Necrotizing Fasciitis

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Necrotizing fasciitis (NF) is a rapidly progressive, life-threatening soft tissue infection characterized by necrosis of fascia and subcutaneous tissue with relative sparing of overlying skin (initially) and underlying muscle. It represents a surgical emergency where early recognition and aggressive debridement are the only interventions that improve survival. [1]

Definition: Necrotizing fasciitis is a necrotizing soft tissue infection (NSTI) involving the fascial planes, spreading along the relatively avascular fascia with thrombosis of perforating vessels leading to secondary skin necrosis. Unlike cellulitis, the infection travels in the deep fascial planes, making surface examination misleadingly benign. [2]

Epidemiology:

• Incidence: 0.4-0.9 per 100,000 population per year [3]
• Increasing incidence: 2-4 fold increase over past 20 years
• Mortality: 20-40% overall; up to 70-80% with delayed treatment or toxic shock syndrome
• Male:Female ratio: 2-3:1
• Age: Bimodal - peaks in neonates and adults over 50 years
• Fournier's gangrene (perineal NF): 40% mortality

Historical Context:

• First described by Confederate surgeon Joseph Jones in 1871 during American Civil War
• Term "necrotizing fasciitis" coined by Wilson in 1952
• Previously known as "hospital gangrene," "streptococcal gangrene"
• Remains associated with military trauma, natural disasters, and IV drug use epidemics

Mechanism of Tissue Destruction:

Necrotizing fasciitis spreads along fascial planes because:

1. Fascia is relatively avascular - fewer immune cells reach infection
2. Bacteria produce enzymes (hyaluronidase, lipases, collagenases) that digest connective tissue
3. Thrombosis of perforating vessels leads to skin ischemia (explains pain out of proportion)
4. Toxin production causes systemic toxicity and shock

Type I (Polymicrobial) Pathophysiology:

• Synergistic infection with aerobic and anaerobic organisms
• Aerobes consume oxygen, creating hypoxic environment
• Anaerobes thrive in hypoxia, produce gas (crepitus)
• Typically occurs in compromised tissue (diabetes, PVD, post-surgical)
• Enzymes from multiple organisms accelerate tissue destruction

Type II (Monomicrobial - GAS) Pathophysiology:

• Group A Streptococcus produces multiple virulence factors:
  • Streptolysin O and S: Pore-forming toxins causing cell lysis
  • Streptococcal pyrogenic exotoxins (SPE-A, B, C): Superantigens causing massive cytokine release
  • M-protein: Antiphagocytic, promotes adherence
  • Streptokinase: Activates plasminogen, promotes spread
• Streptococcal Toxic Shock Syndrome (STSS): Superantigen activates 20-30% of T-cells (vs 0.01% in normal antigen response) causing cytokine storm
• The Eagle Effect: At high bacterial loads, GAS enters stationary phase and stops dividing. Beta-lactams (which work on dividing bacteria) become less effective. Clindamycin works by inhibiting protein synthesis (including toxin production) regardless of growth phase.

Type III (Gas Gangrene/Clostridial) Pathophysiology:

• Clostridium perfringens produces alpha-toxin (lecithinase)
• Alpha-toxin lyses cell membranes, causing massive tissue necrosis
• Rapid gas production (CO2, H2) causes crepitus
• Extremely rapid progression - can be fatal within hours

Vibrio vulnificus:

• Gram-negative rod found in warm seawater
• Enters through minor wounds during seafood handling or swimming
• Produces cytolysins and proteases
• Particularly severe in patients with liver disease or haemochromatosis (iron overload feeds bacterial growth)
• Mortality 50-60% if septicemic

The Clinical Challenge: Early necrotizing fasciitis mimics cellulitis. The key is recognizing the discordance between patient symptoms (severe) and examination findings (relatively minor).

History

Classic Presenting Symptoms:

1. Pain out of proportion - THE cardinal feature

   • Severe pain that seems excessive for appearance
   • Pain extending beyond area of visible erythema
   • Inadequate response to analgesia
   • May paradoxically improve as nerves undergo necrosis (ominous sign)

2. Rapid progression

   • "It wasn't like this 4 hours ago"
   • Erythema spreading despite antibiotics
   • Blisters appearing over hours

3. Systemic symptoms

   • Fever, rigors, sweating
   • Nausea, vomiting, diarrhea
   • Confusion, altered consciousness
   • "Feeling like I'm going to die"

Precipitating Events:

• Minor trauma (scratch, insect bite, abrasion)
• Recent surgery (abdominal, perineal, orthopaedic)
• Injection (IVDU, intramuscular injection)
• Perianal abscess, pilonidal disease
• Childbirth, episiotomy
• Varicella infection (children)
• NSAID use (may mask early symptoms, promotes bacterial invasion)

Physical Examination

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Key Principle: Investigations should NOT delay surgery if clinical suspicion is high. The operating theatre is both diagnostic and therapeutic.

Laboratory Investigations

LRINEC Score (Laboratory Risk Indicator for NECrotizing fasciitis):

LRINEC Score Interpretation:

• Score less than 6: Low risk (PPV less than 50%)
• Score 6-7: Intermediate risk - high clinical vigilance
• Score ≥8: High risk (PPV 75%+) - strongly consider surgery

CRITICAL LIMITATION: LRINEC was developed retrospectively. A normal LRINEC does NOT exclude NF. Sensitivity is only 60-80%. Clinical judgement remains paramount. [4]

Other Laboratory Tests:

• Blood cultures: Positive in 20-50%, identifies causative organism
• Lactate: Elevated lactate indicates tissue hypoperfusion and worse prognosis
• Creatine kinase (CK): Elevated if myonecrosis (worse prognosis)
• Procalcitonin: May help differentiate bacterial infection from other causes
• Coagulation: PT/INR, APTT, fibrinogen, D-dimer (DIC is common)
• Arterial blood gas: Metabolic acidosis indicates severe sepsis

Imaging

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Plain RadiographCT ScanMRIUltrasound

Plain Radiograph (X-ray)

Role: Quick screening, may show gas in soft tissues

Findings:

• Gas tracking along fascial planes (pathognomonic but only present in 25-50%)
• More common in Type I (polymicrobial) and Type III (clostridial)
• May be absent in Type II (GAS)

Limitation: Low sensitivity; absence of gas does NOT exclude NF

CT Scan

Role: Most useful imaging modality if time permits

Findings:

• Gas tracking along fascial planes (specific but not always present)
• Fascial thickening and enhancement
• Fluid collections along fascia
• Non-enhancement of fascia (indicates necrosis)
• Extent of soft tissue involvement

Advantages:

• Rapid acquisition
• Shows extent of disease for surgical planning
• Identifies gas that may be missed on X-ray

CRITICAL WARNING: CT should NOT delay surgery if clinical diagnosis is clear. A normal CT does NOT exclude NF.

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MRI

Role: Most sensitive imaging modality but rarely indicated acutely

Findings:

• T2 hyperintensity along fascia (edema)
• Fascial thickening greater than 3mm
• Non-enhancement with gadolinium (necrosis)
• Tracking of fluid along fascial planes

Limitations:

• Time-consuming (30-60 minutes)
• May not be readily available after hours
• Should NOT delay surgery
• Reserve for equivocal cases where time permits

Ultrasound

Role: Bedside tool, limited utility

Findings:

• Subcutaneous thickening
• Fascial thickening greater than 4mm
• Fluid along fascial planes
• Hyperechoic foci with dirty shadowing (gas)

Advantages:

• Bedside availability
• No radiation
• Can guide aspiration

Limitations:

• Operator dependent
• Limited sensitivity
• Cannot assess deep fascial planes

The Finger Test (Bedside Diagnosis)

Indications: High clinical suspicion for NF but diagnosis uncertain

Technique:

1. Perform under local anaesthesia at bedside or in theatre
2. Make 2cm incision through skin and subcutaneous tissue down to fascia
3. Observe for:
   • Lack of bleeding (vessel thrombosis)
   • "Dishwater" gray pus (pathognomonic)
   • Necrotic fascia - gray, stringy, easily separates with finger dissection
   • "Finger test" positive - can easily pass finger along fascial plane with no resistance

If positive: Proceed immediately to extensive debridement

📊 Management Algorithm

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The Three Pillars of NF Management:

1. Resuscitation - Aggressive fluid, vasopressor support, ICU admission
2. Debridement - Early, extensive, repeated
3. Antibiotics - Empiric broad-spectrum, include clindamycin for toxin inhibition

The Definitive Treatment: Surgery is both diagnostic and therapeutic. No amount of antibiotics can substitute for adequate debridement of necrotic tissue.

Debridement TechniqueSecond-Look SurgeryAmputationWound Reconstruction

Surgical Debridement Technique

Timing:

• Operate within 6-8 hours of admission (ideally sooner)
• Every hour delay increases mortality by 9%
• Do not delay for imaging if clinical diagnosis clear

Principles:

• Aggressive, extensive debridement
• All necrotic tissue must be removed
• Healthy tissue bleeds - debride until you see bleeding edges
• Fasciotomies if compartment syndrome suspected

Step-by-Step Approach:

1. Incision

   • Longitudinal incision over area of maximal involvement
   • Extend beyond visible erythema to healthy tissue

2. Assess Fascia (Finger Test)

   • Necrotic fascia is gray, stringy
   • Easily separates from underlying muscle with finger dissection
   • Healthy fascia is glistening white and adherent

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3. Debride Fascia

   • Excise all necrotic fascia with no resistance
   • Continue until fascia bleeds and is adherent
   • May need to extend incisions to follow necrosis

4. Assess Muscle

   • Healthy muscle: Pink, contracts to stimulation, bleeds when cut
   • Necrotic muscle: Dull, non-contractile, does not bleed
   • Debride non-viable muscle (myonecrosis = worse prognosis)

5. Assess Skin

   • Initially viable skin may become necrotic over 24-48 hours
   • Preserve skin if viable (can excise at relook)
   • Excise overtly necrotic skin

6. Wound Management

   • Leave wounds open
   • Apply saline-soaked dressings or NPWT
   • Plan for return to theatre

Planned Re-Look Surgery

Timing:

• Return to theatre at 24-48 hours
• Earlier if clinical deterioration

Purpose:

1. Assess adequacy of initial debridement
2. Debride any newly demarcated necrotic tissue
3. Assess tissue viability (muscle, skin)
4. Repeat until all necrosis excised and patient improving

Endpoints for Completion:

• No further necrotic tissue
• Healthy, bleeding wound bed
• Viable granulation tissue forming
• Patient systemically improving

Average Number of Debridements:

• Most patients require 2-4 debridements
• Some require more (especially Fournier's gangrene)
• Underestimating need for re-look is common error

When to Amputate

Indications for Primary Amputation:

• Life-threatening sepsis refractory to debridement
• Extensive circumferential limb involvement
• Associated vascular injury precluding limb salvage
• Myonecrosis involving entire limb compartments

Decision-Making:

• "Life over limb" principle
• May need multiple debridements before decision clear
• Early senior input essential
• Discuss with patient/family early if amputation likely

Level of Amputation:

• Must be proximal to all necrotic tissue
• Healthy bleeding muscle at amputation site
• Leave stump open for monitoring
• May need revision if residual infection

Amputation Decision

Amputation is a life-saving procedure in fulminant NF. Delay in amputation to "try to save the limb" can result in patient death. The principle is "life over limb". Early discussion with family about this possibility is essential.

Wound Closure and Reconstruction

Timing:

• Only after all infection controlled
• All necrotic tissue removed
• Healthy granulating wound bed
• Patient systemically stable

Options:

Secondary Intention:

• For small wounds
• NPWT to promote granulation

Split-Thickness Skin Graft (STSG):

• Most common closure method
• Once healthy granulation tissue present
• May be meshed for large defects

Dermal Substitutes:

• For large defects with exposed critical structures
• Integra, Matriderm, etc.
• Two-stage procedure with STSG

Flaps:

• For defects with exposed bone, tendon, vessels
• Local, regional, or free flaps
• Require plastic surgery input

Perineal Reconstruction:

• Fournier's gangrene often requires complex reconstruction
• Scrotal/penile skin grafts
• Testicular transposition
• Gracilis flaps for perineal defects

Complications

Immediate/Early:

• Septic shock - multi-organ failure, DIC, death
• ARDS - acute respiratory distress syndrome
• Acute kidney injury - from sepsis, rhabdomyolysis
• Limb loss - amputation required in 15-20%
• Exsanguinating hemorrhage - from eroded vessels
• Toxic shock syndrome - especially Type II (GAS)

Late:

• Chronic wounds - prolonged healing, skin grafts
• Scarring and contractures - may limit function
• Chronic pain - phantom limb pain if amputated
• Psychological morbidity - PTSD, depression, body image issues
• Functional impairment - particularly after limb amputation

Prognostic Factors

Factors Associated with Increased Mortality:

Survival Outcomes

Overall Mortality:

• Historical: 70-80% (pre-antibiotic era)
• Current: 20-40% with modern treatment
• Early recognition and aggressive surgery: 10-25%
• Delayed treatment: 50-70%

Factors Improving Survival:

• Recognition within 24 hours of symptom onset
• Surgery within 6-8 hours of presentation
• Adequate debridement (multiple re-looks)
• ICU care with multi-organ support
• Clindamycin in antibiotic regimen
• IVIG in streptococcal toxic shock

Epidemiology in Australia

Necrotizing fasciitis occurs across Australia with some specific patterns relevant to local practice:

Incidence and Demographics: Australia has an incidence similar to other developed nations at approximately 0.4-1.0 per 100,000 per year. However, there are notable risk factors in the Australian population including high rates of diabetes mellitus (particularly in Indigenous Australians and Pacific Islander communities), obesity, and peripheral vascular disease. Remote and rural communities face additional challenges related to delayed presentation and access to surgical facilities. [1]

Organism Patterns: Type I polymicrobial NF predominates in Australia, particularly in diabetic patients and those with peripheral vascular disease. Type II GAS infections occur sporadically, with occasional clusters in schools or communities. Vibrio vulnificus is a concern in tropical northern Australia where seawater exposure during the warm months (October-April) poses a risk. Aeromonas hydrophila should also be considered in freshwater exposures, particularly in northern Queensland.

Management Considerations

Healthcare System Access: In Australia, necrotizing fasciitis is managed within the public hospital system with emergency surgical services available at major metropolitan and regional centres. The Australian Commission on Safety and Quality in Health Care recognizes sepsis (including NSTI) as a priority condition requiring rapid recognition and treatment. Patients presenting to smaller regional or rural hospitals may require urgent retrieval to centres with ICU and surgical capability.

Antibiotic Selection: The Therapeutic Guidelines (eTG) provide Australian recommendations for empiric antibiotic therapy in necrotizing soft tissue infections. Standard empiric regimens include piperacillin-tazobactam or meropenem combined with clindamycin and vancomycin. For confirmed GAS infection, benzylpenicillin plus clindamycin remains first-line. All antibiotics discussed are available on the Pharmaceutical Benefits Scheme (PBS) for in-hospital use.

Indigenous Health Considerations: Aboriginal and Torres Strait Islander Australians have higher rates of diabetes, chronic kidney disease, and skin infections, placing them at increased risk for NF. Cultural considerations in wound care, the importance of family involvement in healthcare decisions, and the challenges of remote healthcare access should inform management plans. Renal dosing adjustments are commonly required given the high prevalence of CKD.

Smoking Cessation: Australia has a comprehensive tobacco control framework. For NF survivors requiring wound healing, referral to Quitline (13 7848) and nicotine replacement therapy can support cessation, which is critical for wound healing and graft success.

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2. Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med. 2017;377(23):2253-2265. doi:10.1056/NEJMra1600673

3. Arif N, Yousfi S, Vinnard C. Deaths from necrotizing fasciitis in the United States, 2003-2013. Epidemiol Infect. 2016;144(6):1338-1344. doi:10.1017/S0950268815002745

4. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004;32(7):1535-1541. doi:10.1097/01.ccm.0000129486.35458.7d

5. Wilson MP, Schneir AB. A case of necrotizing fasciitis with a LRINEC score of zero: clinical suspicion should trump scoring systems. J Emerg Med. 2013;44(5):928-931. doi:10.1016/j.jemermed.2012.09.039

6. Kobayashi L, Konstantinidis A, Shackelford S, et al. Necrotizing soft tissue infections: delayed surgical treatment is associated with increased number of surgical debridements and morbidity. J Trauma. 2011;71(5):1400-1405. doi:10.1097/TA.0b013e31820db8fd

7. Mascini EM, Jansze M, Schouls LM, et al. Penicillin and clindamycin differentially inhibit the production of pyrogenic exotoxins A and B by group A streptococci. Int J Antimicrob Agents. 2001;18(4):395-398. doi:10.1016/s0924-8579(01)00413-7

8. Darenberg J, Ihendyane N, Sjölin J, et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial. Clin Infect Dis. 2003;37(3):333-340. doi:10.1086/376630

9. May AK, Stafford RE, Bulger EM, et al. Treatment of complicated skin and soft tissue infections. Surg Infect (Larchmt). 2009;10(5):467-499. doi:10.1089/sur.2009.012

10. Therapeutic Guidelines Limited. Therapeutic Guidelines: Antibiotic. Melbourne: Therapeutic Guidelines Limited; 2019.