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!
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…
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.
My patient was a 29 yo female with a MRSA bacteremia, query infectious endocarditis with septic emboli. She weighed 49.8 kg and her SCr was 48 and stable. The previously ordered dose in emerg by the pharmacist was: vancomycin 1.5 g IV q8h. From her current weight the dose seemed a bit high but a level was taken and the trough was 15.4 mg/L. This reflected steady state as it was before the 4th dose.
What occurred was the ID service was following her, and instructions were to “weigh the patient, then page, ID to adjust vanco”. ID changed the dose to 1 g IV q24h. This prompted me to check the MAR and see if all doses were administered on time, and to double check whether the renal function had changed. This patient received all doses on time, and her renal function was stable. Her blood cultures had still not cleared MRSA. I wrote a pharmacy order to cancel the previous orders and continue vancomycin at 1.5 g IV q8h, and to take a level on Thursday (one week after the last level). She had missed one dose of her vancomycin due to the change, but by the time the next level is taken on Thursday, she would have achieved steady state again by then.
During my medicine rotation at SPH I was involved in the care of a gentleman with a past medical history of (amongst other conditions) bipolar I, T2DM, and recurrent episodes of DKA who presented to the ED in hyperosmolar hyperglycemic state. During his stay in hospital, he required bolus insulin significantly beyond his basal insulin glargine (on the scale of 60-80 units of lispro per day in addition to 90 units of glargine nightly at bedtime).
The main barrier to discharge for this gentleman was an inability to adhere to his insulin and PO drug therapy as his medications were frequently stolen from him. The idea of daily dispensing (including the insulin) and safe storage of his medications was floated to the team. I liaised with the community pharmacy and ensured that they would follow up with him and reinforce the importance of taking his antihyperglycemic medications to avoid further trips to hospital. I also prepared the discharge prescriptions and discussed the implementation of a simple, once-daily insulin regimen, taking into account insulin bolus usage in hospital and nutrition differences upon discharge (as this gentleman is homeless and would not have reliable access to food in the community).
A bit late posting this…first couple days on CTU Pink at St. Paul’s has been busy! It’s certainly interesting what rolls in through the door and the different issues that come up. Here are the goals I set for myself prior to starting the rotation..mostly borne out of the feedback I received from BCCA in regards to my process:
Goal #1: Improve my ability and confidence to provide verbal recommendations to the team. Objectives to meet this goal:
- Attend team bedside rounds and have my recommendations ran by my preceptor and ready to go by then
- Structure my rationale in terms of efficacy and safety
- Have a plan B recommendation prepared in case my first one is not accepted with a good rationale
Goal #2: Be more comprehensive with my alternatives list for resolution of DTPs. Objectives to meet this goal:
- Include and consider continuing current management, or different doses or dosing forms of medications in my alternatives
- Do not leave a DTP without a medical issue attached to it, e.g. adjust the bowel protocol for renal dysfunction, attached to AKI as a problem
Goal #3: Become more systematic in gathering info and reporting in regards to daily updates. Objectives to meet this goal:
- Utilize the same format and process in updates as in the initial workup, e.g. ROS, vitals, labs, new problems, DTPs, alternatives, plan
- Consistently solicit feedback from preceptor on how to streamline thought process to be more comprehensive
Goal #4: Develop a strong knowledge base on the most common set of conditions that are encountered on a general medicine ward. Objectives to meet this goal:
- Seek out new opportunities to fill in gaps in knowledge; personally, substance abuse disorders and acute conditions not well covered in the undergrad curriculum, e.g. CHFE, DKA, sepsis, hepatitis C
- Perform personal mini didactics on unfamiliar conditions, structured similarly to how conditions were learned in pharmacy school, e.g. pathophys, lab and physical, treatment alternatives, landmark trials/evidence, monitoring
- Continue to record nuggets of knowledge in notebook to reconcile with previous knowledge of conditions, and reflect how one would treat the condition with differing circumstances
I look forward to further developing my thought process and being more confident in formulating plans.
Currently on project week, but attended a seminar conducted by one of the graduate PharmD candidates on the use of DOACs in valvular A-fib. Personally, I had come across a couple of patients on my 489 rotation and also a patient on Clinical Orientation who had some form of valvular stenosis (don’t recall which valve was affected), and upon further review of an NEJM review paper, I always assumed the following: mechanical valve = no DOACs allowed. These patients were on warfarin or put on warfarin upon discharge. Turns out it is always a bit more complicated than that…here are some highlights:
- The definition of valvular A-fib varies, depending on where you are. In Canada: mitral stenosis, or bioprosthetic/mechanical valves qualify as valvular A-fib.
- The original warfarin vs placebo trials excluded patients with mitral stenosis as warfarin was already standard of care…hence DOAC vs warfarin subgroup analyses that were conducted after RE-LY, ARISTOTLE, ROCKET-AF excluded mitral stenosis pts as well
- The subgroup analyses of the 3 landmark DOAC trials are based on small sample sizes on the scale of n = 200 or so
- The most reassuring data comes from RE-LY and ARISTOTLE in terms of stroke, systemic emboli, and major bleed rates when it comes to testing for interaction between having various forms of valvular disease or not having valvular disease
- Dabigatran = no differences in stroke, emboli, or bleed whether you had valvular disease or not; HOWEVER, the RE-LY re-analysis included patients with moderate and severe mitral stenosis – i.e. the patients more likely to be admitted.
- Rivaroxaban = may have increased bleeds with atrial or mitral regurg…but that may be due to bigger sample size
- Apixaban = no differences in stroke, emboli or bleed whether you have valvular disease or not
- Bottom line: dabigatran appears to have the most reassuring data, with the caveat that atrial regurg or stenosis, or mitral regurg drove the results
- Bottom line: mechanical heart valves still are a no-go for DOACs. Trials are ongoing, however.
After this seminar, it definitely opened my eyes and I would look harder into whether a DOAC can be used, as now current practice appears to be shifting towards being a little looser with their use. Also, as a bonus, Pharmacare coverage can be obtained as long as the valvular disease is not rheumatic in nature, as long as it isn’t mitral stenosis, and as long as it isn’t a prosthetic heart valve.
Hey, that wasn’t so bad now, was it? First clinical rotation complete! I think I am starting to fully understand what previous residents say – as soon as you start feeling somewhat comfortable with a ward, it’s time to move on to the next rotation. However, it is all to make you a more adaptable and proficient clinician. I thoroughly enjoyed my time at BCCA, and I had so many great opportunities, such as to observe procedures such as lumbar punctures and bone marrow biopsies, and take a trip down to RadOnc to see the machines and learn more about radiation-specific adverse effects.
I also became more comfortable with formulating medical problem and DTP lists and prioritizing them. I think overall, I never expected to be an expert in oncology by the end of it, but I think I met my overarching goal which was to “become marginally closer to being a competent clinician” – yay for achieving things! How about my goals that I came up with before the rotation?
Goal #1: Develop a head to toe approach to assessing a patient for adverse drug events secondary to chemotherapy, or supportive agents for chemotherapy – yes, did this. Went back to my review of systems, and my preceptor helped me work through the laundry list of side effects that one may experience, depending on the chemotherapy agent that is being used, and at which dose.
Goal #2: Be able to provide executable recommendations upon demand for proactive nausea and vomiting management based on the BCCA protocol the patient is on – achieved this. I had a patient in my last week with a pancreas primary that was locally advanced to her GI system who had intractable nausea and vomiting, but unfortunately was non-compliant to diet restrictions recommended by the RD. It was very tricky discerning which medications or non-pharm measures were actually effective for her, but it was rewarding working with the Pain and Symptom medical team, even if it was brainstorming medication regimens that we hadn’t tried with her. My roadmap going forward will be to go back to the fundamentals – have an alternatives list to every recommendation – then you won’t miss anything.
Goal #3: Develop a process for counselling oncology patients on either a new chemotherapy regimen or supportive care medications – I did prepare a medication calendar for a couple of patients during the course of the rotation, and counselled on changes to therapy, and also symptoms of oncologic emergencies to watch out for, such as fever (heralding febrile neutropenia), or bilteral numbing in extremities (heralding spinal cord compression). Most of the patients I came across were already midway or further through their treatment regimen.
Back from the Sunshine Coast and enjoying my vacation week so far – Gen Med next…
On August 30th, I delivered a case presentation around a topic that is commonly encountered by the clinical pharmacist in an oncology setting – non-painful chemotherapy-induced peripheral neuropathy (CIPN). As quite a number of patients on the ward I was on were receiving platinum agents or vincristine, I encountered it in every single of those patients as well. It triggered a clinical question in me that I sought to answer – is there anything that I could recommend to help these individuals, and when would I recommend it?
Perhaps not surprisingly, most of the evidence for treatment of CIPN is centered around either painful CIPN, or extrapolated from evidence in non-chemotherapy induced peripheral neuropathy of other etiologies, such as diabetes.
Here are the things that I thought went well:
– I think that my literature search was sound and thorough
– I was able to fully rationalize my decision-making after some prompting by questioning after the presentation
– I felt at ease delivering the presentation
Here are things that I would like to work on for my next seminar:
– I say “uh” at lot. I think I just need to pause at certain places to gather my thoughts.
– Don’t go fidgeting for answers during question period
– Be a more effective pharmacist by anticipating next steps after this therapeutic decision: what if this doesn’t work? How long to treat?
Upon the advice of Dr. Abadi, this may turn into a publishable case study that I will continue to keep in touch with my primary preceptor, and follow-up on this patient’s response to therapy. I also, depending on the patient’s response and follow-up, may turn this into a BC-wide case presentation (after some serious cutting – 20 minutes is short!)
Here are my slides: Oncology Case Presentation
This was a brand new experience for me – facilitating that is, but I had attended other journal clubs. For this one, I opted for a PowerPoint presentation format as I wanted to give some background to the trial and the drug used before delving into the actual paper.
This was a journal club on the REMARC trial – comparing lenalidomide maintenance therapy vs placebo after standard-of-care R-CHOP for diffuse large B-cell lymphoma, looking at progression-free survival.
Here’s what I thought went well:
– Apparently I appeared confident. Well, fake it till you make it. =)
– The process I used for clinically appraising the paper felt right, and I intend on using that process for future journal clubs. Harking back to EBM week, using a checklist like CONSORT certainly helps.
Areas for improvement for next time:
– Could do a better job anticipating future directions in terms of other comparators, for example lenalidomide vs. salvage chemotherapy, or longer follow-up
– Use a more interactive format next time
Overall, I thought it went pretty well and I look forward to building upon this foundation going forward for future journal clubs.
My slides: Oncology Journal Club Presentation