Necrotizing Soft Tissue Infection
(Necrotizing Cellulitis or Fasciitis; Necrotizing Subcutaneous Infection)
Necrotizing soft tissue infection (NSTI) is typically caused by a mixture of aerobic and anaerobic organisms that cause necrosis of subcutaneous tissue, usually including the fascia. This infection most commonly affects the extremities and perineum. Affected tissues become red, hot, and swollen, resembling severe cellulitis, and pain develops out of proportion to clinical findings. Without timely treatment, the area becomes gangrenous. Patients are acutely ill. Diagnosis is by history and examination and is supported by evidence of overwhelming infection. Treatment involves antibiotics and surgical debridement. Prognosis is poor without early, aggressive treatment.
(See also Overview of Bacterial Skin Infections.)
There are three subtypes of NSTI. Type I NSTI, typically involving the torso and perineum, results from infection with group A streptococci (eg, Streptococcus pyogenes) as part of a polymicrobial infection or a mixture of aerobic and anaerobic bacteria (eg, Bacteroides sp). These organisms typically extend to subcutaneous tissue from a contiguous ulcer or infection, or after trauma. Streptococci can arrive from a remote site of infection via the bloodstream. Perineal involvement (also called Fournier gangrene) is usually a complication of recent surgery, perirectal abscess, periurethral gland infection, or retroperitoneal infection resulting from perforated abdominal viscera. Patients with diabetes are at particular risk of Type I NSTI.
Type II NSTI is caused by group A beta-hemolytic streptococci alone or together with staphylococcus. Patients tend to be younger with few documented health problems but may have a history of IV drug use, trauma, or recent surgery. The infection has the potential for rapid local spread and systemic complications such as toxic shock.
Type III NSTI is usually associated with aquatic injuries sustained in warmer coastal areas. Vibrio vulnificus is the usual pathogen. Type III infections share clinical similarities to Type II infections and may spread rapidly.
NSTI causes tissue ischemia by widespread occlusion of small subcutaneous vessels. Vessel occlusion results in skin infarction and necrosis, which facilitates the growth of obligate anaerobes (eg, Bacteroides) while promoting anaerobic metabolism by facultative organisms (eg, Escherichia coli), resulting in gangrene. Anaerobic metabolism produces hydrogen and nitrogen, relatively insoluble gases that may accumulate in subcutaneous tissues.
The primary symptom is intense pain. In patients with normal sensation, pain out of proportion to clinical findings may be an early clue. However, in areas denervated by peripheral neuropathy, pain may be minimal or absent. Affected tissue is red, hot, and swollen and rapidly becomes discolored. Bullae, crepitus (resulting from soft-tissue gas), and gangrene may develop. Subcutaneous tissues (including adjacent fascia) necrose, with widespread undermining of surrounding tissue. Muscles are spared initially. Patients are acutely ill, with high fever, tachycardia, altered mental status ranging from confusion to obtundation, and hypotension. Patients may be bacteremic or septic and may require aggressive hemodynamic support. Streptococcal toxic shock syndrome may develop.
Diagnosis, made by history and examination, is supported by leukocytosis, soft-tissue gas on x-ray, positive blood cultures, and deteriorating metabolic and hemodynamic status.
NSTI must be differentiated from clostridial soft-tissue infections, in which cellulitis, myositis, and myonecrosis often occur. Such infections are anaerobic. Anaerobic cellulitis produces lots of gas but little pain, edema, or change in skin; it very seldom travels into the muscle. Necrotizing myositis manifests with fever, pain, and muscle swelling without early skin changes; later, skin may develop redness, warmth, purpura, and bullae.
Treatment of early NSTI is primarily surgical, which should not be delayed by diagnostic studies. IV antibiotics are adjuncts, usually including 2 or more drugs, but regimens vary depending on results of Gram stain and culture (eg, penicillin G 4 million units q 4 h combined with clindamycin 600 to 900 mg q 8 h or ceftriaxone 2 g q 12 h). Evidence of bullae, ecchymosis, fluctuance, crepitus, and systemic spread of infection requires immediate surgical exploration and debridement. The initial incision should be extended until an instrument or finger can no longer separate the skin and subcutaneous tissue from the deep fascia. The most common error is insufficient surgical intervention; repeat operation every 1 to 2 days, with further incision and debridement as needed, should be carried out routinely. Amputation of an extremity may be necessary.
IV fluids may be needed in large volumes before and after surgery. Antibiotic choices should be reviewed based on Gram stain and culture of tissues obtained during surgery. Adjuvant hyperbaric oxygen therapy may also be of benefit; however, evidence of its effectiveness is inconclusive. IV immune globulin has been suggested for streptococcal toxic shock syndrome with NSTI.
NSTI can develop from a contiguous ulcer or infection, hematogenous spread, or after trauma.
Consider NSTI in patients with characteristic findings or pain out of proportion to clinical findings, particularly patients with diabetes or other risk factors.
Arrange surgical therapy while instituting IV fluid and antibiotic therapy and without delaying for testing.
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