Are You Confident of the Diagnosis?
Necrotizing fasciitis is a rare, severe, life-threatening soft tissue infection that in its early stages may be indistinguishable from less severe skin and soft tissue infections such as cellulitis (Table I), with few clues as to the deeper spread of the infection. The “fascia” referred to in the name “necrotizing fasciitis” includes primarily the superficial fascia, which comprises all of the subcutaneous tissue between the skin and underlying muscles.
|Syndrome||Predominant HostPredisposiition||Tissue Layers Involved||Anatomical Location||Microbiology|
|Necrotizing fasciitis Type 1 (NEF1)||Diabetes, abdominal and perineal surgery, perineal infections||Subcutaneus tissues including superficial and deep fascia||Anywhere but most commonly extremities followed by trunk and perineum||Mixed including non-spore forming anaerobic bacteria, enteric gram-negative rods and others|
|Synergistic necrotizing Celluitis||Similar to NEF1||As NEF1 but more often includes muscle involvement||Similar to NEF1||Similar to NEF1|
|Fournier’s gangrene||A subset of NEF1||As NEF1||Scrotum and perineum, penis, vulva||As NEF1|
|Ludwig’s angina||A subset of NEF1||Subcutaneous tissues and fascia of the neck and floor of the mouth||Submandibular space of the neck and floor of the mouth||often polymicrobial: may include oral Streptococci, group A beta hemolytic streptococci, staphylococci, oral anaerobic bacteria|
|Clostridial myonecrosis||Local trauma or surgery||Subcutaneus tissues, fascia, and muscle||Any Site||Clostridial species especially C perfringens|
|Hemolytic streptococcal gangrene (necrotizing fasciitis Type 2)||Can affect Nomal hosts, diabetes, peripheral vascular disease, cirrhosis, corticosteroids||Subcutaneous tissues, fascia, and muscle||Any Site||Group A beta-hemolytic streptococci|
|Staphylococcal necrotizing fasciitis||Can affect normal hosts, minor trauma, surgery||Subcutaneous tissues, fascia, and muscle||Any Site||Staphylococcus aureus especially Community associated MRSA|
|“Saltwater” necrotizing fasciitis||Saltwater and shellfish exposure, Cirrhosis and liver disease||Subcutaneous tissues, fascia, and muscle||Most commonly in the limbs||Vibrio vulnificans and other vibrios|
Proper diagnosis requires maintaining high clinical suspicion for the possibility of this diagnosis as well as careful attention to clues in the history and physical examination, as management differs significantly from other soft tissue infections. In addition to the clues that are relevant for the more common presentations of mixed polymicrobial necrotizing fasciitis found in patients with a variety of immunosuppressive illnesses , there are also unique epidemiologic clues relevant for the specific monomicrobial necrotizing fasciitis syndromes caused by Group A beta-hemolytic streptococci, Vibrio vulnificans, and community-associated Methicillin-resistant Staphylococcus aureus (MRSA).
What you should be alert for in the history
Extension from a primary skin lesion, often minor, is reportedin 75-80% of cases. Some examples of initial skin foci include abrasions and puncture wounds, insect bites, minor skin boils, and injection sites in intravenous drug users; necrotizing fasciitis can also occur as a complication of surgical procedures. Predisposing host risk factors include mild to moderately immune-compromising states such as diabetes mellitus, chronic renal insufficiency, cirrhosis and malignancy as well as other more severe immunosuppressive illnesses. Historical clues for particular pathogens may include history of prior boils or MRSA skin abscesses, exposure to individuals with strep throats or other streptococcal infections, or exposure to coastal waters or shellfish ingestion in patients with suspected V vulnificans infections.
Characteristic findings on physical examination
Findings on physical examination may initially only include the typical findings of cellulitis such as erythema, warmth, and swelling. The pathogenesis involves spread of infection through deep tissue layers and fascia, but evidence of this deep tissue invasion may not be readily apparent on physical examination. Systemic toxicity out of proportion to localized findings, including altered mental status, may be an important clue to suggest the diagnosis. Other skin changes can include thickening, induration, and pain out of proportion to the extent of visible inflammation. Many reports describe localized hypoasthesia or anesthesia. Other local manifestations include bullous lesions and skin necrosis or ecchymosis. Variants of necrotizing fasciitis that involve specific areas of the body include Fournier’s gangrene, which involves the scrotal area and penis or vulva, and Ludwig’s angina or cervical necrotizing fasciitis.
The earlier stage physical findings of erythema, warmth, swelling and localized tenderness overlap with many other diagnoses. Intermediate stage findings including blistering, fluctuance and induration of the skin, and late findings of bullae, localized anesthesia and crepitance, and necrosis have higher specificity for the diagnosis (Figure 1).
Expected results of laboratory studies
There is no single diagnostic laboratory test that can definitively establish a diagnosis of necrotizing fasciitis, other than operative findings. Routine laboratory findings and other studies may provide important clues for the early suspicion of the diagnosis and may help differentiate necrotizing fasciitis from less severe skin and soft tissue infections. White blood count (WBC) is elevated in 84% of patients, and typically markedly elevated. A WBC of over 15,400 in one study and greater than 20,000 in another study differentiated necrotizing fasciitis from less severe infections.
Other important clues reported in various studies include elevated Creatine phosphokinase (CPK, (> 600 IU/L), elevated C-reactive protein (CRP), low serum Na, and elevated blood urea nitrogen (BUN) and creatinine.A Laboratory Risk Indicator for Necrotizing Fasciitis has been proposed ithat includes elevated CRP > 150 mg/dl (4 points) , elevated WBC > 25,000/mm3 , hemoglobin < 11 g/dl, Serum Na < 135 mmol/L, creatinine > 141 mol/L (each 2 points) and glucose > 10 mmol/L ( 1 point) (Table II).In one retrospective analysis, scores of >= 6 in patients with severe soft tissue infections were highly predictive of necrotizing fasciitis, and would be indications for further testing.
|C-Reactive Protein > 150 mg/dl||4|
|WBC > 25,000 cells/mm3||2|
|Hemoglobin < 11 g/dl||2|
|Serum Na < 135 mmol/L||2|
|Creatinine > 141 mol/L||2|
|Glucose > 10 mmol/L||1|
WBC, White blood cell.
Scores of >== 6 in patients with severe soft tissue infection should increase suspicion for the diagnosis of necrotizing fasciitis.
Plain X-ray studies may reveal gas in the soft tissues in up to one-third of necrotizing fasciitis patients but is insensitive as a tool to exclude the diagnosis. Computed tomography (CT) scan and magnetic resonance imaging (MRI) may show findings of soft tissue air and edema of involved tissues (Figure 2), but sensitivity and specificity of these findings have not been adequately characterized. MRI may be overly sensitive for presence of deep tissue involvement and cannot necessarily distinguish cellulitis from fasciitis. Imaging studies can provide evidence to support clinical suspicion, but even if negative due not eliminate the need for surgical assessment in patient management.
Other tests proposed tor establishing the diagnosis include fine needle aspiration, the “finger test,” bedside incisional biopsy with frozen section and gram stain, and measurement of tissue oxygen saturation. A positive fine needle aspirate that yields pus from the tissue confirms the diagnosis and provides material for rapid gram stain and culture but is insensitive in excluding the diagnosis. The “finger test” consists of a 2-cm incision into the deep fascial layer under local anesthesia. In a positive finger test, there is lack of bleeding from the incision, findings of murky “dishwater” pus, and lack of resistance to blunt finger dissection, all of which are highly indicative of necrotizing fasciitis.
A bedside incisional biopsy with immediate frozen section and gram stain and culture is also highly specific for the diagnosis of necrotizing fasciitis, and may be useful for detection of early-stage disease. However, the diagnosis is usually apparent by gross appearance when biopsy is performed in patients with more advanced infection; thus, there is probably only a limited need for obtaining frozen section in in most cases.
Decreased tissue oxygen saturation (< 70%) measured by near-infrared spectroscopy was very sensitive and specific in differentiating necrotizing fasciitis from other skin and soft tissue infections of the lower extremity in otherwise healthy patients with lower extremity infections, but these studies excluded those with shock, peripheral venous or arterial disease, or systemic hypoxia.
The definitive diagnosis of necrotizing fasciitis is still made in the operating room. Operative findings include gray appearing, necrotic fascia, lack of bleeding and lack of adherence of fascial tissue during blunt dissection, and findings of murky or gray colored, often foul-smelling “dishwater” pus (Figure 3). Histopathology is helpful for diagnosis of an early or equivocal case, but in most instances gross appearance alone is adequate to establish the diagnosis. Tissue samples should be sent for gram stain and culture to guide antimicrobial therapy.
Who is at Risk for Developing this Disease?
True necrotizing fasciitis is an uncommon disorder. The Centers for Disease Control (CDC) estimates that there are from 500-1500 cases of necrotizing fasciitis reported in the United States each year, and a recent review of insurance databases in the United States provided an estimate of 0.04 cases of necrotizing soft tissue infections per 1000 person years, but the true number is unknown due to the confusing terminology and lack of specificity for the diagnosis.
Estimates for monomicrobial necrotizing fasciitis syndromes. such as that due to group A streptococcus, are more reliable than estimates for necrotizing fasciitis as a whole. A recent population based study from Ontario reported 0.40 cases of group A streptococcal necrotizing fasciitis per 100,000 population per year. Reports suggest recent increases in prevalence of both group A streptococcal and MRSA necrotizing fasciitis over the past decade.
Risk factors to consider in the evaluation for possible necrotizing fasciitis include (1) host-immune factors that contribute to the development of more serious or invasive tissue infection; (2) factors related to increased risk for local tissue damage, localized superficial infection or other initiating events that may progress to necrotizing fasciitis; and (3) risk factors related to exposure to some of the specific virulent pathogens described below.
Seventy percent of patients have one or more chronic illnesses: important host-immune factors reported in studies include diabetes mellitus, peripheral vascular disease, immunosuppression, chronic renal disease, cirrhosis and other chronic liver disease, malignancy, alcoholism and injection drug use. Other proposed risk factors include older age, obesity and malnutrition.
Fifty percent of patients will have some history of skin trauma prior to presentation. Commonly reported predisposing events in addition to penetrating or blunt trauma include injection drug use, medication injections, insect bites, surgery and other invasive procedures, as well as a wide variety of local infections. The most important inciting events will vary with site of infection. For example, dental, peritonsilar and salivary gland infections are risks for cervical necrotizing fasciitis; infected Bartholin’s cysts, pilonidal abscesses and perirectal abscesses are risks for necrotizing perineal infection; and urethral strictures and manipulations are risks for Fournier’s gangrene in men. Most cases by time of presentation will have a readily apparent primary skin or soft tissue focus of the infection, but there may be no apparent primary focus in 20%.
Variants of monomicrobial necrotizing fasciitis due to specific organisms may have unique epidemiologic clues. Disease due to V vulnificans occurs in immunosuppressed patients, especially those with cirrhosisafter ingestion of raw shellfish or from trauma in warmer coastal waters. Community-associated methicillin-resistant S aureus (CA-MRSA) necrotizing fasciitis may occur in those with personal history of or contacts to individuals with boils, folliculitis, or other draining skin lesions. HIV infection has also been associated with staphylococcal necrotizing fasciitis as well as staphylococcal myositis. Group A streptococcal necrotizing fasciitis remains the most common cause of necrotizing fasciitis in children. Specific risk factors in childhood Group A streptococcal necrotizing fasciitis include recent varicella infection.
What is the Cause of the Disease?
Necrotizing fasciitis has been subdivided into several types based on microbiology, though there is no single uniform classification scheme. Necrotizing fasciitis Type 1 infections, the most common form of the disease, are polymicrobial infections that typically include a mixture of anaerobic, aerobic and facultative bacteria, and are usually seen in patients with diabetes or other underlying immune compromise.
Type 2 infections are predominantly group A streptococcal infections but some authors also include monomicrobial disease due to other beta hemolytic streptococci, S aureus (especially CA-MRSA), Streptococcus pneumoniae, and others. Streptococcal necrotizing fasciitis can occur in any age group and may occur in otherwise healthy individuals without major underlying immune compromise. Streptococcal infections are most often mono-microbial but can include other organisms, most commonly S. aureus. Some streptococcal infections have significant component of myonecrosis (so called “streptococcal myonecrosis”) rather than just fasciitis.
Some authors also include a Type 3 disease, referring specifically to clostridial myonecrosis or gas gangrene. Clostridial myonecrosis is due to contamination of traumatic or surgical wounds with spores of members of the obligate anaerobic clostridial species, most commonly C. perfringens but also a variety of other clostridial species that are ubiquitous in soil and dust but can also colonize mucosal surfaces and the gastrointestinal tract.
Some necrotizing fasciitis variants, such as monomicrobial disease due to marine vibrios, also called “saltwater necrotizing fasciitis”, do not fit neatly into any of the above categories. V vulnificans and less commonly other marine vibrio species, including V. haemolyticus, V.alginolyticus and non-01 strains of V.cholerae cause a syndrome of necrotizing fasciitis from either contamination of wounds with seawater, or from ingestion of raw shellfish and systemic sepsis in patients with immune deficiencies, most notably cirrhosis. A similar syndrome of necrotizing soft tissue from brackish or fresh water is caused by Aeromonas species.
Necrotizing fasciitis is caused by invasion of bacterial organisms through the superficial and deep layers of the subcutaneous tissues. Bacteria gain access to the deep tissues directly through the skin, or less commonly by hematogenous spread. Once bacteria access the subcutaneous tissues they proliferate and spread through the fascial layers.The specific mechanisms of bacterial proliferation are unknown, but issue invasion is facilitated by both defects in host immunity and expression of bacterial virulence factors.
Bacterial virulence factors include a bacterial toxins as well as other secreted bacterial enzymes including proteases, lipases, hyaluronidases and others that contribute to breakdown of fat and connective tissues. Necrosis of tissues results in further local inflammation and tissue edema, endothelial activation and thrombosis of small arteries. Arterial thrombosis results in further tissue necrosis and liquefaction as well as the infarction of cutaneous nerves that leads to hypoesthesia. Infection spreads rapidly through the subcutaneous tissue planes, but is often less readily apparent on the skin surface, thus extent of infection and necrosis can be much greater than suggested by clinical appearance. Tissue necrosis and release of organisms and bacterial toxins into the bloodstream contribute to development of sepsis syndrome.
Prior use of non-steroidal antiinflammatory agents has been epidemiologically associated with more severe presentations of necrotizing soft tissue infections, especially group A streptococcal necrotizing fasciitis, but the significance of these observations as well as the mechanism by which this might occur remains uncertain.
Specific Bacterial Virulence Factors
Type 2 necrotizing fasciitis due to group A beta-hemolytic streptococcal infection is associated with strains expressing particular streptococcal M proteins. In the United States, these are most commonly Type 1 and 3 but also Types 12 and 28. Strains also produce soluble exotoxins A and B. Some of these toxins act as superantigens that stimulate T-cells to produce large amounts of cytokines such as TNF, and this cytokine storm may also contributes the severe systemic manifestations of the disease.
There is overlap between patients with streptococcal toxic shock syndrome (TSS) and streptococcal necrotizing fasciitis, with highest mortality on those with both TSS and necrotizing fasciitis. Streptococcal necrotizing fasciitis in children is less often associated with toxic shock syndrome and has a better prognosis than disease in adults.
The specific virulence factors contributing to staphylococcal necrotizing fasciitis remain poorly characterized. Strains isolated from these infections have most commonly been USA 300 CAMRSA strains that express the Panton-Valentine leukocidin and other virulence traits, but the specific roles of these toxins and the pathogenesis of these severe staphylococcal skin and soft tissue infection remains uncertain.
Clostridial species that cause gas gangrene produce at least 20 characterized exotoxins, the most important of these appears to be the alpha toxin, a potent, lethal toxin with phospholipase activity.
V vulnificans produces a potent hemolysin and a variety of exoproteases. Iron uptake systems have also been suggested as important in regulating the virulence of vibrio infections,
Systemic Implications and Complications
Necrotizing fasciitis is a rapidly progressive infection characterized by severe systemic manifestations including fever, tachycardia, hypotension, and mental status changes. Without appropriate treatment, disease progresses to septic shock and death, although rates of progression may vary with organism and underlying host status.
Mortality rates of necrotizing fasciitis overall are high, ranging from 24-34% in most series, with higher rates of up to 67% in patients with Type 2 Group A streptococcal disease with concurrent toxic shock syndrome. Factors associated with worse mortality include older age, shock, leukopenia with left shift, positive blood cultures and higher APACHE-2 scores. Fournier’s gangrene has a lower overall mortality rate than other syndromes; disease caused by V vulnificans and Aeromonas have higher overall mortality.
The most important predictor of survival found in multiple studies is the time to diagnosis and initiation of necessary surgical therapy. Overall mortality was decreased to 12% in one study when diagnosis of necrotizing fasciitis was made within 4 days of onset of initial symptoms, although some syndromes such as gas gangrene and Vibrio infections may progress more rapidly than others. Even with appropriate diagnosis and initiation of therapy, including surgery, there is tremendous morbidity. Outcomes for survivors may include amputation or severe surgical disfigurement as result of the surgeries required to eliminate the source of sepsis and control the spread of infection (Figure 4).
Treatment options are summarized in Table III.
|Medical Therapy||Surgical Therapy||Physical Modalities|
|Broad spectrum intravenous antimicrobial therapy targeted at suspected pathogens||Diagnostic surgical procedure to confirm diagnosis of necrotizing fasciitis||Hyperbaric oxygen|
|Hemodynamic support and intensive care monitoring||Aggressive debridement of all necrotic tissue|
|Pain control||Amputation if Indicated to control infection|
|intravenous immunoglobulin (IVIG) for streptococcal necrotizing fasciitis with toxic shock syndrome||Frequent return to the operating room to assess adequacy of debridement|
Specific Antibiotic Recommendations for Necrotizing Fasciitis Syndromes
For suspected polymicrobial infections (Necrotizing fasciitis type 1), choices would include a broad spectrum agent or combination of antimicrobial agents targeted at streptococci, anaerobes and enteric gram negatives. Initial choices might include beta-lactam plus beta-lactamase inhibitor (ampicillin-sulbactam or piperacillin-tazobactam) plus clindaymcin, a third generation cephalosporin plus clindamycin or metronidazole, or a carbapenem such as imipenem. For patients with recent hospitalizations and antibiotic exposures, or other specific risk for more resistant organisms, a carbapenem may be the preferred choice.
Standard adult dosing for commonly prescribed parenterally administered antimicrobial agents are listed below. Dosing of many of these agents may need to be adjusted for impaired renal function.
Clindamycin: 600 to 900mg every 8 hours
Metronidazole: 500mg every 8 hours
Ampicillin-sulbactam: 3g every 6 hours
Piperacillin-Tazobactam: 3.375g every 6 hours
Cefepime: 1g every 12 hours
Ceftriaxone: 1g every 24 hours
Imipenem: 500mg every 6 hours
Doripenem: 500mg every 8 hours
Meropenem: 1g every 8 hours
Ertapenem: 1 fgram every 24 hours
Vancomycin: 15 mg/kg every 12 hours
Linezolid: 600mg every 12 hours
Ciprofloxacin: 400mg very 12 hours
The recommended empiric treatment for suspected beta-hemolytic streptococcal infections is a combination of a penicillin plus clindamycin. Clindamycin, a protein synthesis inhibitor, is a potent inhibitor of bacterial toxin production responsible for some of the severe clinical manifestations of streptococcal necrotizing fasciitis and in vitro and in vivo data support the inclusion of this agent in the treatment regimen.
For treatment for suspected primary staphylococcal necrotizing fasciitis, or where staphylococcus is suspected as a component of a mixed infection, initial empiric therapy should target MRSA in addition to other pathogens. Empiric MRSA therapy should include vancomycin or linezolid; daptomycin is another alternative for confirmed MRSA infections. Clindamycin is an alternative for strains known to be susceptible, but rates of clindamycin resistance are increasing. Options for known methicillin-susceptible S aureus infections would include nafcillin or cefazolin; other beta-lactams including the beta-lactam inhibitor drugs also are active against methicillin-susceptible staphylococci.
When clostridium infections are suspected, antibiotics should include clindamycin, a penicillin or a carbapenem. Empiric treatment for suspected V vulnificus and other Vibrio infections includes a combinaion of a third-generation cephalosporin plus doxycycliine. For patients with history of multidrug resistant organisms or with drug allergies, expert consultation should be obtained
Optimal Therapeutic Approach for this Disease
The diagnostic and therapeutic strategies for management of suspected necrotizing fasciitis are deeply intertwined. Treatment for all patients with necrotizing fasciitis includes antibiotics and surgery. Antibiotics are also appropriate initial therapy for nearly all of the alternative diagnoses in the differential diagnosis of necrotizing fasciitis; thus, it is the consideration for surgery and how urgent the need for surgery is that depends on the severity of the clinical presentation. A stepwise therapeutic approach is as follows:
Systemic antimicrobial therapy targeted at likely pathogens. Initial empiric antibiotics should be targeted at the specific syndrome and suspected primary pathogens, based on clinical scenario, anatomic location, and preliminary gram stain results, if available. Antibiotics should be administered in appropriate doses and should be administered intravenously during the initial management phase. Antibiotics should be adjusted based on culture and susceptibility data
Necessary supportive measures: including fluid resuscitation, blood pressure support, and intensive monitoring and critical care management, including ventilatory support if necessary. Patients will also require aggressive pain control.
Early surgical consultation
Rapid assessment of likelihood of the diagnosis of necrotizing fasciitis based on physical findings and laboratory values.
Timely surgical intervention is contingent on early consideration of the diagnosis. Clinical features suggesting need for early and aggressive surgical management include:
Patients not responding to antibiotics as characterized by ongoing fever, toxicity and progression of infections after a reasonable trial
Those with severe systemic toxicity and shock with progressive infection
Those with skin necrosis and easy local dissection along fascial planes
Those with gas in the soft tissues, indicating tissue necrosis
Those with physical findings consistent with more advanced stages of necrotizing fasciitis (bullae, skin fluctuance, skin necrosis, crepitance, skin anaesthesia) should go immediatedly to the operating room for for exploration and debridement. These patients may not need extensive radiographic studies, which may only delay potentially life-saving surgery. If operative findings confirm the diagnosis, further management includes aggressive surgical debridement
Patients with physical findings of possible early stage disease without severe systemic toxicity should have imaging studies, including plain films and CT scan or MRI studies. Those with gas in the tissues or other findings suggesting tissue necrosis should then go for immediate surgical exploration, as above.
Patients whose diagnosis is still uncertain without obvious physical findings indicative of intermediate to later stage disease, severe systemic toxicity, or imaging findings should continue to recieve broad spectrum antibiotic therapy and close monitoring. Those with progression under observation should go for surgical exploration as above. Those with failure to improve after a reasonable period of careful monitoring are candidates for more limited diagnostic operative procedure.
Surgical management should include debridment of all visibly necrotic tissue, with adequate margins beyond the resected tissue. Repeat operative evauation of the wound to assess for need for further debridement should be done within 12-24 hours. Most patients will require mulitple reoperations until the infection is controlled and all necrotic tissue is removed. Necrotizing fasciitis caused by V vulnificans and Aeromonas may require even more aggressive surgical intervention.
Later surgical management for those who survive once infection is controlled may include flaps and skin grafting for closure of large wound deficits.
Intravenous immunoglobuin (IVIG) has been evaluated as an intervention for toxin-producing necrotizing soft tissue infections caused by group A beta-hemolytic streptococci, and has also been discussed as an intervention for severe community-acquired MRSA infections. An observational study demonstrated better outcomes in patients who received IVIG but another blinded, placebo-conrolled trial did not confirm the benefits of IVIG.
The evidence of benefit as measured by decreased mortality with use of IVIG may be stronger for toxic shock syndrome due to group A streptococci , which is often associated with necrotizing fasciitis, than for with those with only necrotizing fasciitis without concurrent toxic shock syndrome, perhaps due to the extremely high mortality of this syndrome with standard therapy. At this time treatment with IVIG for suspected or confirmed group A streptococcal necrotizing fasciitis is not routinely recommended.
Adjunctive Therapies: Hyperbaric Oxygen: This intervention is passionately advocated by some experts for severe cases in addition to antimicrobial therapy and surgical debridement, but evidence that this improves outcomes is limited and the logistics of providing hyperbaric therapy may limit the ability to provide close surgical follow-up and timely debridements of the surgical site. Thus, use of hyperbaric oxygen is not routinely recommended.
Patients with suspected recrotizing fasciitis require intensive clinical monitoring, including hemodynamic monitoring and support and careful observation of the area of skin and soft tissue involvement. Patients and families need to be informed early in the treatment course about the severity and high mortality of this disease process and the need in many instances for aggressive and disfiguring surgery, which may include limb amputation.
Antibiotic therapy should be initiated early, but the critical managment decision is the decision to perform either a diagnostic or a theraputic surgical exploration. Once the diagnosis of nectotizing fasciitis is confirmed, there is no alternative to aggressive surgical debridement, the extent of which will be dictated by operative findings. This often includes multiple trips to the operating room to ensure that all necrotic tissue is debrided. In most studies, survival from necrotizing fasciitis correlates with completeness of surgical debridement. In nearly all instances, patients with confirmed necrotizing fasciitis will be admitted to an intensive care unit for hemodynamic support, ventilatory support, and pain control.
Unusual Clinical Scenarios to Consider in Patient Management
Evaluation of patients with suspected necrotizing fasciitis includes careful attention to features in the history that might suggest risks for or exposures to unusual or atypical pathogens. Consideration of V vulnificans from salt water exposures or ingestion of shellfish, or Aeromonas from fresh water exposures, impact on the choice of antimicrobial agents and will affect decisions on aggressivenss of initial surgical management, as these are rapidly progressive and highly lethal syndromes.
Management of patients with necrotizing fasciitis due to group A streptococcal infections may also be complicated by concurrent group A streptococcal toxic shock syndrome, which has an even worse prognosis than other group A streptococcal necrotizing infections. The proposed clinical case definitions for streptococcal toxic shock syndrome, in addition to isolation of S pyogenes from cultures, includes hypotension plus two or more of the following: evidence of necrotizing fasciitis, myositis or gangrene, renal impairment, coagulopathy, elevated liver enzymes, adult respiratory distress syndrome, and generalized macular erythematous rash that may desquamate.
Use of IVIG for this syndrome remains controversial. An observational study demonstrated better outocmes in patients who recieved intravenous immunoglobulin but another blinded, placebo-controlled trial did not confirm the benefits of IVIG. The evidence of benefit as measured by decreased mortality with use of IVIG may be stronger for toxic shock syndrome due to group A streptococci, which is often associated with necrotizing fasciitis, than for with those with only necrotizing fasciitis without concurrent toxic shock syndrome, perhaps due to the extremely high mortality of this syndrome with standard therapy. Howevere, at this time treatment with IVIG for suspected or confirmed group A streptococcal necrotizing fasciitis is not routinely recommended.
What is the Evidence?
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. vol. 32. 2004. pp. 1535-41. (Description of a retrospectively derived clinical scoring system that predicts those patients with severe soft tissue infections who are candidates for early surgical intervention.)
Wall, DB, deVirgilio, C, Black, S, Klein, SR. “Objective criteria may assist in distinguishing necrotizing fasciitis from non-necrotizing soft tissue infection”. Am J Surg. vol. 179. 2000. pp. 17-21. (Description of a sensitive but not very specific clinical rule using WBC and serum sodium that has excelllent negative predictive value but poor positive predictive value for the diagnosis of necrotizing soft tissue infection.)
Wong, CH, Yang, YS. “The diagnosis of necrotizing fasciitis”. Curr Opin Infect Dis. vol. 2. 2005. pp. 01-6. (Good review of multiple staging systems and modalities studied for improved diagnosis of necrotizing fasciitis and the limitations of all of these.)
Stevens, DL, Bisno, AL, Chambers, HF, Everett, ED, Dellinger, P, Goldstein, EJC. “Practice guidelines for the diagnosis and management of skin and soft tissue infections”. Clin Infect Dis. vol. 41. 2005. pp. 1373-1406. (The most recent Infectious Diseases of America practice guidelines for management of skin and soft tissue infections that includes focused discussions of the severe skin and soft tissue infection syndromes and current recommendations for managment. An update of these guidelines is currently in progress with anticipated publication in Spring 2012).
Wong, CH, Chang, HC, Pasupathy, S, Khin, LW, Tan, LJ, Low, CO. “Necrotizing fasciits: clinical presentation, microbiology and determinants of mortality”. J Bone Joint Surg Am. vol. 85. 2003. pp. 1454-60. (One of several studies demonstrating the critical importance of early surgical intervention on outcome of patients with necrotizing fasciitis. Also includes a good representation of recent microbiology in this series of patients.)
Biltin, BD, Zibari, GB, McMillan, RW, Aultman, DF, Dunn, G, McDonald, JC. “Aggressive surgical management of necrotizing fasciitis serves to decrease mortality: a retrospective study”. Am Surg. vol. 64. 1998. pp. 397-400. One of several studies that demonstrate the importance of early and complete surgical debridement on outcome and mortality of necrotizing fasciitis.)
Kaul, R, McGeer, A, Low, DE, Green, K, Schwartz, B. “Population-based surveillance for group-A streptococcal necrotizing fasciitis: clinical features, prognostic indicators, and microbiologic analysis of seventy seven cases. Ontario Group A streptococcal study”. Am J Med. vol. 103. 1997. pp. 18-24. (Well- done population-based study of epidemiology and clinical features of group A streptococcal necrotizing fasciitis in Canada in which authorsalso describe their experience with use of intravenous immunoglobulin for this population.)
Stevens, DL. “Streptococcal toxic shock syndrome associated with necrotizing fasciitis”. Annu Rev Med. vol. 51. 2000. pp. 271-88. (Excellent review including pathogenesis, molecular biology, clinical features, and management controversies for group A streptococcal necrotizing fasciitis/toxic shock syndrome.)
Chen, SC, Chan, KS, Chao, WN, Wang, PH, Lin, DB, Ueng, KC. “Clinical outcomes and prognostic factors for patients with Vibrio vulnificans infections requiring intensive care: a 10-year retrospective series”. Crit Care Med. vol. 38. 2010. pp. 1984-90. (Retrospective review of a large series of cases of Vibro vulnificans infections that defines clinical presentations and confirms the decreased mortality with very early surgical intervention.)
Miller, LG, Perdreau-Remington, F, Rieg, G, Mehdi, S, Perlroth, J, Bayer, AS. “Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles”. N Engl J Med. vol. 352. 2005. pp. 1445-53. (Retrospective review of patients presenting with skin/ soft tissue cultures that grew MRSA to identify those who had necrotizing fasciitis. This is the first large report describing the emergence of staphylococcal necrotizing fasciitis concurrent with the epidemic of community-associated MRSA infections.)
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