Being on CCU currently, I don’t think that I’ll get a chance to outperform the cardiologists in terms of interpreting an ECG, but I hope to take these skills to CTU or Critical Care and try to apply findings to drug therapy. The main take-home points I got:
– Have an approach: rate, rhythm, axis, conduction, hypertrophy, injury/infarction/ischemia
– Examine leads systematically: doesn’t matter which ones first, just have an approach
– Have a checklist in mind of what pertains to drug therapy
– Look for things that will kill the patient first, e.g. big ST-elevations in anterior leads
If nurses and paramedics can do it, why not us?
Bit of a late entry. I was on my Emergency Medicine rotation and I had a patient (72 year old female) who came in the previous evening with respiratory failure and suspected pneumosepsis. ICU was consulted, and the team is covering empirically with pip/tazo + vancomycin. This patient has a prior history of ESRD (on hemodialysis) – but there is no intention to dialyze the patient currently, given her guarded prognosis! She was empirically given 1 gram vancomycin at 2240h the previous evening. I arrive in the ED at 0800h with instructions for Pharmacy to dose.
The next step I took was to add a random vancomycin level to the patient’s morning bloodwork (the patient was anuric and not going to undergo dialysis at least for the next few days) as the patient was not clearing any vancomycin and by that time (10 hrs post-dose) distribution would have been complete. The level came back at 10.9 mg/L, which was subtherapeutic. Given that a typical therapeutic range for vancomycin is 15-20 mg/L for sepsis, after discussing it with the team I decided to give the patient an extra 750 mg IV vancomycin and to take another random level the following morning. This, by theory, should bring the level up to around 19 mg/L.
What eventually happened was that vancomycin was discontinued the following day as MRSA pneumonia was no longer on the differential, but it was still a useful exercise in what to do regarding vancomycin dosing in a patient who might not perfectly fit the nomogram.
For this case presentation, I presented a case involving a gentleman who came into Emergency complaining of nausea. Upon interview by the EP, he divulges that he consumed an unknown amount of anti-freeze following an ill-conceived bet with a friend. The team starts fomepizole and consults Pharmacy to dose. How to do this?
What I think I did well:
– I gradually have grown more confident during case presentations and can anticipate some of the questions
– Presented the patient with pertinent positives and negatives, taking care not to clutter the presentation
What I can improve on:
– Too many “uhs” and “uhms”; pacing could be slower
– I could have faced my audience more, given that my slides were on the laptop and I did not need to turn around
– For a large study such as a systematic review, possibly delving more into baseline patient characteristics would have lent more colour to my interpretation of the results.
My slides can be found here
Goal #1: Gain a better understanding of the role of the pharmacist in the Emergency Department beyond medication reconciliation: I think I got to see the EM slant of a pharmacist here. Getting involved with RSIs and procedural sedation, and observing how a pharmacist may contribute to helping in a trauma opened my eyes to the full extent of a practicing pharmacist in the ED setting.
Goal #2: Become proficient in condensing information for patient handover from Emergency to ward pharmacist: There were a few instances where I had to provide handover to the evening pharmacist covering Emergency, or to the ward pharmacist covering CTU.
Goal #3: Be able to provide recommendations on workup and pharmacotherapy for the most common conditions/procedures in the ED, e.g. acute pain, stroke, seizure, ACS, arrhythmias, tox overdoses, sedation: I was very fortunate to encounter a variety of cases during this rotation, but strangely there weren’t many hot NSTEMIs or STEMIs… mostly unstable anginas. However, I got to brush up on emergency management of A-fib in the ED, provide seamless discharge when we discharged a patient home on rivaroxaban for newly diagnosed A-fib, and got to see seizures of varying etiologies, from withdrawal to EtOH, to unclear diagnosis, to TBI, to possibly progression of brain mets.
This was an ADS that was more geared for a primer to diabetes care in hospital. Some take-home points I got:
- Overall, poor glycemic control in the hospital setting leads to delayed wound healing, increased stay in hospital, and other negative outcomes (retrospective data)
- NICE-SUGAR showed that in the ICU setting, aiming for <10 mmol/L as a BG target resulted in less mortality vs. more strict control (4.5-6 mmol/L)
- RABBIT-2 showed that despite more control with blood glucose and less hypoglycemia, there were no differences in length of stay between basal-bolus-correctional and sliding scale only insulin regimens. However, for seamless care, a BBC-based regimen would afford more glycemic control in the long run for a diabetic who is primarily dependent on insulin.
- DKA and HHS are mostly managed in the same manner: fluids, insulin, and potassium supplementation.
Overall, this was a good rehash of DKA and HHS (which I went over in detail with Dr Zed in Emerg), and a good reminder of the importance of the varying recommendations in glycemic control depending on the care setting.
My patient was a 91 year old gentleman who was found down by his son, shaking on the ground, more pronounced on the right side. No prior seizure history, however had a history of ICH in the right anterior parietal lobe. On arrival, he was convulsing and unable to obey commands, with rhythmic movements on the left side. He received lorazepam 2 mg IV x one, and a phenytoin load of 900 mg IV x one (at 25 mg/min), with 300 mg PO daily starting tomorrow. A CT head was pending to rule out expansion of his ICH. Overall, he appeared mildly cachectic. Neurology was consulted and they were going to see later today.
I ordered a phenytoin level to be drawn at 1315h (3 hours post-load), and serum albumin. The phenytoin level came back at 61 umol/L and the serum albumin was 38 mg/L. Considering that:
Corrected phenytoin = 61 / (0.02*38 + 0.1) = 70 umol/L, which is in the therapeutic range of 40-80 umol/L, and that he had not seized since receiving the load, the decision was made to continue with phenytoin 300 mg PO daily, while awaiting further workup and investigations by Neurology.
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.
On the eve of the new year, I find myself actually apprehensive of this upcoming rotation. Having been off a clinical rotation since early November, and despite great experiences at DPIC and with the Therapeutic Initiative, I still feel out of practice with the process. The mock oral exam was also a kick in the behind for me; I hope that this upcoming rotation will allow me to further hone the tools that I have acquired and also streamline my process.
I’m also quite fond of documentaries, in any shape or form, and I often watch them to relax (my friends think I’m crazy). One such documentary I came across was Emergency Room: Life + Death at VGH, which follows the frenetic, hectic careers of the emergency physicians, nurses, and allied health in the VGH ED. Am I excited? Of course! Those folks are experienced and seasoned; hopefully I can learn a lot from them without getting in their way :D.
Goal #1: Gain a better understanding of the role of the pharmacist in the Emergency Department beyond medication reconciliation. Objectives to meet this goal:
– Complete all medication reconciliation procedure logs by the end of this rotation
– Shadow at least 2 other allied health in the ED, including EMS if possible
Goal #2: Become proficient in condensing information for patient handover from Emergency to ward pharmacist. Objectives to meet this goal:
– Continue to hone process and deliver a patient presentation to preceptor without “jumping” back too often
Goal #3: Be able to provide recommendations on workup and pharmacotherapy for the most common conditions/procedures in the ED, e.g. acute pain, stroke, seizure, ACS, arrhythmias, tox overdoses, sedation. Objectives to meet this goal:
– Quality over quantity: no trying to learn all conditions at once!
– Learn by doing: by week 4 of rotation, be proficient at handling 50% of practicing ED pharmacist patient load
– Be able to distinguish based on clinical presentation and radiological findings, between conditions that may mimic one another or cause one another, such as ischemic stroke and hypoglycemia, or hyponatremia and hypoglycemia causing seizure.
Liver disease was one of those topics that wasn’t really covered during undergrad, yet through furiously reviewing for PEBCs, and encountering patients with hepatitis and alcoholic cirrhosis throughout rotation, I’ve gotten exposure to it at least. However, I found it immensely helpful to get it in ADS format, so that I at least have an approach to managing complications of liver disease.
What I found surprising was that I did not know how much of a medical emergency variceal bleeds can be, and I learned how they come about, how they are diagnosed, and the role of pharmacotherapy (usually only think about this after initial stabilization and emergency care).
What I think will come in handy for my Emergency med clerkship coming up is that usually if patients present with a suspected upper GI bleed and they don’t know if it is variceal or non-variceal, the team will usually start the patient on both octreotide and an IV PPI pending surgery or a scope. The main therapeutic controversy that was discussed was whether to continue beta-blockers in the setting of secondary prevention of variceal bleed with concurrent refractory ascites. Generally, the benefit for beta-blockers in secondary prevention of variceal bleed is so dramatic (NNT = 3-4, NNT = 10 for primary prevention) that leaving a mini-dose of propranolol (10-20 mg daily) will usually be done.
Overall, this was a useful session with a few stimulating discussions through working with the cases that were provided.
This session for me was an excellent reminder of what was covered during undergrad, with additional information on management of A-fib in the emergency department – it also was great to review my V-W antiarrhythmic classes. Actually, it made me think of my Toxicology rotation. Certain classes of antiarrhythmics influence certain ion channels in myocytes, which may affect the ECG. I thought back to certain toxicities – sodium channel = prolonged QRS complex, which potassium channel = prolonged QTc interval.
What I found really valuable from this presentation were actually the series of flashcard-like slides, which were a good reminder of the ADRs associated with each of the medications used for rhythm control (flecainide, amiodarone, dronedarone, sotalol). I hope to apply what I learned during this ADS to my upcoming Emergency rotation.