Complicated infections are:
- Those involving deeper soft tissues necessitating surgical intervention, such as infected ulcers, burns, major abscesses, or an underlying disease state that complicates the response to treatment (eg, peripheral arterial disease, chronic kidney disease, diabetes mellitus)
- Superficial infections or abscesses in sites, such as the rectal area, where the risk of anaerobic or gram-negative pathogen involvement is higher.
- Overall, Staphylococcus aureus is the pathogen most frequently isolated from complicated SSTIs.
- This pathogen typically is associated with the production of virulence factors not common to methicillin-sensitive S. aureus (MSSA) isolates or to hospital-associated HA-MRSA isolates, including the Panton-Valentine leukocidin (PVL) toxin.
- These superficially spreading infections involving the skin are caused almost exclusively by β-hemolytic streptococci.
- Antibiotic therapy: for moderate to severe infections, parenteral penicillin is the agent of choice (1C).
- Treatment failures may occur if β-lactam agents are used alone in severe cases (1C).
- Protein synthesis-inhibitory agents alone—eg, clindamycin or a macrolide— or in combination with cell wall-active agents should be given in severe cases (1B/C).
- Increasing macrolide resistance among streptococci introduces concern about the value of these agents (1C).
- Other regimens that may be considered are antistaphylococcal penicillins, cefazolin, and ceftriaxone (2B/C).
- Simple abscesses may respond to incision and drainage (I&D) alone (2B).
- More complex abscesses and those with substantial cellulitis require adjuvant antibiotic therapy (1C).
- Inadequate response to therapy should prompt evaluation of the adequacy of drainage (1C).
- Empiric antibiotic therapy should be directed toward the most likely pathogens (1B).
- Agents directed at CA-MRSA should be considered in most settings (1B).
- Suspected polymicrobial infections should be managed with coverage of enteric gram-negative and anaerobic pathogens (1B).
Necrotizing Skin and Soft Tissue Infections
- Delays in diagnosis increase both the morbidity and the mortality rate (1C).
- The presence of gas in soft tissues is specific for necrotizing infections and more sensitive than physical examination (1C).
- Computed tomography and MRI improve the detection of soft tissue gas (1B).
- Radiographic findings of tissue fluid and edema are neither sensitive nor specific for necrotizing infection (1C).
- Clinical features strongly suggestive of necrotizing infection (1C):
- pain disproportionate to the findings at physical examination
- tense edema
- skin ecchymosis/necrosis
- cutaneous anesthesia
- systemic toxicity
- progression despite antibiotic therapy
- Laboratory values predictive of the presence of necrotizing infection (1C):
- white blood cell (WBC) count >14×109/L
- serum sodium concentration <135 mmol/L
- blood urea nitrogen (BUN) concentration >15 mg/dL
- Early appropriate antibiotic coverage of inciting pathogens is indicated (1C).
- Timely surgical debridement improves outcome (1C).
- Although no randomized or important non-randomized studies in NSTIs exist to direct therapy specifically, adequate surgical debridement of involved tissue is confirmed to improve the outcome (1C).
- Frequent re-evaluation or return to the operating room within 24 hours should be undertaken to ensure adequacy of debridement and lack of progression (1C).
- Empiric antibiotic therapy should be directed toward the likely pathogens (1C). The likely pathogens differ depending on the clinical setting, inciting pathophysiology, and previous exposure to antibiotics (1C).
- Necrotizing infections are more frequently polymicrobial and may involve aerobic and anaerobic gram-positive and gram-negative pathogens (1C).
- Assuming that relevant pathogens are covered appropriately, several single-agent regimens probably are effective, including imipenem/cilastatin, meropenem, ertapenem, piperacillin/tazobactam, ticarcillin/clavulanic acid, tigecycline, and minocycline (2C).
- Increasing resistance of gram-negative bacilli to ampicillin/sulbactam raises concern about the use of this agent unless local sensitivities are known (1C).
- Numerous combinations of agents probably are equally effective in the treatment of NSTIs provided appropriate coverage of relevant pathogens is ensured (2C).
Rapidly Progressive Soft Tissue Infections
More rapidly progressive soft tissue infections can be caused by a variety of virulent pathogens characterized by significant toxin production including:
- S. pyogenes, Clostridial species, CA-MRSA, Vibrio and Aeromonas spp., and S. aureus species that produce toxic shock syndrome toxin 1 (TSST-1).
All these infections require early and aggressive antibiotic therapy and surgical debridement and drainage (1C).
Combination therapy that includes protein synthesis inhibitory agents to which the organism is sensitive should be provided (1C).