One of the scenarios that I found myself scratching my head over the past few months on rotation is this: what are the pharmaceutical implications for a patient receiving TPN or enteral nutrition (EN)? Does it matter? Is there a difference? Do we need to care, as pharmacists?
Spoiler alert – Yes, we do.
Some take-home points:
– Don’t overcomplicate. TPN = EN except by delivery system
– There are tons of different kinds of tubes depending on entrance and exit points. For pharmacists, we just have to make sure it goes down the thicker lumen
– 25 kcal/kg total calories –> divide 50% carbs, 30% fat, 20% protein
– Carbs and protein roughly are 4 kcal/g; fat is 10 kcal/g
– The commercially available MVI and Micro +6 concentrate will do the job for vitamins and minerals
– MAINTAIN ELECTROLYTES WITH TPN/EN, SUPPLEMENT REACTIVELY THROUGH DIFFERENT ACCESS
– As a pharmacist, for a clogged EN tube, you can save the day by recommending Cotazym (make sure it’s NOT enteric-coated – 1 capsule should do it given through the tube), but you should give it ASAP before the clogged stuff becomes hard rock!
– A lot of things such as nausea, vomiting, constipation are blamed on the tube. Do not succumb to this temptation, and reassess for other causes (medical conditions, MEDICATIONS, procedures)
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?
I personally feel that Cardiology has been my toughest rotation so far – the sheer volume of trials and information to incorporate, synthesize and apply has been quite challenging. It was quite fortunate that we had this ADS to round out my experiences so far on CCU. Throughout the seminar, I tried to relate the material back to the patients I encountered, and relate the guidelines to what is actually done in practice.
I won’t go over take home points since there are numerous ones, but rather say that Cardiology is like peeling back an onion – no matter how well you think you know the material, there is always another layer to the trial or concept, or another clinical situation where in the absence of good RCTs, clinical decisions have to be made. We all try to fit patients into compartments and boxes and fit them into typical patient profiles for trials, but it most often doesn’t work that way.
This ADS was a good reminder of the main things that one may encounter in a CKD or ESRD patient dependent on HD or PD. It was a bit of a challenge digging out what I learned during the renal elective in undergrad, and all the antibiotic recommendations for line infections in HD and peritonitis in PD… some take-homes I got:
- The ferritin target is higher in HD vs non-HD patients (including PD)
- For MBD: lower the PO4, lower the iPTH, lower the Ca, but DON’T raise the Ca unless the patient is symptomatic.
- The contraindication of malignancy in patients receiving ESAs depends on the type of malignancy – solid tumours are at higher risk
- Double-cephalosporin coverage is recommended as first line for peritonitis in PD
- Fluconazole 100 mg PO daily is recommended as fungal prophylaxis if the patient has had peritonitis in the past, has had exposure to broad spectrum ABX recently, had recent GI surgery, or is immunocompromised
- Vancomycin +/- gentamicin (if unstable) is recommended for HD catheter-related infections – I assume the vancomycin is preferred over cefazolin because it would cover Enterococcus faecium.
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.
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.
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!)
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.
Personally, I felt that being on CTU has been great for my progression through the program. Maybe it is because the conditions that I encountered were somewhat familiar since I had come across them either in undergrad or Clinical Orientation, but I felt more confident in formulating medical problem lists and prioritizing interventions than when I was in Oncology.
Goal #1: Improve my ability and confidence to provide verbal recommendations to the team: I definitely feel like I have improved in this respect. I attended both bedside and table rounds with the medical team and actively participated in them. Although there is a lot of work still to be done to refine my recommendations and rationale when it comes to verbalizing them to the team, I think I’ve made a good start.
Goal #2: Be more comprehensive with my alternatives list for resolution of DTPs: I think I have grown a bit in regards to this. I have learned to group some interventions under a “Renal Function” or “AKI” medical problem and the like.
Goal #3: Become more systematic in gathering info and reporting in regards to daily updates: Maybe this is more of an IT issue, but I felt way more comfortable keeping abreast of the new diagnostics and labs that were pending for my patients once I learned how to do that on Sunrise Clinical Manager (the computer system at SPH). However, I found out that what works best for me is to group my workflow into two parts: monitoring in the morning by body system, then interventions by medical problem.
Goal #4: Develop a strong knowledge base on the most common set of conditions that are encountered on a general medicine ward: Sometimes it got a bit too busy to actively record every little nugget of knowledge in my book, but I felt like I had a good framework by which to rapidly get up to speed on an unfamiliar condition such as warm autoimmune hemolytic anemia, and its considerations when it comes to drug therapy.
I am looking forward to applying these skills in a more focused approach during ID/Antimicrobial Stewardship!