INTRODUCTION

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Background

Necrotizing fasciitis (NF) is an insidiously advancing soft tissue infection characterized by widespread fascial necrosis. A number of bacteria in isolation or as a polymicrobial infection can cause NF. The organisms most closely linked to NF are group A beta-hemolytic streptococci, although the disease may also be caused by other bacteria or different streptococcal serotypes.

NF was first described in 1848. In 1920, Meleney identified 20 patients in China in whom hemolytic streptococcus was the sole organism. Wilson coined the term necrotizing fasciitis in 1952 and found no specific pathologic bacteria related to the disease.

A few distinct NF syndromes should be recognized. The 3 most important are type I, or polymicrobial; type II, or group A streptococcal; and type III gas gangrene, or clostridial myonecrosis. A variant of NF type I is saltwater NF, in which an apparently minor skin wound is contaminated with saltwater containing a Vibrio species.

NF may occur as a complication of a variety of surgical procedures, including cardiac catheterization.¹ Familiarity with NF may facilitate earlier diagnosis and initiation of appropriate therapy.

A related Medscape CME course that may be of interest is The New York Course 2007: Developments in Infectious Diseases—Community-Acquired Methicillin-Resistant Staphylococcus aureus Infections. A related eMedicine article is Necrotizing Fasciitis (emergency medicine focus). Finally, an article available through Medscape that may be helpful is Maggot Debridement Therapy in Necrotizing Fasciitis Reduces the Number of Surgical Debridements.

Pathophysiology

Organisms spread from the subcutaneous tissue along the superficial and deep fascial planes, presumably facilitated by bacterial enzymes and toxins. This deep infection causes vascular occlusion, ischemia, and tissue necrosis. Superficial nerves are damaged, producing the characteristic localized anesthesia. Septicemia ensues with systemic toxicity.

Important bacterial factors include surface protein expression and toxin production. M-1 and M-3 surface proteins, which increase the adherence of the streptococci to the tissues, also protect the bacteria against phagocytosis by neutrophils.

Streptococcal pyrogenic exotoxins (SPEs) A, B, and C are directly toxic and tend to be produced by strains causing NF. These pyrogenic exotoxins, together with streptococcal superantigen (SSA), lead to the release of cytokines and produce clinical signs such as hypotension. The etiological agent may also be a Staphylococcus aureus isolate harboring the enterotoxin gene cluster seg, sei, sem, sen, and seo but lacking all common toxin genes, including Panton-Valentine leukocidin.² The poor prognosis associated with NF has been linked to infection with certain streptococcal strains. Community-acquired methicillin-resistant S aureus has also been associated with NF.³

Mortality/Morbidity

The mortality rate can be as high as 25%. Cases of NF with sepsis and renal failure have a mortality rate as high as 70%.

Age

Approximately one half of the cases of streptococcal NF occur in young and previously healthy people.

CLINICAL

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History

NF tends to begin with constitutional symptoms of fever and chills. After 2-3 days, erythema is noted, and supralesional vesiculation or bullae formation ensues. Serosanguineous fluid may drain from the affected area. NF may develop after skin biopsy; at needle puncture sites in those use illicit drugs; and after episodes of frostbite, chronic venous leg ulcers, open bone fractures, insect bites, surgical wounds, and skin abscesses. However, in many cases, no association with such factors can be made. NF may also occur in the setting of diabetes mellitus, surgery, trauma, or infectious processes.

In a pediatric NF series, clinical features began 1 week after the initiating event, beginning with edema and induration, which was followed in 24-48 hours by erythema or a violaceous discoloration.⁴ Pain and, occasionally, crepitation, was also noted early. The latter indicates the presence of gas produced by aerobic and anaerobic bacteria and is highly suggestive of the diagnosis of NF. In a series of 39 pediatric cases, the most common initiating factor in 13 of them was varicella.⁵

• Type I, or polymicrobial NF, usually occurs after trauma or surgery.
• • This form may initially be mistaken for a simple wound cellulitis. However, severe pain and systemic toxicity reflect widespread tissue necrosis underlying apparently viable skin.
  • This disease process may also be observed in association with urogenital or anogenital infections (see Physical, below).
• Type II, or group A streptococcal NF, is the so-called flesh-eating bacterial infection.
• Type III NF, or clostridial myonecrosis, is gas gangrene. This skeletal muscle infection may be associated with recent surgery or trauma.

Physical

• General findings may include the following:
  

  • From a rapidly advancing erythema, painless ulcers may appear as the infection spreads along the fascial planes. A black necrotic eschar may be evident at the borders of the affected areas.
  • Metastatic cutaneous plaques may occur.
  • Septicemia is typical and leads to severe systemic toxicity and rapid death unless appropriately treated.
  • In individuals with diabetes, crepitus is often evident, as are nonclostridial anaerobic infections.
• In type II NF, the widespread tissue necrosis underlying the apparently viable skin can be demonstrated by passing a probe through the tissue.
• • The condition may appear similar to a simple wound cellulitis; however, the severe pain and systemic toxicity reflect the widespread tissue necrosis underlying the apparently viable skin. Surgically confirmed NF cases were compared with 12 patients with superficial soft tissue infection.⁶ NF patients were more likely to have skin areas of ischemia or necrosis, fluid-filled vesicles, and severe sepsis or septic shock.
  • Gas may be evident.
  • This process may also be observed in the perineum in association with urogenital or anogenital infections (eg, Fournier gangrene).
• In type II NF, gas usually is not evident in affected tissues.
• Although the following features can occur with cellulitis, they may suggest NF instead:
  • Rapid progression
  • Poor therapeutic response
  • Blistering necrosis
  • Cyanosis
  • Extreme local tenderness
  • High temperature
  • Tachycardia
  • Hypotension
  • Altered level of consciousness

Causes

• Group A beta-hemolytic streptococci is not the only cause of NF. Haemophilus aphrophilus and S aureus are also associated with the condition, and some patients have mixed infections involving multiple species of bacteria, including mycobacteria, or fungi.
• • A synergistic infection with a facultative anaerobic bacterium may be significant.
  • In 1 patient, Phycomycetes appeared to be responsible for NF.
  • Diabetes mellitus and immunosuppression predispose patients to NF.
  • However, approximately one half of the cases of streptococcal NF occur in young and previously healthy people.
• In type I NF, anaerobic and facultative bacteria work synergistically to cause what may initially be mistaken for a simple wound cellulitis. A variant of type I NF is saltwater NF in which an apparently minor skin wound is contaminated with saltwater containing a Vibrio species.
• In type II NF, varicella infection and the use of nonsteroidal anti-inflammatory drugs may be predisposing factors.
• Type III NF is usually caused by Clostridium perfringens. When type III NF occurs spontaneously, Clostridium septicum is more likely to be the etiologic agent; these cases usually occur in association with colon cancer or leukemia.
• Rapidly progressive NF following a stonefish sting has been described in 2 patients.⁷

DIFFERENTIALS

Section 4 of 11  

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WORKUP

Section 5 of 11  

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Lab Studies

• Examination by an experienced surgeon is critical. NF may be associated with a WBC count more than 14,000/µL, a serum sodium less than 135 mmol/L, and a blood urea nitrogen level greater than 15 mg/dL; however, these parameters cannot be relied upon in a clinical setting.
• Laboratory tests, along with appropriate imaging studies, may facilitate the diagnosis of NF.
• Although the laboratory parameters may vary in a given clinical setting, the following may be associated with NF:
• • The WBC count may be elevated. It may be more than 14,000/µL.
  • The blood urea nitrogen level may be elevated. It may be greater than 15 mg/mL.
  • The serum sodium level may be reduced. The level may be less than 135 mmol/L.
• New techniques include rapid streptococcal diagnostic kits and a polymerase chain reaction (PCR) involving SPE genes (eg, SPE-B).

Imaging Studies

• Standard radiographs are of little value unless free air is depicted, as with gas-forming infections.
• Some authors believe CT may be more sensitive than plain radiography in demonstrating subcutaneous air.
• B-mode and possibly color Doppler ultrasonography, contrast-enhanced CT, and the appropriate laboratory tests, may facilitate the rapid diagnosis of NF.
• T2-weighted MRIs may show well-defined regions of high signal intensity in the deep tissues.
• More importantly, MRI or CT delineation of the extent of NF may be useful in directing rapid surgical debridement.
• MRI can be used to identify NF, but its sensitivity exceeds its specificity.⁸

Other Tests

• Excisional deep skin biopsy may be helpful in diagnosing and identifying the causative organisms.
• Cultures of the affected tissue obtained at initial debridement may be helpful.
• Gram staining of the exudate may provide a clue as to whether a type I or type II infection is present; the type influences the antibiotic therapy.

Histologic Findings

Sections show superficial fascial necrosis with blood vessels occluded by thrombi. A dense infiltration of neutrophils may be observed in deeper parts of the subcutaneous tissue and fascia. Subcutaneous fat necrosis and vasculitis are also evident. Eccrine glands and ducts may be necrotic. Alcian blue or periodic acid-Schiff staining with diastase may show clusters of bacteria and fungi. Excisional deep skin biopsy may be helpful in diagnosing and identifying the causative organisms.

TREATMENT

Section 6 of 11  

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Medical Care

Once the diagnosis of NF is confirmed, initiate treatment without delay. Because of the complexity of this disease, a team approach is best (see Consultations). Ideally, the patient should be moved to the surgical intensive care unit, and his or her hemodynamic parameters should be closely monitored.

The medical care of a patient with NF may involve the administration of antibiotics, hyperbaric oxygen (HBO), and/or intravenous immunoglobulin.

• Antibiotics: Gram staining of the exudate may provide a clue as to whether type I or type II infection is present; the type influences antibiotic therapy. Empirically, broad-spectrum antibiotics should be administered immediately. A foul smell in the lesion strongly suggests the presence of anaerobic organisms.
• • Combination therapy: This approach involves the use of 2 or 3 antibiotics. To cover aerobes (usually gram-negative organisms), ampicillin and gentamicin are useful. For anaerobes, clindamycin or metronidazole has been used. In group A streptococcal infections, clindamycin has been used, specifically in combination with beta-lactam antibiotics.
  • Single antibiotic coverage: Broad-spectrum beta-lactam drugs such as imipenem cover aerobes, including Pseudomonas species. Ampicillin sulbactam also has broad-spectrum coverage, but it does not cover Pseudomonas species. The maximum doses of the antibiotics should be used, with consideration of the patient's weight and liver and renal status. Once culture and sensitivity results are available, the antibiotic coverage should be reevaluated.
  • Vancomycin: The use of vancomycin to treat methicillin-resistant S aureus is often discussed and may depend on the clinical situation. For example, use may depend on whether a nasocranial infection is present, or it may need to be avoided in patients, who are likely to be carriers of methicillin-resistant S aureus (eg, those with diabetes, those who use illicit drugs, those undergoing hemodialysis).
• HBO therapy^{9, 10}: Once other modalities, including surgical debridement and antibiotic administration, have been used, HBO therapy may be considered. Some believe that treatment reduces the mortality rate related to necrotizing soft tissue infections. A small retrospective analysis of HBO therapy associated its use with a marked reduction in mortality as part of an aggressive treatment regimen for NF.¹¹
• Intravenous immunoglobulin: In severe streptococcal infections associated with NF, the use of intravenous immunoglobulin (IVIG) may be a useful adjunct treatment. To the author's knowledge, no randomized trials have been reported in the literature, but results from anecdotal cases strongly support its use.

Surgical Care

In all patients, examination by an experienced surgeon is critical.

• Once the diagnosis is made, immediate surgical debridement is necessary. This regimen outlined below is continued until further tissue necrosis stops and the growth of fresh viable tissue is observed. If a limb or organ is involved, amputation may be necessary because of irreversible necrosis and gangrene or because of overwhelming toxicity, which occasionally occurs. Prompt surgery ensures a higher likelihood of survival.
• The surgical incisions should be deep and extend beyond the areas of necrosis until viable tissue is reached.
• The entire necrotic area should be excised.
• The wound should be well irrigated.
• Hemostasis should be maintained, and the wound should be kept open.
• Surgical debridement and evaluations should be repeated almost on a daily basis.
• The wound should be inspected in the operating room.

Consultations

• A team approach is the best method of treating this complicated disorder. Team members should include the following: a surgeon, an infectious disease specialist, a pathologist, and a microbiologist.
• Depending on the area involved, the team may also include a urologist; a specialist in plastic surgery; or an ear, nose, and throat surgeon in cases of infections of the cervical area.
• The specialists and subspecialists involved should discuss the patient's condition and determine a comprehensive plan of treatment.

MEDICATION

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The goals of pharmacotherapy are to eradicate the infection, prevent complications, and reduce morbidity.

Drug Category: Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of this clinical setting.

Drug Name	Gentamicin (Garamycin, Jenamicin)
Description	Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Not the DOC. Consider if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms. Dosing regimens are numerous; adjust dose with CrCl and changes in volume of distribution. Monitor drug levels and renal function at regular intervals, and adjust dose or discontinue accordingly.
Adult Dose	3 mg/kg/d IV/IM divided tid q8h
Pediatric Dose	<28 wk gestational age: 2.5 mg/kg IV q24-36 h 28-32 wk gestational age: 2.5 mg/kg IV q18 h 33-42 wk gestational age: 2.5 mg/kg IV q12 h Term neonates >1 wk and infants and children <5 y: 2.5 mg/kg IV q8h >5 years: 2-2.5 mg/kg IV q8h
Contraindications	Documented hypersensitivity to this class of antibiotics and to sulfites; do not use in non–dialysis-dependent renal insufficiency
Interactions	Neurotoxic, ototoxic, and nephrotoxic medications; general anesthetics and neuromuscular blocking agents; coadministration with other aminoglycosides, cephalosporins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents (prolonged respiratory depression may occur); coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; irreversible hearing loss of varying degrees possible (monitor regularly); concomitant penicillin and aminoglycoside therapy reported to result in inactivation of aminoglycoside both in vivo and in vitro (amikacin appears to possess the greatest stability in presence of penicillins; half-life of amikacin is minimally affected by presence of carbenicillin; appears that in treatment of severely ill patients requiring both penicillin and aminoglycoside therapy, amikacin is aminoglycoside of choice); concomitant magnesium and aminoglycosides can produce neuromuscular weakness and possibly paralysis; high incidence of renal failure (serum creatinine increase >50%) observed in patients treated with polygeline 3.5% and gentamicin for elective coronary artery bypass graft If antibiotic therapy necessary during BCG treatment, consider antibiotic with low activity against bacillus Calmette Guérin (eg, amoxicillin, TMP-SMZ, cephalosporin)
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Narrow therapeutic index (not intended for long-term therapy); preexisting inner ear or renal impairment, especially if patient recently received ototoxic or nephrotoxic medications; caution in local irrigation; caution in renal failure (patient not on dialysis); caution in myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment; may cause fetal deafness; age (very young/very old), and dehydration; risk factor for toxicity

Drug Name	Clindamycin (Cleocin)
Description	Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes and arresting RNA-dependent protein synthesis.
Adult Dose	600-1200 mg/d IV/IM divided bid/tid/qid; not to exceed 600 mg per single IM injection or 1200 mg/h IV More severe infection: 1200-2700 mg/d IV/IM divided bid/tid/qid Serious infection: 2700-4800 mg/d IV/IM divided bid/tid/qid
Pediatric Dose	<1 month: 15-20 mg/kg/d IV/IM divided tid/qid >1 month: 20-40 mg/kg/d IV/IM divided tid/qid
Contraindications	Documented hypersensitivity
Interactions	Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Caution in premature infants (may contain benzyl alcohol as a preservative); regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis; adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile; dysgeusia; monitor periodic blood counts and renal and hepatic function if use prolonged; rare cardiopulmonary adverse reactions possible with rapid IV administration

Drug Name	Metronidazole (Flagyl)
Description	Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for C difficile enterocolitis).
Adult Dose	Loading dose: 15 mg/kg IV infused over 1 h (approximately 1 g for 70-kg adult) Maintenance dose: 7.5 mg/kg infused over 1 h q6h (approximately 500 mg for 70-kg adult) for 7-10 d or longer if necessary; not to exceed 4 g/d
Pediatric Dose	Initial loading dose: 15 mg/kg IV infused over 60 min Term infants: 7.5 mg/kg IV q24h, starting 48 h after initial dose Term infants (1-4 wk), maintenance: 7.5 mg/kg IV q12h starting 24 h after initial dose Infants and children, maintenance: 30 mg/kg/d IV divided q6h, not to exceed 4 g/d
Contraindications	Documented hypersensitivity to drug or components; first trimester of pregnancy
Interactions	May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity; phenytoin or phenobarbital may reduce levels; disulfiram reaction may occur with ethanol ingestion; metronidazole may increase toxicity of amprenavir oral solution (avoid concurrent administration); cholestyramine decreases effects; increases adverse effects of fluorouracil
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy; caution in history of CNS disease or fluid retention; fluid retention with corticosteroids; GI discomfort; dysgeusia; GU discomfort; leukopenia or thrombocytopenia

Drug Name	Imipenem and cilastatin (Primaxin)
Description	For treatment of infections due to multiple organisms in which other agents do not have wide-spectrum coverage or are contraindicated because of potential for toxicity.
Adult Dose	500-1000 mg IV/IM q6-8h depending on the severity of disease and the infecting organisms
Pediatric Dose	<1 week: 25 mg/kg IV q12h 1-4 weeks: 25 mg/kg IV q8h 1-3 months: 25 mg/kg IV q6h >3 months: 15-25 mg/kg IV q6h Not to exceed 4 g/d
Contraindications	Documented hypersensitivity
Interactions	Coadministration with cyclosporine may increase CNS adverse effects of both agents; coadministration with ganciclovir may result in generalized seizures; avoid use with probenecid
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Adjust dose in renal insufficiency; avoid use in children <12 y; CNS adverse effects (eg, seizures) possible; pseudomembranous colitis; monitor renal, hepatic, and hematopoietic systems with prolonged use; not recommended if patient <30 kg with renal impairment (data lacking); not recommended in children with CNS infections (increased seizure risk); not recommended if CrCl <5 mL/min/1.73 m2 unless hemodialysis performed within 48 h

Drug Name	Ampicillin and sulbactam (Unasyn)
Description	Combination of beta-lactamase inhibitor with ampicillin. Covers skin, enteric flora, and anaerobes. Not ideal for treatment of nosocomial pathogens.
Adult Dose	1.5-3 g IV/IM q6h; not to exceed 4 g/d sulbactam
Pediatric Dose	<12 years: 100-200 mg/kg/d (ampicillin component) IV/IM divided q6h; not to exceed 4 g sulbactam/d >12 years: Administer as in adults
Contraindications	Documented hypersensitivity to this and other beta-lactam antibiotics
Interactions	Probenecid and disulfiram increase ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Adjust dose in renal failure; evaluate rash; adjust for renal insufficiency; differentiate from hypersensitivity reaction; may cause diarrhea, pseudomembranous colitis, and false-positive results with urine glucose test or other laboratory tests (eg, liver, hematologic, albumin, total protein, renal); administer on empty stomach when given orally at least 0.5 h ac or 2 h pc

Drug Name	Vancomycin (Lyphocin, Vancoled, Vancocin)
Description	Antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin-structure infections. Indicated for patients who cannot take or whose conditions fail to respond to penicillins and cephalosporins or those with infections with resistant staphylococci. To prevent toxicity, current recommendation is to assay vancomycin trough levels after third dose, with samples obtained 0.5 h prior to next dose. Use CrCl to adjust dose in renal impairment.
Adult Dose	2 g IV divided 500 mg q6h or 1 g q12h; administered at a rate of <10 mg/min or over 60 min
Pediatric Dose	<1 year: 15 mg/kg initial dose IV, followed by 10 mg/kg IV q12h ( <1 wk old) or q8h (1-4 wk old); administer over at least 60 min >1 year: 10 mg/kg per dose IV q6h; administer over at least 60 min
Contraindications	Documented hypersensitivity; corn allergy
Interactions	Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; concurrent administration of other potentially ototoxic, nephrotoxic, or neurotoxic agents (eg, aminoglycosides, paralytic agents) may increase risk of the same adverse event; coadministration with trospium may result in increased serum concentrations of either drug
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Caution in renal failure, neutropenia; adjust dose in renal insufficiency; caution in history of hearing loss or recent ototoxic agent; may cause ototoxicity, neutropenia, local necrosis, or phlebitis about infusion or injection site, chemical peritonitis possible if administered via peritoneal dialysis; red man syndrome caused by too-rapid IV infusion (dose administered over only few min) but rare with 2-h or PO or IP administration (red man syndrome is not an allergic reaction); pseudomembranous colitis; avoid IM administration

FOLLOW-UP

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Complications

• Sepsis and renal failure are possible complications.
• Metastatic cutaneous plaques may occur.
• Septicemia is typical and leads to severe systemic toxicity and rapid death unless appropriately treated.

Prognosis

• The poor prognosis in NF has been linked to infection with certain streptococcal strains.
• The mortality rate can be as high as 25%.
• Aeromonas infection, Vibrio infection, cancer, hypotension, and band form WBC count greater than 10% were found to be independent positive predictors of mortality in patients with NF, while streptococcal and staphylococcal infections were not identified as predictors of mortality. Hemorrhagic bullae appeared to be an independent negative predictor of mortality. However, accuracy of these factors needs to verified.¹²

MISCELLANEOUS

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Medical/Legal Pitfalls

• Missing this diagnosis may prove fatal for the patient and lead to obvious medicolegal repercussions for his or her health care providers.

MULTIMEDIA

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Media file 1:  Left upper extremity shows necrotizing fascitis in an individual who used illicit drugs. Cultures grew Streptococcus milleri and anaerobes (Prevotella species). Patient would grease, or lick, the needle before injection.
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Media type:  Photo

Media file 2:  Left lower extremity in a 56-year-old patient with alcoholism who was found comatose after binge drinking. Surgical drainage was performed to treat the pyomyositis-related, large, non–foul-smelling (sweetish) bullae. Gram staining showed the presence of gram-positive rods. Cultures revealed Clostridium perfringens. The diagnosis was clostridial myonecrosis.
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Media type:  Photo

Media file 3:  Sixty-year-old woman who had undergone postvaginal hysterectomy and repair of a rectal prolapse has a massive perineal ulceration with foul-smelling discharge. Cultures revealed Escherichia coli and Bacteroides fragilis. The diagnosis was peroneal gangrene.
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Media type:  Photo

Media file 4:  Necrotizing fascitis at a possible site of insulin injection in the left upper part of the thigh in a 50-year-old obese woman with diabetes.
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Media type:  Photo

Media file 5:  Necrotizing fascitis of entire thoracolumbar posterior area in 20-year-old patient with chronic myelogenous leukemia and neutropenia (WBC count, 680/mL). Cultures revealed gram-negative Pseudomonas species and Bacteroides fragilis.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

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1. Federman DG, Kravetz JD, Kirsner RS. Necrotizing fasciitis and cardiac catheterization. Cutis. Jan 2004;73(1):49-52. [Medline].
2. Morgan WR, Caldwell MD, Brady JM. Necrotizing fasciitis due to a methicillin-sensitive Staphylococcus aureus isolate harboring an enterotoxin gene cluster. J Clin Microbiol. Feb 2007;45(2):668-71. [Medline].
3. Cheng NC, Chang SC, Kuo YS, Wang JL, Tang YB. Necrotizing fasciitis caused by methicillin-resistant Staphylococcus aureus resulting in death. A report of three cases. J Bone Joint Surg Am. May 2006;88(5):1107-10. [Medline].
4. Fustes-Morales A, Gutierrez-Castrellon P, Duran-Mckinster C, Orozco-Covarrubias L, Tamayo-Sanchez L, Ruiz-Maldonado R. Necrotizing fasciitis: report of 39 pediatric cases. Arch Dermatol. Jul 2002;138(7):893-9. [Medline].
5. Ford LM, Waksman J. Necrotizing fasciitis during primary varicella. Pediatrics. Jun 2000;105(6):1372-3; discussion 1373-5. [Medline].
6. Zahar JR, Goveia J, Lesprit P, Brun-Buisson C. Severe soft tissue infections of the extremities in patients admitted to an intensive care unit. Clin Microbiol Infect. Jan 2005;11(1):79-82. [Medline].
7. Tang WM, Fung KK, Cheng VC, Lucke L. Rapidly progressive necrotising fasciitis following a stonefish sting: a report of two cases. J Orthop Surg (Hong Kong). Apr 2006;14(1):67-70. [Medline].
8. Arslan A, Pierre-Jerome C, Borthne A. Necrotizing fasciitis: unreliable MRI findings in the preoperative diagnosis. Eur J Radiol. Dec 2000;36(3):139-43. [Medline].
9. Korhonen K. Hyperbaric oxygen therapy in acute necrotizing infections with a special reference to the effects on tissue gas tensions. Ann Chir Gynaecol Suppl. 2000;(214):7-36. [Medline].
10. Korhonen K, Kuttila K, Niinikoski J. Tissue gas tensions in patients with necrotising fasciitis and healthy controls during treatment with hyperbaric oxygen: a clinical study. Eur J Surg. Jul 2000;166(7):530-4. [Medline].
11. Krenk L, Nielsen HU, Christensen ME. Necrotizing fasciitis in the head and neck region: an analysis of standard treatment effectiveness. Eur Arch Otorhinolaryngol. Mar 6 2007;[Medline].
12. Hsiao CT, Weng HH, Yuan YD, Chen CT, Chen IC. Predictors of mortality in patients with necrotizing fasciitis. Am J Emerg Med. Feb 2008;26(2):170-5. [Medline].
13. Afifi RY, El-Hindawi AA. Acute necrotizing fasciitis in Egyptian patients. Int J Surg. Jan 28 2008;[Medline].
14. Akcay EK, Cagil N, Yulek F, Anayol MA, Cetin H, Cag Y, et al. Necrotizing fasciitis of eyelid secondary to parotitis. Eur J Ophthalmol. Jan-Feb 2008;18(1):128-30. [Medline].
15. Anwar UM, Ahmad M, Sharpe DT. Necrotizing Fasciitis After Liposculpture. Aesthetic Plast Surg. 12 2 2004;[Medline].
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Article Last Updated: Mar 14, 2008