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Necrotising soft tissue infections

Section: Skin and soft tissue Sub-section: Skin infections and breakdown Curriculum: Curriculum, page 53

  • Necrotizing soft tissue infections (NSTIs) include necrotizing forms of faѕciitiѕ, myositis, and ϲellսlitiѕ
  • These infections are characterized clinically by fulminant tissue destruction, systemic signs of toxicity, and high mortality. Accurate diagnosis and appropriate treatment must include early surgical intervention and antibiotic therapy.

Necrotising faѕciitiѕ

Definition

  • A life threatening clinical syndrome of aggressive bacterial infection of soft tissues with progressive tissue necrosis
  • Predominantly affecting deep fascia & subcutaneous tissue layers
  • a.k.a. “Flesh-eating bacteria”, suppurative fasciitis, hospital gangrene, necrotizing erysipelas, haemolytic streptococcus gangrene

Incidence

  • 0.4 cases per 100,000
  • Increasing incidence
  • M > F 2-3:1
  • Mean age 38-44
  • Rare in children

Classification

  • Type 1 – Polymicrobial
  • Type 2 – Monomicrobial

Type 1

  • Polymicrobial
    • Average 4 micro-organisms
  • Anaerobes and Aerobes work synergistically
    • Anaerobic species
      • Most commonly Bacteroides, Clostridium, or Peptostreptococcus
    • Enterobacteriaceae
      •  Escherichia coli, Enterobacter, Klebsiella, Proteus
    • Facultative anaerobic
      • Streptococci - other than group A Streptococcus 
  • More common in trunk & perineum
  • More common in
    • Immunocompromised
    • T2DM
    • PVD

Type 2

  • Monomicrobial:

    • Gram positive Cocci
      • Group A Strep (S. pyogenes – Beta- hemolytic)
        • Group A strep is associated with higher rate of bacteremia & TSS
          • Hence more rapid progression
      • Staphylococcus aureus
    • Gram negative rods
      • Aeromonas species (Aeromonas hydrophila)
        • Freshwater exposure
      • Vibrio species (Vibrio vulnificus)
        • Salt water exposure

  • Some authors include type 3 and 4 - Uptodate does not.

    • Type 3
      • Clostridial myonecrosis (Gas gangrene)
      • Or classify the gram negative water born bacteria (Aeromonas or Vibrio) as 3 and not gas gangrene
    • Type 4 - Fungal

Risk Factors

  • DM
  • PVD
  • Immunosuppression
  • Smoking
  • IVDU
  • Obesity
  • Chronic renal failure
  • Alcohol abuse
  • Trauma
  • Insect bites/animal bites
  • Surgical incision
  • Chickenpox
  • Indwelling catheters
  • Perforation of GI Tract

Clinical Presentation

  • HIGH INDEX OF SUSPICION = KEY TO DIAGNOSIS
    • Erythema 66-100%
    • Pain or tenderness beyond margin of erythema 73-98%
    • Swelling 75-92%
    • Crepitus or skin necrosis 13-31%
    • Bullae 23-42%
    • Fever 32-53%
    • Hypotension 11-18%
    • 10-40% - Hx of trauma or break in skin
  • May present as fulminant, acute or sub-acute
    • Patients with fulminant disease progress to shock
  • Earliest clues
    • Local pain out of proportion to the apparent severity of cellulitis
    • Erythema and oedema - spreading diffuse inflammatory reaction, that blends into the surrounding tissue
    • Overlying skin is shiny & tense, without sharply demarcated borders
    • Speed of spread
    • Skin may be anaesthetic
    • Crepitus may be present (late)
      • Gas: Clostridium, E. coli, Peptostreptococcus, Bacteroides
  • Low grade fever, tachycardia = Common
  • Patients anxious & sweaty
  • In later stages: Skin necrosis may become evident → Skin turns purple / black
    • Manifests sooner in areas of thinner skin (perineum)
  • In adults: limbs most commonly affected
  • 14-35% initially diagnosed as simple cellulitis or abscess

Pathology

  • Initiating event
    • Infection usually begins through a break in the skin
  • Bacteria spread and invasion through tissue
    • Initially through skin and subcutanous tissue
    • Then infection spreads rapidly along the muscle fascia due to its relatively poor blood supply
  • Spread is aided by:
    • Endotoxin - components of bacterial cell membranes that illicit an inflammatory response
    • Exotoxin - compounds secreted by bacteria & enzymes
      • Hyaluronidase, Collagenase, Streptokinase, Lipase
      • Enable horizontal extension through fascial planes
  • This results in
    • Vascular thrombosis due to activation of Coagulation Cascade
    • Tissue ischaemia and necrosis
    • Further spread, facilitated by ischaemic microcirculation
  • Host immune response
    • Local response is ineffective due to vascular compromise and necrosis
    • Systemic response is triggered
      • Exaggerated inflammatory response caused by cytokines TNFa and IL-1, IL-6
    • Progression
      • This results in SIRS, Sepsis, multi-organ dysfunction, shock, DIC, Death.

Specific toxins

  • Clostridium
    • Releases α toxin
  • Group A Streptococcus
    • Surface M proteins
      • Inhibits phagocytosis/opsonization by complement
    • Many Exotoxin including Spe A, C, G, Streptolysin O, Streptococcus Superantigen (TSS)
      • Trigger cascade of cytokines by activating T-Cells and Macrophages
      • Strep toxins trigger profound cellular/tissue damage
  • Staphylococcus
    • Toxic shock syndrome toxin-1
      • superantigen
    • Staphylococcal enterotoxins A, B, C, D, E, G, H
    • Staphylococcal hemolysins

Investigations

  • Clinical diagnosis
  • Bloods: FBC, UEC, CRP
    • If both WCC & serum Na are normal, necrotising fasciitis is unlikely
      • (NPV = 99%)
  • X-ray: May demonstrate air (?50% sensitive)
  • CT: 80% sensitivity (even without IV contrast)
  • MRI more sensitive but less specific – fascial enhancement
  • USS no good
  • Bedside FNA, incisional biopsy for culture – high false –ve rate
  • LRINEC score
  • At operation – “the finger test”

LRINEC Score

  • Biochemical scoring system based on a retrospective observational study
    • Gives probability of necrotizing soft tissue infection
  • Points for
    • CRP
    • WCC
    • Hb
    • Na+
    • Creatinine
    • Glucose
  • Score of ≥ 6 used as a cut-off for nec fasc
    • PPV 92%, NPV 96%
    • Note 10% of patients with nec fasc had LRINEC <6!
  • Must use with caution
    • No prospective trials validating LRINEC
    • Validation studies have not replicated same results as original study

Operative Test

  • “Finger Test”
  • 2cm incision in skin, to deep fascia
  • Lack of bleeding / exudate
  • Insert index finger, if subcutaneous tissue is easily dissected off the fascia (to which it is normally densely adherent), the test is +ve
    • Pathognomonic for necrotizing fasciitis
  • Liquefactive necrotic tissue or pus (“dishwater”) can also be found in between the fascial planes

Management

  • Resuscitation
  • Broad spectrum antibiotics (as per local guidelines)
    • UTD recommends
      • Carbapenem (Meropenem 1g IV Q8hrs), or Tazocin
      • anti-MRSA – Vancomycin
      • Clindamycin (antitoxin effects)
  • Te Whatu Ora Waitemata Guidelines:
    • Benzylpenicillin 2.4g (4MU) IV Q4Hly
    • Clindamycin 600mg IV Q8H
    • Gentamicin as per dose guidelines
    • Can tailor further therapy to culture sensitivities
      • e.g. Penicillin + Clindamycin/Metronidazole
      • +/- Gentamicin for gram negatives
  • Surgical debridement
  • ICU care

Surgical Debridement

  • Beyond margins of infection
    • Boundary should be as wide as rim of cellulitis, back to healthy bleeding tissue
    • Most important determinant of mortality is time & adequacy of debridement
  • x 9 increase in MR if delayed > 24 hours
  • x 7 increase in MR if debridement incomplete
  • ± Relook / serial debridement
    • Average of three needed – 12-36 hours apart
  • ± Fasciotomy
  • Amputations needed in 20%
  • Staged reconstruction of defects
  • Vac dressing
  • May require grafting

ICU Care

  • Fluids (aggressive)
    • Avoidance of vasopressors if possible
  • Nutritional support
  • ± Hyperbaric Oxygen
    • ?↓ mortality (conflicting reports in literature, data limited)
    • 100% oxygen at 2.8x atmospheric pressure for 95mins up to 3x/day for 6 days
    • Arterial oxygen 2000mmHg (versus 300mmHg in normobaric)
    • Tissue oxygen 300mmHg versus 75mmHg
    • Used to target anaerobes (Clostridium etc.)
    • In theory inhibits anaerobic growth & exotoxin production & enhance killing abilities of leucocytes

Prognosis/Natural History

  • Mortality rates: 30-50%
    • Higher mortality if head, neck, chest or abdo are involved
  • Predictors of Mortality
    • Time to operative intervention
    • Age > 60
    • WCC > 30
    • Creatinine > 200
    • Shock
    • DM

Necrotizing Cellulitis

  • Cellulitis without fasciitis
  • Can have frankly necrotic centre
  • Systemic symptoms will be less
  • Management principles the same

Necrotizing Streptococcal Myositis

  • Rare
  • Group A streptococcus
  • Necrotising infection involving muscle
  • Early Symptoms
    • Pain in the muscle, that worsens over 24-48hrs
    • High rate of bacteraemia & subsequent Toxic Shock Syndrome
  • USS / CT:
    • Swelling ± air in muscle (some say NO gas with this problem)
  • Management
    • Aggressive surgical debridement
    • High dose penicillin & clindamycin (+/- vanc for MRSA)
  • MR 80-100%

Fournier’s gangrene

Gas gangrene

Toxic Shock Syndrome

  • Superantigen
    • Bacterial protein from Staphylococcus
      • Polyclonal T-lymphocyte activators
      • Induce prolific cytokine cascades
    • Streptococcus pyogenic superantigen
      • Generates toxic shock syndrome via profound cytokine cascade through macrophage activation
  • Endotoxins
    • Bacterial wall lipopolysaccharides that are released when cell wall degraded
    • Create the manifestations of septic shock
  • Low doses
    • Activates Monocytes & Macrophages (via TNF, IL-1, IL-6, Chemokines)
  • Moderate doses
    • Cytokine-induced secondary effectors (NO) become important
    • Systemic effects of TNF, IL-1 (fever, acute phase reactants)
    • Inhibits thrombomodulin & TFPI – tips cascade toward thrombosis
  • High doses
    • Same cytokines cause
    • Systemic vasodilation, diminished myocardial contractility, widespread endothelial injury & activation
    • ARDS, activation of coagulation system, DIC, MSOF

Dog and Cat Bite Infections

Dog Bite Organisms

  • Pastuerella spp.
  • Staph aureus
  • Strep pyogenes
  • Capnocytophaga canimorsus
  • Anaerobes

Cat Bite Organisms

  • Pasteurella multocida
  • Staph aureus
  • Strep pyogenes
  • Anaerobes
  • Bartonella henselae – causative agent in Catscratch Disease

Rodent Bite Organisms

  • Streptobacillus moniliformis
  • Spirillum minus
  • Salmonella spp.

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