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)
4/ Starting with nomenclature:
Anti-diuretic hormone, desmopressin, DDAVP, vasopressin, AVP, Pitressin, Vasostrict – are they really all the same?
Not quite.
5/ Anti-diuretic hormone (ADH) and arginine vasopressin (AVP) can be used interchangeably for the neurohypophyseal hormone secreted by the posterior pituitary.
10/
You can remember that V2⃣ receptors increase H2⃣O retention.
AVP and DDAVP both bind here, but DDAVP has a much stronger affinity to these receptors.
11/ In the NeuroICU, we’re primarily using ADH in this context to treat central DI resulting from transsphenoidal adenomectomy (TSA) or cerebral herniation resulting compression of pit stalk/gland.
A vasopressin bolus and gtt are usually the initial choice for DI treatment.
12/ We often given vasopressin 2.5-5unit IV while waiting for the gtt, and then give 0.25-1 unit/hour which is titrated to Uosm, UOP, and serum sodium.
All of which need to be very, very closely monitored!
13/ Long term, DI is managed with desmopressin (DDAVP) given PO, nasally, subQ or IV.
As a PO drug, its absorption can be unpredictable. Finding right dose requires some trial & a lot of monitoring.
Typical:
PO dose: 0.1mg qHS - 0.3mg TID.
IV doses: 1-2mcg qHS to BID
14/ Totally counterintuitively ADH can also regulate the correction of Na+ in chronically hypovolemic hyponatremic patients
If that seems incredibly ludicrious (…why would we give a patient with ⬇️sodium H2O retention drug??) read: tinyurl.com/5fydkkh7 from @ibookCC.
15/ So… ADH can be used to treat hypernatremia in central DI and prevent overcorrection of sodium in chronic hypovolemic hyponatremia. Vasopressin or desmopressin work for these purposes.
16/ How does ADH result in vasoconstriction?
This is mediated by binding of ADH to V1⃣ receptors located in smooth muscles which triggers catecholamine-independent vasoconstriction.
Image: tinyurl.com/46yhekft
17/ Doses here are fixed @ either vasopressin 0.03 or 0.04 units/min.
Remember, the DI dose is vasopressin 0.5-1 unit/*hour*
I remember thinking that they were orders of magnitude different, but because of the time denominator, the shock dose is actually ~2-5x larger
18/ Finally, both vasopressin and desmopressin/DDAVP have intrinsic platelet activating properties
DDAVP has the added effect of releasing von Willebrand factor & F VIII from endothelial cells.
Image reminding u of the importance of vWF (image @NEJM)
19/ Since the 1970s desmopressin was used to prevent bleeding in pt w/ 🔽vWF
The bleeding dose is a 1x IV Desmopressin 0.3mcg/kg (~20-30mcg).
For comparison, the anti-diuretic dose is 1-3mcg IV. The hemostasis dose is thus x10 higher.
Effect is max @ ~30 mins. last 6-8hr
20/ In the neuroICU we very commonly see patients with ICH who were taking ASA. PATCH trial (Lancet 2016) demonstrated worse outcomes in patients who received platelet transfusion to “reverse” ASA’s effect.
Given DDAVPs' platelet activating effect, this a good alternative?
21/ Maybe?
Retrospective Assessment of Desmopressin Effectiveness & Safety in Patients w Antiplatelet-Associated Intracra pubmed.ncbi.nlm.nih.gov/31567345/
Early Admin of Desmopressin and Platelet Transfusion for Reducing Hematoma Expansion in Patients With Acut… pubmed.ncbi.nlm.nih.gov/32304415/
1/WE'RE BACK!
A 52 yo architect presents with a year of difficulty with memory & planning.
At work, she can't adapt to the new software.
Family notes she “forgot” steps in planning their annual vacations (“she didn’t book the hotel!”)
She's increasingly irritated & withdrawn.
2/ At work this had led to significant trouble and her manager has asked her to cut back on hours. She became increasingly anxious at work and irritated.
Her primary care doctor ordered an MRI which was reported as normal, particularly noting normal hippocampus volume.
3/ She underwent a neuropsychological assessment which underscored impairments in executive functions and cognitive flexibility.
However, she did poorly across many tests, including validity measures.
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