Necrotising Fasciitis: Comprehensive Clinical Overview
Epidemiology and Risk Factors
Necrotising fasciitis is a rare but life-threatening soft tissue infection with mortality rates of 50–70% when patients progress to hypotension and multi-organ failure, despite no significant decrease in mortality over the past century. 1
- Approximately two-thirds of cases involve the lower extremities, making leg trauma a particularly high-risk scenario. 1
- Diabetes mellitus is the most common comorbidity, present in approximately 70.8% of cases, and is a significant clinical predictor of limb amputation. 2, 3
- Advanced age and the presence of two or more comorbidities adversely affect outcomes. 3
- The disease is often underestimated or misdiagnosed in 85–100% of cases during initial evaluation due to the paucity of specific cutaneous findings early in the disease course. 4, 3
Clinical Presentation and Diagnostic Features
Cardinal Early Signs
Severe pain disproportionate to physical findings is the hallmark early symptom and the most critical diagnostic clue distinguishing necrotising fasciitis from simple cellulitis. 5, 1
- A hard, "wooden" feel of subcutaneous tissue extending beyond visible skin involvement is pathognomonic and distinguishes fasciitis from cellulitis, where tissues remain palpable and yielding. 5, 1
- Edema or tenderness extending beyond the area of cutaneous erythema is present in approximately 80% of cases and represents a cardinal sign of deeper tissue involvement. 1
- Failure to respond to initial antibiotic therapy after 24–48 hours is a key indicator mandating immediate surgical exploration. 5, 1
Advanced Clinical Features
- Systemic toxicity with altered mental status, profound toxicity with fever or hypotension during antibiotic therapy. 5, 1
- Skin necrosis, ecchymoses, or bullous lesions are present in 70% of cases. 1
- Crepitus (gas in soft tissues) on examination. 5, 1
- Erythema occurs in 90% of cases but is also common in simple cellulitis, making it less diagnostically useful. 1
Intra-operative Diagnostic Findings
- Swollen, dull-gray fascia with stringy areas of necrosis. 5
- Thin, brownish exudate with absence of true pus even after deep dissection. 5, 1
- Extensive undermining of surrounding tissues. 5
- Tissue planes that dissect easily with a gloved finger or blunt instrument. 5
Diagnostic Work-Up
Clinical Assessment Priority
Clinical judgment remains the paramount diagnostic tool; imaging or laboratory tests must never delay surgical exploration when necrotising fasciitis is suspected. 5, 1
Bedside Diagnostic Maneuvers
- Finger test (exploratory incision): When diagnosis is uncertain, a small exploratory incision under local anesthesia can be performed at the area of greatest concern; positive findings include minimal resistance to finger dissection, lack of bleeding, presence of necrotic tissue, and emergence of murky gray ("dishwater") fluid. 5, 1
- Necrotising fasciitis becomes evident by gross inspection without the need for frozen-section pathology. 5
Laboratory Investigations
- The Laboratory Risk Indicator for Necrotising Fasciitis (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
- The quick Sequential Organ Failure Assessment (qSOFA) score should be applied on presentation to gauge severity; a score ≥2 (respiratory rate ≥22 breaths/min, altered mentation, or systolic BP ≤100 mmHg) signals increased risk of organ dysfunction but must not delay operative exploration. 5
- Serial procalcitonin (PCT) measurement can guide discontinuation: a day-1 to day-2 PCT ratio >1.14 predicts successful surgical source control with sensitivity of ≈83% and specificity of ≈71%. 5
Imaging Studies (Only If Surgery Is Not Delayed)
- Bedside ultrasound: sensitivity ≈88% and specificity ≈93%; predictive finding includes diffuse subcutaneous thickening with fluid accumulation >4 mm deep to the fascia. 5
- Computed tomography with IV contrast: sensitivity 100% and specificity ≈81%; typical findings are fascial thickening, non-enhancing fascia on contrast, and gas within tissues. 5, 1
- Magnetic resonance imaging is not recommended in the emergency setting due to time constraints. 5
Microbiological Sampling
- Deep-tissue (rather than superficial) specimens must be obtained for Gram stain and culture, as superficial wound flora do not reliably represent the deep-tissue infection. 5
- Polymicrobial synergistic infection is the most common cause (53.9% of cases), with streptococci and Enterobacteriaceae being the most common isolates. 3
- Group A Streptococcus is the most common cause of monomicrobial necrotising fasciitis. 3
Emergent Management Strategies
Surgical Management: The Definitive Treatment
Immediate aggressive surgical debridement is the definitive treatment for necrotising fasciitis; any delay—including awaiting imaging or antibiotics—is directly linked to higher mortality and multi-organ failure. 5
- Timing is critical: Surgical debridement should be performed within 12 hours of presentation; each hour of delay is associated with increased mortality. 5, 1
- Inadequate initial debridement is associated with a mortality rate of 38% versus 4.2% when aggressive early surgical management is performed. 5
- Multivariate analysis demonstrates that only a delay in surgery of more than 24 hours is correlated with increased mortality (p <0.05; relative risk = 9.4). 3
Operative Protocol
- Perform radical debridement of all necrotic tissue, including skin, subcutaneous fat, and fascia. 5
- 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. 5, 6
- The mean number of surgical interventions is approximately seven. 2
- In cases with fecal contamination (Fournier's gangrene), fecal diversion (e.g., colostomy or fecal tube system, optionally combined with negative-pressure therapy) should be performed. 5
Empiric Antimicrobial Therapy
Initiate empiric broad-spectrum antibiotics immediately upon suspicion, covering MRSA, gram-negative organisms, and anaerobes. 5
Polymicrobial Necrotising Fasciitis (Most Common)
- One MRSA-active agent (vancomycin, linezolid, or daptomycin) plus one of the following combinations:
- When local epidemiology shows high prevalence of extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae, carbapenems should be preferred over piperacillin-tazobactam. 5
- In clinical practice, aminopenicillin ± sulbactam in combination with clindamycin and/or metronidazole has shown 93% sensitivity to initial treatment. 2
Group A Streptococcal Necrotising Fasciitis
- Clindamycin 600–900 mg IV every 8 hours plus penicillin is the recommended regimen. 5, 6
- Clindamycin is essential because it suppresses toxin production even after bacterial growth has ceased. 5
Duration of Antimicrobial Therapy
- Continue antibiotics until all three of the following criteria are met:
- Typical duration of IV therapy ranges from 5–14 days, with total antibiotic therapy typically 2–3 weeks for deep soft tissue infections. 6
Transition to Oral Antibiotics
- Transition criteria include clinical improvement, afebrile for 48–72 hours, ability to tolerate oral intake, and hemodynamic stability. 6
- Oral options for MRSA coverage include 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. 6
- For streptococcal infections, oral penicillin V 500 mg four times daily is appropriate. 6
Aggressive Fluid Resuscitation and Hemodynamic Support
Aggressive intravenous fluid administration is as critical as surgical debridement for patient survival in necrotising fasciitis. 5
- Infected wounds exude large volumes of tissue fluid, frequently leading to septic shock. 5, 6
- Patients require continuous hemodynamic monitoring in an intensive-care setting and, when needed, vasopressor support. 5
- Mean hospitalization is approximately 32 days, including 8 days in the intensive care unit. 2
Multidisciplinary Team Approach
From the moment of diagnosis, a coordinated multidisciplinary team—including surgeons, intensivists, and infectious-disease specialists—must be engaged to optimize decision-making and reduce mortality. 5
- Ongoing involvement of wound-care, reconstructive surgery, physical therapy, and rehabilitation specialists is required for long-term recovery after the acute phase. 5, 6
Differential Diagnosis
Primary Differentials
- Cellulitis typically responds to initial antibiotic therapy, while failure to respond after 24–48 hours is a key indicator of necrotising fasciitis. 1
- Abscesses have localized fluctuance and discrete pus collection, whereas necrotising fasciitis shows no true pus even after deep dissection, with only a thin, brownish exudate. 1
- Severe cellulitis/erysipelas, pyomyositis, and deep vein thrombosis can initially mimic necrotising fasciitis but lack the characteristic features of deeper tissue involvement and systemic toxicity. 1
Algorithmic Approach to Differentiation
- When evaluating a patient with suspected soft tissue infection, systematically assess: pain severity relative to examination findings, tissue consistency on palpation, extent of edema/tenderness, presence of systemic toxicity, and response to antibiotics. 1
- If any two or more of these features are present, proceed immediately to surgical exploration rather than continuing conservative management, as delay in diagnosis correlates directly with poor outcomes and mortality. 1
Critical Pitfalls to Avoid
- Do not postpone surgical exploration while awaiting imaging studies; clinical judgment should drive immediate operative intervention. 5, 1
- Preadmission treatment with antibiotics can modify the initial clinical picture and often mask the severity of the underlying infection. 3
- The LRINEC score should not be used to rule out necrotising fasciitis due to its poor sensitivity. 1, 6
- Early recognition and urgent operation are the most critical factors for reducing mortality; delay is directly correlated with poor prognosis and multi-organ failure. 6, 3