1. Salcido, Richard "Sal" MD, EdD

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Necrotizing soft tissue infections (NSTIs) are uncommon, severe, and potentially lethal infections, characterized by rapid subcutaneous spread through the fascial planes.1-3 Necrotizing fasciitis (NF) is an example of an NSTI and the subject of this issue's CME activity.

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In the United States, NTSI incidence is 0.4 case per 100,000 population.1,2 Most NSTIs are difficult to diagnose in early stages, which may account for the high rates of morbidity and mortality, including the likelihood of a lifesaving amputation to ameliorate the infection. Despite advances in clinical management, mortality ranges from 8.3% to 76%1,2 and is highest when NSTI is accompanied by shock and/or host factors such as advanced age, comorbidities, or an impaired immune system. Compared with white patients, the incidence rate of NF-associated death was greater in black, Hispanic, and American Indian patients and lower in Asian patients.


These NSTIs are not new. Hippocrates first described NSTI in the fifth century BCE.4 He characterized it as a complication of acute streptococcal infection, a malady that caused many to lose limbs. In the late 18th century, NSTI was known as phagedenic ulcer; phagedena gangrenous; gangrenous, malignant, or putrid ulcer; or "hospital gangrene" during the US Civil War.5 In 1883, Dr Jean-Alfred Fournier described a necrotizing infection of the perineum and scrotum; today, the eponymous Fournier gangrene endures.3


Typically caused by toxin-producing bacteria, the main causative pathogen of NSTIs is invasive group A streptococcus. The variable amounts of early or late systemic toxicity depend on the strain of bacteria and toxins produced and the immune system of the patient.


The progression of NSTI is characterized by what may initially be evaluated as a nonspecific swelling or erythema.3,6 After the initial local finding, the sequence or progression of the disease can be measured in mere hours. As the infection disseminates, patients develop pain and signs of systemic toxicity disproportionate to the findings of skin examination, and practitioners must maintain a high index of suspicion for NSTI. Early diagnosis and treatment are crucial to patient survival and a functional outcome.6


These infections arise primarily in the dermis and epidermis, but they more commonly affect the deeper layers of adipose tissue, fascia, or muscle. The toxic nature of the infection facilitates rapid passage through fascial plains, discrete compartments, or local and regional anatomical structures. Of particular anatomical interest are the vital structures that occupy the "fascial planes," bounded or enveloped by the fascia and deep tissues. A starting point for conceptualizing deep tissues begins with reviewing the vital structures that constitute the deep anatomic systems and their clinical relationships. The fundamental structures contained in the deep tissue include nerves, arteries, veins, and lymph (NAVAL), as well as the supportive connective tissues.7 Any disruption to the form, function, or flow of the NAVAL structures puts the muscles at inherent risk. And in the case of NSTIs, the deep tissues form an anatomical pathway for infection and toxins to travel through these critical compartments and spaces.


Wong et al8 created an evaluation tool for diagnosing NF called the Laboratory Risk Indicator for Necrotizing Fasciitis. The indicator score can supplement good clinical judgment in differentiating soft tissue infection from NF. The tool was internally validated using a small cohort, revealing a sensitivity of 90%, specificity of 95%, positive predictive value of 92%, and negative predictive value of 96% for detecting early NF. Indirect laboratory measurements can often be nonspecific.8


Given the biochemical, fluid/gas, and functional structures involved in NSTI, an imaging technology that is portable and delivers real-time results would enhance diagnostic accuracy. One such diagnostic modality is a bedside ultrasound. Providers can evaluate the image using the following mnemonic: STAFF (subcutaneous thickening, air, and fascial fluid). More work needs to be done in comparing the efficacy of ultrasound to other imaging modalities.8,9


As noted in this month's CME article, Learning from Clinical Experience with Necrotizing Fasciitis, the mainstay of treatment for NSTIs is early and aggressive surgical debridement, broad-spectrum antibiotics,5 and intensive care support for resultant shock. I encourage you to read the full article for more in-depth information about this unique skin infection.




1. Bonne SL, Kadri SS. Evaluation and management of necrotizing soft tissue infections. Infect Dis Clin North Am 2017;31(3):497-511. [Context Link]


2. Arif N, Yousfi S, Vinnard C. Deaths from necrotizing fasciitis in the United States, 2003-2013. Epidemiol Infect 2016;144(6):1338-44. [Context Link]


3. Misiakos EP, Bagias G, Patapis P, Sotiropoulos D, Kanavidis P, Machairas A. Current concepts in the management of necrotizing fasciitis. Front Surg 2014;1:36. [Context Link]


4. Descamps V, Aitken J, Lee MG. Hippocrates on necrotising fasciitis. Lancet 1994;344(8921):556. [Context Link]


5. Lamb MM, Lloyd A. Necrotizing soft-tissue infection: disease overview and updated treatment strategies. US Pharm 2017;42(4):HS16-20. [Context Link]


6. Hakkarainen TW, Kopari NM, Pham TN, Evans HL. Necrotizing soft tissue infections: review and current concepts in treatment, systems of care, and outcomes. Curr Probl Surg 2014;51(8):344-62. [Context Link]


7. Salcido RS. Inside the deep tissues: nerves, arteries, veins, and lymph. Adv Skin Wound Care 2011;24(8):344. [Context Link]


8. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med 2004;32(7):1535-41. [Context Link]


9. Castleberg E, Jenson N, Dinh VA. Diagnosis of necrotizing faciitis with bedside ultrasound: the STAFF exam. West J Emerg Med 2014;15(1):111-3. [Context Link]