2/We heard that the patient had 5 days of diarrhea, but heard little more about that symptom. If the diarrhea had been profound then we could see a normal gap acidosis, therefore the labs suggest modest diarrhea.
125/4.5/83/26
Disappointing to me, we were not given BUN or creat
3/ Let's think about the Na of 125. That is low enough to cause altered mental status. Even patients who slowly lower their Na to that level often become confused.
The main differential for decreased sodium starts with volume contraction, euvolemia or edematous sate.
4/ Another nerdy, yet important point - by definition w/ a Na of 125 the patient is overhydrated. Volume contraction & dehydration are not synonyms. So the patient is overhydrated. Given the urine osms > 400 we can exclude primary polydipsia, beer potomania and "tea & toast"
5/ ADH is involved - is it appropriate or inappropriate
Appropriate ADH is like the post-op state - volume contraction, stress, pain, nausea, opiates. So we should be evaluating the patient's volume - hence I'm missing the BUN, creatinine and urinalysis.
6/ We might initially infer volume contraction with the elevated serum Hgb (17.9). While caring for this patient, I would want to see the Hgb decrease with volume.
7/ Towards the end we are given a clue that the patient actually has SIADH. If the patient had volume contraction, giving volume would increase the serum Na, but the Na decreased. This will only happen if the elevated urine osms persist. The explanation is a bit complex.
8/ Let's assume either LR or NS. They each have around 300 osms /liter. But if the urine osms are great than that, the patient will excrete the given osms in less urine than the IV fluids. The difference in volume is the equivalent of adding water to the intravascular space.
9/ If in fact the patient has SIADH (and small cell has SIADH in the 6-17% range), then what should we do? If money is no object, you can correct with Tolvaptan. When money matters you can try demeclocycline. With either, trying to normalize the Na is challenging.
10/ I hope that working through these labs and sharing my interpretations might help you with a future patient. Please ask questions in case I am guilty of the Curse of Knowledge and therefore did not explain things clearly enough.
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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?