Necrotizing fasciitis

Author: Faculty Reviewer:

Publish date: Posted on
Last updated: April 1, 2021

Keywords #

necrotizing fasciitis
necrotizing soft tissue infection

Diagnosis #

Necrotizing fasciitis (NF) is a severe infection of the deep soft tissue including the muscular fascia, subcutaneous tissue, and overlying skin.[1] Also known as “flesh-eating bacteria syndrome,” it is a limb- and life-threatening diagnosis with a reported mortality rate ranging from 20-40%.[2,3] NF typically begins with a breach in the epidermal surface and development of severe pain out of proportion to physical exam findings. This eruption quickly reveals shiny, tense red erythema and edema, then violaceous/grey discoloration.[4] Bullae and subcutaneous emphysema (“gas gangrene”) may also be present and systemic symptoms—such as fever—are common. The infection is classified according to the underlying organism(s):[4,5]

Type I: Polymicrobial, with various gram-positive cocci, gram-negative rods, and at least one anaerobic organism (especially Clostridium spp.)

  • Most common class of NF
  • Affects the trunk and perineum
  • Patients are often older and with more medical comorbidities (e.g. immunosuppression, diabetes)

Type II: Monomicrobial, most commonly with Group A Streptococcus (GAS).

  • Classically affects the extremities
  • Affects more healthy/immunocompetent adults
  • Patients often with history of trauma, surgery, or IV drug use (IVDU)
  • Associated with toxic shock syndrome
  • Some categorize monomicrobial infections further: classifying gram-negative marine organisms as Type III, classically Vibrio vulnificus, and fungal organisms as Type IV.[6]
Key Concepts #
  • NF is a life-threatening infection of the fascia that rapidly progresses to necrosis of the overlying skin and subcutaneous tissue
  • Signs and symptoms include severe pain, fever, erythema and/or purple discoloration of the wound, bullae, and subcutaneous emphysema
  • Hyponatremia and leukocytosis are common laboratory findings
  • Risk factors include immunosuppression, diabetes, obesity, alcoholism, IVDU, peripheral artery disease, chronic kidney disease, cirrhosis, and malignancy; however, NF also affects young and healthy patients
  • Early diagnosis and treatment with IV antibiotics and surgical debridement is critical
Epidemiology #

NF is a relatively rare diagnosis, with an incidence of approximately 1,000 cases per year (0.04 cases per capita) in the United States.[7]

Clinical Features #
  • The common signs and symptoms of NF at the time of admission include erythema, pain/tenderness beyond the margins of erythema, swelling, fever, bullae, hypotension, crepitus, skin necrosis, induration, and fluctuance.[5]
  • Infections with Clostridial species may also present with subcutaneous emphysema.
  • Hyponatremia and leukocytosis are the most common lab abnormalities.[8]
  • NF tends to affect the limbs, trunk and genitalia—the latter termed Fournier gangrene. Necrotizing head and neck infections may also occur.[1]
  • Early NF may appear clinically similar to cellulitis, erysipelas, or abscess; however, NF can be differentiated from these conditions by the presence of bullae or blisters, degree of associated pain, and rapid progression.[2,5]
  • Prompt diagnosis of NF is critical due to its propensity for rapid escalation to sepsis and multiorgan failure.
Differential Diagnoses #
  • Myonecrosis
  • Pyomyositis
  • Phlebitis
  • Deep vein thrombosis
  • Hematoma formation and neutrophilic dermatoses (such as necrotizing Sweet’s syndrome and pyoderma gangrenosum). The latter is important to recognize as surgical intervention may lead to significant morbidity related to pathergy. [2,5]

Diagnostic Workup #

The diagnosis of NF is traditionally made clinically, with the “gold standard” for diagnosis being operative exploration.[5] Frank tissue necrosis, malodorous discharge, and easily dissectible fascia are all suggestive of NF. Intraoperative biopsy and gram stain may be utilized in the case of any uncertainty.

Laboratory findings may also prove useful in the diagnosis of NF. One study reported Na < 135 with WBCs > 15,400 has positive and negative predictive values of 80% for detecting NSTI.[8] More recently, a scoring system (“Laboratory Risk Indicator for Necrotizing Fasciitis”, LRINEC) for diagnosing NF has been developed using the variables C-reactive protein, WBC count, hemoglobin, sodium, creatinine, and glucose.[9]

Plain x-ray, CT, and MRI are all capable of detecting some features of NF, but with low sensitivity and/or low specificity.[5] Plain x-ray may detect subcutaneous emphysema but not deeper fascial gas; furthermore, subcutaneous emphysema is present in only a minority of patients. CT can detect inflammatory changes (e.g., fascial thickening) in addition to subcutaneous emphysema, with a reported 80% sensitivity for detecting necrotizing soft tissue infections (NSTIs) in general.[10] MRI has a reported 90-100% sensitivity and 50-85% specificity for detecting NSTIs, but MRI is often not feasible in critically ill patients.[11]

Treatment #

The mainstay treatments for NF are early and aggressive surgical debridement, IV antibiotics, and critical care.[9] Surgical intervention is critical as a delay in time to debridement is associated with an increase in mortality rate.[12] IV antibiotic therapy should empirically cover broadly including streptococci, staphylococci, gram-negative bacilli and anaerobes.[5] Of note, clindamycin is a useful agent due to its inhibitory effects on toxin synthesis by GAS. Antibiotics are generally narrowed according to culture results and continued until systemic signs of infection resolve and no additional surgical debridement is needed. Additional treatment modalities for NF include IV immune globulin (IVIG) and hyperbaric oxygen therapy; however, their role and efficacy remain poorly studied and controversial.

References #
  1. Salcido RS. (2007) Necrotizing fasciitis: reviewing the causes and treatment strategies. Adv Skin Wound Care. 20(5): 288-93.
  2. Levine EG, Manders SM. (2005) Life-threatening necrotizing fasciitis. Clin Dermatol. 23(2): 144-7.
  3. McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. (1995) Determinants of mortality for necrotizing soft-tissue infections. Ann Surg. 221(5): 558-65.
  4. Hakkarainen TW, Kopari NM, Pham TN, Evans HL. (2014) Necrotizing soft tissue infections: review and current concepts in treatment, systems of care, and outcomes. Curr Probl Surg. 51(8): 344-362.
  5. Sarani B, Strong M, Pascual J, Schwab CW. (2009) Necrotizing fasciitis: current concepts and review of the literature. J Am Coll Surg. 208(2): 279-88.
  6. Howard RJ, Pessa ME, Brennaman BH, Ramphal R. (1985) Necrotizing soft-tissue infections caused by marine vibrios. Surgery. 98(1): 126-30.
  7. Simonsen SME, Van Orman ER, Hatch BE, Jones SS, Gren LH, Hegmann KT, Lyon JL. (2006) Cellulitis incidence in a defined population. Epudemiol Infect. 134(2): 293-299.
  8. Wall DB, de Virgilio C, Black S, Klein SR. (2000) Objective criteria may assist in distinguishing necrotizing fasciitis from nonnecrotizing soft tissue infection. Am J Surg. 179(1): 17-21.
  9. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. (2004) The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 32(7): 1535-41.
  10. Wysoki MG, Santora TA, Shah RM, Friedman AC. (1997) Necrotizing fasciitis: CT characteristics. Radiology. 203(3): 859-63.
  11. Schmid MR, Kossmann T, Duewell S. (1998) Differentiation of necrotizing fasciitis and cellulitis using MR imaging. AJR Am J Roentgenol. 170(3): 615-20.
  12. Bilton BD, Zibari GB, McMillan RW, Aultman DF, Dunn G, McDonald JC. (1998) Aggressive surgical management of necrotizing fasciitis serves to decrease mortality: a retrospective study. Am Surg. 64(5): 397-401.