Goals and objectives: Toxicology rotation

Goal #1: Develop an approach to evaluating the poisoned patient. Objectives to meet this goal:
– For each toxidrome, have a framework for which abnormal lab findings, signs and symptoms I would expect to see, head to toe
– Work on obtaining collateral for which substance was ingested and timeline from ingestion
– Become familiar with various laboratory and radiologic findings for ingestion of certain toxins

Goal #2: Become confident in providing triage, and if applicable, recommendations for ingestion of a variety of toxins. Objectives to meet this goal:
– Come in with prior knowledge of how to navigate the DPIC Poison Management Manual efficiently
– For common poisoning agents (acetaminophen, TCAs, ethanol, polyethylene glycol, etc), be able to describe the toxidrome and severity of each agent.
– Be able to address the elements of supportive care (i.e. https://lifeinthefastlane.com/fast-hugs-in-bed-please/ – FAST HUGS IN BED PLEASE) in the poisoned patient

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ADS – Anticoagulation

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)

Reflections on ID and Antimicrobial Stewardship

I honestly had so much fun on the antimicrobial stewardship service. Apart from learning all about diagnostics, assessing fluid samples, shadowing wound care, attending microbiology rounds, and having a process to assess infection, I think where I grew the most on this rotation was communicating with the medical team. This rotation forced me to be 100% comfortable with my recommendations (at least when it came to antibiotics) and it was valuable for me to be thrown right in and defend those recommendations. Goals and objectives. Did I meet them?

Goal #1: Develop a framework and approach to assessing the patient with a suspected infection. I think I achieved this – for a variety of infections (CNS, SSTI, pulmonary source, endocarditis, GI source, cystitis and pyelonephritis, C diff) I became familiar with how a diagnosis of an infectious process is reached.

Goal #2: Begin to have a framework for correlating clinical presentation to specific microbiological etiologies. Although this is not always possible, in the case of pneumonia or cellulitis, sometimes one can have a higher pre-test probability of a suspected bug based on radiological findings or clinical presentation. See Nuggets of Knowledge for more.

Goal #3: Develop a convincing yet professional approach to communicating interventions from Antimicrobial Stewardship to physicians and other health professionals who are most responsible for the patient. Yep. Definitely feel better about this. It was helpful for me to bounce recommendations off Michelle and have her play the physician. What if the response is “my patient got better on antibiotics”, but you feel like the patient does not even have an infection? What if the response is “I’m gonna keep him on vancomycin ‘just in case'”, even though the patient has never swabbed positive for MRSA and doesn’t have any other risk factors?

C3.5 R2: Prepare and deliver educational seminar to pharmacists (#3)

As part of my Antimicrobial Stewardship rotation, I delivered a presentation on aggressive (4.5 g IV q6h) versus non-aggressive (3.375 g IV q6h or 4.5 g IV q8h) dosing of pip/tazo for Pseudomonas infections in adult patients without CF and with good renal function. I decided to focus my presentation on a few sources of infection. This presentation triggered a lot of debate among the pharmacists, which was good to see.

What I thought I did well on this presentation:
– Tackled a topic that had a lot of grey to it! I think I never expected the evidence to be great but it was new for me to draw clinical conclusions based on the level of data I encountered
– I thought I was more prepared with questions from the audience compared to my Medicine presentation, although Michelle and Tien (the ID fellow with us on rotation) had to jump in on occasion.
– My pace was more relaxed, and I did not feel like I was rushing through the presentation

What to work on for next presentation, and BC-wide:
– Need to refine slides to make them more viewer-friendly, especially when going over large amounts of literature
– Need to be more clear on conditions of my recommendations and rationale, i.e. HAP vs VAP, same source, same bugs…therefore same dose!
– Be more economical with what I say, versus what appears on the slides. People need to listen as well as read!

My slides

ADS – Electrolytes

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!)

Nuggets of Knowledge: When to treat a urinary candidiasis or a catheter tip-isolated positive Candida culture, and osteomyelitis tidbits

I have a patient who, after a bout in ICU and after 3 weeks of hospitalization, had Candida albicans growing in the urine (with no flank pain, or urinary urgency or discomfort), and also on her central venous catheter tip (only growing in 1 of 2 bottles). She has a Foley in and suffers from urinary incontinence. She also presents with symptoms of an URTI (query HAP query COPDE) However, blood cultures are negative in all bottles. Do you treat with fluconazole?
Risk factors for candiduria: elderly, female, indwelling urinary device, on broad-spectrum ABX, diabetes.
IDSA says: if blood cultures are positive, then definitely treat. However, asymptomatic candiduria is NOT treatable unless neutropenic, an infant, or will undergo urologic surgery. In other patients, treatment does NOT affect mortality. Definitely try and pull the Foley!
Data is lacking regarding negative blood cultures and positive cath tip cultures: data from this paper would seem to indicate that you would NOT treat just a positive cath tip culture. Given that this patient also does not present with symptoms of a UTI (she has urinary incontinence at baseline), it would seem that fluconazole treatment is NOT warranted.
UPDATE (Oct 21): so I found out that it is “common practice” to treat for 2 weeks after central catheter removal with an echinocandin (if you don’t know it’s an azole-susceptible Candida sp.) or fluconazole (if indeed Candida albicans). I guess it is playing it safe – catheter tip in the blood…treat AS IF it is a candidemia.

Osteomyelitis XR and CT “language”
– “Periosteal reaction” = usually means new bone is growing from destructed old bone due to either injury or infection
– “Osteolysis” = can be from inflammatory etiology or malignancy
– “Subperiosteal abscess” or “subcutaneous gas” = anaerobic involvement

In diabetic patients only, a probe to bone of an infected wound automatically means that the patient has osteomyelitis. No imaging is necessary.

Also learned that wound care nurses can be your best friend on an ID or AMS service…look for the “wet ones” to be infected, and “dry eschar” or the like to be infection mimics! Of course though, always correlate with clinical status and imaging.

C3.5 R2: Prepare and deliver educational seminar to pharmacists (#2)

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.

Nuggets of Knowledge: CAP radiography, beta-lactams, 5th generation cephalosporins,and atypical coverage

Few things learned today…

Causative organisms and imaging
– Staphylococcus aureus 
is not a common cause of CAP, but one is at higher risk if a patient had influenza prior to developing a pneumonia
– S. aureus pneumonia can be correlated with cavitations (indicating an abscess) on a CXR…but then again, cavitations could also reflect group A strep or S. pneumoniae pneumonia.
– Combined with risk factors of course, Pseudomonas aeruginosa pneumonia could be gathered by bronchiectasis on the CXR

Edit (Nov 3rd, 2017): More pneumonia radiography and clinical pearls:
Anatomically, the right side of the bifurcation from the trachea is superior to the left side…so naturally, bacteria take the path of least resistance and end up in the right lower lobe for the typical consolidation one sees on the CXR
– The CXR will usually lag behind clinical signs and symptoms by a day…so if a patient is a quick presenter to ED, sometimes you can’t visualize the consolidation until you repeat the CXR a day later!
– Depending on local resistance rates, at St Paul’s, levofloxacin covers Pseudomonas, and usually a cipro susceptible strain will be levo susceptible (levofloxacin has the added advantage of covering usual CAP bugs whereas cipro poorly covers Streptococcus pneumoniae).
– The reverse cannot be said – levo susceptible strains are not necessarily cipro susceptible
– Cipro resistant strains may be levo susceptible…but you will need to call your micro lab to get that info.

Atypical coverage is only warranted if one feels that the host immune system will not be able to overcome such an infection, such as in the case of immunocompromised patients, or those with structural lung disease.

Beta-lactams and coverage of a CAP
– High-dose amoxicillin (1 g PO TID) is only recommended if intermediate Strep is suspected…and local resistance rates indicate that it is not a worry here
– Risk factors for a beta-lactam resistant Strep pneumo: patient <2 or >65 yo, beta-lactam therapy within last 3 months, alcoholism, medical comorbids, immunosuppressed, exposure to child in daycare centre.
– For outpatients only: amoxicillin, amoxi/clav, cefuroxime are all acceptable alternatives. IDSA guidelines recommend adding a macrolide or doxycycline for atypical coverage, but practically, only if immunocompromised or structural lung disease is present.
– For inpatients: cefotaxime, ceftriaxone, ampicillin. Respiratory FQs ONLY USED FOR TRUE BETA-LACTAM ALLERGY.

Haemophilus influenzae can produce beta-lactamases. Which cephalosporins and penicillins overcome these enzymes?
Cefuroxime is more active than cefazolin to H. influenzae and M. catarrhalis that produce beta-lactamases
– 3rd generation cephalosporins are distinguished by stability against beta-lactamases of Gram-negative bacilli

Ceftaroline is a 5th gen cephalosporin with activity against MRSA, VISA, and S. pnuemoniae resistant to penicillin or CTX. It does NOT cover ESBL, Pseudomonas aeruginosa, Acinetobacter baumanii, or B. fragilis

Goals and Objectives: Infectious Diseases and Antimicrobial Stewardship rotation

Goal #1: Develop a framework and approach to assessing the patient with a suspected infection. Objectives to meet this goal:
– Develop a head to toe approach to evaluating whether the patient actually has an infection or not
– Know the common clinical and radiographical presentations for pneumonia, cellulitis, infective endocarditis, sepsis, UTI, septic arthritis, and osteomyelitis.
– Develop a monitoring plan to assess drug therapy for each intervention made during my time on the AMS service.

Goal #2: Begin to have a framework for correlating clinical presentation to specific microbiological etiologies. Objectives to meet this goal:
– For each infectious syndrome, where it is possible, acquire knowledge on distinguishing factors on radiography or clinical presentation that would differentiate between different causative pathogens.
– Attempt to interpret dictations from 1-2 X-rays or CT scans, i.e. “pulmonary infiltrates”, “ground glass lesions”, per day.

Goal #3: Develop a convincing yet professional approach to communicating interventions from Antimicrobial Stewardship to physicians and other health professionals who are most responsible for the patient.
– Practice, practice, practice. Become involved in that aspect of the service.
– Incorporate pharmaceutical teaching into interventions.

Reflections on General Medicine

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!