1/
What is the most worthless electrolyte on the BMP, and why is it chloride?

Agree?
A #tweetorial 🧵 to change your mind…

And if you’re thinking, why in the world is this a #neurotweetorial? Read on. #neurotwitter @MedTweetorials
2/
First, this #tweetorial is based on a lecture given in @emoryneurocrit didactics by one of our *awesome* teachers: Dr. Ofer Sadan (@neuro_intensive), and is shared in #tweetorial format w/ his permission.
3/
So, again, why is a #neurologist interested in chloride?

Because neurologists ❤️ giving chloride.

Ur thinking, “No. I have literally never ordered chloride.” … But, think of all the 23.4% and 3% sodium you have ordered.

All that sodium comes with a bystander: Chloride.
4/
Most intensivists agree there is nothing “normal” about 0.9% NS.

The SMART Trial (NEJM 2018) does NS might lead to more adverse renal events? tinyurl.com/4bzw2rb9

15K pts received resusc w/ 0.9%NS vs. Plasma-Lyte/LR.
EndPoint: death, renal replacement tx, Cr⬆️>200% b/l
5/
In the balanced group, 14.3% had a primary endpoint vs. 15.4% in the saline group. Which is a small, but sig diff (P=0.04). Given 5 million people are admitted to ICUs each year, that percentage point adds up.

Graphic: @tscquizzato
6/
A major diff in the 2 groups was the plasma HCO3- and Cl- levels (see 🔽).

Note: Serum Cl- levels about same on presentation, but the NS group got NS in ED/OR, reflected in a higher “ICU admission” Cl- in the NS group (red).
7/
Why do⬆️Cl- levels lead to ⬆️ rates of AKI? Prev studies have shown that ⬆️Cl- =⬆️acidosis, inflammation, & renal vasoconstriction.

Ex: ⬇️ in mean renal artery flow velocity (P = 0.045) & renal cortical tissue perfusion (P = 0.008) after saline, but not after Plasma-Lyte 🔽
8/
But, doesn’t Plasma-Lyte cost a lot more??

No. Plasma-Lyte =$4.50, NS =$2. tinyurl.com/twjv7n38
Renal replacement therapy: upwards of $3k. PER DAY. tinyurl.com/yjszx8wf

EMcrit has a great post about the evils of Cl- for gen ICU
emcrit.org/pulmcrit/smart/
9/
But what about NeuroICU patients? Are they getting AKIs & if so, is it Cl- related? @neuro_intensive took a look in our SAH cohort from 2009-14 (n=1672 that’s a lot of SAH pts @emoryneurocrit!) to answer this!

1,267 aSAH pts included in the study, 212 pts developed an AKI.
10/
In this cohort, those that developed an AKI were more likely male, w/ HTN, CAD, DM. They also had ΔCl- of 9.24 vs 3.77 during their admission.

Serum Cl (not Na) was associated w/ AKI, OR=1.2 [1.12-1.29].
11/
Ok. So maybe increasing chloride tracks with AKI… but, we are giving 23.4% to save the brain!

(and obviously, little biased here but brain🧠> kidney… I mean, the kidney doesn’t even have an emoji)

And since the brain needs all that sodium, kidney be damned. Right?
12/
The❓is, is there a better hypertonic solut?

Which brings us to the ACETatE trial.

Low-Cl- vs high-Cl-containing HTS for the treatment of SAH–related complications: The ACETatE (A low ChloriE hyperTonic solution for brain Edema) Randomized Trial

tinyurl.com/3c9ap34s
13/
The ACETatE trial was a single center pilot study comparing use of 30cc NaCl (23.4%) & 50cc NaCl/Na-acetate (16.4%) in aSAH pt at risk of AKI (Cl- >109).

Fluid comp shown ⬇️. NaCl/Na-Acetate solution: ⬆️ in vol & absolute Na content, but ⬇️ in Na conc. & has 33% less Cl-.
14/
32 pts were randomized. 15 to the NaCl “normal” 23.4% and 17 to NaCl/Na-Acetate 16.4%. In those that got the more balanced hypertonic, the ΔNa+ trended higher and ΔCl- trended lower.
15/
In the 2º outcomes: AKI rate was ⬆️ in the NaCl group compared to the NaCl/Na-Acetate group & most patients had hyperchloremia bf AKI. Importantly, there was no difference in outcomes. Both lowered ICP by the same degree (p=0.6) & had the same sustained effect (p=0.4)
16/
While small and ultimately underpowered for funding reasons, the pilot demonstrated the safety of replacing 23.4% NaCl with a chloride-lean solution and both had similar effects on ICP and outcomes and the AKI rates were lower with the “balanced” HTS solution.
17/
So, does this matter in the neuroICU?

In @EmoryNeuroCrit SAH cohort, mortality rate is sig. higher in patients with AKI (28.3% vs 6.1% in the non-acute kidney injury group [p < 0.001]).
18/
True in other groups.
In 458 mod-severe TBI unadjusted mortality was ⬆️ for pt w/ time weighted average Cl->125 mmol/L & TWA Na>160 mmol/L. When adjusted for the burden of hyperNa & hyperCl-, only hyperchloremia was independently associated w/ in-hosp mortality.
@SMuehlschMD
19/
Take aways:
⭐️0.9%NS =not normal. Balanced fluids👍
⭐️HyperCl may ⬆️ acidosis, inflammation, renal vasoconstriction, & AKI
⭐️Neurologist can inadvertently ⏫ Cl- w/ 23.4%
⭐️“Balanced” HT solutions ⬇️ ICP & may prevent AKI
⭐️We must be thoughtful about the solutions we give

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More from @caseyalbin

29 Apr
A #tweetorial #medtweetorial
@MedTweetorials

1/
3 AM: Pager Pager Pager

Me [very groggily]: Hey, what’s up?

Awesome overnight APP: Sorry to wake you! But, Mrs. Very-Small-Stroke-NIHSS-2-Had-Been-Clinically-Stable-All-Day just PEA arrested.

Me [not so groggily]:
2/
Awesome APP: We successfully got ROSC (bc team
@emoryneurocrit
= Flexed bicepsStar-struck) and have him stabilized. Going to scan now!

So, #neurotwitter, where’s the lesion?
3/
Trick question.

All of these areas through neurologic pathology – stroke/seizure/bleed - could all have caused a sudden death (or at the very least sudden LOC).
Read 24 tweets
31 Mar
1/
Attending: “But never anticoagulation for an intracranial dissection!”

Me as a resident: “Of course. Totally!”

Also me ⬇️: [googling “where do the internal carotid arteries and vertebral arteries become intracranial?”]

Feel familiar? A #tweetorial @MedTweetorials
2/
With the TREAT-CAD trial, lots of talk about dissection treatment. Whether your team anti-platelets or team anticoagulation (🙋🏻 Must. Give. Heparin (@MGHNeurology) 4 ever. I know you feel this, @namorris!) consideration about the location of dissection is possibly important.
3/
Also, regardless of your team… TREAT-CAD was not able to demonstrate non-inferiority of ASA, just saying.

Aspirin versus anticoagulation in cervical artery dissection (TREAT-CAD): an open-label, randomised, non-inferiorit… pubmed.ncbi.nlm.nih.gov/33765420/
Read 12 tweets
26 Mar
1/
Your patient that is “over breathing” the vent may still be dead by brain criteria.

A #tweetorial #medtweetorial for providers in #criticalcare #EM #neuro #neurocriticalcare. @MedTweetorials
2/
First and foremost, let’s be clear that to be dead by brain criteria, the patient must have cessation of ALL brain function *INCLUDING absence of respiratory drive.*

Thinking "But... I thought you just said...."?
3/
The contradiction here lies in that ventilators are sometimes too sensitive.
Read 13 tweets
18 Feb
1/ Alright, #Neurotwitter, the votes for today’s #neuroDDxThursday were overwhelmingly in favor of multiple cranial neuropathies!

Thought about one slide, but this needs a #tweetorial! So that you aren't 😬😬😬 when confronted with this:

#MedEd #FOAMed @MedTweetorials
2/
Reminder: The 12 cranial nerve nuclei are located in the brainstem, and if you have trouble remembering where they are, welcome to the club. Here’s a reminder! Will post the medulla section Monday, stay tuned.
3/
We’ll move from central to peripheral etiologies.

The brainstem is like Times Square in NYC- so much going on in a very small space.

A small insult can easily cause damage to multiple cranial nerves. amiright, #stroketwitter?
Read 15 tweets

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