Most commonly referred to as flesh-eating bacteria, necrotizing fasciitis is a progressive, rapidly spreading inflammatory infection located in the deep fascia that destroys fascia and fat with secondary necrosis of subcutaneous tissue. Also referred to as hemolytic streptococcal gangrene, acute dermal gangrene, suppurative fasciitis, and synergistic necrotizing cellulites, necrotizing fasciitis is most commonly caused by the pathogenic bacteria Streptococcus pyogenes, also known as group A Streptococcus (GAS), although other aerobic and anaerobic patho-gens may be present.
This severe and potentially fatal infection may begin at the site of a small insignificant wound or surgical incision. It's characterized by invasive and progressive necrosis of the soft tissue and underlying blood supply. The high mortality rates associated with it have been attributed to the emergence of more virulent strains of streptococci caused by changes in the bacteria's deoxyribonucleic acid.
This would account for an increase in the frequency and severity of the cases reported since 1985, following a 50- to 60-year span of clinical insignificance. Noted for decades and described in medical literature since the Civil War, necrotizing fasciitis accounts for 8% of reported cases of invasive GAS infections today. The mortality rate is very high, at 70% to 80%. Mortality drops significantly and prognosis improves with early intervention and treatment. Cases treated aggressively with surgery, antibiotics, and hyperbaric oxygen (HBO) therapy have seen mortality rates reduced to as low as 9% to 20%.
More than 80 types of the causative bacteria S. pyrogenes are in existence, making the epidemiology of GAS infections most complex. 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.
In necrotizing fasciitis, group A beta-hemolytic Streptococcus and Staphylococcus aureus, working alone or together, are most commonly the primary infecting bacteria. They can enter the host via local tissue injury or through a breach in the integrity of a mucous membrane barrier. Other aerobic and anaerobic pathogens, including Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella, may be pres-ent. They can proliferate in an environment of tissue hypoxia caused by trauma, recent surgery, or medical compromise. The end product of this invasion is necrosis of the surrounding tissue, which accelerates the disease process by creating an even more favorable environment for the organisms.
Men are three times more likely to develop this rare condition than women, and the disease rarely occurs in children except in countries with poor hygienic practices. The mean age of the population contracting the disease is 38 to 44 years.
Pain, out of proportion to the size of the wound or injury it's associated with, is usually the first symptom of necrotizing fasciitis. It generally presents before all other physical findings.
The infective process will usually begin with a mild area of erythema at the site of insult, which will quickly progress within the first 24 hours. During the first 24- to 48-hour period, the erythema changes from red to purple in color and then to blue, with the formation of fluid-filled blisters and bullae that indicate 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. In later stages, hypotension and respiratory insufficiency, which are signs of overwhelming sepsis requiring supportive care, occur. In the most severe cases, necrosis advances rapidly until several large areas of the body are involved. This may cause the patient to become mentally cloudy, delirious, or even unresponsive secondary to the intoxication rendered.
Other complications include renal failure, septic shock with cardiovascular collapse, and scarring with cosmetic deformities. Without treatment, involvement of deeper muscle layers may occur, resulting in myositis or myonecrosis.
Tissue biopsy is the best method of diagnosing necrotizing fasciitis. Cultures of microorganisms can be obtained locally from the periphery of the spreading infection or from deeper tissues during surgical debridement. Gram's staining and culturing of biopsied tissue are useful in establishing the type of invasive organisms and the effective treatment against them.
Radiographic studies can pinpoint the presence of subcutaneous gases, and computed tomography scans can locate the anatomic site of involvement by locating the necrosis. In combination with clinical assessment, magnetic resonance imaging determines areas of necrosis and the need for surgical debridement.
Other supportive studies include laboratory values such as complete blood count with differential, electrolytes, glucose, blood urea nitrogenand creatinine, urinalysis, and arterial blood gas levels.
Other conditions to consider in the differential diagnosis include cellulitis, testicular torsion, epididymitis and orchitis (as related to Fournier's gangrene), gas gangrene, hernias, and toxic shock syndrome (TSS).
Prompt and aggressive exploration and debridement of suspected necrotizing fasciitis is mandatory for early, definitive diagnosis and to improve prognosis. Ninety percent of patients that present with clinical signs and symptoms will need immediate surgical debridement, fasciotomy, or amputation.
Penicillin, clindamycin, metronidazole, ceftriaxone, gentamicin, chloramphenicol, and ampicillin are among the medications given orally, I.V., or I.M. to treat the organisms involved with necrotizing fasciitis. The specific drug is determined by the sensitivity of the cultured organisms. When the infection is polymicrobial, medications must be used in combination. Recommendations for specific drugs continue to change as new antibiotics are developed and new resistance emerges.
Reports suggest that the use of HBO therapy decreases the mortality rate, significantly improves the tissues defense against infection, and prevents the necrosis from spreading by increasing the normal oxygen saturations of infected wounds by a thousandfold, causing a bactericidal effect. Typical treatment involves aggressively starting HBO therapy after the first surgical debridement and continuing for a total of 10 to 15 sessions.
❑Antibiotic therapy should be initiated immediately.
❑Accurate and frequent assessment of the patient's pain level, mental status, wound status, and vital signs is essential in order to recognize the progression of the wound changes or the development of new signs and symptoms. Changes must be reported and documented immediately.
❑The need for supportive care, such as endotracheal intubation, cardiac monitoring, fluid replacement, and supplemental oxygen should be assessed and provided as warranted.
❑Care of postoperative patients and patients with trauma wounds requires strict sterile technique, good hand hygiene, and barriers between health care providers and patients to prevent contamination.
❑Health care workers with sore throats should see their physician to determine if they have a streptococcal infection. If they are diagnosed positive, they should'nt return to work until 24 hours after the initiation of antibiotic therapy.
❑Risk factors for contracting necrotizing fasciitis include patients with advanced age, human immunodeficiency infection, history of alcohol abuse, and varicellar infection. Patients with chronic illnesses, such as cancer, diabetes, cardiopulmonary disease, and kidney disease requiring hemodialysis, and those using steroids are more susceptible to GAS infection due to their debilitated immune response.
Alert Be alert for signs and symptoms of TSS, which is associated with any streptococcal soft tissue infection, and the development of shock, acute respiratory distress syndrome, renal impairment, or bacteremia, any of which can lead to sudden death.
Review other book chapters online related to Necrotizing fasciitis:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Professional Guide to Diseases (Eighth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2005 ISBN: 1-58255-370-X 
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