Recommendations
Key Recommendations
Refer the patient for emergency surgical debridement as soon as you suspect necrotising fasciitis and get an early review from the critical care team; this is a life-threatening surgical scenario.[3][5]
Surgical debridement should be performed as soon as possible, but at least within 12 hours of hospital admission, to reduce the number of subsequent debridements, progression to organ failure, and mortality.[3][56]
Start empirical antibiotics as soon as you have obtained blood cultures and ensure the patient has adequate haemodynamic support (intravenous fluids ± vasoactive drugs) and analgesia.[3][35]
Urgently discuss choice of antibiotic with an infectious disease or microbiology specialist.
Once culture results are available and the causative organism is identified, tailor the patient’s antibiotics accordingly.[3]
This topic covers the diagnosis and management of necrotising fasciitis in adults only.
Refer the patient immediately to the surgical team; necrotising fasciitis requires rapid debridement of the infected subcutaneous tissues in combination with empirical antibiotic therapy.[2][3][4][20]
The infected subcutaneous tissue is devitalised, so expedited surgical removal of all infected tissue, drainage of infected fluids, and removal of infected devices or foreign bodies is critical for successful treatment.[3] Surgical debridement should be performed as soon as possible, but within 6-12 hours of hospital admission.[3][15][46][57]
Surgical specimens including tissue and fluid should be obtained for microbiological culture.[2][3]
A multidisciplinary approach (including a surgeon, an infectious disease or microbiology specialist, and critical care) is required.[15][53]
While the patient is waiting for surgery, monitor them for systemic toxicity (e.g., signs of end-organ damage), as well as local signs and symptoms of extension of the area of necrotising fasciitis.[4]
Consider the need for additional debridement or alterations in antibiotic or antifungal therapy, based on culture results from subcutaneous tissue or blood, the patient’s clinical condition, and discussion with the multidisciplinary team.[2][3][4] See Surgical re-exploration below.
More info: Surgical debridement
When surgical debridement is performed, incisions should extend beyond the areas of visible necrosis and the entire necrotic area excised.[4] 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 are lacking; a reasonable approach may be serial debridement every 12 to 24 hours until minimal or no remaining necrotic tissue is encountered.[3]
Get an early review from the critical care team. Some patients will need critical care support, depending on the degree of surgical resection and their physiological state.
Give intensive haemodynamic support with intravenous fluids, and vasoactive drugs if needed.[2][3][4]
Check local protocols for specific recommendations on fluid choice. Evidence from critically ill patients in general (not specifically people with necrotising fasciitis) suggests that there is no difference in benefit between normal saline and a balanced crystalloid (such as Hartmann's solution [also known as Ringer’s lactate] or Plasma-Lyte®), and therefore either choice of fluid is reasonable.[58][59]
Ensure the patient has adequate analgesia.[3] Morphine is used in practice.
Practical tip
Be aware that large volumes of normal saline as the sole fluid for resuscitation may lead to hyperchloremic acidosis.
Also note that use of lactate-containing fluid in a patient with impaired liver metabolism may lead to a spuriously elevated lactate level, so results need to be interpreted with other markers of volume status.
Evidence: Choice of fluids
Evidence from two large randomised controlled trials (RCTs) suggests there is no difference between normal saline and a balanced crystalloid in mortality at 90 days, and therefore either option is a reasonable choice for the resuscitation of critically ill patients.
There has been extensive debate over the choice between normal saline (an unbalanced crystalloid) versus a balanced crystalloid (such as Hartmann’s solution [also known as Ringer’s lactate] or Plasma-Lyte®). Evidence from critically ill patients points to no benefits from using a balanced crystalloid in preference to normal saline. Clinical practice varies widely, so you should check local protocols.
In 2021 to 2022 two large double-blind RCTs were published assessing intravenous fluid resuscitation in intensive care unit (ICU) patients with a balanced crystalloid solution (Plasma-Lyte) versus normal saline: the Plasma-Lyte 148 versus Saline (PLUS) trial (53 ICUs in Australia and New Zealand; N=5037) and the Balanced Solutions in Intensive Care Study (BaSICS) trial (75 ICUs in Brazil; N=11,052).[58][59]
In the PLUS study 45.2% of patients were admitted to ICU directly from surgery (emergency or elective), 42.3% had sepsis and 79.0% were receiving mechanical ventilation at the time of randomisation.
In BaSICS almost half the patients (48.4%) were admitted to ICU after elective surgery and around 68% had some form of fluid resuscitation before being randomised.
Both found no difference in 90-day mortality overall or in prespecified subgroups for patients with acute kidney injury (AKI), sepsis, or post-surgery. They also found no difference in the risk of AKI.
In BaSICS, for patients with traumatic brain injury, there was a small decrease in 90-day mortality with normal saline - however, the overall number of patients was small (<5% of total included in the study) so there is some uncertainty about this result. Patients with traumatic brain injury were excluded from PLUS as the authors felt these patients should be receiving saline or a solution of similar tonicity.
One meta-analysis of 13 RCTs (including PLUS and BaSICS) confirmed no overall difference, although the authors did highlight a non-significant trend towards a benefit of balanced solutions for risk of death.[60]
Previous evidence has been mixed.
One 2015 double-blind, cluster-randomised, double-crossover trial conducted in four ICUs in New Zealand (N=2278), the 0.9% Saline vs. Plasma-Lyte for ICU fluid Therapy (SPLIT) trial, found no difference for in-hospital mortality, AKI, or use of renal-replacement therapy.[61]
However, one 2018 US multicentre unblinded cluster-randomised trial - the isotonic Solutions and Major Adverse Renal events Trial (SMART), among 15,802 critically ill adults receiving ICU care - found possible small benefits from balanced crystalloid (Ringer’s lactate or Plasma-Lyte) compared with normal saline. The 30-day outcomes showed a non-significant reduced mortality in the balanced crystalloid group versus the normal saline group (10.3% vs. 11.1%; odds ratio [OR] 0.90, 95% CI 0.80 to 1.01) and a major adverse kidney event rate of 14.3% versus 15.4% respectively (OR 0.91, 95% CI 0.84 to 0.99).[62]
One 2019 Cochrane review included 21 RCTs (N=20,213) assessing balanced crystalloids versus normal saline for resuscitation or maintenance in a critical care setting.[63]
The three largest RCTs in the Cochrane review (including SMART and SPLIT) all examined fluid resuscitation in adults and made up 94.2% of participants (N=19,054).
There was no difference in in‐hospital mortality (OR 0.91, 95% CI 0.83 to 1.01; high-quality evidence as assessed by GRADE), AKI (OR 0.92, 95% CI 0.84 to 1.00; GRADE low), or organ system dysfunction (OR 0.80, 95% CI 0.40 to 1.61; GRADE very low).
Empirical antibiotic therapy
Start empirical intravenous antibiotic therapy as soon as you have obtained blood cultures.[2][3][35] Urgently discuss choice of antibiotic with an infectious disease or microbiology specialist.
Use high-dose broad-spectrum antibiotics that target the most common aetiologies of:
Type I infection
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
Type II infection
Group A streptococcus.
Consider local resistance and epidemiological patterns (including extended-spectrum beta-lactamase or carbapenemase-producing organisms).
Appropriate antibiotics include piperacillin/tazobactam, a carbapenem (e.g.,meropenem), a cephalosporin (e.g., ceftriaxone), or a fluoroquinolone such as ciprofloxacin (if the patient is allergic to penicillin).
Always add vancomycin, linezolid, tedizolid, or daptomycin for MRSA cover.[3]
Add antibiotics that inhibit toxin production until group A streptococcus involvement is excluded.[3] Evidence for clindamycin is strongest.[2][37]
Fungal pathogens (Mucorales, Candida) are rare causes of necrotising fasciitis; empirical antifungal agents are not recommended.
Continue empirical antibiotics until the causative organism has been determined. Once these results are available, tailor antibiotic therapy accordingly.
Drug safety alert: Fluoroquinolones
Fluoroquinolones have been associated with serious, disabling, and potentially irreversible adverse effects, including tendonitis, tendon rupture, arthralgia, neuropathies, and other musculoskeletal or nervous system effects.[64] Warnings have also been issued about the increased risk of aortic dissection, significant hypoglycaemia, and mental health adverse effects in patients taking fluoroquinolones.[65][66]
Pathogen-targeted antibiotic therapy
Once culture results are available, tailor the patient’s antibiotics to target the causative organism.[4] Always consult an infectious disease or microbiology specialist (this is particularly important if the patient has multi-drug resistant necrotising fasciitis or is allergic to penicillin) and consider local epidemiological patterns.
Continue antibiotics until further debridement (see Surgical re-exploration below) is no longer necessary, the patient has clinically improved, and fever has resolved for 48 to 72 hours.[3][67]
Type I infection (polymicrobial)
Type I infection involves aerobic and anaerobic organisms.[3] It is most commonly seen in older patients and in those with underlying illnesses.[8]
Suitable antibiotic regimens include piperacillin/tazobactam, a carbapenem (e.g., meropenem), a cephalosporin (e.g., ceftriaxone), or a fluoroquinolone such as ciprofloxacin (if the patient is allergic to penicillin).
Continue vancomycin, linezolid, tedizolid, or daptomycin if MRSA is confirmed. Continue an antibiotic that inhibits toxin production until group A streptococcus involvement is excluded.[3] Evidence for clindamycin is strongest.[2][37]
Drug safety alert: Fluoroquinolones
Fluoroquinolones have been associated with serious, disabling, and potentially irreversible adverse effects, including tendonitis, tendon rupture, arthralgia, neuropathies, and other musculoskeletal or nervous system effects.[64] Warnings have also been issued about the increased risk of aortic dissection, significant hypoglycaemia, and mental health adverse effects in patients taking fluoroquinolones.[65][66]
Type II infection
Monomicrobial: group A streptococcus or Staphylococcus aureus
Type II infection is most commonly due to group A streptococcus; clindamycin plus a penicillin is recommended.[2][37]
If the patient has a penicillin allergy, vancomycin monotherapy may be used.
S aureus may also cause type II infection.[3]
Use antibiotics that are active against MRSA until cultures confirm susceptibilities; options include vancomycin, linezolid, tedizolid, or daptomycin. Ceftaroline or dalbavancin are also reasonable choices.[2][3] In practice, tigecycline may also be used.
Flucloxacillin or cefazolin may be used if methicillin susceptibility is confirmed.[2]
Monomicrobial: gram-negative or clostridium organisms
Monomicrobial infection with gram-negative or clostridium organisms is rare.[5] It includes infection with:
Vibrio vulnificus: predisposing risk factors include hepatic disease, diabetes mellitus, chronic renal insufficiency, and adrenal insufficiency[9]
Aeromonas hydrophila: most common in patients with immunosuppression, burns, and trauma in an aquatic setting[10]
Klebsiella pneumoniae, in South East Asian countries, in particular Taiwan[11]
Clostridium: can also cause gangrenous necrotising fasciitis – see Gangrene.
Doxycycline should be included in the management of necrotising fasciitis due to V vulnificus or A hydrophila.[2]
Fungal infection
Fungal infection is rare and is the result of infection with pathogens such as Mucorales and Candida species. Seek advice from an infectious disease or microbiology specialist. Liposomal amphotericin-B is usually the primary treatment option.
If the patient develops streptococcal toxic shock syndrome (TSS), seek urgent advice from a senior colleague. Consider intravenous immunoglobulin (IVIG) as an adjunctive therapy for these patients.[3][4] See Toxic shock syndrome. IVIG may also have a role in managing patients with streptococcal infection without TSS.[3]
More info: IVIG
Efficacy data for use of IVIG for necrotising fasciitis are conflicting. Some studies suggest modest benefit; however, one Cochrane review showed no clear benefit on adverse events or mortality.[68][69][70][71][72][73]
The World Society of Emergency Surgery consensus recommendations suggest consideration of IVIG in patients with necrotising fasciitis due to group A streptococcus.[3][4]
The Infectious Diseases Society of America guidelines do not include a recommendation regarding the use of IVIG in patients with necrotising fasciitis with streptococcal toxic shock syndrome, citing the need for additional efficacy studies.[2]
Consider the need for additional debridement or alterations in antibiotic or antifungal therapy, based on culture results from subcutaneous tissue or blood, the patient’s clinical condition, and discussion with the multidisciplinary team.[2][3][4][53]
Surgical re-exploration to assess the need for further debridement should be performed at least every 12 to 24 hours after the initial debridement.[3] However, re-exploration may be needed sooner in some patients; inform the surgical team urgently if the patient has clinical signs of worsening infection (local or systemic), or worsening laboratory markers (particularly white blood cell count).[3]
Re-exploration should be repeated until the patient has no necrotic tissue remaining.[3][4]
If the patient has functional or cosmetic disability due to extensive surgical debridement, reconstructive surgery may be required. However, this should only be considered when the patient is stable and the infection has been completely eradicated.
[Figure caption and citation for the preceding image starts]: Small areas of skin necrosis in a young woman with cellulitis and necrotizing fasciitis of her lower abdomen 5 days after a cesarean sectionFrom: Hasham S, Matteucci P, Stanley PRW, et al. Necrotising fasciitis. BMJ. 2005 Apr 9;330(7495):830-3 [Citation ends].
Use of this content is subject to our disclaimer