Necrotizing Fasciitis: Current Concepts and Review of the Literature

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Necrotizing Fasciitis: Current Concepts and Review of the Literature Necrotizing Fasciitis: Current Concepts and Review of the Literature Babak Sarani, MD, FACS, Michelle Strong, MD, PhD, Jose Pascual, MD, PhD, C William Schwab, MD, FACS Necrotizing soft-tissue infection (NSTI) was first described crotizing infection and stated that fascial necrosis is the sine by Hippocrates circa 500 BC, when he wrote, “Many were qua non of this process.8 More recently, the term necrotiz- attacked by the erysipelas all over the body when the excit- ing soft tissue infection has been advocated to encompass all ing cause was a trivial accident . flesh, sinews, and bones forms of the disease process because necrotizing infection fell away in large quantities . there were many deaths.”1 of all soft tissue involves a similar approach to diagnosis and Despite many advances in our understanding of this disease treatment regardless anatomic location or depth of infec- and great improvements in medical care, the mortality as- tion. This single, all-encompassing name, facilitates under- sociated with NSTI has not changed in the last 30 years and standing and assurance of proper management.9 It should remains 25% to 35%.2 Mortality is directly proportional to be noted that mortality increases with the depth of the time to intervention.3-6 In addition, prevalence of this dis- primary site of infection. ease is such that the average practitioner will see only one or two cases in his or her career. Physicians cannot be suffi- Incidence and classification ciently familiar with NSTI to proceed rapidly with accurate NSTI has an incidence of approximately 1,000 cases per diagnosis and the necessary management. The purpose of year in the United States or 0.04 cases per 1,000 person- this article is to provide an evidence-based review of the years.10 The incidence of NSTI increased between 1980 microbiology, pathophysiology, diagnosis, and treatment and 2000, although the exact reason for this remains spec- of NSTI. Because there are no adequately powered, ran- ulative.11 Possible explanations include increased microbial domized, and blinded studies, the recommendations are virulence and resistance because of excessive use of antibi- based on retrospective and nonblinded study data otics, better disease reporting, or both. Regardless, al- available. though it remains rare, NSTI is a highly lethal condition NSTI was described as “hospital gangrene” by British requiring early aggressive intervention for salvage. Naval surgeons in the 18th and 19th century. Dr Joseph NSTI can be classified based on anatomy, depth of in- Jones, a Confederate Army surgeon, was the first person to fection, or microbial source of infection (Table 1). Al- describe this disorder in a large group of patients in 1871, though these classification systems are not clinically useful when he reported on 2,642 cases and found a mortality rate because they do not affect diagnosis or treatment, they are of 46%.7 In 1883, the French physician, Jean Alfred useful in providing a common language for research. In Fournier, described a similar NSTI of the perineum in five addition, as noted here, the depth of the primary site of male patients—a process that continues to bear his name. It infection correlates with mortality. is now described in both male and female patients. In the ensuing years, many other terms, such as necrotizing erysip- elas, streptococcal gangrene, and suppurative fasciitis, have Microbiology and risk factor for disease been also been used. Because the gas-forming organism, Three basic microbial subtypes of NSTI are described (Ta- Clostridium perfringens, can be associated with this infec- ble 1). Type I infections are the most common form of tion, it has also been referred to as “Clostridial gangrene” or disease and are polymicrobial in nature. Tissue isolates “gas gangrene.” demonstrate an average of four different organisms in most In 1951, Dr Wilson proposed the term necrotizing fasci- wounds. Approximately 55% to 75% of all NSTI result itis to include both gas-forming and nonϪgas-forming ne- from type I infection and the causative microbes are a com- bination of gram-positive cocci, gram-negative rods, and 4,6,12,13 Disclosure Information: Nothing to disclose. anaerobes. Two recent, single-center retrospective studies have characterized the prevalence of these organ- Received June 14, 2008; Revised August 27, 2008; Accepted October 30, 2,9 2008. isms in type I NSTI (Table 2). Less commonly, the in- From the Division of Traumatology and Surgical Critical Care, Depart- fection might be caused by a species of bacteroides or clos- ment of Surgery, University of Pennsylvania, Philadelphia, PA. tridium. Despite its historic prevalence, C. perfringens is Correspondence address: Babak Sarani, MD, Division of Traumatology and Surgical Critical Care, Department of Surgery, 3440 Market St, First Floor, now a rare cause of NSTI because of improvements in Philadelphia, PA 19104. email: [email protected] sanitation and hygiene. Clostridia septicum, a bacterium © 2009 by the American College of Surgeons ISSN 1072-7515/09/$36.00 Published by Elsevier Inc. 279 doi:10.1016/j.jamcollsurg.2008.10.032 280 Sarani et al Necrotizing Fasciitis J Am Coll Surg Table 1. Classification of Necrotizing Soft Tissue Infection Abbreviations and Acronyms Classification factor Comment HBO ϭ hyperbaric delivery of 100% oxygen Anatomic location Fournier’s gangrene of perineum/scrotum MRSA ϭ methicillin-resistant Staphylococcus aureus Depth of infection Necrotizing adipositis (most common), NSTI ϭ necrotizing soft-tissue infection fasciitis, myositis SC ϭ subcutaneous Microbial cause Type I: Polymicrobial (most common) Type II: Monomicrobial (Staphylococcus, Streptococcus, Clostridia sp) that is endogenous to the colon, is a very rare cause of NSTI Type III: Vibrio vulnificus* in patients with perforated carcinoma of the colon. *Classification of Vibrio vulnificus necrotizing infection as type III is not universally agreed on. Type I infections tend to occur in the perineal and trunk areas and are often diagnosed in immunocompromised pa- tients, particularly diabetics and patients with peripheral particularly chronic hepatitis B infection. Although this is vascular disease.12 Other risk factors for this type of NSTI the least common type of NSTI, it is associated with a include obesity, chronic renal failure, HIV, alcohol abuse, fulminant course and must be recognized quickly by the abscess, IV drug use, blunt or penetrating trauma, insect surgeon to minimize the time to operative intervention. bites, surgical incisions, indwelling catheters, chicken pox, Multisystem organ failure will develop within 24 hours of vesicles, and (rarely) perforation of the gastrointestinal infection and the disease is uniformly fatal if not promptly tract (eg, carcinoma or diverticulitis).14-17 Despite the recognized and treated. plethora of risk factors, there is no specific inciting event identified for 20% to 50% of patients.2,6,13 In addition, the Pathophysiology relative importance of each risk factor is unknown because It is generally agreed that microbial invasion of the subcu- studies evaluating this demonstrate wide variance between taneous (SC) tissues occurs either through external trauma study populations and design. or direct spread from a perforated viscus (particularly co- Type II NSTI is a monomicrobial infection caused by lon, rectum, or anus) or urogenital organ. Bacteria then group A Streptococcus (Streptococcus pyogenes) either alone or track SC, producing endo- and exotoxins that cause tissue in association with Staphylococcus aureus. As such, type II ischemia, liquefactive necrosis, and often systemic ill- NSTI is unique because it might be associated with toxic ness.11,26 Infection can spread as fast as 1 inch per hour with shock syndrome. In addition, in the last 5 years, there has little overlying skin change. been an increasing incidence of community-acquired Production of various exotoxins can enhance a particular methicillin-resistant Staphylococcus aureus (MRSA) soft- microbe’s virulence and accelerate progression of infection. tissue infection reported, particularly in IV drug abusers, The Clostridium species produce ␣-toxin, which cause ex- athletes, and institutionalized groups.18-20 Today, MRSA is tensive tissue necrosis and cardiovascular collapse. Staphy- cultured in up to 40% of necrotic wounds. Additionally, lococcus aureus and Streptococci elaborate surface proteins group A streptococci can survive and replicate in macro- M-1 and M-3, exotoxins A, B, C, streptolysin O, and su- phage, thereby escaping antibiotic therapy even in tissues perantigen. The M proteins increase the microbes’ ability that remain well-perfused and amenable to antibiotic to adhere to tissue and escape phagocytosis. Toxins A and B penetration.21,22 damage endothelium, cause loss of microvascular integrity, Type II NSTI is far less common than type I infection and escape of plasma, resulting in tissue edema, and im- and tends to occur in otherwise healthy, young, immuno- paired blood flow at the capillary level. These toxins, along competent hosts. This infection is classically located on the with streptolysin O, stimulate CD4 cells and macrophages extremities, although truncal involvement is well-reported. to produce large bursts of tumor necrosis factorsϪ␣, Frequently, there is a history of recent trauma to or opera- interleukin-1, and interleukin-6.27,28 Systemic release of tion on the area. IV drug abusers are at risk for either type these cytokines produces the systemic inflammatory
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