Infection of the chronic wound how to decide

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Text of Infection of the chronic wound how to decide

  • 1. Lee C. Ruotsi, MD, FACCWS, UHM

2. SIGNS AND SYMPTOMSPRIMARY SECONDARY Rubor (erythema) Delayed healing Dolor (pain) Changes in wound bed color Calor (warmth) Friable/hyper granulation Edema/swelling Abnormal/increased odor Purulence Increased drainage Fever 3. RISK FACTORS FOR WOUND INFECTIONSYSTEMICLOCAL Vascular disease Large wound area Edema Increased wound depth Malnutrition Degree of chronicity Anatomic location Diabetes Foreign bodies Alcoholism Necrotic tissue Prior surgery or radiation Mechanism of injury Drugs i.e. corticosteroids Degree of contamination Immune deficits Reduced perfusion 4. CONTAMINATION TO INFECTIONINFECTION LOCAL/SYSTEMIC CRITICAL COLONIZATION COLONIZATIONCONTAMINA- TION 5. WOUND CONTAMINATION Presence of non-replicating micro-organisms onthe wound surface that evoke no clinical hostresponse All chronic wounds are contaminated Bacterial colony counts low Wound healing occurs in spite of presence of bacteria Not the presence of bacteria but interaction with host thatdetermines their impact on wound healing 6. WOUND CONTAMINATION 7. WOUND COLONIZATION Presence of replicating micro-organisms within a wound in the absence of any detectable host injury Most organisms are normal skin flora Staph epi and other coag negative staph,corynebacterium, propionibacterium, Gram negatives; Proteus and Pseudomonas 8. WOUND COLONIZATION 9. SUPERFICIAL CRITICAL COLONIZATION Replicating microbial burden in the wound surface compartment with subtle clinical signs of host injury aka: covert/localized infection, increased bacterialburden 10. SUPERFICIAL CRITICAL COLONIZATION 11. DEEP WOUND INFECTION Level of microbial burden or virulence has overwhelmed the host responses and the micro-organisms cause clinical injury by invading locally or deeply below the wound base Stage before systemic sepsis 12. DEEP WOUND INFECTION 13. SYSTEMIC SEPSIS (BACTEREMIA) Relatively uncommon as a result of woundinfections Found in 10-20% of severely infected wounds;diabetic foot wounds and deep pressure ulcers aremost common Small wounds, if infected with Group A Strep orMRSA can rapidly progress from contamination tosystemic infection (sepsis) Example- MRSA outbreaks in athletes 14. CONFOUNDING VARIABLES Pain;may be absent in infected diabetic foot wound Warmth; may be absent with ischemia Erythema;may be absent in diabetes and ischemiamay be venous insufficiency, not infection Purulence;may be normal exudates produced by healthy granulation tissue Fever; may be absent in compromised host Edema; may be manifestation of venous disease rather than infection 15. INCREASED BACTERIAL BURDEN May only appear as mild erythema and hyperemia Objectively- wound may not appear infected Bacteria compete for nutrients and oxygen Exotoxins, endotoxins and proteases impairnormal cellular functions Wound Healing is compromised when:a) more than 4 pathological species presentb) tissue bacteria levels > 105 16. PATHOGENS AS A FUNCTION OF TIME Early Acute 4 weeks Long Term Chronic 17. EARLY ACUTE Predominance of usual skin flora Staph aureus and Beta Hemolytic strep follow in early weeks 18. 4 WEEKS Facultative anaerobic gram rods begin to colonize Most common: Proteus, E. Coli, Klebsiella As wound deteriorates, deeper structures become affected and anaerobes become more common Environment becomes more polymicrobial (4-5 sp.) 19. LONG TERM CHRONIC Often more anaerobic than aerobic Also, aerobic Gram rods:PseudomonasAcinetobacterXanthomonas 20. LONG TERM CHRONIC 21. THE WOUND ENVIRONMENT Chronic wounds differ biochemically from acute ones Prolonged inflammatory response leads to increase in inflammatory cytokines and MMPs Debridement, control of infection and inflammation, moisture control and excision of wound edges and callous Sharp debridement gold standard 22. DEBRIDEMENT Excisional or selective Excisional: surgical removal ofclearly identifiable tissue bycutting outside wound margins Selective: removal of devitalizedtissue, ie slough, fibrin, crusts,exudates Debridement changes woundphysiology; chronic to acute Universally accepted and shouldrely on intuition Better healing with morefrequent debridement (Wellsupported) 23. SURGICAL / SHARP DEBRIDEMENTScalpel, Curette ADVANTAGES: DISADVANTAGES Fastest and most effective Requires skill andmethod of removal of advanced trainingdevitalized wound tissue Can damage blood vessels, Very selective Nerves, tendons, etc Stimulates wound healing Can be painful and maythrough release ofinflammatory cytokines require anesthesia 24. ENZYMATIC DEBRIDEMENTCollagenase Advantages: Disadvantages Most selective of non- Slowsurgical methods Expensive Painless Requires prescription Low risk of damage to May cause inflammationother structuresbut rare Daily, patient appliedtherapy 25. AUTOLYTIC DEBRIDEMENTProteolytic enzymes, Hydrogels Advantages Disadvantages Occurs naturally, to some Slowextent, in all moist wounds Wound must be monitored Can be augmented withclosely for signs ofhydrogels, etc infection anaerobic if Safe occlusive dressing used Selective Inexpensive 26. MECHANICAL DEBRIDEMENT Wet to dry, Pulse lavage, Whirlpool Advantages Disadvantages Inexpensive Non-selective Can be effective short-term Traumatizes and debridesin proper setting healthy as well asdevitalized tissue Painful 27. MISCELLANEOUS Pseudomonas: Frequently cultured from deteriorating wounds and tends not to be invasive unless in compromised host Enterococcus: Frequently cultured and need not be treated unless only organism cultured and wound clinically infected Candida: Same as above for Enterococcus 28. CULTURE METHODS Quantitative Deep tissue Gold standard Biopsy Culture >105 org/gm of tissue Any level B Hemolytic Strep Invasive Usually requires local Caution with PAD Time consuming/$$$ for lab 29. CULTURE METHODS Levine swab technique Best supportive evidenceoutside quantitativebiopsy culture1) Cleanse/irrigate wsaline2) Firm pressure of swabtip in cleanest portionof wound base3) Rotate 360 degrees4) Transport media 30. NERDS AND STONEES Cross sectional validation study of 112 patients Studied clinical assessment variables to determinepresence and quantity of wound bacteria Wounds evaluated using mnemonics to assess for: 1) Critical colonization (NERDS) 2) Infection (STONEES) Results compared to semi-quantitative swab cultures 31. NERDSN Non-healing wound - Wounds that are not 20% - 40% smaller in 4 weeks by hx or recordsE Exudative wound - Increase in wound exudate with >50% of dressing stained with exudateRRed and bleeding Wound bed tissue bright red with exuberant granulation tissue. Bleeds easily with gentle manipulationDDebris Presence of discolored granulation tissue, slough and necrotic / nonviable tissue.S Smell Unpleasant or sweet, sickening odor 32. STONEESS Size - Wound size is increasing. Longest length x widest width (right angles). Only very deep wounds and most stage III / IV pressure ulcers should have depth measured with probe.TTemperature increased Increased periwound margin temperature by > 3 F difference between mirror image sites.OOs (Probes to or exposed bone) - Wounds that have exposed bone or probed to bone at time of examNNew areas of breakdown or satellite lesionsEErythema/Edema Reddening/swelling in periwound skinEExudate - Increased amount of drainageSSmell - Unpleasant or sweet, sickening odor 33. RESULTS Predictability compared to semi-quantitative cultures obtained via Levine Technique 34. RESULTS Suggest that level of bacterial growth can be assessedusing the clinical variables in the mnemonicsNERDS: Scant to light growthSTONEES: Moderate to heavy growth When any 3 clinical signs were combined in eithergroup: Sensitivity = 73% for scant/light (NERDS) Sensitivity = 90% for mod/heavy (STONEES) Woo, Sibbald; OWM 2009;55(8):40-48 35. I.D.S.A. D.F.U. CLASSIFICATIONClinical DescriptionIDSA Class Wound without purulence or any Uninfectedmanifestations of infection >2 of following:(purulence, erythema, Mildpain, tenderness, warmth, induration).Cellulitis 1 of following:Cellulitis >2 cm, lymphangitis, deep tissue Moderateabscess, gangrene, muscle, tendon, boneinv. Systemic toxicity/metabolic instability Severe(fever/chills, tachy, hypotension,confusion, vomiting, increased WBCs 36. ACCURACY OF SYMPTOMS AND SIGNS 2 studies from Gardner, et al showed that likelihood of infection increases when increased pain present. Absence of pain was not a useful predictor of absence of infectionGardner, Hillis, Frantz; 2009 Gardner, Frantz, Doebbeling; 2001 37. ACCURACY OF SYMPTOMS AND SIGNS Purulent exudate, erythema, heat and edema (classicsigns) not helpful in diagnosing infection in chronicwounds Wounds without serous exudates or those healingrapidly were less likely to be infected Foul odor did not significantly predict infection Examined application of IDSA DFU scale to chronicwounds 46% and 52% sensitivity. Not helpful.Gardner, Hillis, Frantz; 2009 38. ACCURACY OF NONINVASIVE TESTS Four studies evaluated utility of swab cultures and labmarkers compared with deep tissue biopsy culture. 4 studies included 198 patients Levine Technique: Positive culture predictive ofinfection and negative culture predictive of absence ofinfection Z - Technique: Not useful in predicting or excludingwound infection Reddy, Gill, Wu, Kalkar, Rochon; JAMA 2012 39. DR. OTTO VON SCRATCHANSNIFF 40. BOTTOM LINE Classic signs of infection not particularly helpful indiagnosing infection in chronic wound Serous exudate more predictive (higher LR) thanpurulent exudate in predicting infection Combinations of findings (IDSA DFU) not useful forpredicting chronic wound infection Increasing pain is the most useful indicator ofinfection when there is suspicion of infection butabsence of pain does not predict absence of infection 41. MORE BOTTOM LINE Qu