the meta-analysis detected a barely significant increase in "clinically significant bleeding" in patients treated with steroid. there was *no* difference in bleeding of any severity. why this discrepancy? let's dig deeper...(2/7) ncbi.nlm.nih.gov/pubmed/31501997
the primary endpoint ("clinically significant" bleeding) was only reported in 25 trials. most are small. nearly *half* of the power in this analysis comes from a single trial, Roberts 2004... what was going on here? (#rantorial 3/7)
digging into the supplemental data shows that the Roberts 2004 trial involved giving astronomically massive doses of steroid for traumatic brain injury! of course that caused GI bleeding! (#rantorial 4/7)
the primary analysis is missing some major studies (ADRENAL etc). perhaps these studies didn't specifically record "clinically significant" bleeds, so they weren't included. this causes the primary endpoint to be dominated by wierd studies like Roberts 2004 (#rantorial 5/7)
the secondary endpoint, GI bleeding of any severity, included a lot more studies (55 vs. 25). this may explain the discrepancy between the primary endpoint versus the secondary endpoint (which *didn't* find harm from steroid)(#rantorial 6/7)
this study illustrates the a classic pitfall of meta-analyses: blenderizing together profoundly heterogenious studies to achieve a barely significant result (p=0.04) and then suggesting that it means something. (#rantorial 7/7)
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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)