Everything You Ever wanted to Know About Necrotizing Fasciitis

NF refers to a group of life-threatening infections of the skin, soft tissues, and muscles which progress rapidly along fascial planes, at a rate of 2–3 cm/hr.¹ NF is rare, with an incidence of 0.4 in 100,000 people per year.² NF is a surgical diagnosis with OR findings including friability of superficial fascia, “dishwater” grey exudate, and absence of pus.

Type 1 ¹

– Polymicrobial

– Aerobic + anaerobic 

– Typically 4-5 organisms involved 

– Often gas-producing

– 70-90% of cases ³

– Immunocompromised patient (e.g., DM, ESRD, IVDA) 

Type 2 ³

– Monomicrobial

– Gram + (Group A Strep, Staph aureus)

– Virulence factors result in toxicity producing systemic symptoms

– Occurs at any age

– Healthy or immunocompromised patient 

Type 3 ¹

– Monomicrobial

– Clostridium, E. coli, Aeromonas hydrophila, Vibrio vulnificus 

– Risk factors include: IVDA, deep puncture wound, crush injury

Type 4 ¹

– Fungal

– Candida spp. and Zygomycetes

– Immunocompromised host

Yes. The median mortality 21.5%¹ (range 8.7% to 76%). Without treatment, mortality is reportedly almost 100% (though there is no evidence for this estimate).

There are two major mechanisms through which group A strep is thought to cause NF. The first is through a defined portal of entry. In this mechanism, bacteria gain entry to deep tissue through superficial cutaneous lesions. This starts with mild erythema of the superficial skin, followed by extensive inflammation, and finally dusky/purple skin and bullae, gangrene, severe systemic symptoms. This occurs rapidly over 24-72 hours.³

A second, much harder to detect and often missed mechanism is through NO defined portal of entry. In these cases, there is an inciting event such as a simple muscle strain or bruise, followed by deep local tissue destruction, infection, and exotoxin release. Exotoxin release can cause the patient to feel ill with nonspecific symptoms such as malaise, myalgias, nausea, vomiting, diarrhea, and anorexia. The patient will likely have pain at the site of this deep infection but will lack cutaneous manifestations. With these nonspecific systemic symptoms and lack of significant skin findings, patients are often misdiagnosed (e.g. viral syndrome, gastroenteritis) at this stage. When bullae and ecchymosis develop, significant tissue destruction and systemic disease are already present. Therefore, patients have a high mortality rate of >70% as the correct diagnosis is often only made in later stages.³

NF is a difficult diagnosis to make but there are certain red flags that should put NF higher on your differential:⁴

– Pain disproportionate to exam

– Failure to respond to initial antibiotics

– Findings extending beyond the area of external skin involvement, i.e. deep induration, “woody” texture or tenderness beyond external margins of erythema

– Systemic symptoms

– Crepitus

– Bullous lesions

– Skin necrosis or ecchymoses

Labs are not specific for the diagnosis of NF. Common lab findings include WBC >20, bun >18, cr >1.2, and elevated CK, but none are useful in ruling in or ruling out the diagnosis. Blood cultures are positive in only 25% of cases, and surgical cultures are positive in 80%.¹

It can’t help you either. 

The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score was developed as a screen for necrotizing fasciitis. 

In the development study, a score ≥ 6 had a PPV 92% and NPV of 96%. But, 10% of patients in the study who had necrotizing fasciitis had a score < 6. ⁵

Validation studies have generally shown poor sensitivity and specificity for the LRINEC score. ^6,7,8,9  There is also poor performance in pediatric patients.¹⁰  It is not uncommon for fatal NF cases to have scores ≤ 2.¹¹ Therefore, the score has no utility in diagnosis or ruling out necrotizing fasciitis. Most importantly, the score has only been studied retrospectively and never validated prospectively.

Imaging should be pursued in cases with equivocal findings, although it is not always necessary and could delay treatment.¹

X-ray has limited utility. Soft tissue gas on plain films has a sensitivity of 48.9% and specificity 94%.¹²

CT is the most commonly used imaging modality. The findings of fascial involvement and absence of fascial enhancement with IV contrast are sensitive (>90%) ¹³ but are somewhat nonspecific. We often look for fascial gas as a marker for the diagnosis, but this finding only has a sensitivity of 88.5% and a specificity of 93.3%.¹² Remember, not all types of NF produce gas, so do not be falsely reassured by its absence.

Percutaneous biopsy has been proposed to make the diagnosis but has been found to be a poor substitute for open surgical inspection and biopsy.³

The finger test is another bedside test that can be performed. Under local anesthesia, a 2 cm incision is made down to the deep fascia, followed by gentle probing with a finger looking for dishwasher pus, a lack of bleeding or a lack of tissue resistance.¹ Although multiple papers in the surgical literature refer to this test, we were unable to find data supporting its use and its comparison to the gold standard of true operative exploration.

No. The presence of fever has low sensitivity (46%) and specificity (77%).²

In addition to aggressive resuscitation and prompt operative intervention, antibiotics are important in the treatment of NF. It is thought that without surgical intervention, antibiotics have little benefit on their own. Ischemia and hypoxia of infected tissue may limit their delivery,¹ however data supporting this is limited. 

Recommended initial antibiotic regimens:

Vancomycin or linezolid AND piperacillin/tazobactam or carbapenem or ceftriaxone + metronidazole⁴

For suspected Group A Strep treatment: 

Penicillin + clindamycin (suppresses streptococcal toxin and cytokine production)⁴

For suspected Type 4 (fungal):

Add amphotericin B or fluconazole

Surgery is the mainstay for diagnosis and treatment of NF. Therefore, early surgical consultation in suspected cases is essential. In the operating room patients undergo surgical debridement, necrosectomy, fasciotomy, and gram stain to help determine the cause and guide treatment.¹

The timing and extent of debridement is a key determinant of mortality in these cases. One study found that a 24-hour delay in surgical intervention increased the relative risk of death by 9.4 and that timing to surgery was the only modifiable risk factor for mortality.¹⁴

After the initial surgery, additional operative inspection and debridement are done every 1-2 days until necrosis and infection have stopped progressing.