Patient was continued on an antibiotic regimen of IV vancomycin, clindamycin, and piperacillin-tazobactam. Vasopressor support was gradually reduced and respiratory support weaned until both were finally discontinued on postoperative day 2. Soon thereafter, she was transferred to the surgical floor. Negative pressure wound vacuum-assisted closure therapy was applied to the left thigh and was maintained for one week.
The operative cultures were positive for group A Streptococcus (GAS) pyogenes. Upon discharge, antibiotic regimen was adjusted and limited to oral amoxicillin-clavulanate for 14 days until completion. After a 2-week hospital stay, patient was transferred to an acute rehabilitation facility in stable condition and remained there for one week. Follow up was maintained for a total of 6 months, during which time she had no lasting effects from either illness or resultant interventions other than cosmetic concerns from the surgical wounds. In a follow-up phone discussion with patient 10 months after recovery, she reported that she had returned to work as a registered nurse and had been without any functional disability or discomfort.
Discussion
Originally described by Hippocrates in the 5th century as a complication of erysipelas, necrotizing fasciitis later became known as the “malignant ulcer.” It was subsequently described in the United States in 1871 as “hospital gangrene” by Confederate surgeon Joseph Jones.1-3 In 1952, the name was later modified to necrotizing fasciitis by Wilson.4
Today, necrotizing fasciitis is an uncommon disease process, yet one that must be recognized and treated immediately. If not dealt with promptly and aggressively, the virulent and toxin-producing bacteria— most commonly GAS pyogenes— will cause severe systemic toxicity and may lead to death.5
Incidences and Outcomes
According to the US Centers for Disease Control and Prevention (CDC), about 9,000 to 11,500 cases of invasive GAS disease occur each year in the United States, resulting in approximately 1,000 to 1,800 deaths annually. Necrotizing fasciitis comprises an average of 6% to 7% (540- 805) of these invasive cases per year.6
The incidence of necrotizing fasciitis rose sharply in the mid-1980s to the early 1990s but has remained steady over the past 10 years, with 2012 CDC statistics reporting 72 cases per 32,777,740 persons through its voluntary surveillance program. This extrapolates to an estimated 686 cases of GAS-associated necrotizing fasciitis in the United States, with a reported mortality rate of 20% to 25%.7
The highest incidence of disease occurs in the elderly and in patients with diabetes, immunosuppression, and peripheral vascular disease. In children, varicella infection is a known risk factor.8
Other risk factors include obesity, alcohol use, malnutrition, and smoking, as well as corticosteroid use and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs). Despite the large number of predisposing factors that have been identified, half of all cases of necrotizing fasciitis occur in healthy individuals.9-14
Etiology
Necrotizing fasciitis is thought to be caused by at least two distinct bacteriologic entities. Type I is considered polymicrobial, with Bacteriodes, Clostridium, and Peptostreptococcus, in combination with anaerobic Streptococcus (other than GAS) and Enterobacteriaceae (eg, Escherichia coli, Klebsiella), being the most common infecting species. Type II causative agents include GAS and other β-hemolytic streptococci— alone or with other species of Staphylococcus aureus, including methicillin- resistant S aureus.8 In rare instances, the causative agent is fungal.
Treatment
In a review of patient medical records, Wong et al15 demonstrated that prompt recognition and surgical management of necrotizing fasciitis (ie, within 24 hours of presentation) resulted in improved outcomes. Since the particular causative agent of necrotizing fasciitis in each case is usually unknown, initial treatment should include broad-spectrum IV antibiotics— which are active against grampositive, gram-negative, and anaerobic bacteria—with special consideration for GAS and Clostridium (Table). It is not recommended that initial empiric therapy include antifungals. In this case, the patient was in the OR within 10 hours from presentation, was started immediately on antibiotic regimens for hospital-specific sepsis, and was given appropriate resuscitative measures.
Hyperbaric oxygen therapy is mentioned in the literature as an adjunct to surgery and antibiotics in the treatment of necrotizing fasciitis. Acting as a bactericidal/ bacteriostatic agent against anaerobic bacteria by increasing formation of free oxygen radicals, this therapy is thought to restore the bacterial killing capacity of leukocytes in a hypoxic wound by increasing oxygen tension. Treatment with hyperbaric oxygen may also better define necrotic tissue, facilitating more precise amputation and debridement. Although there are no randomized controlled studies in humans, several authors have shown a reduction in mortality and morbidity with the use of hyperbaric oxygen therapy, in conjunction with early antibiotic and surgical treatment, in animal models and in retrospective studies of patients. 19 When available, hyperbaric oxygen can be initiated once antibiotics have been started and debridement has been performed. The use of hyperbaric oxygen therapy should not delay definitive surgical debridement.