SKIN AND SOFT TISSUE INFECTIONS: NECROTIZING FASCIITIS
Pathophysiology
In necrotizing fasciitis, fulminant bacterial infection of the subcutaneous tissue results in liquefactive necrosis of the superficial fascia, subcutaneous fat, and deep fascia. Historic and modern terms referring to the infection and its subtypes include hospital gangrene, phagedena, hemolytic streptococcal gangrene, progressive synergistic bacterial gangrene, and many others. Superficial skin initially remains intact as the necrosis extends along fascial planes in as little as a few hours. The exudate is thin and often described as “dishwater pus. Vascular thrombosis leads to necrosis of large areas of skin.
Necrotizing fasciitis can affect any area of the body, but abdominal wall, extremities, and perineum are the most common. The infection begins with the introduction of pathogens into the subcutaneous fascia. Possible routes include trauma, injections, cutaneous infections (including cellulitis, ulcers, abscesses, and varicella), insect bites, deep infections, or hematogenous spread from distant sites. Inciting trauma may be minor and even unnoticed; some cases are idiopathic.
Abdominal wall necrotizing fasciitis is usually a postoperative complication, particularly after fecal contamination of the abdominal cavity. Abdominal wall infections have also occurred after gut perforation, or secondary to other abdominal pathologies. Fournier’s gangrene typically refers to necrotizing fasciitis of the male genitalia and perineum, usually secondary to local infections (genitourinary, intra-abdominal, or perianal), trauma, or instrumentation. Vulvar involvement in women has been described and has similar causes. Head and neck cases are rare but particularly dangerous, given the possibility of spread along cervical fascial planes and involvement of major blood vessels and the mediastinum.
Microbiology
Culture of microorganisms from infection sites reveals two major types of necrotizing fasciitis. Type I is polymicrobial, involving a mix of anaerobic and facultative bacteria, often including Enterobacteriaceae and non-group A streptococci. Type II infections are caused by group A B-hemolytic streptococci (primarily Streptococcus pyogenes) alone or with staphylococci. Increased virulence of some group A streptococcal strains may be related to exotoxins, surface proteins, and variable levels of immunity among hosts.
Abdominal and perineal infections tend to be type I in nature and are typically caused by enteric pathogens. Common bacteria include gram-negative enteric bacilli, enterococci, and anaerobic species, such as Bacteroides and Clostridium species. Most studies have shown that necrotizing fasciitis of the extremities and idiopathic cases tend to be type II in etiology. However, many observational studies may not have used rigorous anaerobic bacteria isolation methods, and one large case series described mostly polymicrobial infections predominated by anaerobes in any site.
Marine Vibrio species, most notably Vibrio vulnificus, may cause necrotizing fasciitis following contact with seawater, fish, or shellfish. Other causes include group В streptococci, Pasturella multocida, and Candida species.
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