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Soft tissue infections Thomas Genuit, MD,MBA, FACS Sinai Hospital of Baltimore 2006 Definitions and Etiologies Soft tissue infections were first defined slightly more ... – PowerPoint PPT presentation

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1
Soft tissue infections
  • Thomas Genuit, MD,MBA, FACS
  • Sinai Hospital of Baltimore
  • 2006

2
Definitions and Etiologies
  • Soft tissue infections were first defined
    slightly more than a century ago. In 1883,
    Fournier described a gangrenous infection of the
    scrotum that continues to be associated with his
    name. In 1924, Meleney documented the pathogenic
    role of streptococci in soft tissue infection.
    Shortly thereafter, Brewer and Meleney described
    progressive polymicrobial postoperative infection
    of the muscular fascia with necrosis (the term
    necrotizing fasciitis was not introduced until
    the 1950s). The association between toxic-shock
    syndrome and streptococcal soft tissue infection
    was delineated as this disease reemerged in the
    1980s.

3
Definitions and Etiologies
  • Diverse group of diseases that involve the skin
    and underlying subcutaneous tissue, fascia, or
    muscle.
  • May be localized to a small area or may involve a
    large portion of the body.
  • May affect any part of the body, though the lower
    extremities, the perineum, and the abdominal wall
    are the most common sites of involvement.
  • Some are relatively harmless if treated promptly
    and adequately others can be life-threatening
    even when appropriately treated.

4
Definitions and Etiologies
  • Symptoms and signs
  • Pain (localized tendernes) ? loss of sensation
  • erythema, edema / induration
  • Blisters, crusted plaques
  • (Epi)dermal erosion and necrosis
  • Fluctuation, crepitus
  • Systemic signs of SIRS/Sepsis
  • fever, tachycardia, hypotension, organ dysfuction

5
Definitions and Etiologies
  • Simple vs. complex
  • Primary vs. secondary vs. tertiary
  • Cellulitis vs. abscess
  • Superficial vs. deep
  • Necrotizing vs. non-necrotizing
  • Traumatic vs. non-traumatic
  • Dermatitis, fasciitis, myositis ( combinations)
  • Single vs. multiple pathogens
  • Classic syndromes
  • Rapidly progressive infections
  • toxic shock syndromes
  • Specific etiologies or pathogens

6
Definitions and Etiologies
  • Non-traumatic - Spontaneous
  • Glandular infection (folliculitis, furuncle,
    carbuncle, hidradenitis, perianal-, perineal-, )
  • Micro-trauma (cuts, insect bites, )
  • Trauma (wounds - including surgical)
  • Clean Wounds An uninfected operative wound in
    which no inflammation is encountered and the
    respiratory, alimentary, genital, or uninfected
    urinary tracts are not entered.
  • Clean-Contaminated Wounds Operative wounds in
    which the respiratory, alimentary, genital, or
    urinary tracts are entered under controlled
    conditions and without unusual contamination.
  • Contaminated Wounds Includes open, fresh,
    accidental wounds. In addition, operations with
    major breaks in sterile technique (e.g., open
    cardiac massage) or gross spillage from the
    gastrointestinal tract, and incisions in which
    acute, non-purulent inflammation is encountered
    are included in this category.
  • Dirty or Infected Wounds Includes old traumatic
    wounds with retained or devitalized tissue and
    those that involve existing clinical infection or
    perforated viscera.

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8
Superficial infections
  • Majority of soft tissue infections
  • Involve epidermis, dermis and/or subcutaneous
    tissues
  • Pyoderma
  • general term bacterial infection of the skin.
  • several subcategories

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Superficial infections
  • Impetigo
  • highly contagious, confined to the epidermis
  • usually face or extremities.
  • most common in infants and preschool children
  • more frequently in patients with preexisting skin
    conditions (e.g., eczema, atopic dermatitis,
    varicella, angular cheilitis, scabies).
  • usually in areas of skin breakdown
  • warm and humid weather, crowded living, and poor
    hygiene contribute
  • dominant pathogen is S. aureus, less common S.
    pyogenes
  • bullous or a nonbullous form of the disease
  • Bullous numerous blisters or bullae that rapidly
    become pustules -gt rupture within 1 to 2 days -gt
    thick, honey-colored, crusted plaque remains for
    days to weeks.
  • Nonbullous erythema and tiny, less prominent
    vesicles -gt crusted erosions in the skin. skin
    lesions are intensely pruritic, local spread as a
    result of scratching and release of infected
    fluid associated regional lymphadenopathy is
    common.

11
Superficial infections
  • Impetigo
  • Glomerulonephritis may complicate
    streptococcal-induced impetigo.
  • diagnosis by Gram stain and culture of vesicular
    fluid or crusted plaque.
  • skin lesions usually resolve spontaneously within
    2 to 3 weeks.
  • antibiotic therapy accelerates the resolution
  • Mupirocin ointment (2)
  • Erythromycin and clindamycin ointments are
    alternatives
  • with disseminated impetigo, disease of the mouth
    and in pts in whom topical therapy fails, a
    7-day course of oral Abx. Is indicateddicloxacill
    in, cephalexin, cefadroxil, erythromycin, or
    clindamycin may be used

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Superficial infections
  • Erysipelas
  • principally involves the dermis.
  • infection extends through the dermal lymphatic
    vessels
  • tender, pruritic, intensely erythematous,
    hyperthermic, sharply demarcated, and raised
    plaque
  • most cases preceded by influenzalike
    symptomspain (local, myalgia) , often high
    fever, and leukocytosis.
  • lymphangitis and -adenopathy sometimes present
  • lower leg most common site, followed by face,
    arms, and upper thighs.
  • predisposing factors local conditions as
    athlete's foot, leg ulcers, and venous stasis
    dermatitis, presence of lymphedema, diabetes
    mellitus, alcoholism, immunocompromise, and
    obesitymore likely to recur when associated
    diseases are inadequately treated (10 within 6
    months, 30 within 3 years)
  • almost invariably caused by S. pyogenes.

14
Superficial infections
  • Erysipelas
  • antibiotic treatment
  • uncomplicated erysipelas penicillin,
    amoxicillineffective in at least 80 of cases.
    Oral and intravenous antibiotic regimens are
    equally efficacious.
  • patients with erysipelas of the lower extremity
    should be placed on bed rest, and the involved
    leg should be elevated
  • once the patient is able to resume normal
    activities, he or she should be fitted with
    elastic stockings, to help reduce the recurrence
    of edema and lower the risk of lymphedema.
  • For patients with tinea pedis, a topical
    antifungal agent is used to treat the infection
    and prevent recurrence.

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16
Superficial infections
  • Folliculitis
  • infection of the hair follicle
  • painful, tender, erythematous papule with a
    central pustule single or multiple lesions in
    the skin of any hair-bearing area
  • Predisposing factors shaving, plucking, waxing,
    heat and humidity, the use of corticosteroids or
    antibiotics, immunosuppression, and occlusion of
    the skin by clothing, adhesives, etc.
  • typically caused by S. aureus. It is
    characterized by a. In rare cases, Pseudomonas
    aeruginosa, Klebsiella species, Enterobacter
    species, Proteus species, yeasts, and fungi.
  • Pseudomonas folliculitis exposure to
    inadequately chlorinated water (swimming pools,
    hot tubs, or whirlpools) folliculitis with fever
    and malaise appearing 6 hours to 3 d p. exposure.
    Klebsiella, Enterobacter, and Proteus speciesin
    patients receiving long-term Abx. therapy for
    acne vulgaris. Yeast folliculitis and fungal
    folliculitis occur in immunocompromised pts.

17
Superficial infections
  • Folliculitis
  • most resolve spontaneously within 7 to 10 days.
  • topical therapy clindamycin, erythromycin, or
    mupirocin ointments chlorhexidine or
    benzoyl peroxide warm soaks may
    accelerate resolution Isotretinoin can be used
    to treat gram-negative folliculitis. Gentamicin
    cream may be helpful in Pseudomonas folliculitis
  • with refractory or disseminated follicular
    infections oral antibiotics S. aureus
    dicloxacillin, erythromycin, cephalexin,
    cefadroxil, or clindamycin (cave up to 20-30
    prevalence of MRSA in certain pts.) Gram neg
    oral ciprofloxacin more aggressive therapy with
    systemic symptoms of sepsis
  • Elimination of predisposing factors to reduce
    likelihood of recurrence.

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19
Superficial infections
  • Furuncles and carbuncles
  • deeper infections of the hair follicle that
    extend into the subcutaneous tissue.
  • furuncle, or boil small abscess
  • firm, tender, erythematous nodule
  • occurs in skin areas exposed to friction ( inner
    thighs and the axilla). also face, neck, upper
    back, and buttocks.
  • predisposing factors increased friction and
    perspiration (obese individuals or athletes),
    corticosteroid use, diabetes mellitus, and
    inherited or acquired defects in neutrophil
    function
  • Initial treatment warm compresses to help
    promote drainage oral antimicrobial agent
    effective against S. aureus incision-and-drainage
    necessary when lesions do not drain
    spontaneously. Failure to drain these lesions
    adequately may result in recurrence, as well as
    in progression to a more serious infection.

20
Superficial infections
  • Carbuncle deep cutaneous infection involving
    multiple hair follicles
  • characterized by destruction of fibrous tissue
    septa and formation of a series of interconnected
    abscesses. Patients commonly present with
    relatively large skin lesions (confluence)
    associated with chronic drainage, sinus tracts,
    and scarring
  • typically painful, red, tender, indurated area of
    skin with multiple sinus tracts.
  • Systemic manifestations (e.g., fever and malaise)
    are common.
  • occurs most frequently on nape of the neck, upper
    part of the back, or the posterior thigh.
  • Therapy incision-and-drainage w. thorough search
    for loculated areas should be undertaken Wide
    local excision of the involved skin and
    subcutaneous fat is often necessary to prevent
    recurrent disease. oral antistaphylococcal agent

21
Bites
  • 50 of all Americans bitten by animal or human
    during lifetime
  • 1 of all emergency department visits.
  • soft tissue infection is the most common
    complication
  • risk of infection depends on type of bite, site
    of injury, time elapsed, host factors, and
    management of the wound
  • hand or foot or over a major jointscalp or the
    face of an infantpuncture wounddelay in
    treatment gt 12 hrimmunosuppression, chronic
    alcoholism, diabetes mellituscorticosteroid use,
    preexisting edema in affected extremity
  • overall risk of infection 5 - 15 patients who
    seek medical attention
  • 2 - 20 for dog bites,
  • 30 to gt 50 for cat bites,
  • 10 - 50 for human bites.

22
Bites
  • Animal bites
  • dog 80 to 90, cat 3 to 15, non-domestic
    animals 1 to 2
  • Infection typically significant pain, soft
    tissue swelling, and tenderness associated
    injuries to nerves, tendons, bones, joints, or
    blood vessels. Hand bites associated with an
    increased risk of tenosynovitis, septic
    arthritis, and abscess formation.
  • Infections are usually polymicrobial, aerobes and
    anaerobes.
  • P. multocida 50 to 80 cat bites and 25 dog
    bites.Infection with acute severe pain,
    tenderness, and swelling, within 12 to 18 hours
  • Capnocytophaga canimorsus in immunocompromized
    pts.can be serious, w. overwhelming sepsis
    associated mortality is 25 to 30.

23
Bites
  • Therapy
  • Immediate wound toilet wash w. soap and water,
    irrigate, debride devitalized tissue
  • close lt 6 hoursolder than 12 hours, cat bites,
    and bites on the hand should be left open.
  • In all cases of infection get aerobic and
    anaerobic cultures
  • Determine tetanus immune status and immunize when
    appropriate.
  • non-domestic carnivore bites (e.g., bats, skunks,
    raccoons, foxes, or coyotes) irrigate with
    povidone-iodine and immunize against rabies
  • w. established soft tissue infection and/or risk
    factors Abx effective against aerobic and
    anaerobic organismsAmoxicillin-clavulanate ,
    trimethoprim-sulfamethoxazole, doxycycline,
    and/or ciprofloxacinP. multocida penicillin V,
    amoxicillin, cefuroxime, or ciprofloxacin C.
    canimorsus pcn, ampicillin, cipro, erythromycin,
    or doxycycline.

24
Bites
  • Human bites
  • occlusional bites (teeth puncture the skin) or
    clenched-fist injuries (contact with
    teeth).occlusional bites carry same risk of
    infection as animal bites, clenched-fist
    injuries and all hand injuries are associated
    with higher risk of infection.
  • Soft tissue infections are polymicrobial, mixture
    of aerobes and anaerobes. On avg. five different
    microorganisms isolated concentration of
    bacteria in the oral cavity is higher in humans
    bacteroides species are more common and often
    produce b-lactamases. predominant aerobic
    organisms are S. aureus, Staphylococcus
    epidermidis, a- and b-hemolytic streptococci and
    corynebacteria
  • contact with blood or saliva may transmit
    hepatitis B and C, Mycobacterium tuberculosis,
    and HIV.

25
Bites
  • Therapy
  • thorough high-pressure irrigation, with 1
    povidone-iodine (bactericidal viricidal).
  • aerobic and anaerobic cultures
  • debride devitalized tissue leave wound should
    open, infected or not.
  • extremity should be immobilized and elevated.
  • Abx for all infected hand wounds
    amoxicillin-clavulanate or doxycycline
  • Assess tetanus status and immunize as appropriate
  • Admit and IV Abx w. systemic signs of infection
    , severe cellulitis, compromised immune
    status diabetes mellitus significant
    associated joint, nerve, bone, or tendon
    involvement infection refractory to oral Abx.
    therapy

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27
Superficial infections
  • Cellulitis
  • acute bacterial infection of the dermis and
    subcutaneous tissues
  • primarily lower extremities - can affect all
    other areas
  • common causes
  • puncture wounds from injection of illicit drugs,
    foreign bodies or bites
  • secondary infection of preexisting skin lesions
    (eczema tinea pedis decubitus, venous stasis,
    or ischemic ulcers)
  • Less common extension of a subjacent infection
    (e.g., osteomyelitis)bacteremia from a remote
    site of infection.
  • Predisposing factors
  • lymphatic disruption or lymphedema, interstitial
    edema, previous irradiation of soft tissue,
    peripheral vascular disease diabetes mellitus,
    malnutrition, immunocompromise

28
Superficial infections
  • Cellulitis
  • Nonnecrotizing Form overwhelming majority
  • typically pain, soft tissue erythema, and
    constitutional symptoms (e.g., fever, chills, or
    malaise)
  • erythema with advancing borders, skin warmth,
    tenderness, edema. /-Lymphangitis or -adenitis
  • usually single aerobic pathogen
  • In otherwise healthy adults S. pyogenes and S.
    aureusS. pyogenes - more common (esp w.
    lymphangitis)S. aureus - often w.
    underlying chronic skin disease. Other H.
    influenzae - children or adults infected with
    HIVS. pneumoniae - pts with diabetes mellitus,
    alcoholism, nephr.
    syndrome, SLE, or hematol. malignancies.P.
    multocida - dog or cat bites. S.
    epidermidis - immunocompromised pts, (incl. HIV
    txplants)V. vulnificus - pts who ingested
    raw seafood or who had soft tissue
    trauma and sea water exposure A. hydrophila -
    w. soft tissue trauma fresh water exposure

29
Superficial infections
  • Cellulitis
  • Nonnecrotizing Form
  • Gram negatives and anaerobes
  • in decubital ulcers, diabetic, perianal/perineal
    infections
  • Therapy empirical antibiotic regimen attempts
    to isolate pathogen are usually unsuccessful
    needle aspiration / skin biopsy at advancing
    margin positive lt 15 / 40 bacteremia is
    uncommon blood cultures positive lt 2 to 4
    unless Sx of sepsisIn an otherwise healthy
    adult, uncomplicated cellulitis w/o systemic
    manifestations oral antibiotic on an outpatient
    basis

30
Superficial infections
  • Cellulitis
  • Nonnecrotizing Form
  • Therapy
  • majority of Strep and Staph are PCNase
    dicloxacillin, augmentin, cephalexin,
    cefadroxil, erythromycin, or clindamycin
  • margins of erythema should be marked
  • reduced activity and elevation
  • appropriate analgesic agents should be given.
  • diabetic or immunocompromised pts. and w. high
    fever orrapidly spreading cellulitis /
    cellulitis refractory to oral Abx (gt48 h)
    admission for I.V. Abx.Nafcillin, Cefazolin or
    ampicillin-sulbactam Clindamycin for suspected
    MRSA and PCN allergies Vancomycin, other Abx.
    and combination regimen

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32
Deep infections
  • Cellulitis
  • Necrotizing form superficial vs. deep
  • Superficial necrotizing cellulitis
  • similar etiology and pathogenesis to
    nonnecrotizing cellulitis
  • Predominantly in PVD, diabetes, pressure ulcer,
    venostasis, lymphedema or neglected primary
    cellulitis
  • more serious and often progressive
  • pathogens similar anaerobesclostridia,
    peptostreptococcus, bacteroides,
  • Therapy broad-spectrum Abx.urgent operative
    debridement is indicated/- hyperbaric O2 therapy

33
Deep infections
  • Cellulitis
  • Necrotizing form
  • Deep necrotizing cellulitis Necrotizing
    dermatitis, fasciitis, myositis
  • extension of superficial infection or
  • primary deep space infection
  • crush / penetration / neglect / hematogenous
  • does not have to have skin necrosis
  • often lack of specific early signs Sx, delayed
    diagnosis
  • host and pathogen factors
  • most are polymicrobial
  • early localized pain, tenderness, mild edema /
    erythema may be subtle -gt cave systemic illness
    gt local signs
  • Later bullae, intense erythema, skin necrosis,
    crepitus

34
Deep infections
  • Cellulitis
  • Necrotizing form
  • Deep necrotizing cellulitis
  • Necrotizing fasciitis
  • angiothrombotic microbial invasion and
    liquefactive necrosis of deep subqutaneous
    tissues, fascia /- muscle
  • Hallmark dishwater tissue fluid, thrombosis of
    vesselsfrank necrosis occurs later initially,
    tissue invasion proceeds horizontally,
  • Myonecrosis
  • rapidly progressive life-threatening infection
  • indicates involvement of Clostridium species.
  • gas formation common but not sine qua non
  • short incubation severe progressive disease in lt
    24 h
  • acute severe pain, often minimal physical
    findings
  • systemic signs of toxicity/ sepsis

35
Deep infections
  • Cellulitis
  • Necrotizing form
  • Deep necrotizing cellulitis
  • Therapy
  • broad-spectrum Abxto include MRSA, Gr. Neg and
    Clostridiabacteriocidal agents!
  • when clostridia suspected or confirmed,
    penicillin G, 2 to 4 million U every 4 hours
    immediately clindamycin, 900 mg every 8 hours,
    should be added. hyperbaric O2
    therapyoperative debridement.

36
Special infections
  • Rapidly progressive Cellulitis flesh eating
    bacteria
  • Strep. And Staph with Hyaluronidase, elastase,
  • Other exotoxins hemolysins, fibrinolysins, and
    streptolysins cause severe SIRS, hemolysis,
    intravascular thrombosis -gt DIC
  • Often extremely short progression time to MOF
  • Therapy as with deep necrotizing infections
  • broad-spectrum Abx to include MRSA, Gr. neg and
    Clostridiabacteriocidal agents! cave Eagle
    effect and toxin production during lag phase
  • hyperbaric O2 therapy
  • wide operative debridement.

37
Special infections
  • Streptococcal Toxic-Shock Syndrome
  • hemolytic streptococci of group A (S. Pyogenes)
  • more than 60 of patients with STSS have
    bacteremia.
  • current incidence 1.5 per 100,000 - STSS 10 to
    15, necrotizing fasciitis in 6.
  • typically extremity infection
  • only 50 have a demonstrable portal of entry
  • severe pain is the most common initial
    symptomsudden onset / generally precedes
    physical findings gt rapid progression.
  • hypotension invariably develops within 4 to 8
    hours after presentation -gt Shock, ,MOF, ARDS
  • Hemoglobinuria and an elevated serum creatinine,
    even w. adequate resuscitation

38
Special infections
  • Streptococcal Toxic-Shock Syndrome
  • S. pyogenes classified into gt 80 different
    strains, or M types
  • M proteins impede phagocytosis and induce
    vascular leakage by forming complexes with
    fibrinogen. They cleave (NAD), interrupting
    elemental cellular processes. The M proteins M1
    and M3 are associated with the majority of
    streptococcal necrotizing soft tissue infections.
  • Streptococcal pyrogenic exotoxins (SPEs) produced
    by most streptococci cause severe soft tissue
    infection can be transmitted by bacteriophages
    to different M types. They are the cause of the
    fever, shock, and tissue injury SPE-A and SPE-B
    induce synthesis of TNF-a, IL-1b, and IL-6.
  • M proteins or SPEs may act as superantigens.
    stimulate T cell responses direct binding to the
    Vb region of the T cell receptor, bypassing the
    normal antigen presentation pathway they do not
    undergo phagocytosis this pathway can stimulate
    more than a thousand times more T cells than the
    conventional antigen pathway and trigger a
    massive release of cytokines.

39
Special infections
  • Streptococcal Toxic-Shock Syndrome
  • clinical treatment failure sometimes w.
    penicillin alone attributable to the large
    inoculum size Eagle effect large inocula reach
    the stationary growth phase very quickly.
    Penicillin and other b-lactam antibiotics are
    ineffective in the stationary growth phase
    because of the reduced expression of
    penicillin-binding proteins)
  • toxin production is not inhibited by b-lactam
    antibiotics during the stationary growth phase.
    -gt add Abx. that inhibit protein synthesis
  • Clindamycin is more effective than b-lactam
    agents it suppresses bacterial toxin synthesis
    and inhibits M-protein synthesis, Clindamycin
    also suppresses synthesis of penicillin-binding
    proteins, and it can act synergistically with
    penicillin.

40
Surgical Site Infections
  • NNIS data on nosocomial infections
  • Surgical site infection 37
  • Urinary tract infection 27
  • Pneumonia (NP, VAP) 15
  • Primary BSI 7
  • All other sites 15
  • VA NSQIP data on nosocomial infections
  • Surgical site infections 5.1
  • Pneumonia 3.6
  • Urinary tract infection 3.5
  • Sepsis/systemic BSI 2.1

41
Surgical Site Infections
  • SSI impact
  • Procedures SSI No. deaths
    Cost (M)
  • Cardiac Surgery 383,000 15,000
    11,000 83.5Colorectal Surgery
    250,000 15,500 11,500
    127.0Other Surgery gt500,000 7,900
    4,500 63.0
  • In 2002 CDC and CMS initiated Surgical Infection
    Prevention Project(SIPP) now core benchmark
    for hospital performance, monitored by JCHAO and
    other organizations (WWW.SURGICALINFECTIONPREVENTI
    ON.ORG)

42
Natl. Acad. Sciences Research Council
Classification of wounds
43
NNIS risk factors for SSI
  • risk factors in addition to wound class
  • location of operation (abdomen or chest)
  • duration of operation
  • condition of wound at end of case
  • American Society of Anesthesiologists (ASA) class
    III, IV or V
  • patient clinical status (three or more diagnoses
    on discharge).

Endogenous bacteria are more important source of
SSI than exogenous pathogens Personnel is the
most important source for exgenous bacteria
44
Surgical Site Infections
  • SSI prevention is key!
  • Avoid elective surgery in the presence of remote
    infection
  • Proper selection and timing of peri-op Abx.
  • Strict adherence to infection control
  • Facilities, instruments, practices
  • Providers Hands, protection,
  • Modification of host factors
  • Nutrition, tight diabetic control
  • Immunosuppressants

45
Parenteral Antibiotics Recommended for
Prophylaxis of SSI
  • For coverage against aerobic gram-pos /-
    gram-neg organisms Cefazolin 1g I.V. or I.M.
    (I.V. preferred)
  • If patient allergic to cephalosporins or if MRSA
    suspectedVancomycin 1g I.V. Clindamycin
    600 mg I.V. or
  • Combination regimens for gram-neg aerobes and
    anaerobesMetronidazole 500 mg I.V.
    plus Aminoglycoside) 1.5 mg/kg I.V.
  • For single-agent coverage against gram-neg
    aerobes and anaerobes Cefoxitin 12 g I.V.
    or Cefotetan 12 g I.V.
  • Must be given ½ to 1 hour prior to incision!

46
Surgical Site Infections
  • SSI prevention is key!
  • Modification of host factors
  • Bowel preparation mechanic vs. SGD ?
  • Antimicrobial shower / baths (chlorhexidine) ?
  • Preoperative skin decontamination !
  • Clip rather than shave !
  • Preoperative nutritional optimization ?!
  • Peri-op tight diabetic control esp. week one !
  • Post operative O2 therapy !
  • Smoking cessation !

47
Surgical Site Infections
  • SSI prevention is key!
  • Modification operative factors
  • Decrase duration of OR ?!
  • Avoid hypotension/hypoxia ?!
  • Minimize use of Electrocautery !
  • Reduce talking !
  • Reduce tension on wound edges !
  • Reduce ischemia reperfusion !
  • Post operative O2 therapy !
  • Reduce need for blood transfusion ?!
  • Avoid drains ?!

48
Surgical Site Infections
  • SSI Therapy
  • Open the wound
  • Culture the wound
  • Ampiric Abx. therapy if significant cellulitis
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