Necrotizing Fasciitis

Pathogenesis: Infection, either apparent or inapparent, results from a breach in integrity of the skin or mucous membrane barriers and can be associated with malignancy, a diverticulum, hemorrhoids, or an anal fissure.
- - In the case of infections with no obvious portal of entry, transient bacteremia is thought to seed sites of nonpenetrating trauma (e.g., bruise, muscle strain).
- - Infection spreads to the deep fascia and along fascial planes through venous channels and lymphatics.
Microbiology: Necrotizing fasciitis is caused by S. pyogenes, mixed aerobic and anaerobic bacteria, or Clostridium perfringens; methicillin-resistant S. aureus (MRSA) strains that produce the Panton-Valentine leukocidin have also been reported as an occasional cause.
Clinical manifestations: The timing of cutaneous manifestations (e.g., violaceous bullae; friable, necrotic skin; induration; brawny edema) depends on whether the infection began superficially (rapid onset) or in deeper structures (slower onset).
- - Early in the disease course, severe pain and unexplained fever may be the only findings.
- - Thrombosis of blood vessels in dermal papillae leads to ischemia of peripheral nerves and anesthesia of the affected area.
- - In later stages, pts appear toxic and often develop shock and multiorgan failure.
Diagnosis: Diagnosis is based on clinical presentation. Other findings may include gas detected in deep tissues by imaging studies (particularly with clostridial species but rarely with S. pyogenes) and markedly elevated serum CPK levels (in the case of concomitant myositis).
Treatment: Emergent surgical exploration to deep fascia and muscle, with removal of necrotic tissue, is essential. Table 84-1 provides recommendations for adjunctive antibiotic therapy.

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