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!
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.
Upper GI bleeds (UGIB) – I always thought that the colour of the stool is a good indicator of whether it is an UGIB or lower GIB (LGIB). However, I learned that it wasn’t a sensitive indicator, although it can aid in the diagnosis. General management for a non-variceal bleed is as follows:
– IV PPI (increases gastric pH –> stabilizes blood clots –> improves survival). Is intermittent dosing better, or continuous infusion better? This meta-analysis seems to say that there is a 28% RRR (2.64% ARR) for re-bleed within 7 days for intermittent dosing, although the results were pooled from a variety of intermittent regimens.
– Prokinetics: only warranted if endoscopy is needed to rule in or rule out UGIB. Erythromycin 3 mg/kg IV over 20-30 mins, 30-90 mins pre-procedure.
– Somatostatin and octreotide: clinical efficacy proven, but PPIs and prokinetics (with endoscopy) are much cheaper and there is more clinical experience.
Splenic infarcts and abscesses: when are antibiotics indicated?
Splenic INFARCTS: due to a whole bunch of different diseases, such as underlying cancer, embolic disease (such as A-fib or IE), splenomegaly, trauma. Treat the underlying cause.
Splenic ABSCESS: usually results from an endocarditis. May be accompanied by left-sided pleural effusion. This requires drainage + antibiotics +/- splenectomy. Usually the abscess is polymicrobial – usually E coli, Streptococcus spp, Enterococcus spp, and anaerobes.
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.
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!
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.
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.