Necrotising fasciitis

Contents

Classification

Necrotising fasciitis (NF) is a rapidly progressive, life-threatening infection of the deep fascia with secondary necrosis of overlying skin and subcutaneous tissue.

Type I — Polymicrobial (70–90%)

  • Synergistic infection with mixed aerobic and anaerobic bacteria
  • Risk factors: diabetes mellitus, obesity, immunosuppression, peripheral vascular disease, recent surgery or instrumentation
  • Typical sites: perineum, abdominal wall, lower extremities
  • Includes Fournier's gangrene (perineal/genital Type I)

Type II — Monomicrobial (10–30%)

  • Most commonly Group A Streptococcus (Streptococcus pyogenes)
  • Can affect young, otherwise healthy individuals (no predisposing condition)
  • Rapid, aggressive progression; highest mortality
  • Associated with streptococcal toxic shock syndrome (strep TSS)
  • Other monomicrobial organisms: Staphylococcus aureus (including MRSA), Klebsiella pneumoniae (in immunocompromised, particularly in South-East Asia), Aeromonas hydrophila (fresh water exposure), Vibrio vulnificus (salt water, shellfish)

Type III — Gram-Negative Monomicrobial

  • Marine organisms: Vibrio vulnificus — associated with seawater, raw shellfish consumption; particularly dangerous in liver disease (cirrhosis); characteristic haemorrhagic bullae
  • Gas gangrene (clostridial myonecrosis): Clostridium perfringens → myonecrosis rather than fascial necrosis; overlapping spectrum

Microbiology

Type I Polymicrobial Flora (typical)

  • Aerobes: E. coli, Klebsiella, Proteus, Enterococcus, S. aureus
  • Anaerobes: Bacteroides, Peptostreptococcus, Clostridium spp.
  • Synergistic: anaerobes consume O₂ and create reducing environment → facilitates anaerobic gas production and inhibits phagocytosis; aerobes provide toxins and enzymes that allow deeper tissue invasion

Group A Streptococcus (Type II)

  • Produces numerous virulence factors: streptolysin O and S (cell lysis), hyaluronidase (tissue spread), M protein (anti-phagocytic), streptococcal superantigens (M1, M3 strains — trigger massive non-specific T-cell activation → cytokine storm → toxic shock)
  • Streptococcal TSS: hypotension + organ failure + skin involvement; mortality >50%

Clinical Recognition

NF is a clinical diagnosis confirmed at surgery. External skin signs may be minimal or absent early — the fascial necrosis runs ahead of the overlying skin changes.

Cardinal Features

Feature Notes
Pain out of proportion to appearance Hallmark early sign; intense disproportionate pain over the affected area
Systemic toxicity Disproportionate tachycardia, fever, hypotension relative to local findings
Skin changes (late) Erythema → oedema → skin discolouration (dusky/violaceous) → bullae → frank necrosis
Wooden consistency Induration and "woody" feel of subcutaneous tissues on palpation
Crepitus Gas in soft tissues (not always present; highly specific)
Anaesthesia of skin Overlying cutaneous nerves destroyed → skin numbness (late)

Rapid clinical deterioration despite apparently limited local findings should raise suspicion.

Surgical ("Finger") Test

On surgical exploration: blunt dissection along fascial planes encounters no resistance (normal fascia does not separate this easily); absence of bleeding from necrotic tissue; "dishwater" grey fluid in the fascial planes; grey necrotic fascia. These findings confirm NF.

LRINEC Score

The Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC score) combines laboratory markers to estimate the probability of NF:

Variable Points
CRP >150 mg/L +4
WBC 15–25 ×10⁹/L +1; >25 ×10⁹/L = +2
Haemoglobin 11–13.5 g/dL +1; <11 g/dL = +2
Sodium <135 mmol/L +2
Creatinine >141 µmol/L +2
Glucose >10 mmol/L +1

Score ≥6: high risk (positive predictive value ~75%); score <6: lower risk.

Critical limitations:

  • Poor sensitivity — NF can present with scores <6, particularly early in the disease
  • The LRINEC score should never be used to exclude NF — clinical suspicion mandates surgical exploration regardless of score
  • Useful for raising clinical index of suspicion, not for ruling out the diagnosis

Investigations

Imaging

Plain X-ray or CT:

  • Gas in soft tissues on plain X-ray or CT: pathognomonic when present — however, gas is absent in up to 50% of cases (particularly Type I without gas-producing organisms)
  • CT is more sensitive than X-ray: thickening of fascia, asymmetric fascial thickening, air tracking along fascial planes, fluid collections
  • CT does NOT exclude NF — a normal CT in the setting of strong clinical suspicion should not delay surgical exploration
  • MRI: most sensitive imaging modality; not practical in an emergency

Microbiology

  • Blood cultures (aerobic and anaerobic) ×2 before antibiotics
  • Wound swabs: limited value pre-debridement (surface contamination)
  • Tissue samples and fascial biopsies intraoperatively: frozen section histology can confirm necrosis; culture guides antibiotic de-escalation

Other Investigations

  • FBC (severe leucocytosis or paradoxical leucopenia in severe sepsis)
  • CRP (markedly elevated), procalcitonin
  • CK: markedly elevated if myonecrosis component
  • LFTs (systemic toxin effect)
  • Glucose, creatinine, electrolytes (LRINEC variables)
  • Clotting: DIC may co-exist

Management

1. Emergency Surgical Debridement

Surgical debridement is the single most important determinant of survival. Delay is the primary driver of mortality.

  • Immediate surgical exploration on clinical suspicion — do not wait for imaging results if the patient is deteriorating
  • Wide excision of all necrotic tissue: resect to viable bleeding margins; leave no necrotic tissue
  • Repeat debridement: mandatory at 24–48h (often multiple returns to theatre required); necrosis can extend rapidly
  • Definitive wound management: VAC (vacuum-assisted closure), grafting, or reconstruction after infection controlled

2. Antibiotics

Broad-spectrum empirical coverage from the outset, targeting both aerobic and anaerobic organisms:

Empirical regimen (UK practice, based on type and local guidelines):

  • Piperacillin/tazobactam 4.5 g IV 6-8-hourly (broad aerobic/anaerobic cover)
  • PLUS clindamycin 1.2 g IV 6-hourly: crucially important — inhibits bacterial ribosomal protein synthesis → inhibits toxin production (particularly streptolysin, superantigens in Group A Strep); bacteriostatic effect on rapidly dividing organisms
  • If Group A Strep suspected or confirmed: add benzylpenicillin 2.4 g IV 4-hourly (or ampicillin) — synergistic with clindamycin; high-dose penicillin kills actively dividing organisms
  • If MRSA risk: replace pip-tazo with meropenem + vancomycin or teicoplanin
  • Tailor based on intraoperative cultures as results return

Duration: continue broad-spectrum antibiotics until necrosis controlled, patient stable, and cultures guide de-escalation.

3. ICU Resuscitation

  • Aggressive haemodynamic resuscitation (septic shock physiology)
  • Vasopressors (noradrenaline), organ support (RRT for AKI, mechanical ventilation)
  • Nutrition: early enteral nutrition; high protein requirements during wound healing phase

Fournier's Gangrene

Fournier's gangrene is Type I necrotising fasciitis specifically involving the perineum, scrotum, penis, or vulva.

  • Mixed polymicrobial infection; typically in diabetics, elderly, or immunocompromised
  • High mortality (15–40%) from systemic sepsis; genital loss is common
  • Management: same principles — urgent surgical debridement (including orchiectomy if scrotal involvement; testes themselves are usually spared as they have a separate blood supply via spermatic cord), antibiotics, ICU support
  • Defunctioning colostomy: sometimes required to divert faecal contamination from perianal wounds
  • Urinary diversion: suprapubic catheter if urethral involvement
  • Wound care: frequently requires multiple dressing changes, VAC therapy, skin grafting

Adjunctive Therapies

Intravenous Immunoglobulin (IVIG)

  • Rationale: streptococcal superantigens drive massive T-cell activation → cytokine storm in strep TSS; IVIG contains polyclonal antibodies that neutralise bacterial superantigens and toxins
  • Evidence: small case series and observational data suggest benefit in streptococcal TSS; no large adequately powered RCT
  • Current use: considered in confirmed Group A Strep NF with TSS features (hypotension + organ failure); dose 1 g/kg day 1, 0.5 g/kg days 2–3; discussed with microbiologist/immunologist

Hyperbaric Oxygen (HBO)

  • Rationale: increases tissue oxygen partial pressure → enhances neutrophil bactericidal activity against anaerobes; may reduce necrotic spread
  • Evidence: limited RCT evidence; observational studies suggest possible mortality benefit
  • Current use: adjunctive only in specialist centres with facilities; must never delay surgical debridement; logistically difficult in critically ill patients

Viva Questions

1. How do you clinically recognise necrotising fasciitis early and what is the significance of pain out of proportion?

Necrotising fasciitis is notoriously difficult to diagnose early because external signs lag significantly behind the extent of fascial necrosis. The hallmark early sign is pain disproportionate to the visible skin findings — this occurs because the deep fascia is richly innervated while the overlying skin may appear relatively normal or only mildly inflamed. The intense pain reflects deep tissue ischaemia and inflammatory infiltration of the fascia. As the disease progresses, the overlying skin nerves are destroyed by the spreading necrosis, paradoxically causing anaesthesia — at this stage the skin may appear necrotic but is no longer painful, which is a late and sinister sign. Systemic toxicity out of proportion to local signs (disproportionate tachycardia, hypotension, fever) is another key feature. Gas on imaging is pathognomonic but absent in up to 50% of cases. The LRINEC score supports clinical suspicion but should never be used to exclude NF. If there is strong clinical suspicion, the only appropriate response is urgent surgical exploration — a negative exploration is preferable to a delayed diagnosis.

2. Why is clindamycin included in the antibiotic regimen for necrotising fasciitis, even when piperacillin/tazobactam provides broad-spectrum coverage?

Clindamycin serves a specific and critical role beyond its bacterial coverage: it is a protein synthesis inhibitor (binds the 50S ribosomal subunit and prevents peptide elongation). This means it inhibits the production of bacterial toxins and virulence factors — particularly important in Group A Streptococcal NF, where the clinical syndrome is driven as much by superantigen-mediated immune activation (leading to streptococcal TSS) as by the bacteria themselves. Even organisms in a non-replicating state (which are less susceptible to cell-wall active agents like penicillin/pip-tazo) continue to produce toxins — and clindamycin inhibits this toxin production. The combination of a cell-wall active agent (benzylpenicillin for GAS, or pip-tazo for polymicrobial) with clindamycin therefore addresses two different pathophysiological mechanisms: bacterial killing AND toxin suppression. This combination is also synergistic — the cell-wall agent kills actively dividing organisms while clindamycin limits virulence factor production. In Type I polymicrobial NF, clindamycin's anaerobic coverage is an additional benefit.

3. A 52-year-old diabetic presents with a painful, erythematous, swollen left thigh with no obvious breach and moderate systemic upset. CT shows fascial thickening but no gas. How do you manage this?

I am concerned about NF until proven otherwise. The absence of gas on CT does not exclude NF — gas is only present in a minority of cases and its absence should not reassure. I would not wait. My priority is to discuss immediately with the surgical team for theatre. While awaiting theatre: blood cultures, broad-spectrum IV antibiotics (pip-tazo + clindamycin), resuscitation with IV fluids and vasopressors as needed, and full organ function assessment. I would not repeat imaging or perform further tests if they would delay theatre — the surgical exploration is both diagnostic and therapeutic. If the surgeon performs a "finger test" at the bedside under local anaesthesia and finds easy dissection along fascial planes with lack of bleeding and dishwater fluid, this confirms the diagnosis and mandates immediate formal debridement. In the ICU context, I would simultaneously prepare for the patient's return post-debridement: ICU bed, vasopressors, plan for repeat theatre in 24–48h (multiple debridements are the rule, not the exception). IVIG should be considered if Group A Strep is confirmed with toxic shock syndrome features.