Toxic Shock Syndrome (TSS)

Source control is the operation - You will usually meet TSS on the way to an emergent debridement, washout, or removal of a retained foreign body. Pulling the source (tampon, nasal packing, infected wound) and debriding devitalized tissue is the treatment, and early surgical management is what changes outcome. Don't let the workup delay the incision.

This is vasoplegia, not just hypovolemia - Cytokine-driven systemic vasodilation plus capillary leak. Aggressive crystalloid comes first; norepinephrine is the recommended first-line pressor for shock that stays refractory after fluid. Target a MAP above 65 mmHg, the approximate critical perfusion pressure for heart and kidney, and follow lactate and ScvO2 rather than blood pressure alone.

Send an ionized calcium - Life-threatening hypocalcemia runs throughout this disease and has to be repleted. Recheck it after citrate-containing blood products, because low ionized calcium worsens exactly the vasoplegia and myocardial depression you are already fighting.

Coagulopathy gates regional - Anemia, thrombocytopenia, and prolonged coagulation times are common, and platelets under 100,000 is one of the CDC multisystem criteria. Get a CBC and coagulation studies before you consider neuraxial, and before a lumbar puncture if one is being discussed for altered mental status.

The airway mucosa is part of the syndrome - Mucous membrane hyperemia, strawberry tongue, and conjunctival erythema are diagnostic features, so expect swollen, friable oropharyngeal tissue. Instrument gently and have a smaller tube within reach.

Full stomach every time - Vomiting and diarrhea are part of the multisystem criteria and these patients arrive emergently. RSI.

Look at the CK before reaching for succinylcholine - Creatine phosphokinase greater than twice the upper limit of normal is one of the CDC criteria. Where rhabdomyolysis is in the picture, use rocuronium rather than succinylcholine to avoid a hyperkalemic response.

Clindamycin is the one that matters - Broad-spectrum coverage goes in after cultures, and most institutions add vancomycin or linezolid for MRSA. Clindamycin is added specifically to suppress toxin production and improves outcomes when included, but it is bacteriostatic and never goes alone. Initial therapy also covers gram-negatives, since you cannot tell early whether the infection is polymicrobial.

IVIG for shock that outlives your pressors - IVIG neutralizes circulating toxin. Optimal dosing is not established, but high dose at 2 g/kg is accepted, and observational data show reduced mortality compared with antibiotics alone.

Skip the steroids - Corticosteroids are not currently recommended as adjunctive therapy in TSS. An older study showed reduced illness severity but no mortality benefit. Don't reach for them the way you might in refractory septic shock.

Renal and hepatic dysfunction change your dosing - BUN or creatinine and bilirubin or transaminases at twice the upper limit of normal are part of the case definition. Assume prolonged effect from renally cleared drugs and titrate to effect.

Plan on the ICU - All of these patients get admitted to intensive care. Plan to leave them intubated and hand off to an intensivist; infectious disease and surgery will both already be involved.

Toxic shock syndrome (TSS) is an acute toxin-mediated illness defined by fever, hypotension, a sunburn-like rash, and end-organ damage. It is caused by superantigen-producing Staphylococcus aureus or group A Streptococcus (Streptococcus pyogenes). Superantigens bypass the normal pathway for T-cell activation and drive massive cytokine release, so the patient loses vascular tone and leaks intravascular volume through the capillaries at the same time.

Classically tied to high-absorbency tampons, but non-menstrual sources now matter just as much: post-surgical wound infections, abscesses, burns, retained nasal packing, dialysis catheters, necrotizing fasciitis. Staphylococcal TSS usually follows a localized infection; streptococcal TSS follows bacteremia, cellulitis, or necrotizing fasciitis. Onset is fast, and the difference matters for how worried you are: streptococcal case fatality can exceed 50%, non-streptococcal is under 3%.