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.
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
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
20/ ⭐️Every number on the BMP matters. (Yes, even chloride.)
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/
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.
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?