eMedicine Specialties > Dermatology > Bacterial Infections

Necrotizing Fasciitis

Author: Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Coauthor(s): Rajendra Kapila, MD, MBBS, Professor of Medicine, Department of Medicine, UMDNJ, New Jersey Medical School
Contributor Information and Disclosures

Updated: May 5, 2009

Introduction

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 necrotizing fasciitis.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.

Necrotizing fasciitis 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 necrotizing fasciitis 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 necrotizing fasciitis type I is saltwater necrotizing fasciitis, in which an apparently minor skin wound is contaminated with saltwater containing a Vibrio species.

Necrotizing fasciitis may occur as a complication of a variety of surgical procedures or medical conditions, including cardiac catheterization,² among others.^3,4,5,6,7,8 Familiarity with necrotizing fasciitis may facilitate earlier diagnosis and initiation of appropriate therapy.

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 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.⁹ The poor prognosis associated with necrotizing fasciitis has been linked to infection with certain streptococcal strains. Community-acquired methicillin-resistant S aureus has also been associated with necrotizing fasciitis.¹⁰

Mortality/Morbidity

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

Age

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

Clinical

History

Necrotizing fasciitis 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. 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. 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.

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.¹¹ 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 necrotizing fasciitis. In a series of 39 pediatric cases, the most common initiating factor in 13 of them was varicella.¹²

• 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 (see Physical, below).¹³
• Type II, or group A streptococcal necrotizing fasciitis, is the so-called flesh-eating bacterial infection.⁵
• Type III necrotizing fasciitis, 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.
  • Purpura with or without bullae formation, occasionally with a lack of cutaneous erythema and heat, may be found, which does not preclude the diagnosis of necrotizing fasciitis.¹⁴
• 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. Surgically confirmed necrotizing fasciitis cases were compared with 12 patients with superficial soft tissue infection.¹⁵ Necrotizing fasciitis 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 necrotizing fasciitis, gas usually is not evident in affected tissues.
• Although the following features can occur with cellulitis, they may suggest necrotizing fasciitis 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 necrotizing fasciitis. 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.^16,17
  • A synergistic infection with a facultative anaerobic bacterium may be significant.
  • In 1 patient, Phycomycetes appeared to be responsible for necrotizing fasciitis.
  • Diabetes mellitus and immunosuppression predispose patients to necrotizing fasciitis.
  • However, approximately one half of the cases of streptococcal necrotizing fasciitis occur in young and previously healthy people.
  • Streptococcus pneumoniae is a rare cause of necrotizing fasciitis.¹⁸ 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, Clostridium septicum is more likely to be the etiologic agent; these cases usually occur in association with colon cancer or leukemia.
• Rapidly progressive necrotizing fasciitis following a stonefish sting has been described in 2 patients.¹⁹

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