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Emergency and Acute Medicine – Toxic Shock Syndrome (TSS)
Toxic shock syndrome (TSS) is a severe, acute, life-threatening illness caused by toxin-producing bacteria, most commonly Staphylococcus aureus and less commonly Group A Streptococcus (referred to as streptococcal toxic shock syndrome, STSS). These organisms produce exotoxins such as toxic shock syndrome toxin (TSST-1) and streptococcal pyrogenic exotoxins, which act as superantigens. These toxins trigger massive cytokine release, leading to fever, immune dysregulation, and profound vasodilation with capillary leak, ultimately resulting in hypotension and shock.
The etiology of TSS has evolved over time. Initially associated with menstruating women using highly absorbent tampons, modern cases are now frequently nonmenstrual. These include infections related to surgical wounds, postpartum infections, burns, nasal packing, mastitis, osteomyelitis, and soft tissue infections. Many individuals are asymptomatic carriers of S. aureus in areas such as the nasal passages, skin, or genital tract. In streptococcal TSS, infection often follows minor trauma and may present with severe pain even before visible signs of infection appear.
Clinically, TSS is diagnosed using criteria established by the CDC. Patients typically present with high fever (>38.9°C), hypotension, and a diffuse blanching macular erythroderma rash. This rash is followed 1–2 weeks later by desquamation, especially of the palms and soles. Multisystem involvement is a hallmark and includes gastrointestinal symptoms (vomiting, diarrhea), musculoskeletal involvement (severe myalgias or elevated creatine phosphokinase), mucosal hyperemia (conjunctival, oral, or vaginal), renal dysfunction, hepatic involvement, hematologic abnormalities such as thrombocytopenia, and central nervous system symptoms including confusion or hallucinations.
Streptococcal TSS differs slightly in presentation and diagnostic criteria. It requires isolation of Group A Streptococcus from a sterile site, hypotension, and evidence of organ dysfunction such as renal failure, coagulopathy, liver dysfunction, acute respiratory distress syndrome, or soft tissue necrosis. A key distinguishing feature is severe pain, often out of proportion to physical findings, which may indicate deep soft tissue infection such as necrotizing fasciitis.
Laboratory findings are nonspecific but reflect systemic inflammation and organ dysfunction. These may include leukocytosis or leukopenia, elevated creatinine and liver enzymes, thrombocytopenia, electrolyte abnormalities (such as hypocalcemia), and elevated creatine phosphokinase. Cultures from blood or suspected infection sites should be obtained, although blood cultures are not always positive in staphylococcal TSS. Imaging such as chest radiography or CT may help identify the source of infection or complications.
The differential diagnosis includes Kawasaki disease, Scarlet fever, Stevens-Johnson syndrome, Rocky Mountain spotted fever, and meningococcemia. Differentiation is essential because management strategies differ significantly.
Management of TSS is a medical emergency and focuses on rapid stabilization and source control. Prehospital care includes airway management, IV access, and fluid resuscitation. In the emergency department, aggressive management of shock is critical, often requiring large volumes of intravenous fluids (up to 4–20 L in the first 24 hours). If hypotension persists, vasopressors such as norepinephrine or dopamine are initiated.
Identifying and removing the source of infection is essential, such as removing tampons, nasal packing, or infected wound material. Early surgical consultation is necessary if drainage or debridement is required, particularly in cases of suspected necrotizing infection.
Antibiotic therapy should be initiated promptly. Regimens typically include clindamycin or linezolid to suppress toxin production, combined with agents such as vancomycin for broad coverage. For confirmed methicillin-sensitive S. aureus, oxacillin or nafcillin may be used. In streptococcal TSS, broader-spectrum regimens including beta-lactams and clindamycin are recommended. Intravenous immunoglobulin (IVIG) may be considered, particularly in streptococcal TSS or refractory shock.
All patients with TSS require hospital admission, and most require intensive care due to the risk of rapid progression to multiorgan failure.
Key clinical pearls include recognizing the combination of fever, rash, hypotension, and multisystem involvement, and initiating aggressive supportive care immediately. Early antibiotic therapy, toxin suppression, and prompt source control are critical for survival.
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