Rhinosinusitis | Clinical Medicine

0:01[snorts]

0:08What's up, ninja nerds? In this video

0:09today, we're going to be talking about

0:10rhino sinusitis. This is part of a

0:12clinical medicine series. And if you

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0:37that out there. All right, let's talk

0:38about rhinositis. So a lot of times

0:40people will actually just say, "Oh, it's

0:41well it's sinusitis technically, Zach,

0:43right? It's an infection. It's

0:45inflammation of the paranasal sinuses."

0:48And that that that is true, but oftent

0:49times more than not, I'd say when

0:53patients have sinusitis, it's almost

0:54always they have concominant rhinitis.

0:56And so we should actually define that

0:58very very simply. So in rhinitis it's

1:00really just inflammation of the nasal

1:01cavity right and in this case it's

1:03usually due to an infectious process. So

1:05inflammation of said nasal cavity

1:10whereas when we talk about sinusitis

1:12it's the inflammation of the paranasal

1:14sinuses and

1:16technically when we talk about paranasal

1:19sinuses some will include the mastoid. I

1:21like to say that as more of an exception

1:22in this kind of scenario where we're not

1:24going to talk about the the mastoid

1:26sinus that was more in the ear

1:27infections lectures but parinasal

1:30sinuses and again these this

1:32inflammation is usually due to an

1:34infectious eeologies which we'll get

1:35into. Now in chronic rhinositis that may

1:38not always be the case where it's it is

1:40more kind of like a chronic inflammatory

1:42process that we'll get into that's

1:43usually due to either polyps or no

1:45polyps. I promise we'll get there. When

1:47we talk about rhinitis, it's really when

1:50you look at the nasal cavity, all of

1:52this is lined with a mucosal tissue.

1:54That's pseudoratified siliated columnar

1:56epithelial tissue. That's a mouthful,

1:57right? Heck of a word. But really,

2:00that's all this is. It's all of this

2:01kind of tissue everywhere in here.

2:06This is all inflamed. So that's really

2:08what we have. And it's even these kind

2:09of what we call the conch. So you have

2:11your superior, middle, your inferior

2:12nasal cone, the miatuses. All of those

2:14are inflamed. So that's rhinitis. Now

2:17the sinuses are really important to

2:19remember that they are connected to your

2:22nasal cavity. They're not just this

2:23hollow cavity in your skull that doesn't

2:25connect with the nasal cavity. There's

2:26like little holes. And I don't want to

2:28go too crazy on the anatomy component,

2:30but you know here we have this is our

2:32superior nasal conche. This one here.

2:34And then this one here in the middle. I

2:35bet you can't guess it. Yeah, it's the

2:37middle nasal conche. And this one is the

2:38inferior nasal conche. Well, the grooves

2:40in between them are called the miatus.

2:43So you have here the superior I'm sorry

2:46um the superior miatus the middle miatus

2:47and the inferior miatus. Now when

2:51patients who have sinusitis it's

2:53important to remember that the most

2:55common exit point for the sinuses in the

2:58middle miatus. And so for example here

3:01is this frontal sinus. There's an

3:02anterior ethmoidal sinus and a middle

3:04ethmoidal. Those all really and I'm just

3:07going to represent with this blue arrow.

3:09They drain where? Well again think about

3:10it. This is your superior mus, middle

3:12mius. These usually have a little kind

3:15of exit point where they empty. I'm

3:19going to kind of bring it underneath

3:20here right here. So there's a little

3:23kind of like exit point called the

3:24middle miatus. And that's really where

3:26the frontal sinus and the anterior

3:28middle ethmoidal sinuses empty in. The

3:31sppheninoid sinus has another like

3:33little hole here. There's this tiny

3:35little hole and it empties it into this

3:37recess called the sppheninoethmoidal

3:39recess. Again, I don't want you guys to

3:41get too bogged down with that. All I

3:43want you to know is that this has an

3:46exit point here. And so, what I'm what

3:48I'm trying to get at here is that this

3:51sinus is continuous with the nasal

3:53cavity. So, it's almost impossible for

3:55you to have a rhino almost impossible

3:58for you to have a sinocitis without

3:59involving to some degree the nasal

4:01cavity mucos. That's why patients often

4:03we call it rhinocitis. So, it's me just

4:05be getting into more semantics, but

4:07let's kind of remind ourselves of again

4:09what these sinuses are. So, this sinus

4:12right here is going to be called the

4:14frontal paranasal sinus, right? This one

4:17here is the ethmoid.

4:20And technically, the ethmoid, if you

4:21want to be particular, is broken into

4:22anterior, middle, and posterior

4:23ethmoidal sinuses or that's more for

4:26anatomy. And then this right here is

4:27going to be your

4:30sppheninoid sinus. So, you're probably

4:32thinking, "Okay, Zach, there's another

4:34one. I know it. You told me that don't

4:35worry about the mastoid. There is one.

4:37You can't really see it in this diagram

4:38very well, but it's the maxillary. But

4:40here we have the spphenoid, we have the

4:42ethmoid, and we have the frontal

4:43sinuses. And what I already told you is

4:45that the frontal and the anter middle

4:47ethmoidal, they empty into the middle

4:49mus. The sppheninoid empties out into

4:51the spphenino ethmoidal recess. If I

4:54wanted to be particular, I'm not going

4:56to be, but I'm going to mention it

4:57verbally. The posterior ethmoidal sinus

5:00does empty into the superior miatus. I'm

5:03not going to go that far. I'm just going

5:04to let you guys know that. But this is

5:07what I want you to understand that since

5:08a patient develops inflammation of their

5:10nasal cavity, if it can find these

5:13little entryways, it can travel up into

5:15the sinuses. And if it travels up into

5:17those sinuses, what are you going to

5:18get? You're going to get an inflamed

5:22paranasal sinus. So that's what I want

5:25you to understand. They can find their

5:26ways into these paranasal sinuses. Now,

5:29here's another view. So this is looking

5:31at a sagittal view which is involving

5:33inflammation of the nasal cavity and

5:35these visible paranasal sinuses through

5:37there little holes. We'll talk about a

5:40little bit later but that little hole is

5:41called an oa and it's in the miatus and

5:44so we call it an osteommeatal complex.

5:46We'll get into it. I promise we'll get

5:48into it as we get deeper into this. But

5:49the next component here is just to take

5:51another look. So another view that we

5:52often times see here is this view which

5:54is kind of looking at the patient from

5:56the front on but I'm kind of making them

5:57look like a weirdo but I'm cutting off

5:58their nose. But we can see into the

6:00nasal cavity nice and clearly. If you

6:02could imagine here this is going to be

6:05there

6:06septum which is formed by the

6:08perpendicular plate of the ethmoid bone

6:09the vulmer and then on the sides here we

6:11have the again superior middle inferior

6:13nasal conche superior miatus middle

6:16miatus and then you'll have below this

6:17the inferior miatus. What you'll notice

6:20is what that these sinuses which ones

6:22are this is the maxillary sinus this is

6:25the ethmoid sinus and this is the

6:27frontal sinuses. All of those they come

6:30down and they dump into that what

6:32component? The middle miatus. And so

6:34again it's just giving you another view.

6:35Now we actually should bring this down

6:36though right here to below right below

6:41that conje.

6:43But you get the point. So the view from

6:46here is kind of interesting because you

6:47can kind of see this as well. If you

6:49have inflammation

6:52of this nasal cavity

6:55and there's this little hole, this

6:56little oa, what can it do? It can travel

7:01and it can involve these sinuses here.

7:04It can travel

7:06and involve these sinuses. You get the

7:08point.

7:10Now,

7:12whenever you kind of involve these

7:14sinuses,

7:16you're going to end up with some

7:17symptoms. But again, real quick here,

7:19just so we can kind of appreciate this

7:20anatomy here. We already talked about

7:22this. This is your frontal,

7:25right? This one is your ethmoid

7:28and this one is your maxillary.

7:32And again, we can appreciate the

7:33spphenoid better over there. But what

7:36I'm trying to get at here is that

7:37whenever a patient has rhinitis, they

7:39almost always have an associated

7:41sinusitis. And you can kind of say that

7:43vice versa with the sinusitis.

7:45Now in this scenario, if a patient has

7:48inflammation of their nasal cavity and

7:50their sinuses, what would that present?

7:52How if a patient came to the hospital,

7:53they came to the clinic, they came to

7:54you to see you, what would be their

7:56initial complaints that would make you

7:57even think that it could be rhinocyitis?

7:59Because then once you determine that

8:00it's a it's possibly a rhinocyitis, I

8:02got to determine if it's viral,

8:04bacterial, fungal, or if it's chronic.

8:06And that's what we're going to get into.

8:07But for right now, what I want you to

8:09understand is often times

8:12this is going to be usually some type of

8:15nasal discharge. There's going to be a

8:17pretty common type of complaint. So a

8:19patient will present with some degree of

8:21nasal discharge. This discharge is

8:25because of a lot of the mucus

8:26production. So whenever you have

8:28inflammation

8:30of the nasal cavity, inflammation of the

8:32sinuses, your natural reaction is to

8:33start kind of bringing blood flow and

8:35and white blood cells to the area to

8:36fight off whatever that infectious

8:37ethology is. And that causes sometimes

8:40more of that discharge to become

8:42present. Usually we use the term perent

8:46to describe more of that bacterial

8:48component, but for right now I just want

8:50you to think about nasal discharge. The

8:53second kind of symptom here is going to

8:56be congestion. So there'll be some

8:58degree of congestion. Now the congestion

9:01is because as a patient gets a lot of

9:03rhinitis, they get tons and tons and

9:05tons of inflammation of this nasal

9:07cavity. Think about having to breathe

9:09through your nose when everything is

9:11super super small and tiny. You got a

9:13tiny little lumen. Now that's the key

9:15behind this. So the congestion is more

9:17of that nasal obstruction just due to

9:19nasal cavity inflammation.

9:21The next symptom here is going to be

9:25interesting. All right. So, we got nasal

9:27discharge is usually inflammation

9:28causing fluid and mucus to come out of

9:30the sinuses, out of the nasal cavity,

9:33out of the nose. Congestion,

9:35inflammation of that nasal cavity,

9:37obstructing air flow. The third one is

9:40facial pain and pressure. So, facial

9:44pain and pressure. I want you to just

9:47think about this for a second. If a

9:49patient has inflammation of these

9:52sinuses, the maxillary sinuses or the

9:55ethmoid and the frontal sinuses, these

9:58are normally very hollow cavities. They

10:00decrease the weight of the skull. You

10:02fill it with mucus and potentially pus

10:04and a lot of liquid. What's going to

10:05happen? It's going to get heavy and

10:06you're going to feel that, man. It's

10:08going to really hurt. And so that facial

10:10pain and pressure is very common.

10:11Usually maxillary is going to be here

10:12around that kind of cheek area, right?

10:14Sometimes it can even cause dental pain.

10:16When you get things like particularly

10:18ethmoid and maybe spphenoid, those are a

10:19little bit deeper, but they might cause

10:20pain really more retroorbbitally. And

10:22then whenever you have pain and pressure

10:24of the forehead, that could be the

10:25frontal sinuses. But it's all because

10:27those sinuses are filled with mucus and

10:29fluid and potentially pus and that's

10:31causing those to distend. What you know,

10:33nerves, cranial nerves actually

10:34innervate these. And so if you have

10:36things like your your uh nerves actually

10:38innervating those and they get pushed

10:39from stretch, that's going to cause

10:41those signals is that's going to give

10:42that kind of pain and pressure

10:43sensation. And often times we kind of

10:45add on to this on the vignette. If you

10:47see a patient who comes in congestion,

10:49discharge, facial pain and pressure

10:51that's worse whenever they lean forward,

10:53it's because all of that mucus is

10:55shifting. It's creating that weight and

10:57that's going to cause that symptom to

10:59become more escalated. The fourth one is

11:01kind of like a possibility and it

11:04screams more of the chronic picture. But

11:06there's one other thing about the nasal

11:08cavity beside it having that

11:09pseudoratified siliated columnar which

11:11does what? The basic definition is that

11:14when air comes in you want it to warm

11:16the air, moisten the air and and you

11:18also want to trap any kind of particles

11:20that are coming in the air. But there's

11:22one other thing. When you have air

11:24coming in, if you want to smell

11:26something like a bag of dog poo or some

11:28type of like really good steak or food,

11:30that smell is in the nasal cavity. So

11:33because of that, in patients who have

11:35significant amounts of inflammation and

11:37mucus, what if you block those smells

11:39from hitting the alactory epithelium?

11:41That can cause a decrease in smell. What

11:43do we call that whenever there's a

11:44decrease in smell? We call it hyposmia.

11:46And in worst case scenario, sometimes

11:50it can even cause anosmia which is no

11:53smell. Right? So sometimes you may even

11:55have anosmia. This is due to the

11:58olfactory nerves and epithelium being

12:00affected. All right. What I got out of

12:03this here is rhinitis, inflammation of

12:05the nasal cavity, sinusitis,

12:06inflammation of the paranasal sinuses.

12:08Which part of the paranasal? Frontal,

12:10ethmoid, sppheninoid and maxillary, not

12:12mastoid. How do the sinuses get inflamed

12:15if a patient has rhinitis? Because they

12:17run through the oste. The oste is the

12:20little hole that connect with those

12:22sinuses. They get filled with fluid and

12:23mucus. How will they present? They'll

12:26have nasal discharge, congestion, facial

12:28pain, pressure, hyposmia.

12:30Now there is a difference between acute

12:33onset and chronic onset rhinocyitis.

12:36What I want you to know here is for

12:38acute, this is usually something that

12:40developed within, we often define less

12:43than four weeks. So we really want to

12:46have like a timeline between these two.

12:48This one is usually it's been going on

12:52for not really a long time, less than

12:55four weeks. And oftent times the

12:56patients are presenting very very soon.

12:58It's usually a couple days. People don't

13:00like have to I'm not going to live with

13:01this pain and pressure and all this

13:03stuff, this discharge. They're not going

13:04to be doing that. Chronic rhinocyitis.

13:07This is a patient coming in who's been

13:08dealing with this for a really long

13:10time. Oftentimes we say greater than 12

13:13weeks. And so that's a timeline that

13:16more likely establishes how long they've

13:18been dealing with these symptoms. The

13:21really really important point is when

13:22they come in very very soon. It hasn't

13:24been something they've been dealing with

13:25for more than four or 12 weeks. It's

13:28easier for us to figure it out. So

13:31usually there's a couple different

13:33subtypes here. There's what's called

13:34acute viral

13:37rhinocyusitis. All right. So acute viral

13:40rhino

13:42sinocitis. This is by far the most

13:47common cause of a patient presenting

13:49with acute rhinocerositis overall.

13:52Another one is acute bacterial and this

13:55would be the second most common cause.

13:58And then the last one is going to be

14:00fungal. So acute viral definitely the

14:02most common and we'll talk about this in

14:04a second but acute viral oftent times

14:06sets the stage for a person to develop

14:09bacterial

14:11rhino uh sinocitis.

14:15The last one is extremely rare and

14:18usually it's only common in certain

14:20types of patients which we'll get into

14:21but it's called acute and we like to

14:22really add this in invasive meaning

14:25[laughter] this thing is super super

14:28rough dude. fungal

14:31rhino

14:33sinocitis. So the the the benefit of

14:36this is that it's extremely rare. The

14:38downside is for those people who do end

14:39up getting it, it causes significant

14:42damage. And that's why it's really

14:44important for us to understand that

14:46chronic rhinocyitis, you've been dealing

14:47with this for a while. This isn't a

14:48patient who just all of a sudden came

14:50about and had this. This is something

14:51they've been dealing with for a long

14:52time. The thing that you need to start

14:54to determine and really the best way of

14:56doing that is if they come in with

14:57symptoms, you then need to figure out

15:01is the patient having nasal polyps or

15:03not? That's really it. So whenever a

15:05patient comes in with these symptoms,

15:06you then have to determine is it acute,

15:08chronic. I look at the timelines from

15:10there. I then have to determine if it's

15:11viral, bacterial, and fungal, and what

15:13we'll get into and we'll try to figure

15:15and navigate out that component. For

15:17chronic, it's been going on for a while.

15:19How do I determine the differences

15:20between the two? We kind of define this

15:22in two different subtypes. So it's

15:24chronic. So we'll put CRS CRS

15:28without

15:30nasal polyps.

15:33And then we have, you guessed it, CRS

15:36with

15:38nasal polyps. And that's really all it

15:41comes down to. So what I want to do is I

15:42kind of want to highlight this component

15:45here is that is the differentiating

15:47factor between these two. And we'll get

15:48into this because simply all I would

15:51need to know is is if I looked into the

15:53nose and I evaluated, if I saw nasal

15:55polyps, I could talk about this one. If

15:56I didn't see it, I would think about

15:58this one. And I start getting into

15:59what's causing it and how to treat it.

16:02So now that we've done that, we got a

16:03patient who comes in, they're presenting

16:04with again facial pain and pressure,

16:06perent, maybe just nasal discharge,

16:08we'll say for now. They present with

16:11congestion,

16:13maybe they present with a decrease in

16:14smell. You need to then figure out okay

16:17it's less than four weeks which one of

16:18these three is it for acute viral

16:21rhinositis we already know it's the most

16:23common and we know that it's a virus so

16:26but the question is is what kind of

16:27viruses oftent times more than not these

16:30viruses are usually going to be like

16:32your common cold viruses rhino virus is

16:35extremely common adno virus is extremely

16:38common but in those scenarios where

16:41patients we know there is some nasty

16:43ones that can really really hurt and

16:45cause not just that kind of natural

16:47presentation of sinusitis but they cause

16:49diffuse symptoms. What are those really

16:51really rough ones that we're going to

16:52have a dedicated lecture as to influenza

16:55and SARS Kovv2. So influenza can also

16:59cause this

17:01and there's also going to be your SARS

17:04Kovv2

17:06which is going to cause COVID 19. So,

17:08the whole point I'm trying to make for

17:10you guys is that this is your most often

17:13cause. Out of these, which ones are

17:16probably going to be the ones that you

17:17want to associate it with? More often

17:19than not, guys, I'm not kidding. It's

17:21usually rhino virus and it's the common

17:23cold one. And that's really it. We're

17:25not going to have a patient presenting

17:26with anything kind of like significant.

17:28Oftent times, it's that one. And they

17:30will get better. The reason why I

17:31mentioned these two is because these two

17:34they actually will be really important

17:35for us to differentiate because we could

17:37change our management if it is those

17:38two. But let's say for example patient

17:42has how would you get these? H how would

17:44these pathogens work their way into the

17:49nasal cavity? And the problem with these

17:51things is that they cause damage along

17:53their path. They don't just move in one

17:55direction. They often times will damage

17:57tissues along their path. This is via

18:01respiratory droplets. So via these

18:03respiratory droplets.

18:06So someone is talking to you, they

18:08cough, they spit, I don't either way,

18:10these things are flopping around in the

18:13air and they make their way

18:16into your airway. When they get into the

18:18airway, this is where they're going to

18:19inflict damage. So what I want to do is

18:22I want to zoom in

18:25on this area and take a look see. Let's

18:27do that. As we zoom in, these viruses,

18:31they're sneaky little sons of guns. They

18:33have special receptors, and I'm not

18:35expecting you to memorize this part, but

18:38they do have Oh, there goes the purple.

18:39We'll use this one here.

18:42We have special receptors that are

18:45present on the epithelium and it can

18:48bind to it. And these receptors

18:52are called your ICAM receptors. You

18:54don't have to remember that. I wouldn't.

18:56I'm just being kind of extra. So, you

18:59have these ICAM receptors. When the

19:02virus binds to this, what it does is it

19:04gets taken into these cells, right? It

19:07gets taken into these cells and it

19:09starts to replicate. When it does that,

19:12it can cause two different issues. So,

19:14let's say that this thing gets taken

19:16into these cells. When it gets taken

19:19into these cells, there's two results

19:20that will happen.

19:22One is that the virus will replicate and

19:25replicate and replicate in these cells.

19:27And what we know is that eventually

19:31these cells will undergo licis. They

19:34will die. So you'll end up with some

19:36cell death, right? So you're going to

19:38end up with some cell death. So that's

19:40one thing. So you're going to be

19:41damaging mucosal cells via cell death.

19:44All right? So we'll say that we're going

19:45to get some type of viral cells. That's

19:48one thing that's going to happen is

19:50we're going to get some cell

19:52death via lis because that virus is

19:55going to be replicating and growing

19:56within the cell and eventually it's

19:57going to pop out so it can spread. The

20:00other component here is these viruses,

20:03dude, they're interesting. So what they

20:05can do is is they can actually as they

20:07kind of grow in they kind of develop

20:09inside of these cells, they tell the

20:12psyia to stop functioning. So, in in

20:15essence, what it does is it causes

20:18something called psilio

20:21stasis. You're like, "Nah, you're you're

20:22being silly." No, I promise I'm not. No

20:25pun intended. What happens is these

20:28little dudes here,

20:30you stop functioning. The psyia stop

20:33working. And that's really critical

20:35because our goblet cells, what do they

20:37do? What do goblet cells do? Goblet

20:40cells naturally produce mucus.

20:44And this mucus is supposed to kind of

20:46coat the airway

20:48and it's also supposed to trap

20:50particles.

20:51But in this patient who has this viral

20:55infection, the psyia are not going to be

20:58able to move the mucus. And because of

21:00that, mucus will start to build up. So

21:03the cilioasis leads to mucus buildup.

21:06And that's really, really important. All

21:09right? So we're going to get a lot of

21:11mucus buildup.

21:13and that's going to contribute to some

21:14of this kind of overall issue. So,

21:16you're going to get mucus buildup

21:19and you're just going to get some

21:20generalized inflammation from this cell

21:22death. So, all of this is going to cause

21:25your inflammation. It's going to really

21:27just it's going to jack things up, dude.

21:29It's going to make everything kind of

21:30inflamed. All that mucosa. So, let's

21:32actually define that you're going to get

21:34mucosal

21:36inflammation. And that's really where

21:38all of this comes down to is the cells

21:40die. So, you're damaging the mucosal

21:42tissue. you're causing a lot of mucus to

21:44build up because the psyia ain't working

21:46now and that inflammation is going to

21:48become problematic. Now, where is this

21:50inflammation occurring? That's where I I

21:52really want you guys to think about this

21:54inflammation is occurring in the

21:56respiratory mucosa. Again, if you guys

21:58remember this tissue, what is this

21:59tissue here? So, this is your

22:01pseudoratified ciliated columnar

22:03epithelial tissue. So, these are the

22:04pseudoratified epithelial cells, which

22:06are the blue ones. And what are these

22:08like green ones? These are called your

22:09goblet cells. So, the goblet cells

22:11produce the mucus. the psyia, the

22:13siliated cells, those are the ones that

22:15have the cyia help to beat the mucus,

22:17right? And that's really important. So

22:18when you get this viral infection and it

22:20gets its way into the cell, it can stop

22:22the psyia from working and kill the

22:24mucosal cells. So the goblet cells are

22:25producing mucus, but you don't have the

22:27ability to move them. That's going to

22:29cause problems. Now that inflammation

22:32is really where we see issues. So let's

22:34pretend here that this is the epithelial

22:36cells here. And now what's going to

22:38happen is you guys remember I just I

22:40took one sinus. Let's just pretend this

22:42is the frontal. This that's all it is.

22:43This is just the frontal paranasal sinus

22:45and it's going to come down and it's

22:47going to empty into the middle neiatus.

22:49Right? If we get inflammation, which I'm

22:52going to represent the thickening of

22:54this mucosal tissue, maybe there's some

22:56mucus there as well right here. Look at

22:59this. You see how this is happening?

23:02You should understand now why all of

23:05this occurs. I have inflammation. What

23:07did it just do? It caused a narrowing of

23:10the osteomiatal complex. I told you we

23:14would come back to that, right? I done

23:16told you. So now we have this narrowing

23:19of the osteomiatal complex and that's

23:22where we start to see some problems. So

23:23narrowing

23:26of and I'm going to abbreviate it the

23:28osteomiatal

23:30complex. Now, when that happens,

23:35the sinuses produce kind of a mucousy

23:38fluid.

23:39That fluid is supposed to be able to

23:41move out into the nasal cavity, and air

23:44is supposed to run from the nasal cavity

23:46into these sinuses. All that's going to

23:48happen is all this mucus

23:51and fluid is going to start building up

23:54and building up and building up. And

23:57this cavity is going to start becoming

23:59filled with mucus. And what happens when

24:02you fill a cavity that can't actually

24:03drain? It starts to distend and stretch.

24:08And then you start to get some degree of

24:11some sinus kind of like pressure. And

24:13that's where we start to see some

24:14worsening issues. So now I have this

24:16sinus filling. I have this sinus cavity

24:21is going to be under high pressure

24:26and it's going to have a lot of mucus

24:30buildup.

24:33And that's the two problems here that

24:35set us up for the stage for the next

24:36component here. So now this sinus cavity

24:38is filled with mucus and it's really

24:41going to start building up some pressure

24:43and that's where we start to see some of

24:45the issues. All right. So you probably

24:48are we're getting to a little critical

24:50component here. We talked about acute

24:54viral rhinocinusitis. I've led you to

24:56kind of see how it causes all of this

24:57pathophysiological response which

24:59inflames the nasal cavity, inflames the

25:01sinuses, gives you all the symptoms. But

25:03Zach, you said that it was going to be

25:04something that would really help me to

25:05think about it. I would be able to

25:07differentiate viral from bacterial.

25:10Here's what's interesting about this

25:12one. And patients who have this viral

25:15rhinocinusitis,

25:17one of the key things is that oftent

25:19times their symptoms aren't just usually

25:22defined to the nasal cavity themselves.

25:25Remember I told you that these can move

25:27throughout the respiratory tract. So

25:29this isn't the key thing, but I want you

25:31to understand that it can cause you know

25:33things like a sore throat. You know it

25:36can cause things like fngitis for

25:37example. It may cause things like a

25:40cough or it may because it can cause

25:43things like laryngitis. It may cause

25:45cough or horarsseness.

25:50Those are definitely possibilities. But

25:52here here's the critical thing which I

25:54think is really important because again

25:55along the way it is going to be damaging

25:58not just the nasal cavity. It can damage

26:01other tissues. So you can get like a

26:02sore throat from fingitis. You can get

26:04some laryngitis and cause a cough and

26:05horarsseness. The key thing is that this

26:09goes away very quickly. That's what I

26:12want you to take away from acute viral.

26:14So, I know that that seems like Zach,

26:16you kind of spent all this time for

26:18what? Well, it's leading you up to the

26:19bacterial part. I promise. But what I

26:22want you to trust me for now is that

26:24with acute viral, usually this is

26:27self-limited. It goes away. And so

26:30oftent times this will improve

26:35in less than 10 days is kind of our cut

26:39off. If it doesn't then we start to

26:43think it may not be viral. If a patient

26:46has some sinus symptoms and they also

26:48have things like a sore throat, maybe

26:50they have a cough, horseness of their

26:52voice, it could be an unspecified kind

26:55of upper respiratory tract infection

26:56which just so happened to involve the

26:57sinuses as well. And that definitely

27:00does suggest more of a viral case. If

27:02you see other areas of the upper

27:03respiratory tract, but this is really

27:06the critical point, more important than

27:08the other kind of tissue involvement is

27:10the time for improvement. Viral

27:13infections are self-limited and they

27:15will go away on their own. Bacterial on

27:17the other hand, they don't behave the

27:20same way like that. bacterial decide to

27:23say I I do what I won't and what I mean

27:26by this is usually when a patient gets

27:29bacterial rhinositis there's a viral

27:32infection that pushes them into it so in

27:35other words a patient had a viral

27:37rhinoscinitis maybe they got a rhino

27:39virus infection and then what happened

27:41is

27:43you created the perfect culture medium

27:46with all of this mucus and no ox how

27:50does how do you know bacteria Some of

27:51them need oxygen. If I plug this dang

27:54osteomal complex, how's any air going to

27:56get up there to the bacteria? The

27:58bacteria going to be in a perfect

28:00culture medium, dark, lots of fluid. The

28:02pH is probably going to be changed and

28:04they ain't got no dang oxygen. So these

28:06things in those scenarios, it just

28:08allows for the perfect kind of culture

28:10medium for them. Perfect culture medium.

28:12So essentially what I want you to take

28:14away from this is viral

28:17the viral

28:19infection

28:22basically sets up

28:25bacterial

28:28infection

28:30because at this point when a person had

28:32this all set up all they did was they

28:35already did all the narrowing for the

28:37person and I promise I'm going to get

28:38into all of this but now all of this

28:40inflammation is here from that viral

28:42infection. All that narrowing

28:45of the osteomatal complex is there. All

28:48right? All of this is still present. And

28:51now you got the perfect culture medium.

28:54You got hypoxic conditions.

28:56You got all this mucus building up. And

28:59now any bacteria that are a part of our

29:02normal flora in here can grow. So that's

29:05the question. What are those bacteria?

29:09So, the key thing here is is we have a

29:11couple different types of pathogens that

29:12I want you guys to know. And you can

29:14remember it by, man, I'm shaking my dang

29:17head. All right, shake my head. So, this

29:19is going to be Let's actually write

29:20these out. There's actually shake my

29:22head. We'll put shake my head. So, the

29:27first one is going to be by far the most

29:30common. This is going to be strepto

29:34caucus

29:36pneumonia. All right. The next one is

29:39called Moraxella

29:41catateralis. And the next one is called

29:45hmophilus

29:47influenza. And this is the non-typable

29:50version. These are going to be the most

29:53common bacterial pathogens. Now, here's

29:56the thing which is really interesting.

29:58These bacteria, they don't just like,

29:59oh, oh, I'm I'm coughing, I'm sneezing,

30:01I'm spreading this pathogen. These

30:04bacteria are natural colonizers. Let me

30:06I have right here. This is a natural

30:09colonizer. So, this is going to be found

30:11naturally in the nasal cavity. This is

30:13this is kind of a normal bacteria. And

30:14if it's in the nasal cavity, how else

30:16could it get into the sinuses? The

30:18osteo. And so, this thing's here. It's

30:21sitting right there, right? And if you

30:24create an opportunity to shut off any

30:26kind of air flow, you have it sitting a

30:28lot of fluid and mucus, it's going to

30:30grow. So, now that pathogen is sitting

30:32right there, dude. Now, what I want to

30:34do is I I know I drew these green, but I

30:37got all this mucus here in green. So,

30:38let's change the color of the bacteria.

30:40But for a second, I just want you to

30:41trust me that this bacteria is sitting

30:43here.

30:45And now, because you created the perfect

30:48environment for it, it's going to start

30:51growing

30:52and growing and this is going to cause

30:55some particular issues. So, what happens

30:56is the viral infection sets up the

30:59perfect environment. What is that

31:00environment? This is going to be a sinus

31:02cavity is going to be under pressure.

31:03It's going to have lots of mucus

31:04buildup. And on top of that, it's going

31:06to be hypoxic conditions. There's not

31:07going to be as much air flow through

31:08there. This allows for the bacteria that

31:11are sitting in there, the bacteria to

31:14actually undergo excessive growth

31:17because these are naturally going to be

31:19there. But because these things now are

31:21in the perfect culture medium, oh baby,

31:24these things are going to grow like like

31:26wildfire. They're going to replicate

31:27like bunnies. And because of that, guess

31:30what? the bacteria eventually going to

31:31do. They're going to start causing some

31:33nasty damage. And so they release

31:35obviously different types of toxins.

31:37They cause tissue damage and that's

31:40going to start really really ramping up

31:42this inflammation much more so than this

31:45viral case, right? The viral case,

31:46you'll definitely get a little bit of

31:48inflammation, right? You're definitely

31:50going to have inflammation,

31:52but viruses aren't going to be as like

31:54toxic as we should say as something

31:56compared to a bacterial infection. These

31:59are going to produce more of a toxic

32:01appearance. The bacterial growth in

32:03itself is kind of interesting how this

32:05kind of all works. Let's say here I'm

32:08just taking this and I'm zooming in on

32:10it. That's all I'm doing. I'm taking

32:11this area and I'm zooming in on it. So

32:14now I have the bacteria sitting in this

32:17perfect culture medium. Right here's

32:19some of these bacteria

32:21and they're sitting in this perfect

32:23culture medium and they're they're just

32:25they're ripping things up, dude. They're

32:27kind of they're maybe releasing toxins.

32:28They may be causing different types of

32:30destruction of these cells. Whenever

32:31that happens, these cells signal your

32:34immune system, right? And they signal

32:37the immune system in two different ways.

32:39They're going to release different types

32:40of cytoines.

32:43And two things that these cytoines will

32:45do, right? when it releases these

32:47cytoines and I don't need you guys to

32:49know all this dang stuff is it's going

32:51to cause vasoddilation

32:55and it's going to cause a capillary

32:58leak. In other words, this thing is

33:00going to be filled to the gills and it's

33:02going to be leaking like a seieve. And

33:04because of that, you're going to get

33:05lots of blood flow to the area and

33:07that's going to cause what? Well, if you

33:09got lots of blood flow coming to this

33:11area, what that's going to do is

33:15you're going to allow for things like

33:16fluid and proteins and stuff like that

33:19to start leaking out. So now I'll

33:21represent that fluid with the kind of

33:22this bluish color. You're going to start

33:24causing all of this fluid to really

33:26occur here.

33:28And what's that going to do

33:31around this kind of sinus area? It's

33:33going to cause swelling, right? So, as a

33:35result, you're going to start getting a

33:36lot of swelling

33:39and that's going to worsen the pain,

33:41dude. That's going to definitely worsen

33:42the pain in these patients.

33:44But there's another component here as

33:46well, the cytoines.

33:49And that reaction over here with the

33:50viral, it's natural inflammatory

33:53reactions that your immune system will

33:54kind of just process and it'll get

33:55eventually get over, but they don't

33:57bring in tons of neutrfils on viral

33:59infections. bacterial infections,

34:02there's some serious cytoines that any

34:04kind of neutrfils that are called to the

34:06area in an area that's really leaky and

34:08it's getting a lot of blood flow,

34:10they're going to respond to. And so now

34:12these neutrfils that are kind of just

34:13rocking through the bloodstream, it's

34:15going to say, "Oh, dang sister, we got

34:17some inflammation over here." And it's

34:19going to start leaking out. The problem

34:21with neutrfils is that they are great

34:23immune system cells, but they often

34:25times can cause destruction to the

34:28tissue that they're also trying to

34:29protect. And that's kind of the

34:31downside. So now these cytoines are

34:33going to pull these neutrfils out into

34:34this area. And what happens is the

34:36neutrfils will kind of find their way

34:38out here to fight. All right? So again,

34:41cytoines cause vasoddilation, capillary

34:43leak that kind of worsens the overall

34:45swelling within the sinuses and the

34:48nasal cavity. So again that swelling is

34:49in which tissues the sinuses and the

34:52nasal cavity they get super super

34:54swollen. The other component here is

34:56that the cytoines trigger the neutrfils

34:59to come to the area. So again these

35:01cytoines also pull

35:04neutrfils

35:06out into this area to come and fight.

35:07They say all right time to fight guys.

35:09When the neutrifils get out here the

35:11neutrfils they basically release a bunch

35:13of different types of like proteases and

35:15all different types of things. And these

35:18neutrfils are basically going to turn

35:20this mucus when they start fighting and

35:22kind of trying to destroy these

35:23bacteria.

35:25Basically what happens is it turns that

35:28mucus into more of a dead pus exa

35:33exudative type of like debris.

35:35Essentially what happens is after all of

35:38this starts to take place it converts

35:40this mucus into more of a mucco

35:44perent

35:47discharge.

35:49And some would argue that that's not

35:51always the case, but this is kind of

35:54just explaining the pathophysiological

35:57mechanism is if you bring in lots of

35:59neutrfils into a tissue, this is going

36:01to cause more of that exudative type of

36:04effect. And so the reason why I say that

36:06is that then this mucopirulent discharge

36:09is going to cause them to really drain

36:11out of the sinuses and the nasal cavity.

36:13So the perulent discharge is really

36:16maybe screaming more of the bacterial

36:18picture than the viral picture, but

36:20that's not always perfect. The other

36:22thing is that they'll have significantly

36:24more swelling than the viral picture

36:26will. And so technically you would say

36:28the pain and the pressure would be worse

36:31as well. So the reason why I'm telling

36:33you this is that if you have the

36:35mucopulent discharge in this particular

36:38scenario for bacterial that's one thing

36:42the swelling we could theoretically

36:44argue that it increases the pain and the

36:48pressure factor

36:50increases the pain and the pressure

36:52factor and if I increase the pain and

36:55the pressure that may scream more of a

36:57bacterial picture not perfect but it

36:59could there's one other thing that I

37:02will say

37:04in all of these inflammatory reactions

37:06cytoines are released

37:09and usually bacterial rhinocyitis when

37:12these cytoines get out into the

37:13bloodstream there's another thing that

37:16happens what do we know about cytoines

37:17theoretically these cytoines

37:21not only kind of alert the immune system

37:24not only do they cause vasoddilation but

37:26they also precipitate

37:29a fever

37:31And so that is one really important

37:33thing about these cytoines is that when

37:34these cytoines get into the bloodstream

37:36especially things like interlucan one

37:37tumor necrotic factor alpha they go to

37:40the we've done this lecture so many

37:42times you guys know this already the

37:44hypothalamus they turn up the thermostat

37:46and the patient starts to present with a

37:49fever. You can still get this in the

37:51viral picture. It's just not going to be

37:53as severe. So that's why patients who

37:55have more of that higher kind of like

37:57fever, they have significant pain and

38:00pressure and that mucoperulin discharge

38:03is another potential factor. It screams

38:06more of the bacterial thing. But here's

38:08the thing, a lot of people would argue

38:10that is not really the way that we think

38:12about acute bacterial. The way that we

38:15think about acute bacterial is the

38:17timeline. Yeah, guess what? In viral you

38:21could have mucoperin discharge. In viral

38:22you could have a lot of pain and

38:24pressure. In viral you could have a

38:25fever especially things like influenza

38:27and COVID. So is that a good argument?

38:29Not really. The best argument is that

38:32viral is self-limited and it should go

38:34away. With bacterial it may not go away

38:38and so it does not

38:42improve

38:46in less than 10 days. Oftent times it

38:48extends. There's another argument though

38:50too. So, not only is it just in less

38:52than 10 days, but you know, I often said

38:54that viral infection sets the stage.

38:56Well, viral infection usually it gets

38:58better pretty quick, probably in a

38:59couple days. So, if a patient had an

39:01initial viral infection that then caused

39:04a superimposed bacterial infection and

39:06let's say that this was it's getting

39:07ready to go away by day four and five,

39:09what would you see? You'd see an

39:10improvement because the viral infection

39:12is resolving. And then you you would

39:15think, oh, it was viral. And then what

39:16would happen is the bacteria would

39:18eventually start to cause things to get

39:19worse to catapult up to catapult up and

39:21you would see them get worse again. So

39:22what we see is is not just in a lack of

39:25improvement in 10 days some patients

39:27especially with this viral co- infection

39:29another option is so we'll say this or

39:33or

39:35they have what's called a double

39:38worsening.

39:42All that means is is they originally

39:46they had symptoms

39:48initially they got better and then they

39:50had a spike in their symptoms again.

39:52Right? So within that 10day time frame

39:54essentially if I were to do like a graph

39:56let's say here here is kind of like

39:59here's time right and here's their

40:02symptoms. What we would notice is is

40:04that you would see that their symptoms

40:06would start off and then it would get

40:08better and then all that would happen is

40:11it would get worse. Right? That's that

40:13double worsening type of presentation is

40:15they would have the symptoms, they would

40:17get better and all of a sudden they

40:18would again get worse. That's classic

40:20for acute bacterial rhinocyitis.

40:24Okay, I think we really like hit this

40:27one pretty hard. So let's let's move on

40:29now and talk about the next component.

40:32The next component here is fungal.

40:34Fungal is uh it's it's a son of a gun.

40:36Like I told you, it's pretty rare. So

40:38when a patient comes in, they present

40:39with facial pain, pressure, they present

40:41with nasal discharge, they present with

40:43congestion,

40:45um maybe some hyposmia. And the way that

40:48you really have learned to differentiate

40:49viral from bacterial is really more

40:51particularly on the lining of symptom

40:54duration, right? Less than 10 days. If

40:57it's not improving in 10 days or they're

40:59double worsening or they theoretically

41:00have a high fever, pain and pressure

41:02that's not going away, you could make

41:04that argument. Fungal, dude, this is

41:06this is the one where you'll be able to

41:08see it. It's it's blaringly obvious in

41:11this scenario when it's invasive. There

41:13is two different types of fungal

41:15species. Um but I would argue that the

41:18um the risopus is going to be the more

41:21aggressive one. So there there is two.

41:22I'll I'll write it out. can have things

41:24like um for example, you can have

41:26aspergillis.

41:29This this can cause it. I'd say it's not

41:32going to be as aggressive and it can

41:34even occur in patients. They can have

41:35what's called an allergic like a fungal

41:38rhinocinitis due to aspiggil spores. The

41:40more common one is the riseus

41:44and riseus essentially I'm going to

41:46write this out. It causes something

41:48called mucor

41:50micosis. So, this might start ringing a

41:52bell. You guys might have heard about

41:54this in class. Mukor micosis. This stuff

41:57is This stuff is just absolutely insane.

42:00These fungi right here, they're pretty

42:02aggressive, right? So, aspiggillos can

42:05definitely cause some type of an

42:07invasive picture, but it's not going to

42:09be as is the one I really want you to

42:11associate it with. The one I really want

42:12you to associate it with is going to be

42:14more the risopus.

42:17Now, there's one other thing. This

42:20doesn't happen in everybody. People

42:22become exposed to fungal spores all the

42:24time. So these these fungal spores I

42:27need uh my orange marker.

42:30All right, I have an orange marker here.

42:32>> I got you. [laughter]

42:36>> Thanks, man. The next component here is

42:39whenever you have patients who have

42:40rises

42:42mucor micosis, we're exposed to fungal

42:44spores all the time, right? So these

42:46things basically could be within the

42:48airways, they could be within the

42:49sinuses, you could have them there,

42:52right? But immunompetent

42:55individuals clear these things. All

42:57right, that's the key. So you got to

42:59find this in a person who has a specific

43:01risk factor. Acute viral can happen in

43:03anybody who just got exposed to someone

43:04sneezing a coffin on them. Acute

43:06bacterial can happen if they got a viral

43:07infection. They don't have to be immuno

43:09compromised, anything like that. This

43:12patient has to have something that puts

43:13them at risk. And that's what I want you

43:14to look for in the clinical vignette or

43:15in their history. And so there's two

43:18scenarios for this one. The risk factors

43:21that really put a patient into this

43:23bucket is two. One is diabetic keto

43:27acidosis. And that's the one that I

43:28really want you to associate this with.

43:30The other one is any type of amuno

43:35suppression. And oftent times on the

43:37exams they use things like neutropenia

43:41as an example. So this is another one to

43:43look for. So don't forget that one. But

43:45again, the particular risk factors that

43:48make a patient get something like this

43:49because again, you are exposed to this.

43:52This is a natural thing. It can find its

43:54way into the nasal cavity, find its way

43:56into the sinuses. It's there. It's just

43:59if you give it the perfect opportunity.

44:01Yeah, you heard that term opportunity.

44:03So they're more likely to be

44:04opportunistic infections. If you give it

44:07the opportunity with this, the risk

44:09factors, it will do what it needs to do.

44:11So let me explain why this happens

44:14in DKA which is the most important one.

44:18This is really the thing that is going

44:20to drive this right. So this is the the

44:23particular thing. So let's actually take

44:24this into consideration. What uh happens

44:27here is um let's actually just bring DKA

44:29over here. In patients who have DKA

44:32the big thing I want you to remember is

44:35that it obviously causes acidosis.

44:38So it's going to cause acidosis, but

44:40you're also going to have a patient have

44:41high glucose levels. So this is going to

44:43be the things you have acidosis, and

44:45that's usually due to the ketone bodies,

44:46and you have high amounts of glucose.

44:49So this high amounts of glucose and

44:50acidosis, they really they create some

44:53dang problems.

44:55One of the things that happens here is

44:58acidosis. Essentially, what it does is

45:01is you have a protein, it's called

45:03transferin, right? There's a protein

45:05here called transferin. That's really

45:07the the thing I want. I'll put a little

45:08hole in there. What do you think that

45:10hole that transfer holds on to?

45:13Don't don't say trans or something like

45:15that. It holds on to iron, right? So

45:17transferin holds on to that iron. Now,

45:20whenever a person has and I want you to

45:22remember this person has an acidotic

45:25scenario, that iron is going to be

45:28liberated. The transfer kind of like

45:29disassociates from it. And so you're

45:31probably like, "Zack, do I really need

45:33to know this?" Probably not, but I think

45:34it's cool. [laughter]

45:35It's going to release the iron. And now

45:39I have these high levels

45:41of free iron. When iron is free, guess

45:44who loves iron?

45:47Come on. I'm I'm I'm setting you up here

45:49to spike this thing risopus. And so now

45:53this creates an opportunity to do what

45:55to that actual this fungus. This thing

45:58starts growing like crazy. And so now

46:01you take this thing and it starts bop

46:03bop bop bop. And now all I did was I

46:07just made this thing proliferate.

46:10And that's what iron really does is it

46:11creates the perfect kind of like medium

46:14for fungal growth. And now I got a

46:17fungus growing like crazy.

46:20Now here's the next component.

46:23Not only does the acidosis make the

46:25opportunity for the fungus to become

46:27more intense by growing, but the glucose

46:31and the acidosis increase the expression

46:33of different receptors, which is crazy.

46:36So whenever you have high glucose and

46:38acidosis, it increases the expression of

46:41receptors on epithelial cells and

46:43endothelial cells. So that's what's the

46:44next thing is you're going to have

46:46increased. So I have this increased

46:47glucose, it increases expression of

46:50receptors. So now here you're going to

46:53have increased expression

46:56of

46:58epithelial

47:01receptors and you're going to have

47:03increased expression

47:07of indo and you're probably like dude I

47:09don't why is all of this that important

47:11to talk about? I promise we're going to

47:13get there. When we have all of this

47:16increased expression, you then create an

47:19opportunity because on that fungus, it's

47:21got a little receptor, a little protein

47:22that it needs to click into these. If

47:25you give it a gateway, a door, it will

47:27come in. So the glucose, that high

47:30glucose increases the expression of

47:31these things. So now I have two of these

47:33things and I'm opening up two doors. One

47:36is for the fungus to bind here, then

47:39travel, and then get here, and then

47:42guess what it does? it travels into the

47:45blood vessel. So this thing is going to

47:48be getting into the blood vessel. Why is

47:50that a problem? Because now we have

47:52something called angio invasion.

47:55[clears throat]

47:56Now when I have all of this fungi

48:00in the blood vessel and we triggered

48:02something called angio invasion, guess

48:04what this fungus does? The fungus then

48:07starts triggering clotting cascades.

48:10And now what happens is this fungus gets

48:12here it under goes what is this called

48:15again? When it gets into the blood

48:17vessel this is called angio invasion.

48:18Let's actually write that out. So what

48:20happened here? We triggered something

48:21called angio

48:23invasion. It invaded the blood vessels.

48:25That's all it means. Use these receptors

48:27to get to the blood vessels. Right? Then

48:30once in here it then triggers the

48:32clotting cascade and then you get clots

48:35that start to form here.

48:37So then we're going to cause this fungus

48:39will then lead to an increase in we'll

48:41just call thrombosis.

48:43We'll say it causes thrombosis of these

48:46vessels. And where where is all of this

48:47occurring dude? In the nasal cavity and

48:50in the sinuses. All of this is happening

48:51in the vessels that are surrounding the

48:53nasal cavity and the sinuses.

48:55If I have thrombosis now so this thing

48:58causes a clotting cascade, right? Which

49:01leads to thrombosis. The next thing here

49:04is that blood is supposed to move to

49:06particular tissues. And as blood kind of

49:08runs through here,

49:11it's going to come into contact with

49:13this this clot and it's going to make it

49:16harder

49:18for oxygen to get to the tissues beyond

49:21it. [snorts] And so what's going to

49:22happen is this patient is going to have

49:24decreased O2 delivery. That's going to

49:28lead to eskeeia.

49:30And eskeeia is going to lead to

49:33necrosis.

49:35Now, here's why I'm mentioning all of

49:36this.

49:38This fungus led to thrombosis. So, it

49:42stimulates thrombosis. That then drops

49:44O2 delivery. That then increases

49:46eskeeia. That then increases necrosis.

49:48Necrosis of what tissues? The sinus

49:52cavities and the nasal cavities. So now

49:54I'm going to have necrosis of again

49:56which tissues of sinuses

50:01and the nasal cavity. And boy oh boy

50:05that sounds absolutely horrific. So now

50:08let's pretend here for a second we're

50:09going to have all of this happening in

50:10these blood vessels. So here here's all

50:12these blood vessels that are going to

50:14the the actual nasal cavity like your

50:15turbineates for example and then going

50:17to the sinuses.

50:19All of these, the fungus got its way

50:23through the mucosa into the actual blood

50:26vessels and caused them to claw off.

50:28Let's draw like little dots here. Here's

50:31a little dot there, a little dot there.

50:34We'll see. There's one here, one there,

50:37one there, one there, one there. You're

50:39blocking all of these off. If that

50:42happens, you can't get oxygen. All of

50:44these start to undergo necrosis. And I'm

50:47going to draw that with this black

50:48tissue. So now all of this is going to

50:49undergo gangrous necrosis and it's going

50:52to be all over the turbineates. It might

50:55get over the septum. It's going to be in

50:57the nasal cavities. I mean I'm sorry in

50:59the sinus cavities. Dude, this is

51:01absolutely horrific. Right. The problem

51:05with this is two things. One is can you

51:09imagine if I have all of this necrotic

51:11tissue, I would definitely be able to

51:13see this, right? 100%. When you look

51:16into someone's nasal cavity, the first

51:18thing that you'll notice is these things

51:21called black escars. So you'll see these

51:24like black

51:26necrotic

51:28escars

51:30and that's all because of this process.

51:32It's going to be over the turbineates.

51:33It's going to be over the septum. You're

51:35going to see that. The other thing is

51:37there's blood vessels. Dude, imagine

51:41I cause all this necrosis and I eat away

51:44at some of these vessels. What could I

51:47potentially have an opportunity for? If

51:49I erode into a nearby vessel, that

51:52erosion will then cause this vessel to

51:54startot

51:57toots and you're going to end up with

52:00epistaxis.

52:02That's why I wanted you guys to

52:04understand this. So the necrosis can

52:06then cause necrotic escars over the

52:09turbinates the septum all over the dang

52:11place but also they may come in

52:13presenting with epistaxis

52:19that's why I really wanted you guys to

52:21understand this right so when I talk

52:23about a patient coming in who says I got

52:25man I got the facial pain pressure I got

52:28congestion man can't smell nothing I got

52:31discharge and then all of a sudden you

52:33look in their nasal cavity. They say,

52:34"I've been having some nose bleeds." And

52:36then you look up, you say, "Uhoh,

52:38there's necrotic escars." You look at

52:40their history, it says, "Oh my gosh,

52:41they're diabetic or they're immunos

52:42compromised." That is an emergency. This

52:45patient will get very, very sick and

52:47have disfigurement if you don't get to

52:49the bottom of this. The crazy thing, and

52:51I don't I can't imagine how these fungi

52:53get this ability. This thrombosis is

52:55protective.

52:57Think about this. If I have all these

52:58thrombi, basically what happens is all

53:00these thrombi kind of wall off. that

53:02kind of blocks drugs from getting to the

53:05fungi. They're smart. And that's why

53:08sometimes guess why the only way that we

53:10can kind of like stop this necrosis from

53:11spreading we got to cut it out and

53:13debride it. That's why this is so

53:14aggressive. And the reason other thing

53:17component here is that since this

53:18necrosis is so aggressive, guess what it

53:21can do? This is one of the most likely

53:24types of infections for it to spread

53:26beyond the sinuses, spread beyond the

53:29nasal cavity. So this one can easily

53:32easily spread. So what I want you to

53:34remember is this has the highest

53:37risk

53:42of we call it syonesal spread

53:48and we'll get into that when we get into

53:49the complications. And so that's what I

53:52really want you to think about is

53:53because this thing can cause so much

53:54aggressive necrosis, this thing can very

53:57very quickly spread outside of the nasal

53:59cavity, outside of the sinuses to your

54:01orbit, to your brain, to your bones, and

54:04that's what makes this one uh not

54:05delicious, dangerous. All right, you

54:08guys get the point for this one. That's

54:09what I want you to take away with this

54:11one. Usually you're going to have need

54:13this presence, which I kind of explained

54:15how that comes into play. The biggest

54:16thing if you don't remember all that is

54:17that it gets into the vessels, clots

54:19them, causes necrosis and you get these

54:21necrotic escars. It can erode into the

54:23vessels and cause epistaxis and it can

54:25spread very very quickly. All right, we

54:29hit the acute ones. You're like, dude, I

54:31I I I just wanted to know about sinus

54:33infections. I didn't need to know all

54:34this this stuff. I promise it'll come

54:37into play. We make better clinicians

54:38when we understand things, I believe.

54:41So, chronic rhinocyitis, we're now at

54:44the other end. This is a patient who's

54:45been dealing with this for a while.

54:46They've been dealing with those symptoms

54:47that we talked about for a bit.

54:51We said that in these patients really

54:52what it comes down to is knowing if they

54:54have polyps or not. That really helps

54:56you to distinguish potentially the

54:58underlying cause. It also helps you to

55:00distinguish like really what would be

55:01the best treatment. So for those who

55:04don't have polyps, usually the cause of

55:06this is it's usually twofold. And what

55:08do I mean by this? Chronic rhino

55:11sinusitis

55:14in its own entity is not an infectious

55:16eeteology

55:18which you're probably like wait what why

55:19are we talking about this an infectious

55:20disease bro it's not only an infectious

55:23eeology usually it's a chronic

55:26inflammatory condition and so in this

55:29scenario we have patients who have

55:31certain types of abnormalities one is

55:34maybe they have something which is like

55:36super rare but it's called cona

55:39Bossa

55:41and I told you guys something. There was

55:44the most important turbineate or the

55:46most important concha where a lot of

55:48those sinuses empty in. Do you guys

55:49remember which one it was? It was just

55:52beneath the middle turbineate or the

55:54middle conce.

56:00So that's what we call conchoa. It's

56:01like it's like pumatization essentially

56:03of it. It's it's pretty rare. It's not

56:05super con. And I know you're probably

56:06like, "Oh, why am I talking about it?"

56:08But you get a very interesting component

56:10here. And patients who have this

56:13concha

56:16blossa.

56:18You see here that they have this large

56:22middle conche. And what is it doing at

56:25that osteomal complex? It's leading to

56:29blockage. So, it's blocking

56:33the osteomal complex, which is going to

56:35do all that stuff that we talked about.

56:37It's going to lead to a buildup

56:41of mucus.

56:44And then what happens is the buildup of

56:45mucus allows for bacteria that do live

56:47in those areas to start to grow, but

56:49they cause these things called bofilms.

56:52So, you get what's called bacterial

56:54bofilms, and usually it's things like

56:55staff orius, and that's also the

56:58contributors. So that kind of just

57:00worsens the overall inflammation. But

57:02you get the point. The contraosa does

57:04what? It kind of narrows this opening.

57:07And if you narrow the opening, you kind

57:08of affect the drainage pathway, right?

57:10So this drainage pathway is blocked. By

57:14doing that, we already talked about

57:16this. You block that, you build up the

57:18mucus and you can cause bacterial

57:20bofilms, which then leads to

57:22inflammation. And that's where we get

57:23the chronic rhinocinitis. Right? So

57:26that's one component here. So it's

57:28usually a combination of some type of

57:30anatomical obstruction

57:33and a bacterial biophilm which is most

57:35often which one if you had to remember

57:38one it's usually staflacccusarius but I

57:41don't I don't want you guys to go too

57:42crazy on this because I really want you

57:43to more associate because you'll find

57:45something interesting chronic rhinocitis

57:46if it was an infection what would we

57:48treat it with antibiotics chronic

57:50rhinocitis we don't really treat with

57:51antibiotics we treat with steroids

57:53oftent times or surgical procedures or

57:55saline irrigation we don't give them

57:56antibiotics unless they have acute

57:58exacerbation on top of their disease.

58:00That's why it's important.

58:02Another one is going to be a deviated

58:06septum. So, a deviated septum.

58:11Now, over time, when you have chronic

58:13inflammation, what's a natural reaction?

58:14Just a just out of adding a little

58:16component here. If you have chronic

58:18inflammation, what does it lead to?

58:19Fibrosis. And sometimes over time, these

58:21patients will develop some kind of

58:23fibrodic reactions.

58:25with deviated septum. Think about this.

58:28Let's say that I have this, and again,

58:29I'm kind of skewing my my my diagram

58:31here for a reason, but let's say that I

58:33had someone, you know, they got conked

58:34in the nose. They caught like a, you

58:36know, a good old hook from Floyd

58:38Mayweather or, you know, I don't know,

58:40Mike Tyson, they took one right to the

58:42right to the noggin, right on the nose,

58:44and they popped that septum. They

58:46deviated the septum. And now this

58:48thing's more curved than most people's

58:50toenails. In that scenario, what is it

58:52doing? It's blocking the osteomiatal

58:55complex. If you block the osteomiatal

58:58complex, are you going to allow for the

59:01drainage?

59:03No. If you don't allow for the drainage,

59:05what happens? Mucus builds up. Bacterial

59:07bofilms that contain staff orius builds

59:08up. You cause inflammation over time.

59:10That leads to fibrosis. And that's what

59:12makes it hard for you to ever come back

59:14from. So you guys are getting the point

59:16here, right? That with this one, it's

59:17the same thing. It's an anatomical

59:19obstruction. But both of them are going

59:23to be possibilities.

59:25But usually this is associated with

59:28these two things. So we'll do this.

59:30We'll put or

59:33plus

59:35bacterial

59:38bofilms. The last component here is you

59:40get a deviated septum or you get

59:42concoalosa. You block the oatal complex,

59:44build up mucus, you cause bacterial

59:45bofilms. That combination leads to

59:47inflammation. The biggest thing here is

59:48that over time that inflammation can

59:50possibly lead to fibrosis and that will

59:54then make this a little bit more hard

59:56for a patient to ever kind of get better

59:58from. All right, so that's the plus or

59:59minus is that over time you may start to

1:00:02experience some fibrosis and that

1:00:04fibrosis that's what really makes this a

1:00:06little bit more of a challenging

1:00:07picture. If I start to get really really

1:00:09fibrodic tissue here, it makes it to

1:00:11where a lot of things are going to be

1:00:13hard and we're going to possibly need

1:00:15surgical interventions. These are ones

1:00:17that would respond very well to a

1:00:20surgical intervention. If a patient has

1:00:21a deviated septum and they have a conco,

1:00:23you could go in and actually surgically

1:00:25fix these things. But you want to get to

1:00:27it before they get to that fibrodic

1:00:29process. All right.

1:00:31Chronic rhinocyitis with polyps. This

1:00:35one's it's very interesting. Usually in

1:00:38this scenario, this is patients who have

1:00:41the best way of saying it is they got

1:00:42like immune systems that are a little

1:00:44bit ADHD. All right. So, for example,

1:00:48couple scenarios here is I would think

1:00:49about this in what's called AERD.

1:00:53This is basically aspirin exacerbated

1:00:56respiratory disease. Another term for

1:00:59this um we call it the SERS triad if you

1:01:04really want to remember this one. And I

1:01:06think it is actually helpful because

1:01:08it's kind of it's kind of cool. So, the

1:01:10Sampers Triad, do you guys remember

1:01:12this? Let's see if you guys remember

1:01:13this. So Sanders triad

1:01:16is consisting of three particular

1:01:18points. What is that? One is you have a

1:01:22patient who has asthma, you have a

1:01:26patient who has aspirin sensitivity and

1:01:30I'll explain what this means in a

1:01:31second. And the last thing is you have a

1:01:34patient who has polyps and usually these

1:01:36are nasal polyps. That's called your

1:01:37Stor triad. A lot of this triad is built

1:01:41upon the pound built upon the foundation

1:01:44of like a metabolic defect and an

1:01:48overactive immune system. Another

1:01:51eeology besides this one is usually some

1:01:54type of fungus. So usually this is where

1:01:57we talk about aspiggilis. So aspergillis

1:02:00it actually does have fungal spores and

1:02:02it basically creates these kind of like

1:02:05essentially like an immune reaction. Let

1:02:06me let me explain what happens here.

1:02:09in these patients who have uh this kind

1:02:12of samp aspirin does let's go back and

1:02:14remind ourselves aspirin

1:02:17basically does what? So we have these

1:02:19pathways right? So you have what's

1:02:20called um we can actually remember it

1:02:22like this we have arachidonic acid and

1:02:24eventually you get something called

1:02:26lucatryins and you get something called

1:02:27prostaglandins right and this is kind of

1:02:30the basic simple reaction. So going to

1:02:32lucatryins is the lipooxygenase going to

1:02:34the prostaglandins is the cylo oxygenase

1:02:37right? So here is the cox enzymes and

1:02:40here is the lipo oxygenase enzymes. When

1:02:43you give someone aspirin, right, and

1:02:45they also have an underlying history of

1:02:46things like asthma, you also increase

1:02:48the risk of polyps, the concept behind

1:02:51this is that aspirin basically is going

1:02:54to kind of like inhibit these patients

1:02:57COX enzyme. When you inhibit the COX

1:03:00enzyme,

1:03:02basically you shut down this pathway.

1:03:04And then what happens is arachidonic

1:03:06acid, if it can't get pushed into this

1:03:08pathway, it gets pushed hard into this

1:03:11pathway. And lucatrien are some nasty

1:03:14little son of a guns that in patients

1:03:15who have any kind of like sensitive

1:03:18immune system especially if they have

1:03:19things like underlying asthma whatever

1:03:21it may be they are super super sensitive

1:03:25and so here's what I want you to

1:03:26remember patients who have things like

1:03:28for example the aspirin exacerbated

1:03:30respiratory disease they get exposed to

1:03:33things like aspergillis

1:03:35uh fungal spores

1:03:38we have immune system cells one is

1:03:41called your tea helpper er two cells and

1:03:43the other one are called your innate

1:03:44lympoid cells type two. I don't go

1:03:46crazy. All I want you to know is they

1:03:48got some super sensitive immune system

1:03:49cells. All that happens here is that

1:03:52these things are really like a pretty

1:03:53intense trigger. And this basically

1:03:56through things like lucatryins or things

1:03:58like aspiggillospores, you create kind

1:04:00of immune reactions that activate these

1:04:02cells. When these cells are activated,

1:04:05they do two things. One

1:04:08is they both pump out something called

1:04:12interlucan 5 and interlucan 5 is a very

1:04:17powerful stimulator of who are these

1:04:19cool dudes with their ray bands? These

1:04:21are your eocinophils.

1:04:24These are eocinophils, right? So what

1:04:27the interlucan 5 does is it really helps

1:04:30to activate eosinaphils. eosinaphils,

1:04:33dude, these things are like they don't

1:04:34they don't play no games. They ain't

1:04:36around here to play no games. And they

1:04:38come to these cells basically

1:04:41and they they just release things like

1:04:43major basic protein and all of that and

1:04:45it causes basically a lot of an

1:04:47inflammatory reaction.

1:04:50All right. So you're going to get a lot

1:04:51of inflammatory reactions. The concept

1:04:52behind this is that you want eosinaphils

1:04:54to fight against things like fungus and

1:04:55and patients who have like some type of

1:04:57like hyperimmune uh inflammatory

1:04:59responses, things like aspirin,

1:05:00exacerbated respiratory diseases,

1:05:02eosinaphils are very very heavily

1:05:03involved. Usually these patients have

1:05:05high eosinaphil levels that causes a lot

1:05:07of destruction to the actual mucosal

1:05:09tissue. So what do I get? I get mucosal

1:05:15tissue

1:05:17injury.

1:05:19The other component here is it also

1:05:22releases something

1:05:24another cytoine

1:05:26called interlucan 13.

1:05:30And interlucan 13 does two things.

1:05:34One I'm not going to get too crazy about

1:05:36but you know we have these things called

1:05:37goblet cells and goblet cells they

1:05:40respond very very nicely to interlucan

1:05:4213 and one of the things that it will do

1:05:44is it'll increase

1:05:46your your mucus production right so

1:05:48whenever you have lots of interlucan 13

1:05:51it will increase mucus production but

1:05:54that's not the big thing I want you guys

1:05:55to focus on the thing it also does

1:05:57besides this here I will you know what

1:05:58heck I'll add it in it will stimulate

1:06:00mucus production but the other thing I

1:06:01really want you to know is its comes

1:06:03here and it makes the vessels that are

1:06:06going to that damaged mucosal tissue

1:06:09really leaky. When it gets leaky,

1:06:14all this fluid

1:06:16and exudate

1:06:18and eocinophils

1:06:21start leaking out of the vessels into

1:06:24this sub mucosal space. So, I'm going to

1:06:26have fluid. And what other kind of cells

1:06:27am I going to have here? I'm going to

1:06:28draw them in red. What other kind of

1:06:30cells? I'm going to have eocinophils.

1:06:32They're going to be all up in this dang

1:06:34thing, right? What's going to happen is

1:06:37that this sub mucosa starts kind of

1:06:38getting bigger and bigger and bigger and

1:06:41bigger and eventually you start lifting

1:06:43this thing up and up and up and it's

1:06:44just it's just boop boop and eventually

1:06:47this is what ends up forming. You kind

1:06:50of bubble off

1:06:53the mucosa

1:06:56and then it kind of forms this like

1:06:57little bubble. All of this is that fluid

1:07:01and eocinophils. Isn't that cool? Ain't

1:07:03that cool? Come on. You know it is. So

1:07:05all of this is all that fluid.

1:07:08And what else is in there? The

1:07:10eosinaphils.

1:07:11And they're kind of they're poking out.

1:07:13It's like a hemorrhoid in the nose. What

1:07:15is this thing? That's a nasal polip. So

1:07:18you get the point here. The big thing I

1:07:20want you to remember is that in patients

1:07:22who have things like maybe they have

1:07:23allergies or ex this really critical

1:07:26thing for the exam is the samp triad or

1:07:28they have aspiggilis fungal spore

1:07:30exposure. The big thing here is that

1:07:32usually polyps are most often associated

1:07:34with kind of an eocinophilic allergic

1:07:36type of reaction and that pushes these

1:07:39cytoines to bring fluid mucus and on top

1:07:43of that eocinophils into the tissue and

1:07:45bubble out to the mucosa creating

1:07:47polyps.

1:07:49If that polip bulges out there, think

1:07:53about this. Come on. What is it doing? I

1:07:57want you to think for a second. This

1:07:58polip is bulging out,

1:08:02right? What's it doing? What is it

1:08:04blocking the osteomiatal complex? You

1:08:07guys, this is this is like I think the

1:08:09foundation of it, right? Is that it's

1:08:10going to block the osteomatal complex

1:08:14and and I don't need to go through it.

1:08:15I've done it like 3,000 times already

1:08:16that at this point we understand that by

1:08:18blocking that osteomatal complex you

1:08:20create mucus buildup [snorts] you create

1:08:22inflammatory bofilms and you create an

1:08:25an opportunity for chronic rhinocinitis.

1:08:28The reason why I say all of this is that

1:08:31because in these conditions they're

1:08:33going to respond really well to shutting

1:08:35down inflammation like with what

1:08:37steroids.

1:08:39Steroids are going to be really good for

1:08:40these sometimes if they get too big

1:08:42where they're literally ball valving

1:08:43this thing. What you have to do

1:08:45sometimes though you may have to cut

1:08:46those polyps out because we don't want

1:08:48to block the otoal complex but if you

1:08:50can get steroids to shrink the

1:08:51inflammation down you may be okay that's

1:08:53why this is not really an infectious

1:08:55disease in its own it's kind of like a

1:08:57superimposed bacterial bofilm on chronic

1:09:00inflammatory conditions I don't want to

1:09:03go too crazy but I don't want you guys

1:09:04to forget that chronic rhinocyitis also

1:09:07especially for the exams I want to add

1:09:09this last little tidbit don't forget

1:09:12that this can be it just doesn't fit

1:09:14into the definitions that we talked

1:09:16about it with. It is also associated

1:09:21and I think it's really cool to

1:09:22understand this. It's associated with a

1:09:25condition called cystic fibrosis. And

1:09:28this should make perfect sense. What

1:09:29does cystic fibrosis do? It makes mucus

1:09:32thick. If you get lots of thick mucus

1:09:34that block off the osteomatal complex,

1:09:36what's going to happen? It's the same

1:09:38concept. Another one is

1:09:42primary siliary diskynasia. What is

1:09:45primary silary diskynesia?

1:09:47It's basically you see these thingies

1:09:49here, these pseudoratified epithelial

1:09:50cells, they have celia. They don't work.

1:09:55If they don't got cyia that work, can

1:09:56you beat mucus out of the sinuses? No.

1:10:00The whole point I want you to associate

1:10:01with these is that these cause blockages

1:10:04of the otoal complex, but it's not

1:10:05through a polip. And it's not well

1:10:08that's not true. Cystic fibrosis can

1:10:09cause polyps if I want to be particular

1:10:11but it's not via a polip and it's not

1:10:14via some type of anatomical obstruction.

1:10:16It's usually a lot of mucus blockage. So

1:10:19that's the one thing I want to add is

1:10:20that these do that particularly through

1:10:22which type of concept is that cystic

1:10:24fibrosis or primary diskynesia? They

1:10:28cause a mucus blockage.

1:10:32And I think always on the exam if you

1:10:35want to remember this primary silary

1:10:37diskynesia they'll present it one

1:10:39particular way. They'll say that you

1:10:41have a young child who has a bunch of um

1:10:45uh who has chronic rhinocyitis

1:10:48and on top of that their heart is

1:10:50flipped to the other side. So they have

1:10:53situs inversis and they have

1:10:56bronchiacttois. That's the things I want

1:10:58you to remember for primary silary

1:10:59diskynesia. There's something a triad

1:11:01called cardigan's triad which is you'll

1:11:03have a patient a young child who

1:11:04presents with chronic rhinositis

1:11:06bronchiacttois and a flipped heart. All

1:11:08you have to see is the flipped heart and

1:11:10it'll make you think about this one.

1:11:11Oftent times with a lot of these if it's

1:11:13viral usually it's self-limited goes

1:11:15away. In certain scenarios like pretty

1:11:18like heavy bacterial rhinositis or an

1:11:22especially acute invasive fungal

1:11:24rhinositis. stuff can spread outside of

1:11:27the sinus, outside of the nasal cavity

1:11:30and that's where we start seeing some

1:11:31problems. So for example when we talk

1:11:34about these osteomiitis it's not

1:11:36something I would always see but I would

1:11:38see it for the exams with um especially

1:11:41frontal sinusitis. So, think about this

1:11:44here. Let's say that you have a patient

1:11:45who has some infection, some

1:11:48inflammation

1:11:49of their frontal sinuses. And again,

1:11:51it's supposed to kind of basically drain

1:11:54out right into the nasal cavity. You get

1:11:56a lot of inflammation, you get mucus

1:11:57build up, you get bacteria. All right,

1:11:59cool. What can happen? Well, one of the

1:12:02things here is that this can spread. I

1:12:04mean, think about this. The sinus is

1:12:06just a hollow cavity sitting in a bone.

1:12:08What bone? The frontal bone. this a

1:12:11hollow cavity sitting inside of a bone.

1:12:13It's the sppheninoid bone. So when

1:12:15patients get infection of that sinus,

1:12:17all it has to do is literally just

1:12:20spread to the bone. And whenever you

1:12:23spread to the bone, that's when you

1:12:24start getting an infection

1:12:27and inflammation of the bone tissue. And

1:12:31so that's really the difference is all

1:12:33that's really happened is you had

1:12:34pathogens that spread

1:12:40from where?

1:12:42From the sinus

1:12:46to the bone tissue.

1:12:48Now here's here's the thing I would add.

1:12:52oftentimes when you get infections that

1:12:55really are spreading into the bone. The

1:12:58downside to this is that this will

1:13:00definitely intensify the pain. Right?

1:13:02So, a couple different kinds of clinical

1:13:04signs that I would be looking out for.

1:13:06So, if I were to be looking out for what

1:13:08kind of clinical kind of presentation

1:13:10would really make me even think about

1:13:12this? Well, the first thing I would add

1:13:17is I would see that the patient would

1:13:18have an increase in pain. Right?

1:13:20Whenever you cause that kind of

1:13:21involvement of the bone, the bone is,

1:13:23you know, it's innervated and it's also

1:13:25going to be one of those that it doesn't

1:13:26allow for a lot of expansion very much.

1:13:29And so, you're going to definitely see

1:13:30an increase in the pain. That's

1:13:34definitely going to be pretty obvious,

1:13:35right? The other component here is that

1:13:38this is a bacterial infection. Whenever

1:13:40you get bacterial infections, what do

1:13:42they do? Well, they cause tissue damage.

1:13:44What's the response to that tissue

1:13:46damage? Well, one of the things is that

1:13:48this will then lead to cytoine release.

1:13:51And what kind of cytoines? Well,

1:13:52whenever you have an infection of a

1:13:53tissue, you really amplify things like

1:13:55interlucan one. You amplify things like

1:13:57tumor necrotic factor alpha much more

1:14:00than in the sinuses. And so, what would

1:14:02you also start to expect? You might

1:14:04start to see things like an increase in

1:14:06their white count and a fever. And so,

1:14:09that high amount of that cytoine storm,

1:14:11it can really push up what kind of

1:14:13things? it can push up their white blood

1:14:15cell count and it can also drive up a

1:14:18fever. So if I have a patient whose pain

1:14:21is more intense in the localized area

1:14:23especially the frontal bone and then I

1:14:25look at their kind of lab work and I

1:14:27find that they have an increase in their

1:14:28white blood cell count an increase in

1:14:30their fever that may make me a little

1:14:32bit more concerned. There's one other

1:14:34thing though and this is I think the the

1:14:36telltale signs obviously the pain right

1:14:38and it's going to be painful at rest

1:14:40it's going to be painful when you

1:14:41palpate it but in some scenarios

1:14:45you can actually cause this infection it

1:14:47kind of starts to kind of get around

1:14:49it's just beneath the perryioium

1:14:51and sometimes let's actually draw it

1:14:53like this you can actually have a I

1:14:56guess the best way of saying it is you

1:14:58can kind of form like a sub

1:15:01perryostial

1:15:04abscess.

1:15:06And all this means is that when you look

1:15:09at this patient, you will see a a little

1:15:12bit of a bump right there on their

1:15:14forehead. That's really what will

1:15:16happen. And so with this scenario, if I

1:15:18were to kind of imagine this, let's say

1:15:19that I kind of drew this out here,

1:15:23you'll see here

1:15:25from this that they'll have that sinus

1:15:28or that bone. It'll kind of like start

1:15:31pushing out. So, here was the the sinus

1:15:33back here.

1:15:35All right. Here's the sinus. And you'll

1:15:38notice

1:15:40that the sinus was the source, right?

1:15:44The sinus was the source.

1:15:46And then

1:15:48the infection spread

1:15:51and spread and it got just beneath the

1:15:53perryostium and it caused this kind of

1:15:56like big bumpy little appearance to

1:15:58occur. And so it'll be kind of like a

1:16:00large indurated area that as you push on

1:16:01it, it'll it'll have like a little bit

1:16:03of fluctuance to it. We give that

1:16:05subperostial abscess a very specific

1:16:08name for the exams. And we call this

1:16:11a pot puffy tumor.

1:16:14It's just something to think about for

1:16:16the exam is a pot puffy tumor. It's not

1:16:21a tumor. It is an abscess that's formed

1:16:24from an actual frontal sinus that spread

1:16:26to that area and it's just beneath. If I

1:16:28were to draw this in like a pinkish

1:16:29color here, this is the perryioium. So

1:16:32just right here, just beneath the

1:16:34perryostium, we're seeing this fluctuant

1:16:37type of abscess forming, which is just

1:16:39basically an absess that walled itself

1:16:40off inside of the bone just beneath the

1:16:42perryioium. So that's something I would

1:16:44think about here. So osteomiitis

1:16:47usually it's an infection that spreads

1:16:49to the bone. So the pain's going to be

1:16:50worse. They may have some evidence of

1:16:54systemic inflammation which is that they

1:16:56may have a increase in their white count

1:16:59and they may have a fever. So increased

1:17:03white blood cell may be a potential

1:17:05trigger and they may have

1:17:08a fever and that fever may be persistent

1:17:11and in certain scenarios which really is

1:17:13going to give it away is that you'll

1:17:15feel kind of like a um indurated but

1:17:18fluctuant type of like a tissue right

1:17:20off on that actual frontal bone where

1:17:21the sinuses usually lie. All right? And

1:17:23that would be a pot puffy tumor. So,

1:17:25this is something that you would have to

1:17:26actually get like a CT scan, um,

1:17:28sometimes MRIs to see the actual extent

1:17:31into the bone. And these patients are

1:17:33oftentimes going to have to be on

1:17:34antibiotics for a pretty decent amount

1:17:36of time. So, that's something I want you

1:17:37guys to think about. Orbital cellulitis

1:17:39is another complication. And really,

1:17:41it's any kind of orbital complication.

1:17:44It doesn't have to be orbital

1:17:45cellulitis. It could be preceptal,

1:17:47right? Which is just in front of the

1:17:48actual orbital septum. So, that would

1:17:51usually cause the eyelid edema and

1:17:52arythemma and they would get a good

1:17:54amount of swelling. orbital cellulitis

1:17:55is behind the orbital septum and that's

1:17:57going to cause a significant amount of

1:17:58swelling where the eye just going to

1:17:59bulge out and then you can't move the

1:18:01eye as much. Sometimes you can get

1:18:03abscesses inside of the orbital cavity.

1:18:05So it's not just one thing. There's

1:18:06actually a thing called a chandler

1:18:08classification that really digs into

1:18:09that more. We're not going to get into

1:18:10that. So orbital cellulitis

1:18:13the most common trigger here is going to

1:18:15be from ethmoid sinusitis. So you see

1:18:17how here we have the ethmoid bone and

1:18:19here we have these ethmoid sinuses.

1:18:21These little suckers, dude, they got a

1:18:23thin little bone that they can just

1:18:26spread right across and get into the

1:18:29orbital cavity. Thin little bone. Do you

1:18:31guys know what that's called? It's the

1:18:33lamina paparatier.

1:18:35So whenever a patient gets ethmoid

1:18:39sinocitis,

1:18:42it travels. So it moves

1:18:45across. What is the structure called?

1:18:48the lamina

1:18:50paparati

1:18:52and it gets into the orbital

1:18:55cavity.

1:18:58That is really kind of the overall

1:19:00mechanism here. So a patient has ethmoid

1:19:02sinocitis. That ethmoid sinusitis allows

1:19:04for the infection to spread across the

1:19:06bone. Very thin bone gets into the

1:19:07orbital cavity starts just wrecking

1:19:10things dude. So all we have to do here

1:19:11is draw here is the inflamed sinus.

1:19:14this thing gets in here,

1:19:17bye-bye.

1:19:19And that's really what we got to be

1:19:20scared about. So, if a patient came in

1:19:22and they had maybe some again nasal

1:19:24congestion, they had some facial pain

1:19:25and pressure, maybe it was kind of

1:19:26situated around the eye, maybe they had

1:19:29um also some nasal [clears throat]

1:19:30discharge and all of a sudden they can't

1:19:32move their eye, their eyes really

1:19:33swollen, you should be concerned about

1:19:34something like orbital cellulitis. So,

1:19:37clinically, whenever the orbital cavity

1:19:39gets inflamed, so this is going to cause

1:19:40orbital cavity inflammation. Obviously,

1:19:44like I said, this could form as just

1:19:45cellulitis. It could even become an

1:19:47abscess, but it starts to damage

1:19:48particular structures. So, the

1:19:50structures that we got to worry about is

1:19:52it causes enlargement

1:19:56of two things. One is the enlargement of

1:19:58the um orbital fat. There a lot of

1:20:01orbital fat tissue. And the other one is

1:20:04it's going to cause enlargement, but

1:20:06usually that enlargement is going to

1:20:07cause meioitis or enttrapment. Either

1:20:09way, there's going to be, let's actually

1:20:11say, um, enttrapment

1:20:15is one thing or myioitis, which is just

1:20:18basically inflammation of the extra

1:20:21ocular muscles. All right, those are the

1:20:24two things that are going to be in the

1:20:25orbital cavity there. If that happens,

1:20:27the clinical presentation will be pretty

1:20:29straightforward. So, what would that

1:20:31clinical presentation be? The clinical

1:20:33presentation comes down to usually this

1:20:35would be proptosis.

1:20:38So you would have the eye bulging

1:20:40forward and that would be pretty

1:20:42problematic. So that would really make

1:20:44you think about one thing, right? The

1:20:46other thing here is that it's often

1:20:48times going to be in combination with an

1:20:49entrapment or inflammation of the

1:20:51muscles that move the eye. And so what

1:20:53would that be associated with? It would

1:20:55also be restricted

1:21:00and painful

1:21:03extracular movements. The combination of

1:21:07these two is what really should make you

1:21:09think about orbital cellulitis. You'd

1:21:11have to get some imaging here, like a CT

1:21:13scan to really see if it's just the

1:21:15cellulitis or if there is an abscess or

1:21:17anything else that's really going on

1:21:19here because that would need to be

1:21:20addressed. These patients would need to

1:21:21be on IV antibiotics. These patients may

1:21:23have to be on IV antibiotics initially,

1:21:25but then eventually gets transitioned

1:21:27over to oral. But you're you're getting

1:21:29the difference here that often times

1:21:30patients who have things like sinusitis,

1:21:31we treat them with oral antibiotics,

1:21:33especially if it's bacterial. we don't

1:21:34need to do IV. We don't need to do any

1:21:36kind of surgical interventions usually.

1:21:38But in the scenario where it does spread

1:21:40to the orbit or it spreads to the bone

1:21:42or it spreads to other scary areas, we

1:21:44may have to reach for those IV

1:21:45antibiotics and do some other types of

1:21:47interventions. So that's what I want you

1:21:48to take away from this one. Cavernous

1:21:51sinus thrombosis is kind of like a

1:21:52similar concept.

1:21:55Usually [sighs and gasps]

1:21:57cavernous sinus is interesting. So

1:21:58here's here's what I want you to

1:21:59remember. You have some veins here and

1:22:02and this is not going to be perfect the

1:22:04way you would view it, but I want you

1:22:06guys to just I guess trust me for now

1:22:09that there is opthalmic veins and the

1:22:12opthalmic veins are essentially kind of

1:22:14like uh you have the superior and

1:22:16inferior and again it probably looks

1:22:17like that's the case but but it's medial

1:22:19lateral just trust me for right now that

1:22:21you have some superior and some inferior

1:22:23abdomic veins and what they do is they

1:22:26drain from the orbit into the cavernous

1:22:29sinus.

1:22:31If a patient started off with ethmoid

1:22:36sinusitis

1:22:38and that ethmoid sinusitis

1:22:40did [clears throat] what? Spread. Where

1:22:43does it spread? Spreads across the

1:22:46laminina

1:22:48and it gets into the orbital cavity. So

1:22:51now I have all of this inflammation

1:22:53here. Obviously we just talked about

1:22:54what that would be orbital cellulitis.

1:22:57But these veins, they're valless, which

1:23:02means that things can kind of flow in

1:23:04different directions. It's not always

1:23:05one directional flow. The pathogens can

1:23:09hop in to these veins and travel their

1:23:13way into the retrograde

1:23:17into the cavernous sinus.

1:23:20When they get to the cavernous sinus,

1:23:22they can cause inflammation. they can

1:23:24clot off the vessels and that's when we

1:23:27start seeing some issues. So here's what

1:23:29I want you to remember to kind of follow

1:23:31this process. First thing is you have

1:23:34ethmoid

1:23:36sinusitis

1:23:38and then what happens it spreads to the

1:23:40orbital cavity

1:23:43from here it flows via what the opalic

1:23:46veins. So then infection

1:23:51spreads

1:23:54via the opthalmic veins

1:24:00and where do they dump into the

1:24:02cavernous sinus and then they empty

1:24:07into

1:24:09cavernous

1:24:11sinus.

1:24:13So here's what we've done so far. We

1:24:14have an infection in the ethmoids.

1:24:16They cross the laminoperation get to the

1:24:18orbital cavity. They hijacked the actual

1:24:22opthalmic veins and then spread to the

1:24:25actual cavernous sinus in the cavernous

1:24:27[clears throat] sinus. What happens? You

1:24:31get inflammation of the cavernous sinus

1:24:32but also the cavernous sinus is sneaky

1:24:34dude. This infection

1:24:37it kind of causes clots to form

1:24:41especially where these opthalmic veins

1:24:42want to dump in. So two things really

1:24:44happen here. One thing is once they

1:24:47empty in one is you get septic thrombi.

1:24:52So you get basically a septic

1:24:55thrombi

1:24:58in the cavernous sinus and that's where

1:25:00we call this cavernous sinus thrombosis.

1:25:04Now think about this for a second. If

1:25:06you clot this off blood is supposed to

1:25:07be coming from the eyes and emptying

1:25:09into the cavernous sinus. But you got

1:25:11clots there. What's going to happen to

1:25:12these dang optodomic veins? They're

1:25:14going to blow up, right? They're going

1:25:16to look like they've been, you know, on

1:25:18steroids and drinking water for a while

1:25:20and they're going to blow up and they're

1:25:21going to get super super engorged. And

1:25:24because of that, what's going to happen?

1:25:27All of this engorgment of the veins are

1:25:29going to cause you're going to get all

1:25:30that swelling in the eye. And so what

1:25:33ends up happening here is that these

1:25:35patients usually have very specific

1:25:37clinical presentations. They get things

1:25:39like we talked about. They get

1:25:41perorbital edema. Their eyes are like

1:25:43they look like they're super swollen.

1:25:46That's one thing. They get proptosis.

1:25:51They also get chemosis, which is

1:25:53basically swelling of the conjunctiva,

1:25:56right? It looks like a blister on their

1:25:57conjunctiva. I'm not kidding. So, these

1:25:59are the the actual big things that I

1:26:01want you to remember because of this.

1:26:02It's backflowing into the opthalmic

1:26:04veins and it's causing all that

1:26:06congestion in the orbital cavity. And

1:26:07so, again, it'll cause perorbital edema.

1:26:10It'll cause proptosis and it'll cause

1:26:12chemosis. All of that is because of the

1:26:15movement, the redirection of it back

1:26:17this way and that's going to cause all

1:26:19this swelling in the orbital cavity.

1:26:20That should make sense, right? The other

1:26:23thing is

1:26:25when you cause inflammation because that

1:26:28that infection when it gets into the

1:26:30cavernous sinus jacks it all up. You're

1:26:32going to get inflammation

1:26:36of the cavernous sinus.

1:26:38Well, it's really really critical to

1:26:40remember what in the heck runs in the

1:26:42cavernous sinus

1:26:45and information of the cavernous sinus.

1:26:47Basically, it kind of um let's say

1:26:50presses on specific structures that run

1:26:53through here. Do you guys know which

1:26:55structures run through here? Let me

1:26:56actually get this. There's a couple

1:26:58different things.

1:27:00One is you have cranial nerve three.

1:27:02Another one is cranial nerve four.

1:27:05Another one is the V1 division of the

1:27:07facial ner trigeminal. Then there's the

1:27:09V2 division. And then there's another

1:27:12one right in here which is cranial nerve

1:27:14six.

1:27:16And then on top of that you also have

1:27:17like a sympathetic plexus and you have

1:27:19an artery. What's that artery? I'm going

1:27:21to kind of inflame this whole thing

1:27:22here. This whole thing is getting

1:27:24inflamed because of the infection,

1:27:27right? And you got the clot there. But

1:27:29there's another structure that runs

1:27:30right next to this this um this nerve.

1:27:33What is that structure? That's called

1:27:34the internal corateed artery. Right? So

1:27:37you have a couple different cranial

1:27:38nerves here. I'll I'll list them again.

1:27:40This is cranial nerve three, cranial

1:27:44nerve four. This is cranial nerve five

1:27:48here. These two, but you have two

1:27:49divisions, V1 and V2. And this one here

1:27:53is cranial nerve six. All right. This

1:27:57one right there. And then you have the

1:27:58artery right there, which is the

1:28:00internal corateed artery. All right. The

1:28:03point I make of all of this is when you

1:28:04get inflammation of the cavernous sinus,

1:28:06it's going to naturally start pressing

1:28:08on those nerves.

1:28:10And because of that, we're not going to

1:28:12go through all of these. We talked about

1:28:13this a lot in other lectures. So, this

1:28:15is just more of a consistent recap that

1:28:17you guys have noticed. You're going to

1:28:19get cranial nerve palsy. So, you'll get

1:28:21things like a cranial nerve three,

1:28:24four,

1:28:26and six pausy.

1:28:28What will that do? Just think about it.

1:28:30Come on. It's going to cause restricted

1:28:32extracular movements. You're not going

1:28:34to be able to maybe uh medially um

1:28:36you're not going to be able to add

1:28:37abduct, maybe look up, maybe look down.

1:28:38All of those things are going to be

1:28:39impeded because you've affected all of

1:28:41these extracular muscles that are

1:28:43supplied by these nerves. You can even

1:28:45have double vision. So that's one thing.

1:28:48The second thing is the facial nerve. So

1:28:51you're going to have cranial nerve five

1:28:54pausy especially for the two divisions

1:28:58the V1 and the V2 division. So you may

1:29:01have decreased sensation, paristhesas,

1:29:03numbness, tingling of the face. And on

1:29:07top of that, you know, the cranial

1:29:08number five also controls the coral

1:29:09reflex. There may be a diminished coral

1:29:11reflex. And if we really had to be

1:29:13particular, there is a plexus that wraps

1:29:16around the what's that called? The

1:29:18sympathetic plexus. What happens if you

1:29:20damage the sympathetic plexus? You can

1:29:22get Horner syndrome. So, another

1:29:25possibility, but we're going to put it

1:29:26as a plus and minus because we don't

1:29:27often see it that often is Horners.

1:29:31But I think it just kind of helps us to

1:29:33be good clinicians if we think about

1:29:34that. So, in patients who have cavernous

1:29:37sinus thrombosis, the big thing is that

1:29:39you start off with an infection of a

1:29:41sinus. Most often this bad boy gets to

1:29:44the orbital cavity, gets into the

1:29:46opdomic veins, gets to the cavernous

1:29:48sinus, clots off the cavernous sinus

1:29:50entry points. Also, cavernous sinus are

1:29:53interconnected.

1:29:55These little suckers, dude, they're

1:29:57smart, man. They interconnect

1:30:00because of that symptoms whenever this

1:30:02develops comes up bilaterally within

1:30:04like 24 to 48 hours. So you get

1:30:07bilateral perorbital edema, bilateral

1:30:09proptosis, chemosis and bilateral

1:30:12cranial nerve palsies. That's why this

1:30:14is important to because it helps you to

1:30:15differentiate a little bit between the

1:30:16orbital cellulitis which is often

1:30:18usually unilateral. Okay, this one

1:30:21really really bad. Really really bad. We

1:30:23have to treat this one with ivy

1:30:24antibiotics. Often times we have to give

1:30:26hepin and we this one's a tough one to

1:30:28kind of treat. You don't want this one.

1:30:31With that being said, you don't want

1:30:32this one either because intraraanial

1:30:34infections are also pretty pretty dang

1:30:35scary, right? With intraraanial

1:30:38infections, there's there's things like

1:30:39meningitis. There's there's there's

1:30:41brain abscesses. You can even get

1:30:43infections in between the different

1:30:45parts of the meningis like subdural

1:30:47empas and epidural abscesses. The thing

1:30:49I want you to understand here is it's

1:30:51it's pretty straightforward. These

1:30:53things they spread they spread two

1:30:56different ways. So let's say that here

1:30:57it spreads into the menes. You can get

1:31:00things like menitis

1:31:02here. It can spread into the brain. You

1:31:05can get things like an abscess. Same

1:31:07thing here. I can spread into the

1:31:08meningis or I can spread into the brain.

1:31:10So the different ways that a patient may

1:31:12present is they may present with where

1:31:15is my green marker here. One way is they

1:31:19may get what is this called? Whenever

1:31:20you have it starts off as cerebritis,

1:31:22but then that cerebritis gets a really

1:31:25really walled off infection here. And we

1:31:27used uh I think orange in the past and

1:31:29it gets filled with all this pus-like

1:31:31material. What is this called? This is a

1:31:34brain abscess. Right? So one

1:31:36presentation. So the different kind of

1:31:37intranial infections here could be

1:31:38things like a brain abscess. That's one.

1:31:41Right?

1:31:43Another way that this could present

1:31:48is that the infection could spread to

1:31:50the different parts of the meninges and

1:31:52you can get infections sometimes in

1:31:54between the in the epidural space and

1:31:56you can get infections into the subdural

1:31:58space. So let's pretend here for a

1:31:59second that I have an infection that's

1:32:01really really deep right here and maybe

1:32:04I have another one that's really really

1:32:05deep right here. Well here I could get

1:32:07things like a subdural impaema and an

1:32:10epidural abscess. So these are also

1:32:11possible. They're definitely way more

1:32:13common with frontal sinusitis though.

1:32:16All right. So again, brain abscess, you

1:32:18can get things like a subdural empa

1:32:21which is obviously an infection that's

1:32:23in the subdural space,

1:32:27empa.

1:32:30And then the other one is an epidural

1:32:32abscess. So an abscess that forms in the

1:32:34epidural space. And then the last one is

1:32:38sometimes it can just be into the

1:32:39subacoid space or affect different parts

1:32:40of the meningis and it's not really an

1:32:42abscess. It's an infection that's kind

1:32:44of like spread throughout the meningis

1:32:45and that can cause something called

1:32:48menitis. Menitis. So these are the

1:32:51different ways that this could all

1:32:54occur is menitis different types of

1:32:56abscesses.

1:32:58And that's what I really really kind of

1:32:59want you to understand here. Now

1:33:02[sighs and gasps] the ways that these

1:33:04infections do this is they spread from

1:33:06the sinuses by something called

1:33:08contiguous spread. So the mechanism the

1:33:11mechanism

1:33:14is something called

1:33:16contiguous spread. And I don't need for

1:33:20us to get all kinds of like crazy on

1:33:23this. It's it's really straightforward.

1:33:27One

1:33:29and two. The infection starts in the

1:33:31sinus, moves through the bone and then

1:33:34gets into the actual meninges. That's

1:33:37it. So the infection

1:33:39infection spreads

1:33:46through the bone.

1:33:48All right? So you get something like an

1:33:49osteomiitis

1:33:51and then as it works its way tracks its

1:33:53way back and get into the epidural

1:33:54space. Get an epidural empa. epidural

1:33:56abscess can track into the subdural

1:33:58space get a subdural empa track into the

1:34:00meninges especially the subacttoid space

1:34:02and you get some menitis you get the

1:34:04point that's one way the infections

1:34:10spread

1:34:13via valveless veins which we kind of

1:34:17already talked about above the athic

1:34:20veins are a perfect example of that so

1:34:23there's two different ones that I want

1:34:24you to think about here. One is that

1:34:27cavernous sinus that's really common for

1:34:29infections like ethmoid, sppheninoid,

1:34:32basically to get to the cavernous sinus

1:34:33and cause these types of infections,

1:34:35right? So, one of those is you kind of

1:34:38have things like we talked about the

1:34:40athalmic veins is a perfect example of

1:34:43how that infection spreads, right? And

1:34:45that was with the ethmoid. That was the

1:34:47perfect example for that one. There's

1:34:49other ones which are in the bone and

1:34:51they kind of interact very interestingly

1:34:54to like deep deep veins. I don't want to

1:34:56go too crazy into it but they're called

1:34:58diploic veins. They're in the bone

1:35:01especially this is very common for

1:35:04frontal. Very common for frontal

1:35:06sinusitis.

1:35:08Essentially what happens [clears throat]

1:35:10is you have a bone here right here's

1:35:13your bone

1:35:14and then you have different layers. So

1:35:16we'll just use the colors here. So we'll

1:35:19say here's the uh you have two different

1:35:21parts of the dura matter here.

1:35:24And then we'll say here is another layer

1:35:26which we'll just we'll just keep the

1:35:28same color here for right now. So

1:35:29there's the perryosta layer and then you

1:35:31have the meningial layer right and then

1:35:35obviously we'll have the arachnoid mo.

1:35:41But here's the big thing.

1:35:44There's these big veins. They call them

1:35:45the dural venus sinuses, right? Here's

1:35:48your dural venus sinuses. Here's the

1:35:50bone. Let's say that this is the frontal

1:35:51bone. And let's say here,

1:35:55here's that sinus that we were kind of

1:35:56talking about. And there's the infection

1:35:58in it. There's small little veins in the

1:36:01bone that basically kind of like capture

1:36:04that and can travel through

1:36:08their way here through the bone and

1:36:11access this space. Tell me that isn't

1:36:14crazy.

1:36:15So now if I have an infection

1:36:19right here of this sinus

1:36:22and the infection spreads

1:36:25through the diploic veins it can access

1:36:29things like the superior sagittal sinus

1:36:31and then from here it can eventually get

1:36:33into your brain tissue. It can get into

1:36:34the meningis you get the point. It's

1:36:36it's almost exactly like we talked about

1:36:38with the cavernous sinus. You're just

1:36:39giving it a gateway. So that's the two

1:36:41ways that these things happen. What I

1:36:44need you to understand is clinically,

1:36:45how would I know that a patient started

1:36:47off with a sinus infection and all of a

1:36:48sudden they came in with something like

1:36:49this? Well, think about this. For

1:36:53example, if a patient cames in

1:36:54clinically, they're going to be sick as

1:36:56crap, man. The clinical presentation

1:36:59really comes down to the area or the

1:37:01type of infection we're discussing. So,

1:37:04for the most part, when I talk about

1:37:06these, the two most common ones are

1:37:08going to be things like menitis and like

1:37:10brain abscesses that they'll probably

1:37:11present. But either way, you're going to

1:37:14see things that are probably like

1:37:15relatively common. I'd say you'll see a

1:37:18patient who's going to have a severe

1:37:20headache. So, a severe headache, it will

1:37:22be definitely one. They may have a fever

1:37:26and there may be neurological

1:37:30deficits

1:37:32and especially when it comes to things

1:37:34like menitis, what else would I

1:37:36potentially see? Not only cortical signs

1:37:37like neurological deficits, but I may

1:37:39see menism. And that menismas is the

1:37:42sign potentially to make you think about

1:37:44menitis. Right? This was a lot. This was

1:37:47a lot. And again, the thing I want you

1:37:48to take away from these types of

1:37:49infections is they are uncommon, but we

1:37:51don't want to miss them. Usually the

1:37:54ones that I get really, really concerned

1:37:55about, especially with orbital

1:37:57involvement and brain involvement, is

1:37:58which one of those acute ones? Acute

1:38:01invasive fungal rhinocyitis. That is the

1:38:04one that can spread rapidly and can kill

1:38:07a patient. It is very very common for

1:38:09that thing to spread to the orbit and

1:38:10then into the brain. Bacteria would be

1:38:12the next one. We talked about a lot of

1:38:15this but now what I want you guys to do

1:38:16is to put it into action. Let's make an

1:38:18application of this knowledge and talk

1:38:20about how to think about these patients

1:38:21clinical presentation and get to a

1:38:23diagnostic certainty. Let's do that now.

1:38:26All right. Let's now talk about the

1:38:27diagnostic approach to sinus infection.

1:38:28So when we talk about this, I think the

1:38:30first thing to kind of ask yourself is

1:38:32when we think about sinus infections,

1:38:34what are the ways that these patients

1:38:36usually present? because a lot of these

1:38:38are diagnosises based upon clinical kind

1:38:41of um gestalt and overall it's a

1:38:44clinical diagnosis essentially. So we

1:38:46have to be good with understanding what

1:38:47that really kind of entails. So let's

1:38:50talk about particularly what is the

1:38:51clinical criteria for an acute

1:38:53rhinoscinoitis and and does the patient