Synopsis
Recognise superantigen-mediated shock, resuscitate organ failure, remove the toxin-producing focus and combine bactericidal therapy with specialist-directed toxin suppression.
- Toxic shock syndrome is a superantigen-driven clinical syndrome of fever, hypotension, rash or soft-tissue focus and multiorgan dysfunction.
- Staphylococcal disease often has diffuse sunburn-like erythroderma, mucosal hyperaemia, vomiting and later palm and sole desquamation; blood cultures may be negative.
- Streptococcal toxic shock commonly accompanies bacteraemia, severe focal pain, necrotising fasciitis or myositis and has high mortality.
- Do not wait for desquamation or full surveillance criteria before treating a clinically compatible shock syndrome.
- Remove the toxin source immediately: tampon, packing and infected device, or operative drainage and debridement of wound, uterus or deep soft tissue.
- Start broad bactericidal intravenous cover plus clindamycin toxin suppression after cultures without delaying sepsis treatment.
- Confirmed susceptible group A streptococcal disease is treated with benzylpenicillin 2.4 g every four hours plus clindamycin 1.2 g every six hours intravenously.
- Intravenous immunoglobulin is not routine; discuss selected refractory severe streptococcal toxic shock with critical care, infection specialists and transfusion services.
Key red flags
Hypotension, rising lactate, confusion, oliguria or hypoxaemia indicates established shock and organ failure.
Severe focal limb or wound pain can be the only early clue to invasive group A streptococcal necrosis.
Diffuse erythema with conjunctival or mucosal hyperaemia and shock suggests staphylococcal toxic shock.
Haemorrhagic bullae, skin anaesthesia, crepitus or rapidly spreading oedema requires immediate surgical exploration.
Tampon, nasal packing, wound packing, device or retained foreign material can maintain toxin production.
Postpartum, postoperative and varicella-associated disease require deliberate examination of concealed wounds and genital or uterine sources.
Fever, hypotension, generalised sunburn-like erythema and conjunctival, oral or vaginal hyperaemia suggests staphylococcal toxic shock.
Abrupt vomiting, diarrhoea, severe myalgia and headache can precede shock and rash, particularly in staphylococcal disease.
Intense limb, wound, pelvic or soft-tissue pain with swelling and early shock may indicate invasive group A streptococcal infection.
Acute kidney injury, thrombocytopenia, coagulopathy, hepatic injury, encephalopathy, respiratory failure and creatine-kinase elevation reflect systemic toxin injury.
Investigation priorities
Identify invasive streptococcal or staphylococcal bacteraemia before antibiotics.
Management branches
Fever, hypotension and compatible rash, focal pain or multiorgan dysfunction makes toxic shock plausible.
- Use ABCDE, provide oxygen when indicated, establish access, measure lactate and glucose, take blood cultures and begin physiology-guided crystalloid resuscitation.
- Start the local severe sepsis and toxic-shock intravenous regimen immediately, including high-dose clindamycin when streptococcal or staphylococcal toxin disease is suspected.
- Begin vasopressor and critical-care support promptly when hypotension persists and monitor urine output, perfusion, acid-base status and respiratory failure.
- Notify surgery, obstetrics, gynaecology, ENT or another source team immediately according to the likely concealed or deep focus.