Review Article
Necrotizing Fasciitis
Joseph M. Bellapianta, MD
Karin Ljungquist, MD
Ellis Tobin, MD
Richard Uhl, MD
Dr. Bellapianta is Chief Orthopaedic
Resident, Albany Medical Center,
Albany, NY. Dr. Ljungquist is
Orthopaedic Resident, Ohio State
University Medical Center,
Columbus, OH. Dr. Tobin is Clinical
Associate Professor, Department of
Medicine, Albany Medical College,
Albany, NY. Dr. Uhl is Professor of
Surgery, Division of Orthopaedic
Surgery, Albany Medical College.
Dr. Uhl or a member of his
immediate family is a member of a
speakers’ bureau or has made paid
presentations on behalf of AO and
has received research or institutional
support from CONMED Linvatec,
DePuy, Smith & Nephew, Stryker,
and Synthes. None of the following
authors or a member of their
immediate families has received
anything of value from or owns
stock in a commercial company or
institution related directly or
indirectly to the subject of this
article: Dr. Bellapianta,
Dr. Ljungquist, and Dr. Tobin.
Reprint requests: Dr. Bellapianta,
Albany Medical College, Suite 202,
1367 Washington Avenue, Albany,
NY 12206.
J Am Acad Orthop Surg 2009;17:
174-182
Copyright 2009 by the American
Academy of Orthopaedic Surgeons.
174
Abstract
Necrotizing fasciitis is a rare but life-threatening soft-tissue infection
characterized by rapidly spreading inflammation and subsequent
necrosis of the fascial planes and surrounding tissue. Infection
typically follows trauma, although the inciting insult may be as
minor as a scrape or an insect bite. Often caused by toxin-
producing, virulent bacteria such as group A streptococcus and
associated with severe systemic toxicity, necrotizing fasciitis is
rapidly fatal unless diagnosed promptly and treated aggressively.
Necrotizing fasciitis is often initially misdiagnosed as a more benign
soft-tissue infection. The single most important variable influencing
mortality is time to surgical débridement. Thus, a high degree of
clinical suspicion is necessary to avert potentially disastrous
consequences. Orthopaedic surgeons are often the first to evaluate
patients with necrotizing fasciitis and as such must be aware of the
presentation and management of this disease. Timely diagnosis,
broad-spectrum antibiotic therapy, and aggressive surgical
débridement of affected tissue are keys to the treatment of this
serious, often life-threatening infection.
A lthough necrotizing fasciitis gar-
nered tabloid fame as a sensa-
tionalistic “new” and dangerous
rotizing fasciitis” in 1952 and de-
scribed the inflammation and necro-
sis of the subcutaneous fat and deep
“flesh-eating bacterium” in the
fascia, with sparing of the muscle,
1990s,1 it was described by Hip- that are the cardinal features of this
pocrates in the 5th century BCE.2 devastating disease.7 This character-
Necrotizing fasciitis has since had ization agrees with the current belief
many names, including phagedena,
that a disease process, rather than a
phagedena gangrenosum, progressive particular organism, is implicated in
bacterial synergistic gangrene, and this condition.
nonclostridial gas gangrene.3 The
first report in the United States was
made in 1871 by Confederate Army Etiology
surgeon Joseph Jones, MD, who de-
scribed “hospital gangrene” with a Necrotizing fasciitis typically follows
an injury to the involved site. Even a
mortality rate of almost 50%.4 In
1883, Fournier5 identified his ep- minor lesion may be sufficient to al-
low bacteria to breach the skin bar-
onymic form of gangrene and so de-
scribed the pathology of necrotizing rier. Necrotizing fasciitis has been as-
fasciitis affecting the perineum and sociated with minor or blunt trauma,
external genitalia. Meleney6 identi- insect bites, surgical incisions,8 cuts,
fied hemolytic streptococcus as the abrasions, contusions, injection sites,
etiologic agent of the disease in cutaneous ulcers, perirectal ab-
1924. Wilson coined the term “nec- scesses, incarcerated hernia,7 burns,
Journal of the American Academy of Orthopaedic Surgeons
 Joseph M. Bellapianta, MD, et al

splinters, childbirth, chicken pox, Figure 1 Figure 2

penetrating injury, and muscle
strains.9 Although the skin is the
most common portal of entry, in
45% of cases, no definitive access
point can be found,10 possibly be-
cause the inciting insult was so mi-
nor as to be forgotten. The extremi-
ties are most commonly involved,
but necrotizing fasciitis can affect
any body part.11 Infections of the
trunk and perineal regions have a
higher mortality rate than those of
the extremities, presumably because
amputation is not feasible as a life-
saving option.7 Developing blisters on the arm in
necrotizing fasciitis. Note the
presence of ruptured bullae
draining serosanguineous fluid in Necrotizing fasciitis of the arm.
Risk Factors the lower left quadrant of the Note the ecchymosis, erythema,
figure. and presence of serous drainage
Any host condition that results in an from ruptured blisters.
immunocompromised state is a risk
quently, the infection is often incor-
factor for necrotizing fasciitis. Diabe-
rectly identified as cellulitis. A high in-
tes mellitus, the most common co-
dex of suspicion is critical to avoid disproportionate to injury seen ear-
morbidity, is present in 18% to 60%
morbidity and mortality because, al- lier in the process gives way to anal-
of cases.8 Other risk factors include
though cellulitis without deeper in- gesia as cutaneous nerves are de-
obesity,12 peripheral vascular dis-
volvement is usually treatable with an- stroyed. Superficial fat and fascia
ease,13 intravenous drug use,13 alco-
tibiotics alone, necrotizing fasciitis necrose, producing the watery, gray-
hol abuse,14 malnutrition,8 smok-
requires surgical débridement.9 The ish, often foul-smelling “dishwater
ing,13 chronic cardiac disease,13,15
triad of swelling, erythema, and inor- pus” characteristic of the disease.20
chronic corticosteroid therapy,16
dinate pain—often disproportionate By this stage, the patient shows con-
chronic immune suppression,17 can-
to the observed lesion—in a patient stitutional symptoms of fever, chills,
cer,17 and age.17 The continued or
who is thought to have cellulitis hypotension, tachycardia, and possi-
chronic use of nonsteroidal anti-
should raise suspicion of necrotizing bly an altered level of consciousness,
inflammatory drugs has been sug-
fasciitis. Pain may precede warming and is critically ill21 (Table 1).
gested as a possible risk factor7 be-
and induration of skin (ie, wooden Acute renal failure is present in 35%
cause it may mask initial symptoms
skin) by several hours.18 Rapid mi- of patients, coagulopathy in 29%, liver
and delay diagnosis.18,19 Although
gration of the margins of erythema function tests are abnormal in 28%,
numerous risk factors have been
and skin induration (>1 cm/hr) de- acute respiratory distress syndrome is
identified, half of all cases of necro-
spite the use of intravenous antibiot- seen in 14%, and bacteremia is seen in
tizing fasciitis occur in previously
ics is another important clue in the 46%.22 The clinician must not be in-
healthy individuals.8
early stages of the disease.3 appropriately reassured by the ab-
Classic signs of necrotizing fasciitis sence of these findings because many
Clinical Presentation develop as the disease progresses. patients may lack these signs on pre-
Blisters and bullae form and drain sentation. In one series, only 47% of
Necrotizing fasciitis typically begins as first serosanguineous and then hem- patients presented with classic skin
a slightly inflamed area of soft tissue orrhagic fluid (Figure 1). The skin changes of bullae, vesicles, and ne-
that suddenly and dramatically may also show violaceous discolora- crosis, and only 51% were febrile.23
progresses to overt fasciitis with sys- tion before turning frankly necrotic Disproportionately severe pain, the
temic toxicity. Early diagnosis is made and sloughing (Figure 2). Crepitus most sensitive symptom, is noted in
difficult by a paucity of skin findings in may be present if there is soft-tissue nearly 100% of patients with necro-
the first stages of disease. Conse- gas. Edema develops rapidly. Pain tizing fasciitis.24

March 2009, Vol 17, No 3 175

Necrotizing Fasciitis
Diagnosis
Diagnosis is primarily clinical, and
no test is as valuable as a high degree
of suspicion. Laboratory and radio-
logic evaluations can be helpful but
are best used for confirmation of the
diagnosis. Pursuing such tests should
never delay surgical intervention. Av-
erage time from onset of initial
symptoms to diagnosis is 2 to 4 days,
although some cases may take weeks
to be correctly identified.25
Laboratory Evaluation
Initial laboratory evaluation should
include a complete blood count,
comprehensive metabolic panel, and
coagulation studies. Blood cultures
should be taken to obtain pathologic
diagnosis of involved microorgan-
isms and antibiotic sensitivities to
guide future targeted antibiotic ther-
apy. Arterial blood gases should be
assessed, especially when signs of
sepsis are present.7 Azotemia, hy-
ponatremia, hypoproteinemia, throm-
bocytopenia, hematuria, elevated
creatine kinase and erythrocyte sedi-
mentation rates, metabolic acido-
sis, hypoalbuminemia, anemia, and
hyperbilirubinemia are commonly
noted. Hypocalcemia secondary to
extensive fat necrosis may be seen.
Few metabolic abnormalities may be
noted early on, but as the disease
proceeds toward sepsis and organ
failure, laboratory findings may be-
come extremely deranged.
In addition to clinical monitoring,
routine laboratory evaluations can
be used to distinguish necrotizing
fasciitis from other soft-tissue infec-
tions. Wall et al26 described a model
based on the white blood cell (WBC)
count and serum sodium levels. They
reported that concurrent findings of
a WBC count >15,400 cells/µL and a
serum sodium level <135 mmol/L are
90% sensitive for necrotizing fascii-
tis. However, this model lacks speci-
176
Table 1 Table 2
Physical Examination Findings in Variables and Scoring of the
Patients With Necrotizing Laboratory Risk Indicator for
Fasciitis Necrotizing Fasciitis (LRINEC)
Finding Patients (%) Value Score
Pain 100 C-reactive protein level
(mg/L)
Erythema 95
<150 0
Edema 82
>150 4
Cellulitis 75
White blood cell count
Fever (>38.5° C) 70
(cells/µL)
Discoloration 49
<15,000 0
Crepitus 25
15,000–25,000 1
Vesicles 16
>25,000 2
Disorientation 14
Hemoglobin level (g/dL)
Adapted with permission from Childers BJ, >13.5 0
Potyondy LD, Nachreiner R, et al: 11–13.5 1
Necrotizing fasciitis: A fourteen-year
retrospective study of 163 consecutive <11 2
patients. Am Surg 2002;68:109-116.
Sodium level (mmol/L)
≥135 0
ficity (76%) and has a poor positive <135 2
predictive value (26%) for necrotiz- Creatinine level (mg/dL)
ing fasciitis, suggesting that it is use- ≤1.6 0
ful only for ruling out the disease. >1.6 2
Another model for evaluating group Glucose level, mg/dL
A streptococcus soft-tissue infections ≤180 0
found that C-reactive protein levels >180 1
>16 mg/dL are 89% sensitive and
Adapted with permission from Anaya DA,
90% specific for necrotizing fasciitis, Dellinger EP: Necrotizing soft-tissue
and that creatine kinase levels >600 infection: Diagnosis and management.
Clin Infect Dis 2007;44:705-710.
U/L are 58% sensitive and 95% spe-
cific for necrotizing fasciitis as op-
posed to cellulitis.18 tissue infections when 6 was used as
Wong et al27 developed the Labora- the cut-off score.27
tory Risk Indicator for Necrotizing
Fasciitis (LRINEC). This method dif- Radiologic Evaluation
ferentiates necrotizing fasciitis from Plain radiographs are most useful for
other soft-tissue infections using the detecting gas in soft tissues. How-
parameters of C-reactive protein ever, their utility is limited, as studies
level, total WBC count, and hemo- are often normal until infection and
globin, serum sodium, creatinine, necrosis are advanced, and in many
and glucose levels (Table 2). The cases, soft-tissue gas never presents.
probability of necrotizing fasciitis is Computed tomography (CT) scans
<50% with a score ≤5, 50% to 75% are more beneficial than plain radio-
with a score of 6 or 7, and >75% graphs. Increased attenuation of the
with a score ≥8 (minimum score, 0; subcutaneous fat with stranding is
maximum, 13). The model had a seen in 80% of cases, and fascial
92% positive predictive value and a thickening may be present.25 Images
96% negative predictive value for may show gas in soft tissues or
detecting early cases of necrotizing tracking along fascial planes.25 CT
fasciitis in patients with severe soft- scans are especially sensitive in iden-
Journal of the American Academy of Orthopaedic Surgeons

tifying soft-tissue edema and often
can be more useful than physical ex-
amination in defining the margins of
infection. However, abnormal CT
findings are not universal, and cases
have been reported of necrotizing
fasciitis with negative CT findings.24
Magnetic resonance imagining
studies have demonstrated a high
sensitivity (93% to 100%) for diag-
nosing necrotizing fasciitis.24 Lique-
factive tissue necrosis and inflamma-
tory edema create fascial fluid that is
detected as abnormally increased sig-
nal intensity on T2-weighted images.
On T1-weighted images, necrosis
and edema present as variably in-
creased signal intensity along thick-
ened deep fascial planes.29 Although
magnetic resonance imaging is very
useful in delineating the extent of in-
fection, it is of lesser priority than
surgical débridement of necrotic tis-
sue when a patient is unstable with
worsening signs of sepsis.
Biopsy
The diagnostic benchmark for necro-
tizing fasciitis is the finding of fascial
necrosis during surgery. Outside the
operating room, tissue-based diag-
nostic procedures may be of use. The
“finger test” is a bedside procedure
that can confirm necrotizing fasciitis.
Under local anesthesia, a 2-cm inci-
sion is made down to the deep fascia,
and a gloved finger is inserted to its
base. The presence of dishwater pus,
lack of bleeding on incision, and lack
of tissue resistance to blunt finger
dissection define a positive test.
Frozen-section biopsy can also be
done at bedside. A small elliptical
section of skin, deep tissue, and fas-
cia is taken from the suspected area,
along with another from the leading
edge of any erythema, induration, or
necrosis. The specimens are then
submitted for Gram stain, frozen sec-
tion, and culture. This method al-
lows an accurate diagnosis of necro-
March 2009, Vol 17, No 3
tizing fasciitis to be made within 15
minutes of biopsy and reduces the
time between onset of symptoms and
diagnosis. Although mortality rates
are lower with this technique, it is
somewhat cumbersome and requires
the immediate availability of an ex-
perienced pathologist.28 Frozen-
section biopsy is best used in cases in
which the diagnosis is unclear and
the patient is stable. Surgical inter-
vention should never be postponed
to perform such a biopsy in cases in
which necrotizing fasciitis is strongly
suspected.
Mortality
There are an estimated 500 to 1,000
cases of necrotizing fasciitis in the
United States annually,8 with mortal-
ity ranging from 6% to 76%.27 A re-
cent review of 147 patients revealed
a mortality rate of 9.3%, suggesting
that outcomes are improving, pre-
sumably because of more effective
patient management.30 Patients aged
<1 year or >60 years have the highest
mortality rates.13 Thrombocytopenia,
abnormal liver function tests, low se-
rum albumin level,31 acute renal fail-
ure, and elevated blood lactate level
are significantly associated with mor-
tality,7 while advanced age, strepto-
coccal toxic shock syndrome, and
immunocompromised status are in-
dependent predictors of death.32 A
study of 99 patients with necrotizing
fasciitis found that the risk of death
increased by 4% for every year of
life.32 However, the most important
clinical variable affecting mortality is
the time from admission to initial dé-
bridement, making rapid diagnosis
of the utmost importance.7
Histopathology
Necrotizing fasciitis is characterized
by necrosis of the superficial fascia,
fat, and nerves, with thrombosis and
Joseph M. Bellapianta, MD, et al
suppuration of the arteries and veins
(Figure 3). Obliterative vasculitis of
the subcutaneous vessels is seen early
in the disease.13 There is expansion
of fibrous septa by edema, mixed in-
flammatory cell infiltrate, and early
fibroblastic proliferation.29 As the
disease progresses, lesions develop
liquefactive necrosis at all involved
tissue levels. A dense neutrophil-
predominant inflammatory infiltrate
is present, and Gram stain of the af-
fected tissues is usually positive.24
Microbiology
Aerobic, anaerobic, gram-positive
and -negative organisms, and even
fungi have been implicated in necro-
tizing fasciitis (Table 3). The infec-
tion can be classified into three
groups based on Gram stain and
bacterial culture results. Type 1 con-
stitutes 80% to 90% of all cases and
is a polymicrobial infection involving
non–group A Streptococcus along
with anaerobes and/or facultative
anaerobes. It often involves entero-
bacteriaceae as well. Typically, four
to five species will be cultured from
the wound. This type is associated
with postoperative abdominal and
perineal infections; it is most com-
mon in immunosuppressed patients.
Virulence is not well understood but
is speculated to be the result of syn-
ergy between bacterial species.
Type 2 necrotizing fasciitis is de-
fined by the presence of group A β-
hemolytic streptococci, typically as a
single agent,20 although Staphylococ-
cus or other organisms may be
present. This is the “flesh-eating”
presentation of necrotizing fasciitis.13
Infection usually occurs in an ex-
tremity and can develop in healthy
individuals.
Type 3 necrotizing fasciitis is caused
by marine vibrios (gram-negative rods).
Vibrio vulnificus is thought to be the
most virulent of these agents. Infection
177
Necrotizing Fasciitis

Figure 3 Table 3
Organisms Identified in
Necrotizing Fasciitis

Gram-positive aerobic bacteria

Group A β-hemolytic streptococci
Group B streptococci
Enterococci
Coagulase-negative staphylococci
Staphylococcus aureus
Bacillus spp
Gram-negative aerobic bacteria
A, Low-magnification photomicrograph demonstrating necrotizing fasciitis. Escherichia coli
Note the skeletal muscle tissue (upper right) encircled on the left and below Pseudomonas aeruginosa
by infected fascial tissues featuring extensive acute suppurative inflammation Enterobacter cloacae
(hematoxylin-eosin, original magnification ×20). B, Higher-magnification
photomicrograph demonstrating the intense infiltrate of neutrophils in the Klebsiella spp
fascial septum, with extension into the adjacent skeletal muscle fibers Proteus spp
(hematoxylin-eosin, original magnification ×100). Serratia spp
Acinetobacter calcoaceticus
Citrobacter freundii
usually begins with a puncture wound ders group A Streptococcus one of Pasteurella multocida
caused by a fish, or a cut or insect bite the most common human pathogens, Anaerobic bacteria
that is then exposed to seawater or ma- and it is capable of producing a vari-
Bacteroides spp
rine animals. Soft-tissue damage is ety of clinical disorders, including
Clostridium spp
thought to be mediated by an extracel- pharyngitis, cellulitis, impetigo, and
Peptostreptococcus spp
lular toxin synthesized by the vibrio scarlet fever. It is among the few bac-
Marine Vibrio spp
organism.20 Klebsiella, Escherichia teria that can cause a wound infec-
Vibrio vulnificus
coli, and other uncommon organ- tion, cellulitis, or necrotizing fasciitis
Vibrio parahaemolyticus
isms have also been reported as caus- within 24 hours following surgery.37
Vibrio damsela
ative agents of necrotizing fasci-
Vibrio alginolyticus
itis.31,33 Recently, cases of necrotizing
fasciitis resulting from community- Treatment Fungi
Candida spp
acquired methicillin-resistant Staphy-
There are five parameters of therapy for Aspergillus spp
lococcus aureus (MRSA) have been
necrotizing fasciitis: early diagnosis and Rhizopus
reported.34,35
débridement, broad-spectrum antibiot-
The microbiology of type 2 necro- Adapted with permission from Green RJ,
ics, aggressive resuscitation, frequent re-
tizing fasciitis is the best character- Dafoe DC, Raffin TA: Necrotizing fasciitis.
evaluation, and comprehensive nutri- Chest 1996;110:219-229.
ized of the three groups. The natural
tional support (Figure 4).
habitat of group A Streptococcus is
human skin and mucosal surfaces. It The initial incision should be made
Surgical Débridement
has coevolved with humans and does directly over the involved skin, paral-
not survive outside a human host. Surgical débridement is the founda- lel to the neurovascular bundles and
The bacterium boasts an enormous tion of management because it is the down to the deep fascia. The surgeon
and evolving molecular diversity, fastest and most effective way to re- may encounter dull, gray, avascular ne-
driven by horizontal transmission duce the bacterial load and halt the crotic tissue demonstrating a lack of re-
among group A streptococci strains necrotic process. This is the only in- sistance to blunt dissection, lack of
and also between group A and other tervention proven to increase the rate bleeding of the fascia, and the presence
streptococci. Acquisition of pro- of survival.8 The goal of surgery is to of foul-smelling dishwater pus.24 The
phages confers virulence through remove at the first débridement all margins of débridement should be
phage-associated factors and in- necrotic tissue, including muscle and advanced until skin and fascia nor-
creases bacterial survival against skin if necessary, in addition to the mally adherent to the deep fascia are
host defenses.36 This diversity ren- involved fascia.11 encountered and must terminate in

178 Journal of the American Academy of Orthopaedic Surgeons

 Joseph M. Bellapianta, MD, et al

Figure 4

Treatment algorithm for necrotizing fasciitis. IVIG = intravenous immunoglobulin G, MRI = magnetic resonance imaging
*Amputation may be indicated at the first surgical intervention if the infection is quickly progressing, necrosis has
consumed most of the involved limb, and limb salvage is deemed impossible.

viable, vascularized tissue. Poorly
perfused tissue will act as a nidus for
continued bacterial proliferation.13
Although amputation does not im-
prove mortality in certain studies,38 it
may be necessary with some very ag-
gressive infections as a first-line sur-
gery to avoid death. Some authors
have described conservative manage-
ment in pediatric patients, allowing
tissue demarcation to occur over a
period of several days before surgical
intervention, but this approach has
not been adopted at our institution
for either adults or children.39
Careful management of the extensive
wounds that often result from this rad-
ical form of surgery is critical. The
wound must be reevaluated daily be-
cause repeated débridement is com-
monly required. The wound should be
kept covered to protect against second-
ary infection, encourage the formation
of granulation tissue, and absorb in-
flammatory exudates. Both alginate and
hydrogel dressings have been used suc-
cessfully. Topical negative pressure ther-
apy can reduce edema and stimulate the
formation of granulation tissue, and
may reduce wound pain.
Once the infection has resolved and
a bed of healthy granulation tissue is
present, the wound may be closed with
skin flaps or split-thickness grafts.7
Many cases will require reconstruc-
tive surgery with possible free-tissue
transfer.13 Wound management tech-
niques developed for burn victims
may be applicable, and the successful
use of the skin substitute Integra (In-
tegra LifeSciences, Plainsboro, NJ)
following surgical débridement for

March 2009, Vol 17, No 3 179

Necrotizing Fasciitis
Table 4
Initial Antibiotic Management for Necrotizing Fasciitis
Initial Empiric Therapy*
Clindamycin plus any of the Clindamycin plus vancomy-
following: imipenem, mero-
penem, ampicillin/sulbactam,
piperacillin/tazobactam
* Before results of Gram stain are available
necrotizing fasciitis has been re-
ported. By providing early wound
coverage, grafting can be delayed un-
til the patient has recovered from the
initial injury.40
Antibiotic Therapy
Antibiotics are an important comple-
ment to surgical therapy but cannot
be the sole treatment because fascia
is poorly vascularized, and the dis-
ease process further reduces its blood
supply. This results in poor antibiotic
delivery to the site of infection. De-
spite having little effect on the
wound itself, antibiotics can reduce
the bacterial load, terminate toxin
production, and help prevent organ
failure. Intravenous antibiotic ther-
apy should be instituted at presenta-
tion after microbial cultures are ob-
tained.
Initially, the infection should be
treated empirically with broad-
spectrum agents with activity against
gram-positive, gram-negative, and
anaerobic organisms until antimicro-
bial sensitivities are obtained (Ta-
ble 4).
Acceptable regimens include imi-
penem, meropenem, ampicillin/sul-
bactam, and piperacillin/tazobactam,
all in combination with clindamycin.
Gram stain of pus or deep wound tis-
sue acquired during surgery should
guide initial adjustments to antibiotic
therapy. The presence of gram-positive
180
Gram Stain Result
Gram-positive Cocci Gram-positive Cocci in
in Clusters Pairs or Chains
Clindamycin plus any of the follow- Clindamycin plus any of the
cin, or monotherapy with ing: piperacillin/tazobactam,
linezolid ampicillin/sulbactam, or high-
dose penicillin
cocci in clusters seen on Gram stain is
adequate to support the use of vanco-
mycin or linezolid because of the in-
creased prevalence of MRSA.34,35,41 In
contrast, Gram stain revealing gram-
positive cocci in pairs or chains is
treated with clindamycin and a
β-lactam antibiotic. When the Gram
stain reveals a polymicrobial flora,
initial empiric therapy should be
continued. As culture results and
sensitivities become available, antibi-
otic therapy should be further ad-
justed if necessary.
Clindamycin is advised at the earli-
est suspicion of group A streptococ-
cal or Staphylococcus aureus infec-
tion because it shuts down bacterial
ribosome function, which inhibits
both M protein and exotoxin pro-
duction. Linezolid also possesses this
ability. This inhibition facilitates
phagocytosis and suppresses the syn-
thesis of tumor necrosis factor-α,
thereby reducing the overzealous im-
mune response.9 The Eagle effect de-
scribes the limits of the efficacy of
penicillin after a streptococcal infec-
tion has reached steady state,37 but
the efficacy of clindamycin is not af-
fected by the size of the bacterial in-
oculum or the stage of growth. Clin-
damycin has been shown to be more
effective than penicillin against strep-
tococcus species.24 One study found
that use of clindamycin reduced the
risk of hospital mortality by 89%
Journal of the American Academy of Orthopaedic Surgeons
Polymicrobial With Gram-
positive Cocci and Gram-
negative Bacilli
following: imipenem, mero-
penem, ampicillin/sulbactam,
piperacillin/tazobactam
among patients with necrotizing fas-
ciitis.42
Supportive Care
Adequate fluid resuscitation and
blood pressure support are essential
because patients with necrotizing fas-
ciitis often are septic at presentation
or become so very quickly. Nutri-
tional support is necessary because
loss of fluid, protein, and electrolytes
from the large surgical wounds are
comparable to those observed in
burn victims. In the acute phase, in-
take of twice the basal caloric re-
quirement is appropriate. A patient
who is unable to tolerate enteral
feedings should receive total
parenteral nutrition.13 Postoperative
care must also address adequate pain
management, such as use of patient-
controlled analgesia.43
Adjunctive Therapies
Adjunctive therapies include intrave-
nous immunoglobulin G (IVIG), hy-
perbaric oxygen (HBO), and recom-
binant human-activated protein C.
The latter has been cited in a case re-
port as a promising new therapy for
sepsis that may reduce mortality in
patients with group A streptococcus
necrotizing fasciitis.44
In both in vivo and in vitro studies,
IVIG has been found to inhibit the ac-
tivation of T-cells by superantigens and

to inhibit the activity of streptococcal
antigens to elicit cytokine production.
Thus, it has been speculated to be of po-
tential use in necrotizing fasciitis caused
by group A streptococcus. The typical
dosage is 1 to 2 g/kg of body weight per
day for 2 days.45 Some studies have
reported decreased mortality with
the use of IVIG in patients with
streptococcal toxic shock syndrome,
but a recent review found no evi-
dence that it improves clinical out-
comes in necrotizing fasciitis.46
HBO therapy has been proved to
be efficacious for clostridial gan-
grene,47 but its use in necrotizing fas-
ciitis is supported only by anecdotal
and retrospective reports. Bacterial
infection is associated with reduced
tissue oxygen tension, and HBO may
be able to reverse several of the
pathophysiologic mechanisms poten-
tiating the necrotizing process. It is
thought that reestablishment of a
normal or elevated partial oxygen
pressure by administration of HBO
can terminate the vicious cycle of in-
fection, ischemia, and reduced host
defense mechanisms. HBO therapy
may also be helpful in identifying in-
fection boundaries, potentially re-
ducing unnecessary débridement.48
Standard therapy is 2.0 to 2.5 atm
for 90 to 120 minutes twice daily un-
til infection progression is halted.
Reported outcomes vary greatly. Es-
cobar et al49 found an 11-fold greater
chance of survival with HBO treat-
ment and a decrease in morbidity
with fewer amputations in a retro-
spective study of 42 patients. Rise-
man et al50 reported that HBO use
reduced mortality from 66% to 23%
in a retrospective study of 29 pa-
tients. Conversely, Brown et al51 con-
cluded that there was no significant
reduction in mortality rate associated
with HBO therapy among 54 pa-
tients with necrotizing fasciitis.
HBO therapy carries risks. Among
the potential complications are claus-
trophobia, tympanic membrane rup-
March 2009, Vol 17, No 3
ture, seizures, and central nervous sys-
tem oxygen toxicity.7 Because of the
lack of randomized, prospective data
regarding the utility of HBO therapy,
currently it is best characterized as
an adjunct therapy of potential bene-
fit that should never delay or inter-
fere with surgical intervention.
Summary
Necrotizing fasciitis is an uncommon
infection of the superficial fascia and
surrounding tissue. It is typically the
result of a mixed infection with viru-
lent, toxin-producing bacteria, or
group A Streptococcus alone. MRSA
appears to be emerging as an addi-
tional microbiologic factor. Early di-
agnosis is essential because the dis-
ease can rapidly progress to severe
systemic toxicity and shock, organ
failure, or acute respiratory distress
syndrome. The single most effective
management tool is a high degree
of clinical suspicion followed by
prompt surgical débridement of all
necrotic tissue, with repeat débride-
ment as needed. Broad-spectrum an-
tibiotic therapy accompanies surgical
management, and clindamycin is sig-
nificantly beneficial when strepto-
coccal or staphylococcal species are
involved. Patients with necrotizing
fasciitis are often critically ill, and in-
tensive supportive care is necessary.
Adjuvant therapies may be benefi-
cial, but further study is needed to
prove their efficacy.
Acknowledgment
The authors would like to thank
Jeffrey S. Ross, MD, for his generous
help preparing the pathology slides.
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