- Author: Richard F Edlich, MD, PhD, FACS, FACEP; Chief Editor: Michael Stuart Bronze, MD more...
Necrotizing fasciitis is a rapidly progressive inflammatory infection of the fascia, with secondary necrosis of the subcutaneous tissues. The speed of spread is directly proportional to the thickness of the subcutaneous layer. Necrotizing fasciitis moves along the fascial plane.[1, 2]
Necrotizing fasciitis has also been referred to as hemolytic streptococcal gangrene, Meleney ulcer, acute dermal gangrene, hospital gangrene, suppurative fasciitis, and synergistic necrotizing cellulitis. Fournier gangrene is a form of necrotizing fasciitis that is localized to the scrotum and perineal area.
Necrotizing fasciitis may occur as a complication of a variety of surgical procedures or medical conditions, including cardiac catheterization, vein sclerotherapy, and diagnostic laparoscopy, among others[6, 7, 8, 9, 10, 11] . It may also be idiopathic, as in scrotal or penile necrotizing fasciitis.
The causative bacteria may be aerobic, anaerobic, or mixed flora. A few distinct necrotizing fasciitis syndromes should be recognized. The 3 most important are as follows:
Type I, or polymicrobial
Type II, or group A streptococcal
Type III gas gangrene, or clostridial myonecrosis
A variant of necrotizing fasciitis type I is saltwater necrotizing fasciitis, in which an apparently minor skin wound is contaminated with saltwater containing a Vibrio species.
Because of the presence of gas-forming organisms, subcutaneous air is classically described in necrotizing fasciitis. This may be seen only on radiographs or not at all.
The frequency of necrotizing fasciitis has been on the rise because of an increase in immunocompromised patients with diabetes mellitus, cancer, alcoholism, vascular insufficiencies, organ transplants, HIV infection, or neutropenia.
Since 1883, more than 500 cases of necrotizing fasciitis have been reported in the literature. There may be an increased incidence in African and Asian countries; however, because of the lack of recorded cases, the true incidence is not known.
The mean age of a patient with necrotizing fasciitis is 38-44 years. This disease rarely occurs in children. Pediatric cases have been reported from resource-poor nations where poor hygiene is prevalent. The male-to-female ratio is 2-3:1.
These infections can be difficult to recognize in their early stages, but they rapidly progress. (see Clinical and Workup). They require aggressive treatment to combat the associated high morbidity and mortality (see Treatment).
Images of necrotizing fasciitis are shown below.
Necrotizing fasciitis was first described by a Confederate Army surgeon, Joseph Jones, during the US Civil War. In 1883, Fournier documented necrotizing fasciitis in the perineal and genital region. Meleney later reported 20 patients he encountered in China in whom necrotizing fasciitis was caused by hemolytic streptococcus. Wilson used the term necrotizing fasciitis without assigning a specific pathologic bacterium that caused the disease.
Smith et al first classified soft tissue infections as either local or spreading. Lewis later further classified soft tissue infections into either necrotizing or non-necrotizing. He further subdivided these infections into either focal or diffuse.
Recent collective reviews
In 2010, a team of scientists and surgeons from the Legacy Emanuel Shock Trauma Center in Portland, Oregon, wrote a collective review on the diagnosis and treatment of necrotizing fasciitis. These scientists and surgeons found extensive wide debridement of all tissues that can be easily elevated off the fascia with gentle pressure should be undertaken. The use of adjunctive therapies, such as hyperbaric oxygen therapy (HBO), continue to receive considerable attention as a integral parts of the life-saving therapies.
In 2011, Drs Rausch and Foca wrote an exciting report focusing on necrotizing fasciitis in a pediatric patient. At the end of the report, the authors pointed out that all pediatricians must be aware of the possibility of severe infections in pediatric patients with necrotizing fasciitis who had vascular lymphatic malformations.
In 2012, a team of scientists and surgeons from Turkey wrote a comprehensive collective review on necrotizing fasciitis. At the end of their report, they emphasize that early diagnosis of necrotizing fasciitis may be life saving.
At the Imperial College in London, United Kingdom, 5 scholars wrote a comprehensive 5-year review of necrotizing fasciitis. They emphasize that necrotizing fasciitis is a life-threatening disease that is often difficult to diagnose. The authors guide the readers to make the correct diagnosis as soon as possible in order to save lives.
National Necrotizing Fasciitis Foundation (NNFF) 
The cofounders of this distinguished Foundation are necrotizing fasciitis survivors, Donna Batdorff and Jackie Roemmele. In the 16 years since these 2 women have teamed up to be leaders in this Society, they have diligently worked in concert with a dedicated volunteer staff to fulfill the Foundation’s mission to increase awareness about necrotizing fasciitis. Foundation activities include public speaking and outreach efforts regarding necrotizing fasciitis throughout the world to educate the medical community and to help save lives from this often misdiagnosed, rapidly fatal disease. See National Necrotizing Fasciitis Foundation.
Necrotizing fasciitis is characterized by widespread necrosis of the subcutaneous tissue and the fascia. It was once considered an uncommon clinical entity. In the 1990s, the media popularized the idea that this infection was caused by "flesh-eating bacteria." Although the pathogenesis of necrotizing fasciitis is still open to speculation, the rapid and destructive clinical course of necrotizing fasciitis is thought to be due to multibacterial symbiosis and synergy.
Historically, group A beta-hemolytic Streptococcus (GABS) has been identified as a major cause of this infection. This monomicrobial infection is usually associated with an underlying cause, such as diabetes, atherosclerotic vascular disease, or venous insufficiency with edema. GABS usually affects the extremities; approximately two thirds of the GABS infections are located in the lower extremities.
During the last 2 decades, researchers have found that necrotizing fasciitis is usually polymicrobial rather than monomicrobial.[26, 27, 28] Anaerobic bacteria are present in most necrotizing soft-tissue infections, usually in combination with aerobic gram-negative organisms. Anaerobic organisms proliferate in an environment of local tissue hypoxia in those patients with trauma, recent surgery, or medical compromise.
Facultative aerobic organisms grow because polymorphonuclear neutrophils (PMNs) exhibit decreased function under hypoxic wound conditions. This growth further lowers the oxidation/reduction potential, enabling more anaerobic proliferation and, thus, accelerating the disease process.
Carbon dioxide and water are the end products of aerobic metabolism. Hydrogen, nitrogen, hydrogen sulfide, and methane are produced from the combination of aerobic and anaerobic bacteria in a soft tissue infection. These gases, except carbon dioxide, accumulate in tissues because of reduced water solubility.
In necrotizing fasciitis, group A hemolytic streptococci and Staphylococcus aureus, alone or in synergism, are frequently the initiating infecting bacteria. However, other aerobic and anaerobic pathogens may be present, including the following:
Coliforms (eg, Escherichia coli)
Bacteroides fragilis is usually noted as part of a mixed flora in combination with E coli. B fragilis does not directly cause these infections, but it does play a part in reducing interferon production and the phagocytic capacity of macrophages and PMNs.
A variant synergistic necrotizing cellulitis is considered to be a form of necrotizing fasciitis, but some authorities feel that it is actually a nonclostridial myonecrosis. This condition begins in the same manner as necrotizing fasciitis, but it progresses rapidly to involve wide areas of deeper tissue and muscle at an earlier stage than might be expected. Severe systemic toxicity occurs.
Anaerobic streptococci, occasionally seen in intravenous drug users, cause many forms of nonclostridial myonecrosis (see the image below). Some cases of necrotizing fasciitis can be caused by Vibrio vulnificus. This organism is seen more often in patients with chronic liver dysfunction, and it often follows the consumption of raw seafood. V vulnificus may cause subcutaneous bleeding.
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 necrotizing fasciitis. 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.
The poor prognosis associated with necrotizing fasciitis has been linked to infection with certain streptococcal strains. Community-acquired methicillin-resistant S aureus (MRSA) has also been associated with necrotizing fasciitis.
Single-nucleotide changes are the most common cause of natural genetic variation among members of the same species. They may alter bacterial virulence; a single-nucleotide mutation in the group A Streptococcus genome was identified that is epidemiologically associated with decreased human necrotizing faciitis.
It was found that wild-type mtsR function is required for group A Streptococcus to cause necrotizing fasciitis in mice and nonhuman primates. It was speculated that a naturally occurring single-nucleotide mutation dramatically alters virulence by dysregulating a multiple gene virulence axis.
Severe myositis accompanying septic necrotizing fasciitis may be caused by a Panton-Valentine leukocidin–positive S aureus strain. Immunostaining may document strong binding of the Panton-Valentine leukocidin toxin to necrotic muscle tissues.
Although necrotizing fasciitis most frequently develops after trauma that compromises skin integrity, it may rarely develop in a healthy person after minor trauma such as an isolated shoulder sprain that occurred without a break in skin barrier.
Surgical procedures may cause local tissue injury and bacterial invasion, resulting in necrotizing fasciitis. These procedures include surgery for intraperitoneal infections and drainage of ischiorectal and perianal abscesses. Intramuscular injections and intravenous infusions may lead to necrotizing fasciitis.
Minor insect bites may set the stage for necrotizing infections. Streptococci introduced into the wounds may be prominent initially, but the bacteriologic pattern changes with hypoxia-induced proliferation of anaerobes.
Local ischemia and hypoxia can occur in patients with systemic illnesses (eg, diabetes). Host defenses can be compromised by underlying systemic diseases favoring the development of these infections. Illnesses such as diabetes or cancer have been described in over 90% of cases of progressive bacterial gangrene.
Of patients with necrotizing fasciitis, 20-40% are diabetic. As many as 80% of Fournier gangrene cases occur in people with diabetes. In some series, as many as 35% of patients were alcoholics. However, approximately one half of the cases of streptococcal necrotizing fasciitis occur in young and previously healthy people.
A study by Hung et al suggested that liver cirrhosis is an independent risk factor for necrotizing fasciitis. In a retrospective analysis of hospital data, the investigators determined the incidence of necrotizing fasciitis development in 40,802 patients with cirrhosis and 40,865 control patients, over a three-year follow-up period after each patient’s initial hospitalization. Necrotizing fasciitis occurred during follow-up in 299 patients with cirrhosis (0.7%) and in 160 control patients (0.4%), giving patients with cirrhosis a hazard ratio of 1.98 for necrotizing fasciitis. It was also found that the risk of necrotizing fasciitis was greater in patients with complicated cirrhosis than in those with the noncomplicated type (hazard ratio 1.32).
Studies have shown a possible relationship between the use of nonsteroidal anti-inflammatory agents (NSAIDs), such as ibuprofen, and the development of necrotizing fasciitis during varicella infections. Additional studies are needed to establish whether ibuprofen use has a causal role in the development of necrotizing fasciitis and its complications during varicella infections. This has not previously been described.
Group A beta-hemolytic streptococci have historically been noted as a cause of necrotizing fasciitis, but Haemophilus aphrophilus and S aureus are also associated with the condition, and some patients have mixed infections involving multiple species of bacteria, including mycobacteria, as well as fungi.[35, 36]
A synergistic infection with a facultative anaerobic bacterium may be significant. In 1 patient, Phycomycetes appeared to be responsible for necrotizing fasciitis.
Streptococcus pneumoniae is a rare cause of necrotizing fasciitis. In one patient, S pneumoniae serotype 5 was also isolated. This serotype 5 antigen is included in the polysaccharide 23-valent pneumococcal vaccine, highlighting the value of pneumococcal immunization.
In type I necrotizing fasciitis, anaerobic and facultative bacteria work synergistically to cause what may initially be mistaken for a simple wound cellulitis. A variant of type I necrotizing fasciitis is saltwater necrotizing fasciitis in which an apparently minor skin wound is contaminated with saltwater containing a Vibrio species.
In type II necrotizing fasciitis, varicella infection and the use of nonsteroidal anti-inflammatory drugs may be predisposing factors.
Type III necrotizing fasciitis is usually caused by Clostridium perfringens. When type III necrotizing fasciitis occurs spontaneously, C septicum is more likely to be the etiologic agent; these cases usually occur in association with colon cancer or leukemia.
The reported mortality in patients with necrotizing fasciitis has ranged from 20% to as high as 80%.[39, 26, 28, 40] Pathogens, patient characteristics, infection site, and speed of treatment are among the variables that affect survival.
Poor prognosis in necrotizing fasciitis has been linked to infection with certain streptococcal strains. However, McHenry et al found that monomicrobial infection with S pyogenes was not associated with an increased mortality.
A retrospective study by Hsiao et al found that Aeromonas infection, Vibrio infection, cancer, hypotension, and band form WBC count greater than 10% were independent positive predictors of mortality in patients with necrotizing fasciitis, 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 be verified. .
In another study, preexisting chronic liver dysfunction, chronic renal failure, thrombocytopenia, hypoalbuminemia, and postoperative dependence on mechanical ventilation represented poor prognostic factors in monomicrobial necrotizing fasciitis. In addition, patients with gram-negative monobacterial necrotizing fasciitis had more fulminant s epsis.
The mean age of survivors is 35 years. The mean age of nonsurvivors is 49 years.
A retrospective review by Cheng et al showed that upper extremity necrotizing fasciitis has a high mortality rate. In their review, about 35% of patients died. A state of altered consciousness and respiratory distress at initial presentation were found to be statistically significant factors for eventual mortality. Early diagnosis and referral for aggressive surgical treatment prior to the development of systemic toxic signs are essential for survival.
In a retrospective review of craniocervical necrotizing fasciitis, Mao et al reported a survival rate of 60% for patients with thoracic extension (6 of 10) compared with 100% for those without thoracic extension. Lower overall survival for the patients in the thoracic extension group was attributed to older patient age, greater comorbidity, need for more extensive surgical debridement, and increased postoperative complications.
Better survival of the patients without thoracic extension was attributed to aggressive wound care and surgical debridement, broad-spectrum intravenous antibiotics, and care in the surgical intensive care unit.
A study by Friederichs et al indicated that necrotizing fasciitis tends to have a worse outcome when acquired iatrogenically via injection or infiltration than it does when acquired in other ways, with higher mortality and amputation rates (67% and 73%, respectively) found. The study included 21 patients with injection- or infiltration-related necrotizing fasciitis and 134 patients who were infected with the condition through other means.
In a study by Rouse et al, the overall mortality rate was 73% (20 of 27 patients). They indicated that prompt recognition and treatment of necrotizing fasciitis was essential: Of 12 patients whose treatment was delayed for more than 12 hours, 11 patients died.
Similarly, McHenry et al reported that the average time from admission to operation was 90 hours in nonsurvivors of necrotizing soft-tissue infections; in survivors, this average time was 25 hours. Early debridement of the infection was obviously associated with a significant decrease in mortality.
Necrotizing fasciitis survivors may have a shorter life span than population controls, owing to infectious causes such as pneumonia, cholecystitis, urinary tract infections, and sepsis.
Necrotizing fasciitis has become sufficiently common in the United States that a National Necrotizing Fasciitis Foundation has been formed. The cofounders of this foundation are survivors of necrotizing fasciitis. The goals of this foundation are to increase awareness about necrotizing fasciitis, to educate the medical community, and to help save lives from this often misdiagnosed, rapidly fatal disease.
The Foundation’s Web site has stories about survivors of necrotizing fasciitis with color photographs. The Foundation provides a list of journal articles as well as 8 brief reports on necrotizing fasciitis that can be downloaded at no cost.
Hakkarainen TW, Kopari NM, Pham TN, Evans HL. Necrotizing soft tissue infections: review and current concepts in treatment, systems of care, and outcomes. Curr Probl Surg. 2014 Aug. 51 (8):344-62. [Medline]. [Full Text].
Federman DG, Kravetz JD, Kirsner RS. Necrotizing fasciitis and cardiac catheterization. Cutis. 2004 Jan. 73(1):49-52. [Medline].
Chan HT, Low J, Wilson L, Harris OC, Cheng AC, Athan E. Case cluster of necrotizing fasciitis and cellulitis associated with vein sclerotherapy. Emerg Infect Dis. 2008 Jan. 14(1):180-1. [Medline]. [Full Text].
Bharathan R, Hanson M. Diagnostic laparoscopy complicated by group A streptococcal necrotizing fasciitis. J Minim Invasive Gynecol. 2010 Jan-Feb. 17(1):121-3. [Medline].
Akcay EK, Cagil N, Yulek F, et al. Necrotizing fasciitis of eyelid secondary to parotitis. Eur J Ophthalmol. 2008 Jan-Feb. 18(1):128-30. [Medline].
Anwar UM, Ahmad M, Sharpe DT. Necrotizing fasciitis after liposculpture. Aesthetic Plast Surg. 2004 Nov-Dec. 28(6):426-7. [Medline].
Bisno AL, Cockerill FR 3rd, Bermudez CT. The initial outpatient-physician encounter in group A streptococcal necrotizing fasciitis. Clin Infect Dis. 2000 Aug. 31(2):607-8. [Medline].
Gibbon KL, Bewley AP. Acquired streptococcal necrotizing fasciitis following excision of malignant melanoma. Br J Dermatol. 1999 Oct. 141(4):717-9. [Medline].
Sewell GS, Hsu VP, Jones SR. Zoster gangrenosum: necrotizing fasciitis as a complication of herpes zoster. Am J Med. 2000 Apr 15. 108(6):520-1. [Medline].
Tung-Yiu W, Jehn-Shyun H, Ching-Hung C, Hung-An C. Cervical necrotizing fasciitis of odontogenic origin: a report of 11 cases. J Oral Maxillofac Surg. 2000 Dec. 58(12):1347-52; discussion 1353. [Medline].
Kihiczak GG, Schwartz RA, Kapila R. Necrotizing fasciitis: a deadly infection. J Eur Acad Dermatol Venereol. 2006 Apr. 20(4):365-9. [Medline].
Quirk WF Jr, Sternbach G. Joseph Jones: infection with flesh eating bacteria. J Emerg Med. 1996 Nov-Dec. 14(6):747-53. [Medline].
Fournier A. Gangrene foudroyante de la verge. Semaine Med. 1883. 3:345.
Meleney FL. Hemolytic streptococcus gangrene. Arch Surg. 1924. 9:317-364.
Wilson B. Necrotizing fasciitis. Am Surg. 1952 Apr. 18(4):416-31. [Medline].
Smith AJ, Daniels T, Bohnen JM. Soft tissue infections and the diabetic foot. Am J Surg. 1996. 7S:172(Suppl.6A).
Lewis RT. Soft tissue infections. World J Surg. 1998 Feb. 22(2):146-51. [Medline].
Edlich RF, Cross CL, Dahlstrom JJ, Long WB 3rd. Modern concepts of the diagnosis and treatment of necrotizing fasciitis. J Emerg Med. 2010 Aug. 39(2):261-5. [Medline].
Rausch J, Foca M. Necrotizing fasciitis in a pediatric patient caused by lancefield group g streptococcus: case report and brief review of the literature. Case Rep Med. 2011.
Vayvada H, Demirdover C, Menderes A, Karaca C. [Necrotizing fasciitis: diagnosis, treatment and review of the literature]. Ulus Travma Acil Cerrahi Derg. 2012 Nov. 18(6):507-13. [Medline].
Bratdorff D, Roemmele J. National Necrotizing Fasciitis Foundation (NNFF) 1997-2009. Available at http://www.nnff.org. Accessed: April 17, 2013.
Bahebeck J, Sobgui E, Loic F, Nonga BN, Mbanya JC, Sosso M. Limb-threatening and life-threatening diabetic extremities: clinical patterns and outcomes in 56 patients. J Foot Ankle Surg. 2010 Jan-Feb. 49(1):43-6. [Medline].
Stone DR, Gorbach SL. Necrotizing fasciitis. The changing spectrum. Dermatol Clin. 1997 Apr. 15(2):213-20. [Medline].
Rouse TM, Malangoni MA, Schulte WJ. Necrotizing fasciitis: a preventable disaster. Surgery. 1982 Oct. 92(4):765-70. [Medline].
Andreasen TJ, Green SD, Childers BJ. Massive infectious soft-tissue injury: diagnosis and management of necrotizing fasciitis and purpura fulminans. Plast Reconstr Surg. 2001 Apr 1. 107(4):1025-35. [Medline].
Morgan WR, Caldwell MD, Brady JM, Stemper ME, Reed KD, Shukla SK. Necrotizing fasciitis due to a methicillin-sensitive Staphylococcus aureus isolate harboring an enterotoxin gene cluster. J Clin Microbiol. 2007 Feb. 45(2):668-71. [Medline]. [Full Text].
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. 2006 May. 88(5):1107-10. [Medline].
Olsen RJ, Sitkiewicz I, Ayeras AA, et al. Decreased necrotizing fasciitis capacity caused by a single nucleotide mutation that alters a multiple gene virulence axis. Proc Natl Acad Sci U S A. 2010 Jan 12. 107(2):888-93. [Medline]. [Full Text].
Lehman D, Tseng CW, Eells S, et al. Staphylococcus aureus Panton-Valentine leukocidin targets muscle tissues in a child with myositis and necrotizing fasciitis. Clin Infect Dis. 2010 Jan 1. 50(1):69-72. [Medline].
Hung TH, Tsai CC, Tsai CC, et al. Liver cirrhosis as a real risk factor for necrotising fasciitis: a three-year population-based follow-up study. Singapore Med J. 2014 Jul. 55(7):378-82. [Medline].
Tang WM, Ho PL, Yau WP, Wong JW, Yip DK. Report of 2 fatal cases of adult necrotizing fasciitis and toxic shock syndrome caused by Streptococcus agalactiae. Clin Infect Dis. 2000 Oct. 31(4):E15-7. [Medline].
Parcell BJ, Wilmshurst AD, France AJ, Motta L, Brooks T, Olver WJ. Injection anthrax causing compartment syndrome and necrotising fasciitis. J Clin Pathol. 2011 Jan. 64(1):95-6. [Medline].
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). 2006 Apr. 14(1):67-70. [Medline].
Simsek Celik A, Erdem H, Guzey D, et al. Fournier's gangrene: series of twenty patients. Eur Surg Res. 2011. 46(2):82-6. [Medline].
Hsiao CT, Weng HH, Yuan YD, Chen CT, Chen IC. Predictors of mortality in patients with necrotizing fasciitis. Am J Emerg Med. 2008 Feb. 26(2):170-5. [Medline].
Lee CY, Kuo LT, Peng KT, Hsu WH, Huang TW, Chou YC. Prognostic factors and monomicrobial necrotizing fasciitis: gram-positive versus gram-negative pathogens. BMC Infect Dis. 2011 Jan 5. 11:5. [Medline]. [Full Text].
Cheng NC, Su YM, Kuo YS, Tai HC, Tang YB. Factors affecting the mortality of necrotizing fasciitis involving the upper extremities. Surg Today. 2008. 38(12):1108-13. [Medline].
Mao JC, Carron MA, Fountain KR, et al. Craniocervical necrotizing fasciitis with and without thoracic extension: management strategies and outcome. Am J Otolaryngol. 2009 Jan-Feb. 30(1):17-23. [Medline].
Friederichs J, Torka S, Militz M, Buhren V, Hungerer S. Necrotizing soft tissue infections after injection therapy: higher mortality and worse outcome compared to other entry mechanisms. J Infect. 2015 Jun 3. [Medline].
Light TD, Choi KC, Thomsen TA, et al. Long-term outcomes of patients with necrotizing fasciitis. J Burn Care Res. 2010 Jan-Feb. 31(1):93-9. [Medline].
Olafsson EJ, Zeni T, Wilkes DS. A 46-year-old man with excruciating shoulder pain. Chest. 2005 Mar. 127(3):1039-44. [Medline].
Iwata Y, Sato S, Murase Y, et al. Five cases of necrotizing fasciitis: lack of skin inflammatory signs as a clinical clue for the fulminant type. J Dermatol. 2008 Nov. 35(11):719-25. [Medline].
Simonart T, Simonart JM, Derdelinckx I, et al. Value of standard laboratory tests for the early recognition of group A beta-hemolytic streptococcal necrotizing fasciitis. Clin Infect Dis. 2001 Jan. 32(1):E9-12. [Medline].
Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin Infect Dis. 2014 Jul 15. 59(2):147-59. [Medline]. [Full Text].
Drake DB, Woods JA, Bill TJ, et al. Magnetic resonance imaging in the early diagnosis of group A beta streptococcal necrotizing fasciitis: a case report. J Emerg Med. 1998 May-Jun. 16(3):403-7. [Medline].
Fugitt JB, Puckett ML, Quigley MM, Kerr SM. Necrotizing fasciitis. Radiographics. 2004 Sep-Oct. 24(5):1472-6. [Medline].
Chao HC, Kong MS, Lin TY. Diagnosis of necrotizing fasciitis in children. J Ultrasound Med. 1999 Apr. 18(4):277-81. [Medline].
Sharif HS, Clark DC, Aabed MY, Aideyan OA, Haddad MC, Mattsson TA. MR imaging of thoracic and abdominal wall infections: comparison with other imaging procedures. AJR Am J Roentgenol. 1990 May. 154(5):989-95. [Medline].
Sandner A, Moritz S, Unverzagt S, Plontke SK, Metz D. Cervical Necrotizing Fasciitis-The Value of the Laboratory Risk Indicator for Necrotizing Fasciitis Score as an Indicative Parameter. J Oral Maxillofac Surg. 2015 Jun 5. [Medline].
Namias N, Martin L, Matos L, Sleeman D, Snowdon B. Symposium: necrotizing fasciitis. Contemp Surg. 1996. 49:167-78.
Lille ST, Sato TT, Engrav LH, Foy H, Jurkovich GJ. Necrotizing soft tissue infections: Obstacles in diagnosis. J Am Coll Surg. 1995. 182(1):7-11.
Ramirez-Schrempp D, Dorfman DH, Baker WE, Liteplo AS. Ultrasound soft-tissue applications in the pediatric emergency department: to drain or not to drain?. Pediatr Emerg Care. 2009 Jan. 25(1):44-8. [Medline].
Wronski M, Slodkowski M, Cebulski W, Karkocha D, Krasnodebski IW. Necrotizing fasciitis: early sonographic diagnosis. J Clin Ultrasound. 2011 May. 39(4):236-9. [Medline].
Parenti GC, Marri C, Calandra G, Morisi C, Zabberoni W. [Necrotizing fasciitis of soft tissues: role of diagnostic imaging and review of the literature]. Radiol Med. 2000 May. 99(5):334-9. [Medline].
Beltran J, McGhee RB, Shaffer PB, et al. Experimental infections of the musculoskeletal system: evaluation with MR imaging and Tc-99m MDP and Ga-67 scintigraphy. Radiology. 1988 Apr. 167(1):167-72. [Medline].
Tang JS, Gold RH, Bassett LW, Seeger LL. Musculoskeletal infection of the extremities: evaluation with MR imaging. Radiology. 1988 Jan. 166(1 Pt 1):205-9. [Medline].
Rahmouni A, Chosidow O, Mathieu D, et al. MR imaging in acute infectious cellulitis. Radiology. 1994 Aug. 192(2):493-6. [Medline].
Craig JG. Infection: ultrasound-guided procedures. Radiol Clin North Am. 1999 Jul. 37(4):669-78. [Medline].
Arslan A, Pierre-Jerome C, Borthne A. Necrotizing fasciitis: unreliable MRI findings in the preoperative diagnosis. Eur J Radiol. 2000 Dec. 36(3):139-43. [Medline].
Childers BJ, Potyondy LD, Nachreiner R, et al. Necrotizing fasciitis: a fourteen-year retrospective study of 163 consecutive patients. Am Surg. 2002 Feb. 68(2):109-16. [Medline].
Stamenkovic I, Lew PD. Early recognition of potentially fatal necrotizing fasciitis. The use of frozen-section biopsy. N Engl J Med. 1984 Jun 28. 310(26):1689-93. [Medline].
Bakleh M, Wold LE, Mandrekar JN, Harmsen WS, Dimashkieh HH, Baddour LM. Correlation of histopathologic findings with clinical outcome in necrotizing fasciitis. Clin Infect Dis. 2005 Feb 1. 40(3):410-4. [Medline].
Uman SJ, Kunin CM. Needle aspiration in the diagnosis of soft tissue infections. Arch Intern Med. 1975 Jul. 135(7):959-61. [Medline].
Francis J, Warren RE. Streptococcus pyogenes bacteraemia in Cambridge--a review of 67 episodes. Q J Med. 1988 Aug. 68(256):603-13. [Medline].
Crew JR, Thibodeaux KT, Speyrer MS, et al. Flow-through Instillation of Hypochlorous Acid in the Treatment of Necrotizing Fasciitis. Wounds. 2016 Feb. 28 (2):40-7. [Medline].
Chelsom J, Halstensen A, Haga T, Hoiby EA. Necrotising fasciitis due to group A streptococci in western Norway: incidence and clinical features. Lancet. 1994 Oct 22. 344(8930):1111-5. [Medline].
Edlich RF, Wind TC, Heather CL, Thacker JG. Reliability and performance of innovative surgical double-glove hole puncture indication systems. J Long Term Eff Med Implants. 2003. 13(2):69-83. [Medline].
Wang KC, Shih CH. Necrotizing fasciitis of the extremities. J Trauma. 1992 Feb. 32(2):179-82. [Medline].
Kaufman JL. Clinical problem-solving: necrotizing fasciitis. N Engl J Med. 1994 Jul 28. 331(4):279; author reply 280. [Medline].
Adams EM, Gudmundsson S, Yocum DE, Haselby RC, Craig WA, Sundstrom WR. Streptococcal myositis. Arch Intern Med. 1985 Jun. 145(6):1020-3. [Medline].
Edlich RF, Wind TC, Heather CL, Thacker JG. Reliability and performance of innovative surgical double-glove hole puncture indication systems. J Long Term Eff Med Implants. 2003. 13(2):69-83. [Medline].
Edlich RF, Woodard CR, Pine SA, Lin KY. Hazards of powder on surgical and examination gloves: a collective review. J Long Term Eff Med Implants. 2001. 11(1-2):15-27. [Medline].
Gear AJ, Hellewell TB, Wright HR, et al. A new silver sulfadiazine water soluble gel. Burns. 1997 Aug. 23(5):387-91. [Medline].
Frame JD, Still J, Lakhel-LeCoadou A, et al. Use of dermal regeneration template in contracture release procedures: a multicenter evaluation. Plast Reconstr Surg. 2004 Apr 15. 113(5):1330-8. [Medline].
Wainwright DJ. Use of an acellular allograft dermal matrix (AlloDerm) in the management of full-thickness burns. Burns. 1995 Jun. 21(4):243-8. [Medline].
Stevens DL, Yan S, Bryant AE. Penicillin-binding protein expression at different growth stages determines penicillin efficacy in vitro and in vivo: an explanation for the inoculum effect. J Infect Dis. 1993 Jun. 167(6):1401-5. [Medline].
Yan S, Bohach GA, Stevens DL. Persistent acylation of high-molecular-weight penicillin-binding proteins by penicillin induces the postantibiotic effect in Streptococcus pyogenes. J Infect Dis. 1994 Sep. 170(3):609-14. [Medline].
Gemmell CG, Peterson PK, Schmeling D, et al. Potentiation of opsonization and phagocytosis of Streptococcus pyogenes following growth in the presence of clindamycin. J Clin Invest. 1981 May. 67(5):1249-56. [Medline]. [Full Text].
Stevens DL, Bryant AE, Yan S. Invasive group A streptococcal infection: New concepts in antibiotic treatment. Int J Antimicrob Agent. 1994. 4:297-301.
Stevens DL, Bryant AE, Hackett SP. Antibiotic effects on bacterial viability, toxin production, and host response. Clin Infect Dis. 1995 Jun. 20 Suppl 2:S154-7. [Medline].
Edlich RF, Winters KL, Woodard CR, Britt LD, Long WB 3rd. Massive soft tissue infections: necrotizing fasciitis and purpura fulminans. J Long Term Eff Med Implants. 2005. 15(1):57-65. [Medline].
Lota AS, Altaf F, Shetty R, Courtney S, McKenna P, Iyer S. A case of necrotising fasciitis caused by Pseudomonas aeruginosa. J Bone Joint Surg Br. 2010 Feb. 92(2):284-5. [Medline].
Barry W, Hudgins L, Donta ST, Pesanti EL. Intravenous immunoglobulin therapy for toxic shock syndrome. JAMA. 1992 Jun 24. 267(24):3315-6. [Medline].
Yong JM. Necrotising fasciitis. Lancet. 1994 Jun 4. 343(8910):1427. [Medline].
Darenberg J, Ihendyane N, Sjolin J, et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial. Clin Infect Dis. 2003 Aug 1. 37(3):333-40. [Medline].
Norrby-Teglund A, Muller MP, Mcgeer A, et al. Successful management of severe group A streptococcal soft tissue infections using an aggressive medical regimen including intravenous polyspecific immunoglobulin together with a conservative surgical approach. Scand J Infect Dis. 2005. 37(3):166-72. [Medline].
Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis: current concepts and review of the literature. J Am Coll Surg. 2009 Feb. 208(2):279-88. [Medline].
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. 7-36. [Medline].
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. 2000 Jul. 166(7):530-4. [Medline].
Krenk L, Nielsen HU, Christensen ME. Necrotizing fasciitis in the head and neck region: an analysis of standard treatment effectiveness. Eur Arch Otorhinolaryngol. 2007 Aug. 264(8):917-22. [Medline].
Sugihara A, Watanabe H, Oohashi M, et al. The effect of hyperbaric oxygen therapy on the bout of treatment for soft tissue infections. J Infect. 2004 May. 48(4):330-3. [Medline].
Green RJ, Dafoe DC, Raffin TA. Necrotizing fasciitis. Chest. 1996 Jul. 110(1):219-29. [Medline].
Riseman JA, Zamboni WA, Curtis A, Graham DR, Konrad HR, Ross DS. Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery. 1990 Nov. 108(5):847-50. [Medline].
Brown DR, Davis NL, Lepawsky M, Cunningham J, Kortbeek J. A multicenter review of the treatment of major truncal necrotizing infections with and without hyperbaric oxygen therapy. Am J Surg. 1994 May. 167(5):485-9. [Medline].
Monestersky JH, Myers RA. Hyperbaric oxygen treatment of necrotizing fasciitis. Am J Surg. 1995 Jan. 169(1):187-8. [Medline].