1
Soft tissue infections

• Thomas Genuit, MD,MBA, FACS
• Sinai Hospital of Baltimore
• 2006

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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.

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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.

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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

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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

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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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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.

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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.

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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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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.

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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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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.

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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

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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.

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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.

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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.

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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.

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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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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

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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

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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

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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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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

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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

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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

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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.

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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.

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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

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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.

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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.

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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

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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)

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Natl. Acad. Sciences Research Council
Classification of wounds
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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
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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

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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!

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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 !

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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 ?!

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Surgical Site Infections

• SSI Therapy
• Open the wound
• Culture the wound
• Ampiric Abx. therapy if significant cellulitis