Toxic shock syndrome

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Epidemiology

1-2/100,000 cases/yr


Etiology

S. aureus strain that produces toxic shock syndrome toxin-1 (superantigen)

Superantigens stimulate T-cell proliferation independent of antigen-specific binding --> massive cytokine production

Also effect neutrophil chemotaxis suppression, blockage of reticuloendothelial system


RF

postop pts, nasal packing, abscess, burns, tampons...IUDs!

Definition

I. Fever: temperature >38.9°C

II. Rash: diffuse macular erythroderma

III. Hypotension: systolic blood pressure <90 mm Hg (adults) or <5th percentile for age (children younger than 16 years), or orthostatic hypotension, dizziness, or syncope

IV. Multisystem dysfunction: at least 3:

    A. Gastrointestinal: vomiting or diarrhea at onset of illness
    B. Muscular: severe myalgias, or serum creatine phosphokinase level (CPK) greater than twice the upper limit of normal
    C. Mucous membranes: vaginal, oropharyngeal, or conjunctival hyperemia
    D. Renal: blood urea nitrogen or creatinine level greater than twice the upper limit of normal, or pyuria (5 leukocytes per high-power field), in the absence of urinary tract infection
    E. Hepatic: total serum bilirubin or transaminase level greater than twice the upper limit of normal
    F. Hematologic: platelets<100,000/L
    G. Central nervous system: disorientation or alteration in consciousness but no focal neurologic signs at a time when fever and hypotension are absent.

V. Desquamation: One to 2 weeks after the onset of illness (typically palms and soles)

VI. Evidence against an alternative diagnosis: If obtained:

    1. negative culture results for blood, throat, or cerebrospinal fluid
    2. absence of an increase in antibody titers to the agents of leptospirosis, measles, or Rocky Mountain spotted fever.


  • “Confirmed” case meets all 6 criteria; “probable” case meets 5 of the 6.

†Blood culture may be positive for S aureus.


Treatment

Abx, including Clindamycin, Vanc

Supportive, pressors often


Source

AnnalsofEM Nov 2009