Necrotising fasciitis

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"necrotizing fasciitis"[MeSH Terms] AND management

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"necrotizing fasciitis"[MeSH Terms]

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Necrotising Fasciitis

Necrotising fasciitis (NF) is a rapidly progressing, life-threatening deep soft tissue infection causing necrosis of the subcutaneous tissues, fascia, and eventually overlying skin. Without aggressive treatment, mortality approaches 70%.

Classification

TypeMicrobiologyDetails
Type IPolymicrobial (most common)Mixed aerobic + anaerobic organisms
Type IIMonomicrobialGroup A beta-haemolytic Streptococcus (GAS), ± S. aureus
Type IIIGram-negative (marine)Vibrio vulnificus - associated with seawater exposure
Type IVFungalCandida spp. - immunocompromised patients
Named variants:
  • Fournier's gangrene - perineal/scrotal involvement
  • Meleney's gangrene - abdominal wall; synergistic bacterial gangrene

Microbiology

Common organisms include:
  • Streptococcus pyogenes (group A Streptococcus) - most feared monomicrobial cause
  • Staphylococcus aureus (including MRSA)
  • Escherichia coli, Pseudomonas, Proteus, Klebsiella
  • Anaerobes: Bacteroides, Clostridium (gas-forming)
Clostridial infection produces rapid, gas-forming, necrotic infection (gas gangrene / clostridial myonecrosis) and carries especially high mortality.

Pathophysiology

Organisms enter via trauma, surgery, or a skin breach and spread along fascial planes, causing:
  1. Acute inflammatory infiltrate in subcutaneous tissue
  2. Thrombosis of microvascular supply → ischaemia
  3. Tissue necrosis spreads contiguously along fascial planes (occasionally "skip lesions" that later coalesce)
  4. Toxin release + systemic sepsis → septic shock, multiorgan failure
The ischaemia explains the hallmark disproportionate pain and the relative absence of lymphangitis (lymphatics traverse the dermis, which is initially spared).

Risk Factors / Predisposing Conditions

  • Diabetes mellitus (most common comorbidity)
  • Penetrating trauma or recent surgery
  • Immunosuppression (steroids, chemotherapy, HIV)
  • Intravenous drug use
  • Obesity, peripheral vascular disease
  • Perineal infection (perianal abscess, Bartholin's cysts)
  • Pressure sores, bites, boils, varicella
Up to 30% of patients may have no identifiable comorbidities. 80% have a history of prior trauma/infection and >60% of cases begin in the lower extremities.

Clinical Features

Early (may resemble cellulitis)

  • Erythema, warmth, swelling, pain
  • Fever, tachycardia

Classical signs

  • Disproportionate pain relative to visible skin changes (early hallmark)
  • Oedema extending beyond the visible erythema
  • Woody-hard subcutaneous texture - inability to distinguish fascial planes
  • Skin turns dusky-blue/purple-black (progressive thrombosis)
  • Skin vesicles and bullae (Figure below) - contain dark purple/haemorrhagic fluid
  • Soft-tissue crepitus (gas-forming organisms)
  • "Dishwater" (grey/brown) drainage from wound
  • Fixed skin staining

Late / severe

  • Cutaneous gangrene and frank skin necrosis
  • Hypotension, septic shock
  • Renal failure (hypovolaemia + cardiovascular collapse)
  • Absence of lymphangitis
"Hard" signs (crepitus, skin necrosis, bullae, hypotension, gas on X-ray) are present in less than half of patients at presentation - Tintinalli's Emergency Medicine
NF of anterior abdominal wall showing central necrosis with surrounding erythema
Necrotising fasciitis of the anterior abdominal wall - Bailey and Love's Surgery, 28th Ed.
NF at presentation - buttock/lower back with dusky skin necrosis
NF at initial presentation - Bailey and Love's Surgery, 28th Ed.
NF after 24 hours - rapid progression with massive tissue destruction
Rapid progression after 24 hours - Bailey and Love's Surgery, 28th Ed.
NF of arm with bullae and extensive tissue destruction
Typical bullae and induration in NF of the arm - Bailey and Love's Surgery, 28th Ed.

Diagnosis

This is primarily a clinical diagnosis. Do not delay surgical treatment if suspicion is high.

Investigations

Laboratory (LRINEC Score):
The LRINEC (Laboratory Risk Indicator for Necrotising Fasciitis) score uses routine labs:
VariableValuePoints
CRP (mg/L)<1500
≥150+4
WBC (×10³/mm³)<150
15-25+1
>25+2
Haemoglobin (g/dL)>13.50
11-13.5+1
<11+2
Sodium (mmol/L)≥1350
<135+2
Creatinine (µmol/L)≤1410
>141+2
Glucose (mmol/L)≤100
>10+1
Maximum score: 13
  • Score ≥6: PPV 92%, NPV 96% - raise suspicion, carefully evaluate
  • Score ≥8: Strongly predictive of NF
  • Caution: LRINEC ≥6 misses many cases (especially Vibrio species and neck infections). It should NOT be used in isolation to exclude the diagnosis. - Tintinalli's Emergency Medicine
Other lab findings: Elevated creatinine kinase (often enormously elevated), hyponatraemia, thrombocytopaenia (especially Vibrio), lactic acidosis, elevated band count.

Imaging

  • Plain X-ray: May show gas in soft tissues - do NOT delay surgery for this
  • CT: Useful for showing gas tracking along fascial planes, but MRI is preferred
  • MRI: Best modality - superior soft-tissue contrast, shows fascial plane involvement without radiation; can map extent for surgical planning
  • Ultrasound: Can detect abnormal muscle echo texture; useful in children and resource-limited settings
"Relevant imaging must therefore be performed immediately" - emergency surgical debridement cannot wait - Grainger & Allison's Diagnostic Radiology

Operative diagnosis

Intraoperative findings confirm the diagnosis:
  • "Finger test": Lack of resistance to blunt finger dissection along fascial planes
  • Absence of bleeding (devascularised tissue)
  • Grey/necrotic fascia that peels easily from underlying muscle
  • "Dishwater" fluid
Biopsy of fascial layers confirms the histological diagnosis.

Management

1. Resuscitation (simultaneous with surgical planning)

  • Aggressive IV fluid resuscitation
  • Haemodynamic monitoring (ICU admission)
  • Oxygen supplementation; intubation if airway compromised
  • Correct electrolyte derangements

2. Antibiotics (IV, broad-spectrum, started immediately)

  • High-dose penicillin G + third-generation cephalosporins (e.g., cefotaxime) + metronidazole (anaerobic cover)
  • Add clindamycin for GAS (inhibits toxin production via ribosomal mechanism - "Eagle effect")
  • Cover MRSA if suspected (vancomycin/linezolid)
  • Adjust based on wound cultures and sensitivities

3. Surgery (cornerstone of treatment - must not be delayed)

"This is a surgical emergency and the diseased area should be debrided as soon as possible until viable, healthy, bleeding tissue is reached." - Bailey and Love's Surgery
  • Radical surgical debridement: Remove all devitalised tissue generously, going beyond the zone of induration
  • Wound is lightly packed open with gauze/dressings
  • Planned re-look in 24-48 hours - necrosis is prone to spread; multiple debridements are typically required (daily until healthy bleeding tissue is reached)
  • Vacuum-assisted closure (VAC) dressings after initial debridement
  • Early skin grafting in selected cases to minimise protein/fluid losses

4. Adjuncts

  • Hyperbaric oxygen (HBO): Increasingly used; reduces mortality from 30-50% (without HBO) to 9-20% (with HBO). Mechanism: enhances neutrophil killing of anaerobes, promotes wound healing
  • IVIG may be considered for streptococcal toxic shock syndrome

Prognosis / Mortality

Setting30-day Mortality1-year Mortality
Without aggressive treatmentup to 70%-
With treatment26-40%up to 50%
With HBO9-20%-
Independent predictors of mortality: Age >60, WBC >30,000, creatinine >2 mg/dL, cardiac disease, septic shock, clostridial infection, high ASA class, dialysis dependence.
Limb loss occurs in ~26% of extremity cases. Independent predictors: cardiac disease, shock at admission, clostridial infection.

Key Summary Points

(Bailey and Love's Surgery, 28th Ed.)
  • Surgical emergency - primarily a clinical diagnosis
  • Polymicrobial synergistic infection (or monomicrobial with GAS)
  • 80% have a history of previous trauma or infection
  • Rapid progression to septic shock
  • Treat with urgent resuscitation, IV broad-spectrum antibiotics, and radical surgical debridement
  • LRINEC score is a useful adjunct but must not replace clinical judgement
  • Re-debridement planned at 24-48 hours; multiple procedures are the norm
  • Mortality 30-50% even with treatment
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