Lea Alhilali, MD Profile picture
Sep 8, 2022 12 tweets 7 min read Read on X
1/Controversy in radiology gets tense! The Mt Fuji sign for tension pneumocephalus is under scrutiny.When should you call it?
A #tweetorial about #imaging this important #neurosurgery complication
#medtwitter #FOAMed #FOAMrad #medstudent #neurorad #radres #meded #neurotwitter Image
2/Some believe that the peaked, mountain like appearance of the frontal lobes is a critical sign of a life-threatening complication & should be called & reported. Others believe it is too non-specific, is commonly seen when there isn’t tension & should be retired. Who’s right? Image
3/First, let’s clarify about what the Mt Fuji sign actually is. Most are familiar with the fact that large collections of pneumocephalus can compress the frontal lobes—making them look like the slopes of a mountain. But this isn’t actually enough to call Mt Fuji. Image
4/You also need to see frontal lobe separation. This means the subdural air tension is greater than CSF surface tension between the frontal lobes--one of the highest liquid surface tensions—so you know pressure is high. This little V is why it looks like Mt Fuji, not any mountain Image
5/Why do we get tension pneumocephalus? 3 main ways. (1) Upside down coke bottle effect w/a CSF leak. As liquid drips out w/a CSF leak, nature abhors a vacuum, so air rushes in to replace it. If outside pressure is higher than CSF pressure, more air will come in & create tension Image
6/Here’s a skullbase CSF leak creating pneumocephalus. As CSF leaks out, air replaces it. If air pressure is higher than intracranial pressure, more air will come in. The worst tension pneumocephalus I ever saw was a pt w/an unknown sphenoid sinus skullbase leak they put on CPAP! Image
7/Next mechanism is the ball valve mechanism. Air gets in through a defect (from trauma, surgery, etc). Increased pressure eventually pushes down on the brain, causing the brain to close the defect so the air can’t escape. This is the same mechanism seen w/tension pneumothorax. Image
8/Final mechanism is use of nitrous oxide in neuroanesthesia. If the pt has a subdural collection (usually w/air in the operative setting), nitrous oxide enters the subdural 34 times faster than it diffuses out as nitrogen into the blood stream—creating increased pressure/tension Image
9/This is why nitrous oxide is no longer commonly used in neuroanesthesia. Decreased use of nitrous oxide is also why tension pneumocephalus is less common in the post-operative setting now than it was in the past. Image
10/So how helpful is the Mt Fuji sign for determining tension pneumocephalus post-operatively (a time when pneumocephalus is common)? Well it turns out, the sign can be seen in 1/3 pts without a neurosurgical emergency. So it is not very specific and can cause overcalling Image
11/More importantly is how the pt is doing clinically. Significant pneumocephalus can be seen post op—but if the pt is not declining, even large amounts of pneumocephalus can be managed by putting the pt on 100% O2--just like w/a pneumothorax--w/good results. Image
12/So remember it isn’t just one sign—it is the whole picture of how the pt is doing clinically. Don’t lose sight of the forest for the mountain!

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More from @teachplaygrub

Dec 5
1/They say form follows function!

Brain MRI anatomy is best understood in terms of both form & function.

Here’s a short thread to help you to remember important functional brain anatomy--so you truly can clinically correlate! Image
2/Let’s start at the top. At the vertex is the superior frontal gyrus. This is easy to remember, bc it’s at the top—and being at the top is superior. It’s like the superior king at the top of the vertex. Image
3/It is also easy to recognize on imaging. It looks like a big thumb pointing straight up out of the brain. I always look for that thumbs up when I am looking for the superior frontal gyrus (SFG) Image
Read 12 tweets
Dec 1
1/To call it or not to call it? That is the question!

Do you feel a bit wacky & wobbly when it comes to calling normal pressure hydrocephalus on imaging?

You don’t want to overcall it, but you don’t want to miss it either!

Let me help you out w/a thread about imaging in NPH! Image
2/First, you must understand the pathophysiology of “idiopathic” or iNPH.

It was first described in 1965—but, of the original six in the 1965 cohort, 4 were found to have underlying causes for hydrocephalus.

This begs the question—when do you stop looking & call it idiopathic? Image
3/Thus, some don’t believe true idiopathic NPH exists.

After all, it’s a syndrome defined essentially only by response to a treatment w/o ever a placebo-controlled trial.

However, most believe iNPH does exist--but its underlying etiology is controversial. Several theories exist Image
Read 19 tweets
Nov 21
1/Time to go with the flow!

Hoping no one notices you don’t know the anatomy of internal carotid (ICA)?

Do you say “carotid siphon” & hope no one asks for more detail?

Here’s a thread to help you siphon off some information about ICA anatomy! Image
2/ICA is like a staircase—winding up through important anatomic regions like a staircase winding up to each floor Lobby is the neck.

First floor is skullbase/carotid canal. Next it stops at the cavernous sinus, before finally reaching the rooftop balcony of the intradural space.Image
3/ICA is divided into numbered segments based on landmarks that denote transitions on its way up the floors.

C1 is in the lobby or neck.

You can remember this b/c the number 1 looks elongated & straight like a neck. Image
Read 10 tweets
Nov 4
1/The 90s called & wants its carotid imaging back!

It’s been 30 years--are you still on NASCET?

Feeling vulnerable about plaque vulnerability?

This month’s @theAJNR SCANtastic has what you need to know about carotid plaque

ajnr.org/content/46/10/…Image
2/Everyone knows the NASCET criteria:

If the patient is symptomatic & the greatest stenosis from the plaque is >70% of the diameter of normal distal lumen, patient will likely benefit from carotid endarterectomy

But that doesn’t mean the remaining patients are just fine! Image
3/Yes, carotid plaques resulting in high-grade stenosis are high risk

But assuming that stenosis is the only mechanism by which a carotid plaque is high risk is like assuming that the only way to kill someone is by strangulation. Image
Read 13 tweets
Oct 24
1/Having trouble remembering how to differentiate dementias on imaging?

Is looking at dementia PET scans one of your PET peeves?

Here’s a thread to show you how to remember the imaging findings in dementia & never forget! Image
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On PET, AD demonstrates a typical Nike swoosh pattern—with decreased metabolism in the parietal & temporal regions Image
3/The swoosh rapidly tapers anteriorly—& so does hypometabolism in AD in the temporal lobe. It usually spares the anterior temporal poles.

So in AD look for a rapidly tapering Nike swoosh, w/hypometabolism in the parietal/temporal regions—sparing the anterior temporal pole Image
Read 16 tweets
Oct 17
1/My hardest thread yet! Are you up for the challenge?

How stroke perfusion imaging works!

Ever wonder why it’s Tmax & not Tmin?

Do you not question & let RAPID read the perfusion for you? Not anymore! Image
2/Perfusion imaging is based on one principle: When you inject CT or MR intravenous contrast, the contrast flows w/blood & so contrast can be a surrogate marker for blood.

This is key, b/c we can track contrast—it changes CT density or MR signal so we can see where it goes. Image
3/So if we can track how contrast gets to the tissue (by changes in CT density or MR signal), then we can approximate how BLOOD is getting to the tissue.

And how much blood is getting to the tissue is what perfusion imaging is all about. Image
Read 18 tweets

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