The end of a journey marks the beginning of a new adventure!


The clinical teaching unit (CTU) really is an ideal learning environment for medical residents, students and in this case a pharmacy resident! CTU was fast paced learning environment. With the help of my preceptors I was able to adapt and transition into a more independent practice as expected during my final rotation in the practice residency. During this rotation it felt like each of my experiences in the residency had led up to this and each day I felt more prepared to contribute and to help optimize patient care. Although the learning will continue throughout my career this experience in CTU helped to build my confidence in independent practice. I learned when to reach out to colleagues (and in this case my preceptor) and when I felt I had enough information and knowledge to make a recommendation to the team. The volume and turn over challenged me to refine my process and each day was an opportunity to improve. I feel that this rotation enhanced my ability to contribute meaningfully to direct patient care as part of an interdisciplinary team.

This is the final chapter of this journey, thank you for accompanying me along the way. I do not yet know what the future has in store. I do know one thing for sure: I am ready.

General dosing guidelines in hemodialysis patients make dosing straightforward right?

I am certain you know where this is going…let’s take the treatment of confirmed influenza as an example. Oseltamivir 75mg PO post-HD for five days is recommended for treatment of influenza onset within the past 48h. Since oseltamivir is removed by high-flux HD, this can mean post-HD x 2 or 3 doses depending on the number of days between sessions. To simplify this, I have been recommending 3 doses (in cases where a clinical pharmacist is not readily available). This avoids under dosing however may result in a longer treatment time. The consequences of a prolonged influenza infection in this population include nausea, vomiting, diarrhea, missed HD sessions, increased risk of complications and acute hospital admission. Consequences of extended treatment include an increase in medication cost for the hospital (one capsule per incidence) and increased side effects such as headache (2-17%), nausea (8-10%) and vomiting (2-16%). With the knowledge that simplicity can reduce under dosing for a medication not routinely ordered, this generalized recommendation seems justifiable although an assessment of treatment days would be ideal.

Gentamicin pharmacokinetic assessment

A 45 year old female hemodialysis patient I had been following was febrile during her nocturnal dialysis session. That night an order for gentamicin 80mg IV post-HD had been ordered. She has polycystic kidney disease and the concern was infection from a ruptured cyst could quickly turn fatal. I completed an assessment of the order the following day and the empiric dosing had not taken into consideration the patient’s dry weight of 110kg at a height of 5’4. She did recover quickly following a gentamicin dose of ~1mg/kg and the cause was likely not bacterial. After speaking with the nephrologist, I documented the assessment in her chart including her adjusted body weight (ABW), calculations to reassess if her weight changes significantly and suggestions to consider for dosing. She is considered at high risk of a cyst rupture requiring timely and effective antibiotic dosing. Given a long list of drug allergies which include antibiotics, gentamicin would likely be employed if this occurred. Her antibiotic allergies are cephalexin (hives/vomiting), ciprofloxacin (hives/anaphylaxis), sulfa drugs (anaphylaxis), vancomycin (hives/anaphylaxis). So I wanted to share this if only to solidify it in my own head. Just to be clear, I am not in anyway implying that the nephrologist need the equations written in the chart. It’s just that as long as she remains on nocturnal dialysis, there is the possibility of a 2 am call and no matter how brilliant you are, EVERYONE deserves an equation sheet at 2 am.

Given her weight and height, an adjusted weight of 76.8kg was calculated. Firstly a loading dose (LD) of 2-3mg/kg for an infection of this etiology was recommended. A LD would more quickly approach steady state concentrations (not steady state!). Gentamicin exhibits concentration dependent killing whereas adverse drug reactions are generally time dependent. Gentamicin 160mg IV post-HD as a LD was suggested rather than 200mg IV on the higher end of the spectrum. This was in part in an effort to protect any residual kidney function and in part because it seems like a very high dose (very scientific, I know). When determining an appropriate maintenance dose, the most likely pathogens from a burst cyst are reportedly E. coli (75%) or another gram negative rod (UptoDate). The suggested dosing for this was gentamicin 1.5-2mg/kg. This gives a maintenance dose of 120mg IV post-HD or alternately 100mg IV post-HD (1.3mg/kg) which is a safer dose in the absence of gentamicin level and close to the reference range. Optimally, the maintenance dose is guided by a pre-HD trough (target 2.5-5mg/L in HD patients).

Quinine no more!

This presentation focused on de-prescribing quinine in hemodialysis patients. It is difficult to see the de-prescribing flow chart I created to outline of my approach when de-prescribing quinine in this patient population and so I have added it as well. The time frames are guidelines and may be adjusted as appropriate for a given patient. One way this approach differs from others is that I do not recommend restarting quinine at the lowest effective dose if cramping occurs. Rather, I would consider another treatment first. Re-initiating quinine at the lowest effective dose may be employed if necessary before introducing additional therapy however I believe this needs to be done mindfully with a de-prescribing strategy in mind. My concern is a patient may inadvertently be continued on two therapies for muscle cramps both with side effects (such as concurrent quinine and gabapentin).

Another question was regarding discontinuing prn quinine on hemodialysis as a last step. It was rightly noted that the pharmacokinetics of quinine suggest that prn dosing for muscle cramps may not be very effective clinically. However this is in patient already using prn doses at differing times during the hemodialysis session. Quinine prn dosing may be effective if taken at hemodialysis initiation in anticipation of muscle cramps in the last half-hour. This may be done if a large fluid volume is removed. In situations where it is truly a prn dose in response to muscle cramps, my justification is building patient trust. Discontinuing a medication that may have been effective at a time during the course of dialysis can require a step wise approach. In my experience, discontinuing the dose during hemodialysis last has been the most acceptable to patients. Possibly because during hemodialysis is where the patient is most likely to experience cramps (or associate with muscle cramps). This is just one possible approach and I welcome any feedback.

Quinine De-Prescribing

De-prescribing Flow Chart

Fun fact: Can drinking tonic water improve muscle cramps? Drinking 10 cans of tonic water would provide enough quinine to potentially yield therapeutic benefit and harm…not so great for fluid restrictions though! (yes, this was a real question)




Up date: the project name may be changed from QSTOP to Quiditch, brilliant!

Nephrology, two ears to listen and 2 kidneys to filter


March 9th was World Kidney Day! After a one month rotation in the hemodialysis unit, I definitely appreciate my kidneys enough to give them a whole day. Filter the blood, regulate potassium, phosphate and calcium, promote red blood cell production, help activate vitamin D (so it can do its thing), indirectly keep calcium in my bones and not in my arteries….I think they deserve a week rather than a day next year. In all seriousness, the World Kidney Day is a global campaign for kidney health awareness and so I do digress. In terms of drug therapy and drug dosing, nephrology can be a whole other world. Nephrology, where uncommon drugs are used commonly and common drugs are used uncommonly. In hemodialysis (HD), vancomycin and gentamicin are relatively common empiric IV antibiotics. The dosing of these renally cleared medications is simplified as the extended half-life allows outpatients to be dosed each HD rather than daily. The target/accepted pre-HD gentamicin trough is also elevated at 2.5-5mg/L with the assumption that at least half of the drug is removed by hemodialysis (giving a post-HD trough of 1-2.5mg/L or less).

Decreasing or de-prescribing medications such as PPIs and H2RAs has required a little more investigation prior to a recommendation. A patient with polycystic kidney disease was taking rabeprazole 20mg PO bid for GERD caused by the pressure of her enlarged kidneys on the stomach (a fairly solid indication). The dose was reduced as her last flare was in the fall however until her kidneys are removed (hopefully during a transplant) she may require the high dose PPI in the future. Cases of severe GERD are not uncommon however re-evaluation and de-escalation of drug therapy is often warranted as conditions change. Terazosin, indicated for BPH, may act as a two-fer for the management of refractory hypertension. Heparin, replavite, alfacalcidol, IV iron, calcium carbonate (Tums), domperidone and quinine are seemingly the rule rather than the exception.

Management of disease states can differ as well. There have been three trials assessing the CV benefit of statins in HD patients. The 4-D, AURORA, and SHARP trials have failed to demonstrate a significant reduction in cardiovascular events despite reduction in LDL cholesterol. This may be secondary to the proposed mechanism of cardiovascular disease in these patients. Rather than atherosclerotic, vascular calcification is thought to be the predominant pathological change resulting in increased cardiovascular risk however, like osteoporosis and bone mineral disease, these two can co-exist. As a general rule, statins are not started in HD patients however they are continued if the statin preceded HD. A cardiology consult may change this when the harm of not treating may be substantial however questionably evidence based.

Stroke prevention in non-valvular atrial fibrillation (not to be confused with vavular atrial fibrillation or VTE treatment) is another good example. Warfarin appears to pose a greater bleed risk than stroke reduction in HD patients. It may even contribute to stroke risk. Warfarin inhibits the synthesis of vitamin K dependent clotting factors and it also inhibits the activation of matrix gla. Matrix gla is a protein which promotes bone calcification (rather than blood vessels). Hence the association of warfarin with calciphylaxis! Interestingly, in rat models, supplementation with vitamin K reduces warfarin associated vascular calcification. Could this benefit HD patients with atrial fibrillation and a mechanical valve??

I have to admit that I will miss the patients in the hemodialysis unit. They are truly inspiring individuals with a unique story and complicated, fascinating medication management needs.





For your enjoyment, I will leave you with this. You’re welcome 🙂


Last but definitely not least: the Clinical Teaching Unit

My final rotation will be in the clinical teaching unit (CTU). I am excited for the experience of working as the CTU blue team pharmacist. The patients admitted to CTU are generally acutely ill and often have a clinically interesting condition to facilitate the learning of the medical residents and students. My learning goals for this rotation are to explore the pharmacotherapy and therapeutic alternatives for managing conditions such as pericarditis, diabetic ketoacidosis, cirrhosis, acute heart failure, metabolic acidosis and alkalosis. If you have been reading my ePortfolio at all, you’ll know that I generally speak my mind. So here it is: I am so excited for this challenge and learning opportunity that I have butterflies. So wish me well and I will update you soon!

It’s Valentine’s Day, time for those three little words…thyroid stimulating hormone! 

Thyroid stimulating hormone (TSH), plays an important role in thyroid function and consequently metabolic function. It is the most common lab measurement ordered to determine thyroid function (and with low thyroid function, where would you get the energy to make dinner for your sweetheart?).

One of my learning goals was to look at diagnostic tests and their role in medication management. Originally I was thinking of diagnostic imaging however the diagnostic value of TSH measurements in acutely ill patients has resurfaced time and time again during my clinical re-orientation. This was especially true in patients previously diagnosed with hypothyroidism.

On your floor, a patient with previously controlled hypothyroidism was admitted through the ER where  a TSH was ordered. The TSH is low however there are no signs or symptoms of clinical hyperthyroidism…at least none that cannot be explained by another mechanism. Do we dose adjust the levothyroxine?

Now, I do not claim to have all the answers to this question but it was helpful for me to create a short write-up and to create a table of how I would approach TSH (and FT4 if available) measurement with what I now know today. This includes patients believed to be euthyroid prior to admission. I would love feedback from others to know how you approach this.