Necrotising Fasciitis

Necrotising Fasciitis

Author: Tamsin Nicholson, Swansea, 1st year GEM

5 Key Points

  • Necrotising fasciitis is a life-threatening bacterial infection affecting superficial and deep fascia and muscle.
  • Progression can be rapid, up to 3cm of tissue loss per hour.
  • Necrotising fasciitis can be differentiated from cellulitis by pain being disproportionate to the visible skin inflammation.
  • The finger test enables quick identification of necrotising fasciitis.
  • Radical surgical debridement must be undertaken as soon as possible.

What is necrotising fasciitis?

Necrotising fasciitis is a life-threatening bacterial infection of subcutaneous tissues, fascia and muscle. It is intensely painful, progresses rapidly, and the infection tracks along the layers of tissue.

Clinical anatomy

Necrotising fasciitis affects the hypodermis, deep fascia and muscle. The hypodermis, also known as the superficial fascia, is the deepest layer of the skin. The deep fascia lies underneath the hypodermis. The deep fascia is dense fibrous tissue that envelopes muscle. In necrotising fasciitis, the infection tracks along these layers of tissue. It is for this reason, that the extent of the infection and associated tissue damage may be much greater than the visible area of inflammation from the surface.


Bacteria enters subcutaneous tissues via trauma, surgical incision or bowel perforation. The bacteria proliferate, releasing toxins and enzymes that cause thrombosis. The impaired blood supply leads to local ischaemia, cell death and tissue necrosis. Skin appears normal in early stages, with necrosis occurring later due to thrombosis affecting dermal capillary beds(1).


Necrotising fasciitis is most commonly classified according to the causative organism(1, 2). The majority (70-80%) of cases are Type 1, and 20-30% are Type II. Type III and IV necrotising fasciitis occur infrequently(1).



Who’s at risk?

Type I

  • Polymicrobial
  • Bowel-derived bacteria
  • Mixed anaerobes and aerobes
  • Elderly
  • Immunocompromised
  • Peripheral vascular disease & diabetes

Type II

  • Often monomicrobial
  • Skin or throat derived bacteria
  • Group A streptococcus
  • Staphylococcus aureus
  • Healthy patients with recent trauma or surgery
  • IV drug users

Type III

  • Gram-negative
  • Often marine-related bacteria
  • Vibrio species 
  • Patients with exposure to seafood or marine life 
  • Wound exposed to contaminated water

Type IV

  • Fungal
  • Usually associated with trauma
  • Candida species in immunocompromised patients
  • Zygomycetes in immunocompetent patients
  • Burns patients
  • Healthy patients with recent trauma
  • Severely immunocompromised

Clinical features

Patients appear generally unwell, presenting with severe pain, fever and dermatological symptoms. Repeated examination is important. As the infection progresses, dermatological features become more severe and patients may develop signs of sepsis.

The dermatological features are classified into three stages:(1)

  1. Erythema with tenderness extending beyond the erythema, swelling, and heat
  2. Blistering, skin bullae, skin fluctuation
  3. Crepitus, skin necrosis, gangrene, haemorrhagic bullae.

Progression is variable, but can be up to 3cm of tissue loss per hour(3). It is helpful to mark the boundaries of inflammation, to identify the rate of progression(4). In rapidly progressing disease, death can occur within hours of presentation(1).

Necrotising fasciitis vs cellulitis

The clinical features of necrotising fasciitis are very similar in the early stages. Therefore, misdiagnosis is common, but associated with increased morbidity and mortality. The primary distinguishing feature is that necrotising fasciitis induces severe pain that is disproportionate to the visible inflammation(5).


Surgical exploration and biopsy confirm diagnosis of necrotising fasciitis.

The finger test(6)

A surgeon makes a small incision under local anaesthetic and inserts a finger down to the deep fascia(7). This reveals features of necrotising fasciitis including:

  • ’Dishwater’ pus
  • Lack of fascial resistance - normally the superficial fascia would adhere to the dermis
  • Visible necrosis of fascia and muscle(1).

Other signs include:

  • Significantly elevated CRP and white cell count(5)
  • Blood cultures positive for group A streptococcus in Type II necrotising fasciitis(5)
  • Signs of sepsis
  • Histology reveals underlying thrombosis, necrosis and bacteria(1).


On admission

Patients have high risk of sepsis and may require haemodynamic resuscitation to optimise tissue perfusion(1).

Surgical debridement

Aggressive surgical debridement is required as soon as possible. Imaging should not delay surgery. Debridement aims to remove all affected tissue and the source of infection. Amputation may be necessary. Multiple debridements are often required to eradicate infection. Significant blood loss and difficulties closing wounds can occur. Reconstructive surgery may be considered at a later date.


Antibiotic choice should be guided by a senior microbiologist. Broad spectrum antibiotics should be used.

  • Tazocin or a carbopenem may be used in combination with clindamycin(1)
  • For group A streptococcus, penicillin and clindamycin may be used(5).


Necrotising fasciitis is a life-threatening disease with a mortality rate over 30%(8). Significant loss of soft tissue is the most common cause of mortality, associated with loss of limb and infection(9). Different causative organisms have variable mortality rates. Other factors impairing patient outcome include:

  • Increased age
  • Uncontrolled diabetes
  • Immunosuppression
  • Delayed surgery(8)
  • Malnourishment
  • Hypertension
  • Malignancy(10)

Necrotising fasciitis also leads to significant functional deficits in surviving patients. Surviving patients will likely require input from the multidisciplinary team including physiotherapists, psychologists, trauma counsellors, prosthetists etc.


1. Davoudian P, Flint NJ. Necrotizing fasciitis. Continuing Education in Anaesthesia Critical Care & Pain. 2012;12(5):245-50.

2. Morgan MS. Diagnosis and management of necrotising fasciitis: a multiparametric approach. Journal of Hospital Infection. 2010;75(4):249-57.

3. Misiakos EP, Bagias G, Patapis P, Sotiropoulos D, Kanavidis P, Machairas A. Current concepts in the management of necrotizing fasciitis. Front Surg. 2014;1:36.

4. Kiat HJ, En Natalie YH, Fatimah L. Necrotizing Fasciitis: How Reliable are the Cutaneous Signs? J Emerg Trauma Shock. 2017;10(4):205-10.

5. Kumar PJ, Clark ML. Kumar & Clark Clinical Medicine: Elsevier Saunders; 2020.

6. Andreasen TJ, Green SD, Childers BJ. Massive infectious soft-tissue injury: diagnosis and management of necrotizing fasciitis and purpura fulminans. Plast Reconstr Surg. 2001;107(4):1025-35.

7. Lau JK, Kwok K, Hung Y, Fan C. Validation of finger test for necrotising soft tissue infection. Journal of Orthopaedics, Trauma and Rehabilitation.0(0):2210491720961546.

8. Wallace HA PT. Necrotizing Fasciitis 2020 [Available from:

9. Khamnuan P, Chongruksut W, Jearwattanakanok K, Patumanond J, Tantraworasin A. Necrotizing fasciitis: epidemiology and clinical predictors for amputation. Int J Gen Med. 2015;8:195-202.

10. Wang JM, Lim HK. Necrotizing fasciitis: eight-year experience and literature review. Braz J Infect Dis. 2014;18(2):137-43.

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