAL COMPARTMENT • pH-modulating matrix • Chronic wounds have higher pH (alkaline) • Weakly acidic environment promotes wound healing • Proteases levels are high in chronic wound • Proteases activity can be lowered by reducing wound pH to around 5 pH DEPENDANT ENZYME ACTIVITY LEVELS OF PROTEASES IN WOUNDS Schultz G, Mozingo D, Romanelli M, Claxton K. Wound healing and TIME; new concepts and scientific applications. Wound Rep Regen 2005;13(4): S1-11

24. TREATING INFECTIONDEEP COMPARTMENT ADAPTED FROM DOW 2001

25. TREATING INFECTIONDEEP COMPARTMENT

26. SUMMARY • Bacteria in all chronic wounds • Host resistance is the most important factor which determines whether there will be infection or not • To diagnose infection is a clinical skill • Superficial / deep compartment = different treatment strategies • Remember other Wound Bed Preparation measures to reduce both bacterial and cellular burden

27. THANK YOU! ØVERLI

28. NIFS-SEMINAR 2006 • TOPIC: ”If wounds are not healing” • WHERE: SAS Radisson Hotel, Tromsø / Norway • WHEN: February 2nd and 3rd, 2006 • INFORMATION: Guro Vaagbø, Seksjon for hyperbar medisin, Haukeland Universitetssykehus, N-5021 Bergen; http://www.nifs-saar.no