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Pathology and aetiology

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

This condition can be classified microbiologically into 4 groups :

  • type I - polymicrobial infection, 70%-80% of cases
    • also known as synergistic NF
    • typically a slow process that evolves over days
    • affects immunocompromised patients or those with an underlying abdominal pathology
    • a mixture of aerobic and anaerobic organisms can be seen, common pathogens include pseudomonas, haemolytic staphylococcus, bacteroides, coliforms (2)
    • more indolent better prognosis and easier to recognize clinically
  • type II - monomicrobial, 20%-30% of cases
    • progresses more rapidly
    • approximately 50% of type II NF cases are associated with the exotoxin driven disease - toxic shock syndrome
    • generally due to gram positive organism e.g. - group A streptococci (most common), Clostridium perfringens, Staphylococcus aureus (1)
  • type III
    • commoner in Asia
    • caused by gram negative organism (often marine related organism) e.g - Vibrio spp such as V. damselae and V. vulnificus
  • type IV
    • caused by fungal infection
    • usually it is associated with traumatic wound and burns (1)

Some known risk factors of NF include (1,2,3):

  • diabetes and other chronic medical diseases
  • immunosuppressive drugs
  • malnutrition
  • advanced age e.g. - age >60 years
  • IV drug use
  • peripheral vascular disease
  • obesity
  • underlying malignancy

Clinicians should obtain specific history form patient to gather information about any precipitating events which might have caused NF. e.g. -

  • traumatic event - surgery, IV drug use, penetrating injury
  • non traumatic - soft tissue infections, burns, childbirth etc (1)

Notes:

  • the underlying pathogenesis reflects the evolution of clinical signs over time:
    • subcutaneous infection spreads from either a breach in the soft tissue or haematogenous spread
      • causes erythema and swelling (mimics features occurring in a soft tissue infection)

    • pathogen then spreads along the horizontal planes
      • causes infarction of the nutrient vessels and nerves
      • and then consequent induration and disproportionate pain

    • in the final stage the infarction leads to oedematous changes in compartments, forming haemorrhagic bullae and then the appearance of gas gangrene

Reference:


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