REVIEW ARTICLE

Necrotizing fasciitis: Classification, diagnosis, and management

Luca Lancerotto, MD, Ilaria Tocco, MD, Roberto Salmaso, MD, Vincenzo Vindigni, MD, PhD,
and Franco Bassetto, MD, Padova, Italy

ABSTRACT: Necrotizing fasciitis (NF), a life-threatening rare infection of the soft tissues, is a medical and surgical emergency. It is
characterized by subtle, rapid onset of spreading inflammation and necrosis starting from the fascia, muscles, and subcutaneous
fat, with subsequent necrosis of the overlying skin. Once suspected, immediate and extensive radical debridement of necrotic
tissues is mandatory. Appropriate antibiotics and intensive general support avoid massive systemic diffusion of the infective
process and are the key for successful treatment. However, early diagnosis is missed or delayed in 85% to 100% of cases in large
published series: because of the lack of specific clinical features in the initial stage of the disease, it is often underestimated or
confused with cellulitis or abscess. Mortality rates are still high and have shown no tendency to decrease in the last 100 years.
Unfortunately, the prevalence of the disease is such that physicians rarely become sufficiently confident with NF to be able to
proceed with rapid diagnosis and management. This review covers the literature published in MEDLINE in the period 1970 to
December 31, 2010. Particular attention is given to the clinical and laboratory elements to be considered for diagnosis. A wide
variety of diagnostic tools have been described to facilitate and hasten the diagnosis of NF, but the most important tool for early
diagnosis still remains a high index of clinical suspicion. (J Trauma. 2012;72: 560 566. Copyright 2012 by Lippincott Williams
& Wilkins)
KEY WORDS: Necrotizing fasciitis; subcutaneous tissue; fascia; soft tissue infection; skin.

N ecrotizing fasciitis (NF) is a rare infection of the soft

tissues, characterized by rapid but subtle onset of
spreading inflammation and necrosis starting from the fascia,
involving muscles and subcutaneous fat, with subsequent
necrosis of the overlying skin. Hippocrates (500 BC) gave an
early description as diffused erysipelas caused by trivial
accidents, [where] flesh, sinews, and bones fell away in large
quantities, [leading to] death in many cases. NF features and
rapidity are such that it continues to attract peoples imagi-
nation and the attention of the mass media.1 Once suspected,
rapid, extensive radical debridement of necrotic tissues, ap-
propriate antibiotics, and intensive general support avoid
massive systemic diffusion of the infective process and are
the key for successful treatment.2,3 However, the lack of
specific clinical features and skin changes in the initial stage
of the disease easily lead to underestimation or misdiagnosis
as cellulitis or abscess.4 6 For this reason, mortality rates
have remained almost unchanged through the centuries. Un-
fortunately, the prevalence of the disease is such that physi-
cians rarely become sufficiently confident with NF to be able
to proceed with rapid diagnosis and management.
Submitted: May 28, 2011, Accepted: August 12, 2011.
From the Clinic of Plastic Surgery (L.L., I.T., V.V., F.B.), University of Padova,
Padova, Italy; and Department of Pathology (R.S.), University Hospital of
Padova, Padova, Italy.
Address for reprints: Luca Lancerotto, MD, Clinic of Plastic Surgery, Uni-
versity of Padova, Via Giustiniani 2, 35128 Padova, Italy; email:
luca.lancerotto@unipd.it.
DOI: 10.1097/TA.0b013e318232a6b3
MATERIALS AND METHODS
This review is based on a search of the literature on NF
and related skin diseases (necrotizing and nonnecrotizing soft
tissue infections) published in MEDLINE in the period 1970
to December 31, 2010, and bibliographies of retrieved arti-
cles. Key words searched were necrotizing fasciitis (NF),
cellulitis, fascia, subcutaneous tissue infection, group A
Streptococcus, and necrotizing soft tissue infection. Reviews,
randomized controlled trials, observational studies, and case
reports in English or French were considered. Data were
extracted independently by three reviewers, and any disagree-
ment was resolved by consensus.
Epidemiology
NF is a rare disease. The US Center for Disease Control
and Prevention estimates that 500 to 1,000 cases of NF are
diagnosed each year in the United States (population
309,000,000).7 The incidence of NF in adults is reported to be
0.40 cases per 100,000 population.8 It progressively increases
among patients aged 50 years and older, reaching 12 per
100,000 over the age of 80.9 A seasonal fluctuation has been
observed, with higher incidence in cold months (January to
April).9 No significant difference in incidence is observed
between men or women. Authors report periodical peaks in
the population, partially explained by increased microbial
virulence and resistance to antibiotics.9,10 The results of
population-based surveillance suggest that 85% of invasive
infections occur sporadically in the community, 10% are
hospital acquired, 4% occur in residents of long-term care
facilities, and 1% after close contact with a case.11 The results
of population-based active surveillance in Ontario, Canada,
suggest that the rate of secondary cases of streptococcal toxic

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shock syndrome (STSS) or NF infection is 2.9 cases per 1,000
household contacts, which is 200 times the baseline risk in the
community; but the 95% confidence interval around this esti-
mated rate are wide (0.8 7.5 per 1,000).11
NF is a predominantly adult disorder: it has been reported
in 0.08 per 100,000 children per year. However, in children, it
has a fulminant course with a high mortality rate.12
The hospital admission rate for NF is 2.73 per 10,000
admissions.2,13,14 An Australian study reported that the mean
hospital length of stay for survivors of NF was 36 days, and the
average cost per patient during hospital stay was AUS$64.517
(47.0265; US$47.0265).15 For 63% of their patients admitted to
the intensive care unit (ICU), the average length of stay in the
ICU was 11 days. A similar average duration of hospitalization
(34 days) was reported from Taiwan.16
Classification
NF is classified into two types, based on microbiology
(Table 1). Type I NF is a polymicrobial infection, with at
least one anaerobic species in combination with one or more
facultative anaerobic species, such as nontypable streptococci
and members of Enterobacteriaceae.17 It is typically located
at the trunk, abdominal wall, perianal and groin areas, and in
postoperative wounds.5 In newborns, type I NF can be a
life-threatening complication of omphalitis.18 Approximately
55% to 75% of all NF result from type I infection.
Type II NF is a monomicrobial infection, most commonly
caused by invasive group A Streptococci (GAS)-pyogenes, less
frequently by other streptococci or staphylococci.
Type II is associated with minor cutaneous/muscular
injuries in otherwise healthy, immunocompetent patients.
Predominant isolation sites are the head/neck and extremities.
GAS NF may present together or complicate with streptococ-
cal toxic shock syndrome (STSS) in about 30% of cases
(Table 2).13,14,19 No difference in mortality rates is observed
between type I and type II.20
Recently, authors have also described a third type because
of marine Vibrio species, reported as following minor injuries
exposed to salt water, i.e., fish stings and bites or shellfish
injuries. This third type is associated with a fulminant course,
with development of multiorgan failure within 24 hours if not
treated.10,20,21 When affecting the scrotum/perineum, NF is
known by the name of Fourniers gangrene, from Jean Alfred
Fournier who first described it in 1886.22
TABLE 1. Necrotizing Fasciitis Classification
Type Species Localization
Type 1 Polimicrobial: at least one Trunk, abdomen,
anaerobic facultative anaerobes and perineum
(Enterobacteriaceae, nongroup A
streptococci)
Type 2 Monomicrobial: group A -hemolytic Extremities
streptococci and/or other
streptococci staphylococci
Type 3 Marine Vibrios Extremities
Modified from Low and McGeer.5
2012 Lippincott Williams & Wilkins
Lancerotto et al.
TABLE 2. Diagnostic Criteria of Streptococcal Toxic Shock
Syndrome
Isolation of group A Streptococcus (pyogenes) from a normally sterile site
(e.g., blood and liquor) and hypotension (90 mm Hg) and two or
more of:
Renal impairment (creatinine 2 normal)
Coagulopathy (CID) or platelets 100.000/mm3
Liver involvement (AST, ALT or bilirubine 2 normal)
Adult respiratory distress syndrome
Generalized erythematous rash that may desquamate
Soft tissue necrosis (NF, myositis, or gangrene)
Modified from Davies.13
Microbiology
From an examination of recent case series, bacteria of the
Streptococcus species seem to be the most common single
causative organism. Staphylococcus aureus stands as the second
most frequently isolated aerobic bacteria, followed by Entero-
coccus species, Lactobacillus, and Corinebacterium species.
Escherichia coli and Klebsiella were the commonest facultative
anaerobic bacteria isolated, followed by anaerobic cocci. Clos-
tridium species are now a rare cause of NF, despite their
historical prevalence, as a result of improved sanitation. How-
ever, hundreds of single reports are found in the literature in
which cases of NF were caused by an extremely high variety of
microorganisms. Indeed, the clinical manifestations known by
the name of NF are the common angiothrombotic and necrotiz-
ing outcomes of a spectrum of invasive soft tissue infections, in
which a common element is the primary involvement of fascial
structures.
In the last 6 years, an increasing incidence of methicillin-
resistant S. aureus soft tissue infections has been reported, so
that today methicillin-resistant S. aureus is cultured in up to
40% of necrotic wounds.23 In general, polymicrobial infec-
tions tend to have longer incubation periods than monomi-
crobial infections, thus making them difficult to detect at an
early stage.
Sites of Infection
The most common sites of infection are extremities,
particularly the upper limb, primary site in 10% to 48% of NF
in large series. Lower extremities (28%), perineum (21%),
trunk (18%), and head or neck (5%) follow.14 In newborns,
necrotizing soft tissue infections most commonly involve the
abdominal wall as the initial site, followed by the thorax,
back, scalp, and extremities including the thigh and groin.24
Predisposing Factors
More than half the patients developing NF have preexist-
ing medical conditions, 35% at least two.25 The most common
predisposing risk factors include diabetes mellitus (30%), im-
mune suppression (17%), end-stage renal failure, liver cirrhosis,
pulmonary diseases (6%), malignancy (5%), and use of injection
drugs.2,14,26 A recent Varicella infection has been identified as a
risk factor for GAS NF among children.13 Blunt trauma has long
been anecdotally associated with higher risk of NF, and two
recent case-control studies seem to confirm this observation in
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the case of invasive GAS disease. Interestingly, the same studies Clinical Presentation
found no significant association between blunt trauma and cel- The term necrotizing fasciitis, first coined by Wilson
lulitis.27 Bryant et al.28 suggested that, at least in case of GAS, in 1952, is perhaps the most accurate in describing the key
this may be due to the higher exposure of vimentin on the features of the infectious process.31
surface of injured muscle cells, which would act as binding The most constant initial clinical feature is pain out of
protein for the bacteria. proportion to physical findings, in which case NF should
In newborns, several underlying conditions have been definitely be considered in differential diagnosis. Wang et
identified as contributing to the development of NF, including al.32 developed a clinical staging system based on a retro-
omphalitis, mammitis, balanitis, fetal scalp monitoring, post- spective evaluation of 22 patients (Table 3). At initial assess-
operative complications, septicemia, and necrotizing entero- ment (day 0), almost all patients presented with erythema,
colitis.24 Overall, 16% of NFs in children are associated with tenderness, warm skin, and swelling (Fig. 1). Blistering
a chronic underlying illness, patients with leukemia having an occurred in 41% of patients at presentation, whereas late
increased risk above all.29 signs such as skin crepitus, necrosis, and anesthesia were
infrequently seen (0 5%). As time elapsed, more patients had
Diagnosis blistering (77% had blisters at day 4) and eventually the late
Establishing the diagnosis of necrotizing soft tissue signs of NF, skin crepitus, necrosis (Fig. 2), and anesthesia
infections is not easy. In early stages, cases of NF are easily (9 36%). It is important to emphasize that these hard signs,
confused with cellulitis or abscesses. Early diagnosis is although typical and specific, are observed in only 10% to
missed in 85% to 100% of cases in large published series14 40% of patients.4,14,33 Moreover, they can quickly progress
and it is reported as the single cause of fatal outcomes.30 A within 24 hours to 48 hours, especially when NF is substained
wide variety of diagnostic tools have been described and by Streptococcus species. The absence of respiratory symp-
tested to facilitate and hasten the diagnosis of NF, based on toms, the presence of focal pain, and a recent history of
the close relation of rapid diagnosis and clinical outcome. penetrating or blunt trauma may be helpful diagnostic
clues.13,14,19,34 Introduction of the pathogen into the subcuta-
neous space may occur via any disruption of the overlying
skin (cut, abrasion, burn, laceration, contusion, bite, injection,
TABLE 3. Necrotizing Fasciitis Signs and Symptoms or surgical incision).
NF of the upper limb has a rapid centripetal diffusion to
Early Late
shoulder, neck, and trunk, which is facilitated by the rich
Local vascularity of the elbow region and of the fascial planes of
Skin puncture or injury Hematic/gas bullae arm and forearm.3537 Involvement of the chest area is asso-
Erythema Necrosis ciated with a negative outcome and must be prevented.38,39 A
Warmness Purple/blue skin colour combination of lesions in the perineal and lower extremities
Tenderness Crepitus has rarely been documented.
Myalgia Hypoesthesia
Hypersensitive skin Sensory/motor deficit Laboratory
Systemic Laboratory findings are nonspecific: 1white blood
Pain out of proportion Fever (sometimes hypothermia) cell count (WBC), 1creatine phosphokinase, 2albumin,
Swelling Hypotension 2sodium (Na), 1prothrombin time, or activated partial
Fever Mental confusion thromboplastin time have been suggested as useful param-
Multiorgan failure eters to identify NF cases, but are not exclusive.13,34 Wall
Modified from Wang et al.32 et al.26 suggested WBC 15.4 109 and Na 135
mmol/L, the former more important than the latter, as

Figure 1. Case 1 (A) Edematous, tender appearance of the arm, elbow, and upper half of forearm at referral; (B) same case,
exploration of right arm revealed partially liquefied, foul smelling, darklooking fascia, and necrosis of bicep.

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Figure 2. Case 2 (A) Detail of right elbow, edematous, tender, and blistered (arrows); small necrotic area visible at wrist (*).
(B) Surgical exploration and fasciotomy of right upper limb extending from neck to hand, with drainage of fluids and debride-
ment of necrotic tissues. Skin and subcutaneous tissue necrosis is visible at wrist.

laboratory parameters to distinguish NF from nonnecrotiz-
ing soft tissue infections. More recently, Wong et al.40
proposed a scoring system (laboratory risk indicator for
necrotizing fasciitis [LRINEC]) based on C-reactive pro-
tein, WBC, hemoglobin, Na, serum creatinine, and serum
glucose levels at admittance, which classifies patients in
low-, intermediate-, and high-risk categories of NF in the
early course of the disease (Table 4). A recent retrospec-
tive study on 209 patients by Su et al.41 demonstrated
increased rates of both mortality and amputation in pa-
tients with LRINEC score 6. Although helpful in under-
standing which patients are most at risk of a fatal outcome,
care should be taken in the use of such indexes, because
the relationship between the LRINEC score and outcomes
remains unclear. Of the LRINEC parameters, glucose and
C-reactive protein are considered predictors of mortality in
critically ill patients, in relation to sepsis hyperglycemia and
end-stage acute renal failure. A recent article reports the retro-
spective analysis of the case notes of all patients admitted to the
ICU, Townsville Hospital, Townsville, between January 2002
and December 2005 with the admission diagnosis of NF and the
application of the LRINEC score to the initial blood tests. With
a cutoff score of 6, the LRINEC score had a sensitivity of
80%, specificity of 67%, a positive predictive value of 57%,
and a negative predictive value of 86% in distinguishing
patients with proven NF from those with severe soft tissue
infections.42

TABLE 4. Laboratory Risk Indicator for Necrotizing Fasciitis Imaging

(LRINEC) Score System Confirmatory radiographic studies may be helpful.
LRINEC Score Magnetic resonance imaging is suggested to be the most
adequate radiologic technique to differentiate necrotizing and
LRINEC
Variable Value Score Points nonnecrotizing soft tissue infections.43 Specific findings for
NF include hyperintense signal on T2-weighted images at the
C-reactive protein (mg/L) 150 0
deep fascia and within muscles. Soft tissue thickening is also
150 4
a characteristic finding, but it may also be noted after trauma.
WBC (cells/mm3) 15 0
Whether its use may have an impact on morbidity or mortal-
1525 1
ity has not yet been assessed. Observation of gas in subcu-
25 2
taneous tissues, often associated with the isolation of aerobic
Hemoblobin (g/dL) 13.5 0
coliforms such as Enterobacteriaceae44 on X-ray or com-
1113.5 1
puted tomography scan, is reported in 17% to 29% of
11 2
patients.14,20,33 This is a very specific but not very sensitive
Sodium (mmol/L) 135 0
finding in patients with NF. Computed tomography is more
135 2
sensitive than X-ray in identifying signs of NF because it
Creatinine (mg/dL) 1.6 0
can show inflammatory changes such as abscesses or
1.6 2
fascial thickening, which a retrospective study associated
Glucose (mg/dL) 180 0
with 80% sensitivity for diagnosis of NF.45 Ultrasound
180 1
examination is an alternative to detect superficial ab-
LRINEC Score
Points, Sum Risk Category NF Probability scesses, although it is considered neither sensitive nor
specific for diagnosis of NF.
5 Low 50%
67 Intermediate 5075% Microscopic Features
8 High 75%
Microscopic reports typically show necrosis of the
LRINEC score system by Wong et al.; for intermediate- and high-risk patients, the superficial fascia with polymorphonuclear infiltration and
model has positive predictive value of 92% and negative predictive value of 96%.40
edema of reticular dermis, subcutaneous fat, and superficial

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Lancerotto et al.
Figure 3. Histological features of NF. (A) Almost pure neu-
trophil inflammation involving fascia (hematoxylin-eosin
80); (B) intense edema of papillary dermis and neutrophil
infiltrate of reticular dermis (hematoxylin-eosin 62); (C)
presence of many gram-positive cocci (Grams stain200);
(D) extensive areas of necrosis (hematoxylin-eosin200);
(E) angiothrombosis encountered at all levels, also with sec-
ondary vasculitic alterations (hematoxylineosin200); and
(F) inflammation and necrosis involving adjacent muscle
(hematoxylin-eosin50).
fascia of tissue excised in the operating theater (Fig. 3).
Intraoperative tissue biopsy should be obtained from the
interface between live and dead tissue. The disease is char-
acterized by angiothrombosis of the perforating vessels to the
skin, caused by the local hypercoagulable state. Liquefactive
necrosis of the superficial fascia initially spreads horizontally,
then involving muscles and the overlying skin, the extent of
the infection being usually much greater than that indicated
by skin findings alone (Figs. 1 and 3).46,47
Surgical Exploration
Surgical exploration remains the most sensitive and
specific option to confirm or exclude NF. Suggestive macro-
scopic findings at surgical exploration include detection of
gray necrotic tissue, gross fascial edema (Fig. 1), thrombosed
vessels, watery, thin, often foul-smelling fluid described as
dishwater pus, noncontracting muscles, and a positive fin-
ger test result, which is characterized by the possibility of
dissecting the subcutaneous tissue off the deep fascia with
minimal resistance.2,20 Surgery also represents a mandatory
life-saving therapy for affected patients, and although a major
operation can be necessary in cases of confirmation, limited
cutaneous access is needed as an initial step. In consideration
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Volume 72, Number 3
of the prognostic importance of missed diagnoses, we think
that, in dubious cases, surgical exploration should not be
avoided or delayed.
If no surgery is performed, the presence of cutaneous
necrosis together with classical clinical presentation and
pathogen isolation is needed for definitive diagnosis.5,48
Treatment
Surgery
Surgical debridement is a mandatory life-saving step
and should be performed as soon as possible. The most
important determinants of mortality are the timing and ade-
quacy of debridement: Wong et al.14 reported a ninefold
increase in mortality if the procedure is delayed more than 24
hours after hospital admission. Bilton et al.49 found increased
mortality from 4% to 38% in incomplete versus complete
debridement, and also Voros et al.50 reported dramatically
increasing mortality with delay and inadequate surgical
intervention.
Surgical debridement must be done until brisk bleeding
occurs from adjacent overlying subcutaneous tissues and
underlying muscles, if involved.10 All necrotic tissues, in-
cluding fascia, must be removed to reduce the bacterial load,
stimuli to inflammation, and facilitate recovery. In addition,
as it exposes tissues to oxygen, surgery may prove antago-
nistic to anaerobic bacteria. The wound should be bluntly
probed in all directions, especially in highly suspected areas
such as any pockets or subcutaneous or submuscular exten-
sion of infection. Repeated debridements may be necessary
(as dictated by the state of the wound) until the infection is
adequately controlled. Tissues are often edematous and
highly secreting, so wounds are usually left open after de-
bridement. Sterile dressings with normal saline-soaked gauze
once or twice each day may be used to cover the wound in the
interim. At our Institution, iodine gauze is preferred, because
it combines antiseptic action with a stronger desiccative and
foreign body effect which stimulates production of healthy
granulation tissue. Some authors recommend a second surgi-
cal exploration 24 hours to 48 hours later as mandatory to
ensure that the infectious process has not extended. If the
patient is stable, we prefer reevaluation during dressing
changes, the patient being brought back to the operating room
only in case of need. Reconstructive surgery should be
considered only once the patients general conditions are
stable and the infection fully eradicated. Wound coverage,
when not possible by direct suture, can be achieved by either
split thickness skin grafting or tissue transfer. Negative pres-
sure therapy may be used to promote healing and wound
closure, and this has helped in reducing the size of larger
defects. Other forms of surgery, such as amputation, may
result necessary for necrotizing infections of the extremities.
Antibiotic Therapy
Empirical broad-spectrum antibiotic coverage should
be supplied as soon as NF is diagnosed. Several multidrug
regimens have been described, including high-dose penicillin,
high-dose clindamycin, and a fluoroquinolone or aminogly-
coside for coverage of gram-negative bacteria. Penicillin
should always be included in consideration of possible GAS
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etiology. Because of the emergence of penicillin-resistant
staphylococci, third-generation cephalosporin, alone or in com-
bination with an aminoglycoside and metronidazole, must be
considered to provide adequate cover.33 Subsequent modifica-
tions can be made according to the organisms isolated and the
sensitivities obtained at antibiogram. It is suggested that, in cases
of NF complicated by streptococcal toxic shock syndrome
(STSS), the use of protein synthesis inhibitors such as clinda-
mycin prove more effective than penicillin; they inhibit M
protein and exotoxin synthesis by group A Streptococcus, thus
controlling the inflammatory response. Duration of antibiotic
therapy is recommended to last until the patient no longer
manifests signs of systemic inflammation, which generally
results in a 14-day course.14,17,20,33 Antibiotic therapy is
certainly of help, but not sufficient in itself to stop the spread
of the infection, because the angiothrombotic character of the
disease limits access of the drug to the affected areas. Indeed,
it has been shown that, when treatment is based only on
antimicrobial therapy and support, mortality approaches
100%. Reported risk factors that should serve as a trigger for
more aggressive surgical care and antimicrobial therapy are
truncal involvement, leukocytosis, acidosis, hypoalbumine-
mia, and hypocalcemia.
Other Therapies
Intravenous immunoglobulin therapy has been used
with some success in STSS.19,51 It is mostly theoretical, and
based on binding staphylococcal- and streptococcal-derived
exotoxins, thereby limiting the onset of a systemic inflam-
matory response syndrome.52
Postsurgery hyperbaric oxygen (HBO) therapy is a
generally accepted possibility.2,53 A recent study using an
experimental rat model receiving HBO exposure at 2.5 ATA
pressure proved that subcutaneous tissue oxygen tension
levels increased fivefold and the carbon dioxide tension levels
twofold compared with initial levels. Results were confirmed
in six NF patients in normobaric conditions and during HBO
therapy with PO2 even regularly higher in the vicinity of the
infected area than in healthy tissues.54 However, there are no
definitive clinical data to support the benefit of adjuvant HBO
therapy for NF. A recent retrospective study of 67 cases was
reviewed to compare the outcomes of adjuvant HBO therapy
versus non-HBO therapy: it did not find any differences
between the groups in mortality and average length of hospital
stay. However, the HBO group had significantly lower amputa-
tion rates.55 Multicenter, prospective, case-control studies should
be performed to assess the possible benefit of adjuvant HBO2
therapy for NF. Certainly, HBO therapy should not jeopardize
standard therapy for NSTIspecifically, adequate and timely
debridement.
Outcome
Mortality rates are high and have remained almost
unchanged in the past century. From analysis of the series
published between 1924 and 1988, it is assessed at 25% to
30%, with no significant variations through the decades; 30%
occur as early deaths due to sepsis.4,33 The risk of death from
NF is reported as increasing by 4% for every year of life.38
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Lancerotto et al.
The overall mortality rate in most of the published pediatric
series ranges between 5% and 10%.56
Extensive tissue necrosis may result in poor, often fatal,
outcomes, because of the development of septic syndrome.
Untreated, the disease is almost invariably fatal. The mortality
rate of STSS-complicated NF doubles with dramatic progression
to multiorgan failure.9 The association of the two conditions is
reported to have fatal outcomes in up to 70% of patients
occurring in 76 hours to 92 hours. Significant associations with
negative outcomes have been detected for a large number of
factors, like extremes of age (60 and 1), immunologic
compromise, and systemic diseases. The main factor recognized
to influence prognosis negatively is late surgical debride-
ment.10,14,33,38 Moreover, patients with infection by Clostridia
have a fourfold increased risk of death and limb loss compared
both with polymicrobial and other monomicrobial infections.57
Anaya et al.58 created a clinical scoring system that categorizes
patients with NSTI according to the risk of death, based on six
independent parameters at admission: age 50 years, heart rate
110 bpm, temperature 36C, WBC count 40,000/mcL,
serum creatinine concentration 1,5 mg/dL, and hematocrit
50%; the accuracy of this model was 86.8%. Complications of
the illness and its treatment are common. Widjaja et al.15
reported infections in other parts of the body as the most
common complication, followed by pneumonia, urinary tract
infection, and heart failure.
CONCLUSION
NF is a rare condition with poor prognosis unless
promptly treated. Characteristic clinical presentations are ob-
served only late while initial findings may be misleading. NF
should always be considered in differential diagnosis in cases
presenting with local pain and/or inflammation, even in patients
with no apparent predisposition. A high index of clinical suspi-
cion is needed, together with appropriate resuscitation and sur-
gery to have any effect on the very high mortality.
DISCLOSURE
The authors declare no conflict of interest.
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