Academic Day Seminar – HIV

I really enjoyed this session by Dr. Sandra Chang! 🙂 I thought she provided a very practical and comprehensive overview on HIV and did an excellent job in helping us form an approach to managing patients with HIV!

Some key points from this session are:

  • Initial therapy consist of triple drugs – combining medications for different HIV targets helps decrease the risk of resistance…but also requires pts to be able to commit/adhere to a regimen. Assess and help address any barriers!
    • Ensure seamless administration with 100% adherence with good tolerability:
      (1) Continuing from home
      (2) While in hospital
      (3) On discharge
  • Drug interactions – consider ALL types of medications, including street drugs
    • Useful resources: liverpool, HIVclinic
    • Lexicomp: not the most accurate, but can be used for comparison with above resources
      • Do not use lexicomp for renal dose adjustment!
    • RAL has more data in chemo DDIs, but DTG likely tno expected to interact with chemo

(Misc) Blood work to consider in hospital:

  • HIV plasma viral load, CD4 cell count, hsCRP, RPR
  • Investigation of hepatitis immune status
    • Hepatitis A (anti-HAV, total)
    • Hepatitis B (anti-HBs)
  • Acute viral hepatitis undefinited etiology:
    • Hepatitis A (anti-HAV, IgM)
    • Hepatitis B (HBsAg, plus anti-HBc if required)
    • Hepatitis C (anti-HCV)
  • Chronic viral hepatitis undefined etiology:
    • Hepatitis B (HBsAg, anti-HBc, anti-HBs)
    • Hepatitis C (anti-HCV)

Subclinical Hypothyroidism

ID: 83 yo female with refractory hypertension (on multiple antihypertensives with SBP ~170)

  • Has subclinical hypothyroidism which is being treated with levothyroxine (?link to refractory hypertension)


  • Primary hypothyroidism is characterized by a high serum thyroid-stimulating hormone (TSH) concentration and a low serum free thyroxine (T4) concentration
  • Subclinical hypothyroidism is defined biochemically as a normal free T4 concentration in the presence of an elevated TSH concentration. Secondary (central) hypothyroidism is characterized by a low serum T4 concentration and a serum TSH concentration that is not appropriately elevated

Primary hypothyroidism: 95%

  • TSH high, serum free T4 is low; subclinical (TSH high, serum free T4 normal)
  • Chronic autoimmune/lymphocytic (Hashimoto’s) thyroiditis: most common cause of hypothyroidism. Mainly older women. Anti-TPO (thyroid peroxidase) antibodies present in 75% of cases.
  • Iatrogenic: radioiodine, external Neck radiation, thyroidectomy
  • Iodine: deficiency (urine iodone <45 mcg/d) or excess
  • Drugs: rifampin, carbamazepine, phenobarbital, phenytoin, valproate, estrogen, cholestyramine, sucralfate, FeSO4, AlOH, CaCO3, lithium, interferon alpha, sunitinib, PPI? coffee?. Numerous mechanisms.
  • Infiltrative diseases: hemochromatosis, scleroderma, leukemia, tuberculosis, PCP

Hashimoto’s thyroiditis:

  • Presence of high serum concentrations of abs to thyroid peroxidase (TPO) and thyroglobulin
  • Do not routinely measure TPO abs in patients with primary overt hypothyroidism because almost all have chronic autoimmune thyroiditis – can be measured in subclinical hypothyroidism to predict likelihood of progression to permanent overt hypothyroidism

Secondary hypothyroidism: <1 %

  • TSH deficiency
  • Pituitary necrosis (eg. Sheehan’s syndrome), trauma, pituitary tumors
  • Treat with Thyrotropin (TSH, Thyrogen). Usually also need to replace other pituitary hormones.

Tertiary (central) hypothyroidism: <1%

  • TRH deficiency
  • Hypothalamic damage from tumors, trauma, radiation therapy, or infiltrative diseases.
  • Treat with Protirelin (TRH, Relefact TRH). Usually also need to replace other pituitary hormones.

In hypothyroidism caused by hypothalamic or pituitary disease, TSH secretion does not increase appropriately as T4 secretion falls. As a result, the symptoms and the serum free T4 value must be used to make the diagnosis. Thus, we measure both serum TSH and free T4 if pituitary or hypothalamic disease is suspected (eg, a young woman with amenorrhea and fatigue)

Hypothalamus — TRH –> Anterior Pituitary — TSH –> Thyroid Gland

Signs and symptoms:

CNS Fatigue, weakness, paresthesia, depression, cognitive dysfunction, decreased hearing, slow speech
HEENT Periorbital edema, tongue enlargement
RESP Dyspnea on exertion, pleural effusion, sleep apnea
CVS Bradycardia, diastolic hypertension, pericardial effusion, nonpitting edema (severe hypo), ↑ risk of CVD (HF, CHD, stroke, lipids)
GI Constipation, decreased taste
GU/Renal Menorrhagia, pubertal delay, galactorrhea, hyperprolactinemia
LIVER Ascites
ENDO Weight gain, ↑ LDL, ↑ total cholesterol
Lytes/HEME Hyponatremia (rare, only in severe), normochromic, normocytic hypoproliferative anemia
MSK/Bone Growth delay, myalgia, cramps, weakness, bradykinesia, carpal tunnel syndrome
DERM Dry, coarse skin, eczema thinning of hair, loss of eyebrows, cold sensitivity, brittle nails

The clearance of many drugs, including antiepileptic, anticoagulant, hypnotic and opioid drugs, is decreased in hypothyroidism. Thus, drug toxicity may occur if drug dose is not reduced. In addition, drugs that are administered at effective doses in patients who are hypothyroid may become less effective during T4 replacement.

Goal: Normalize TSH, T4, T3 + eliminate S&Sx.


  • Synthetic Levothyroxine (T4):
    • Young healthy adults: Start “full replacement dose”: 1.6 mcg/kg/d (50-200ug/d)
    • ELDERLY: Start 50 mcg/d; may be 1 ÎĽg/kg/d in elderly (50-100 ÎĽg/d).
    • CAD: Start 12.5-25 ÎĽg/d and monitor for angina.
    • 12.5-25 mcg/d dosage adjustments. Initiate with T4 monotherapy.
  • T4+T3 not superior to T4 alone on body weight, lipids, symptoms, cognition, QOL.
  • IV formulation available (500ÎĽg/vial = $125)

Do you treat in subclinical hypothyroidism?:

  • TSH > 10 mU/L: treat to prevent progression to overt hypothyroidism
    • data linking subclinical hypothyroidism with atherosclerosis and myocardial infarction and the increased risk of progression to overt hypothyroidism
    • supported by ATA, AACE, European thyroid association guidelines
  • TSH 7-9.9 mU/L: treat most under age 65-70 yo d/t association of increased CV mortality in younger patients. ?benefit in older patients and concerns of safety in older pts (↑ risk of exacerbation and induction of angina and CAD)
  • TSH ULN-6.9mU/L: treat <65 to 70 who have sxs suggestive of hypothyroidism. Consider if high titers of anti-TPO abs, and patients with goiter. For older patients, these levels of TSH may be age-appropriate.

  • Infertility or attempting pregnancy: suggest initiating T4 replacement (TSH values above 1st trimester-specific normal reference range with normal free T4)


  • Re-measure TSH 4-8 weeks after initiation or dose change.
  • Questionable role for fT4, no role for T3 in routine monitoring.
  • TSH annually once stable & when conditions change.
  • Avoid chronically low TSH even if asymptomatic due to osteoporosis risk (TSH <0.1 to 3.6 x ↑ in hip fracture risk & 4.5 x ↑ in vertebral fracture risk vs. normal TSH in women >65 y/o. [Ann Intern Med 2001;134:561-568, BMJ 2011;342:d2238].)
  • NOTES: Targeting lower half of TSH range no better than upper half w.r.t. Sx, QOL, cognition. [JCEM 2006:91: 2624 –2630].
  • Factors possibly requiring UPWARD dosage adjustment: worsened thyroid function, pregnancy, hi-fiber diet, concurrent rifampin, carbamazepine, phenobarbital, phenytoin, estrogen, cholestyramine, sucralfate, FeSO4, AlOH, CaCO3, lithium, nephrotic syndrome
    • ASSESS ADHERENCE (most common reason)
  • Factors possibly requiring DOWNWARD dosage adjustment: nephrotic syndrome, weight loss, androgen therapy.

Primary Hypothyroidism & Pregnancy:

  • Screening in normal healthy women: no consensus.
  • Recommendations range from screen all women before pregnancy (AACE) to screen only if high-risk (family history or goiter).
  • TREAT with T4 if TSH > ~4 mU/L.
  • If not on T4 therapy prior to pregnancy, no consensus about optimal initial dose. Some have suggested 1.2-1.4 mcg/kg/d initially. A retrospective study showed T4 50mcg/d (avg) was associated with reduced pregnancy loss and increased preterm delivery, preeclampsia, gestational diabetes.
  • Women with pre-existing primary hypothyroidism: Counsel women with primary hypothyroidism before pregnancy. If already on T4 before detecting pregnancy: Increase L-thyroxine intake by 20-30% immediately + contact caregivers urgently. [e.g. take an extra L- thyroxine dose twice weekly beginning immediately]
  • MONITORING: TSH ~q4 weeks until ~20 weeks, and at least once ~30 weeks. T4 requirements go up as early as 4-6 weeks of pregnancy, and increase through weeks 16-20, then plateau until delivery. 50 and 85% of LT4-treated hypothyroid women need a dose increase during pregnancy. Target TSH: 0.4-2.5 mU/L throughout pregnancy. Return to preconception T4 dose following delivery, TSH @ 6 weeks.

Considering patient’s refractory hypertension which is uncontrolled on multiple antihypertensives, trialing treatment of subclinical hypothyroidism to manage hypertension is appropriate (go low and slow).

C3.5 R3: Practice-Based Teaching


C3.5 R3(b): Demonstrate skill in the MODELING form of practice-based teaching

C3.5 R3(c): Demonstrate skill in the COACHING form of practice-based teaching

During residency, I was paired up with a 3rd year pharmacy student through the TMP-SMX program. I had the opportunity to model patient interviews when she shadowed me during my psychiatry rotation. During my ICU rotation, we briefly discussed patient work-ups and how to perform physical assessments. After our discussion, she performed some physical assessments on a patient while I supervised.



Academic Day Seminar – Total Parenteral and Enteral Nutrition

This was a really great session to have, and Jan did an absolutely terrific job going over this large topic and giving us practical take-away points on nutrition. This was definitely a very heavy topic and I’m glad I have a TPN rotation to try to apply the knowledge and concepts from this session.

I. The Basic Five for Enteral and Parenteral Nutrition:

  1. Equations
  2. Monitoring
  3. Tube/Access
  4. Delivery
  5. Formula

II. When you have the choice to decide between TPN and EN, EN is the 1st Choice!

  • Enteral Nutrition does not necessarily have lower risk than TPN
  • Risks of EN include:
    • Aspiration pneumonia (inability to protect airway)
    • Tube placement complications (e.g. perforation of GI tract)
    • Tube maintenance complications (esp with enteric tubes which migrate upwards and feeds to esophagus, potentially leading to aspiration)
    • GI intolerance
    • Inadequate intake (mean % received is usually 60% of what is prescribed)
    • Drug interactions (e.g. phentoin)
  • Risks of PN include:
    • Infectious complications (e.g. line infections)
      • Risk is now lower with better glucose control and stricter criteria to decide who gets PN
    • Catheter-related complications
    • Higher risk of refeeding syndrome (risk is still present with EN but with PN tend to be more aggressive with refeeding so risk is higher)
    • Liver dysfunction (PNALD = Parenteral Nutrition Associated Liver Disease)
    • Fluid/electrolyte/glucose imbalance (as increased tendency to be more aggressive with refeeding)
    • Gut mucosal atrophy (PN does not contain glutamine and GI is not being used)

✔ Enteral Nutrition

What are some barriers to providing EN?:

  • Developing procedures for safe EN practice
  • Thought that tube feeds cause diarrhea
  • CHIME: Constipation, History, Infection, Medications, Equipment


I. Energy

  • Factors that ↑ metabolic rate: lean body mass, physical activity and exercise, growth and development, being male, height (overall size), digestion)
  • Factors that ↓ metabolic rate: aging, fat mass (which is not metabolically active), starvation and dieting, sedentary living, being female (due to less muscle mass), sleep
  • % REE (= resting energy expenditure): as injury escalates (e.g. elective surgery → skeletal trauma → sepsis/peritonitis → major burns), the REE and metabolic response increases ..and when patients are in starvation, % REE decreases
  • Depends on the goal, which is usually: weight maintenance (vs. gain or loss)
  • Predictive equations: accuracy rate of 40-75% (compared to IC)
    E.g. Harris Benedict, Ratio Method
  • In ICU: Indirect calorimetry
  • What weight to use?:
    Adjusted body weight – highly debated in literature
    ADJ W = ((ABW-IBW)x25)+*IBW
    *Use BMI 25


  • Calculating protein needs:
    Most patients require 1.2-1.5g/kg/d of proteins, 20% total kcal


  • Multiple points of interface with water:
    1. Hydration, 2. Flushing EAD, 3. Dilution (medications, powdered formula)
  • Methods:
    • mostly done by age:
      20-55 yo: 35 mL/kg/day
      55-75 yo: 30 mL/kg/day
      >75 yo: 25 mL/kg/day
    • but this is just a starting point and will have to think of other IV fluids, current volume status, etc.
  • None of the formulas have been validated against a gold standard. No recommendations. Closely monitoring patients for optimal water intake regardless of which formula is chosen!


  • No tube = No nutrition (since no access)
  • No tube = No medication


Nasoenteric Tubes: Insertion site: Nose → GI tract

  • Irritant to nose…and risk of fistulas due to exposure of feeds
  • Nasogastric tube
  • Nasoduodenal tube (post-pylori)
  • Nasojejunal tube (post-pylori)

Enterostomy: Insertion site: GI tract → GI tract

  • Gastrostomy: Stomach → Stomach
  • Jejunostomy: Small bowel → Small bowel
  • Gastrojejunostomy: Stomach → Small bowel

Endoscopic Placement:

  • PEG: Percutaneous (through the skin) Endoscopic Gastrostomy
  • PEG-J: Percutaneous Endoscopic Gastro-jejunostomy
  • PEJ: Percutaneous Endoscopic Jejunostomy

Radiologic Placement:

  • PRG: Percutaneous radiologic gastrostomy
  • PRG-J: Percutaneous radiologic gastrojejunostomy
  • PRJ: Percutaneous radiologic jejunostomy

Radiologic vs. Endoscopic Placement: both equally successful (90-95%) with low mortality rates


  • anything less than French 12 should NOT be used for medications (d/t occlusion)
  • French 8 vs 12 = no difference in comfort for patients
  • MEDS ⇒ FRENCH 12
  • Internal diameter ~ External diameter


  • want larger diameters
  • need to allow tract to mature and form nice fistula tract (textbook typically states ~2 to 4 weeks but in reality it usually takes 4 weeks and might be longer for pts with impaired wound healing like diabetes)


Tube feeding routes:

  • Insertion site: Expected duration
    – if longer duration, should be away from nostril
    – enterostomy tubes: tend to be larger bore tubes
  • Terminus: Gastric function

Orogastric tubes: insertion site is mouth

  • Indication: trauma to nostril, sinus issues
  • more commonly seen in ICU (and some evidence suggesting decreased risk of VAP, but weak evidence)
  • if patients are conscious…may chew on the tube…but in ICU, use oroendotracheal tube which are larger and harder to chew

If < 4-6 weeks:

  • GASTRIC → NG (gastric) tube
  • If Gastric contraindicated (e.g. gastric stasis) → ND tube
  • CI: surgically altered gastric anatomy, delayed gastric emptying, GERD, increased aspiration risk, gastric outlet or duodenal obstruction, gastric or duodenal fistula

If 4-6 weeks:

  • GASTRIC → G (gastrostomy) tube
  • If gastric contraindicated → GJ tube or J tube (tube tip lies depending on whether the stomach is emptying)
  • Basal gastric acid secretion: 2.4-3L per 24 hrs
    • if patient has obstruction pre-pyloric, patient will be vomiting this you would want a tube tip to lie in J tube and a port in the stomach to decompress and get rid of acid


Delivery schedules: Important to know for dosing of medications!

  1. Continuous: run over 24 hours (start at lower rate and then titrated)
  2. Cyclic: a set rate that runs over less than 24 hours (usually a term used for nocturnal feeding…feed during night and disconnect during the day…may be because don’t want to be hooked up all day…or nocturnal feeds may be a supplement)
  3. Intermittent: larger volume of feeds delivered over shorter time (~1-2 hrs) (e.g. given at meal times)
  4. Bolus: similar to intermittent…taking larger volumes of feed delivered over a SHORTER time (~20 mins)

Most patients will be getting continuous delivery as possible fluid/electrolyte disturbances, gastric stasis and/or hemodynamic instability make more rapid administration potentially hazardous

Drug interactions:

  • Phenytoin
  • Ciprofloxacin

Dieticians don’t like post-pyloric tubes as cannot tolerate large volumes over a short time (e.g. diarrhea)

PICKING FORMULAS: Efficacy studies not required before products can be manufactured

  • Classifications: polymetric (everything is intact → fluid, fiber, protein), disease-specific, modular

When should a fluid restricted formula be used?

  • Renal dysfunction
  • RFS risk
  • Liver compromise
  • Cardiac compromise
  • Post-op fluid retention/redistribution

When should a fibre containing formula be used?

  • Fibre = good to help GI tract and lyte absorption…but not a lot of evidence
  • Insufficient data to support routine use of fiber in critically ill pts. Concerns re how fibre might be associated with harm in some pts (hemodynamically unstable, bowel ischemia risk, suppressed bowel motility)

When would a higher protein formula be used?

  • Depends on the patient’s injury


  • there are renal products (low protein) for CKD who are not on dialysis
  • for pulmonary compromise (e.g. someone intubated), high fat low carbohydrate = more CO2 is generated with carbohydrate → but evidence is weak
    – main thing is to not overfeed the patients
  • for hepatic products (e.g. encephalopathic patients) → have to show that correct fluid/lyte balance, metabolic stress, maximum therapy e.g. lactulose → if encephalopathic then may be a role for these products (removed from formulary at VGH)
  • for diabetic products: less carbohydrate and higher fibre with fat → this helps to slow gastric emptying…but no evidence supporting efficacy


Mnemonic: Good Monitoring Methods Improve Nutrition

  • GI: abdominal distension constipation, diarrhea (even for patients on PN since you want to know when we can use the gut, for example in patients who were put on PN d/t ileus)
  • Metabolic
  • Mechanical
  • Infection: tube site
  • Nutrition: mean % prescribed, ins and outs (e.g. feeds are held due to medications)
    • Do not look at albumin (since negative actue phase reactant and a measure of ILLNESS and not nutrition)
    • Do not look at weight (since measure of hydration)

DIARRHEA: B5 JG Diarrhea 2017 final


Potential causes include:

  1. Poorly crushed meds
  2. Liquid meds with low pH – the pH of the formula is ~ 7…therefore, if a protein rich environment = causes precipitation of protein and occludes the tube…so liquid medications may not always be better (as well ingredients like sugars, preservatives, thickening agents can cause significant SEs)
  3. Viscious liquid medications
  4. Failure to flush tube before/between/after medications are given

Prevention includes:

  • Never add meds directly to feed or bag
  • If there is both a G and J port present, use the G port for meds
    (e.g. for dual lumen tubes – 1 lumen terminates in J port and 1 lumen terminates in the G tube for decompression)
    …if gastric stasis has resolved, and gastric emptying has improved = would want to use the G port since it is the larger bore and it is more physiologically better to access medications
  • If tube lumen < 12 Fr. Do not use for meds
  • Always flush medications

REFEEDING SYNDROME: B5 EN RFS Monitoring March 2017

  • period of under nutrition, associated with fluid and electrolyte shifts and metabolic complications
  • Electrolyte replacement – consider comorbidities (e.g. renal failure pt)
  • For extreme risk at RLS (need to go slow with nutrition) to provide more time to replete electrolytes
  • Thiamine: water soluble (few stores in our body…can be depleted within 11-21 days)
    • deficiency: Wernicke’s encephalopathy (200-300mg daily)

Possible contributing factors of underfeeding:
1. Incorrect energy calculation
2. Too infrequent monitoring
3. Incorrect formula
4. Feed delivery interruptions (e.g. medication delivery)

If EN is to be held for meds, can consider:
1. PAD EN rate for time off pump
2. Consider switching to nocturnal feeds if drug dose during the day as BID or QID doses
3. Discuss with pharmacist re reduced drug dose frequency
4. Change to more energy dense formula

Other references:

✔ Total Parenteral Nutrition

  • KEY POINT: PRO 20%, CHO 50%, LIPID 30%
    • These % are generally safe as they will land you in between minimum and maximum dose
  • Average length: 6-10 days of TPN
  • Indications:
    • malnourished or at risk for malnutrition
    • contraindication to EN
    • patient cannot tolerate adequate EN
    • lacks sufficient bowel function to maintain or restore nutrition status due to GI dysfunction

Contraindications to EN:

  1. Severe hemodynamic instability
  2. Prolonged ileus, vomiting, diarrhea or persistent GI bleed
  3. Bowel obstruction
  4. Significant GI ischemia
  5. High-output fistula (if fistula that is gastric/small-bowel → can still enterically feed the patient by bypassing..but if too far down the GI tract where not enough surface area…may have to give it up)

Reasonable time frame for initiating PN when EN is not feasible in ADULTS:

  1. Initiate PN after 7 days for well-nourished, stable patients who have been unable to receive significant (>50% est requirements) oral or enteral nutrients
  2. Initiate PN within 3-5 days in those who are nutritionally at risk and unlikely to achieve desired oral intake with EN
  3. Initiate PN as soon as is feasible for patients with baseline moderate or severe malnutrition in whom oral intake or EN is not possible or sufficient
  4. Delay the initiation of PN in a patient with severe metabolic instability until the patient’s condition has improved


I. Protein:

  • Provide substrate to support organ structure/function; promote wound healing; support immunity
  • Energy value (same as enteral): 4kcal/g

II. Carbohydrate:

  • Source of energy
  • Composition: Dextrose monohydrate
  • Energy value: 3.4kcal/g
  • Min: 100g/d (for main organs  – e.g. CNS)
  • For peripheral access, higher mosmol/L = increased risk of thrombophlebitis
    For central access, osmolality is not an issue = can see D20W and D50W

III. Lipid injectable emulsion or ILE

  • Provides essential fatty acids and energy
  • Several types commercially available
    Differ in:
    1. Percent emulsion: 20%, 30%
    2. Type of oil: soybean, olive, other
  • Long chain omega acids thought to be immunosuppressive…but…as critical ill patients are malnourished…don’t worry too much about that

Electrolytes: requirements vary with: body weight, nutritional status, degree electrolyte depletion, organ function, ongoing electrolyte losses, acid/base balance, medications, disease process, carbohydrate composition

Nutrition – With refeeding syndrome, always start at LOWER doses (e.g. if patient needs 2000 cal → will give 1000 cal and then follow the PRO 20%, CHO 50%, LIPID 30%  = no issue even though carbohydrate drives refeeding syndrome more since will be at lower dose)

  • Most products are transitioning to not contain electrolytes
    (the values listed on the basic 5 facts are based on a healthy individual)
  • Managing short term electrolyte deficits by addition to the PN solution is not ideal
    • baseline/maintenance lytes (if needed) should be in TPN
      But…when in doubt, leave it out!
  • Electrolytes can be lost in NG suction!

Thiamine + Vit C: not unusual to add on additional thiamine and Vit C

  • FDA recommended that not enough vitamin C in products
  • Usually add on additional 100mg Vit C and 100-300mg Thiamine

Trace elements:

  • FH + VCH: Use Micro + 6 Concentrate
  • In short-term, standard is okay..but in longer term, concern about accumulation in trace elements especially in patients with altered liver dysfunction (but generally rare to not see the standard amounts of trace elements)
  • Iron not routinely added to PN solutions (as not stable and concern about infusion reactions)
  • PPN: Osmolarity < 900 mOsmol/L, limit 14 ds, have to rotate site
  • CPN: highly concentrated hypertonic solutions, may be used indefinitely

Compounding – PN product type:

  • Commerical pre-mixed: solution (lipid, CHO, PRO) and each macronutrient is kept in a separate entity…roll the bag and break membranes and get a 3 in 1 and with standard electrolytes for ~70kg
    – can add additional electrolytes and trace elements
  • Standard compounded
  • Custom compounded

!!Appropriate monitoring parameters shall include!!:

  • Fluid requirements
  • Serum electrolyte concentrations
  • Serum glucose concentrations
  • Hepatic function
  • Renal function
  • Serum triglycerides
  • Signs/ symptoms of access device complications

FYI: In pts with Anorexia Nervosa – albumin will be normal (as pt has adjusted)

  • if hit by truck = catecholamine response and for sick pts → albumin will be low


  • Potassium chloride and potassium acetate
  • Before adjusting the PN, what would you adjust?
    • If IV running…and then PN gets started and nobody has written TFI “Total Fluid In”… so if NS running where Cl: 154 mmol/L is going in → causing acid-base disorder

Impact of overfeeding with PN (since bypassing GI tract) → PNALD

  • Altered LFTs common
    • other factors can also affect liver dysfunction: sepsis, meds, etc.)
  • Lack of oral intake or EN: not stimulating gall bladder contraction to release bile
    • increase risk of stones
  • PNALD typically improves with the advancement of EN and discontinuation of PN
    • e.g. can we start trickling feeds to allow for stimulation of gall bladder and biliary tract
  • Some evidence that long-term soybean-based IVFE = increased risk with PNALD
    • Intralipid emulsion = starting to be taken off formulary (d/t liver concerns)
  • Some evidence that continuous PN is not physiologically normal and may be affecting liver function → may go with cyclical to give liver a break


Academic Day Seminar – Anti-fungals

I can’t believe it’s our last resident-led ADS. Julianna and Rob did a great job facilitating the session! They provided many clinical pearls and an excellent overview on anti-fungals!

My notes can be found here: Antifungal 2017 ADS Notes

Important tidbits to keep in mind when approaching anti-fungal infections:

  • Amphotericin B
    • Achieves high levels in kidney, primarily stored in kidney and slowly released (= long terminal half-life ~ 15ds) –> potential for renal toxicity (hypoMg, hypoK, and eventually renal tubular acidosis)
    • Liposomal Amphotericin B – ↓ nephrotoxicity, ↓ incidence of infusion reactions
      • At VGH and most other BC sites…tend to use liposomal right off the bat due to concerns with nephrotoxicity, regardless of baseline renal function
      • Deoxycholate has poor CNS penetration, Liposomal may have better CNS penetration and would be the alternate formulation in CNS aspergillosis
  • Flucytosine
    • *SAP* Indication for cryptococcal meningitis in combination with Amphotericin B
    • Possibly de-aminated to 5-FU (might be cause of bone marrow suppression and GI intolerance)..also causes hepatic suppression
  • Voriconazole – Candida, Aspergillus
    • Non-linear kinetics – half-life ~6 hrs (VARIABLE)
    • Hepatically metabolized by CYP2C9, 2C19 and 3A4
    • + Inhibits the above enzymes 2C9, 2C19 and 3A4
  • Itraconazole – role is limited due to moderate F, poor distribution…but has a broad spectrum of activity and may serve as salvage therapy for patients who have not recovered on other azoles
    • Posaconazole – “improved version of itraconazole” – and roles includeProphylaxis of invasive fungal infections in neutropenic patients, Refractory invasive fungal infections, Zygomycetes
  • Activity – triazoles (fungistatic to yeasts, fungicidal to aspergillosis); echinocandins (fungistatic to aspergillosis, fungicidal to candida)
  • Echinocandins – all highly protein bound, distributes well into tissues but has NO CSF penetration
    • large molecules = difficult to cross through CNS = won’t use for CNS infections
  • Therapeutic drug monitoring for flucytosine, voriconazole, posaconazole
    • Voriconazole + posaconazole levels sent to SPH (done once weekly)
  •  *remember to renally adjust* – Flucytosine, Fluconazole
    • Risk of toxicity via accumulation of IV vehicle in voriconazole in renal impairment – if appropriate, change to PO voriconazole
    • ?adjusting for renal dysfunction for amphotericin B – complicated
  • Do not consider candida as a contaminant in BCx (even if 1/4 or 2/4 +, would still treat)
  • SAP drugs – Isavuconazole, Flucytosine

Learning Objectives – Ambulatory Cardiology

I am incredibly excited to be heading to JPOSC this upcoming week for my ambulatory cardiology rotation. The following are my learning objectives:

  1. Perform at least 1 physical assessment per day and provide interpretations of my findings to my preceptor and team
    1. In particular, I would like to be able to comfortably and competently assess JVPs by the end of this rotation
  2. Be able to use available evidence (e.g. trials, PICO) to support my recommendations and to explain risk vs. benefits to my patients
  3. Complete the following procedure log: C3.5 R2: Prepare and deliver educational seminar to nurses, physicians or other allied health care members



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