そんなこんなで、蜂窩織炎 時々 復習
Cellulitis and erysipelas
Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth in the absence of underlying suppurative foci. Erysipelas has more distinctive anatomic features than cellulitis; erysipelas lesions are raised above the level of surrounding skin so that a clear line of demarcation between involved and uninvolved tissue is usually present.
Predisposing factors include disruption to the skin barrier as a result of trauma (such as penetrating wounds or injection drug use), inflammation (such as eczema or radiation therapy), preexisting skin infection (such as impetigo or tinea pedis), and edema (due to venous insufficiency).
The diagnosis of cellulitis is based upon clinical manifestations. Cultures are necessary only in patients with systemic toxicity, extensive skin involvement, underlying comorbidities, special exposures (animal bite, water-associated injury), or recurrent or persistent cellulitis.
The most common causes of cellulitis are beta-hemolytic Streptococcus (groups A, B, C, G, and F), and other pathogens include Staphylococcus aureus; gram-negative aerobic bacilli are identified in a minority of cases. Beta-hemolytic streptococci are the predominant cause of erysipelas.
Management of cellulitis and erysipelas should include supportive measures, such as elevation of the affected area and treatment of underlying predisposing conditions.
Patients with mild cellulitis may be treated with oral antibiotics. We recommend that patients with signs of systemic toxicity or erythema that has progressed rapidly should be treated initially with parenteral antibiotics (Grade 1B). Parenteral therapy is also appropriate for patients with persistence or progression of symptoms despite 48 to 72 hours of appropriate oral therapy.
Patients with nonpurulent cellulitis should be managed with empiric therapy for infection due to beta-hemolytic streptococci and methicillin-susceptible S. aureus (MSSA). Patients with nonpurulent cellulitis and additional risk factors for methicillin-resistant S. aureus (MRSA) should be managed with empiric therapy for infection due to beta-hemolytic streptococci and MRSA.
Patients with purulent cellulitis (eg, cellulitis associated with purulent drainage or exudate, in the absence of a drainable abscess) should be managed with empiric therapy for infection due to MRSA, pending culture results.
Treatment of cellulitis for neonates usually requires initial parenteral therapy. Therapy is usually administered for 7 to 10 days.
Patients with erysipelas and systemic manifestations (such as fever and chills) should be treated with parenteral therapy. Patients with mild infection or those who have improved following initial treatment with parenteral antibiotic therapy may be treated with oral therapy.
The duration of therapy should be individualized depending on clinical response. In general, 5 days of therapy is appropriate for patients with uncomplicated cellulitis whose infection has improved within this time period. Extension of the duration (up to 14 days) may be warranted in the setting of severe infection and/or slow response to therapy.
We suggest administration of suppressive antibiotic therapy for patients with recurrent cellulitis who have predisposing factors that cannot be alleviated (Grade 2B).
Group A streptococcal (GAS) bacteremia
Group A streptococcal (GAS) bacteremia occurs following development of infection at a primary site of infection; GAS bacteremia occurs most commonly in the setting of skin and soft tissue infection. Other forms of infection include pharyngitis, pneumonia, and postpartum endometritis, and toxic shock syndrome.
Streptococcal bacteremia is most common in the very young and in older adults, although infection may occur in patients of any age, and most patients are not immunosuppressed. Risk factors in adults under 40 include postpartum infection, intravenous drug use, and HIV infection.
The most common source of GAS bacteremia in adults is skin and soft tissue infection, including cellulitis, erysipelas, pyoderma, injection drug use, burns, varicella virus infection, necrotizing fasciitis, and spontaneous gangrenous myositis. Deep soft tissue infections may also be associated with shock and organ failure.
Treatment of GAS bacteremia requires a multidisciplinary approach including antibiotic management, surgical debridement (if warranted), and management of septic physiology (if present).
We recommend penicillin G (4 million units intravenously every four hours in patients with normal renal function) and clindamycin (900 mg intravenously every eight hours) for treatment of GAS bacteremia (Grade 1C). Clinical failures of penicillin therapy for streptococcal infections do occur; in these settings, clindamycin is especially useful, both because its efficacy is not affected by inoculum size or stage of growth and because it suppresses toxin production.
The duration of antibiotic therapy for GAS bacteremia should be individualized.
We suggest the use of intravenous immune globulin in patients with invasive GAS infections who develop signs of shock.
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