Cellulitis

Empiric treatment of Cellulitis

Cellulitis

Cellulitis is an inflammation of the subcutaneous tissue characterized by invasion without definite localization. Thin exudate spreads through the cleavage planes of tissue spaces. It usually involves the extremities and identifiable portal of entry is detectable. The most common etiologic organisms are Beta hemolytic streptococci, Staphylococci, Clostridium perfringens.

The invasiveness of this organism is due to the production of hyaluronidase and streptokinase, which dissolve the intercellular matrix and the fibrin inflammatory barrier respectively. Characteristically, the skin is dark red with local oedema and heat; it blanches on pressure. There may be vesicles and, in severe cases, cutaneous gangrene. Cellulitis is often accompanied by lymphangitis and lymphadenitis, and there may be an associated septicaemia.

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Clinical Features

There is usually an identifiable portal of entry which can be a surgical wound, puncture site, skin ulcer or dermatitis. Other features include:

  • Local signs of inflammation, which may be very intense
  • Poorly defined brown-red edema
  • Blebs and bullae in severe cases; tissue destruction and ulceration may follow
  • Central necrosis and suppuration may occur late in some complicated cases
  • Systemic signs of bacteremia and toxemia due to spread and toxin release

Empiric treatment

The bacterial etiology of cellulitis depends on the location of the infection and any special exposures associated with its cause. For example, cellulitis following exposure of a wound to salt water suggests Vibrio vulnificus as an etiology. Cellulitis associated with foot ulcers in diabetic patients is caused by a mixture of aerobic gram-positive, aerobic gram-negative, and anaerobic bacteria.

However, most cellulitis cases in immunocompetent hosts result from inoculation of skin organisms through breaks or disruption in the epidermis. Thus, uncomplicated cellulitis in an immunocompetent patient without a history of unusual exposures is usually caused by Staphylococcus aureus, Streptococcus pyogenes, or other streptococci.

Because it is difficult to determine the specific bacterial etiology of cellulitis in individual patients, treatment is usually empiric and consists of agents with potent activity against gram-positive bacteria. The increasing resistance of Staphylococcus aureus and Streptococcus pyogenes to antibiotics, however, has complicated treatment choices.

In general, severe infections should be treated in the hospital with intravenous antibiotics, whereas mild-to-moderate infections may be treated with oral antibiotics in the outpatient setting. In regions where methicillin-resistant Staphylococcus aureus (MRSA) is common or when other risk factors for this pathogen are present (e.g., previous MRSA infection, recent antibiotic therapy), parenteral options include glycopeptides (vancomycin, telavancin), linezolid, daptomycin, tigecycline, and ceftaroline. Doxycycline, trimethoprimsulfamethoxazole, linezolid, and clindamycin are oral agents that can be used. If the likelihood of MRSA is low, suitable choices for parenteral therapy include antistaphylococcal penicillins (nafcillin, oxacillin), first-generation cephalosporins (cefazolin), or clindamycin.

Oral agents include dicloxacillin, oral first-generation cephalosporins (cephalexin, cefadroxil), clindamycin, or a macrolide (azithromycin, clarithromycin, erythromycin). In all situations, the actual choice should be guided by local resistance patterns.

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