Overview
Necrotizing fasciitis is a severe, insidiously advancing, soft-tissue infection characterized by widespread fascial necrosis (see the image below). A number of bacteria in isolation or as a polymicrobial infection can cause this condition.[1] The organisms most closely linked to necrotizing fasciitis are group A beta-hemolytic streptococci, although the disease may also be caused by other bacteria or different streptococcal serotypes. In Texas from 2001-2002 and from 2009-2010, a rising incidence of necrotizing fasciitis of 5.9 versus 7.6 cases per 100,000 population has been documented, although hospital mortality (9.3%) was unchanged.[2] A nationwide French study identified 1537 patients with a median age of 60 years, with 23.7% dying.[3] Owing to an increasing litigious climate in many countries, necrotizing fasciitis has become the subject of numerous malpractice suites,[4] including from disability after successful outcomes from life-saving extensive surgery.[5, 6]
View Image | Left upper extremity shows necrotizing fascitis in an individual who used illicit drugs. Cultures grew Streptococcus milleri and anaerobes (Prevotella.... |
See also the following:
Types of Necrotizing Fasciitis
Familiarity with necrotizing fasciitis may facilitate earlier diagnosis and initiation of appropriate therapy. This infection may occur as a complication of a variety of surgical procedures or medical conditions, including cardiac catheterization,[7] vein sclerotherapy,[8] and diagnostic laparoscopy,[9] among others.[10, 11, 12, 13, 14, 15] Necrotizing fasciitis can appear in a variety of sites after a number of encounters, including a stonefish sting,[16] following a shoulder sprain in a previously healthy person,[17] on a swollen breast,[18] and as a complication of acne appearing initially as lip cellulitis.[19]
Type I, or polymicrobial necrotizing fasciitis, 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 below).[20]
Type II, or group A streptococcal necrotizing fasciitis, is the so-called flesh-eating bacterial infection.[12]
Type III necrotizing fasciitis, or clostridial myonecrosis, is gas gangrene. This skeletal muscle infection may be associated with recent surgery or trauma.
Type IV can be designated as fungal necrotizing fasciitis. Since necrotizing fasciitis is rarely caused by or complicated by a fungus, the authors of this Medscape Reference article (Schwarz and Kapila) have designed it as type IV. In any case, early fungal smear and culture should be considered.[21] Candidal species may be etiologic,[22] possibly combined with a bacterial etiology such as Streptococcus pyogenes.[23]
Clinical Evaluation
In a study of 20 patients with necrotizing fasciitis with a median age was 52.5 years, the overall mortality rate was only 8.3%, attributed to early diagnosis and treatment.[24] Half had a comorbidity such as diabetes mellitus or congestive heart failure.
Patients with necrotizing fasciitis tend to present with erythema and supralesional vesiculation or bullae formation 2-3 days following constitutional symptoms of fever and chills. Serosanguineous fluid may drain from the affected area.
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, and metastatic cutaneous plaques may occur.
Purpura with or without bullae formation, occasionally with a lack of cutaneous erythema and heat, may be found, but this does not preclude the diagnosis of necrotizing fasciitis.[25] Gas may be evident; this process may also be observed in the perineum in association with urogenital or anogenital infections (eg, Fournier gangrene).
Necrotizing fasciitis 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. It has even been described affecting the perineum and genital region due to excessive masturbation in an otherwise healthy man with severe scrotal pain and swelling and frequent masturbation who had used soap as a lubricant, resulting in recurrent penile erythema and minor skin abrasions.[26]
See the images below.
View Image | Massive perineal ulceration with foul-smelling discharge in a 60-year-old woman who had undergone postvaginal hysterectomy and repair of a rectal prol.... |
View Image | 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. |
However, in many cases, no association with such factors can be made. Necrotizing fasciitis may also occur in the setting of diabetes mellitus, surgery, trauma, or infectious processes.
Necrotizing fasciitis causes thrombosis of fascial blood vessels, producing a true surgical emergency. Although thickening of the deep fasciae as a result of fluid accumulation and reactive hyperemia may be visualized using computed tomography and magnetic resonance imaging, these findings are not specific for necrotizing fasciitis.[27] Thus, although imaging studies can confirm the diagnosis and evaluate spread, they should not delay emergency surgical treatment.
In type II necrotizing fasciitis, 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. When surgically confirmed necrotizing fasciitis cases were compared with 12 patients with superficial soft-tissue infection, the patients with necrotizing fasciitis were more likely to have skin areas of ischemia or necrosis, fluid-filled vesicles, and severe sepsis or septic shock.[28]
Gas usually is not evident in affected tissues in type II necrotizing fasciitis. Although the following features can occur with cellulitis, they may instead suggest necrotizing fasciitis:
Pediatric cases
In a pediatric necrotizing fasciitis 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.[29] Pain and, occasionally, crepitation, was also noted early. Crepitation indicates the presence of gas produced by aerobic and anaerobic bacteria and is highly suggestive of the diagnosis of necrotizing fasciitis; this finding is often present in patients with diabetes and in those with nonclostridial anaerobic infections. In a series of 39 pediatric cases, the most common initiating factor in 13 of them was varicella.[30]
Differential Diagnosis
Limb- and life-threatening hand and foot infections, including necrotizing fasciitis, in diabetic patients account for substantial morbidity and mortality.[31] Of 56 patients in one series, 17 (30.36%) had necrotizing cellulitis, 12 (21.43%) had wet gangrene, 9 (16.07%) had acute extensive osteomyelitis, 5 (8.93%) had dry gangrene, 5 (8.93%) had gas gangrene, 4 (7.14%) had necrotizing fasciitis, and 4 (7.14%) had diffuse hand infections. In diagnosing necrotizing fasciitis, computed tomography is better than plain radiography. Nevertheless, clinical suspicion suggests use of early surgical consultation to facilitate diagnosis.[32]
Other conditions that should be considered when evaluating a patient with suspected necrotizing fasciitis include the following:
Acute Febrile Neutrophilic Dermatosis
Acute Hemorrhagic Edema of Infancy
Cellulitis
Erythema Induratum (Nodular Vasculitis)
Postsurgical pyoderma gangrenosum[33]
Author
Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School
Disclosure: Nothing to disclose.
Coauthor(s)
Rajendra Kapila, MD, MBBS, Professor, Department of Medicine, Rutgers New Jersey Medical School
Disclosure: Nothing to disclose.
Specialty Editors
Michael J Wells, MD, FAAD, Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology
Disclosure: Nothing to disclose.
Van Perry, MD, Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio
Disclosure: Nothing to disclose.
Chief Editor
Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Janet Fairley, MD, Professor and Head, Department of Dermatology, University of Iowa, Roy J and Lucille A Carver College of Medicine
Disclosure: Nothing to disclose.
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