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.
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!)
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!
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/
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!
Few tidbits from the ADS on ID.
- Presence of polymorphonuclear cells (PMNs) indicates inflammation
- Beware of epithelial cell contamination in a sample
- Coagulase-negative Staphylococcus spp is often a contaminant of blood cultures
- A C&S will NEVER have PO susceptibility data due to concerns with bioavailability. Consult microbiology if you need direction.
- Eosinophilia increases suspicion of allergic reactions or parasitic infections
- Lymphocytosis increases suspicion of malignancy or bacterial infections
- Acute phase reactants are non-specific but add to the overall picture
- Pearl: cellulitis treated with ABX will appear to worsen for 2-3 days due to killing of bacteria and subsequent release of endotoxins
- Some antibiotics perform poorly in acidic environments, so therefore will not penetrate and treat an abscess.
- When do you consult microbiology?
- Need more specific identification on an organism
- Need additional susceptibility or MIC data
- Need guidance on which test to use to identify a bug
And of course, this fun gem: