Necrotising Soft Tissue Infections

Necrotising soft-tissue infections are aggressive, life-threatening infections characterised by rapidly progressing necrosis of subcutaneous tissue and fascia, with relative sparing of underlying muscle. NSTI:

Epidemiology and Risk Factors

Predisposing factors for necrotising soft tissue infection include:

  • Abnormal anatomy
    • Previous trauma
    • Previous surgery
    • Obesity
    • Lymphedema
    • Chronic venous insufficiency
    • DVT
  • Vascular damage
    • PVD
    • Diabetes
    • Smoking
  • Immunosuppression
    • Alcoholism
    • Steroid use
  • Route of entry
    • IV drug use
    • Pre-existing infection

Risk factors associated with ↑ mortality include:

  • Age
    Especially in >70 age group.
  • Illness severity
  • Organism
    Higher mortality seen with:
    • Group A Streptococci
    • Enteric organisms

Pathophysiology

Necrotising fasciitis involves:

  • Rapid proliferation of subcutaneous bacteria
  • Leukocyte proliferation
  • Thrombosis of fascial vessels
    Leads to ischaemia and necrosis of tissue.

Toxic shock syndromes also contribute to haemodynamic instability in both Streptococcal and Staphylococcal infections.

Clinical Manifestations

Typically present as cellulitis that:

  • Affects the relatively young and well
  • Follows a history of minor trauma
  • Is initially indistinguishable from an uncomplicated soft tissue infection, but fails to improve on antibiotics
  • Has disproportionate pain to the degree of injury
    • Hard, “woody” oedema of affected areas

Additional features include:

  • Fever
    Surprisingly rare.
  • Crepitus Associated with gas-forming organism infection (generally Clostridia, classically C. Perfringens) but may also occur with other bacteria such as E. Coli.

Diagnostic Approach and DDx

Investigations

Bedside:

  • ABG
    • Lactic acidosis

Laboratory:

  • Bloods
    • FBE
    • UEC
    • CMP
      • Hypocalcaemia
    • Coag
      • DIC

Imaging:

  • XR
    • Gas in soft tissue planes
  • CT
    • Fascial thickening
    • Contrast enhancement
    • Fascial fluid collections
    • Gas in soft tissue planes
  • US
    • Fascial fluid collections
    • Gas

MRI may reveal fascial thickening and hyperintense T2 signal; however MRI is not the ideal investigation for a time-critical surgical diagnosis.

Other:

  • Operative findings
    • Gray necrotic fascia
    • Lack of bleeding
      Due to microvascular thrombosis.
    • “Dishwater” pus

Management

  • Standard sepsis resuscitation
  • Aggressive, early, surgical debridement
  • Broad spectrum antibiotics with Streptococcal cover

Resuscitation:

  • C
    • Noradrenaline almost always required in a “true” NSTI

Specific therapy:

  • Pharmacological
    • Antimicrobials
      • Broad-spectrum agent
        • Meropenem 1g Q8H
        • Amoxacillin/clavulanate 1.2g Q6-8H
      • Streptococcal cover
        • Clindamycin 300-450mg Q6H
      • MRSA cover
        • Vancomycin
    • IVIG
      • Associated with ↓ hospital mortality
  • Procedural
    • Aggressive surgical debridement
      Single most important management strategy.
      • Outcome improves with surgeon experienced in management
      • Early debridement is critical for a good outcome
      • Aggressive debridement to healthy tissue
  • Physical
    • Hyperbaric Oxygen Therapy
      • Controversial
      • Associated with a ↓ in mortality and number of debridements, although evidence is conflicting
      • Use should never delay surgical debridement
      • Significant logistic impediments to use
        • Availability
        • Transfer of critically ill into an isolated environment
      • Evidence is conflicting and some retrospective studies do not demonstrate mortality benefit

Antimicrobial therapy should be adjusted for known resistance patterns.

Clindamycin suppresses Streptococcal toxin production, which may ↓ severity of septic shock and is strongly associated with ↓ mortality.

The mechanism of HBOT is uncertain, possibilities include:

  • ↑ Viability of marginal tissue
  • ↓ Bacterial toxin production
  • Inhibits anaerobic bacterial growth
    ↑ Tissue oxidation reduction potential.
  • Potentiates antibiotic function
  • ↑ Efficacy of neutrophil respiratory burst

Disposition:

  • ICU
    Obviously required for shock requiring vasoactive support.

Complications

Prognosis

  • 30% mortality with aggressive surgical intervention and appropriate antibiotics
  • Frequent surgical debridements
  • Long hospital stay
  • Large soft tissue defects

References

  1. Devaney B, Frawley G, Frawley L, Pilcher DV. Necrotising soft tissue infections: the effect of hyperbaric oxygen on mortality. Anaesth Intensive Care. 2015 Nov;43(6):685-92. PubMed PMID: 26603791.
  2. Levett D, Bennett MH, Millar I. Adjunctive hyperbaric oxygen for necrotizing fasciitis. Cochrane Database of Systematic Reviews 2015, Issue 1. Art. No.: CD007937.
  3. Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.