Necrotizing Soft Tissue Infections:
A Primary Care Review
ADRIENNE J. HEADLEY, M.D., University of Medicine and Dentistry of New Jersey–Robert WoodJohnson Medical School, New Brunswick, New Jersey
Patients with necrotizing soft tissue infections often present initially to family physicians. These infections must be detected and treated rapidly to prevent loss of limb ora fatal outcome. Unfortunately, necrotizing soft tissue infections have no pathognomonic signs. Patients may present with some evidence of cellulitis, vesicles, bullae,
edema, crepitus, erythema, and fever. They also may complain of pain that seems outof proportion to the physical findings; as the infection progresses, their pain may
decrease. Magnetic resonance imaging and laboratory findings such as acidosis, anemia, electrolyte abnormalities, coagulopathy, and an elevated white blood cell count
may provide clues to the diagnosis. No single organism or combination of organisms
is consistently responsible for necrotizing soft tissue infections. Most infections arepolymicrobial, with both anaerobic and aerobic bacteria frequently present. Fungal
infections also have been reported. Generally, bacterial and toxin-related effects converge to cause skin necrosis, shock, and multisystem organ failure. Aggressive debridement of infected tissues is critical to management. Antimicrobial therapy is importantbut remains secondary to the removal of diseased and necrotic tissues. (Am Fam Physician 2003;68:323-8. Copyright© 2003 American Academy of Family Physicians.)N

ecrotizing soft tissue infections are a broad category ofbacterial and fungal skininfections. Descriptive terms
vary based on the location,
depth, and extent of infection (e.g., Fournier’s
gangrene [necrotizing perineal infection],
necrotizing fasciitis [deep subcutaneous infection]). Depending on the depth of invasion,
necrotizing soft tissue infections can cause
extensive local tissue destruction, tissue necrosis, systemic toxicity, and even death. Despite
surgical advances and the introduction of
antibiotics, reported mortality rates for necrotizing soft tissue infections range from 6 percent to as high as 76 percent.1
Patients with necrotizing soft tissue infections frequently present initially to primarycare physicians. Because of the importance ofReported risk factors for necrotizing soft tissue infections
include age greater than 50 years, peripheral vasculardisease, diabetes mellitus, malnutrition, atherosclerosis, highcomorbid index scores, obesity, and intravenous drug abuse.

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early diagnosis and treatment, family physicians need to maintain a high index of suspicion for these infections and should be awareof possible presenting features.
Anatomic Factors and Time Course
Anatomic factors are important in explaining the facility with which necrotizing soft tissue infections cause damage.2-5 Most bacteria
and fungi can multiply within viable tissue,
but fibrous attachments or “boundaries”
between subcutaneous tissues and fascia(e.g., scalp, hands) can help limit the spreadof infection. The natural lack of fibrous
attachments in the larger areas of the body(e.g., trunk, extremities) facilitates widespread infection.2-4
The time course for necrotizing soft tissue
infections varies. Infection can progress overdays to weeks; more often, however, limbthreatening or life-threatening sequelae manifest within only a few hours after the infection
begins.2 Furthermore, seemingly limited
infections may result in massive systemic
effects. Many bacteria, such as group A streptococci, secrete virulence-enhancing toxins orproteins that can trigger multisystem organ
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Although necrotizing soft tissue infections canbe monomicrobial, they usually are synergistic
polymicrobial infections.

failure and septic shock.6 Therefore, the physician can beconfronted unexpectedly with a rapidly deteriorating
patient who has no overt or only minimal signs of extensive skin infection.
Risk Factors
Reported risk factors for necrotizing soft tissue infections
include age greater than 50 years, peripheral vascular disease, diabetes mellitus, malnutrition, atherosclerosis, highcomorbid index scores (i.e., Acute Physiology and Chronic
Health Evaluation [APACHE] or Surgical Infection Stratification System), obesity, hypoalbuminemia, chronic alcoholism, and intravenous drug abuse (Table 1).1-3,7-10 Manyof these risk factors reflect an immunocompromised state.
Trauma, postoperative infections, occult diverticulitis,
strangulated femoral hernia with subcutaneous extravasation of infected contents, cancer, and even acupuncture
have been cited as precipitating events in necrotizing soft
tissue infections.3 In addition, diabetic ketoacidosis, neutropenia, high-dose corticosteroid therapy, and burns canincrease the risk of cutaneous mucormycosis-induced
necrotizing skin infections.3,7
Etiology
Although necrotizing soft tissue infections can bemonomicrobial, they usually are synergistic polymicrobial infections. Investigators in one study11 found that
only 28 of 182 patients developed necrotizing skin infections from single pathogens; the other 154 patients had
polymicrobial infections (average of 4.4 organisms in theoriginal wound cultures). In this series, the majority ofmonomicrobial infections were caused by streptococcal
isolates such as -hemolytic streptococci (namely group
A streptococci or Streptococcus pyogenes). Other frequently cited causes of monomicrobial necrotizing soft
tissue infections include Staphylococcus aureus andClostridium perfringens.11
The organisms isolated most often in polymicrobial
necrotizing soft tissue infections are combinations ofstaphylococci (especially Staphylococcus epidermidis with
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Risk Factors for Necrotizing Soft Tissue Infections
Age greater than 50 years
Atherosclerosis
Burns
Cancer or otherimmunocompromised state
Chronic alcoholism
Corticosteroid use
Diabetes mellitus
Hypoalbuminemia

Intravenous drug abuse
Malnutrition
ObesityOccult diverticulitis
Peripheral vascular disease
Postoperative infection
Strangulated femoral herniawith content extravasation
TraumaInformation from references 1 through 3 and 7 through 10.

-hemolytic streptococci), enterococci, Enterobacteriaceae
species (commonly Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae, and Pseudomonas aeruginosa), streptococci, Bacteroides/Prevotella species, anaerobic gram-positive cocci, and Clostridium species.11,12
In one study,1 69 percent of necrotizing soft tissue infections were found to be polymicrobial, and 29 percent werecaused by single pathogens. In 2 percent of infections, noorganisms grew from intraoperative culture. Investigatorsin another study13 found that more than 90 percent of
nonclostridial polymicrobial necrotizing soft tissue infections involved β-hemolytic streptococci or coagulase-positive staphylococci; the remaining 10 percent of infections
were attributed to gram-negative enteric bacteria.13,14
Another series15 reported that 59 percent of necrotizing
soft tissue infections were polymicrobial. A review16 of
necrotizing soft tissue infections in 163 patients revealed
that 71 percent of the infections were polymicrobial. In
some instances, fungi have been cultured from polymicrobial infections.11
Perhaps the only generalization that can be made about
polymicrobial necrotizing soft tissue infections is that aerobic and anaerobic organisms are frequently found incombination. Because of culture results, necrotizing soft
tissue infections have previously been categorized as type Ior type II infections. Type I infections are mixed infections
generated by anaerobic and facultative bacteria, whereas
type II infections generally are caused by group A streptococci. Staphylococci also may be found in conjunction
with group A streptococci.12

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Physical Examination
The physical examination should cover all body surfaces.
This thorough approach is especially important in patientswith deterioration of mental status as a result of conditions
such as diabetic ketoacidosis. Sepsis from an infection
must be considered in the perineum and other areas thatare concealed by clothing.
Most necrotizing soft tissue infections occur in theextremities, abdomen, groin, and perineum.2 In at least
one series,3 these infections were discovered in theextremities (53 percent of cases), perineum or buttocks(20 percent), trunk (18 percent), and head and neck
(8.9 percent).
Because necrotizing skin infections begin in deep tissue
planes, the epidermis may appear relatively unscatheduntil late in the course of infection. Therefore, it can be difficult to differentiate necrotizing soft tissue infection from
nonnecrotizing infection or simple cellulitis.17 However,some clinical clues are available (Table 2).1-3,17-20
One group of investigators1 noted that soft tissue edema,
erythema, severe pain, temperature greater than 38°C
(100.4°F), bullae, or necrosis may signify a necrotizing soft
tissue infection (Figure 1).17 Other investigators3 havefound some correlation between necrotizing soft tissue
infection and preexisting cellulitis (76 percent of cases) andTABLE 2Clinical Clues to the Diagnosis of Necrotizing
Soft Tissue Infections
Skin
Erythema
Tense edema
Grayish or otherdiscolored wounddrainage
Vesicles or bullae
Necrosis
UlcersCrepitus

Pain
Pain that extends past margin of apparent
infection
Severe pain that appears disproportionate
to physical findings
Decreased pain or anesthesia at apparent
site of infection
General features
Fever
Tactile temperature
Diaphoresis
Tachycardia
Toxic delirium

Information from references 1 through 3 and 17 through 20.

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FIGURE 1. Right leg edema and erythema extending over
the anterior tibia and medial malleolus in a 59-year-old
woman. Violaceous bullae without evidence of obvious
trauma were observed over the medial malleolus andmedial calf.17

vesicles, bullae, or necrosis (47 percent of cases). Painful
skin ulcers with gangrenous margins may be a feature of
mixed bacterial infections.2 The presence of crepitus isvariable. In one series,18 crepitus was present in only 18
percent of patients with necrotizing fasciitis and was a lateclinical sign. Thus, signs of soft tissue edema, erythema,
ulceration, bullae, or necrosis should prompt the inclusionof necrotizing soft tissue infection in differential diagnoses.
Complaints of pain beyond the visible limits of skin erythema or out of proportion to visible signs of skin infection also should arouse clinical suspicion for necrotizing
soft tissue infection. Patients with systemic infection may
be diaphoretic, febrile, and tachycardic, and they may
manifest toxic delirium. In addition, they may become
hypotensive and demonstrate signs of renal failure andhemolytic anemia.2
Because of the paucity of distinct findings, necrotizing
soft tissue infections still may be missed. Bullae and skinnecrosis, for example, may not be present in 66 to 70 percent of patients with occult infections.19
Diagnosis
The differential diagnosis of necrotizing soft tissue infections includes staphylococcal bacteremic skin lesions andlocal infections resulting from erysipelas, nonnecrotizing
cellulitis, impetigo, furuncles, carbuncles, folliculitis, candidal septicemia, and insect or other bites (e.g., brownrecluse spider).2
Physical findings are not sufficient to identify the organ-

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Signs of soft tissue edema, erythema, ulceration,bullae, or necrosis should prompt the inclusionof necrotizing soft tissue infection in differential
diagnoses.

isms that cause these infections. For example, althoughclostridial myonecrosis can present with a thin, brownish
discharge, a wound culture should be performed to confirm the identity of the pathogen.21
The gold standard for detecting necrotizing soft tissue
infections is tissue biopsy obtained at the time of wound
exploration and surgical debridement. During wound
exploration, tissue integrity and depth of invasion also canbe evaluated. The findings of fascial necrosis and myonecrosis are indicative of necrotizing infection. Loss of fascial integrity along tissue planes and frank evidence ofmuscle involvement are also diagnostic.12 Note that the useof frozen sections at the time of biopsy may not always
provide accurate information about the depth of tissue
involvement.
Demonstration of necrotic tissue on fine-needle aspiration of infected tissue also is important in establishing thediagnosis of necrotizing soft tissue infection. In addition,other modalities have been investigated as diagnostic tests.
However, with the exception of wound exploration andculture, negative results on these tests cannot exclude
necrotizing skin infections.
One investigative team3 noted a correlation between
necrotizing soft tissue infections and subcutaneous air on

The Author
ADRIENNE J. HEADLEY, M.D., is assistant professor in the Department
of Family Medicine at the University of Medicine and Dentistry of New
Jersey (UMDNJ)–Robert Wood Johnson Medical School, New
Brunswick. Dr. Headley received her medical degree from the State University of New York Health Science Center, Brooklyn, and had several
years of residency training in general surgery at Beth Israel Medical
Center, New York, N.Y. She completed a family practice residency anda family practice fellowship in obstetrics and gynecology at UMDNJ–
Robert Wood Johnson Medical School.
Address correspondence to Adrienne J. Headley, M.D., Department of
Family Medicine, University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School, Medical Education Building,Second Floor, 1 Robert Wood Johnson Place, New Brunswick, NJ
08901. Reprints are not available from the author.

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radiographs (25 percent of cases) and white blood cellcounts higher than 20,000 per mm3 (20  109 per L;
49 percent of cases). However, an absence of soft tissue gas
on radiographs does not exclude these infections.17 Furthermore, neither the presence nor absence of gas onradiographs of infected sites correlates with the presence ofspecific pathogens.4
Magnetic resonance imaging (MRI) can be a helpful
diagnostic adjunct because of its soft-tissue and multiplanar-imaging capabilities.22 In these respects, MRI is
superior to ultrasonography or plain-film radiography indetecting tissue inflammation and necrosis. The use ofgadolinium MRI (T2-weighted images) has been reported
to yield hyperintense intramuscular and deep fascial signals and rim enhancement compatible with necrotizing
soft tissue infections; however, such findings are nonspecific for these infections.22 More investigation is needed
to clarify the type of MRI findings and weighted images
that can reliably distinguish necrotizing from nonnecrotizing skin infections.
Elevated polymorphonuclear leukocyte counts may
reflect systemic infection. One team of investigators1
reported that white blood cell counts higher than 16,300
per mm3 (16.3  109 per L), anemia (hemoglobin level
lower than 10 mg per dL [100 g per L]), hypocalcemia (corrected to a serum calcium concentration of less than 8.4 mg
per dL [2.10 mmol per L]), acidosis (pH less than 7.35),
crepitus, or the presence of soft tissue gas may alert physicians to the presence of necrotizing soft tissue infections.
Another investigative team23 found that 76 percent ofpatients with necrotizing soft tissue infections had platelet
counts below 150  103 per mm3 (150  109 per L) or prothrombin and partial thromboplastin times more than
1.5 times higher than normal control values. Prolonged
prothrombin times were associated with a higher mortality rate.
If findings such as tense skin edema, crepitus, bullae, andradiologic and laboratory abnormalities are present, they
provide additional impetus to obtain urgent surgical consultation for wound exploration.24
Treatment
SURGICAL DEBRIDEMENT

Controlled surgical debridement of necrotic and diseased tissues remains the cornerstone of treatment and canincrease survival in patients with necrotizing soft tissue
infections. In one series,18 patients who underwent surgicalwww.aafp.org/afp

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Necrotizing Soft Tissue Infections
TABLE 3

Antibiotics Commonly Used to Treat Necrotizing
Soft Tissue Infections
Penicillin or ampicillin plus an aminoglycoside (e.g., gentamicin[Garamycin]) and anaerobic coverage (e.g., clindamycin [Cleocin]
or metronidazole [Flagyl])
Ampicillin-sulbactam (Unasyn)
Ticarcillin-clavulanate potassium (Timentin)
Piperacillin-tazobactam (Zosyn)
Imipenem-cilastatin (Primaxin)
Antipseudomonal cephalosporin (e.g., ceftazidime [Fortaz])and clindamycin or metronidazole
Nafcillin (Unipen) plus anaerobic and gram-negative coverage
Vancomycin (Vancocin) plus anaerobic and gram-negative
coverage (e.g., an aminoglycoside or aztreonam [Azactam],or a third-generation cephalosporin): used mainly in patientswith penicillin allergy
Adapted with permission from Elliott D, Kufera JA, Myers RA. The
microbiology of necrotizing soft tissue infections. Am J Surg
2000;179:365, with additional information from reference 2.

debridement more than 12 hours after hospital admission
had higher amputation and mortality rates. Another investigation25 also found higher mortality rates when diagnosis and surgical debridement were delayed. Factors noted
to be critical to patient survival include prompt recognition of infection, nutritional support, surgical debridement, wound reexploration, and soft tissue coverage.18
With the resolution of the necrotizing infection and theestablishment of granulation tissue, surgical attention canbe directed toward coverage of tissue defects caused by theinfectious process.3
ANTIBIOTIC OR ANTIFUNGAL THERAPY

Empiric antibiotic therapy can be employed until woundculture isolates are identified. Depending on the culture
results, antibiotic selection can be modified. Because of
likely colonization, superficial wound cultures are not helpful in determining appropriate antibiotic therapy.
Because most necrotizing soft tissue infections arepolymicrobial, broad-spectrum coverage is advisable.12
Options include combinations such as ampicillin, gentamicin (Garamycin), and clindamycin (Cleocin) or
metronidazole (Flagyl).2,3 Ampicillin-sulbactam (Unasyn), ticarcillin-clavulanate potassium (Timentin), andpiperacillin-tazobactam (Zosyn) also provide adequate
anaerobic and aerobic coverage. The advantages ofpiperacillin-tazobactam or ticarcillin-clavulanate potassium therapy include gram-negative and pseudomonalcoverage.2 Patients with necrotizing soft tissue infections
also have been treated with nafcillin (Unipen) plus agentswith anaerobic and gram-negative coverage.11
Imipenem-cilastatin (Primaxin) provides extensive
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The gold standard for detecting necrotizing soft
tissue infections is tissue biopsy obtained at the timeof wound exploration and surgical debridement.

broad-spectrum coverage. This combination agent is
active against nosocomial gram-negative bacilli such asEnterobacter species, Citrobacter species, Acinetobacter
species, Proteus vulgaris, P. aeruginosa, and Serratia
marcescens.2 Because of this coverage, imipenem-cilastatinand -lactam and -lactamase inhibitors have been usedsuccessfully as single agents in the treatment of necrotizing
soft tissue infections.2
Broad-spectrum coverage is likely to combat thepathogens that can cause necrotizing soft tissue infections.
For example, enterococci are associated with these infections. In one study,11 however, 16 of 198 patients with necrotizing soft tissue infections received suboptimal broad-spectrum antibiotic coverage; 13 of these patients did not receive
an antibiotic that was active against enterococci.
Treatment with intravenously administered amphotericin B (Abelcet) can be used with surgical debridement
to control fungal skin infections.2
Agents commonly used to treat necrotizing soft tissue
infections are listed in Table 3.2,11 Treatments for gas gangrene are summarized in Table 4.26

TABLE 4

Antibiotics Commonly Used to Treat Gas Gangrene
Penicillin G: 24 million units per day in divided doses every
4 to 6 hours IV
andClindamycin (Cleocin): 900 mg every 8 hours IV
orCeftriaxone (Rocephin): 2 g every 12 hours IVorErythromycin: I g every 6 hours IV (not by bolus)
IV = intravenously.
Adapted with permission from Gilbert DN, Moellering RC Jr, Sande
MA. The Sanford guide to antimicrobial therapy. 32d ed. HydePark, Vt.: Antimicrobial Therapy, 2002:31.

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Necrotizing Soft Tissue Infections

WOUND REEXPLORATION

If infection progresses despite surgical debridement andthe use of broad-spectrum antibiotic or antifungal therapy,
surgical reexploration is necessary. The possibility of adjacent or deeper sites of occult necrosis and infection must
be excluded.
OTHER TREATMENTS

Hyperbaric oxygen therapy has been a controversial
adjunct in the management of necrotizing soft tissue infections. It is not recommended as a replacement for surgicaldebridement or intravenous antibiotic therapy.27
Information should be obtained about the tetanus
booster status of patients with necrotizing soft tissue infections. If immunization is inadequate, appropriate tetanus
prophylaxis should be administered.
The author indicates that she does not have any conflicts of interest. Sources of funding: none reported.
Figure 1 from Meltzer DL, Kabongo M. Necrotizing fasciitis: a diagnostic challenge. Am Fam Physician 1997;56:145-9.
The author thanks Alfred Tallia, M.D., M.P.H., and Niranjan V. Rao,
M.D., University of Medicine and Dentistry of New Jersey–Robert
Wood Johnson Medical School, New Brunswick, N.J., for reviewing the manuscript.
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