Academic Day Seminars

ADS – Delirium, Presentation Skills, Patient Advocacy & LFTs

Today was a great day of reflecting on common topics relevant for residency:


  • Hyperactive: Hallucinations, delusions, agitation, disorientation.< 5% of ICU delirium are purely hyperactive motoric subtype.
  • Greater than 75% of delirium cases are either hypoactive or mixed
  • Hypoactive: Confusion, sedation, less often has psychotic features, often misdiagnosed as depression or dementia OR unrecognized.
  • Mixed: periods of quiet, followed by periods of agitation/restlessness
  • Delirious pts have an increased risk of mortality.
  • Once the delirium resolves, for the subsequent year, the pt continues to have inc. mortality, and can still have brain deficits. In post-delirium ICU pts can have a PTSD of the memories of the delirium in the ICU
  • As pharmacists a huge role for us is de-prescribing – and looking at whether any of the medications are contributing (e.g. anticholinergics, benzos, etc.) and ensuring their concurrent disease states are well-managed by medications if indicated.
  • Precipitating factors: PRIMES
    P Pain Assess pain management
    Poor Nutrition Dehydration, malnutrition, Assess albumin/protein, lytes, vit def
    R Retention Urinary retention, assess fluid in/outs
    Restraints Minimize, explore alternatives
    I Infection / Injury Consider UTI, pneumonia, wound, diarrhea.   MI, CHF, hypoxemia (COPD).  Recent surgery, trauma, stroke
    Immobility Change from premorbid function
    M Metabolic Assess acid-base, lytes, renal fx, glucose, albumin
    Medications Polypharmacy, anticholinergic meds, BZDs, opioids, antiemetics, glucocorticoids, withdrawal syndromes, toxicity (dig, phenytoin)
    E Elimination Constipation / impaction
    Environment Unfamiliar place, no exposure to daylight
    S Sleep Altered sleep/wake cycle
    Skin Assess for skin breakdown/wounds
    Sensory Sensory deficits – does pt have hearing aids, glasses, dentures?

Presentation Skills:

  • Today was a useful introduction on how to do a case presentation (with particular focus on our BC wide cases upcoming)
  • Some tidbits I took away were:
    • If I am not including every article that came up in my search strategy, briefly mention why not – so to show that I did this thoughtfully as opposed to forgetfully.
    • Ensure that I come up with the meat and focus and direction of my presentation first, and then make powerpoint slides
    • If my recommendations based on the evidence do not match, then have two slides explaining what happened (e.g. team rejected recommendations b/c of “x”). In this situation monitoring parameters should match what happened as opposed to what I would have liked to have happened.
    • Make sure that I explain all the therapeutic alternatives and why I have ruled each one out, as opposed to having the audience be uncertain if this was thought about or forgotten!

Patient advocacy:

This was a very interesting lecture, which was much more “soft-skill” orientated. It was refreshing to have a patient’s mom give us her interpretation of how we interact as healthcare professionals with her and her child (who is commonly hospitalized). Some tips that really resonated with me are:

  • How to interact with a patient (KIDS acronym):
    • K-Knock
    • I-Introduce yourself
    • D-describe what you are there to do
    • S-sit down, slow down
  • Always introduce myself, and ask “Do you have some questions for me” as opposed to “any” questions – to encourage questions.
  • Ask the child questions directly (as opposed to addressing the parents solely)

Liver Function Tests:

This was a great review of LFTs and how to be able to quickly assess the predominant factor affecting my patient’s liver function. Some takeaways included:

  • Elevations of aminotransferases/ALP/GGT are only markers of liver injury, not liver dysfunction
  • LFT “normals” are based on the mean + 2 SDs, so there is ~ 2.5% of the population who have an elevated baseline LFTs
  • Look at trend of enzyme alteration & magnitude of enzyme alteration:
    • Mild – <5 times
    • Moderate – 5-10 times
    • Marked – >10 times

Markers of hepatocellular damage: AST & ALT

  • In acute injury in the first 24-48 hours: AST rises more quickly and higher than ALT.
  • After 24-48 hours: ALT > AST in injury
  • AST/ALT ratio:
    • <1: majority of cases of acute hepatocellular injury
    • > 1: alcoholic liver disease (often >2), drug-induced injury, malignancy, cirrhosis, non-liver disease
  • ALT and AST require vitamin B6 as a cofactor in order to convert certain enzymes however when you have alcoholism it results in a deficiency of vit B6 levels. ALT is more dependent on B6, so when you have alcoholic liver disease they have B6 deficiency so cannot synthesize as much ALT which is why your AST/ALT ratio favours AST in alcoholic liver disease.

Markers of cholestatic predominance:

  • ALP (>4x normal) and elevated bilirubin
  • If GGT is also elevated, liver cause is most likely; If not than bone origin is likely.

Markers of liver synthetic function: Increased INR, decreased albumin.


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