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This infection causes rapid necrosis and liquefaction of fascia, muscle, and tendon. Most cases involve Clostridium perfringens; Streptococcus pyogenes accounts for most of the remaining cases. Myonecrosis is classically associated with trauma (including surgery) and diabetes. There is edematous bronze or purple discoloration, flaccid bullae with watery brown nonpurulent fluid, and a foul odor. The classic presentation is pain out of proportion to physical findings. Systemic signs are also typically present and may develop rapidly into shock.
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Crepitus and appearance of gross air pockets in the tissue are appreciated but may not be present early. The incubation period for clostridia ranges between 1 and 4 days, but can be as early as 6 hours. Decreased tissue oxygen tension and wound contamination are required for the infection to progress. Crepitant cellulitis, synergistic necrotizing cellulitis, acute streptococcal hemolytic gangrene, and streptococcal myositis are some conditions that may be mistaken for clostridial myositis. Often, surgical exploration of the fascia and muscle is required to make the correct diagnosis.
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Management and Disposition
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Treatment includes aggressive resuscitation, broad-spectrum antibiotics (including clindamycin), and tetanus prophylaxis. Surgical debridement or amputation is the mainstay of therapy. Hyperbaric oxygen may have a synergistic effect in preventing the progression of infection and toxin production.
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Shock and multiorgan failure may be rapidly progressive. Mortality is 80% to 90% if untreated and 10% to 25% when treated appropriately.
Clindamycin may improve survival by inhibiting toxin production.
Gram stain of gram-positive bacilli with a relative lack of leukocytes may rapidly confirm suspected clostridial myonecrosis.
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