Before I could even blink, it’s already seven months through the residency year. I definitely do not feel ready to enter practice without the comforting safety net of a preceptor (and I shouldn’t; there’s so much more to learn and experience)…so this ADS was a bit of an awakening for me. I may be expected to precept students in the next year, along with the rest of my colleagues! Isn’t that scary?
What is comforting is that if I know what makes a good preceptor, I can model myself to be that way too, but it takes practice and commitment. I’ve done teaching and mentoring before, but never in a clinical or pharmaceutical context. Some take-home messages I got:
– Always understand your student has a life outside of their rotation, and even if they’re putting in 110% into the rotation, life happens, and sometimes they’ll slip, and that’s okay.
– Don’t use the sandwich method: it’s insincere and belittles positive feedback.
– Instruct, model, coach, facilitate, repeat.
– My preceptors wrestle with a lot of dilemmas on a daily basis: do I step back and observe? Do I let my resident make this recommendation on their own? Should I give them the answer, or have them find it on their own without compromising patient care?
Excited to get my first student already – and hopeful that I’ll be up to the challenge when the time comes.
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.
Before attending this session…full disclosure, I had no clue how to manage a patient with hemorrhagic stroke, be it SAH or ICH. I did not have a patient with either of those during my General Medicine rotation (although I did have a patient with a chronic subdural hematoma…completely different). Overall, here are the take home messages that I got:
– SAH (subarachnoid hemorrhages) carry a much higher rate of mortality and are seen more often in younger patients. Beware of the patient who presents to Emerg with a “thunderclap” headache, most often described as “worst of their life”. Nimodipine and pravastatin are used to manage this (although if pt is already on mod-high intensity statin, don’t be the pharmacist who recommends switching to prava…)
– ICH (intracranial hemorrhages) are best managed by controlling the BP, holding all antiplatelets/anticoagulants (reverse PRN), treat seizures, and possibly surgery.
This session was also a good reminder of the acute management of ischemic stroke and options for antiplatelet therapy for secondary prevention, with a good overview of the landmark trials. I especially found a few slides as quite helpful in summarizing large amounts of information – I intend on using those in my future rotations and possibly in practice.
I think the bottom line for this ADS is “Adam, you need to review your primary literature for anticoagulation”. The session certainly brought up a lot of primary literature, but also raised a couple of clinical controversies. The take-home messages I got were:
– Basically anyone who is immobile, has recently had surgery, or has cancer or another medical condition predisposing to clots requires DVT prophylaxis. Harking back to Clinical Orientation, the words of Mike: “You need to talk yourself out of DVT prophylaxis rather than into DVT prophylaxis”.
– Hip surgery > knee surgery for clot risk, therefore treat longer.
– The BRIDGE trial only included A-fib patients with a mean CHADS2 of 2, so only consider bridging therapy for high-risk clotters…in terms of other high-risk clotting scenarios, there is less to no evidence.
– CONTROVERSY: the rivaroxaban EINSTEIN-PE trial, although it showed non-inferiority to warfarin, had a wide confidence interval (CI), whereas AMPLIFY had a tighter CI when showing non-inferiority to warfarin.
– I always thought VTE treatment in cancer patients was always with indefinite duration until malignancy is resolved, but it turns out it is >6 months. PO options for this population are pending trials (MATISSE subgroup)
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!
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.
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/