Category: Academic Day Seminars

ADS – Electrolytes

I always felt from undergrad that electrolytes as a topic was some sort of nebulous concept… your patient has low potassium, so what are you gonna do? Replace it of course! Also, in the renal elective we got a run-down of hypo and hyperkalemia, derangements in acid/base balance (including anion and non-anion gap acidosis), but this ADS dove a bit deeper into how all those parameters interplay with each other. Some take-home messages I got:
– Digoxin and electrolyte balance are quite closely interrelated. Basically you need extracellular potassium to work the pump, and you need magnesium as a cofactor for the pump. Digoxin binds to that pump. Less K = more dig can bind = less Na-K pump activity.
– Low Mg can result in low K, Na, PO4, and low Ca. In other words – no matter what you do, replace the magnesium along with the others.
– I finally learned what “refeeding syndrome” actually means. I encountered a couple of cases on my Oncology rotation, but never grasped the mechanism behind it. Basically if you are in a ketogenic state and making your carbs from ketones and free fatty acid breakdown (>72 hrs after your last bite of food), if you aggressively refeed the patient, glycolysis intermediates contain phosphorylated compounds, which need phosphate —> high demand = low PO4.

I also enjoyed the cases, as they allowed us to put everything together. I can now appreciate the importance of the magnesium, and can confidently recommend replenishment strategies (after memorizing a couple of products and doses!)

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ADS – Fluid and sodium balance

This was a highly enjoyable session conducted by Dr. Loewen. His one-pager outlines the process one may follow when assessing fluids. Although it is a non-traditional activity for a pharmacist to order IV fluids for resuscitation purposes, and it would be difficult to incorporate this into a daily workflow if one is a clinical pharmacist covering 40-50 beds…it is still good to keep this in mind if only to reassess orders that have been written. I will apply myself to learn how to do a JVP and perform a volume assessment if someone has not done it already…and now I know where various IV crystalloids end up!

The main thing I wanted to know was discussed – screening for drug-caused SIADH. Euvolemic hyponatremia is the main filter, as if a patient presents with that, the list of things that can cause SIADH is quite extensive, which include CNS or respiratory insults – i.e. pneumonias. Hopefully I come across a case of euvolemic hyponatremia so I can put this to practice!

ADS – Presentation Skills

BC-wide is looming in the distance…I respect those of us who need to present these next month! Wow! Overall, this session answered some of the questions I had regarding the nitty-gritty logistical concerns, such as whether my recommendation had to have been accepted to be BC-wide worthy. I think that the more presentations I do, the more I will be confident. I will take and apply the following pointers:
– Don’t try and fit the evidence to the recommendation
– Present ALL applicable evidence if your patient would have been included, don’t just present 1 RCT “because there is no time”
– This isn’t a journal club, no need to go into exhaustive detail <— (I was anxious about this…how much detail? This was reassuring.)

The search is on for a case presentation for this rotation…

ADS – Interpretation of LFTs

This was a helpful seminar conducted by two of our fellow residents on the interpretation of LFTs.

Prior to the session I knew that LFTs should be reported not as absolute values, but magnitudes above the upper limit of normal, increased AST/ALT reflected hepatocellular damage, and increased GGT reflected chronic alcohol use. Also, during Clinical Orientation, I learned that albumin and PTT/INR are good actual measures of liver function…as coagulation factors are manufactured in the liver; therefore, less coag = increased PTT/INR.

Major take-homes from this session:
– It’s always a process in residency. 1) Is this cholestatic/biliary or hepatocellular?
2) How much are the tests elevated above the ULN? Is this acute or chronic?
3) Where is the trend going? 4) What clinical correlations are possible?
5) TREAT THE PATIENT/CAUSE, NOT THE LEVEL!
– AST/ALT, GGT/ALP, and INR (PTT)/albumin are good duets of tests to consider together to get a sense of what is going on
– AST and ALT may be normal in the context of chronic liver damage as increases are only acute and reflect NEW liver cell damage
– Non-alcoholic fatty liver disease is a thing. Suspect it in a mildly (2-5x) elevated AST/ALT and AST:ALT <1 panel with a Hx of metabolic syndrome and obesity.
– The liver can be “bright” on ultrasound in the context of fatty liver disease

I intend on practicing these techniques constantly; I started today with a patient who came in with a Dx of acute pancreatitis and a Hx of hepatitis C. In chronic viral hepatitis, the AST and ALT may hang around the ULN, and the INR is high and albumin low over time. Her case was complicated by a history of alcohol use disorder, hence her GGT was 10x ULN and the bilirubin was highly elevated at 31, and the GGT:ALP ratio was >2.5.

ADS – Phenytoin and Digoxin Pharmacokinetics

We meet again, University of Kentucky Clinical Pharmacokinetics Manual…although phenytoin and digoxin are two drugs which are not used that often (phenytoin definitely not used as often as it was before), it’s two tools that would be helpful in a clinical pharmacist’s arsenal in order to deliver timely, effective and safe pharmacotherapeutic care. The following is what I gathered from the session in order to deliver EFFICIENT and SAFE care (not necessarily perfectly calculating every patient’s individual PK parameters). I look forward to tackling some phenytoin and digoxin PK conundrums on my rotations!

Phenytoin – the skinny on how it is dosed and adjusted – my flowchart
Remember: mg/L * 4 = umol/L
1) Is the patient actively seizing?
YES – load immediately with 15-20 mg/kg IV phenytoin, max rate 50 mg/minute. You don’t have time to calculate a load! Take a level two hours after giving the dose. If the patient is actively seizing while on phenytoin, may give diazepam to abort the seizure.
NO – may load empirically with 13-15 mg/kg PO/IV phenytoin depending on whether they are post-ictal, and start a maintenance dose 8-12 hours after depending on what trough you are aiming for. For PO, take a level 24 hours after giving for a peak.
2) What maintenance dose do I give?
EMPIRICALLY – 5-7 mg/kg
THE LONG WAY (use only if you are unable to achieve adequate troughs with multiple attempts) – look up the patient’s Km (more likely to be stable), calculate the Vm given the Css and dose you have. Back-calculate the necessary dose given the Vm you just calculated.
3) My patient is hypoalbuminemic – what do I do?
ESRD – observed phenytoin/(albumin*0.02 + 0.1) = corrected phenytoin
NO ESRD – observed phenytoin/(albumin*0.01 + 0.1) = corrected phenytoin
4) Do I need to give a mini-load?
IT DEPENDS – on if the patient is near the top of their 5-7 mg/kg empiric range, if they recently seized, if they are experiencing phenytoin-specific toxicity, i.e. drowsiness is NOT a specific symptom
5) My patient is exhibiting phenytoin toxicity and has trough levels exceeding 80 umol/L – how long do I wait for the level to drop below 80?
RULE OF THUMB – 1 day, for every 20 umol/L over 80. Exceptions are if the patient is extremely supratherapeutic (>>120 umol/L), in which case order daily phenytoin levels.
6) At which serum levels would I expect to see certain toxicities?
>120 umol/L = nystagmus and ataxia
>160 umol/L = altered mentation
>200 umol/L = coma.

Digoxin – the skinny on how it is dosed and adjusted – my flowchart
1) How do I load a patient on digoxin? (not really recommended in heart failure…)
EMPIRICALLY – 8-12 mcg/kg IV of LEAN (ideal) body weight
THE LONG WAY – Vd = 7 L/kg, C = 0.6-1 ng/mL for HF, 1.2-1.5 ng/mL for A-fib, F = 0.7 for tablets, S = 1. Calculate PO dose = (Vd * C)/(SF).
REGARDLESS OF HOW YOU CALCULATE, load 1/2 the dose stat, then 1/4 x 2 doses Q6H.
2) When and how much do I give digoxin for maintenance?
0.125-0.25 mg PO daily, or 2.4-3.6 mcg/kg IV daily.
3) Do I need digoxin levels? – no. Do them if and only if you suspect toxicity.
4) How do I give Digibind? – https://lifeinthefastlane.com/ccc/digibind/may need to repeat dosing later due to extensive distribution and high volume of distribution. Take repeat levels to assess response.

Another gem for digoxin toxicity from one of my favourite blogs, which I am sure will come in handy for Emerg rotation – https://lifeinthefastlane.com/ccc/digoxin-toxicity/

ADS – Heart Failure

Two of our fellow residents delivered a very helpful seminar on the diagnosis, presentation, and treatment of HFrEF (more emphasis on this) and HFpEF. For me, it was a helpful reminder of the landmark trials, as well as a great therapeutic update on the recent SHIFT and PARADIGM-HF trials for ivabradine and sacubitril/valsartan, respectively. Here are some of the take-home messages I got:
– A useful way to assess orthopnea is to ask the patient how many pillows they use at home to achieve adequate comfort while breathing
– Triple (ACEI/ARB + BB + MRA) therapy to target doses plus loop diuretic titrated to benefit is still the backbone of HFrEF pharmacotherapy
– The only reason furosemide does not have a RCT demonstrating mortality benefit is that it would be unethical to withhold loop diuretics from HF patients
– CLINICAL PEARL: for renal impairment, effective dose of furosemide may be estimated by calculating SCr divided by 2!
– HFpEF therapy = treat the comorbids and risk factors for HF in general (i.e. smoking, HTN, COPD, liver and renal disease…)
– Hydralazine and ISDN, together, are thought to mimic ACEI action – may be more beneficial in patients of African-American descent
– Ivabradine is kind of like a new digoxin in terms of its effects on heart rate and its morbidity but no mortality benefit, but it only has chronotropic effects
– Anecdotal evidence quips that many patients cannot tolerate the doses of sacubitril/valsartan that was used in the trial (200 mg PO BID)

I’m confident I will encounter numerous HF patients during my various rotations, so I’m glad that this ADS came up relatively early so that I can be more efficient in identifying DTPs – already on clinical orientation and my 4th year hospital rotation I came across two patients who had NEVER been tried on ACEI or ARB for their HFrEF despite not having any absolute or relative contraindications…these patients would certainly benefit from intervention!

ADS – Acid-base disorders

During EBM week, we learned that one of the most common reasons why learners motivate themselves to learn something that they don’t otherwise want to learn is a fear of failure or humiliation. Not that I didn’t want to learn this, as acid-base disorders was an area that weren’t touched upon in the undergrad curriculum (except for one lecture in the renal elective), but Dr. Brown’s lecturing style certainly motivates one to do the pre-readings and do them well.

I won’t go over WHAT was taught as I feel that I have a good grasp on what was covered and I just need to practice it – any patient who has labs drawn, or arterial blood gases done, I will try to evaluate them and see if there is an acid-base disorder. I have a good idea of what causes each of the disorders, and how that will influence drug therapy – example is a metabolic acidosis where replenishment of bicarb is necessary… but bicarbonate is reconstituted in a bag of NS…which has 154 mEq/L. Not nice!

Normal pCO2 = 40 mm Hg
Normal HCO3 = 24 mm Hg (21-28)
Normal anion gap = 10 (8-12)… ADJUST NORMAL down by 2 for every 10 g/L drop in serum albumin (N = 42-46 g/L)

One pearl I must record though is that potassium usually follows blood pH changes due to shunting of potassium (a cation) into or out of the cell to maintain ion balance.
– As pH DECREASES in acidemia, potassium INCREASES
– As pH INCREASES in alkalemia, potassium DECREASES

I’m more a systems kind of person and I like a systematic way of evaluating anything. For that reason, I found acid-base disorders to be easy to wrap my head around. As long as I have the labs, the blood pH is the main anchor and will let me determine whether it is an acidemia or alkalemia. The corroborating signs, symptoms, and labwork will allow me to confirm that the drug therapy for the appropriate diagnosis is the best for the patient.

ADS – Clinical pharmacokinetics approach to aminoglycoside and vancomycin dosing

I found myself repeating the old adage from 2nd year pharmacokinetics that Dr. Ensom said: “if you want the chicken to be finger lickin’ good, you have to use the Colonel’s recipe!” For the majority of patients, the “recipe”, i.e. dosing protocol will work just fine, but this session was mostly me trying to remember how the heck I even knew how to use those equations in The Kentucky Manual…anyway, here are some pertinent points I got from the morning’s session.

Aminoglycosides (Vd = 0.2-0.3 L/kg and t1/2 = 2 hours for adults);  – use the VCH dosing protocol for traditional or extended interval dosing. Do NOT use extended interval in: pregnancy, burns >20% BSA, pts on dialysis, or septic shock. Basically anyone who would have increased clearance such that the post-antibiotic effect will not extend to 24 hours.
To load or not to load? – YES, unless you are doing once-daily extended interval dosing.
When do you take a level? – before the 3rd dose within 30 mins, and 30 mins after the half-hour infusion (4th dose). No levels for extended interval dosing as the trough will be undetectable anyway.
How do you monitor for toxicities? – vestibular toxicity manifests in 1-2 weeks, so get audiology involved if you suspect it. Nephrotoxicity happens quicker.
Adjusting doses based on levels – if your patient’s renal function is stable, and their clinical course is stable, and they have received all their doses and are at steady state… you can use the “cheat” method for a peak level. For everything else, there’s Masterca- The Kentucky Manual. Also useful if the levels were not drawn correctly at the right time.

The “cheat” equation: New dose = old dose * (desired level/actual level) 

Vancomycin (Vd = 0.6-0.8 L/kg and t1/2 = 4-6 hours for adults) – use the VCH/PHC dosing protocol.
To load or not to load? – YES…although in the course of doing the literature search for my project, I found that the evidence of a loading dose is not very extensive, but if a patient’s bacteremic, or they have meningitis, you wouldn’t deny them a load, right?
When do you take a level? – I thought this was cut and dry, before the 4th dose then use the cheat equation above to adjust the dose. HOWEVER, Dr. Loh presented an interesting case where one would have to improvise. A level may not even be warranted for an otherwise healthy patient who may not get vanco past 7 days. Post-levels are usually not indicated, and only reserved for unique cases such as in the case of renal failure or burns, or unstable clinical status warranting calculation of individual PK parameters.
In the setting of fulminant renal failure, it might be advisable to give a “mini-load” for the patient if a suboptimal dose was given in Emerg. After that, a random vanco level may be the best option just to see how the patient is clearing the drug.
If a load was given in Emerg, technically you could take a level pre-3rd dose assuming that the patient’s clinical status has remained stable. – the half-life of vanco is 4-6 hours, so steady state should be reached in 20-30 hours… assuming q12h dosing, that would fall within before the 3rd dose.
How do you monitor for toxicities? – there are some that are dose-related, i.e. red man syndrome and ototoxicity, and some that are not, such as nephrotoxicity (but really…vanco is not that nephrotoxic, one would be more worried about the other medications on board that may be nephrotoxic). NEUTROPENIA actually occurs in 1-10% of patients (as per Lexicomp) but it only manifests after 1-2 weeks of treatment.

Overall, I feel more confident than when I walked in that morning in terms of my ability to evaluate a patient’s AMG or vancomycin regimen. I also learned that sometimes you may have to improvise and think clinically to solve dosing issues – but that’s why we are on the ward! If everything were perfectly protocolized, physicians wouldn’t need us!

ADS – Community-acquired and hospital-acquired pneumonia

I quite enjoyed this session. Going back to Dr. Nishi’s session on an intro to ID, where she kept saying that for undergraduates, we are trained to treat ID as a cookie cutter system. Cellulitis gets cephalexin or cefazolin, full stop! However, real life is never that black and white, and this session revealed that. Dr. Brown introduced a case where the medical resident asks you what is good to treat someone with fever and cough. This was a good session to follow the morning one as we got into the mindset of first asking if there was an infection or not. It was a bit like a general workup. Vitals, ROS, med Hx, conditions, labs, and HPI. Once we were convinced it was a pneumonia, it turned to a roundtable discussion where we each had to provide a regimen and defend it! In total there were almost 30 regimens. After, we went through each and every choice, and the pros and cons of each regimen.

This was a great reminder of what to consider when recommending a medication (or not) for an ID patient. Definitely not cookie cutter. It also made us recall knowledge from the bugs and drugs table from undergrad, along with more up to date antibiograms. 

The process was repeated, albeit abridged, for HAP and VAP. The main point I got was that >48 hours exposure to the hospital setting or health care setting coupled with S/S suggestive of pneumonia increases your suspicion of HAP. In addition, there is much to keep in mind including if they had surgery and what type of surgery they had, prior exposure to broad spectrum ABX…kind of like a regular workup! The biggest pearl I got was that generally, double covering for Gram-negatives is not necessary. This encouraged me to think beyond the guidelines, while also thinking about the usual hospital bugs you’d be worried about such as Enterobacteriaceae, Acinetobacter, and MRSA pneumonia.

This session provided a good framework by which to approach other types of infection I will encounter, including UTIs, intraabdominal infections, meningitis, and others.

ADS – Introduction to Infectious Diseases

I’m writing this on public transit so I don’t forget most of the things (it’s amazing what you think you retain right after but then lose shortly thereafter!). Here are some of the more pertinent points I got from today’s morning session:

– Always be skeptical of a specimen: when it was obtained, where the sample was taken from, and (where I think I’d miss the most) how the sample was obtained. Harking back to my hospital rotation, I know that I’d skip to the C&S.

– The white blood cell count (and sometimes the temperature) can be deceiving: but a fever and leukocytosis indicate infection, I cry! It was a good reminder that there are multiple causes for these signs.

– Source control is sometimes the most important way to treat an infected patient: it’s great that you treat an intraabdominal abscess with cipro and metronidazole, but antibiotics don’t penetrate that well into abscesses. It shows how medicine and pharmacy can work together.

– The fundamental question is “does my patient have an infection?”: Again, it was good to build upon undergraduate knowledge and it gave me some tools to critically assess the culture, physical findings, and antibiotic choice that may be on board already. Just because an organism grows (and sometimes heavily) on a C&S does not mean that organism is causing the infection.

This was a great primer (full of clinical pearls that I will update with in Nuggets of Knowledge) to my upcoming ID/AMS rotation, which I am really looking forward to. It allowed me to rustle through the depths of 2nd year knowledge, and should prove to be a good background by which to base further learning from.