C3.5 R2: Prepare and deliver educational seminar to pharmacists

During my ICU rotation, I presented on the management and use of fibrinolytics in submassive and massive PEs. The evidence regarding this topic is not very clear-cut and it was a great learning experience to try to figure out what I can help my audience take away from the available evidence and implement in their clinical practice.

Things that went well:

  • Flow of the presentation was fairly easy to follow and organized
    • Placed title slides for each section and provided and outline
    • Slides were generally not too text heavy
  • Paused at each section to check in with my audience and to see if there were any questions

Things I could improve on:

  • Continue to practice, practice and practice for my future presentations…I definitely still get very nervous and stumble during my presentation, but overall, I still feel that my delivery skills are improving with each presentation
  • Thinking back to my presentation… I realized that I had my back faced to a few of my audience members (whoops) and only turned back occasionally to ask if there were any questions.
    • For future presentations, I will try to position myself in a way that I’m not blocking the presentation and am able to observe most of my audience to better gauge their understanding

My preceptor kindly helped me prepare for my presentation and provided me with lots of pearls to keep in mind for future presentations:

  • Provide your own critique for each of the studies you present
    • Use the risk of bias domain tool to help present on the quality of the evidence (including internal and external validity)
    • Strength of a DB RCT shouldn’t be that it is randomized and double-blinded
    • Provide your own summary of each trial and your own conclusion
      • Consider the inclusion and exclusion criteria
      • Consider the type of patient population that was eventually randomized
      • Highlight benefits and risks
      • Consider what the audience can or can’t take away from the slide
  • Provide NNT/H only when results are statistically significant
  • When going over goals of therapy and whether the evidence supports it or not, provide more concrete support (e.g. NNH, NNT, citation)
  • When providing comparisons of drugs, include pharmaokinetic information:
    • Also consider: are doses equivalent between options
    • Think about how the drugs are used for other indications
  • Consider my audience and provide some practical application points/pearls
    • For instance, for this topic – providing information on whether or not anticoagulation can be started concomitantly with fibrinolytics and if not, how to decide when to start it? As well as answering what type of PE requires more monitoring and what kind of monitoring?
    • Also for submassive PEs, being able to justify whether you would lyse right away or wait for hemodynamic decompensation before lysing
      • An interesting analogy that my preceptor provided was that if a patient was pre-diabetic, would you prevent them from getting diabetes by giving them the treatment for diabetes?
    • Being able to explain the clinical significance of outcomes studied (e.g. hemodynamic decompensation)
  • If there is a lot of information to cover for trials, place them in the appendix at the end of your presentation
  • Where the evidence is more grey
    • Be able to justify whether you woud lyse or wait until you lyse
  • Studies using ICD-9 codes: good for information where disease states are very uncommon or outcomes are very uncommon

My presentation handout: Submassive+Massive+PE+Final

C3.1 R4(e): Perform & document a pharmacokinetic interpretation (OTHER drug)

Clinical Pharmacy Note RE: Digoxin

ID: 84 yo female admitted for G- bacteremia and hypercapnic respiratory failure

  • PMHx: Afib, HTN, chronic back pain, PVD, scoliosis, recurrent falls and fractures, chronic cellulitis x 8 mos, venous insufficiency ulcers, childhood polio


  • RASS -1, AO x 3
  • Met patient in room to assess for SEs of digoxin:
    • Denies drowsiness, dizziness. Has headaches but this is ongoing from PTA and have not worsened in hospital
    • Denies any visual disturbances and able to identify red and green colours
    • Denies N/V and nurse’s flow sheet shows no diarrhea
    • Denies any change in appetite – ate 1/4 sandwich and 1/3 soup today for lunch
    • At baseline – has muscle weakness to both her arms (L>R) due to childhood polio. Has weak strength of flexion and extension of thigh
  • Denies any chest pain, palpitations or SOB


  • v/s: T 36.3, HR 75, BP 130/65, MAP 93, RR 21 (on 2L NP)
  • ECG (Mar 14): Afib with RVR (130 bpm)
  • ECG (Mar 15): Afib rate controlled (90 bpm), inverted T waves
  • On Mar 14, received digoxin 0.5mg IV at 1340h and 0.25mg IV at 2200h for afib with RVR. No maintenance doses have been ordered
  • Digoxin level on Mar 15 1135h: 4.2 nmol/L (target for afib: 1-2.5nmol/L)
  • Relevant labs (Mar 15): K+ 4.8 mmol/L, eGFR 13 mL/min (eGFR 75 mL/min in Nov 2016)


  1. Digoxin load is effective in controlling her rate for afib
  2. Trough level was taken appropriately and is supratherapeutic, likely due to her AKI
  3. Currently exhibiting no SEs of digoxin. No indication or role for use of digifab at this time
  4. PTA, refused treatment for afib and hypertension.  On admission, afib may have been exacerbated by infection and hypercapnic respiratory failure which are currently being managed. The decision on whether or not to initiate long term management for afib should factor in her goals of therapy for comfort care.

P: Suggest

  1. Not to continue digoxin (no maintenance doses have been ordered)
  2. Daily monitoring for s/s of afib: dizziness, syncope, palpitations, dyspnea (currently no cardiac monitoring d/t goals of therapy for comfort care)
  3. Daily monitoring of safety of digoxin: HR, K+, eGFR, sCr, u/o, worsening of headaches, dizziness, drowsiness, vision changes (flicking lights/halos, blurry or yellow/green vision, red-green colour blindness), worsening of muscle weakness

Other calculations:

  • Dosing of digoxin load IV:
    • LD usually given:
      50% of calculated LD as an IV or PO bolus then 25% of calculated LD q6h x 2

      • Could calculate based on IBW (challenging as wt unknown and pt has scoliosis)
      • If estimate: ~50kg + 5 feet 5, IBW = 56.5kg, CrCl = 16 mL/min,
        LD = 0.56-1.13mg (0.01-0.02mg/kg *IBW/F)
      • If renal impairment (avoid in AKI if possible): reduce loading dose by 50%
        • LD = 0.28-0.56mg
          (Max ~ 0.25mg IV, then 6 hours later – 0.125mg IV Q6H x 2 doses)
      • Could also give PO (F: 07 for tablets)
    • UTD states may generally admin as loading dose: 0.25mg with repeat dosing to a max of 1.5mg over 24hrs
      • In acute renal failure: pt Vd may be increased and reduction in LD may not be necessary; however, maintenance dosing will require adjustment
    • VGH PDTM:
      • Digitalization: 0.01 to 0.015 mg/kg of lean body weight divided into 2 or 3 equal parts and given at 6 hourly intervals
  • Monitoring of digoxin loads:
    • at least 4 -6 hrs after an IV dose
    • at least 6-12 hrs after a PO dose
  • For elderly – consider having max dose as 75% of LD – e.g. 0.5mg IV then 0.25mg IV 6 hours post, or just 1 dose of digoxin 0.5mg IV
  • Other option for rate control in the setting of hypotension and shock:
    amiodarone infusion (no renal dosing adjustment necessary for renal impairment)

C3.1 R4(e): Perform & document a pharmacokinetic interpretation (OTHER drug)

Clinical Pharmacy Note RE: Lithium

ID: 64 yo male admitted for hypoxemic respiratory failure secondary to aspiration pneumonia (also has R sided petroclival meningioma)


  • RASS 0 to -1. AO x3 (to month and year)
  • Squeezed writer’s hand when asked if feeling confused, seeing and feeling things that are not there, feeling very tired, as well as, for dry mouth and increased thirst which is new fo rhim today (Lasix IV BID stopped today and had ++ oral secretions earlier today)
  • Currently on Lithium 300mg PO HS for query bipolar/mood disorder
    • Dose was reduced from 600mg PO HS in ICU due to AKI
    • Lithium level (Mar 13): <0.2 mmol/L, eGFR 97mL/min (stable)
  • According to P’net, was on Lithium 600mg PO HS
    (?compliance as last filled 7 days supply in Dec 2016)
  • Spoke to psych regarding indication and plan for lithium:
    • Psych spoke to his community psychiatrist who did not think the diagnosis for bipolar/mood disorder was strong. According to community psychiatrist, patient was kept on lithium 600mg PO HS in community as patient has failed multiple antidepressants in the past and patient felt that there was some benefit from lithium.
    • Given his clinical state and unclear history of indication and efficacy of lithium, psych suggests continuing on current dose of lithium and reassessing when patient is more stable.


  1. Level drawn appropriately ~12 hours post dose and at steady state
  2. At his current subtherapeutic level, lithium is likely not effective for his query bipolar/mood disorder. However, given his clinical situation (also currently managing his delirium), efficacy of lithium is challenging to assess
  3. If renal function continues to be stable, it is unlikely that levels will become therapeutic with current dose.
  4. There is a potential drug interaction where lithium may enhance neurotoxic effects and EPS symptoms with antipsychotics which is currently used being to manage his delirium. Risk is low as patient is on low doses of antipsychotics (Haldol 2.5mg NG PO Q6H, Nozinan 25mg PO daily at 2100h)

P: Suggest

  1. Continue lithium 300mg PO HS and reassess indication and efficacy of lithium when patient is out of critical care state
  2. When patient is out of critical care state and more stable (e.g. delirium resolved), reassess indication and efficacy of lithium for query bipolar/mood disorder
  3. Daily monitoring of side effects of lithium: ataxia, seizures, tremors, dry mouth, worsening of sialorrhea, N/V/D, and EPS symptoms: spasms, muscle contractions, motor restlessness, tremors
  4. Daily monitoring of renal function (sCr, eGFR) while in ICU


C3.5 R3(d): Prepare and Facilitate a journal club to pharmacists

For my ICU rotation, my journal club was on: Sodium Bicarbonate Versus Sodium Chloride for Preventing Contrast-Associated Acute Kidney Injury in Critically Ill Patients: A Randomized Controlled Trial

Areas of improvement:

  • Build on a systematic approach to performing journal club:
    • What is the evidence to date, and what gap in knowledge is this trial trying to fill?
    • What is the study’s conclusion?
    • What is the application to practice?
      • i.e. what is the inclusion and exclusion criteria, and what are the actual/final patients randomized? How are they similar or different to my patient population?
    • Be specific with my conclusion (e.g. what kind of patients, what kind of monitoring, what kinds of concomitant interventions, etc.)
  • Important to consider how the design of the trial affects the conclusion that I can make about the study. This study was designed as a superiority trial and primary outcome is NSS; however, we cannot say that the two options are comparable as it has not deemed to be non-inferior (non-inferiority trials require more numbers than superiority trial and per-protocol analysis is more conservative in non-inferiority trials)

My handout: HYDRAREA Journal Club



  • Normal: 150-400 x 10^9/L
  • Thrombocytopenia: PLT <150
  • <100: risk of surgical bleeding in high risk surgical patients (i.e. neurosurgery, major cardiac, orthopaedic surgery)
  • <50: risk of surgical bleeding
  • <10-20: risk of severe spontaneous bleeding


  • Post-operative consumption (platelets are being used to help heal wounds post-op)
  • Infections (e.g. HIV, hepatitis C, sepsis with disseminated intravascular coagulation)
    • Thrombocytopenia: independent risk factor for morality in the ICU (sepsis)
  • HIT Type I: not ab mediated (direct effect of heparin) and fall in PLTs (nadir: 100) typically resolves with continued heparin administration
  • HIT Type II: ab-mediated (nadir >20) and may lead to thrombosis until heparin is discontinued
  • Other drug causes: quinine, sulfonamides, acetaminophen, cimetidine, ibuprofen, naproxen, ampicillin, piperacillin, vancomycin, glycoprotein IIb/IIIa inhibitors
  • Nutrient deficiencies (e.g. vitamin B12, folate, copper)
  • Pregnancy

Platelets: also an acute phase reactant (increase in inflammation/infection/trauma)


Currently, I have been seeing patients with hypophosphatemia, and for a few, this has been persistent despite ongoing replacement..

Causes of hypophosphatemia:

  • Acute respiratory alkalosis
    • Rise in intracellular pH stimulates phosphofructokinase activity which in turn stimulates glycolysis → ↑ in demand for phosphate, which is driven intracellularly to form glycolytic intermediate metabolites
      • A similar phenomenon is observed with an increase in intracellular pH, which occurs in metabolic alkalosis
    • Extreme hyperventilation (PCO2 <20mmHg) in normal subjects can also lower serum phosphate concentrations to below 0.32 mmol/L
    • References:
  • Refeeding syndrome
    • Concern of referring syndrome in malnourished, alcohol abuse
  • Stress-induced
    • Dieticians are able to calculate patients’ metabolic needs and assess if the feeds are sufficient in meeting this. Had a patient with status epilepticus with persistently low phosphate levels despite frequent replacement. Dietician calculated her needs and found that it significantly exceeded her feeds. After replacing feeds (and also accounting for the fact that patient is on propofol), phosphate levels were generally WNL
  • Increased losses (e.g. diarrhea, large NG loss)
  • Diabetic Ketoacidosis

Drug causes of hypophosphatemia:

  • Phosphate binders – e.g. calcium supplements
  •  ↑ urinary excretion – e.g. carbonic anhydrase inhibitors, bisphosphonates, corticosteroids
  • Cause vitamin D deficiency or resistance – e.g. phenytoin, phenobarbital
  • IV iron administration
  • Acetaminophen poisoning
  • References: Medicationinducedhypophos

Symptoms of hypophosphatemia:

  • Respiratory failure
  • Cardiac abnormalities
  • CNS dysfunction
  • Difficulty weaning from venilation


  • Address underlying causes
  • Supplement phosphate
    – e.g. NaPO4 IV 15 mmol (=20mmol Na), KPO4 IV 15 mmol (= 22 mmol K+)

    • ICU Rapid Resource at VGH: 20-40 mmol PO4/day
  • Monitor serum levels at least daily
  • Monitor renal function daily – if AKI, risk of accumulation!
  • Monitor for hyperphosphatemia (symptoms: paresthesia, flaccid paralysis, mental confusion, hypertension, cardiac arrhythmias, tissue calcification)

Clinical Pharmacy Note RE: Stroke

Mar 6/17 1330h Clinical Pharmacy Note RE: Secondary Stroke Prevention

ID: 41 yo male admitted with stroke
(Mar 6 Head CT showed established infarct in L side with no signs of hemorrhage)

S/O: v/s: T 36.5, BP 125/65, HR 76, RR 9

  • RASS -1 to 0, aphasia but still able to answer yes/no questions
  • Aspirin 325mg PR load given at 1720 hr on Mar 5, 17 but 80mg daily is held by neurology until infective endocarditis (IE) can be ruled out with negative BCx
  • Due to previous IVDU (on methadone daily, urine + cannabis, opioids, amphetamines), suspecting septic emboli from IE
    • ECHO for IE w/u pending (currently empirically txed with pip/taz and vanco)
    • BCx prelim, results (Mar 5): G+ cocci likely streptococcus or enterococcus
  • Hgb (Mar 6): 78 (stable)


  • Maintenance aspirin is necessary to help ↓ the risk of early and future recurrent ischemic stroke and ↓ the risk of mortality
  • There are no contraindications to use of aspirin with IE. No suspected intracranial hemorhage
  • Patient has no previous history of CVA or TIA, therefore currently no strong need for clopidogrel
  • No significant drug interactions with ASA (low risk of increased bleeding with escitalopram)

P: Suggest

  • Start ASA 80mg daily (life long). Continue Dalteparin SC (VTE Px dose)
  • Monitor for s/s of ischemic stroke: one-sided weakness, numbness, trouble speaking, trouble seeing, severe headache, confusion
  • Monitor for SEs of ASA: bleeding (tarry stools, hematuria), GI upset, hemorrhagic stroke (severe headache, bizarre behaviour), daily CBCs

C3.2 R5: Perform and document a “Best Possible Medication History (BPMH)”

ID: 24 yo female with atypical Angelman syndrome with uncontrolled status epilepticus

HPI: On Feb 25, had seizures on a school trip that did not resolve with use of PRN Lorazepam. Admitted to Squamish hospital then transferred to VGH as LOC was decreasing and seizing q2-3 min (~40 sec per episode). admitted to NICU, given 8mg total ativan, 2mg midazolam, dilantin load x1, valproic acid, levetiracetam titrated up. Phenobarbital bolus was given and then LOC continued to decrease and obstruction. Patient required intubation for airway protection and was brought to ICU.

Anti-epileptics and medications PTA was not clear. Most of Med Rec was verified with: “Per Pharmanet”. Patient also had a fairly recent hospital admission for uncontrolled status epilepticus in Dec 2016, making it difficult to interpret what is current on Pharmanet.

Patient is unable to speak due to her Angelman’s syndrome. Parents were very involved in her care, kept a list of her medications and were able to answer questions. The following is verified by her parents.

Medical Conditions Medications PTA
  1. Focal dyscognitive tonic seizures (characteristics of seizures has been evolving as she has aged)
  2. Acid reflex
  3. Slow GI motility
  4. Neuropathic pain due to scoliosis
  5. Induce amenorrhea
  6. Chronic constipation
All oral medications were taken via G-tube

  1. Topiramate 125mg PO BID
  2. Clobazam 20mg PO AM, 30mg PO HS
  3. Levetiracetam 250mg PO AM, 500mg PO HS (since Jan 17/2017)
    Patient has been managed fairly well on TPM and Clobazam previously but now thought to be no longer effective. Plan with epileptologist is to wean off TPM and Clobazam after appropriate titration of LEV. 
  4. Lorazepam 2-4mg SL PRN (after 2nd clustered seizure)
    Had to use it 3 times in the last month, but parents feel that it is not effective as seizures have generally persisted despite use. Has not used midazolam PTA although filled on P’net 
  5. Lansoprazole Fastab PO BID
  6. Domperidone 10mg (2mL) PO TID
  7. Gabapentin 200mg (2mLs) PO TID
    (Indication purely for neuropathic pain)
  8. Acetaminophen 480mg (15mL) PO Q4H PRN for pain (usually needs 2 times/week)
  9. Loestrin 21 po daily
  10. Microlax (1-2 enemas twice weeky)
  11. Calcium with vitamin D (unaware of dose)

No other non-prescription or alternative medications


  • Even if there is a personal medication list provided, it is important to still verify each medication (dose, route, regimen) and indication. This is especially important for any medications that are currently being titrated up or down. Upon interview with the parents, we were able to identify one discrepancy on the list regarding her anti-epileptics.
  • For medications that have multiple indications, it is important to confirm the intended indication of the medication with the patient and/or caregivers. For example, gabapentin was prescribed purely for her neuropathic pain and not for her seizures. The neurology team had initially considered discontinuing the gabapentin but I was able to let them know it was meant for her pain and gabapentin was continued.
  • I had checked previous consultations on CareConnect after verifying the medications with her parents and found that there were some discrepancies between the consults and my interview. For instance, parents were not aware of the use of phenytoin (filled on Pharmanet) prior to this hospital admission but the most recent consult note stated that it was initiated in Dec 2016 but the plan was to titrate down and discontinue. For patients with more complex histories, medication histories and hospital admissions, it would be important for me to gather as much information from previous admissions and other specialists following them prior to the interview. This would allow me to point out any discrepancies and clarify it with them during a single interview session.
  • When doing medication reconciliations – especially for complex medication histories, I should proactively document on the chart to ensure that the health care team and other specialty teams are aware of the patient’s history.