- 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 Quantitative swab
culture via Levine Technique has highest quality evidence of any
noninvasive test for infection in chronic wounds; both positive and
negative predictive value Presence of increasing pain, along with a
quantitative swab culture, might help physicians estimate the
probability of infection.Reddy, Gill, Wu, Kalkar, Rochon; JAMA 2012
42. 5 QUESTIONS1) Which organisms, regardless of quantity, need to
be treated?2) Which organisms usually do not need to be treated?3)
What are the most reliable clinical indicators of chronic wound
infection?4) What constitutes the best combination of diagnostic
tools (clinical/lab) to diagnose chronic wound infection?5) Is
TMP/SMZ still appropriate, in our community, to treat MRSA wound
infection without systemic illness? 43. Which organisms, regardless
of quantity,need to be treated? Staph aureus; MSSA or MRSA Group A
Strep (S. pyogenes) Group B Strep (S. agalactiae) Group C and G
Strep Pseudomonas aeruginosa E.coli, Klebsiella pneumoniae, Proteus
sp. 44. Which organisms usually do not need to be treated?
Coagulase negative Staph (epi, warneri, capitis) Stenotrophomonas
Acinetobacter species Enterococcus Strep viridans isolates 45. What
are the most reliable clinicalindicators of chronic wound
infection? Pain in immediate periwound area Friable bloody
granulation tissue Advancing pweriwound erythema Malodor Fever or
other systemic signs and symptoms of illnessin absence of other
identifiable source of infection Crepitance in surrounding tissues
46. What constitutes the best combination ofdiagnostic tools
(clinical/lab) to diagnose chronic wound infection Positive swab
(Levine) for appropriate organisms Increasing pain in and around
wound Careful with validity of probe to bone for osteo 47. Is
TMP/SMZ still an appropriate choice, in ourcommunity, to treat MRSA
wound infectionwithout systemic signs/symptoms? Yes 90% Watch for
acute adverse events, ie, Steven-Johnson
