1/ Once upon a time I wrote a #tweetorial about #TCDs. It ended with this great hook feat Beyonce… and… then I got distracted with other things because (⬇️)
(Thinking I don’t remember this post at all, but great! I want to read about TCDs, here you go:
2/ Also, side note, can we talk about Meredith gray’s hair from that tweetorial? If you are in really in medicine and have this perfect blow-out hair, please DM me so I can know your secret.
3/ Takeaways from the last #tweetorial
⭐️TCDs use u/s waves to calculate the velocity of intracranial blood flow
⭐️We measure systolic velocity (PSV), end diastolic velocity (EDV), Pulsatility Index (PI) & mean flow velocity (MFV)
⭐️TCDs are freq used for vasospasm monitoring
4/ But as @namorrismd pointed out, while TCDs are sensitive for vasospasm (90%) and have a good NPV (92%), the PPV is low (57%).
6/ What might be a more useful way to understand cerebral hemodynamics is checking for vascular reactivity w/ a CO2 challenge during TCDs (@namorris). Loss of CVR id'ed pts @ high risk for DCI (sensitivity 91%) this has also been done with acetazolamide. ja.ma/3zZ2P9o
6/ Why these two agents? Because both decrease the pH. Remember low pH is a potent vasodilator.
(The opposition is true of high pH… pls don’t hyperventilate the pt in vasospasm!)
Normal response to CO2 is to increase CBF.
The MCA velocities increase by 2-4% per 1 mmHg of CO2
7/ Wait.
Earlier I said that we are monitoring for increased velocities to detect vasospasm…And now, I'm saying that increased velocities mean more CBF, not less??
So...Are increased velocities good or bad?
So glad you asked!
8/ This gets back to the Lindegaard ratio. Which you’ll recall is the MCA Vmean / ICA Vmean.
🙀Vasospasm causes vasoconstriction solely in the intracranial arteries (LR increases), potentially indicating worsening CBF and a risk for DCI*
*Remember VSP is not the same as DCI
😸Lowering the pH systemically vasodilates the ICA and the MCA, allowing more blood at faster speeds through the entire system.
LR stays normal to slightly elevated
9/ MFV ⬆️(>~120) & LR ⬇️ (<~3-4): suspect hyperemia (usually not a bat thing, but might be problematic in situations w/ impaired cerebral auto-reg or post carotid stenting/CEA)
MFV ⬆️ (>~120) & LR ⬆️ (>~-4-6): suspect vasospasm.
(this is a gradient & clinical context matters!)
10/ But what if the MFV is low?
When I started fellowship and saw a low Vmean, I'd think, "Great! this patient is not in vasospasm! everything is fine!"
11/ That is, unfortunately, not always true.
Why?
Because there is more to TCDs than the Vmean. The waveform matters and one of the ways that that is numerically captured is the pulsatility index.
Pulsatility Index=
(Peak Systolic Vel – End Diastolic Vel)/Mean Flow Vel.
12/ As distal resistance increases the peak systolic velocity increases.
BUT! Because the resistance is high, forward flow drastically slows during diastole.
And you get a waveform that ends up looking like this:
13/ Normal PI is around 1.
Something >~1.5 (or a sudden increase from prior) should clue you in to one of two things:
⭐️Distal vasospasm
⭐️Elevated ICP (causing compressive resistance on distal arteries)
Check out @ghoshal_shivani's noninvasive mini talk instagram.com/tv/CTFFrl2Hy83…
14/ Here's an example:
47 yo W w/ aSAH HH4 post bleed day 4 w/ poor exam despite EVD.
TCD with RMCA Vmeans low (in the 40s)
All good, no vasospasm, right?
15/ Of course not -- No. This is not good at all!
The waveform here is highly abnormal with a dramatically elevated PI in the R MCA territory (other territory PIs were much more modestly elevated, near 1.2-1.5)
16/ STAT CTA demonstrated severe vasospasm in the DISTAL branches of the MCA.
So, elevated PIs in this case clued us into a high distal resistance from spasm.
Pt was treated with IA therapy with mild improvement in velocities and exam.
17/ Another example:
30 yo W aSAH HH4 with large Sylvian hematoma from rupture of an M2 aneurysm (scan ⬇️) PBD 12. Poor exam.
18/ TCDs demonstrate pretty normal V Means
But the PIs are severely elevated in every single window (almost all >2.5)!
17/ Repeat CT scan demonstrated a new EVD tract hemorrhage.
So, here the elevated PI reflected distal downstream compression 2/2 high ICP.
Although the bleed was small, in someone who’s cerebral compliance was already maxed, this was enough to nearly result in herniation.
18/ In this case, EVD had clotted was no longer functional, so we didn't have an invasive ICP monitor. It was the the TCDs waveforms that actually dramatically directed patient care.
Several months after the decompressive crani, this pt came back to the unit to say hi!!
19/ Major take aways:
1⃣ TCDs = sensitive & a good screening tool for vasospasm
2⃣ pH changes vascular flow
3⃣ The pulsatility index and the TCD waveforms are ways to noninvasively look for distal vasospasm & intracranial hypertension
1/ A 20 yo woman comes in because she has recurrent headaches. She describes visual aura, photo-/phonophobia & pain that improves with rest. She also describes a sharp, stabbing, lancinating pain from the back of her head during the episodes.
A #ContinuumCase
2/ What is this?
(PS ChatGPT FTW with "what does an aura look like?" !!)
3/ The patient likely has TWO things:
1⃣Occipital neuralgia causing the pain that radiates from the back of her head
2⃣chronic migraine with aura.
Patients with occipital neuralgia OFTEN have both, and occipital neuralgia is very rarely an isolated headache syndrome
1/ 🥳Big News! This is the 1⃣0⃣0⃣th #CONTINUUMCASE!!
To celebrate? A must know dz, bc w/ this disease:
Time is Spine!
A 39 yo woman with Sjogren’s syndrome comes to the ED with sudden neck pain. Then arm weakness. Then leg weakness. All within 24 hours.
Now she can’t urinate
2/ On your exam, mental status=intact. But she has terrible vision in the right eye, which she reports is from a sjogrens attack.
She has 3/5 arm strength, 2/5 leg strength.
As shown above 🔼 she has a longitudinally extensive lesion w/ contrast at C2 and C3.
Is this Sjogrens?
3/ You complete a spinal tap.
‼️There are 120 WBC with a lymphocytic predominance‼️
A 58 yo woman with breast cancer on active chemo presented with shortness of breath.
She was just found to have (A).
Unfortunately, a head CT reveals (B).
They want to know – can she be a/c’ed? A #ContinuumCase
2/ Thoughts?
3/ Why does this feel like such a common conundrum? A few reasons.
1⃣incidence of brain mets may be 🔼 due to improved detection & better control of extracerebral dz
2⃣VTE is common in cancer patients & may also be 🔼 (more detection, longer life expectancy & novel treatments)
1/ A 35 yo M has lower limb weakness & painful hand & foot paresthesias.
EMG suggested axonal neuropathy and a presumed diagnosis of GBS was made.
After PLEX he was not better, instead he was becoming confused & ataxic.
How might a Thanksgiving Turkey solve this #ContinuumCase?
2/ Note: PLEX does not work immediately. In fact, many pts fail to have a response to immunotherapy during their hospitalization. Many continue to progress DESPITE treatment.
This does not mean that the treatment isn’t working. More is not better!
3/ Ok, off my soap box!
As you should for all confusing cases, you go back to the bedside and the patient tells you that over the last 2 months, he’s had increasing stress that resulted in an escalation of alcohol intake and reduced food intake.