inflammation, wound healing, and infection

Download Inflammation, Wound Healing, and Infection

Post on 24-Feb-2016

60 views

Category:

Documents

0 download

Embed Size (px)

DESCRIPTION

Inflammation, Wound Healing, and Infection. Anne McConville, MD. Why do we care?. Wound infection and failure remain common complications Prolong hospitalization Increased resource consumption Increased costs Increased mortality Influenced by patient factors and perioperative management. - PowerPoint PPT Presentation

TRANSCRIPT

Inflammation, Wound Healing, and Infection

Inflammation, Wound Healing, and InfectionAnne McConville, MD1Why do we care?Wound infection and failure remain common complicationsProlong hospitalizationIncreased resource consumptionIncreased costsIncreased mortalityInfluenced by patient factors and perioperative managementDespite medical advances, wound infection very common cause of complication. Patient factors include: DM, cardiovascular status, and response to stressorsPerioperative management: aseptic technique, appropriately timed ABX, maintaining perfusion and oxygenation2Infection Control: Hand HygieneHand HygieneOften neglectedSemmelweis first noted in with 1847: puerperal infectionsResident vs. Transient floraEven clean procedures can result in contaminationUnfortunately hand hygiene must be mentioned since it is neglected 40% of time.2 L&D clinics in Vienna, med students and drs in 1 and midwives in 2. drs started day with autopsies. Mortality rate 15% vs 2%. When started using chlorinated solution to wash hands at start of day and between patients, mortality decreased to 2%. Long time before this was widely accepted practice. Bacteria always present on skin. Most common resident bacteria are coag-negative staph and diptheroids, usually not pathogenic, in creases of skin.Transient bacteria reside on superficial layers, are easily removed with hand hygiene, and are most likely to cause HCAI. Clean procedures= pulse, applying monitors3Infection Control:Hand HygieneVarious Hand Hygiene ProductsPlain soap and waterAlcohol-based rinses and gelsChlorhexidineIodine and iodophorsChoice depends on expected pathogen, acceptability of HCWs, and cost (usually $1/patient day).

Ideal agent kills broad spectrum of microbes, has antimicrobial activity that persists at least 6 hrs, easy to use with few side effects.Plain soap and water: best for spores (C. diff, Anthrax) and visible dirt. Does not reduce bacterial load, irritating/drying to skin.Alcohol-based: Denatures proteins and is antimicrobial, ethanol most common, best when combined with chlorhexidine. Efficacy depends of volume and duration of contact. Kills gram +, -, HIV, Hep B,C, influenzaChlorhexidine: Disrupts cytoplasmic membranes resulting in precipitation of cellular contents. Kills gram +, -, fungi. Minimally effective against TB. Agent of choice for CVL placement bc persists on skin. May cause corneal damage, ototoxicity, and neurotoxicity.Iodine and iodophors: Impair protein synthesis and cell membrane function. Kills gram +, -, and some spore forming bacteria (inactive against spores themselves), mycobacteria, viruses, fungi. Allergies and skin irritation are common.

4Infection Control: Hand HygieneBarriers to hand hygieneSkin irritationInaccessibilityHCW acceptanceIn ICU, hand hygiene indicated about 20x/hr (probably similar in OR). Cross-contamination in OR from anesthesia personnel VERY common, even to sterile stopcocks.Keep in mind wearing gloves does not obviate need for hand hygiene. Artificial and long fingernails, chipped nail polish are associated with higher bacteria concentrations on hands of HCWs. Should be banned. 5Infection Control:AntisepsisMasksCapsSterile glovesDrapesDecrease OR trafficSite of line placementStudies evaluating efficay of masks in preventing infection show no difference, however studies were small. Mask does protect HCW. Caps are shown to decrease SSI. Study from Israel showed fewer infections from airborne organisms in TKA in those with fewer surgeons and fewer personnel in OR. 1991 study by Mermel sowed increased infection from CVLs placed by anesthesiologist (both in and out of OR). Factors include use of IJ site and less stringency to sterile technique. Maximal sterile barrier technique has improved this. Epidural abscess: use strict aseptic technique particularly needles and catheter. Gown and mask are unlikely to reduce risk. Consider avoiding in patients with bacteremia, or at least wait until appropriate antibiotics started.6Infection Control:Antibiotic ProphylaxisMiles et. al used guinea pig model as proof of principle for antibiotic prophylaxis Knighten et. al assessed the use of high inspired oxygen alone and in addition to prophylactic antibioticsClassen et. al prospective human study showed same results as Miles.Standard for surgeries in which greater than minimal risk of infection Widespread use of ABX began in 1940s-1950s, even then considered their possibility to reduce SSI.Miles: guinea pigs given appropriate ABX 2 hours before or after intradermal injection of bacteria, invasive skin infection and necrosis were prevented. ABX given outside this window were not effective. Also showed that intradermal epinephrine given prior to ABX led to ABX failure, demonstating importance of local perfusion in delivery of ABX to site. Knighton et al showed high inspired O2 concentrations to be as effective as antibiotics and that antibiotics and high FiO2 had additive effects., though oxygen has greater decisive period (may be 6hours or longer according to Knightons study). Classen et. al studied almost 3,000 at LDS hospital Utah with clean and clean-contaminated surgical procedures. Lowest infections when ABX given within 2 hrs of incision. Least when given 0-60 minutes of surgery but not statistically significant, but where our clinical standard today came from.

7Infection Control:Antibiotic ProphylaxisTHA, TKA, extradural ortho and neuro spine, CT, vascular, kidney transplant: CefazolinCranial and intradural spine: CeftriaxoneLiver transplantation: CeftriaxoneColon surgery: CefotetanVaginal and abdominal Hysterectomy: Cefazolin or Cefotetan (if bowel involved)Dosing depends on weight, redosing interval depends on durgs used.Discontinued by 24 hours postoperatively

Antiobiotic chosen should cover the most likely infection and pathogen. Most commonly 1st generation cephalosporin. If anaphylactic to B-lactam, give vanc or clindamycin. . For colon surgery use cipro and flagyl if B-lactam allergy.Hyst: Cipro and flagyl OR gent and clinda.Discontinue to decrease risk of ABX side effects (C. diff)Bc anesthesiologist very present in 60 minutes before surgery, need to take active role in ensuring appropriate ABX, dose and timing are achieved. 8Surgical Site InfectionsSuperficial Incisional (SSI)Deep Incisional SSIOrgan/Space SSIWithin 30 days after operation if no implant left in place and 1 year if implant left in place.Superficial: do not include stitch abscess, burn wounds, episiotomy or circumcision 9Mechanism of Wound RepairInflammationMatrix productionAngiogenesisEpithelizationRemodeling

Repair process is affected by systemic factors: comorbid disease, SNS activity, nutrition, ageLocal factors: bacterial load, degree of inflammation, moisture content, oxygen tension, vascular perfusion****possibly most critical component in wound healing is oxygen supply to the wound (cofactor of enzymymati processes, rate-limiting step for WBC-mediated bacterial killing and collagen formation10Initial Response to InjuryStarts with skin incision creating a woundPhases: hemostasis, inflammation, proliferation, and remodelingEach phase is mediated by contaminants, interaction between cells, cytokines, and other chemical mediatorsFailure of any component or phase may result in wound failurePhases are preserved among species, showing importance of inflammation that directs process of cellular and tissue repair

11Initial Response to Injury: HemostasisPlatelet aggregation and degranulationRelease of chemoattractants and growth factorsCoagulation results

Platelet aggregation at wound and release of chemoattractants and growth factorsWith establishment of coagulation come greater area that is now not perfusedPlatelet degranulation releases: PDGF, TGF-B, IGF-1- all of which initiate inflammatory process

12Initial Response to Injury: InflammationBradykinin, complement and histamine released by mast cellsPMNs arrive almost immediately followed by macrophages in 1-2 daysWBCs continue cycle of inflamamtionCharacterized by erythema and edema of wound edgesThere for WBCs activated by integrins, lactate, hypoxia, infectious agents, and growth factors.These WBCs, macrophages in particular, produce more lactate and growth factors.WBCs also release proteases and collagenases which degrade basement membrane of capillaries to allow inflammatory cells to migrate into the woundLocal blood supply compromised while metabolic demand increased, resulting in a hypoxic and acidotic with high lactate levels represents 3 effectsDecreased O2 supply from vascular damageIncreased demand Aerobic glycolysis by inflammatory cellsResiratory burst by PMNs require O2 to make superoxide which kills bacteriaLocal hypoxia is normal and inevitable part of tissue injury and is stimulus to repair but does infact lead to poor wound healing and increased risk of infection

13ProliferationBegins about 4 days after injuryNeovasularizationAngiogenesisVasculogenesisCollagen and Extracellular Matrix DepositionOxygen dependent processEpithelizationNew blood vessels must replace injured microcirculationAngiogenesis: new vessel growth from mature vessels, ususally post-capillary venulesVasculogenesis: vessel tubules develop from bone marrow derived endothelial precursors that differentiate and connect to existing blood vesselsBoth stimulated by hypoxia and lactateNew blood vessels grow in to the matix that is produced by fibroblasts, matrix helps new vessels grow and mature and without(hypoxic wounds have poor, weak collagen matrix) it prone to hemorhrageEpithelization: 1-3 days in acute, primarily closed wounds. Much longer in open wounds, which requires granulation first and then epithelilizes from edges

14Maturation and RemodelingOngoing remodeling of granulation tissue and increasing tensile wound strengthWound will never achieve tensile strength of uninjured skin/tissueHypertrophic an

Recommended

View more >