Necrotizing Fasciitis

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

Disclosures

Wounds. 2002;14(8) 

In This Article

Pathophysiology

Bacteria are introduced into the skin through a decrease in tissue resistance often as a result of immunosuppression.[12] Bacteria spread through the skin, subcutaneous tissue, and fascia aided by the release of bacterial toxins and enzymes, such as hyaluronidase, collagenase, streptokinase, and lipase. Uninhibited progression of bacterial penetration results in tissue necrosis and thrombosis of the vasculature.

In NF type 2 caused by beta hemolytic streptococcal (BHS) infection, superantigens are thought to be involved in the pathogenesis of disease.[12] BHS secrete superantigens that have the ability to activate T-helper cell lymphocyte clones. T-helper cells secrete various cytokines, such as TNF and - , clotting factors, and complement.[1,8,11,28] This initiates thrombosis and inflammation. Oxygen-free radicals and nitrous oxide are produced. This leads to shock, worsening immunosuppression, depression of myocardial function, and multiorgan failure. BHS may also produce other virulence factors, such as M proteins types 1, 3, 4, 6, 12, and 28. These virulence factors act to depress neutrophilic phagocytosis, thus limiting the body's ability to rid itself of the bacteria. Sharkawy, et al., showed that patients infected with serotype M3 have greater mortality.[4]

Several reports in the literature have implicated nonsteroidal, anti-inflammatory agents (NSAIDS) in the progression of NF; however, this remains controversial.[4] NSAIDS are postulated to potentiate tissue damage by decreasing granulocyte adhesion and phagocytosis and increasing cytokine production. However, even if this occurs, there have been no reports of increased severity of systemic findings of NF.

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