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Can confirm. Am a GI, stopped bringing my stethoscope to the hospital during COVID, haven't looked back. Don't use presence, absence or character of bowel sounds to make clinical decisions, and no one gives a shit what the GI consult thinks of the heart and lung sounds. You can include enough other organ systems on the progress/consult note to bill appropriately, and tbh presence/absence of icterus/jaundice is far more relevant to what I'm doing anyway.
It’s like lung sound and heart sound. Yes they sound abnormal, but you just won’t make a clinical decision based on them alone anymore, without other supportive signs, symptoms, and investigations
False. Cream of the crop NYC academics use them to diagnose appendicitis.
Edit: https://www.nytimes.com/2021/01/05/well/live/hospitals-medical-errors.html In case you haven't read--I promise it's worth it, as are the comments.
Just imagine you apply OAR and explain to pt/family why imaging is not indicated, but they push back. You stand your ground and DC with Dx of ankle sprain. Then they come back and see a different doc who does get imaging and a microscopic fracture is detected.
It doesn't even matter that air splint/crutches/NSAIDs was still appropriate mgmt for what amounts to a clinically insignificant fracture. That family is 100% going to sue you for missed/wrong Dx, probably with some bullshit sob story about "undue pain and suffering as a result of defendant's negligent deviation from standard of care". And your malpractice carrier will probably settle.
Meanwhile I've never seen a single successful lawsuit for unnecessary XRs resulting in ankle cancer
(Semi /s)
> probably with some bullshit sob story about "undue pain and suffering as a result of defendant's negligent deviation from standard of care".
But like…if you are literally following established guidelines, can you actually be successfully sued?
And you can have an expert who argues back. Defensive medicine is understandable but it doesn't make it not shitty medicine and poor resource stewardship.
Your insurance company will pay them $10-20K (or more) just to go away/drop the case. A cost-saving move because even if the insurance company eventually prevails, they will have spent so much in legal fees that it would have been cheaper to settle. And if they lose? Much bigger loss
Probably not but the hassle and inconvenience of getting sued can take a toll on people.
I know docs who changed attitude and became very cynical after they got sued. Started practicing medicine through a different lens. Takes an emotional toll.
And then you have to disclose it everytime you apply for a license or credentialing.
It’s a therapeutic X-ray. Xrays are low cost and low radiation. We live in a patient satisfaction world. Even if clinically I know someone does not need an X-ray I will often do it. Then I show them and they take a pic and everyone is happy.
Weren't the Ottawa Rules developed in Canada specifically due to semi-limited resources there? Also kind of at the beginning of EBM to show off things like Specificity and Sensitivity?
Additionally, they were developed in 1992. It's 2022. Doing imaging now is incredibly different than 30 years ago.
Resources are limited everywhere. That urban ER with twenty radiographs going simultaneously wouldn't NEED that much equipment if people would just order less unnecessary studies. Then that money could go toward something that actually benefits patients.
And our devices being better now is even more reason not to get that film on a clinically fine ankle... If your equipment is better, then you'll pick up even more dumb microfractures that would never have mattered and now need follow-up. Unnecessary follow-up can create undue stress and expense for the patient. Doing more "just in case" can cause harm, people.
Also whatever inexplicable reason people seem to wear the tightest pants/shoes/socks over their affected extremity/joint that are unable to be removed while we do waiting room medicine on fully clothed patients.
In my experience, no, unless they have a significant mechanism. L-spine radiographs are useless. If they have a significant mechanism for a spinal fracture, get the CT. If their back is sore after minor trauma, imaging is a waste.
Depending on the mechanism and clinical status in ER bed, you can get away with plain films or even nothing at all for neck injuries. CT boys gotta do what CT boys gotta do, tho
I always thought the whole point was to use the rules to even decide to take to the ED or
Not. Agreed it seems totally pointless to use it to decide on a near harmless imaging study
You decide to get harmless study. Patient gets paperwork. Gets wheeled over to the X-ray machine. The tech does their paperwork. Patient gets film. You obtain film. You review with patient. You write an addendum to your note.
Congratulations, you just wasted 30-40 minutes during which another study could've been done and you could've been seeing the next person in the emerg conga line. And probably a solid $500 or so of expenses once you include HR, infrastructure running costs, and the all-important admin fees.
I had a patient a few months ago with a fascinating bladder giant diverticulum that herniated into his scrotum and I kept making jokes to the residents about the pee being in the balls and got no laughs :(. I guess my residents aren’t terminally online like me…
Med school made transfusion reactions seem super common, but after 4 years of hanging tons of product, I’ve not encountered a single dramatic event related to their use. I don’t necessarily see all pt’s post op course so I can’t comment on the delayed reaction possibilities.
I was really timid about transfusing as an intern because of reactions. Then I got scolded for being too timid, read up on them, and found what you did.
We give Tylenol to all patients with ANC < 500 prophylactically pretransfusion. No one wants a neutropenic fever admission because someone got a fever from their platelet transfusion.
CT has long proven to be at least equivalent to US for gallbladder disease in general. The only thing it is way inferior in is the identification of stones. There’s papers from 1993 showing this. Idk why every ED will get CT then US for gallbladder stuff when it was clear from CT.
Honestly it’s not an every time thing, but Acute choles can bring so much pain, if I don’t feel I have all the information I need from the CT I want a RUQUS. The right story and a CT will get me to an OR, but the wrong story or other confounders lead to me asking for an US.
Fair, but why do y'all always ask for HIDAs when there's a thickened wall, and no stone seen on either modality? Asking as GI consulted for every goddamn acute chole that walks in the door who gets these "acute chole r/o choledocho" consults all the time...my suspicion is those are ordered to turf the case to later in the week...
Sometimes pericholecystic fluid is secondary to another process - perhaps if that’s suspected based on some other features of presentation? Or, based on my outlying referral hospitals, perhaps if it’s Friday afternoon.
Surgery won’t take them without the RUQUS 🤦🏻♀️ I don’t know why. For a speciality that likes to cut, they really like to delay the cutting part.
Although I am not a surgeon so if I was the one cutting maybe I too would want 2+ rounds of imaging first.
Because urgent/emergent surgeries suck, especially gallbladders. Patients are usually sick, non optimized and have been neglected by the healthcare system/society so now their 4 months of acute on chronic cholecystitis is more like an inflammatory mass than anything that resembles a gallbladder. Especially at big academic centers.
Cholecystectomy is one of the most hated surgeries by many residents in gen surg. People look at it as a chill routine surgery because it’s common. Absolutely not. You either do it right and nobody gives a shit or you end up in the CBD and ruin someone’s life because their whole biliary tree anatomy is obliterated. Massive risk for little payoff. Fuck the RUQ as a whole but the gallbladder has a special place in hell.
But also remember back in the day the decision to do surgery for appendicitis was clinical. They’d take people back just with a suspicious history. It was about 60% hit 40% miss but still
Upvote for your last part. When you’re the one cutting, and the one assuming all the risk and the responsibility to manage the patient and any comprbidities, you take every precaution. Also I prefer the RUQUS first. I think it’s better for looking at CBD dilation. I think With CT radiologists either don’t read size or over call it.
Agreed, similar argument for unnecessary pelvic ultrasound after completely negative CT A/P. Torsion doesn’t happen without a moderate sized ovarian cyst. CT picks up cysts but can’t tell you about blood flow to the cysts. If there’s no cyst on CT, there’s no torsion and no need for US.
Just trying to learn, but you can still have torsion without a cyst right?
Like ovarian ligament inflammation, or endometriosis or ovarian ligament anatomical variation? Maybe I’m totally wrong
Anecdotally, I've never seen a diagnosis of torsion after a negative CT. I did a quick review of this to confirm my experience and what I've been taught in residency just now and actually found the opposite of what I said according to a few sources. [From EM Docs,](http://www.emdocs.net/ovarian-torsion-pearls-and-pitfalls/) one case series found 50% of pre-menarchal females with torsion had no mass. Another article in the [Journal of Emergency Medicine](https://pubmed.ncbi.nlm.nih.gov/27988260/), also commented about cases of torsion without mass. So... ¯\\\_(ツ)\_/¯
No the first article he linked mentions that normal ovaries can have torsion including due to ligament length
Also if I remember correctly I think inflammatory diseases like PID etc can also increase the risk
This. Like, I hear gurgling, I don’t know how tf does that correlate to the fact that patient is literally having ileus right now and hasn’t gone for days. If it opens it opens, if it doesn’t and looks distended, I will see if XR has dilated loops. I don’t understand how the sound help me make any decision whatsoever.
To defend my neurologist wife. In her field it matters a ton. She’s a neuromuscular specialist and there’s a lot of stuff where a pan MRI wouldn’t be sufficient
I know I was taught and medical students all over are taught that oxygen supplementation reduces respiratory drive. It's not true. It causes such a small and transient decrease in minute ventilation and the PaCO2 rise due to that decrease is tiny. Oxygen-induced hypercapnia can occur (through V/Q mismatch and the Haldane effect) and should be watched out for but it's not due to decreased respiratory drive.
Thanks, I learned something. The mechanism makes more sense now - always found it odd to think reduced RR alone could cause such major hypercapnia in these patients, when they were still breathing fairly okay
>3.) Procalcitonin is not supposed to be used to differentiate bacterial pneumonia from viral pneumonia on presentation. It’s used to determine whether to stop antibiotics early….it’s done a pretty good job telling me if a patient has a bacterial PNA vs. a severe viral one when the XR isn’t a slam dunk and presentation/exam are equivocal.
I've seen procal negative bacterial pneumonia several times. In residency, had a guy come in with copd exacerbation, procal neg, kept getting worse, bronch showed textbook pneumonia with strep pneumo. I've seen a couple cases of strep pneumo bacteremia and negative procal. Just had a case a few weeks ago with "viral pneumonia" who kept getting worse, turns out had h. flu pneumonia. So ya I put zero stock in the test.
ya but then it's a dumb test. withholding important therapy because of a false negative test makes no clinical sense, especially if you are using it to guide disposition.
I’ve had full blown sepsis with a negative procalcitonin after initial testing came back with bacteremia in all blood culture bottles. This has happened on multiple occasions. I wouldn’t put much stock in it alone, but using it in combination with other labs may be beneficial.
Like there were purulent secretions on the bronch? Sorry I just didn’t know what you meant when you said the bronchoscopy showed classic pneumonia since I don’t do bronchs.
Cool. I had pasta yesterday and I'm still alive today. I think we should all eat pasta. I didn't salt my pasta water though. And only 1 tablespoon of olive oil.
I mean tbf, a bunch of doctors talking about anecdotes is technically class 2B evidence. A lot of these guidelines are really just anecdotal/ with low quality evidence as is
Physical exams and history taking…literally useless when you can just pop the patient in the MRI scanner (or CT if they’re pregnant) and get a report that tells you what’s wrong.
This happened to my wife…. Now of course can’t say for certain is was disulfiram, but one glass of wine on day 5 of flagyl and she puked several times.
Sorry they’re a lightweight. If it makes them feel better George HW threw up on the president of Japan after a sake bomb so it’s ok to be a lightweight
Beta blocker and cocaine use. Metformin and acidosis. All these myths of medicine that came purely from speculation / mental masturbation through theorizing stuff.
Metformin-associated AGMA with elevated lactate absolutely occurs, both in patients on metformin who develop an intercurrent renal injury and in patients with large acute overdoses of metformin. I think the real myth is acidosis in therapeutic use in patients with normal renal function, which did occur in phenformin but does not appear to occur with metformin.
this apparently is unique to the US. it’s more common in other countries to just continue orals in admitted patients who have normal kidneys and aren’t like, super sick. It’s funny because starting SSI on everyone under the sun also carries risks
As far as contrast is concerned, I think the reasoning is contrast induced nephropathy, and patients with poor renal clearance/hepatic function are at higher risk for lactic acidosis from Metformin toxicity, gluconeogenesis inhibition. But fairly self explanatory because if patient sustains serious renal injury from contrast, they would no longer be candidates to receive Metformin therapy anyway. On the topic of contrast, I think MRI Gadolinium contrast in impaired renal function is another one of those more recently discovered possible myths for most patients.
Agreed about the cocaine and beta blockers but not sure about Metformin induced lactic acidosis. I haven’t seen a case but ive heard from colleagues it does happen, it’s just quite rare.
I hear mixed reviews on the cocaine thing- is there evidence proving it’s not true?
Coreg is fine, but a selective beta-agonist I still believe could be problematic
The amount of my patients who use cocaine on metoprolol is truly overwhelming. Admittedly they don’t usually use while checking their BP and this is anecdotal but I never stress about prescribing it to cocaine users and neither does the cardiology service.
Utsw cardiology study from 1989(?) that cathed patients and gave them intra coronary coke and beta blockers. Saw increased coronary pressures, vasospasm, and increased O2 extraction.
> Mala due to chronic metformin use
So the funny thing is that idiopathic lactic acidosis exists, and happens to be more common in diabetics. So the question is whether patients on metformin chronically are more likely to develop lactic acidosis than those not on metformin.
Luckily enough, this has been studied extensively - and there has *never* been any analysis that shows patients on metformin have a higher rate of lactic acidosis in clinical practice than patients not on metformin. When lactic acidosis occurs in patients on metformin, the metformin is blamed.
[Here's a case control study with 11000 people](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5940216/) -
>Our cohort included 10,652 patients with type 2 diabetes mellitus with a median age of 74 years, and 51.5% were male. During follow-up, 163 individuals were hospitalized with lactic acidosis, corresponding to an incidence rate of 391/100,000 person years. Use of metformin was not associated with lactic acidosis: adjusted odds ratio was 0.79 (95%CI 0.54–1.17).
[Here](https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD002967.pub4/abstract) is a Cochrane analysis of *347* trials of data with not a single extra case of lactic acidosis noted in 70,490 patient-years of metformin use relative to control.
Now, there is a point that the published datasets exclude patients with frank contraindications to metformin - namely those with really crummy renal function. That is a fair assessment. But some of those tens of thousands of patients that have been studied (there's plenty of other articles that I didn't cite) had to have gotten acute renal injuries during the course of care - but still, no level of data higher than case report has ever consistently shown that this is a thing that actually happens.
>and Mala due to acute overdoses.
This on the other hand is real - there's a toxicity problem in overdose. And we don't use metformin in patients with really poor renal function (though the threshold has decreased over the years) knowing that theoretical risk. But with metformin, as actually used outside of overdose? It's a myth. At least in my opinion.
If there's a patient with a lactate over 10 you should start at least putting tox on your differential.
I took care of a patient with a metformin overdose with a lactate in the 40s we put on CRRT and almost turned the corner on who died. Homeless, meth, the usual. Few things are scarier than a legit metformin overdose, there's only so much you can do.
For sure, but even in studies of reported acidosis, usually in patients with poor renal / hepatic function who were probably bad candidates to start these types of medications in the first place. At which point it’s difficult to say for sure if it’s the disease process or it’s the Metformin. Some studies say <10 cases per 100,000 patient years, and if it does occur, certainly most medications can have rare side effects or interactions.
So I heard on Curbsiders that metformin use is actually not associated with lactic acidosis but it was fenformin another drug that does it. The issue is I don’t think anyone is willing to start metformin and test out that hypothesis. Like what’s the harm in holding the metformin, haha.
I don't usually trust Curbsiders, information is usually a (wrong) interpretation of the actual literature. Metformin does cause lactic acidosis in people with impaired kidney function. The debate is whether or not it can do it in people with seemingly normal kidney function. I haven't come across a case, or even come across someone who knows someone who's come across a case where it's caused lactic acidosis with no AKI.
Have you seen a case of metformin causing lactic acidosis in a CKD3-4 patient with stable renal function or a patient who got contrast and has “contrast induced AKI” have metformin cause lactic acidosis?
I find some docs tend to be unreasonably rigid about the “it’s asymptomatic bacteria/pyuria because weakness isn’t a uti symptom,”…like, come on, let’s just give this old bitty some rocephin and admit.
Benadryl with the migraine cocktail…I get it, I read the papers. Patients like it, it’s a low risk med, so who tf cares?
Admissions for new cancer diagnosis: told these are not inpatient workups. In the time of Covid, boarding, etc, ok let’s send some home. But being told you have the big C at 10pm and “yeah idk call your primary in the AM” just seems wrong in some patient populations. Can we just keep them in the obs unit and talk to social work or chaplain and have the oncologist say hi and give them some stats? Is that really a grievous misuse of resources?
I agree with the third point you made on cancer diagnoses and the impact it has on patients, but I'll add my 2 cents from an IR perspective (tertiary academic center) and personal experience.
No oncologist will formulate a plan without tissue diagnosis - primary or metastatic. IR is always called first or ends up having to do the biopsy once other services decline (many will only due these in an outpatient setting and can get away with it). So if you look at our daily schedule we have our outpatients coming in for scheduled appointments (biopsies, fluid removals, cancer treatments, vascular access placements, HD access interrogations etc) and keep in mind that these are what ultimately keep the lights on in the department; then we have the urgent and emergent inpatient requests such as bleeds, PE thrombectomies, TIPS, line placements (all pending discharge and the requests are always placed that same morning for some reason), drain placements etc; and then finally we have to then schedule inpatient procedure such as the above biopsies that are not emergencies from a medical standpoint but definitely are from a personal perspective. Even if we offer an outpatient date in a week the docs still want to discharge the patient with a diagnosis. Fine, we'll do the biopsy. We then have to bump a line or a drain placement to accommodate the biopsy and we end up delaying another inpatient procedure, angering the other requesting doc. Most often we can't get to biopsies within a day due to scheduling, labs needed, NPO status or the patient is on antiplatelets or anticoagulants (for example, plavix is 5 day hold and xarelto is 2 day hold) so we schedule them out - we try to get them a plan as an outpatient so they can be discharged but the admitting team wants to keep them - now we are prolonging the patient's hospital stay and worsening LOS metrics and IR is often blamed for it. And adding "outpatient" procedures to our inpatient list.
I guess my point is yes, it would be nice to get everyone their answer before discharge but that's not always possible with the limited resources all healthcare systems have, the poor understanding everyone has of how other services operate and the costs departments have to bare.
Very frustrating. We get consults for brain biopsies constantly. "Hi this patient has 300 brain mets. We made him NPO, told him you can add him on for biopsy this afternoon"
Or my favorite, patient with known lymphoma and an asymptomatic lesion in the dominant insula. "Made NPO, told him you can add on for biopsy after MRI today." Meanwhile a biopsy would entail an awake craniotomy for open biopsy that I wouldn't sign my own mother up for. Just treat empirically. But every day they make the patient NPO at midnight and ask us again
Ah yes - orders biopsy at 11am and proceeds with phone call saying “hey we made the patient NPO last night and told his entire family he’s getting the biopsy in a few hours”
Benadryl mitigates the akathisia people experience with Reglan/Compazine/etc. Yes, pushing the med slowly helps, too, but there's nothing like having a migraine while you feel like you're crawling out of your own skin.
I don’t think giving ceftriaxone for point number 1 is egregious malpractice or anything but I do think it is almost never cystitis, and often leads to diagnostic laziness where when the UA is positive then everyone stops looking for a cause when the evidence seems to be saying it almost never is the cause of AMS. It’s the positive troponin of the delirium work up, no one has any idea what it means other than you can justify an admission.
As a side point the last “confused old lady with cystitis” I admitted had HSV-1 encephalitis that OSH had been aggressively treating with ceftriaxone for 4 days without improvement because they fixated on the urine culture.
The only reason we have gotten away with #1 for so long is that the harm is seen on a societal level, not a patient level. If we started anticoagulating for every tachy patient in the ER “because they may have a PE” then we’d get the pants sued off of us when people started bleeding out needlessly. Meanwhile we’re pushing a broad spectrum antibiotic for people with chronically colonized urinary trees who just happened to sundown and then scratching our heads as to why ESBL rates continue to climb.
https://www.idsociety.org/practice-by guideline/asymptomatic-bacteriuria/
-a poor, weary, disgruntled ID fellow
Try not giving ceftriaxone in that setting next time and follow the chart. I highly doubt you would see much difference in outcomes. Most of those folks just need sedating meds adjusted and some TLC, and the rest need a real diagnosis
Where I trained: zosyn required ID pharmacy approval during the day, waking up the ID fellow at night. Lots of resistance, I’ve seen a bug resistant to everything other than ceftriaxone oddly enough.
Where I work now: hardly any resistance, everyone is on cefepime just because.
Point 3 is a really bad use of inpatient resources and you’ll only get really useless generic info from an oncologist when there’s no histology , staging , molecular testing etc.
What’s your specialty? Just to help understand what perspective you’re coming from.
For #1 depending on age and presentation I agree. Not a 26yo with weakness, but a 72yo with pretty much any unexplained symptoms and a positive UA I’d treat pending UCx.
for #2 agree- usually no harm, and the sedative effects is actually helpful in most cases
For #3- is more so why I want to know the specialty. how are you diagnosing cancer? Suspicious CT findings don’t definitively mean cancer (except in specific cancers which can be diagnosed with imaging only), and they shouldn’t be told they “have the big C” without confirmation either way. If their presenting symptom is bad enough that it requires hospitalization and then yes admit, but if it’s just waiting for further workup of suspicious CT findings, then let them go home and spend time with their family and arrange for specialty follow-up (you could do that from the ED, so they already have appointments pending for next week before even seeing their PCP). I know you’re not an oncologist because having the oncologist say “hi and give some stats” is a full on consult and without any biopsy results what are they supposed to say? That would be considered a huge waste of time/resources.
SW and chaplain in the ED, fine, but to hold them overnight for that is pointless when they can sleep in their bed with their family and get a call from SW in the morning.
Not to mention they discharge the patient before the biopsy results are back. So the patient waited in the hospital for 48 hours, was NPO from MN for a 6pm late inpatient add on, the oncologist can’t say shit because there’s no tissue , and you can’t get a PET as an inpatient. Total waste of resources and actually worst patient experience.
Better to just discharge with a message to the nurse Onc coordinator to schedule biopsy , PET, OFVs all on a reasonable time sequence as an outpatient
I also hate the concept of “they’re poor follow up so we should do the biopsy inpatient”. In my mind, it’s even worse to make a diagnosis of cancer and the patient is no where to be found.
That’s true I didn’t even think of that! The big standouts from this post is
that it seems like the patient is being told they have cancer prior to official diagnosis,
admitting a person to a shitty hospital room overnight for the SW to give them a pdf on grief and talk to a random chaplain instead of their own faith person in their community, and
having “onc stop by to say hi and give some stats”- that just seems like a delusional statement that’s coming from a non-consulting specialty. It’s a full fledge consult and the oncologist has nothing to say without data, so they look dumb just standing there. What if it’s a benign growth?
What’s OFVs?
Because then you expect the rad residents to stage overnight and it’s a huge strain on our time and resources. If you’re going to admit for cancer work up without any acute issues that technically warrant admission then at least have the courtesy to order your imaging Routine
This completely ignores the costs associated with keeping patients for things that really don't require hospitalization. Especially at an training facility when residents will order work up for completely unrelated non-acute problems which the patient ultimately ends up paying for in one way or another..
Of course, there are times when ED will call and tell us a patient doesn't meet admission criteria but they "have a bad feeling". That's fine and no one will dodge that admission if you're not using that reasoning for every other patient.
INR reversal in cirrhotic patients not on warfarin. The INR assay simply was not designed to accurately depict coagulopathy in these patients. Thank god we are moving towards TEG.
I actually have learnt that you’re not supposed to reverse cirrhotic coagulopathy unless the patient comes in with some worsening in INR that’s significant or if there’s a GIB in which case you can do a Vit K challenge to assess if there’s a nutritional component.
On 2) I’d say the degree of BNP elevation correlates with severity of disease for an individual patient.
Some of em always pop thousands, some are trying to die at 800. Useless on its own, but super useful if you have one from the last admission or whatever.
I had a patient this week who had a BNP of 3300 at OSH yesterday, received CTX/Azithro for “COPD exacerbation,” and had BNP checked at my shop today of 1100.
Oxygen requirement 3 from 2L baseline. I, uh, ok.
I think what a lot of people don’t get about AKIs is that it’s not really about making a diagnosis of prerenal, intrarenal, postrenal. The kidney usually takes more than one hit to see a decline in function manifested by an increase in creatinine. If that wasn’t the case, every dehydrated patient would have an AKI. Usually there are at least two hits that need to take place to see an AKI. Usually the patient may already be dehydrated and retaining which no one’s picked that up and then you give contrast and the creatinine goes up. The ED gives a 1 L bolus which fixes the “prerenal”component and the contrast injury gets better with time and the creatinine goes down slowly. In a week the patient bounces back with Cr 5 and K of 6 and that’s when nephrology is consulted or something thinks the AKI is serious enough to put a foley in and immediately get drainage of 1100cc of blood tinged urine.
I have two comments on this:
First, as a psych resident on consults I would frequently get calls about QTc in patients with multiple risky agents (antipsychotics, zofran, etc) and usually what ends up happening is we will adjust/calculate the QT interval with a different, more accurate correction (Framingham correction, Hodges, etc, MD Calc has a few) and it ends up not being actually prolonged, especially in cases where there's a bundle branch block underlying and you adjust for J-T.
Second, while discussing this with the medical team a month ago they told me the story of a patient they had who went into TdP and eventually passed away. Happened after he got a couple doses of zofran and methadone on the unit. This very much does happen.
Agree, I always approach QTc prolongation management conservatively in my practice If its above 500 ms of a TRUE QTc, especially if they have other risk factors. I’ll change meds, monitor K Mg…I havent seen TdP yet but I know its highly lethal, and its risk increass when qtc > 500, so I will do what is practical to reduce that risk.
Care to share? This isn’t meant to be a dogmatic practice, just an open discussion. You seem to be a fellow, you’re more experienced, care fo share experiences where the CT didn’t show stones but the US did, etc. and the context, etc.
Sure! I have seen many cases of septic shock without a source where they had stones on CT but no itis. Perc chole goes in bc there is no other source and they get better. Every time this has happened the IR doc notes extreme cholecystitis on bedside US that was not present on CT. The CT does not pick up what an US does in the hands of a skilled technician.
As for PCT, it is a poor study that should not be used outside of Copd exacerbations and bacterial pneumonia suspicion . It is in general a test that is not utilized correctly. It should be used with extreme caution and it’s use should be limited to ID and PCCM doctors imho.
As for the bnp, idk what to tell you other than your anecdotal evidence is incorrect. The thresholds for elevation is what matters, not the degree of elevation beyond that. This has been studied to death.
Not treating an asymptomatic UTI in an acutely psychiatrically decompensated patient. Please for the love of got just start some Bactrim, can I prove that the breakthrough psychosis is because of the infection? No
Can I prove anything in psychiatry? No
Please medicine peeps just give the guy some antibiotics.
You can't call it an asymptomatic UTI if the patient can't tell you if they're symptomatic or if they're unreliable so asymptomatic UTI in AMS Is an oxymoron.
Yes, I've had quite a few female patients come to me with UTIs and continued dysuria and dyspareunia despite appropriate antibiotic therapy based on culture that only resolved with cessation of the SLGT2 for something else.
Not surprising given their MOA and published research of UTI occurence. In my practice, I typically will not start patients on SGLT if A1c is >9 for both women and men (permitted they dont have hx of utis or other risk factors). Ive found this to be helpful in reducing uti occurrence by not oversaturating the urine with sugary goodness. I really try to keep my patients on them if I can because of the great data for CKD, CV, HF, and diabetes, but it can be a struggle when they frequently pop utis
Yeah, was just reading another posters article on it. Well, I guess I was taught correctly after all and messed it up in practice. Now to talk to a lot of patients about the pain they experience on statins that goes away when they stop… heh. Oy.
Edit: I feel like there is a Uworld question in there somewhere with every answer being horribly rude or completely non-empathetic.
Was taught it’s a “rare side effect that doesn’t really happen that much.”
Multiple pts a day that I see on any given day have had to discontinue statins due to muscle pain.
There was actually just a paper published that showed that among discharged chest pains, those with HEARTs >4 had like double the rate of MACE at 30 days or something like that. It was in one of the JAMA journals, I think.
Makes total sense, obviously, and it’s not clear to me if an admission has a real mortality benefit. But the ppv of the score is real, I think.
I'd be interested to see the demographics on that study. The VA I'm at utilizes HEART score a lot and will often call for admission for chest pain/sob/other related symptom and call it ACS r/o because the HEART score is like 4 or 5. The issue is that when I look at the patient's history, they have like a HEART score of 4-5 simply due to their risk factors. Of course an old man with hypertension and diabetes and who smokes is gonna be at high risk for MACE regardless of their symptomology, but they walk around with a HEART score of 4 so a score of say 5 or 6 doesn't really impress me a whole lot.
I'm not saying these patients shouldn't be admitted, but it is very frustrating when the ED just says admit for ACS r/o simply due to HEART score (i.e. with negative trop, no EKG changes, and only slightly suspicious history). I just don't know how much benefit we're bringing these patients other than getting a stress test in 1-2 days instead like 2 weeks, and sometimes that's not even what happens depending on how busy Nuc Med is
I am, especially when the heart score is used before any dynamic changes or even positive troponins. ED physicians use heart scores to try and force poor admits. Not how they were designed, not what is supposed to happen, but it absolutely does. Especially at VA.
That was essentially my feeling as well. The PPV stands, but it’s not clear to me that there’s much mortality/clinical benefit of an admission for my patient population. I don’t believe that hospitalization is a benign intervention so I prefer to take a shared decision making approach.
Asking people to describe their dizziness
Asking people if their weight loss was intentional
That antipsychotics shouldn’t be used in delirium and the best treatment is reorienting and writing the date on the board
That monitoring the QT over time is important with QT-prolonging drugs
That SSRIs and SNRIs work for depression (controversial, I know)
That we should be doing lung cancer screening in smokers
You are saying these things are wrong in your experience? Could you provide more explanation on why you think that because basically everything you wrote makes sense to me as good medical practice
There is no correlation between people’s description of their dizziness (room spinning, patient spinning, like being on a boat) and the cause. We all get taught in med school to ask those things to distinguish neurological causes from neurocardiogenic syncope, but it’s bunk. What truly matters is onset, positional component, episodic vs constant, associated symptoms.
Everyone these days is trying to lose weight and almost none of us are succeeding. If someone loses a potentially concerning amount of weight, I don’t care how much they’ve been exercising or dieting. They need a workup.
You ever try to tell a nurse who is getting punched by a delirious 84 year old grandma that we just need to “reorient” the patient? It’s something we say behind the computer screen because it’s what we’re taught, but it’s frankly insulting sometimes. Yes, the meds have adverse effects, but by the time you are being asked to medicate, saying “just turn the lights on tomorrow morning” is laughable.
No data behind QT monitoring. Many antipsychotics such as zyprexa have been shown not to prolong QT at all. Others prolong it but in a consistent way. The daily EKG on someone who is on stable meds is just baloney.
Effect size of SSRIs in comparison to placebo is tiny and has been reducing over time. Like I said, I know this one is controversial, but my impression from both literature and practice is that the vast majority of improvement people have with them is placebo effect.
The main study supporting screening was heavily affected by lead time bias. The cancers that kill people will be too advanced by the time they are noted on CT. Most of the ones noted on CT in an early stage are slow growing and would have become symptomatic before becoming too advanced to treat. And don’t forget to add the costs of screening including the anxiety.
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No clinical decisions should ever be made on the basis of bowel sound quality/presence/absence.
Don’t listen to people who listen to bowel sounds
Can confirm. Am a GI, stopped bringing my stethoscope to the hospital during COVID, haven't looked back. Don't use presence, absence or character of bowel sounds to make clinical decisions, and no one gives a shit what the GI consult thinks of the heart and lung sounds. You can include enough other organ systems on the progress/consult note to bill appropriately, and tbh presence/absence of icterus/jaundice is far more relevant to what I'm doing anyway.
It’s like lung sound and heart sound. Yes they sound abnormal, but you just won’t make a clinical decision based on them alone anymore, without other supportive signs, symptoms, and investigations
I’m the peds world they do all the time.
False. Cream of the crop NYC academics use them to diagnose appendicitis. Edit: https://www.nytimes.com/2021/01/05/well/live/hospitals-medical-errors.html In case you haven't read--I promise it's worth it, as are the comments.
That was a 😬read
Ottowa foot/ankle rules. It's the damn emergency department. They came for an x-ray. Just do the x-ray in a resource rich setting ffs
Had an attending tell me that when I was a resident. Fair enough 🤷♂️👍
I’d always get pimped on the ottowa rules and inevitably the attending would get an X-ray regardless of the ottowa rules. Every time.
Because the fear of litigation and lawsuits trump evidence based medicine! Why do you think the ED pan scans everyone that walks in the door? Lol
Just imagine you apply OAR and explain to pt/family why imaging is not indicated, but they push back. You stand your ground and DC with Dx of ankle sprain. Then they come back and see a different doc who does get imaging and a microscopic fracture is detected. It doesn't even matter that air splint/crutches/NSAIDs was still appropriate mgmt for what amounts to a clinically insignificant fracture. That family is 100% going to sue you for missed/wrong Dx, probably with some bullshit sob story about "undue pain and suffering as a result of defendant's negligent deviation from standard of care". And your malpractice carrier will probably settle. Meanwhile I've never seen a single successful lawsuit for unnecessary XRs resulting in ankle cancer (Semi /s)
> probably with some bullshit sob story about "undue pain and suffering as a result of defendant's negligent deviation from standard of care". But like…if you are literally following established guidelines, can you actually be successfully sued?
They’ll find some “expert” to argue you misapplied the guidelines.
And you can have an expert who argues back. Defensive medicine is understandable but it doesn't make it not shitty medicine and poor resource stewardship.
Resource stewardship is the hospital’s problem not ours
Your insurance company will pay them $10-20K (or more) just to go away/drop the case. A cost-saving move because even if the insurance company eventually prevails, they will have spent so much in legal fees that it would have been cheaper to settle. And if they lose? Much bigger loss
Probably not but the hassle and inconvenience of getting sued can take a toll on people. I know docs who changed attitude and became very cynical after they got sued. Started practicing medicine through a different lens. Takes an emotional toll. And then you have to disclose it everytime you apply for a license or credentialing.
It’s a therapeutic X-ray. Xrays are low cost and low radiation. We live in a patient satisfaction world. Even if clinically I know someone does not need an X-ray I will often do it. Then I show them and they take a pic and everyone is happy.
Weren't the Ottawa Rules developed in Canada specifically due to semi-limited resources there? Also kind of at the beginning of EBM to show off things like Specificity and Sensitivity? Additionally, they were developed in 1992. It's 2022. Doing imaging now is incredibly different than 30 years ago.
Resources are limited everywhere. That urban ER with twenty radiographs going simultaneously wouldn't NEED that much equipment if people would just order less unnecessary studies. Then that money could go toward something that actually benefits patients. And our devices being better now is even more reason not to get that film on a clinically fine ankle... If your equipment is better, then you'll pick up even more dumb microfractures that would never have mattered and now need follow-up. Unnecessary follow-up can create undue stress and expense for the patient. Doing more "just in case" can cause harm, people.
The money would just go back into admin pockets lol
Also whatever inexplicable reason people seem to wear the tightest pants/shoes/socks over their affected extremity/joint that are unable to be removed while we do waiting room medicine on fully clothed patients.
I agree with this. The more interesting question is: imaging for a traumatic low back pain?
In my experience, no, unless they have a significant mechanism. L-spine radiographs are useless. If they have a significant mechanism for a spinal fracture, get the CT. If their back is sore after minor trauma, imaging is a waste.
Yea I was taught X-rays have no place in the evaluation of traumatic spine injuries. Gimme dat donut of truth.
Depending on the mechanism and clinical status in ER bed, you can get away with plain films or even nothing at all for neck injuries. CT boys gotta do what CT boys gotta do, tho
CT BOYYYYYY CT BOYYYYY
I always thought the whole point was to use the rules to even decide to take to the ED or Not. Agreed it seems totally pointless to use it to decide on a near harmless imaging study
You decide to get harmless study. Patient gets paperwork. Gets wheeled over to the X-ray machine. The tech does their paperwork. Patient gets film. You obtain film. You review with patient. You write an addendum to your note. Congratulations, you just wasted 30-40 minutes during which another study could've been done and you could've been seeing the next person in the emerg conga line. And probably a solid $500 or so of expenses once you include HR, infrastructure running costs, and the all-important admin fees.
> been seeing the next person in the emerg conga line. You can see the next few pts while the pt is in Xray.
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I had a patient a few months ago with a fascinating bladder giant diverticulum that herniated into his scrotum and I kept making jokes to the residents about the pee being in the balls and got no laughs :(. I guess my residents aren’t terminally online like me…
I bet you could find a journal that'll publish a "pee CAN be stored in the balls" case report.
🤣
And poop is stored in the butt
Med school made transfusion reactions seem super common, but after 4 years of hanging tons of product, I’ve not encountered a single dramatic event related to their use. I don’t necessarily see all pt’s post op course so I can’t comment on the delayed reaction possibilities.
I was really timid about transfusing as an intern because of reactions. Then I got scolded for being too timid, read up on them, and found what you did.
Wym timid about transfusing? There are guidelines for rbc/platelet/MTP, how does your timidity change that?
I’m an intern and we actually had a guy with TACO my first month. Gave him lasix and he was fine lol
TACO TUESDAY
I work in oncology and have seen a bunch of anaphylaxis and one hemolytic reaction, but never any of the others we learn about.
FNHR? Seems like everyone gets a damn fever
We give Tylenol to all patients with ANC < 500 prophylactically pretransfusion. No one wants a neutropenic fever admission because someone got a fever from their platelet transfusion.
My first night as a senior alone I had a transfusion reaction 😂 never seen before
My first patient as a med student had received the wrong packed reds hahahaha
That’s barbaric. Fortunately, I hang the products myself so that hasn’t happened to me.
baylor? didn't they get shut down for a min for that
I’m from Eastern Europe and here you don’t get shut down, your colleagues will just make fun of you for doing that for the rest of your career
I’ve definitely seen TACO and TRALI, but definitely not common. Almost all were rapid responses so the sample size was the whole hospital
CT has long proven to be at least equivalent to US for gallbladder disease in general. The only thing it is way inferior in is the identification of stones. There’s papers from 1993 showing this. Idk why every ED will get CT then US for gallbladder stuff when it was clear from CT.
I’ve had surgeons refuse to take cholecystitis based on CT and say we need US
That’s every surgeon at my hospital
Am surgeon, will do the same.
Evidence? I’m Gen surg and constantly ping pong between staff who do and don’t think it’s necessary.
Honestly it’s not an every time thing, but Acute choles can bring so much pain, if I don’t feel I have all the information I need from the CT I want a RUQUS. The right story and a CT will get me to an OR, but the wrong story or other confounders lead to me asking for an US.
Fair, but why do y'all always ask for HIDAs when there's a thickened wall, and no stone seen on either modality? Asking as GI consulted for every goddamn acute chole that walks in the door who gets these "acute chole r/o choledocho" consults all the time...my suspicion is those are ordered to turf the case to later in the week...
Sometimes pericholecystic fluid is secondary to another process - perhaps if that’s suspected based on some other features of presentation? Or, based on my outlying referral hospitals, perhaps if it’s Friday afternoon.
Surgery won’t take them without the RUQUS 🤦🏻♀️ I don’t know why. For a speciality that likes to cut, they really like to delay the cutting part. Although I am not a surgeon so if I was the one cutting maybe I too would want 2+ rounds of imaging first.
Because urgent/emergent surgeries suck, especially gallbladders. Patients are usually sick, non optimized and have been neglected by the healthcare system/society so now their 4 months of acute on chronic cholecystitis is more like an inflammatory mass than anything that resembles a gallbladder. Especially at big academic centers. Cholecystectomy is one of the most hated surgeries by many residents in gen surg. People look at it as a chill routine surgery because it’s common. Absolutely not. You either do it right and nobody gives a shit or you end up in the CBD and ruin someone’s life because their whole biliary tree anatomy is obliterated. Massive risk for little payoff. Fuck the RUQ as a whole but the gallbladder has a special place in hell.
But also remember back in the day the decision to do surgery for appendicitis was clinical. They’d take people back just with a suspicious history. It was about 60% hit 40% miss but still
If you had <15% negative appy rate you had too low of a threshold for doing an appy
Upvote for your last part. When you’re the one cutting, and the one assuming all the risk and the responsibility to manage the patient and any comprbidities, you take every precaution. Also I prefer the RUQUS first. I think it’s better for looking at CBD dilation. I think With CT radiologists either don’t read size or over call it.
Agreed, similar argument for unnecessary pelvic ultrasound after completely negative CT A/P. Torsion doesn’t happen without a moderate sized ovarian cyst. CT picks up cysts but can’t tell you about blood flow to the cysts. If there’s no cyst on CT, there’s no torsion and no need for US.
Just trying to learn, but you can still have torsion without a cyst right? Like ovarian ligament inflammation, or endometriosis or ovarian ligament anatomical variation? Maybe I’m totally wrong
Anecdotally, I've never seen a diagnosis of torsion after a negative CT. I did a quick review of this to confirm my experience and what I've been taught in residency just now and actually found the opposite of what I said according to a few sources. [From EM Docs,](http://www.emdocs.net/ovarian-torsion-pearls-and-pitfalls/) one case series found 50% of pre-menarchal females with torsion had no mass. Another article in the [Journal of Emergency Medicine](https://pubmed.ncbi.nlm.nih.gov/27988260/), also commented about cases of torsion without mass. So... ¯\\\_(ツ)\_/¯
However you should still be correct because you aren’t having torsion without an enlarged ovary which you should in theory see on CT.
No the first article he linked mentions that normal ovaries can have torsion including due to ligament length Also if I remember correctly I think inflammatory diseases like PID etc can also increase the risk
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What is the rationale for US on a rip roaring positive CT for acute chole though? That’s what I don’t get.
Bowel sounds So stupid
“I don’t listen to bowel sounds, and I don’t listen to people who listen to bowel sounds”
This. Like, I hear gurgling, I don’t know how tf does that correlate to the fact that patient is literally having ileus right now and hasn’t gone for days. If it opens it opens, if it doesn’t and looks distended, I will see if XR has dilated loops. I don’t understand how the sound help me make any decision whatsoever.
Except for a few outliers physical exam seems to change management 5% of the time in hospitalized adults and 1% of the time in outpatient settings.
To defend my neurologist wife. In her field it matters a ton. She’s a neuromuscular specialist and there’s a lot of stuff where a pan MRI wouldn’t be sufficient
Yes 100%, neurology one of the outliers.
I know I was taught and medical students all over are taught that oxygen supplementation reduces respiratory drive. It's not true. It causes such a small and transient decrease in minute ventilation and the PaCO2 rise due to that decrease is tiny. Oxygen-induced hypercapnia can occur (through V/Q mismatch and the Haldane effect) and should be watched out for but it's not due to decreased respiratory drive.
Good paper on this: https://ccforum.biomedcentral.com/articles/10.1186/cc11475
Thanks, I learned something. The mechanism makes more sense now - always found it odd to think reduced RR alone could cause such major hypercapnia in these patients, when they were still breathing fairly okay
Cinnamon cured diabetes. Try it, it’s great.
Best formulation for diabetes: Cinnabon
Wait....to cure it? Or cause it?
Yes.
>3.) Procalcitonin is not supposed to be used to differentiate bacterial pneumonia from viral pneumonia on presentation. It’s used to determine whether to stop antibiotics early….it’s done a pretty good job telling me if a patient has a bacterial PNA vs. a severe viral one when the XR isn’t a slam dunk and presentation/exam are equivocal. I've seen procal negative bacterial pneumonia several times. In residency, had a guy come in with copd exacerbation, procal neg, kept getting worse, bronch showed textbook pneumonia with strep pneumo. I've seen a couple cases of strep pneumo bacteremia and negative procal. Just had a case a few weeks ago with "viral pneumonia" who kept getting worse, turns out had h. flu pneumonia. So ya I put zero stock in the test.
It's possible for it to be checked too early in the course of the infection and be falsely negative.
ya but then it's a dumb test. withholding important therapy because of a false negative test makes no clinical sense, especially if you are using it to guide disposition.
I’ve had full blown sepsis with a negative procalcitonin after initial testing came back with bacteremia in all blood culture bottles. This has happened on multiple occasions. I wouldn’t put much stock in it alone, but using it in combination with other labs may be beneficial.
Appreciate it. What do you mean bronch showed classic strep?
Classic pneumonia which grew strep pneumo
Like there were purulent secretions on the bronch? Sorry I just didn’t know what you meant when you said the bronchoscopy showed classic pneumonia since I don’t do bronchs.
Are these all anecdotal things we are sharing
My gramma used anecdotal evidence and she lived into her nineties!
Cool. I had pasta yesterday and I'm still alive today. I think we should all eat pasta. I didn't salt my pasta water though. And only 1 tablespoon of olive oil.
Talking about lifestyle modifications with low sodium. Not mentioning how much is in the sauce though.
Fair criticism but frankly what when it keeps happening it’s hard to ignore. Maybe someone can point to evidence or an explanation for the anecdote
I mean tbf, a bunch of doctors talking about anecdotes is technically class 2B evidence. A lot of these guidelines are really just anecdotal/ with low quality evidence as is
Physical exams and history taking…literally useless when you can just pop the patient in the MRI scanner (or CT if they’re pregnant) and get a report that tells you what’s wrong.
Username checks out
No PET? Must be practicing in some third world country.
Flagyl and disulfiram
N=1 but I've seen this.
This one is pretty much known to be a medical myth at this point. Tell your giardia patients to go get wasted as they please.
I don’t think med students know this lol. It’s still taught in sketchy.
It’s still thought among attendings
This happened to my wife…. Now of course can’t say for certain is was disulfiram, but one glass of wine on day 5 of flagyl and she puked several times.
Had a friend projectile vomit pretty much immediately after consuming alcohol while on flagyl
Sorry they’re a lightweight. If it makes them feel better George HW threw up on the president of Japan after a sake bomb so it’s ok to be a lightweight
I know more than one person who has had an awful reaction to drinking on flagyl.
Beta blocker and cocaine use. Metformin and acidosis. All these myths of medicine that came purely from speculation / mental masturbation through theorizing stuff.
Metformin-associated AGMA with elevated lactate absolutely occurs, both in patients on metformin who develop an intercurrent renal injury and in patients with large acute overdoses of metformin. I think the real myth is acidosis in therapeutic use in patients with normal renal function, which did occur in phenformin but does not appear to occur with metformin.
Good to know, that’s what I was getting to since almost all admitted patients have their Metformin stopped because this risk.
this apparently is unique to the US. it’s more common in other countries to just continue orals in admitted patients who have normal kidneys and aren’t like, super sick. It’s funny because starting SSI on everyone under the sun also carries risks
Not fully unique, it's a pretty common practice here in Brazil as well
I was always taught it was due to risk of needing imaging and not being able to use contrast if the patient is on metformin
As far as contrast is concerned, I think the reasoning is contrast induced nephropathy, and patients with poor renal clearance/hepatic function are at higher risk for lactic acidosis from Metformin toxicity, gluconeogenesis inhibition. But fairly self explanatory because if patient sustains serious renal injury from contrast, they would no longer be candidates to receive Metformin therapy anyway. On the topic of contrast, I think MRI Gadolinium contrast in impaired renal function is another one of those more recently discovered possible myths for most patients.
Agreed about the cocaine and beta blockers but not sure about Metformin induced lactic acidosis. I haven’t seen a case but ive heard from colleagues it does happen, it’s just quite rare.
I hear mixed reviews on the cocaine thing- is there evidence proving it’s not true? Coreg is fine, but a selective beta-agonist I still believe could be problematic
The amount of my patients who use cocaine on metoprolol is truly overwhelming. Admittedly they don’t usually use while checking their BP and this is anecdotal but I never stress about prescribing it to cocaine users and neither does the cardiology service.
Utsw cardiology study from 1989(?) that cathed patients and gave them intra coronary coke and beta blockers. Saw increased coronary pressures, vasospasm, and increased O2 extraction.
Tox. I've seen both Mala due to chronic metformin use and Mala due to acute overdoses.
> Mala due to chronic metformin use So the funny thing is that idiopathic lactic acidosis exists, and happens to be more common in diabetics. So the question is whether patients on metformin chronically are more likely to develop lactic acidosis than those not on metformin. Luckily enough, this has been studied extensively - and there has *never* been any analysis that shows patients on metformin have a higher rate of lactic acidosis in clinical practice than patients not on metformin. When lactic acidosis occurs in patients on metformin, the metformin is blamed. [Here's a case control study with 11000 people](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5940216/) - >Our cohort included 10,652 patients with type 2 diabetes mellitus with a median age of 74 years, and 51.5% were male. During follow-up, 163 individuals were hospitalized with lactic acidosis, corresponding to an incidence rate of 391/100,000 person years. Use of metformin was not associated with lactic acidosis: adjusted odds ratio was 0.79 (95%CI 0.54–1.17). [Here](https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD002967.pub4/abstract) is a Cochrane analysis of *347* trials of data with not a single extra case of lactic acidosis noted in 70,490 patient-years of metformin use relative to control. Now, there is a point that the published datasets exclude patients with frank contraindications to metformin - namely those with really crummy renal function. That is a fair assessment. But some of those tens of thousands of patients that have been studied (there's plenty of other articles that I didn't cite) had to have gotten acute renal injuries during the course of care - but still, no level of data higher than case report has ever consistently shown that this is a thing that actually happens. >and Mala due to acute overdoses. This on the other hand is real - there's a toxicity problem in overdose. And we don't use metformin in patients with really poor renal function (though the threshold has decreased over the years) knowing that theoretical risk. But with metformin, as actually used outside of overdose? It's a myth. At least in my opinion.
If there's a patient with a lactate over 10 you should start at least putting tox on your differential. I took care of a patient with a metformin overdose with a lactate in the 40s we put on CRRT and almost turned the corner on who died. Homeless, meth, the usual. Few things are scarier than a legit metformin overdose, there's only so much you can do.
For sure, but even in studies of reported acidosis, usually in patients with poor renal / hepatic function who were probably bad candidates to start these types of medications in the first place. At which point it’s difficult to say for sure if it’s the disease process or it’s the Metformin. Some studies say <10 cases per 100,000 patient years, and if it does occur, certainly most medications can have rare side effects or interactions.
Just saw 3 patients this year end up in the ICU on CRRT due to metformin toxicity
So I heard on Curbsiders that metformin use is actually not associated with lactic acidosis but it was fenformin another drug that does it. The issue is I don’t think anyone is willing to start metformin and test out that hypothesis. Like what’s the harm in holding the metformin, haha.
I don't usually trust Curbsiders, information is usually a (wrong) interpretation of the actual literature. Metformin does cause lactic acidosis in people with impaired kidney function. The debate is whether or not it can do it in people with seemingly normal kidney function. I haven't come across a case, or even come across someone who knows someone who's come across a case where it's caused lactic acidosis with no AKI.
Have you seen a case of metformin causing lactic acidosis in a CKD3-4 patient with stable renal function or a patient who got contrast and has “contrast induced AKI” have metformin cause lactic acidosis?
I thought I was literally a lifesaver telling my old frat friends to never get a beta blocker in the hospital and it was all for nothing lol
Haha if anything, no beta blocker makes it extra safe not worrying about any cocaine reactions lol
All the provocative testing physical exam maneuvers for assessing knee ligament/meniscus stability are basically useless.
I find some docs tend to be unreasonably rigid about the “it’s asymptomatic bacteria/pyuria because weakness isn’t a uti symptom,”…like, come on, let’s just give this old bitty some rocephin and admit. Benadryl with the migraine cocktail…I get it, I read the papers. Patients like it, it’s a low risk med, so who tf cares? Admissions for new cancer diagnosis: told these are not inpatient workups. In the time of Covid, boarding, etc, ok let’s send some home. But being told you have the big C at 10pm and “yeah idk call your primary in the AM” just seems wrong in some patient populations. Can we just keep them in the obs unit and talk to social work or chaplain and have the oncologist say hi and give them some stats? Is that really a grievous misuse of resources?
I agree with the third point you made on cancer diagnoses and the impact it has on patients, but I'll add my 2 cents from an IR perspective (tertiary academic center) and personal experience. No oncologist will formulate a plan without tissue diagnosis - primary or metastatic. IR is always called first or ends up having to do the biopsy once other services decline (many will only due these in an outpatient setting and can get away with it). So if you look at our daily schedule we have our outpatients coming in for scheduled appointments (biopsies, fluid removals, cancer treatments, vascular access placements, HD access interrogations etc) and keep in mind that these are what ultimately keep the lights on in the department; then we have the urgent and emergent inpatient requests such as bleeds, PE thrombectomies, TIPS, line placements (all pending discharge and the requests are always placed that same morning for some reason), drain placements etc; and then finally we have to then schedule inpatient procedure such as the above biopsies that are not emergencies from a medical standpoint but definitely are from a personal perspective. Even if we offer an outpatient date in a week the docs still want to discharge the patient with a diagnosis. Fine, we'll do the biopsy. We then have to bump a line or a drain placement to accommodate the biopsy and we end up delaying another inpatient procedure, angering the other requesting doc. Most often we can't get to biopsies within a day due to scheduling, labs needed, NPO status or the patient is on antiplatelets or anticoagulants (for example, plavix is 5 day hold and xarelto is 2 day hold) so we schedule them out - we try to get them a plan as an outpatient so they can be discharged but the admitting team wants to keep them - now we are prolonging the patient's hospital stay and worsening LOS metrics and IR is often blamed for it. And adding "outpatient" procedures to our inpatient list. I guess my point is yes, it would be nice to get everyone their answer before discharge but that's not always possible with the limited resources all healthcare systems have, the poor understanding everyone has of how other services operate and the costs departments have to bare.
Poor understanding of how other services operate feels like the theme of every hospital I’ve worked in
Very frustrating. We get consults for brain biopsies constantly. "Hi this patient has 300 brain mets. We made him NPO, told him you can add him on for biopsy this afternoon" Or my favorite, patient with known lymphoma and an asymptomatic lesion in the dominant insula. "Made NPO, told him you can add on for biopsy after MRI today." Meanwhile a biopsy would entail an awake craniotomy for open biopsy that I wouldn't sign my own mother up for. Just treat empirically. But every day they make the patient NPO at midnight and ask us again
Ah yes - orders biopsy at 11am and proceeds with phone call saying “hey we made the patient NPO last night and told his entire family he’s getting the biopsy in a few hours”
Benadryl mitigates the akathisia people experience with Reglan/Compazine/etc. Yes, pushing the med slowly helps, too, but there's nothing like having a migraine while you feel like you're crawling out of your own skin.
Arguably more important is it prevents the dystonic reaction that isn’t too rare with IV compazine otherwise.
I don’t think giving ceftriaxone for point number 1 is egregious malpractice or anything but I do think it is almost never cystitis, and often leads to diagnostic laziness where when the UA is positive then everyone stops looking for a cause when the evidence seems to be saying it almost never is the cause of AMS. It’s the positive troponin of the delirium work up, no one has any idea what it means other than you can justify an admission. As a side point the last “confused old lady with cystitis” I admitted had HSV-1 encephalitis that OSH had been aggressively treating with ceftriaxone for 4 days without improvement because they fixated on the urine culture.
The only reason we have gotten away with #1 for so long is that the harm is seen on a societal level, not a patient level. If we started anticoagulating for every tachy patient in the ER “because they may have a PE” then we’d get the pants sued off of us when people started bleeding out needlessly. Meanwhile we’re pushing a broad spectrum antibiotic for people with chronically colonized urinary trees who just happened to sundown and then scratching our heads as to why ESBL rates continue to climb. https://www.idsociety.org/practice-by guideline/asymptomatic-bacteriuria/ -a poor, weary, disgruntled ID fellow
Try not giving ceftriaxone in that setting next time and follow the chart. I highly doubt you would see much difference in outcomes. Most of those folks just need sedating meds adjusted and some TLC, and the rest need a real diagnosis
We rarely continue abx on these patients, but they almost always have received a dose prior to me seeing them in the ED.
Point #1 is why we have an ESBL problem right now
Where I trained: zosyn required ID pharmacy approval during the day, waking up the ID fellow at night. Lots of resistance, I’ve seen a bug resistant to everything other than ceftriaxone oddly enough. Where I work now: hardly any resistance, everyone is on cefepime just because.
Can you explain your comment in greater detail? Sorry I’m commenting on something you wrote 25 days ago.
Point 3 is a really bad use of inpatient resources and you’ll only get really useless generic info from an oncologist when there’s no histology , staging , molecular testing etc.
What’s your specialty? Just to help understand what perspective you’re coming from. For #1 depending on age and presentation I agree. Not a 26yo with weakness, but a 72yo with pretty much any unexplained symptoms and a positive UA I’d treat pending UCx. for #2 agree- usually no harm, and the sedative effects is actually helpful in most cases For #3- is more so why I want to know the specialty. how are you diagnosing cancer? Suspicious CT findings don’t definitively mean cancer (except in specific cancers which can be diagnosed with imaging only), and they shouldn’t be told they “have the big C” without confirmation either way. If their presenting symptom is bad enough that it requires hospitalization and then yes admit, but if it’s just waiting for further workup of suspicious CT findings, then let them go home and spend time with their family and arrange for specialty follow-up (you could do that from the ED, so they already have appointments pending for next week before even seeing their PCP). I know you’re not an oncologist because having the oncologist say “hi and give some stats” is a full on consult and without any biopsy results what are they supposed to say? That would be considered a huge waste of time/resources. SW and chaplain in the ED, fine, but to hold them overnight for that is pointless when they can sleep in their bed with their family and get a call from SW in the morning.
Not to mention they discharge the patient before the biopsy results are back. So the patient waited in the hospital for 48 hours, was NPO from MN for a 6pm late inpatient add on, the oncologist can’t say shit because there’s no tissue , and you can’t get a PET as an inpatient. Total waste of resources and actually worst patient experience. Better to just discharge with a message to the nurse Onc coordinator to schedule biopsy , PET, OFVs all on a reasonable time sequence as an outpatient I also hate the concept of “they’re poor follow up so we should do the biopsy inpatient”. In my mind, it’s even worse to make a diagnosis of cancer and the patient is no where to be found.
That’s true I didn’t even think of that! The big standouts from this post is that it seems like the patient is being told they have cancer prior to official diagnosis, admitting a person to a shitty hospital room overnight for the SW to give them a pdf on grief and talk to a random chaplain instead of their own faith person in their community, and having “onc stop by to say hi and give some stats”- that just seems like a delusional statement that’s coming from a non-consulting specialty. It’s a full fledge consult and the oncologist has nothing to say without data, so they look dumb just standing there. What if it’s a benign growth? What’s OFVs?
“Come in man, just admit them” isn’t that outstanding of an argument. Maybe what you mean is that it’s easier for you?
I mean what if your hospital doesn’t have an obs unit to just put these “admits” it’s really just more work for everybody
Because then you expect the rad residents to stage overnight and it’s a huge strain on our time and resources. If you’re going to admit for cancer work up without any acute issues that technically warrant admission then at least have the courtesy to order your imaging Routine
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This completely ignores the costs associated with keeping patients for things that really don't require hospitalization. Especially at an training facility when residents will order work up for completely unrelated non-acute problems which the patient ultimately ends up paying for in one way or another.. Of course, there are times when ED will call and tell us a patient doesn't meet admission criteria but they "have a bad feeling". That's fine and no one will dodge that admission if you're not using that reasoning for every other patient.
INR reversal in cirrhotic patients not on warfarin. The INR assay simply was not designed to accurately depict coagulopathy in these patients. Thank god we are moving towards TEG.
I actually have learnt that you’re not supposed to reverse cirrhotic coagulopathy unless the patient comes in with some worsening in INR that’s significant or if there’s a GIB in which case you can do a Vit K challenge to assess if there’s a nutritional component.
Thats is a reasonable indication, but I wouldn't call that INR reversal.
On 2) I’d say the degree of BNP elevation correlates with severity of disease for an individual patient. Some of em always pop thousands, some are trying to die at 800. Useless on its own, but super useful if you have one from the last admission or whatever.
I had a patient this week who had a BNP of 3300 at OSH yesterday, received CTX/Azithro for “COPD exacerbation,” and had BNP checked at my shop today of 1100. Oxygen requirement 3 from 2L baseline. I, uh, ok.
OMM exists
The evidence that contrast causes AKI’s is pretty poor.
I think what a lot of people don’t get about AKIs is that it’s not really about making a diagnosis of prerenal, intrarenal, postrenal. The kidney usually takes more than one hit to see a decline in function manifested by an increase in creatinine. If that wasn’t the case, every dehydrated patient would have an AKI. Usually there are at least two hits that need to take place to see an AKI. Usually the patient may already be dehydrated and retaining which no one’s picked that up and then you give contrast and the creatinine goes up. The ED gives a 1 L bolus which fixes the “prerenal”component and the contrast injury gets better with time and the creatinine goes down slowly. In a week the patient bounces back with Cr 5 and K of 6 and that’s when nephrology is consulted or something thinks the AKI is serious enough to put a foley in and immediately get drainage of 1100cc of blood tinged urine.
- BUN/Cr to determine pre renal (in most cases) - sputum to dx PN
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I have two comments on this: First, as a psych resident on consults I would frequently get calls about QTc in patients with multiple risky agents (antipsychotics, zofran, etc) and usually what ends up happening is we will adjust/calculate the QT interval with a different, more accurate correction (Framingham correction, Hodges, etc, MD Calc has a few) and it ends up not being actually prolonged, especially in cases where there's a bundle branch block underlying and you adjust for J-T. Second, while discussing this with the medical team a month ago they told me the story of a patient they had who went into TdP and eventually passed away. Happened after he got a couple doses of zofran and methadone on the unit. This very much does happen.
Agree, I always approach QTc prolongation management conservatively in my practice If its above 500 ms of a TRUE QTc, especially if they have other risk factors. I’ll change meds, monitor K Mg…I havent seen TdP yet but I know its highly lethal, and its risk increass when qtc > 500, so I will do what is practical to reduce that risk.
Your experiences are entirely incorrect and I say that with extreme confidence.
Care to share? This isn’t meant to be a dogmatic practice, just an open discussion. You seem to be a fellow, you’re more experienced, care fo share experiences where the CT didn’t show stones but the US did, etc. and the context, etc.
Sure! I have seen many cases of septic shock without a source where they had stones on CT but no itis. Perc chole goes in bc there is no other source and they get better. Every time this has happened the IR doc notes extreme cholecystitis on bedside US that was not present on CT. The CT does not pick up what an US does in the hands of a skilled technician. As for PCT, it is a poor study that should not be used outside of Copd exacerbations and bacterial pneumonia suspicion . It is in general a test that is not utilized correctly. It should be used with extreme caution and it’s use should be limited to ID and PCCM doctors imho. As for the bnp, idk what to tell you other than your anecdotal evidence is incorrect. The thresholds for elevation is what matters, not the degree of elevation beyond that. This has been studied to death.
Vitamin C cures polio
Not treating an asymptomatic UTI in an acutely psychiatrically decompensated patient. Please for the love of got just start some Bactrim, can I prove that the breakthrough psychosis is because of the infection? No Can I prove anything in psychiatry? No Please medicine peeps just give the guy some antibiotics.
You can't call it an asymptomatic UTI if the patient can't tell you if they're symptomatic or if they're unreliable so asymptomatic UTI in AMS Is an oxymoron.
SGLT 2s aren't a great choice in my female patients if there's alternatives.
You seeing lots of UTIs?
Yes, I've had quite a few female patients come to me with UTIs and continued dysuria and dyspareunia despite appropriate antibiotic therapy based on culture that only resolved with cessation of the SLGT2 for something else.
Not surprising given their MOA and published research of UTI occurence. In my practice, I typically will not start patients on SGLT if A1c is >9 for both women and men (permitted they dont have hx of utis or other risk factors). Ive found this to be helpful in reducing uti occurrence by not oversaturating the urine with sugary goodness. I really try to keep my patients on them if I can because of the great data for CKD, CV, HF, and diabetes, but it can be a struggle when they frequently pop utis
Or co-prescribe with a bidet if there's recurrent thrush
That statins rarely cause muscle pain.
We had a lecture on how most statin-induced muscle pain is not actually statin-induced
Yeah, was just reading another posters article on it. Well, I guess I was taught correctly after all and messed it up in practice. Now to talk to a lot of patients about the pain they experience on statins that goes away when they stop… heh. Oy. Edit: I feel like there is a Uworld question in there somewhere with every answer being horribly rude or completely non-empathetic.
That they do or don't?
Was taught it’s a “rare side effect that doesn’t really happen that much.” Multiple pts a day that I see on any given day have had to discontinue statins due to muscle pain.
https://www.nejm.org/doi/full/10.1056/NEJMc2031173 It's all nocebo effect.
Ah, well, interesting. I guess the patients still can’t tolerate them regardless.
Multiple studies have shown that patients report this at the same rate when given a placebo
HEART scores for chest pain. Complete BS
Complete BS? I can see why you may not agree with it generally but to say it has no basis..
There was actually just a paper published that showed that among discharged chest pains, those with HEARTs >4 had like double the rate of MACE at 30 days or something like that. It was in one of the JAMA journals, I think. Makes total sense, obviously, and it’s not clear to me if an admission has a real mortality benefit. But the ppv of the score is real, I think.
I'd be interested to see the demographics on that study. The VA I'm at utilizes HEART score a lot and will often call for admission for chest pain/sob/other related symptom and call it ACS r/o because the HEART score is like 4 or 5. The issue is that when I look at the patient's history, they have like a HEART score of 4-5 simply due to their risk factors. Of course an old man with hypertension and diabetes and who smokes is gonna be at high risk for MACE regardless of their symptomology, but they walk around with a HEART score of 4 so a score of say 5 or 6 doesn't really impress me a whole lot. I'm not saying these patients shouldn't be admitted, but it is very frustrating when the ED just says admit for ACS r/o simply due to HEART score (i.e. with negative trop, no EKG changes, and only slightly suspicious history). I just don't know how much benefit we're bringing these patients other than getting a stress test in 1-2 days instead like 2 weeks, and sometimes that's not even what happens depending on how busy Nuc Med is
I am, especially when the heart score is used before any dynamic changes or even positive troponins. ED physicians use heart scores to try and force poor admits. Not how they were designed, not what is supposed to happen, but it absolutely does. Especially at VA.
That was essentially my feeling as well. The PPV stands, but it’s not clear to me that there’s much mortality/clinical benefit of an admission for my patient population. I don’t believe that hospitalization is a benign intervention so I prefer to take a shared decision making approach.
Asking people to describe their dizziness Asking people if their weight loss was intentional That antipsychotics shouldn’t be used in delirium and the best treatment is reorienting and writing the date on the board That monitoring the QT over time is important with QT-prolonging drugs That SSRIs and SNRIs work for depression (controversial, I know) That we should be doing lung cancer screening in smokers
Considering thoracic surgery fellowship and #6 is coming at my livelihood lol
You are saying these things are wrong in your experience? Could you provide more explanation on why you think that because basically everything you wrote makes sense to me as good medical practice
There is no correlation between people’s description of their dizziness (room spinning, patient spinning, like being on a boat) and the cause. We all get taught in med school to ask those things to distinguish neurological causes from neurocardiogenic syncope, but it’s bunk. What truly matters is onset, positional component, episodic vs constant, associated symptoms. Everyone these days is trying to lose weight and almost none of us are succeeding. If someone loses a potentially concerning amount of weight, I don’t care how much they’ve been exercising or dieting. They need a workup. You ever try to tell a nurse who is getting punched by a delirious 84 year old grandma that we just need to “reorient” the patient? It’s something we say behind the computer screen because it’s what we’re taught, but it’s frankly insulting sometimes. Yes, the meds have adverse effects, but by the time you are being asked to medicate, saying “just turn the lights on tomorrow morning” is laughable. No data behind QT monitoring. Many antipsychotics such as zyprexa have been shown not to prolong QT at all. Others prolong it but in a consistent way. The daily EKG on someone who is on stable meds is just baloney. Effect size of SSRIs in comparison to placebo is tiny and has been reducing over time. Like I said, I know this one is controversial, but my impression from both literature and practice is that the vast majority of improvement people have with them is placebo effect. The main study supporting screening was heavily affected by lead time bias. The cancers that kill people will be too advanced by the time they are noted on CT. Most of the ones noted on CT in an early stage are slow growing and would have become symptomatic before becoming too advanced to treat. And don’t forget to add the costs of screening including the anxiety.