I got to see a patient in Emerg who had a few medications where she was not taking them as they appeared on Pharmanet, and a couple of things where I had to discuss how to proceed with the attending from Family Practice, who was going to admit her. This patient presented with nausea and vomiting, with worsening spinal and left flank pain. Her CT abdo/pelvis showed a renal stone. She had a prior medical Hx of A-fib (CHADS2 = 2), hypertension, T2DM, spinal stenosis (awaiting orthopedics consult), CKD stage 3a, and fatty liver disease. She was on numerous medications, which included:
– Valsartan 160 mg/HCTZ 12.5 mg PO daily, which was discontinued in community
– Nifedipine XR 30 mg PO daily
– Linagliptin 2.5 mg/metformin 1000 mg PO daily (appeared as BID on Pharmanet)
– Warfarin 1, 2, and 4 mg strengths appeared on her Pharmanet, all with the instructions “take one tablet daily”, but I clarified with the patient that her home dose has been 5 mg PO daily for the past month at least (she had tried 5/6 mg daily alternating days, 4/5 as well in the past), and her INR was 2.3 when she came in (therapeutic for her A-fib). Her diet was self-reported to be erratic, so I provided patient education that consistency is key when considering dietary influences on the INR.
The main thing to reconcile on her MedRec, apart from the warfarin, was polypharmacy on part of analgesics for her spinal stenosis. She was taking gabapentin 300 mg PO BID, diclofenac 2.32% (OTC) gel applied PRN + diclofenac 10% (Rx) gel applied PRN (usually both of these used 2x/week), and acetaminophen 325 mg/methocarbamol 400 mg (Robaxacet) i tab PO HS PRN (usually 2x/week), along with past trials of acetaminophen with codeine +/- caffeine. I discussed this with the physician, and we decided on streamlining her analgesics (diclofenac 10% gel, gabapentin 300 mg PO BID with PRN acetaminophen) referring her to the CPAS service (complex pain and addictions) as increasing her gabapentin was not an option by virtue of her decreased renal function and her intolerance to trials of higher dosages (sedation), possible acetaminophen polypharmacy, and definite diclofenac polypharmacy.
Usually I don’t get to delve into the “Internal Medicine” aspects of a case too deeply in Emerg, but this was a good example of dealing with what she acutely came in with (pain), while cleaning up her medications.
As part of my Antimicrobial Stewardship rotation, I delivered a presentation on aggressive (4.5 g IV q6h) versus non-aggressive (3.375 g IV q6h or 4.5 g IV q8h) dosing of pip/tazo for Pseudomonas infections in adult patients without CF and with good renal function. I decided to focus my presentation on a few sources of infection. This presentation triggered a lot of debate among the pharmacists, which was good to see.
What I thought I did well on this presentation:
– Tackled a topic that had a lot of grey to it! I think I never expected the evidence to be great but it was new for me to draw clinical conclusions based on the level of data I encountered
– I thought I was more prepared with questions from the audience compared to my Medicine presentation, although Michelle and Tien (the ID fellow with us on rotation) had to jump in on occasion.
– My pace was more relaxed, and I did not feel like I was rushing through the presentation
What to work on for next presentation, and BC-wide:
– Need to refine slides to make them more viewer-friendly, especially when going over large amounts of literature
– Need to be more clear on conditions of my recommendations and rationale, i.e. HAP vs VAP, same source, same bugs…therefore same dose!
– Be more economical with what I say, versus what appears on the slides. People need to listen as well as read!
October 12th, I presented a case of an 87 year old female with chronic subdural hematoma whose anticoagulation for her comorbid A-fib was held due to concerns regarding her falling (and possibly hitting her head) and subsequent vertebral fracture. My slides are here.
Overall, I thought it went smoother than my last case presentation. I found that I was eliminating more irrelevant information in presenting the case, and developing a more streamlined process to present multiple studies. I felt at ease delivering the presentation and I felt more comfortable fielding questions from attendees. Where I think I can improve on for next presentation is:
– Anticipating more questions from the audience
– Providing rationale for guideline recommendations where it may be unclear
– Shortening the presentation by eliminating extraneous data from presenting the studies…would also probably help for BC-wide purposes.
With each presentation, I am feeling more confident in delivering them and being more comfortable with the notion that I know the material. I think it comes with being more confident with the fact that you have covered all your bases when researching for the presentation.
Today I was involved in the discharge of an 86 year old female admitted for pancytopenia which was subsequently diagnosed by the hematology service as warm autoimmune hemolytic anemia (AIHA). The main issues with her discharge were whether she should be restarted on antiplatelet therapy and warfarin, whether her ferrous gluconate should be continued, and the choice of her atrial fibrillation rate control therapy.
PMHx significant for:
– STEMI in 2012 that was treated with a CABG –> on ASA 81 mg PO daily upon admission, both held then
– Non-valvular A-fib (CHADS2 = 2), and suspected HFpEF –> on losartan 25 mg PO daily, furosemide 20 mg PO daily, warfarin 2 mg PO daily, and amiodarone 200 mg PO daily. A trial of metoprolol was noted late last year but only for 3 months and upon interview of the patient no reason could be gathered as to why it was discontinued.
She was treated with prednisone 50 mg PO daily for her AIHA, but she was not completely responsive to therapy (platelets still <50) so hematology was considering rituximab.
What the team decided in regards to my recommendations:
– D/C amiodarone
– D/C ferrous gluconate as her anemia was d/t AIHA (high RDW)
– Do not restart ASA as it was 5 years since her STEMI and her platelets were <50, and she has an indication for anticoagulation
– Hold warfarin for now, weekly bloodwork in community, follow-up with GP and restart warfarin at 2 mg PO daily when platelets >50 consistently
– Start metoprolol cautiously at 12.5 mg PO BID for rate control
– Start rosuvastatin 20 mg PO daily for secondary CV prevention as it does not interact with amiodarone which has a half-life of ~50-60 days (unlike atorvastatin), and she had never tried a statin before
– Referral to Healthy Heart Clinic at SPH
My patient was a 75 year old man who was found down, incontinent of urine in a post-ictal state, who had 3 unwitnessed seizures, with a baseline frequency of 1 seizure per day (although none since admission x 8 days now). He was worked up in the ED and the working diagnosis was a pneumonia + uncontrolled seizure disorder. PMHx is significant for T2DM, tonic-clonic seizures, paroxysmal A-fib, left MCA ischemic stroke in 2014 resulting in Broca’s aphasia, had a CABG x 4 in 2000, CKD3b, PUD with prior GI bleed, and hypertension.
He was taking carbamazepine CR 300 mg AM + 200 mg PM daily, and part of his workup involved taking a carbamazepine level. Two levels were done; one upon presentation to the ED on the 26th (36 umol/L), and one at 0545h on the 28th (25 umol/L). Both appeared to be therapeutic (17-51 umol/L). I then enquired about his adherence with him and his family.
Usually a trough level is taken for carbamazepine, and the half-life for repeated dosing (which is what this man was taking, presumably – reports good adherence and is blisterpacked monthly in community) is around 12-17 hours, the level taken at 0545h is not a true trough, but extrapolating using 1st order PK, it would still be technically therapeutic by the time his next dose was due at 0900h (~20-21 umol/L).
Regardless, the purpose of the level was to determine adherence and whether he was underdosed from a pharmacokinetic standpoint – since his baseline seizure frequency was 1 a day, I wrote a note in the health record documenting my thought process and recommended an increase to his carbamazepine to 300 mg CR PO BID, since maintenance doses are usually 600-1200 mg/day, and toxicity (such as more seizures) are not observed until trough levels of >150 umol/L. Neurology has been consulted and will see him on an outpatient basis.
This is a follow-up to the 29 yo female with MRSA bacteremia in my 1st vancomycin interpretation post.
Throughout the course of her hospitalization as she was treated for MRSA bacteremia, she has started to refuse blood work consistently, including vancomycin levels. She was treated with 1.25 g IV q8h. She had a PICC line inserted in preparation for possible discharge and outpatient antibiotic therapy. Consequently, there have been some difficulties in interpretation.
Today, her level (drawn at 0651h for a 0600h dose that was actually given at 0645h) was 45.3 mg/L, which is markedly supratherapeutic compared to the target trough of 15-20 mg/L for a bacteremia. Upon reviewing the MAR (where the dose was initially signed off for 0600h) and the electronic health care record where it indicated the level was drawn at 0651h, I thought initially that it reflected a peak level rather than a trough. However, further discussion with the RN revealed that the previous night nurse hung the dose for a minute, recalled a vanco level was pending, then took the level from the PICC line, where there may have been residual vancomycin.
her SCr has been fluctuating between ~60-80 over the past few days from a baseline of ~45-50, so there is also the possibility that she may be accumulating. Consequently, what was done is her subsequent dose at 1400h was held, and a stat level was taken through the PICC after flushing it with normal saline. That result is currently pending.
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).
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
On my oncology rotation, I came across a patient that I was taking care of who was admitted for hypoxia and SOB when she reported for assessment before her next cycle of chemotherapy for metastatic breast cancer. She was dyspneic, exhausted, and was saturating 89% on room air. She had already received multiple rounds of chemo, including first-line and salvage therapy; unfortunately they have proven not effective. Her chemo drugs were:
– Everolimus 10 mg PO daily
– Exemestane 25 mg PO daily
The medical team decided to treat her for a pneumonia with moxifloxacin 400 mg PO daily for a week based on her signs and symptoms, given initial CXR revealed opacity in the RLL. The timeframe of which she presented with these symptoms was on the scale of weeks, rather than days.
Unfortunately she continued to be dyspneic after the course of antibiotics, and a subsequent CT head and chest revealed ground glass lesions that were suggestive of pneumonitis. A course of prednisone for 9 days has failed to afford much benefit as she still requires 4L of supplemental oxygen on nasal prongs.
As this was a severe adverse effect associated with everolimus, I thought it would be valuable to report it to Health Canada.