4/ Back to the poll choices:
1️⃣ is the VPA being chewed up by fPHT?
I’m sure @theABofPharmaC & @jimmySuhMD are going to do an incredible collab about VPA & PHT.
🛑Spoiler: they do not play nicely together.
5/ In short: VPA displaces PHT from plasma protein binding sites
This significantly ⬆️ FREE phenytoin (as it did in this case, see ⬇️).
But you might not detect this if you are just monitoring TOTAL phenytoin levels, which can stay the same or EVEN DECREASE!
6/ But PHT can also ⬇️ VPA, and the effect is unpredictable.
So -- This is a plausible explanation, but the DRAMATICALLY low VPA would be a bit unexpected.
VPA+fPHT is just a headache. If you really must use, follow free levels closely.
7/ 2️⃣ Is it VPA and warfarin?
No. [Obvi] this patient’s warfarin had been reversed before the burr holes…
But VPA + warfarin can cause issues:
🌟VPA can ⬆️ warfarin by ⬇️ protein binding.
🌟VPA is also an inhibitor of CYP 2C9 = ⬆️ Warfarin
8/ Thanks @MeganRx1 for putting together this awesome chart for the #acuteneurologysurvivalguide. (BTW I swear is going to be published in 2022, hopefully by springtime…).
As you can see warfarin + AEDs also = headache.
9/ So DOACS for patients on AEDs then?
Sadly, those can be tough too. PHT, PHB, & CBZ sig induce the metabolism of DOACs and may result in therapeutic failure.
🛑 Avoid combination of PHT, PHB, or CBZ with DOAC anticoagulants 🛑
10/ 3⃣Was it just VPA wasn’t being absorbed?
Well that would have been true given the state of the gut ⬇️😳But, the VPA was being given IV.
I know that its pentobarbital that gets the bad rap for GI issues, but I find that ileus is a frequent #statusproblem even w/o this med
11/ 4⃣Carbapenem + VPA?
🛎️Bingo!
Carbapenems hate VPA, the whole VPA treatment.
Now, please don’t ask why, no one quite knows the reason.
14/ Finally - The other issue that comes up with VPA is that about ~35% of patients develop hyperammonemia.
Mechanism involves a decrease in carnitine serum concentration (I’m sure @capt_ammonia could explain)!
15/
*Most* pts are asymptomatic, but hyperammonemia encephalopathy/cerebral edema can develop requiring IV L-carnitine 100mg/kg IV x1 f/b 15mg/kg Q4-6H (dosing from peds lits) pubmed.ncbi.nlm.nih.gov/17496767/
For asymptomatic pts can use PO l-carnitine 1000-3000mg/day in divided doses.
16/ Take aways: VPA is a great sz drug but:
💥Does not play nicely with PHT or warfarin
💥Can disappear with even a single dose of a carbapenem
💥Commonly causes hyperammonemia which is usually asymptomatic, but not always
⏸️Use with caution & monitoring in the critically ill.
One day I am going to write a typo-free tweetorial with no misplaced links, no formatting/line issues, no mis-numbered tweets... that day was not today😂.
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Goals for the scroll (⬅️credit @sigman_md 😂):
1⃣ How difficult it can be to diagnose spiral epidural abscesses (SEA)
2⃣ What exactly is the spinal epidural space
3⃣ How these should be treated
4⃣ And why decompress?
3/ Diagnosing SEA = super tricky. The symptoms & labs are so non-specific!
✅Back pain ⏫(but back pain--who doesn't?)
✅Fever is often present, but not always.
✅WBC may be elevated, but sometimes just mildly. ✅Blood cultures are only positive about 60% of the time.
1/ A #tweetorial about simulation in NCC
Today @namorris opened his remarks on Sim in NCC @ #NCS2021 w/ a simple question about the correct first line treatment for SE? Everyone got it.
Then he posed a tougher question.
How often does that happen?
No one voted "always"
2/
Even the most groundbreaking research won’t benefit our patients if we aren’t delivering it correctly.
I so highly encourage you to check out Nick’s talk on-demand if you have access to #NCS2021.
It is 🚨critical🚨 that we teach more effectively!
3/ Convinced?
Some practical, take-aways from this talk about finding right Simulation Solution.
1/🧵
In the early days of fellowship, I remember checking our SAH patients’ transcranial dopplers (TCD), scanning the Vmeans & if they were ~<70 cm/sec throughout thinking:
“Great. Perfect. TCDs globally low. Nothing to worry about here!”
🚨Note. This is not a #tweetorial about if large vessel vasospasm is the cause of DCI or just an epiphenomenon OR if treating vasospasm is the way to improve functional outcomes …That is important!... but that is not this tweetorial. pubmed.ncbi.nlm.nih.gov/21285966/
3/ Given #TCDs is a pretty large topic, this @medtweetorial will be told in 3 parts:
Part 1⃣:
⭐️Basic principles of TCDs
⭐️Use of TCDs to detect Vasospasm
Part 2⃣: The Pulsatility Index - why it matters
Part 3⃣: The Utility of TCDs as an ancillary test in BDT
1/ 1st week of NeuroICU fellowship. A #tweetorial summary:
1⃣ Pt in DI. Give anti-diuretic hormone (ADH), call it “pit drip”
2⃣Pt in distributive shock. Give ADH, call it “vaso”
3⃣Pt on ASA needs EVD. Give ADH (sort of), call it “DDAVP”
4⃣ Fellow postcall & confused, give….
2/ Just kidding… everyone knows the drug for that is
3/ All the names and purposes of ADH had me feeling ⬇️
So – a review of all things ADH including:
✅It’s various aliases
✅Receptors and function
✅Clinical utility in NeuroICU (+general ICUs)
A 70 yo W with history of HTN presented with significant IVH from a ruptured AVM.
Admission EKG showed this:
A #brugada pattern. She had no personal or family history of syncope / sudden death. And on admission (time of this EKG) she was not febrile. About 12 hours later we repeated the EKG:
Trops normal and ECHO later in the day demonstrated a normal EF and grade 1 DD, but no wall motion abnormality. No apical ballooning. There was mildly increase LV wall thickness.