CICM Second Part Exam Practice SAQs 17012018

As prepared by Chris Nickson, here are the practice written questions from a recent CICM Second Part exam practice session at The Alfred ICU, with recommended reading from’s Critical Care Compendium and other FOAM sources:


Discuss the role of apnoeic oxygenation in the management of critically ill patients (100%)

Learn more here:

Apnoeic oxygenation


Compare and contrast toxic epidermal necrolysis (TEN) with acute graft versus host disease (aGVHD) (100%)

Learn more here:

Stevens Johnson Syndrome and Toxic Epidermal Necrolysis

Acute Graft Versus Host Disease

TEN and acute GVHD disease are both multi-system skin disorders that both have high mortality. Though they can usually be distinguished by clinical presentation, histopathology is confirmatory. They may be difficult to distinguish in severe cases occuring after allogenic haematopoietic stem cell transplant.

Cause malignancy (carcinomas and lymphomas)
infection (Mycoplasma pneumoniae, herpes virus, hepatitis A)
drug induced (penicillins, sulfa drugs, quinolones, cephalosporins, anticonvulsants, COX-2, immunosuppressants, allopurinol, corticosteroids)post-SCT/ organ transplantpost-immunisation
Occurs after allogenic haematopoietic stem cell transplant (30-50%) due to graft immune response
Pathophysiology Immune-related cytotoxic reaction aimed at destroying keratinocytes that express a foreign antigen

Results in separation of the epidermis from the dermis

Antigens on the host cells are attacked by the donated T cells

Tissue damage results in cytokine storm

Organs/ sites primarily affected Skin (>30% BSA)

Mucosal membranes



GI tract

+/- other organs (e.g. lung)

Clinical features Occurs 1-8 weeks after cause

Flu-like prodrome (1d-3wks)

Mucositis then after 1-3d

skin rash – macular, with purpuric center, then vesicles, then sheet-like exfoliation

<100d after SCT

puriritic/ painful MP rash +/- vesicles

GI: mucositis, diarrhoea, ileus

Other mucosae and eyes

Complications Sepsis, scarring & strictures, vision impairment, bleeding, fluid loss (e.g. hypovolaemic shock and AKI), capillary leak (e.g. ARDS), death
Diagnosis Clinical presentation

Skin biopsy (early): Necrotic keratinocytes with full-thickness epithelial necrosis and detachment

Clinical presentation

Tissue biopsy: skin (eg, eosinophilic bodies, mononuclear infiltration), liver (eg, necrosis of the bile duct), and gut (eg, crypt-cell degeneration)

CT abdo findings


Specific therapy None proven by high quality trials, but options are:

  • Plasmapheresis
  • Corticosteroids
  • Cyclophosphamide
  • CSA
  • TNF-alpha inhibitors
  • IVIg
First line

  • Corticosteroids
  • +/- other immunosuppressants

Second line options

  • MMF/ CSA/ tacrolimus
  • ATG
  • Ruxilitinib
  • PUVA
  • Etc, etc!
Supportive care and monitoring
  • MDT approach
  • Severe cases referred to burns center
  • Wound care (e.g. dressings)
  • Treat infection (antimicrobials)
  • Analgesia and sedation
  • Eye care
  • Fluid replacement
  • Control bleeding (e.g. blood products)
  • TPN for GI mucosal involvement
Prognosis Predicted by SCORTEN

10-70% mortality (varies with quality of Rx and rapidity of Rx)

Varies with Grade I to IV

20% if complete response to steroids

80% mortality if refractory to steroids

50% develop chronic GVHD


Describe the Stewart (physico-chemical) approach to acid-base disturbances, and discuss the pros and cons of this method. (100%)

Learn more here:

Strong Ion Difference

You can access all the previous practice questions since 2014 here:
See this link on INTENSIVE for exam resources:

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The Bottom Line, ART, and DETO2X-AMI

The Alfred ICU Journal Club has teamed up with The Bottom Line. This means that critical appraisals from our Journal Club discussions are now being published on The Bottom Line, which is rapidly becoming the definitive resource for critical appraisals of the intensive care research.

Recent examples from the Alfred ICU Journal Club production line include summaries of the DETO2X-AMI and ART trials, created by Aidan Burrell and Emma Browne respectively. Here are ‘the bottom lines’:

    • This large MCRCT shows that supplemental oxygen does not make any difference to outcomes in normoxic patients with suspected AMI
    • This result combined with other recent studies that have suggested potential harm from oxygen, plus the fact oxygen is not free, suggests that oxygen therapy in this population is no warranted
    • We await more up to date guidelines that will reflect this
  • ART
    • This trial confirms that protective lung ventilation is the standard of care for moderate-to-severe ARDS and that an open lung approach with recruitment manoeuvres should not be used routinely.
    • The increased mortality due to the intervention in this study is statistically fragile and may lack external validity to other settings
    • Specific subgroups of ARDS patients may benefit from OLA ventilation with recruitment manoeuvres (e.g. adequately resuscitated patients with PEEP-responsive ARDS and few other risk factors for barotrauma or haemodynamic collapse) but identification of such subgroups is uncertain, the evidence for benefit is weak, and there is risk of harm to patients as found in the ART trial


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