Necrotising Fasciitis: Comprehensive Clinical Overview
Etiology and Classification
Necrotising fasciitis is a rapidly progressive, life-threatening bacterial infection of the subcutaneous tissue and fascia that requires immediate surgical intervention to prevent mortality. 1
Microbiological Classification
- Type 1 (Polymicrobial) represents the most common presentation (approximately 54% of cases), caused by synergistic infection with streptococci and enterobacteriaceae, along with anaerobes 2
- Type 2 (Monomicrobial) is most commonly caused by Group A Streptococcus (also termed "streptococcal gangrene" or "flesh-eating bacteria syndrome") 3, 2
- Polymicrobial infections typically involve aerobic and anaerobic organisms working synergistically to cause tissue destruction 1
Anatomical Distribution
- Approximately two-thirds of necrotising fasciitis cases involve the lower extremities, making leg trauma a particularly high-risk scenario 1
- Fournier's gangrene represents necrotising infection of the perineal and genital region, following identical management principles 4
Risk Factors and Comorbidities
- Diabetes mellitus is the most common associated comorbidity, present in approximately 71% of cases 2
- Diabetes mellitus is a significant clinical predictor of limb amputation in patients with necrotising fasciitis 5
- Advanced age and the presence of two or more comorbidities adversely affect outcomes 2
- Any breach in skin integrity (trauma, surgery, injection sites) can serve as a portal of entry 1
Clinical Features and Diagnostic Approach
Cardinal Early Signs (High Diagnostic Value)
Severe pain disproportionate to clinical findings is the hallmark early symptom and the single most important diagnostic clue. 1
- Hard, "wooden" feel of subcutaneous tissue extending beyond apparent skin involvement distinguishes fasciitis from cellulitis, where tissues remain palpable and yielding 1
- Edema or tenderness extending beyond the cutaneous erythema is a cardinal sign of deeper tissue involvement, present in approximately 80% of cases 1
- Systemic toxicity with altered mental status is a critical diagnostic feature 1
- Failure to respond to initial antibiotic therapy after 24-48 hours is a key indicator mandating immediate surgical exploration 1
Cutaneous Manifestations (Later Findings)
- Skin necrosis, ecchymoses, or bullous lesions are present in 70% of cases but represent later findings 1
- Crepitus (gas in tissues) indicates gas-forming organisms 1
- Erythema occurs in 90% of cases but is also common in simple cellulitis, making it less diagnostically useful 1
Critical Diagnostic Pitfall
The paucity of cutaneous findings early in the disease makes diagnosis difficult; only 15% of patients may have a correct diagnosis at admission. 2 Preadmission antibiotic treatment often masks the severity of the underlying infection 2
Diagnostic Work-Up
Clinical Assessment Takes Priority
Clinical judgment remains the paramount diagnostic tool; waiting for imaging can delay definitive diagnosis and treatment, directly correlating with mortality. 1
Immediate Clinical Indicators for Surgery
Proceed immediately to surgical exploration if any two or more of the following are present: 1
- Pain disproportionate to physical findings
- Hard "wooden" feel of subcutaneous tissue extending beyond visible skin involvement
- Lack of response to antibiotics after 24-48 hours
- Systemic toxicity with altered mental status
- Profound toxicity (fever, hypotension) or disease progression despite antibiotics
- Skin necrosis with easy fascial dissection
- Crepitus (gas in soft tissues)
- Bullous lesions or ecchymoses
- Edema or tenderness extending beyond cutaneous erythema
Severity Assessment
- Apply the quick Sequential Organ Failure Assessment (qSOFA) score on presentation: respiratory rate ≥22 breaths/min, altered mentation, or systolic BP ≤100 mmHg signals increased risk of organ dysfunction 4, 6
- The LRINEC score has poor sensitivity (68.2% for ≥6,40.8% for ≥8) and should NOT be used to rule out necrotising fasciitis 1, 6
Imaging (Only If It Does Not Delay Surgery)
- CT with IV contrast demonstrates 100% sensitivity and 81% specificity for detecting necrotising fasciitis 1, 4
- Bedside ultrasound shows sensitivity ≈88% and specificity ≈93%; predictive finding is diffuse subcutaneous thickening with fluid accumulation >4 mm deep to the fascia 4
- MRI is NOT recommended in the emergency setting due to time constraints 4
Bedside Surgical Diagnostic Test ("Finger Test")
When diagnosis is uncertain, perform a small exploratory incision under local anesthesia to assess tissue characteristics: 1
- Positive findings include: minimal resistance to finger dissection, lack of bleeding, presence of necrotic tissue, and emergence of murky gray ("dishwater") fluid 1
Intra-operative Confirmation
The most definitive diagnostic indicator is the appearance during surgical exploration: 1, 6
- Swollen, dull-gray fascia with stringy necrosis
- Thin, brownish exudate (absence of true pus even after deep dissection)
- Extensive undermining of surrounding tissues
- Tissue planes that dissect easily with a gloved finger or blunt instrument
Management
Surgical Management (Primary Treatment)
Immediate aggressive surgical debridement is the definitive treatment; surgical source control must be achieved within the first 12 hours of admission, as each hour of delay is associated with increased mortality. 1, 4
Initial Debridement Protocol
- Perform radical debridement of all necrotic tissue, including skin, subcutaneous fat, and fascia 4
- Inadequate initial debridement is associated with 38% mortality versus 4.2% when aggressive early surgical management is performed 4
- Deep-tissue (not superficial) specimens must be obtained for Gram stain and culture 4
Re-exploration Protocol
- Return to the operating room every 24-36 hours after initial debridement for repeat exploration and further debridement until no additional necrotic tissue is identified 4, 6, 5
- The mean number of surgical interventions is approximately seven 5
Amputation Considerations
- Early amputation of affected tissues may be required in cases of limb involvement with extensive necrosis 5
- Diabetes mellitus significantly increases the risk for amputation 5
Special Consideration for Fournier's Gangrene
- In cases with fecal contamination, perform fecal diversion (colostomy or fecal tube system, optionally combined with negative-pressure therapy) to protect the wound and facilitate healing 4
Antimicrobial Therapy
Initiate empiric broad-spectrum antibiotics immediately upon suspicion, but never delay surgery to start antibiotics. 4
Empiric Regimens for Polymicrobial Necrotising Fasciitis
One MRSA-active agent PLUS one gram-negative/anaerobic combination: 4
MRSA coverage (choose one):
- Vancomycin
- Linezolid
- Daptomycin
PLUS gram-negative/anaerobic coverage (choose one):
- Piperacillin-tazobactam (single agent)
- Carbapenem (meropenem, imipenem-cilastatin, or doripenem)
- Ceftriaxone + metronidazole
- Fluoroquinolone + metronidazole
Alternative empiric regimen: Aminopenicillin ± sulbactam in combination with clindamycin and/or metronidazole has shown 93% sensitivity to initial treatment 5
Special Regimen for Group A Streptococcal Infection
When Group A Streptococcus is confirmed or strongly suspected, use clindamycin 600-900 mg IV every 8 hours PLUS penicillin. 4
- Clindamycin is essential because it suppresses toxin production even after bacterial growth has ceased 4
Local Epidemiology Considerations
- When local epidemiology shows high prevalence of ESBL-producing Enterobacteriaceae, prefer carbapenems over piperacillin-tazobactam 4
Duration of Antibiotic Therapy
Continue antimicrobial therapy until ALL THREE of the following criteria are met: 4, 6
- No further surgical debridement is required
- Clear clinical improvement is evident
- The patient remains afebrile for 48-72 hours
- Typical total duration ranges from 2-3 weeks for deep soft tissue infections 6
Monitoring Antibiotic Efficacy
- Serial procalcitonin (PCT) measurement can guide discontinuation: a day-1 to day-2 PCT ratio >1.14 predicts successful surgical source control with sensitivity ≈83% and specificity ≈71% 4
Transition to Oral Antibiotics
Transition from IV to oral therapy when: 6
- Clinical improvement is documented (stabilization of vital signs, reduction in systemic toxicity, improvement in wound appearance, decreasing inflammatory markers)
- Afebrile for 48-72 hours
- Able to tolerate oral intake
- Hemodynamically stable
Oral antibiotic options (guided by culture results): 6
- For MRSA: Linezolid 600 mg every 12 hours, Tedizolid 200 mg every 24 hours, Trimethoprim-sulfamethoxazole 160/800 mg every 12 hours, or Doxycycline 100 mg every 12 hours
- For streptococcal infections: Penicillin V 500 mg four times daily
Fluid Resuscitation and Supportive Care
Aggressive intravenous fluid administration is as critical as surgical debridement for patient survival. 4
- Infected wounds exude large volumes of tissue fluid, frequently leading to septic shock 4
- Patients require continuous hemodynamic monitoring in an intensive care setting 4
- Vasopressor support is often necessary 4
- Mean intensive care unit stay is approximately 8 days 5
Multidisciplinary Team Approach
From the moment of diagnosis, assemble a coordinated multidisciplinary team including surgeons, intensivists, and infectious disease specialists. 4, 6
- Ongoing involvement of wound-care, reconstructive surgery, physical therapy, and rehabilitation specialists is required for long-term recovery 4
Prognosis and Outcomes
Mortality Determinants
Delay in surgery of more than 24 hours is the single most important factor correlated with increased mortality (relative risk = 9.4). 2
- In patients who progress to hypotension and multi-organ failure, mortality rates rise to 50-70% 1
- Advanced age and two or more comorbidities adversely affect outcomes 2
- Early recognition and urgent operation are the most critical factors for reducing mortality 6
Hospital Course
- Mean hospitalization is approximately 32 days, including 8 days in intensive care 5
- Patients typically require multiple surgical interventions (mean of seven procedures) 5
Pathophysiological Cascade
- Rapid bacterial proliferation and toxin release cause microvascular thrombosis, leading to progressive ischemic necrosis from dermis to deep muscle 4
- This cascade can precipitate systemic inflammatory response, multiorgan failure, and shock within hours 4
- Definitive surgical and medical therapy must be initiated without delay to interrupt this pathophysiologic cascade 4
Critical Pitfalls to Avoid
- Do NOT postpone surgical exploration while awaiting imaging studies—clinical judgment should drive immediate operative intervention 4
- Do NOT rely on the LRINEC score to rule out necrotising fasciitis due to its poor sensitivity 1, 6
- Do NOT wait for fever or dramatic cutaneous findings—pain disproportionate to findings is often the only early clue 1
- Do NOT perform inadequate initial debridement—this is the primary cause of increased mortality 4
- Do NOT delay surgery beyond 12 hours—each hour of delay increases mortality 1, 4