In necrotizing fasciitis, group A beta-hemolytic streptococci and Staphylococcus aureus, alone or together, are most often the primary infecting bacteria. There are more than 80 types of the causative bacteria, S. pyogenes, making the epidemiology of group A streptococci infections complex. Other aerobic and anaerobic pathogens include Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella.

Risk factors for contracting necrotizing fasciitis include advanced age, human immunodeficiency virus (HIV) infection, alcohol abuse, I.V. drug abuse, and varicella infection. Patients with chronic illness, such as cancer, diabetes, cardiac and pulmonary disease, and kidney disease requiring hemodialysis, are also at risk. Those using corticosteroids are more susceptible to group A streptococci infection because of debilitated immune responsiveness.

The infecting bacteria in necrotizing fasciitis enter the host through a local tissue injury or a breach in a mucous membrane barrier. Wounds as minor as pinpricks, needle punctures, bruises, blisters, and abrasions or as serious as a traumatic injury or surgical incision can provide an opportunity for bacteria to enter the body.

The organisms proliferate in an environment of tissue hypoxia caused by trauma, recent surgery, or a medical condition that compromises the patient. The end product of the invasion is necrosis of the surrounding tissue, which accelerates the disease process by creating a favorable environment for these organisms.

High mortality rates associated with necrotizing fasciitis have been attributed to the emergence of more virulent strains of streptococci due to changes in the bacteria’s deoxyribonucleic acid. This accounts for an increase in the frequency and severity of cases reported since 1985, after 50 to 60 years of insignificant clinical disease.

Other complications include renal failure, septic shock with cardiovascular collapse, and scarring with cosmetic deformities. Without treatment, involvement of deeper muscle layers can result in myositis or myonecrosis.

Pain out of proportion to the wound or injury with which it’s associated is usually the first symptom of necrotizing fasciitis and generally presents before all other physical findings.

The infective process usually begins with a mild area of erythema at the site of insult, which quickly progresses within the first 24 hours. During the first 24- to 48-hour period, the erythema changes from red to purple and then blue, with the formation of fluid-filled blisters and bullae appearing, indicating the rapid progression of the necrotizing process. By days 4 and 5, multiple patches of this erythema form, producing large areas of gangrenous skin. By days 7 to 10, dead skin begins to separate at the margins of the erythema, revealing extensive necrosis of the subcutaneous tissue. At this stage, fascial necrosis is typically more advanced than appearance would suggest.

Other clinical symptoms include fever and hypovolemia and, in later stages, hypotension, respiratory insufficiency, and signs of overwhelming sepsis requiring supportive care. In the most severe cases, necrosis advances rapidly until several large areas are involved, causing the patient to become mentally cloudy, delirious, or even unresponsive.

Tissue biopsy is the best method of diagnosing necrotizing fasciitis. Cultures of microorganisms

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