Necrotizing Fasciitis

Jennifer T. Trent, MD, Robert S. Kirsner, MD


Wounds. 2002;14(8) 

In This Article

Signs and Symptoms


NF can affect any area of the body, but in adults it most commonly occurs on the extremities (Figures 1-4).[23] Conversely, in very young children (<1 month of age), the most commonly affected area is the trunk.[3] Distribution of disease is important. There is a higher mortality rate when the head, neck, chest, or abdomen are involved. These areas are more difficult to treat, and critical structures reside within them. Involvement of the genitalia is referred to as Fournier's gangrene (FG) and usually results from a polymicrobial infection. Typically, it occurs as a result of trauma, extension of a urinary tract infection, or an extension of an infection in the perianal or retroperitoneal areas.[24] FG has an abrupt onset with rapid progression of disease, oftentimes without discovering the specific causative microorganism.

Clinical Course

Early on, patients often present with a clinical picture similar to and difficult to differentiate from cellulitis.[4,23] However, one important clue can be used to distinguish NF from cellulitis. Patients will complain of severe pain, usually out of proportion to the clinical appearance of the skin affected. Early diagnosis is critical and may be life saving, as early diagnosis leads to early treatment. It is known that the sooner the diagnosis is made, the lower the mortality. NF may appear similar to cellulitis, with redness and edema, in addition to a spreading, diffuse inflammatory reaction that blends into the surrounding tissue. The overlying skin is shiny and tense without sharply demarcated borders.

In acute cases, infection progresses for two to three days, causing the redness of the skin to turn purple or purple-black, thus heralding the beginning of devastating tissue necrosis.[22] This process may take several weeks in subacute cases. Necrosis occurs presumably as a direct result of thrombosis of the skin's underlying nutrient vessels.[23] This necrotic tissue, in turn, supports the growth and migration of bacteria with subsequent unabated progression of tissue necrosis. If necrosis involves underlying cutaneous nerves, anesthesia may follow pain in the affected skin.[22] Clear or hemorrhagic bullae may develop, but the fluid eventually transforms into a gray, foul-smelling fluid termed dishwater pus. When bullae rupture, a dry, black eschar may develop at the site of rupture.

Over time, as bacterial invasion progresses, worsening infection and frank cutaneous gangrene can be seen.[23] This gangrene extends beyond the skin and into the subcutaneous fat and fascial planes below. Characteristic of NF, a separation of the necrotic tissue along the fascial planes with suppuration occurs. Normal fascia surrounding muscle is thick and forms a protective barrier for the muscle against the overlying infection/necrosis. However, in cases of progressive disease, deeper involvement can develop with invasion of fascia and myonecrosis of the underlying muscle. Lymphadenitis, lymphangitis, crepitation, and venous thrombosis are less commonly seen.

There have been some rare reports of metastatic abscesses developing within the liver, lung, spleen, brain, and pericardium in patients with NF.[6] Metastatic abscesses may occur in the skin, as well as presenting as painless, subcutaneous fluctuant masses, often located over pressure points.[25]

During progression of disease, patients will suffer from systemic complications of NF, including a high fever, chills, and constitutional symptoms ( Table 3 ).[1,13,26,27,28] In fulminant cases, multiorgan system failure will occur, frequently resulting in death.

Hemorrhagic Cellulitis

Hemorrhagic cellulitis (HC) is a variant of NF.[29] HC is characterized by an acute onset of painful erythema and hemorrhage localized to dependent areas of the body, such as the lower extremities, followed by blistering and sloughing of the necrotic areas. Pathogenesis of this condition is related to lipopolysaccharide-induced or bacterial mitogen-induced TNF secreted by activated macrophages. TNF injures endothelial cells and epidermal keratinocytes via neutrophil degranulation and DNAse activation. Therefore, effective treatment for this condition is the combination of antibiotics and corticosteroids, which inhibit secretion of and block cytotoxic effects of TNF .