Question 27

College answer

Syllabus topic/section:

2.1.3 Sepsis and Infections / Rarer infections with specific ICU considerations: Streptococcal Toxic Shock: L1

Discussion:  

Generally, this question was answered well. Candidates who did not demonstrate the standard required provided answers that were very brief, without addressing core concepts such as source control and mentioning antibiotics in only minimal detail.
A discussion of the precise antibiotic regimen with dosages, immunoglobulin therapy with rationale and addressing steroid controversy is required to show competence in managing potentially life-threatening manifestations such as necrotising fasciitis, toxic shock syndrome, severe puerperal sepsis and necrotising pneumonias as well as the less common suppurative pharyngitis, septic arthritis and meningitis.

The marking rubric is included to aid the candidate's future study.

Discussion

a)

Invasive GAS pathologies that should be considered in this patient, judging by the examiners' comments, must have included the following:

• necrotising fasciitis
• toxic shock syndrome
• severe puerperal sepsis
• necrotising pneumonias
• suppurative pharyngitis
• septic arthritis
• meningitis

To be fair, "Invasive GAS pathologies that should be considered" is hard to parse. It sounds like it could be answered with a simple list. "I would consider nec fasc, TSS and purpureral sepsis", etc.  However, this was an "outline" question, and worth 5 marks, which means approximately five minutes (100-120 words or so) would need to be written on this subject. That would have to look like something a bit more meaty. Historically it was hard to know exactly what the examiners expected, but these days often we give you the rubric, and the one in this SAQ suggested that a candidate that meets the pass standard "outlines the features of TSS and necrotising fasciitis in good detail". So it was clinical features they were after? Well:

• Invasive vs. noninvasive:
  • Non-invasive GAS infections are defined as infections where the GAS is identified from a non-sterile site, such as skin or a wound, whereas invasive GAS is found in blood, CSF, pleural or peritoneal fluid, or tissue culture  (Weiss & Laverdière, 1997)
  • Invasive infections include the belowlisted, whereas noninvasive infections with GAS are pharyngitis, tonsillitis, otitis media, skin abscesses, etc.
• Necrotising fasciitis
  • Invasive group A strep in young populations
  • Rapidly progressive critical illness, multiorgan involvement
  • Presents with pain, swelling, blisters, skin creptitus,  but often findings are disproportionately mild to the severity of the pain
• Toxic shock syndrome
  • Common presentation of GAS bacteremia and critical illness
  • CDC criteria are:
    • High fever (> 38.9°)
    • Hypotension and shock
    • Rash consistent with diffuse macular erythroderma
    • Desquamation, particularly of the palms and soles
• Severe puerperal sepsis
  • Usually within 4 days of delivery and usually screened for it antenatally
  • Rapidly progressive
  • Mostly common following vaginal delivery
• Necrotising pneumonia
  • CXR evidence of cavities, haemoptysis
  • More common in diabetics 
  • Not a common organism for pneumonia
• Suppurative pharyngitis
  • Spread through soft tissue spaces, followed by haematogenous spread
  • Less common as a cause of toxic shock syndrome
• Septic arthritis
  • second most common cause of septic arthritis, after S.aureus
• Meningitis
  • rare (~ 2% of invasive GAS infections)
  • Surprisingly low mortality rates in adults

b) Infection-specific management of invasive GAS infection:

• Source control
  • Especially in necrotising fasciitis, essential for survival
  • Debride dead tissue and remove sanitary products responsible
• Antibiotics
  • β-lactam antibiotics:
    • Benzylpenicillin is usually enough
    • or cephazolin/vancomycin where allergic
  • Clindamycin as an adjunct
• Prevention of toxin production
  • Clindamycin (say 600mg tds or 900mg tds IV) is indicated to disrupt bacterial synthesis of the toxic shock protein
• Removal of circulating toxin
  • Intravenous immunoglobulin (to bind circulating TSST)
  • 2g/kg as a single dose
  • IVIG also decreases in the production of proinflammatory cytokines and causes a downregulation of adhesion molecules and chemokines.
• Unproven treatments
  • Corticosteroids are known from case series (Vergis & Gorard, 2007) but are not a part of the established approach