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/ Start with 'is the AMS appropriate for the degree of critical illness?'
Often it is.
But do some digging, did the AMS precede the illness? ...Is it more than what you would expect?
Start with this flow chart⬇️
3/ Is there AMS+ Fever+ headache/meningismus/photophobia or seizures??
(AMS + fever is usually septic encephalopathy)
Add the other findings= reasonable concern for CNS infection... start here⬇️; remember that CNS infections can cause ICP issues and infectious vasculopathy!
1/ A 34 yo M presents with worsening confusion and seizures. He is febrile.
He is intubated and transferred to the NeuroICU.
A #continuumcase about a cause that’s probably low (not) on your DDx.
2/ I’m not even going to ask if you want an LP next, because “Fever, Status, AMS” = I wanted that LP way before this MRI.
You get one and the protein is 80, TNC #155, and glucose 80 (serum 147). Cultures and HSV PCR are pending.
3/ We are clearly in the realm of “inflammation.”
W/ the leptomeningeal enhancement, I’m not ruling bacterial meningitis out (empiric abx until culture back!), but the glucose is reassuringly high for that. Viral meningoencephalitis is a top consideration so bring on acyclovir!
1/ A 75 yo M is brought in by his wife bc he is forgetful & “continues to drop things.”
She notes he's increasingly tearful, forgetful, and has an odd movement in his right hand.
MRI, EEG, LP were all normal.
In the room he keeps doing this with his face:
A #ContinuumCase
2/ What do you worry about most?
3/ Any of these would be reasonable. You could certainly frame this as a rapidly progressive dementia (BTW there is an excellent continuum article on the subject, this is one of the most visited on the website!)
He has been paranoid and confused in the previous weeks.
MRI 👇. A large abdominal mass was identified on imaging.
You know what this is, but do you know why we treat it the way we do?
A #ContinuumCase on immunomodulators
2/ ok ok, everyone gets to vote on what's going on before we dive in on how we are going to treat it and why.
so what do you think?
3/ Anti-NMDA receptor encephalitis is caused by anti-neural antibodies against the cell surface proteins (in this cause the NMDA receptor) this causes in a stereotyped way a progression through
⭐️Psychosis
⭐️Seizures
⭐️Sympathetic storming
⭐️Orofacial dystonias