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The two classic toxic shock syndromes are attributed to Staphylococcus aureus or to group A Streptococcus (Streptococcus pyogenes). Each is a life-threatening illness stemming from toxin production by gram–positive organisms, creating hemodynamic compromise and fulminant multiorgan dysfunction. This cascade makes diagnosis a challenge, with the features looking like the more common entities of sepsis and septic shock. Characteristic epidemiology, pathophysiology, clinical presentations, and management strategies set these syndromes apart (Table 150–1). Early recognition and definitive treatment are the keys to improving patient outcomes.
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STAPHYLOCOCCAL TOXIC SHOCK SYNDROME
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INTRODUCTION AND EPIDEMIOLOGY
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Staphylococcal toxic shock syndrome (TSS) was first described in 1978 in a series of seven children presenting with systemic illness punctuated by fever, headache, confusion, vomiting, diarrhea, scarlatiniform rash, desquamation, hypotension, and multiorgan dysfunction.1 A toxigenic strain of S. aureus isolated from mucosal (nasopharyngeal, tracheal, vaginal) and sequestered sites (abscess, empyema) in five of the patients was the causative organism. During the early 1980s, TSS was linked to tampon use in young menstruating women,2,3 with incidence rates as high as 13.7 per 100,000 menstruating women between the ages of 15 and 24.4 Education on the proper frequency and duration of use of tampons coupled with the removal of highly absorbent tampons from the market are widely credited with reducing menstrual TSS rates, although tampon use remains an important risk factor for menstrual TSS to this day in the United States, Canada, and Western Europe.
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Nonmenstrual TSS is associated with a wide range of skin and soft tissue infections including abscesses, cellulitis, mastitis, and infected surgical and postpartum wounds, including vaginal and cesarean deliveries.5 Sinusitis and superimposed infections of burns, abrasions, and varicella lesions have been described in other cases, particularly in children. Patients with influenza may develop TSS in the setting of secondary S. aureus respiratory tract infections (e.g., pneumonia, tracheitis).6 Because the vagina and nares are known sites of S. aureus colonization, retained foreign bodies, including female barrier contraceptives (e.g., diaphragm, contraceptive sponge) and nasal packing material, are risk factors for developing nonmenstrual ...