Dermatologic Manifestations of Necrotizing Fasciitis 

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.

See also the following:

• Necrotizing Fasciitis
• Emergent Management 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,^[2] vein sclerotherapy,^[3] and diagnostic laparoscopy,^[4] among others.^{[5, 6, 7, 8, 9, 10]} There has even been a report of 2 cases that resulted from a stonefish sting^[11] and 1 case following a shoulder sprain in a previously healthy person.^[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 below).^[13]

Type II, or group A streptococcal necrotizing fasciitis, is the so-called flesh-eating bacterial infection.^[7]

Type III necrotizing fasciitis, or clostridial myonecrosis, is gas gangrene. This skeletal muscle infection may be associated with recent surgery or trauma.

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.^[14] 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 (see the following images). 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 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.^[15]

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:

• Rapid progression
• Poor therapeutic response
• Blistering necrosis
• Cyanosis
• Extreme local tenderness
• High temperature
• Tachycardia
• Hypotension
• Altered level of consciousness

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.^[16] 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.^[17]

Limb- and life-threatening hand and foot infections, including necrotizing fasciitis, in diabetic patients account for substantial morbidity and mortality.^[18] 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.

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)