Toxic Shock Syndrome

Syndrome of severe distributive shock and generalised inflammation that occur secondary to bacterial endotoxin that is produced by some:

Streptococcal and staphylococcal toxic shock syndromes are similar enough to be merged. An overview of these pathogens can be found Streptococci and Staphylococci.

Epidemiology and Risk Factors

General Risk factors:

  • Immunocompromise
  • Pregnancy

Streptococcal toxic shock:

  • Infections
    • Pneumonia
    • Necrotising fasciitis

Staphylococcal toxic shock:

  • Infections
    • Surgical wound
    • Mastitis
    • Sinusitis
    • Osteomyelitis
    • Burns
  • Tampon use
    • Prolonged use of same tampon
    • High-absorbency tampons
    • Within 2 days of menstruation

Pathophysiology

Bacteria secrete endotoxin:

Most people develop antibodies to bacterial endotoxin, TSS occurs in non-immune individuals.

  • Bind to T-cell Major Histocompatibility COmplex
  • Stimulates T-lymphocyte response
    Up to 20% of T-cells may respond, compared to ~0.01% that usually respond to antigens.
  • Leads to massive T-cell activation and large release of T-cell cytokines, in particular:
    • IL-2
    • Interferon-γ
    • TNF-α

Aetiology

Streptococcal toxic shock occurs with invasive streptococcal infection, including:

  • Pneumonia
  • Septic arthritis
  • Peritonitis
  • Obstetric
    • Endometritis
    • Chorioamnionitis
    • Mastitis

Staphylococcal toxic shock syndrome occurs with:

  • Colonisation:
    • Menstrual (~50%)
      Tampon colonisation.
    • Non-menstrual
      • Nasal packing
      • IUD
      • Wounds
        Uninfected wounds can be still colonised with S. Aureus, and be a source of toxic shock.
  • Invasive infection:
    • Pneumonia
    • Soft tissue infection
  • Colonisation without infection

Clinical Manifestations

Diagnostic features:

  • Inflammatory syndrome
    • Fever ⩾39°C
    • Chills
    • Headache
    • Myalgia
    • Sore throat
  • Skin findings
    • Diffuse macular erythrodermic rash
      Sunburn to bright erythema.
    • “Strawberry tongue”
    • Desquamation
      Of palms and soles. Late finding.
  • Multiorgan failure

Suggestive features:

  • Rapid onset
  • Disproportionate:
    • No obvious source with staphyloccal aetiology
    • Otherwise unimpressive infection

Diagnostic Approach and DDx

Consider if:

  • Classical skin findings
  • Known streptococcal infection and sepsis
  • Soft tissue infection and sepsis
  • Flu-like illness with:
    • Significant left-shift
    • Haemodynamic instability despite resuscitation
  • Pregnancy

The US CDC has published diagnostic criteria, which are not reproduced here as they exhibit the unfortunate combination of being both very long and very limited clinical utility.

Investigations

Laboratory:

  • Blood
    • FBE
      • ↑ WCC with left shift
      • Thrombocytopenia
    • CK
      ↑ Secondary to cytokine ↑.
    • UEC
    • LFT
      • ↑ Bilirubin
      • ↑ AST/ALT
    • Coag
    • Cultures

CK may also be ↑ in necrotising fasciitis.

Management

  • Good sepsis resuscitation
    Covered under Management.
  • Specific therapy for toxic shock is relatively benign and a low-threshold to initiate it is appropriate
    Consider with:
    • Known or reasonable likelihood of streptococcal infection
    • Persistent vasopressor requirements

Specific therapy:

This just covers management of toxic shock syndrome; you still need to treat the actual infection with appropriate antimicrobials and source control.

  • Pharmacological
    • Toxin-suppressive antimicrobials
      • Clindamycin 900mg IV Q8H
        • Most evidence
        • Generally broad activity against streptococci and staphylococci
          Combination with a β-lactam recommended for streptococcal infections to avoid potential clindamycin resistance.
      • Linezolid 600mg IV Q12H
        Toxin suppression with better coverage of both streptococci and staphylococci.
    • IVIG
      Neutralise toxic antibodies.
      • 1g/kg on day 1
        Can ↑ to 2g/kg if faiulure of response.
      • 0.5g/kg on day 2 and 3, if required
  • Procedural
    • Source control
      • Debridement of necrotic tissue
      • Removal of tampon

The role and dosing of IVIG in staphyloccal toxic shock is not well elucidated.

Complications

  • C
    • Septic cardiomyopathy
      ↑ Risk in toxic shock.
  • F
    • AKI
  • H
    • DIC

References