great article reminding us not to stop buprenorphine in patients with opioid use disorder who have acute pain. a few key points are worth emphasizing ...1/5
(full article: bit.ly/2L9m8FP)
most important point = don't stop buprenorphine due to acute pain! dividing the bupe dose q6-q8 may improve analgesic effectiveness, so buprenorphine itself can be used as an analgesic. (2/5)
you don't need an X-waiver to prescribe buprenorphine within the hospital. using buprenorphine is now a core clinical competency that all inpatient providers should be comfortable with (3/5)
high-potency full opioids may be added on *top* of buprenorphine to help manage acute pain (e.g. morphine). the dose will need to be increased to compete for receptors, but this can still work (4/5)
don't forget multimodal tx (acetaminophen, ketamine, clonidine, dexmedetomidine, ketamine, gabapentin, did I mention ketamine?). tickling more receptors often better than whaling on the mu-receptors with tons of opioid. more on this in @iBookCC here bit.ly/30JtEOo (5/5)
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how to place a consult: you MUST understand the five stages of consultant grief.
once you can understand this painful and natural process, requesting consults will make a LOT more sense
buckle up, it can be a little rough…
🧵 1/6…
stage 1: denial
- You dont need a consult.
- You called the wrong service.
- 18 years old? consult pediatrics
- I’m not actually on call now
- Everything’s fine, just walk it off…
stage 2: anger
- you should have consulted us earlier/later
- you should have checked this test before calling us
- you’re a terrible doctor/student/human being
this is much better than MINDS (which contained ~90% hypoactive), but probably still not ideal.
(at this point, does anyone actually think that haloperidol helps with hypoactive delirium ??)
other than dilution of the patient population by patients with hypoactive delirium (who are unlikely to benefit & might conceivably be harmed by over-sedation), the methodology seems pretty solid.
I think it's time for a difficult discussion, folks.
Let's talk about CSF lactate 🫣
CSF lactate has been shown to be *superior* to traditional CSF studies in sorting out viral vs. bacterial meningitis in several studies & meta-analyses...
a subset of patients with viral meningitis will initially have a *neutrophilic* pleocytosis.
this can lead to unnecessary admissions & antibiotics
some patients are subjected to repeat LPs 😩
a low CSF lactate could avoid all of this, allowing patients to go home from the ED
CSF lactate measurement is recommended in guidelines from the United Kingdom, Europe, and France.
(it's not recommended in the ID society of America guidelines, but they're from *2004* and require revisions)