Approach

Necrotizing fasciitis is a surgical emergency, requiring rapid debridement of the infected subcutaneous tissues, in combination with empiric antibiotic therapy directed broadly at the likely etiologic agents.[2][3]​​[5]​​[20]​​[38]​​

Tailoring of antimicrobial therapy, as appropriate, is recommended when causative microbial organism(s) are identified via culture.

A combined team approach (surgeon, infectious disease specialist, microbiologist) provides the basis for optimal management.[15][43]​​

This topic covers the diagnosis and management of necrotizing fasciitis in adults only.

Initial management

A surgical consultation should be obtained as soon as the diagnosis is suspected.[2][5]​​[43] Surgical debridement should be performed as soon as possible, but at least within 12 hours of hospital admission.[2][38] The infected subcutaneous tissue is devitalized, so expedited surgical removal of infected tissue is critical for successful treatment. Delay in surgical debridement (>12 hours after admission) has been associated with the need for a greater number of subsequent debridements, higher incidence of organ failure, and higher mortality.​​[3][38][47]

While surgery is awaited, patients should be monitored for systemic toxicity (e.g., signs of end-organ damage), as well as local signs and symptoms of extension of the area of necrotizing fasciitis.[3]​ Empiric antibiotic therapy should be started immediately, then tailored based on culture results from subcutaneous tissue or blood, the patient’s clinical condition, and discussion with the multidisciplinary team.[2]​​​​[3]​​[5]​ An early review from the critical care team should be sought; intensive hemodynamic support with intravenous fluids, and possibly vasoactive drugs, will be needed.​​[2][5]​​[43]

When debridement is performed, surgical incisions should extend beyond the areas of visible necrosis and the entire necrotic area excised.[3]​ Surgical specimens including tissue and fluid should be obtained for pathology and microbiological culture.[2][5]​​​ Further surgical evaluation and debridement is necessary in most cases, and several procedures may be required to ensure that all necrotic tissue is removed. Data to guide optimal timing for surgical re-exploration is lacking; a reasonable approach may be serial debridement every 12 to 24 hours until minimal or no remaining necrotic tissue is encountered.[2]

Streptococcal toxic shock syndrome

For patients who develop streptococcal toxic shock syndrome, the addition of intravenous immunoglobulin (IVIG) may be considered, but efficacy data are conflicting. Some studies suggest modest benefit; however, one Cochrane review showed no clear benefit on adverse events or mortality.[48][49][50][51][52][53]

Infectious Diseases Society of America (IDSA) guidelines do not include a recommendation regarding the use of IVIG in patients with necrotizing fasciitis with streptococcal toxic shock syndrome, citing the need for additional efficacy studies.[5]​ World Society of Emergency Surgery consensus recommendations suggest consideration of IVIG in patients with necrotizing fasciitis due to group A streptococcus.[2][3]

Choice of antibiotics

Until microbial etiology and antimicrobial susceptibilities are known, empiric broad-spectrum antibiotics should be administered targeting the most common etiologies of type I infection (mixed infections with anaerobes such as Bacteroides or Peptostreptococcus with a facultative anaerobe such as certain Enterobacterales [Escherichia coli, Enterobacter, Klebsiella, Proteus], MRSA, or non-group A streptococcus), and also type II infection due to group A streptococcus. Consider local resistance and epidemiologic patterns (including extended-spectrum beta-lactamase or carbapenemase-producing organisms).

When further information is available and the etiologic agent has been determined, antibiotic therapy should be tailored to target the specific agent. As there are currently no definitive clinical trials, the IDSA recommends continuing antibiotics until no further surgical debridement is needed, the patient has improved clinically, and fever has been absent for 48 to 72 hours.[5][54]​​

Recommended empiric regimens

Include vancomycin, linezolid, tedizolid, or daptomycin combined with either: piperacillin/tazobactam or a carbapenem (e.g., meropenem, imipenem/cilastatin, ertapenem). Local resistance patterns (including extended-spectrum beta-lactamase or carbapenemase-producing organisms) should be considered. Vancomycin should be used with caution in patients with renal impairment.

Until group A streptococcus involvement is excluded, antimicrobial agents that inhibit toxin production should be included empirically. Clindamycin should be added to empiric treatment until group A streptococcus involvement has been excluded if linezolid is not already being used as part of the empiric regimen.[5]​​[34]

Fungal pathogens (especially mucorales) are rare causes of necrotizing fasciitis; empiric inclusion of antifungal agents is not recommended.

Recommendations for type I mixed infections

Include vancomycin, linezolid, tedizolid, or daptomycin combined with either: piperacillin/tazobactam or a carbapenem (e.g., meropenem, imipenem/cilastatin, ertapenem). The IDSA supports some of these regimens.​[5]

Recommendations for type II infection

Type II infection is most commonly due to group A streptococcus; clindamycin plus penicillin is recommended.[5]​ For patients with a penicillin allergy, vancomycin monotherapy may be used. When monomicrobial Staphylococcus aureus is the etiologic agent, antibiotics active against MRSA should be used until cultures confirm susceptibilities; options include vancomycin, linezolid, tedizolid, or daptomycin. Ceftaroline, telavancin, or dalbavancin are also reasonable choices, although clinical data are sparse.​​[2][5]

Nafcillin, oxacillin, or cefazolin may be used if methicillin susceptibility is confirmed.

Doxycycline is used in the management of type II necrotizing fasciitis attributable to Vibrio vulnificus and Aeromonas hydrophila.

Fungal pathogens are rare causes of necrotizing fasciitis; lipid amphotericin B is the primary treatment option for patients with mucorales infections.

Subsequent management

In treatment-resistant patients, the need for additional debridement or alteration in antibiotic therapy (based on culture results from subcutaneous tissue or blood) should be considered.​[3][5]

After complete removal of necrotic tissue and final debridement, negative pressure wound therapy may be considered to help with granulation and healing of the wound.[15]

Supportive surgical interventions such as fecal diversion for colostomy in cases of Fournier gangrene with fecal contamination, or tracheostomy for patients with cervicofacial necrotizing fasciitis may be warranted.​[3][18]

Where functional and cosmetic disability results from extensive surgical debridement for necrotizing fasciitis, reconstructive surgery with skin grafting may be required.[3][Figure caption and citation for the preceding image starts]: Late signs of necrotizing fasciitis with extensive cellulitis, induration, skin necrosis, and formation of hemorrhagic bullaeFrom: Hasham S, Matteucci P, Stanley PRW, et al. Necrotising fasciitis. BMJ. 2005 Apr 9;330(7495):830-3 [Citation ends].com.bmj.content.model.Caption@65278086

After prolonged hospitalization and recurrent surgical interventions, physical therapy and rehabilitation may be needed for certain patients.

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