CICM Second Part Exam Practice SAQs 12122019

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 LITFL.com Critical Care Compendium and other FOAM sources:

Q1. 

Regarding central line associated bloodstream infection (CLABSI):

a) Define CLABSI and state the incidence considered acceptable in Australian and New Zealand intensive care units. (20%)

b) Outline measures related to the use and insertion of central venous catheters that help prevent CLABSI (80%)

Learn more here:

Central line infections

Q2. 

Discuss the pharmacological management of convulsive status epilepticus in adults. (100%)

Learn more here:

Glauser T, Shinnar S, Gloss D, et al. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society. Epilepsy Curr. 2016;16(1):48-61. Available at URL: https://journals.sagepub.com/doi/10.5698/1535-7597-16.1.48

Status Epilepticus

Controversies in the acute management of status epilepticus

PulmCrit- All 2nd line conventional anti-epileptics are equally good… or equally bad?

Status epilepticus is continuous seizure activity >10 minutes, or repeat seizure without full recovery; it is a life-threatening emergency. (Definition is controversial!)

  •  longer a seizure lasts the more likely it is to become refractory or recur.
  • High mortality and risk of incomplete neurological recovery if >20-30min

Pharmacological therapy includes:

  • First line benzodiazepine
    • General
      • modulation of the GABA A receptor, which opens the chloride channel and hyperpolarises the cell, leading to postsynaptic inhibition
      • Adverse effects are similar for all benzodiazepines and include sedation, dizziness, weakness, unsteadiness, respiratory depression, and hypotension. There are additive effects when several benzodiazepines are co-administered
      • Cochrane review shows no clear benefit for one agent over another (midazolam, diazepam, lorazepam) https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/29320603/
    • My preference is midazolam 5 to 10 mg (child: 0.2 mg/kg) IV, IM, buccally or intranasally, repeat once 15 minutes later if status epilepticus continues.
      • multiple routes including intramuscular, buccal or intranasal administration if no IV access
      • short elimination half-life
      • may accumulate in patients with renal impairment
      • Familiar
      • Readily available
      • No propylene glycol toxicity
    • diazepam 10 to 20 mg IV, not exceeding 2 to 5 mg/min; repeat once 15 minutes later if status epilepticus continues (child: 0.1 to 0.25 mg/kg IV, over 2 to 5 minutes)
      • Long half life but rapid redistribution from CNS (20-30 min)
      • is diluted with sodium chloride 0.9% before administration, a fine white precipitate may form
      • Propylene glycol diluent – toxicity in high dose
      • Not IM route
      • Can be given via rectal route
    • clonazepam 1 to 2 mg IV, not exceeding 0.5 mg/min; repeat once 15 minutes later if status epilepticus continues (child: 0.25 to 0.5 mg IV, over 2 to 5 minutes)
    • Lorazepam 0.1 mg/kg (4-8mg) IV
      • Longer DOA but shorter half- life than diazepam
      • slower onset of action
  • First line antiepiletpic drug (AED)
    • General
      • Longer acting, so more sustained effect
      • However, typically have slow onset – increasing practice of rapid transition to an induction agent and intubation
      • ESSET trial https://www.nejm.org/doi/10.1056/NEJMoa1905795
        • 384 children with refractory SE
        • Fosphenytoin, levitiracetam, and sodium valproate all were ~45-47% effective (resolved seizure and improvement at 60 mins)
        • No difference in safety (but not powered to detect uncommon events)
        • I.e. current algorithm is not very successful
    • Levetiracetam: 60 mg/kg to 4000 mg over 5–15 min; additional dose 1500–3000 mg
      • Less SE than phenytoin
    • Phenytoin 15 to 20 mg/kg IV, not exceeding 50 mg/min (or 25 mg/min in high-risk patients) (child: 20 mg/kg IV, not exceeding 25 mg/min). Continuous monitoring of the electrocardiogram and blood pressure is essential.
      • Familiar
      • Risk of toxicity if on phenytoin already
      • Drug interactions
      • Propylene glycol toxicity if administered too rapidly
      • Phenytoin has membrane-stabilizing activity and slows inward Na+ and Ca2+  flux during depolarization in excitable tissue; it also delays outward K+ ux.
      • irritant/ tissue damage if IM or extravasates
    • sodium valproate 400 to 800 mg depending on body weight (up to 10 mg/kg) by slow IV injection over 3 to 5 minutes, usually followed by continuous infusion of 1 to 2 mg/kg/hour up to a maximum of 2500 mg/day, according to the patient’s clinical response
      • GABA-ergic inhibition; sodium valproate increases brain GABA levels by inhibition of succinic semialdehyde dehydrogenase in the GABA shunt. Alternatively, it may: 1. mimic the action of GABA at post-synaptic receptors and 2. reduce excitatory inhibition (especially that due to aspartate).
  • Second/ third line agents
    • Alternative first line AED (see above)
    • Induction/ general anaesthetic agents
      • Require intubation due to respiratory depression
      • Short-acting unless infusion
      • Physiologically make most sense for rapid termination of seizures
      • Generally lacking evidence (e.g. animal models, case series)
      • Refractory SE requires cEEG monitoring
    • Barbiturate e.g. Thiopental: loading dose of 2–7 mg/kg (infused at a rate <50 mg/min), with additional doses of 1–2 mg/kg as needed, followed by a continuous infusion at a rate of 0.5–5 mg/kg/h.
      • Rapid acting 
      • GABA receptors on RAS
      • Issues: CVS effects, porphyria, extravasation, intra-arterial toxicity
      • RCT in south Africa favoured phenobarbitone over phenytoin
    • Benzodiazepine infusion (e.g. midazolam, clonazepam)
    • propofol 1.5-2mg/kg IV then 20-200mcg/kg/min
    • Ketamine: loading doses 1–2 mg/kg, every 3–5 min until seizure stop (max 4.5 mg/kg) followed by continuous infusion ranging from 1 to 10 mg/kg/h.
    • Inhalational anaesthetic (e.g. isoflurane)
  • Specific therapies for specific underlying causes
    • magnesium 4 grams IV if eclampsia
    • Pyridoxine for isoniazid toxicity
    • Phenytoin not useful for tox causes
    • Hypertonic saline for hyponatremia
    • NaHCO3 for TCA/ sodium channel blockade
    • Immunosuppressants (eg. methylpred, IV IgG, Rituximab) for autoimmune causes/ NORSE
    • antibiotics/ antivirals

Q3. 

List the typical findings in the following investigation-disease pairs:

a) The nerve conduction findings in ICU-acquired weakness (Critical Illness Polymyoneuropathy). (20% marks)

b) The cerebral spinal fluid findings in Guillain Barre Syndrome. (20% marks)

c) CT brain findings of an acute middle cerebral artery (MCA) occlusion (< 3 hours). (20% marks)

d) MRI brain findings of posterior reversible encephalopthy syndrome (PRES). (20% marks)

e) Plain cervical spine X-ray in acute traumatic central cord syndrome (20% marks)

Learn more here:

Guillain-Barré Syndrome (GBS)
ICU Acquired Weakness (ICUAW)
PRES
https://radiopaedia.org/articles/posterior-reversible-encephalopathy-syndrome-1 https://radiopaedia.org/articles/central-cord-syndrome?lang=us

Critical illness polyneuropathy (CIP) nerve conduction studies shows sensorimotor axonopathy with:

decreased compound muscle action potentials (CMAP) and sensory-nerve action potentials

preserved conduction velocities (CV)

if also present, critical illness myopathy (CIM) shows reduced amplitude and increased duration of CMAPs

GBS CSF

  • elevated protein (only after 5-7 days of disease)
    • sometimes termed ‘cytoalbuminological dissociation’: increased CSF protein in the absence of increased WBCs
      • absence does not rule out GBS or make the diagnosis less likely
    • some patients have oligoclonal banding
    • ~5% of GBS patients have a mild increase in CSF cell count (5–50 cells per μL)

CT brain of hyperacute MCA occlusion

  • The earliest finding of MCA occlusion is hyperdense middle cerebral artery sign – direct visualization of the thromboembolism.
    • Early parenchymal signs include subtle blurring, decreased attenuation and swelling of the grey-white matter junction
    • deep grey matter structures are affected before the cortex (lenticulostriate arteries are end arteries so cytotoxic edema occurs earlier)
      • lentiform nucleus; caudate nucleus
      • insular ribbon
      • surface cortex, including peri-rolandic cortex (usually not evident by 3 h)
    • With time the hypo-attenuation and swelling become more marked, leading to mass effect; before gradually reducing over days

Acute traumatic central cord syndrome

Osseous imaging may be

  • Normal
  • show spondylosis
  • acquired/congenital canal stenosis, or
  • fracture

The presence of an extension teardrop fracture should be a warning sign


You can access all the previous practice questions since 2014 here:
https://docs.google.com/document/d/1_Ta8IvVaVtc5Il7-kJwj6qKGu54OmifJGRUWCXud8dY/edit
See this link on INTENSIVE for exam resources:
//intensiveblog.com/resources/#3

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