2/ KDIGO definition of AKI includes a change in serum creatinine clearance (SCC) within 2–7 days & oliguria for 6 or more hours. The stage is defined by the peak rise in SCC compared w/ previous values & nadir in urine output & is related to risk for complications &prognosis
3/ Thus, when a patient comes to the hospital with an increased creatinine from previous creatinines, that does NOT constitute AKI. When a patient comes in with an increased creatinine, or develops an increase in the hospital you must first determine several things
4/ Is the patient volume contracted - if so, and the patient responds to volume expansion within 2 days - the patient does not have an AKI
Is the patient obstructed? Until we exclude acute obstruction, we should not label the patient with an AKI
5/ If the patient is not oliguric, then the patient does not truly have an AKI, rather perhaps a worsening of CKD. Today in the @CPSolvers#VMR - a patient had a marked creatinine increase from previous labs. Using the term AKI often can confuse evaluation
6/ AKi has become a "catch all" for any creatinine increase. But labeling patients as having an AKI may stall evaluation.
7/ I prefer labeling the patient as having an increased creatinine - and then proceeding with evaluation - volume assessment, obstruction assessment, U/A looking for proteinuria , infection or casts. Today's patient did not have an AKI, rather a new chronic kidney disease.
1/ #UncleBob - on giving formative feedback on rounds. First, make it clear in your expectations discussion (day 1) that you will critique many things and label them as feedback. #MedEd@CPSolvers@uabimres
2/ Especially with new presentations, stop after the HPI and both praise the story and provide suggestions on making the presentation better. Emphasize the role of storytelling as separate from having taken a good history.
3/ Understand that when you ask questions - some are hard and some are easy. When a learner answers a hard question well - praise them and note that you are giving positive feedback.
1/Time for a #UncleBob screed. The question Andrew raises is a very interesting one. First I must provide my understanding of the purpose of teaching ward attending physicians.
I divide this into providing excellent patient care & helping learners grow.
2/ Providing high quality care is a given. Excellent ward attendings evolve with clinical practice (consider the 10,000 hour "rule"). But I would argue that both outpatient clinical practice and inpatient practice are beneficial.
3/ And I believe I learn more in a month of ward attending than if I did a month of solo patient care. Patient care requires attention to detail, diagnostic excellence, management efficiency and proper use of tests and consultants.
2/ Some basic physiology - we metabolize around 1 mEq of H+ daily from our diet. We buffer that acid using titratable (phosphate) and non-titratable (NH4+) acids.
The phosphate pathway does not vary much, but our kidneys can normally control the ammonium pathway
3/ Where does the ammonia come from? Glutamine -> glutamate under the enzyme glutaminase produces NH3
Here is the interesting part. Increased K inhibits this enzyme, thus we produce insufficient NH3 to buffer our dietary intake.
#UncleBob posted this link yesterday. Here are a few thoughts on the article. “I don’t know what’s the matter with people: they don’t learn by understanding; they learn by some other way—by rote or something. Their knowledge is so fragile!”
"The difference between reasoning by first principles and reasoning by analogy is like the difference between being a chef and being a cook. If the cook lost the recipe, he’d be screwed."
This is so relevant to those who grow and those who stagnate.
"Some of us are naturally skeptical of what we’re told. Maybe it doesn’t match up to our experiences. Maybe it’s something that used to be true but isn’t true anymore. And maybe we just think very differently about something." - The best diagnosticians always question previous dx
1/ Here is the story - hopefully instructive. Patient (ESRD w/ dialysis) admitted 3 weeks previously for dyspnea. Portable CXR shows small pleural effusion & some haziness - pneumonia or atelectasis. No fever, no increased WBC, no productive cough. Discussed now w/ radiology
2/ Radiologist teaches our team - pneumonia is a CLINICAL DIAGNOSIS - cannot make the diagnosis by CXR/CT scan.
Patient discharged - readmitted for more dyspnea - now with moderate pericardial effusion and large left pleural effusion. Receive furosemide & then thoracentesis
1/ #UncleBob hopes those on the fence about vaccines will understand this
Weekly COVID-19 death rate via CDC:
Unvaccinated: 9.7 deaths per 100k
Fully vaccinated: 0.7 deaths per 100k
Boosted: 0.1 deaths per 100k
2/ Yes you can get omicron even if you are boosted
BUT
You are less likely to get infected
If you get infected you are much less likely to need hospitalization
If you need hospitalization, you are much less likely to need ICU care, and MUCH less likely to die
3/ Would you turn down medical care if you got sick?
I assume no - almost everyone comes to the hospital and ask for everything
Then why would you not accept a free prevention tool?