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
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