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Michigan State University Department of Radiology Lecture: Larynx Anatomy and Pathology

Michigan State University Department of Radiology Lecture: Larynx Anatomy and Pathology

So the next talk that I’m going to
give is on larynx technique imaging, normal anatomy, and common pathology and
then after this 45-minute talk we’ll take a little break and we’ll have few
talks, have lunch, two talks, take a break, and two talks and we’re done so should be
hopefully a nice relaxing program and hopefully–everybody having fun so far?
Yeah yeah yeah that’s good to hear. So these are the learning
objectives for the next 45 minutes or so is talk a little bit about technique,
anatomy, some tumors, inflammatory and infectious processes, some developmental
lesions and I’ll just say a couple of brief words on vocal cord palsies just
support and give a different perspective on that what Doug mentioned.
So let’s talk a little bit about technique. You know larynx–to be honest with you–is so much easier than it used to be. I remember back when I was a
fellow we’d have different protocols for different types of laryngeal pathologies
but now it’s pretty simple to do it’s multi detector imaging whether you have
a 4, 8, 16, 64 slice. We always acquire everything now by 0.625 millimeters and
we–you know it varies sometimes 2.5 sometimes 1.25 it varies, but it is a bit
of cognitive dissonance in a sense that if you do acquire within section images
and then you view thick images it’s essentially what I did 20 years ago when
we didn’t have multi detector imaging and people say well why do you do that
if you’re going to go ahead and look at the thicker images and really the reason
is for the reformat. So the reason to do the 0.625 acquisition is so you can get
the sagittal and coronal reformats. For contrast we use about a hundred CCs
sometimes it’s even less than that, we use a dual phase injection so we give an
initial 50cc bolus and then we wait for 90 seconds and then we start giving
another 25 to 50 CCs and then we acquire. The reason we do that is that when
multi detector first came out and we gave the contrast and we acquired–you
know–with the 64-slice CT we were essentially doing CTAs on everyone. The
contrast was essentially still in the arterial phase and one of the good
things about the good old days, if you will, I can
now that I trained in the last century, I hate to say that, but I trained in the
last century right? So when I trained in the last century, when we had the
single detector imaging, by the time we acquired the images there wasn’t enough
time for the contrast to actually go into the tumor so that’s one of the
reasons I think in many places are now doing the dual phase and we just do
quiet respiration. Again when I grew up we would do these various maneuvers
Valsalva, Reverse Valsalva, so on and so forth but now we just do quiet
respiration. One of the reasons as I mentioned before to get the reformats
was to do the thin section imaging was to do these reformats. So
again I grew up in the days of axial images and it took me a while to even
look at the sagittal images but when you do do this you know you get a very nice
view of the free margin of the epiglottis. You can see the hyoid bone
here in cross-section, you can see the pre-epiglottic space which is located
here in the true vocal cords and again we’re gonna go over this anatomy in
gross detail so I hope at the very least by the end of this talk you’ll
understand the anatomy on the coronal images. Here’s a free margin of the
epiglottis here’s the false vocal cord, laryngeal ventricle and then the true
vocal cord and again this detailed reformats are really–only can be
acquired with the thin section imaging. This is just an example, anybody want to
take a guess with this? It’s a cystic lesion here involving the larynx, it’s
extending out through the thyrohyoid membrane very nicely seen on the coronal
images and extending out into the soft tissues and neck. Anybody want to take a
guess at what this? What’s that? Laryngeal seal is exactly right
excellent so this is laryngeal seal and we’ll have more to say about that.
Well what about MR–you know–MR can be used, as I say I’ve sort of been around
circles right now I’m–you know–what’s old is new what’s new is old right? So when
CT first came out we did CT then all of a sudden people discovered they could do
MR so everybody rushed to MR and everyone started doing MR but now when I
when I go around and ask people and I’ll just do a show of hands now, how many
people–when you evaluate the larynx–are primarily doing CT as your number one
modality? There’s more than that now! You
residents you can raise your hands here I know what you’ve re–how many people
are doing primarily MR? Okay so yeah so that’s pretty much what I see, even when
I was in Europe last–a few weeks ago, even the Europeans they were one of the
biggest pushers for MR, even now they’re doing more CT. Now having said that if
you do go to your meetings in the US you’re going to see certain institutions
that still do a fair amount of MR which is great. You can do MR very
nicely with 3 Tesla, the reason we do CT is because it’s quicker, it’s less
expensive and also you know I like to– when I’m choosing modalities it’s–if you
do a hundred patients, out of those hundred patients how many are going to
have diagnostic imaging studies that are diagnostic and not limited by some type
of artifact? And so that reproducibility is a major factor why I like CT as
better than MR2 because you know if your sequence is four minutes and after three
minutes and 59 seconds the patient moves all of a sudden your sequence is gone, so
sometimes you have to be pragmatic as well. As I mentioned before in the prior
talk, the crazy thing about head and neck is that, you know, about 80 percent of
what we see in our imaging studies our referring physicians can either see
directly by direct endoscopy or they can palpate. I mentioned before in radiology
we’re sort of programmed to show our worth by listing as many differential
diagnoses as we can and that really doesn’t translate well to head and neck
imaging because the majority of what we see can be seen directly or palpated. So
for instance this is an example of a squamous cell carcinoma, this was
actually tuberculosis, and this was a paraganglioma. You know there’s really no
way to distinguish between squamous cell carcinoma and tuberculosis you know if
you see this paraganglioma and you’re you really love head and neck and you
see this densely enhancing mass, yeah maybe you can suggest that’s a Glomus
tumor but nine times out of ten we really have to depend on our referring
physicians and our pathologists to give us the final diagnosis. So our job as
you’ll see is to really talk more about the spread of the disease as opposed to
given a litany of potential causes of the pathology that we’re
seeing on imaging. Well let’s talk about the anatomy. Now
the anatomy is so so key and if you understand the anatomy then I think
everything else falls into place and I can assure you when I
started my fellowship in the last century I had–that sounds so strange to
me too–but when I started it back in the 1990’s I had no clue about the larynx. I
mean I struggled, I read everything I could, I just didn’t understand it and
then you’ve probably figured out I’m not the sharpest tool in the shed but one
day my 30 watt light bulb went on–went off and everything kind of made sense
to me but now let’s–hopefully I can convince that to you and help you in
your journey and understand the larynx but its standard anatomy for the larynx
is what we’ve learned, it’s the glottic, the supraglottic, and the subglottic
larynx and this is the anatomy of the larynx and that 30 watt light bulb went
on after I realized where all of this complex nomenclature of the anatomic
structures of the larynx arose from and if you start trying to shotgun the
approach and name the different structures of the larynx without an
understanding of the foundation of the larynx you are going to be completely
lost because I can talk to you about cricothyroid thyroarytenoid muscle,
aryepiglottic folds, thyrohyoid notch, hyoepiglottic
ligament and you’re probably completely lost right? It’s, you know, but what I
finally figured out is that if you can understand four or five structures of
the larynx and the reason we don’t understand those four or five structures
the larynx is because, to be honest with you, to be honest with you, we were never
taught this in medical school and I don’t know about where you all went to
med school, but, you know, we spent like six months on the liver and seven months–six weeks on the liver and then four weeks on the leg and a whole bunch of
time on the heart–which a hearts an important organ of course right? A lot of
time on the brain but we just didn’t study the larynx at all and so what I realized
that if you can understand the laryngeal and the bony framework of the larynx and
everything else falls into place so let me give you an example. So what’s the
name of the–what’s the name of this little bone right here that I’m
contouring? The same bone that’s located here.
It’s a hyoid bone right? And then what’s the name of this cartilaginous structure
that’s located here? What’s that? Epiglottis, right. So first of all the
hyoid bone and the epiglottis, those are two of the five framework structures of
the larynx so if you have a ligament that goes from the hyoid bone to the
epiglottis what do you think you’re–that the name of that ligaments going to be?
Take a wild guess. Hyoepiglottic ligament. Okay that’s a
multisyllabic term that if you just throw out there you’re gonna be
completely lost, but the reason it’s called the hyoepiglottic ligament
is just purely based on the anatomy. You have to realize there’s a hyoid bone
and there’s something called the epiglottis and that’s the hyoepiglottic ligament. So let’s take that same approach and say what’s the name of this
cartilaginous structure that I’m looking at right here. Arytenoid exactly what–the
arytenoid cartilage is right so there’s the arytenoid cartilage located here. So
what do you call this fold of tissue which is located here at endoscopy that
goes from the arytenoid cartilage to the epiglottis? Aryepiglottic folds. Simple as that right?
So again another multi-syllabic structure that if you just threw out
there you’d be completely lost, but the reasons called the aryepiglottic folds
because it’s a fold of tissue that goes through the arytenoid to the epiglottis.
What’s the name of this cartilagenous structure that’s located here? Thyroid cartilage, right?
So what do you call the muscle that goes from the thyroid cartilage to the
arytenoid cartilage? Take a wild guess. Thyroid cartilage to the arytenoid cartilage. What muscle would that be?
Thyroarytenoid muscle right? So the muscle that goes to the thyroid
cartilage to the arytenoid cartilage is called the thyroarytenoid muscle and
we’ll see why– what landmark or what level that’s
located. What’s the name of this cartilage structure that’s located right
here? Cricoid–the cricoid cartilage is like the foundation of your house. If you
have no foundation of your house, your house is gonna sink, it’s just going to
completely dissolve and the cricoid cartilage is the signet-shaped ring, a
very tough ring that–which forms the foundation of the larynx because
essentially all of these structures are supported by the cricoid cartilage. So
what do you call this joint that’s located between the cricoid cartilage
and the arytenoid? Cricoarytenoid joint and we’ll see the importance of
identifying the cricoarytenoid joint. And what do you call–what do you think you
call this membrane here that go–this membrane right here that goes from the
thyroid cartilage to the hyoid bone? Thyrohyoid membrane. So now we’re getting
pretty good at this right? So there are five primary structures: hyoid bone,
epiglottis, thyroid cartilage, arytenoid cartilage, and cricoid cartilage right?
So now we see this ligament–this ligament is going from the thyroid
cartilage to the cricoid cartilage so what do you call that ligament then? Cricothyroid ligament or thyroid cricoid
ligament, exactly right. So this is where it all gets the names from and all of
these muscles that you can see that are the muscular structure and the
scaffolding of the larynx again are all derived their names from the cartilage
and the bone that formed the thyroid cartilage. So when we look at this we can
see that this is the endoscopy so this is–what am i pointing at right here? I
know there are ENT surgeons in here. So the radiologists, what do you think this
structure is here? Epiglottis right? What structure is this right here?
Aryepiglottic fold. What are these two white glistening structures that are
located here? Your vocal cord and what’s back here?
Pyriform sinus. This structure right here is the tongue base and what do you
think these saddlebags are here that you can see a little bit of secretions in?
Vallecula. Exactly right. And then this structure that goes from the tongue back
to the epiglottis is called the median glossoepiglottic fold. Alright so
these are the structures that the surgeon see and then as we come down
what we’re gonna do is look at the imaging correlation to what our surgeons
see when they perform endoscopy. So the first thing that we’ll do–again it’s all
anatomy–is to talk about the normal anatomy and show you where it is on
imaging and to use a little bit of pathology to highlight it. So when we
look at the epiglottis, the epiglottis is an anterior and midline structure.
Everybody see the epiglottis is anterior midline so even when I go back to here
you can see that the epiglottis is anterior midline. So the epiglottis is an
anterior and mid line structure, so this is what the surgeons see when they
perform their endoscopy, they can see this aggressive lesion involving the
anterior and midline portion of a larynx, so that’s a primary epiglottic carcinoma.
And when we look at imaging notice how the center of this mass is anterior
midline, so when we see a lesion that’s anterior and midline we–that has to be
involved in the epiglottis. Okay now freeze that picture in your mind and
let’s go to this one. Now what do we see? So, in the endoscopic view, what structure
am i looking at right here where the arrow is? Epiglottis. Where now is this is
this tumor here, is this midline or is it para-midline? Para-midline, exactly right.
Now the–what’s the name of that fold of tissue again that goes in the arytenoid
cartilage to the epiglottis it’s called a what? The aryepiglottic fold. Is that
midline or is that para-midline? Para-midline, exactly right. So now we see this
exophytic aggressive lesion that’s para- midline of the larynx and now we know
that it’s involving what structure? Aryepiglottic folds so how do we
identify that on imaging? So if you look at the
image on the right what structure am I looking at right here that’s anterior
midline? What’s that? Epiglottis, yeah what structure am I looking at here on the
left-hand side? Aryepiglottic fold, exactly right. So everyone see the tumor here
involved in the aryepiglottic fold? See how it’s para-midline? And where is
this air space that’s just lateral to that? Piriform sinus, exactly right. So we
have the epiglottis, the aryepiglottic folds, and the piriform sinus. And what do you think we call the fat right here that’s just anterior to the epiglottis? Area? What’s that?
Preepiglottic fat, that’s exactly right. So all of these complex structures
derive their names on this normal anatomy. And again just to reiterate that
anatomy is the hyoid bone, the epiglottis the hyoid bone–sorry–hyoid bone,
epiglottis, thyroid cartilage, arytenoid cartilage, cricoid cartilage.
Now the way that I eventually learned the anatomy is that–and I really make a plea
to the residents and the fellows–is that for the next two weeks, just the next two
weeks at night before you go to bed just take five minutes and go over those five
structures. For the next two weeks and that’s literally how I did it because
once I got those five structures down then I always remembered the anatomy of the
larynx but it takes a little work up front, but once you emblazon that on
your brain, once it’s embedded, I don’t think you’ll ever forget it. So that’s
a little bit of homework for you. So I have two pieces of homework for you: this
is homework number one and then later on I’ll give you homework number two
okay? Okay so there’s our aryepiglottic fold alright? And, again, the normal
anatomy is epiglottis, aryepiglottic fold, and what’s this black area right here?
This is the what? So the air is the laryngeal ventricle. Now someone stole my
thunder and we’ll talk about now the false vocal cords. So what is the false
vocal cord? Conceptually this is the hardest for me–the hardest piece of
anatomy for the larynx because I struggled over this and even for years,
you know, even once I came into the new century I
still struggled with this and the way that I finally conceptualized it is that
the false vocal cord is essentially the inferior reflection of the aryepiglottic
fold. So the tip of the false vocal cord ends up attaching to the arytenoid
cartilage. So that aryepiglottic fold attaches to the top of the arytenoid
cartilage, but this inferior reflection of the aryepiglottic fold is the false
vocal cord and notice how the false vocal cord is above this airspace which
is what–what was that airspace again here? The laryngeal ventricle, so on a
parasagittal view, here is the false vocal cord. The black here is the
laryngeal ventricle and what’s going to be just below this? What’s that? True vocal
cord. So this red line indicates the level that we are at when we see the
false vocal cord, so notice again as I mentioned before, the aryepiglottic fold comes
down the inferior reflection of the aryepiglottic fold, attaches to the
arytenoid cartilage and this identifies where the false vocal cord is. Now the
key thing is is how do we identify the false vocal cord on a cross-sectional
study? Well remember that anatomy, the aryepiglottic fold comes down and attaches to
the arytenoid cartilage so when we look at a CT scan what we look for is this.
See the top of the arytenoid cartilage? When we see only the top of the arytenoid
cartilage that tells me that I’m at level of the false vocal cord. Now
compare this appearance with this appearance. Do we see any cartilage
here? No not at all but now when we come to this level, then we can see the top of
the arytenoid cartilage. So if I’m at the larynx and I can see the top of the arytenoid
cartilage, then I know I’m at the level of the false vocal cord. Does that make
sense to everyone? Okay that’s the hardest thing. If you got that, everything
for me in the larynx is easier because now we’re at the level of the true vocal
cord and the true vocal cord is very very easy to see because we can see the
cricoid cartilage and the arytenoid cartilage so
we’re at the level of the cricoarytenoid joint. So what does this look like on
imaging? Well here’s a schematic illustration demonstrating the cricoid
cartilage and the arytenoid cartilage and this little tumor here involving the
true vocal cord. So when you see the cricoarytenoid joint you know you’re at
the level of the true vocal cord and here is a schematic illustration of a
verrucous carcinoma involving the true vocal cord and here’s the cricoid
cartilage and the arytenoid cartilage of the cricoarytenoid joint. That tells us
where the true vocal cord is. So just to reiterate again, aryepiglottic fold there’s no
pieces of cartilage, false vocal cord we get the top of the arytenoid cartilage
and then true vocal cord we can see the cricoarytenoid joint. Does that makes sense to
everyone? And finally the subglottis. The subglottis is formed by the signet ring cricoid cartilage. So when you look at
the subglottis, essentially what you look for is the Big O–the formation of
the signet ring. So there’s no cricoarytenoid joint, you just see the
signet ring and when you see the signet ring you know you’re at the level of the
subglottis. So on the parasagittal images, here’s the undersurface of the true
vocal cord and this airway that we’re looking at right here is the cricoid
cartilage, in fact, there’s a part of the signet ring
of the cricoid cartilage here. In fact with a leap of faith you can see the
cricoarytenoid joint on the sagittal images. Here is the shoulder shaped
appearance of the subglottis, here’s the false vocal cord, laryngeal
ventricle, true vocal cord, and now here is the subglottis
and this is a pathologic section of a primary subglottic carcinoma and here is
aggressive appearance here of a primary subglottic carcinoma. So once you get
below and you see the signet ring then you know you’re at the level of the
subglottis. Does that make sense to everyone? Alright,
again it’s anatomy, anatomy, anatomy and then again I’ll make my pleas to my
residents and the fellows in the audience, the fellows I see where you’re
sitting. I see Nick, I see Louis, I see Sam right?
I’m gonna–gonna come bug you guys next week
to ask you about the laryngeal anatomy right? I can still do that
because you’re still fellows right? So let’s go ahead and move on now to tumors
involving the larynx. So, you know, the number one by far away, it’s going to
be squamous cell carcinoma and I showed in the previous portion of the talk the
squamous cell carcinoma, but here’s a type of tumor that’s located here. You
can see this lesion looks like it’s primarily evolving from the cricoid
cartilage. Maybe there’s some rings and circles in here.
Endoscopically the surgeons look down and they see a very very rock-hard mass.
So what do you think the primary diagnosis is going to be here? That’s
exactly right, so this should be–there we go–there’s a chondrosarcoma. So when we
look at the bone algorithms we can see that there is a lot of–this lesion is
primarily arising from the cricoid cartilage.
It’s a submucosa lesion that’s very rock hard and this is a chondrosarcoma. Now
this is a minor salivary gland tumor. Remember the definition of minor
salivary gland tumor? Minor salivary gland tumors is taking salivary gland
tissue and transposing it into a part of the head and neck in which there should be
no native salivary gland. So as a result this can occur anywhere, so remember
the–we talked about an anatomically based differential diagnosis and
essentially the anatomy of the head and neck is similar the anatomy everywhere
else in the body, but the one type of tumor that’s somewhat unique to the head
and neck is the minor salivary gland lesions and remember the most common benign ones
are what? Warthin’s tumors and what was the other one? Anybody? Starts with “p”? Preomorphic
adenoma and then what were the two malignant ones? Mucoepidermoid and what was the other
one? Adenoid cystic carcinoma. Now there are others–different subtypes or other
type of salivary gland tumors that can arise but those if you will are the big
four. So minor salivary gland tumors have the exact same appearance of squamous
cell carcinoma. So number one if you see something like this you probably should
say squamous cell carcinoma and then the pathologist could tell you that you’re
wrong and you can say you’re right I was wrong, thank you
very much, but number one it should be squamous cell carcinoma and this is just
another example–this was happened to be a mucoepidermoid carcinoma involving
the trachea and here on the axial images we can see narrowing of the normal lumen
of the trachea by this mucoepidermoid carcinoma. Again, imaging findings are
completely not distinguishable– indistinguishable I should say–from
squamous cell carcinoma except for this one. This was an interesting case I saw
many years ago, this was a benign–this was actually a pleomorphic adenoma
involving the tongue base. The key thing here is on the gradient echo image it
was very high signal, so I have seen a couple of these, this just happens to be
a pleomorphic adenoma involving the tongue base, again, a minor salivary gland
tumor and the distinguishing feature was the high signal on the gradient echo and
the T2-weighted image, but again, extremely rare. Now this is a bizarre
tumor, this is a granular cell tumor and a granular cell tumor is a tumor that
arises in the larynx and typically we don’t image these, but my my ENT
colleagues–and I have some ENTs in the back there, you can tell me if I’m right or wrong.
The people that I’ve worked in the–in the past say they see this relatively
frequently but what they end up doing is they see them pretty early and they
continue to shave it off, but what happens with some of these granular cell
tumors is that the surgeons will go in and shave it off but these things tend
to have a infiltrate or end up with a growth pattern so by the time that we
see it, everything that’s involving the airway often times has been shaved off
and we end up seeing these as these tumors that extend through the larynx
and in this case extending on the undersurface of the strap muscle so
if I see something that looks like this then I start thinking that this is a
granular cell tumor so this is a non-contrast T1-weighted MR and a
contrast-enhanced T1-weighted MR–again demonstrating this type of growth
pattern. So if I see something like this it almost has a circumferential and
primarily anterior in the larynx and I started thinking of a granular cell
tumor. This is the classic example of a little subglottic hemangioma, so
you know we tend not to image this very frequently. Often times this pediatric
otolaryngologist would tell me they’ll go ahead and see them and if they’re not
obstructing the airway sometimes you can just resolve, but if we do see these on
imaging they’re typically located in the subglottic larynx when you can see dense
enhancement. In this case we can see a little bit of compression of the airway
on the axial and the saggital images. Again the characteristic findings and
the features that we look for that typically in a child–often times a
newborn with a little bit of stridor and when we do the imaging study we can see
this dense enhancement within the subglottic hemangioma.
Well let’s go on to infectious and inflammatory processes. Now you know Wegener’s
granulomatosis is the is the old term for Wegener’s, it now has a new term.
Again, being born in the last century I still use the term Wegener’s
granulomatosis so Wegener’s is a granulomatous vasculitis, it’s primarily
immune mediated, and it has classic forms and the classic forms are necrotizing
granuloma of the upper and lower respiratory tracts. It’s associated with
a systemic vasculitis and it can also result in this necrotizing glomerulonephritis involving the kidneys. Now the laryngeal involvement in Wegener’s
typically is subglottis and results in a narrowing or stenosis and the patients
usually have sore throat, laryngitis, or fevers. Now, in the head and neck, Wegener’s is pretty rare involving the larynx so really where it’s more common is in the
sinuses. I think we’ll probably talk more about that later today. So I’ll give you
my impression about when I think of Wegener’s and the sinuses but just
realize Wegener’s does arise in the larynx it and it’s pretty rare. But again it’s nonspecific, so this was path proven Wegener’s granulomatosis and,
again, what by the way what level are we at right now? Someone tell me. Are we
at the…? Subglottic. See how easy head and neck is?
Subglottic. Why? Because we can see the signet ring of the cricoid cartilage so
now we’re the subglottic area. So when you see the subglottic area you can see
that this circumferential lesion involving the larynx. Yeah could this be squamous
cell carcinoma? Absolutely. Could this be minor salivary gland?
Absolutely. Could this be granular cell tumor?
Absolutely. Could it be Wegener’s? That’s what it
turned out to be. So unfortunately a lot of these things that we see are
nonspecific so we just have to keep this in the back of our minds. Another example,
Wegener’s non-contrast T1-weighted images with contrast we can see diffuse
enhancement in this patients with Wegener’s granulomatosis. Well here’s a,
again, a pretty rare case, this was a case years ago but one of the few cases
where we saw a little abscess involving the free margin of the epiglottis so
could this be a little cyst involved the epiglottis? Absolutely, but this patient
had a very severe fever, a very bad sore throat, we did our CT scan and there’s a
little abscess right here involved on the free margin of the epiglottis. Now
the next stage, if you will, in adults is this concept of supraglottitis. Now in kids
what do we call this? In the kids we typically look for epiglottitis but, if
you will, the adult form of sup– epiglottitis is supraglottitis and these
patients typically present with a fever, sore throat, dysphagia, odynophagia,
muffled voice, and drooling. The pathology can be bacterial or potentially viral as
well but in most cases it’s bacterial and the treatment is airway management
and antibiotics so this is an example of supraglottitus and it looks pretty
ugly right? You look at this and you say you’ve got to be kidding me. But what we
can look at this is–we can identify the normal structures if we just understand
what the anatomy is so let’s take a look. What structure am I looking at right
here? Hyoid bone, exactly. So hyoid bone we
come back and we see this structure right here is this anterior and midline
so what structure is this? Epiglottis. We come back here and now we see the
structure back here and back here so what–you don’t see that as well on this
side, but what structure am I looking at right here? Aryepiglottic fold and what
structure is right back here where my arrow is? Pyriform sinus.
What do we see here? This is the posterior laryngeal wall or the
posterior pharyngeal wall. So once you– excuse me–once you understand the
anatomy then you can understand what the imaging findings are of supraglottitis.
So there’s diffuse enlargement and swelling of the epiglottis, the
aryepiglottic fold, and if we get down to the false vocal cord, the false vocal
cord. There’s diffuse thickening and
enhancement of the mucosa. In this case, there was no obliteration of the pre
epiglottic fat but sometimes you can see that. You can see a lot of edema
involving the retropharyngeal space which is back here, right behind the
pharynx and we can see reticulation and thickening of the platysma muscles so
here’s our platysma muscle here and this is way too thick. So this has a very
aggressive inflammatory appearance to it, so this is supraglottitis and this
just tells us that there are different stages of infections that it can involve.
Not only the neck but everywhere else in the body, so this classification is
ubiquitous. So erysipelas is just an infection of the superficial layers of
the skin. Cellulitis is an infection of the subcutaneous tissues. Necrotizing
fasciitis as we’ll see is destruction of the fascia without skin or muscle
necrosis and then Myositis is involvement of the muscles. So what’s
necrotizing fasciitis? Now, everyone has heard of this. It’s always fascinating to me
there’s a typically increased awareness of necrotizing fasciitis about every 7
years because, you know, Doug’s from New York right? And anytime there’s an
article in The New York Times, the whole population becomes aware of this, so
what’s the other name for necrotizing fasciitis when it hits in New York Times?
Anybody remember that? It’s flesh-eating bacteria so it’s the
old flesh-eating bacteria and all of a sudden there’s an outbreak of
flesh-eating bacteria so that’s–that is necrotizing fasciitis. Now granted it’s a
very severe disease, affects the elderly and the immunocompromised with a
mortality rate of up to 75%. So this is necrotizing fasciitis.
Now the challenges here is what is the– what is the characteristic finding that
tells us it’s necrotizing fasciitis. Here we can see thickening of the area of epiglottic folds, thickening of the posterior laryngeal wall, edema involving
the retropharyngeal space but what’s the characteristic finding that tells us
that’s necrotizing fasciitis? The air, right. So if you have a patient
that’s really sick and they’ve never had radiation or chemotherapy and they
haven’t had a major coughing spell because occasionally if someone coughs
really really hard they can blow a little bronchus or something and the air
can involve the base of the neck, but if you never had someone that’s had recent
surgery, a big coughing spell, or has ever had chemotherapy or radiation therapy–
which is the majority of patients were going to see–if you see this air in the
neck and a pretty sick patient then you have to consider the diagnosis of
necrotizing fasciitis. This on the other hand is a patient that underwent
chemotherapy and radiation therapy and here is air in the neck, but this is due
to chondronecrosis, so if you have a patient treated with
combined therapy, you can actually have gas forming in the soft tissues when you
develop necrosis of the cartilage following this type of treatment. Well
the next couple of things that we’ll talk about, then we’ll take our break, is
a little bit of a developmental lesion. The thyroid gland starts at the tongue
base and it starts at a specific portion of the tongue base. Now does anybody
remember the specific foramen where the thyroid originates or is born? It’s a
foramen cecum, right. So the thyroid gland begins at the foramen cecum and it has,
if you will, a relative descent and I say relative descent because sometimes the
embryologists are not sure whether the thyroid gland falls or the neck grows
superiorly which kind of drags it down so at times it’s debatable, but the thyroid
gland starts at the foramen cecum and has this relative descent to the anterior
portion of the neck and it always gets a little bit confusing as opposed to
what’s lingual thyroid versus what’s thyroglossal duct cysts so the way I try
to explain it is that obviously both of these are related
they’re like first cousins right? So if you have solid
tissue that’s located at the tongue base and anytime that you have residual
thyroid solid tissue, that’s what’s referred to as a lingual thyroid so this
is an example of a lingual thyroid that’s located right where you expect the foramen cecum to be and here we can see it’s densely
enhancing, it looks like there may have a little bit of calcification or within it
and this is the lingual thyroid and when we do a CT scan at the level of where
the thyroid should be we can see that the thyroid is not present, so that’s
classic lingual thyroid. Another example, a patient non-contrast–T2 non-contrast
T1 with enhancement, another example of lingual thyroid and, again, based on that
alone, to be honest with you, I’d probably call that a squamous cell carcinoma, but
on the other hand of the patient is hypothyroid and doesn’t have any thyroid
seen on ultrasound then you have to keep in the back of your mind that this in
fact may be a lingual thyroid. You can do the nuclear medicine studies as seen
here, in this case, here is the sagittal images of a lingual thyroid and this is
the radio iodine study, we can see there’s uptake within the lingual
thyroid gland. So that’s lingual–that’s the lingual
thyroid. Any place where there’s solid thyroid tissue, that’s a lingual thyroid.
So as Doug mentioned, the thyroid gland starts at the foramen cecum and as
it descends inferiorly it has this–I always called it a complex relationship with the
hyoid bone until it ends at the anterior neck. And there was a question earlier
about how do we look at thyroid gland and what are the distinguishing features?
Well at least in my experience, you know, the thyroid–the thyroglossal duct cyst
as we’ve seen here can either be unilocular or multilocular. They can be
midline or para-midline and I’ve seen them superficial or deep to the hyoid
bone and the reason you have that appearance is because of this
relationship right here with the hyoid bone, but the feature that always tells
me–and I’m glad Doug mentioned this before too–is that the thyroid–that the
thyroglossal duct cyst is embedded in the strap muscle so if you see a unilocular or multilocular mass midline or para-midline that’s in the strap muscle,
then that is a thyroglossal duct cyst and the reason is, it’s, you know, we’re–we
do a lot of adult imaging right? You know, the pediatric ENT surgeons and our
pediatric radiologist they obviously do more ultrasound, but the way you distinguish a
kid with a thyroglossal duct cyst is they come in with an anterior neck
mass and they swallow and it moves up and down and the reason it moves up and
down is because it’s in the strap muscles and what do the strap muscles do?
The strap muscles are like the cables in an elevator so when you swallow the
strap muscles are located anterior to the larynx–they’re attached to it and they
contract and they pull the larynx up and they pull the larynx up towards the
tongue base so the epiglottis can flop down so all your food doesn’t go through
the larynx, but it’s that contraction of the strap muscle that causes the larynx
to move. So similarly, if you have an anterior neck mass and it’s embedded in
the strap muscle, clinically you’re going to see movement when the patient
swallows. I think the fancy term is movement with the deglutination. So
that’s the radiological correlate of how thyroglossal duct cysts are made
clinically. So that’s why that key feature is that embedding within the
strap muscle. Doug mentioned before this is the classic Sistrunk procedure, when
they perform the Sistrunk procedure the surgeons have to go in and take a cuff
of the tongue base because they want to make sure that they know the thyroid
gland originates at the frame and cecum, so they need to take that superior cup
of tissue so there’s no residual disease. So what is a laryngocoele? You know
a laryngocoele is dilatation of the laryngeal ventricle and if the laryngocoele
is limited laterally by the thyrohyoid membrane then this is
referred to as a internal or a simple laryngocoele, but if it extends outside
the thyrohyoid membrane into the neck, then this is referred to as a
complex laryngocoele and it’s a key differentiator because if the laryngocoele is located within the larynx this can be removed through an endoscopic
approach. But however if the laryngocoele extends outside the thyrohyoid membrane
into the soft tissues–and this often times requires a cervical
approach–so again that’s how we can we can make our value. Another example of a
laryngocoele, they can be air-filled as is seen here, another one here and
another one here just outside. I am gonna go back real quick because one thing
about laryngocoeles is that, again, when I grew up laryngocoeles were most commonly
seen in glass blowers and trumpet players right?
Anybody remember Dizzy Gillespie when he would blow into his flugelhorn you see these
big things come out? Yeah those are big laryngocoeles right? But the most
common cause of laryngocoele is actually squamous cell carcinomas so anytime that
you see a laryngocoele you have to look for an obstruction–obstructing lesion
that can either be a tumor involving the true vocal cord or the false vocal cord. This is a laryngocoele that became
infected, this is a laryngopyocele, again, it has a similar appearance to the
laryngocoele but clinically you can make the diagnosis. We can also see all of
this reticulation of the fat surrounding the laryngocoele. This was just an
example of an arteriovenous malformation that’s involving the floor of the mouth,
but when we take a look at the larynx we can see that when we take a–this is a
non-contrast T1-weighted image, you can see these flow voids, but when we do a CTA look at this dense enhancement right here. This is all arteriovenous
malformation involving the larynx and when we do an MRV here we can see a
diffuse enhancing lesions on this MRA I should say involving the larynx. The last
thing that I’ll just briefly mention is vocal cord palsy and Doug already talked
eloquently about the recurrent laryngeal nerve. The only couple points I’ll make
about vocal cord palsy is it can be a little tricky. Realize that in chronic
vocal cord palsies you’re going to have asymmetrical dilatation of the laryngeal ventricle.
He talked about the recurrent laryngeal nerve going from top to bottom. The only
couple points that I wanted to make was if you look at a CT scan, you can
potentially determine whether it’s chronic or acute. This is the normal
appearance of the larynx when–someone tell me what level are we at right now? So what–so again let’s not–let’s figure
out what cartilage are we looking at here? Cricoid. Do we see the arytenoid
cartilage. No arytenoid cartilage. So which–what level of the of the larynx
are we at then? Subglottic larynx, exactly right. So here we’re at the level of the
subglottic larynx and realize that there are these constrictor muscles posterior
to it. So one way that we can identify that we’re looking at chronic
denervation atrophy is that these muscles do get some of their branches
from the vagus nerve. So here’s a normal attenuation of the muscle on the left
hand side and we can see that on the right hand side all that fat is
obliterated so if we do have a patient that comes in with a vocal cord palsy and
someone asks you how long is it chronic or is acute, one way to look at it is to
look for the adjacent muscles just posterior to the cricoid cartilage and
the other way that we can look at it too is to look for the little fat right here
involving the left side of the larynx. So here’s the normal appearance here of the,
again, right at the level of the subglottis, but notice how the muscles here are atrophic
and in this case it was due to this bronchogenic carcinoma that’s clipping
the returned vocal cord–a recurrent laryngeal nerve that we illustrated and
if a patient does have a vocal cord palsy then the surgeons can perform some
type of medialization procedure. This can be confusing if you’re not used to
seeing it. This patient had a left vocal cord palsy and this was injection of
teflon. So in this particular case the surgeons went ahead and put teflon in
with medialization of the left vocal cord and this case this was a teflon
granuloma here that was injected and what we see is that this patient had a
left vocal cord palsy, so in order to try to medialize that so this vocal cord is normally moving, but you can see if it moves it cannot
close the airway because this vocal cord is paretic, so what the surgeons can do
is take a little bit of teflon or silicon or whatever they move this vocal
cord medially so this normally moving vocal cord can oppose itself and cause
the sound to occur, but in this case unfortunately this patient developed a large
teflon granuloma after the teflon was injected so one of the potential
complications that you may see. So in summary what we try to do over the last
45 minutes or so is talk a little bit about the technique and remember your
homework right? Homework, homework, homework. It’s look at the normal
cartilages and the bones of the larynx, if you do that for five minutes in the
evening over the next two weeks I don’t think you’ll ever have a problem with
the normal anatomy. We talked a little bit about the tumors, infectious, and
inflammatory process, developmental, and just a little bit about the vocal cord
policies as well, so thank you very much for your attention.

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