Bronchiectasis | Clinical Medicine

0:07What's up ninja nerds? In this video

0:08today we're going to be talking about

0:09bronchiectasis. This is a part of our

0:11clinical medicine section. If you guys

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0:33opportunity. All right, let's start

0:34talking about bronchiectasis.

0:36Bronchiectasis is basically defined as

0:38you have this like massive bronchial

0:40dilation secondary to a lot of

0:42inflammation within the airways. So, we

0:44have to ask ourselves the question when

0:45a patient comes in that we suspect may

0:46have bronchiectasis,

0:48what really is the classic finding that

0:51really would cue you off to think that

0:52this is the cause? Cuz we talked about

0:54in other obstructive lung disease cuz

0:55this is one of them.

0:57Asthma, they come in with potential

0:58findings of maybe uh some particular

1:01dyspnea, maybe they come in with some

1:03wheezing. Whereas those with the COPD,

1:05they come in with either a productive

1:06cough, dyspnea, they come in with

1:08wheezing as well. What's really the

1:10telltale sign to really break this one

1:11off of the obstructive lung diseases?

1:13Really, the classic thing is they have

1:15so much mucus in their airways that

1:17whenever they expectorate and they clear

1:20this mucus, it is really intense. It's

1:22super thick and it smells absolutely

1:24horrific. So, sometimes we say that they

1:26have this thing called a foul

1:30smelling

1:32productive

1:34cough.

1:35So, it's this really nasty mucopurulent

1:37type of sputum that they will

1:39expectorate. And that's usually kind of

1:42this classic finding that we see in

1:44patients who have what's called

1:45bronchiectasis. Now, the question is why

1:47do they have so much mucus that's within

1:49their airways? And why is it so foul

1:50smelling? That probably means that

1:51there's a lot of inflammation, probably

1:52infected material there.

1:55Let's kind of explain that. So, here we

1:56have a patient who has a normal complete

1:58healthy airway.

1:59But then for whatever reason we decide

2:01to bring about a lot of inflammation,

2:04right? So, here we're going to talk

2:05about those causes in a second, but here

2:07this thing right here is really taking

2:09this airway and just turning it on

2:11hyperdrive and saying, "Hey, let's go

2:13either and increase a lot of

2:14inflammation within these airways and

2:16then lead to what? Well, when you

2:18inflame airways, you know what one of

2:19the big things happens? You stimulate

2:21these things called goblet cells. And

2:22goblet cells, they love they love to

2:25produce a ton of mucus. And so, one of

2:27the things that you'll start noticing is

2:28that these patients get a lot of mucus

2:31that builds up within the airways. There

2:32could be other reasons why besides

2:34inflammation, but we'll cover those.

2:36Now, look,

2:37I got this inflamed airway with a ton of

2:40mucus.

2:41The other thing that happens besides

2:43just the mucus is that this inflammation

2:45starts causing other particular

2:46processes to occur. But for right now, I

2:48want you to know that we're going to

2:49trigger this massive increase

2:52in mucus production.

2:54Now, the next thing that happens is this

2:56mucus traps a lot of bacteria. So,

2:59imagine if we trap a lot of bacteria

3:01within this mucus and we also keep

3:03continuing to have inflammation, what's

3:05going to potentially happen? Well, the

3:06inflammation starts kind of destroying

3:08some of the bronchial walls and this

3:10leads to this process called bronchial

3:12dilation. So, then we start seeing

3:14dilation

3:17of the bronchioles.

3:20And not only is this kind of dilation is

3:22occurring, but you still have guess what

3:24else? A lot of mucus lining this

3:26particular airway.

3:28So, it's just this kind of vicious cycle

3:31of inflammation that propagates

3:32increasing mucus production. The mucus

3:35will increase inflammation. The

3:36inflammation will lead to the dilation

3:38of the bronchioles due to a lot of

3:39destruction of the bronchial walls. And

3:41again, this is just kind of this vicious

3:43cycle.

3:45I think one of the big things to

3:46remember is what's the end result of

3:48this? Well,

3:50one of the things that happens as you

3:51build up mucus and inflamed airways and

3:54then dilation is that these airways

3:56become so filled that they become

3:57obstructed. And so one of the primary

4:00themes that I think is important to

4:01remember in patients with bronchiectasis

4:03is they exhibit features of what's

4:04called airway

4:06obstruction. In other words,

4:09these airways are so filled with mucus

4:11and they're collapsed from because of

4:12these bronchial airways being so weak

4:14and destroyed that it is almost

4:15impossible to get things like CO2

4:19out.

4:20And so these patients will potentially

4:22air trap and they can they potentially

4:24can develop features of hyperinflation.

4:26But one of the classic classic features

4:28of these patients is they exhibit

4:29features of what's called airway

4:31obstruction. So bronchiectasis is a part

4:34of the category of diseases called

4:36obstructive pulmonary diseases. And the

4:39reason why is there's mucus that builds

4:42up secondary inflammation, dilation of

4:44the bronchioles, and then bronchial

4:45collapse, and as well as mucus that are

4:47filling up the airways, they can't get

4:49air out in the obstructed airways.

4:52So the question that comes, okay, what

4:54in the heck is the cause of all of this

4:55bronchial inflammation that's

4:57propagating mucus production and

4:58dilation of the arter- of the

4:59bronchioles? Let's come down and talk

5:01about that.

5:02The first thing I want you guys to think

5:04about is that generally there could be

5:06dysfunction of what's called the

5:08mucociliary apparatus.

5:10So you know there's these particular uh

5:13cells and what they're supposed to do is

5:15they're supposed to take things like and

5:16push chloride out. Right? These are

5:19these transmembrane ions.

5:22And in patients who have diseases

5:25such as what's called cystic fibrosis,

5:28so let's say that you have this disease

5:30called cystic

5:32fibrosis,

5:34they have the inability for the cystic

5:37fibrosis transmembrane receptor protein

5:40to be able to

5:41produce chloride.

5:43So they have this defect in these

5:45transporters where chloride will not be

5:48excreted. Why is that important?

5:50Well, whenever goblet cells make mucus,

5:53so let's say here it makes a clump of

5:54mucus.

5:56This mucus that's produced by the goblet

5:58cells can be thinned out by the

6:00chloride.

6:02But if under the circumstances that you

6:04don't have chloride, what's going to

6:06happen to this mucus? It's not going to

6:08be able to get thinned out and what is

6:09the result? They develop a massively

6:12thick kind of mucus that obstructs the

6:14airways. There's one way that we get a

6:16lot of mucus and if mucus gets caught up

6:18within those airways, what can it

6:20entrap? Bacteria. What can bacteria do

6:22to the actual bronchial tissue? Inflame

6:24it. And then with inflammation, that

6:25chronic inflammation will also lead to

6:27dilation and then over time lead to

6:29airway obstruction. So again, big big

6:32problem here is

6:33very very thick [snorts]

6:36mucus because you lose the ability

6:39for these chloride molecules to get

6:41taken up into this actual mucus kind of

6:44molecule right here or mucus clump here

6:46into thin it out.

6:48All right, that's one reason patients

6:49will develop this. So think about the

6:50cystic fibrosis especially in a younger

6:52patient with other history.

6:54Maybe they have a potential history of

6:55exocrine pancreatic insufficiency or

6:57other diseases particularly like

6:59recurrent pulmonary infections and lots

7:01of mucopurulent sputums.

7:04Another particular thing that you want

7:05to think about as a cause here

7:07is a very interesting one and this is

7:09when the cilia stop working. So let's

7:11say that these cilia normally what

7:12they're supposed to do is they're

7:14supposed to beat up mucus and particles

7:17and things to that effect

7:19all the way up like kind of this

7:21escalator.

7:23Right? So if there is a chunk of mucus,

7:25let's say, right here

7:27which has some bacteria in it, it's

7:29going to move it a little bit up here

7:31via the cilia. It'll move it a little

7:33bit up here via the cilia and it'll move

7:36it up here via the cilia.

7:38But now you've destroyed this process.

7:40So now you lose the ability to move and

7:42mobilize this mucus upward so that you

7:45can spit it out or swallow it. And so,

7:47what happens to the mucus? It builds up

7:49and builds up and builds up. And so, as

7:51a result, these patients will build up

7:53mucus.

7:55And if you build up a lot of this mucus,

7:57guess what's going to happen? You end up

7:58with the process that we've just talked

8:00about.

8:02So, the question is, what

8:05So, there's a an There's a build-up.

8:06There's an increased build-up of mucus.

8:09What is the cause of this where the

8:11cilia aren't working?

8:13This is called primary ciliary

8:14dyskinesia.

8:17Another uh term which is thrown around

8:20sometimes is called Kartagener's

8:21syndrome.

8:22But primary ciliary dyskinesia

8:25is one particular thing to think about

8:27here.

8:28What happens here

8:30is also you need to remember that in

8:32primary ciliary dyskinesia or

8:33Kartagener's syndrome, they may also

8:35have other diseases. Usually, uh you

8:37think about situs inversus, and you

8:39think about chronic sinusitis in

8:41combination with bronchiectasis. And in

8:44a patient with cystic fibrosis, you

8:45think about bronchiectasis, frequent

8:47pulmonary infections, as well as maybe

8:50even exocrine pancreatic insufficiency.

8:51Other organs are usually involved as

8:53well in cystic fibrosis.

8:56The last one that causes mucociliary

8:57dysfunction is when you have an airway

8:59obstruction. This could literally be

9:00anything. I'm not I'm not kidding. Let's

9:01say that I'm just going to use this as

9:03this one thing here that there is an

9:05obstructed like substance of some sort.

9:08There's a substrate here.

9:09And it's blocking the movement. It's

9:12similar to like not having cilia if you

9:14want to think about it here.

9:16Cilia is intact, but here we have some

9:18mucus, let's say,

9:20that we want to move along and kind of

9:21clear. But if we can't clear that mucus,

9:25what is it going to do? It's going to

9:26build up.

9:28And so, it's the same kind of concept

9:30here that as these goblet cells produce

9:31mucus, you want to be able to clear that

9:34mucus, but you have something that's

9:35obstructing the movement of the mucus.

9:38There's a lot of different things that

9:39could do that, but it's the same

9:40concept. You're going to build up mucus.

9:42So, over time, this will definitely lead

9:43to the same concept here.

9:45But, you want to know what are those

9:46things? This could be a tumor. I'd say

9:48that's a big one because that's going to

9:49be more of a chronic process, or chronic

9:51obstructive pulmonary disease,

9:52particularly chronic bronchitis. Think

9:54about COPD.

9:55Or maybe some type of foreign body.

9:59This is another one I would definitely

10:00potentially consider as well.

10:02But, these are something that would lead

10:04to mucociliary dysfunction.

10:07The next question that you have to ask

10:08is, "Okay,

10:10these things make sense as to why

10:11there's a ton of mucus. The mucus will

10:13do what again? Carry with it and keep

10:16within it bacteria. Bacteria can cause

10:17tissue damage. Tissue damage then

10:19propagates more inflammation. More

10:20inflammation leads to dilation of the

10:22bronchioles. And then again, with a

10:23combination of mucus build-up, inflamed

10:26bronchioles, and then dilation, you lead

10:29to potentially airway obstruction."

10:31The last thing is, "What if I have

10:33recurrent infections?" That can cause

10:34inflammation, right? So, recurrent

10:36infections are really important. You got

10:37to think about it two ways.

10:39One

10:40is you have a lot of bacteria that

10:42you're being exposed to.

10:44One is called pseudomonas.

10:47And there is a particular disease that

10:48has lots and lots and lots of

10:50pseudomonas that colonizes the airways.

10:51Do you guys know what it is? I want you

10:52to remember an abbreviate. It's called

10:54cystic fibrosis. So, you see how that's

10:56a big one there?

10:57Cystic pseudomonas will definitely lead

10:59to lots of bacteria that then destroy

11:03or inflame the airways.

11:05That's one particular thing. You know,

11:07as you cause airway inflammation, what

11:08do you then do? You stimulate goblet

11:10cells to produce

11:12mucus. And as you increase that mucus

11:15and propagate more of the actual

11:17inflammation of the airways, you'll lead

11:18to this upstream effect that we talked

11:20or the downstream effect that we talked

11:21about up here.

11:23What's another bug?

11:25Another one would be what's called

11:26haemophilus influenza. This is a really

11:29big one. You know what disease carries

11:30this one a lot? COPD.

11:33So, patients with COPD carry or colonize

11:35this bug a lot.

11:37Other ones I think that are important to

11:38remember here is what's called allergic

11:41bronchopulmonary

11:42aspergillosis.

11:44These bugs right here, so this is

11:46usually bacteria. This is more of like a

11:47fungus. I think one of the big things to

11:50remember about allergic bronchopulmonary

11:51aspergillosis is they have these crazy

11:53high IgE levels and they have lots and

11:56lots of eosinophils.

11:58This is like the only type of like air

12:00you know airway disease where there's

12:02tons and tons of inflammation and mucus

12:04that's not due to neutrophilia.

12:06Uh usually asthma and things like

12:08bronchiectasis can have lots of

12:10eosinophils if it's due to this disease.

12:13So, this is lots of bugs.

12:15What if there's not enough immune

12:16function to clear these bacteria or

12:18other types of infections? So, they

12:20don't have a good immune system. So, I

12:22think patients who have very diminished

12:24T cells or very reduced numbers of IgE

12:27antibodies. What if you have decreased

12:29number of T cells or decreased IgE

12:31antibodies? Are you going to be able to

12:32fight off particular bacteria? So, let's

12:34say here's a bacteria.

12:37And this bacteria is going to induce

12:39damage

12:40and injure

12:42these actual respiratory cells which

12:44propagates more mucus production. So,

12:45you get a lot of mucus.

12:49If you don't have the proper immune

12:51system to fight that bacteria off,

12:55right? This will not be able to be

12:57inhibited. Right? And so, this will

12:59continue this bacteria will continue to

13:00destroy the airway tissue. What are

13:02diseases that cause a reduction in T

13:03cells?

13:05HIV.

13:06What's a disease where you have

13:07reduction in IgE antibodies? Various

13:10types of immunodeficiencies. These could

13:12be a hereditary

13:14immuno-

13:15deficiencies.

13:17We can call this like

13:18hypogammaglobulinemia.

13:20But you get the point. There's

13:22destruction of the actual tissue that

13:24leads to an increase in mucus production

13:25as well as more inflammation of the

13:27airways which propagates this process.

13:30The last one is when a patient has

13:31chronic inflammation that's systemic

13:33that maybe damages the lung tissue as a

13:35result. It's not localized, it's

13:38systemic. And then as an adverse effect,

13:41it hits the lungs as a result.

13:43This could definitely be due to a lot of

13:45nasty antibodies. Right? So, usually

13:48this is autoimmune diseases. So,

13:50autoimmune diseases

13:52that carry lots of particular things

13:55like ANAs

13:57or maybe rheumatoid factor, which you'll

14:00see this in diseases like SLE or you'll

14:01see this in diseases like rheumatoid

14:03arthritis, things to that effect, these

14:06will really go and attack

14:09this lung tissue.

14:11And as it injures and inflames the lung

14:13tissue,

14:14there's other disease like scleroderma

14:15as well, it'll do what? Increase, rev up

14:18the production of mucus by the goblet

14:21cells.

14:22And so, these will start making lots of

14:23mucus.

14:25It'll propagate increased inflammation

14:27and then dilation of the airways and

14:29then airway obstruction. So, you guys

14:30get the point. When a patient develops

14:32bronchiectasis, think about that nasty,

14:34foul-smelling productive cough in a

14:36patient who has very dilated but

14:38inflamed, filled airways with mucus due

14:42to mucociliary dysfunction such as in

14:44thick mucus or a problem being able to

14:47move the mucus or recurrent infections

14:50or chronic inflammation. And again, this

14:52is a part of your obstructive lung

14:54diseases. What's the potential

14:55complications of bronchiectasis? Let's

14:58talk about that now. All right, my

14:59friends. So, now we're going to talk

14:59about the complications potentially

15:01associated with bronchiectasis. When a

15:02patient comes in with bronchiectasis, we

15:04already know they get a lot of

15:05foul-smelling productive cough

15:07filled with mucopurulent sputum. We know

15:08the particular pathophysiology. We know

15:10the causes now. What we then have to

15:12watch out for is what are the downstream

15:14negative consequences of this disease?

15:16One of the big ones and I'd say one of

15:17the most common things that you really

15:19want to watch out for on your exam is

15:20hemoptysis. And the reason why is this

15:22is a chronic disease. And so that

15:24chronic inflammation, what will happen

15:26is

15:26the inflammation over time will erode

15:29and eat away at the vessel wall. And so

15:32it'll cause mucosal erosions.

15:35And you know what's right here supplying

15:38the bronchioles?

15:39There's a beautiful artery called the

15:40bronchial artery. 90-95% of the time

15:43bronchial arteries are the most common

15:44cause of the bleeding that rushes into

15:47the actual bronchial tree.

15:49So it leads to

15:50bronchial

15:52artery

15:54ulceration, let's say.

15:56And as you ulcerate that puppy, then you

15:59get hemoptysis.

16:01So then what happens is let's kind of

16:03like see how this kind of all occurs in

16:04sequence. Chronic inflammation, mucosal

16:06erosions, bronchial artery ulceration,

16:08hemoptysis. Watch watch this. Look,

16:10here's all this inflammation where all

16:11the mucus and bacteria and all that

16:13stuff are. Chronic dilation, this starts

16:15eating away at these tiny little

16:18bronchial arteries. And then as that

16:19happens, blood easily enters into the

16:22bronchial tree. And when this enters

16:24into the bronchial tree, it's nice and

16:26irritating to the actual mucosa. What

16:28would you then do?

16:30And this will then lead to them coughing

16:32up

16:33a lot of this type of bloody types of

16:34material. Sometimes some of this blood

16:37could get stuck down here into the

16:38airways. That's not a good thing. That

16:40can definitely lead to respiratory

16:41failure. But that is a possibility. But

16:44often times, they'll cough up some of

16:46that actual material there. And that's

16:48something that you really want to watch

16:50out for. If a patient has hemoptysis,

16:51think about bronchiectasis as a very

16:53common cause.

16:55Okay, what about respiratory failure?

16:57This is another really big one.

16:58Because it's a chronic disease, it leads

17:00to chronic inflammation, mucus

17:02development within the airways. Now,

17:04because of that, think I think of this.

17:07If you have this problem, you got this

17:08big mucus plug.

17:11So mucus plug that's actually developing

17:13within these airways.

17:14What is that going to do

17:16to the actual ventilation to this

17:17alveoli?

17:18The ventilation will be impaired. So,

17:20it's going to be really, really

17:21difficult to get good ventilation into

17:23this alveoli and good ventilation into

17:26this alveoli. So, you'll have a

17:28reduction in ventilation here, but your

17:30perfusion may be normal. What is this

17:33called?

17:35This could be a VQ mismatch, right? But,

17:37here's something really interesting.

17:38Yes, you may have reduction in

17:39ventilation.

17:41But, here's another concept. When these

17:43patients plug up their airways, it is

17:46not only a difficult time getting air

17:48in. You know what else happens? They

17:49have airway obstruction.

17:51And so, from this airway obstruction,

17:52two things happen. They have a kind of a

17:53mixture of the respiratory failure.

17:55One of the things that's really, really

17:57interesting

17:58is as you develop airway obstruction,

18:01what do you do to your lungs?

18:04You cause hyperinflation.

18:06If you obstruct the lung, can you get

18:08CO2 out? No. The lungs build up. They

18:09get big.

18:11As a result, they develop

18:12hyperinflation.

18:13If you hyperinflate your lungs, how

18:16difficult is it going to be to get air

18:19in? Take a deep breath in. Hold it.

18:21Don't exhale. Try to take a deep breath

18:23on top of that. That's what it's like

18:24for these patients. So, as a result,

18:26they develop something called

18:27hypoventilation.

18:30And when they develop this

18:30hypoventilation,

18:32the consequence is is that they don't

18:35actually bring in enough oxygen,

18:38but the other problem here is that they

18:40don't clear

18:41enough CO2.

18:43And as a result, these patients have two

18:44particular problems that ensue as a

18:46result of this.

18:48One

18:50is they have very low O2s, but they also

18:53have very high CO2s.

18:56And so, this is another particular thing

18:57that you want to watch out for. Is

18:59they'll develop features of what's

19:00called hypoxemia and potentially

19:02hypercapnia. What kind of respiratory

19:04failure is this?

19:05This is an example of what's called a

19:06type

19:08two

19:09respiratory failure.

19:11So, this is something to potentially

19:12watch out for with these patients.

19:15All right, what's another thing that can

19:16happen to patients with respiratory

19:17failure due to airway obstruction and

19:18hypoventilation? What could they look

19:20like? They could look terrible. Some of

19:22these patients may exhibit increased

19:24respiratory rate, increased work of

19:25breathing, dyspnea. So, other things

19:27that you want to watch out for is what

19:28do they look like?

19:29And if they're working hard to breathe,

19:30if they're breathing at 50 a minute,

19:32that is also a potential sign of

19:33respiratory distress and therefore

19:35respiratory failure, not just the low

19:36O2. Again, something to watch out for.

19:41Last potential feature here is usually

19:42because of the respiratory failure. So,

19:44patients who have bronchiectasis, this

19:46is usually chronic. They're living with

19:47hypoventilation and VQ mismatch every

19:49single day.

19:50So, because of that, they have

19:52difficulty, again, getting air in

19:55and getting air out.

19:57So, what's the chronic result here in

19:59these patients? They build up oxygen um

20:01they build up CO2 and then they drop

20:03their oxygen.

20:04So, they usually exhibit chronic

20:06hypoxemia.

20:08That chronic hypoxemia as a result of

20:10this hypoventilation and VQ mismatch

20:12leads to

20:13hypoxic vasoconstriction. These vessels

20:16clamp down like a son of a gun.

20:17So, then you get this intense vaso-

20:21constriction.

20:23When this vessel vasoconstricts,

20:27what it does is it makes the pressure

20:28and the resistance I I'm sorry,

20:30resistance in the vessel really high.

20:32So, as a result here,

20:35your peripheral vascular resistance goes

20:36up.

20:38And then the pressure in the arteries go

20:39up. So, these patients develop something

20:40called pulmonary hypertension. And then

20:43what happens is is if your pressures

20:46in the actual pulmonary arteries get

20:48really, really high,

20:50what happens is the right heart has to

20:51develop such a very strong stroke volume

20:53and cardiac output against the high

20:55afterload.

20:56And what happens over time is this will

20:57cause the right heart to really become

20:59strained and begin to fail and develop

21:01features of right heart failure.

21:03Now, if the right heart fails, they have

21:04difficulty getting blood into the heart

21:05and difficulty getting blood out of the

21:07heart. All right? Maybe because of

21:08hypertrophy or dilation or just high

21:10afterload. Because of that, they can't

21:12get blood out of the heart, the pressure

21:14inside of the right heart increases, and

21:16it starts backing up into the vena cava.

21:19And this leads to elevated central

21:20venous pressures. This will back up and

21:22go down and develop many different

21:23features such as

21:25it'll have jugular venous distension via

21:26the superior vena cava.

21:28It'll go down the inferior vena cava and

21:29cause hepatomegaly.

21:32It could even cause ascites.

21:35And last but not least, it may go into

21:36the lower extremities and cause pedal

21:38edema.

21:42So, these are the potential findings

21:43that could develop as a result of

21:46cor pulmonale,

21:48which is usually defined as pulmonary

21:50hypertension due to an underlying lung

21:52disease. You know what type of pulmonary

21:53hypertension this is? This is an example

21:55of type three. So, here, let's write

21:56that down. This is an example of

21:59type

22:01three.

22:03All right.

22:04The last thing that I want to say here,

22:05but it actually should be relatively

22:07common understanding, is that most

22:09patients who develop bronchiectasis, the

22:11common cause is a recurrent infections.

22:14When patients who develop

22:15bronchiectasis, guess what else happens?

22:17They build up mucus,

22:19and they can't clear the actual mucus

22:20from their airways.

22:21Mucus is an area where bacteria love to

22:24colonize and stay.

22:25So, because of that, they have lots of

22:27bacteria developing within their

22:28airways. And in high amounts, that can

22:30cause infections. So, patients with

22:32bronchiectasis are not only can develop

22:34but because of chronic infections, but

22:36they can develop very frequent pulmonary

22:38infections. That's something else to

22:40watch out for as a potential

22:41complication of bronchiectasis. Let's

22:42talk about how to diagnose it. When a

22:44patient comes in, I'd say one of the

22:45biggest things is look for that prod-

22:46productive foul-smelling cough, frequent

22:50pulmonary infections,

22:52um and on top of that, hemoptysis. Those

22:55are the big things. Get a chest x-ray. A

22:57chest x-ray can be kind of helpful

22:59because anytime someone has a nasty

23:01cough or hemoptysis and you know,

23:03potential signs that they could have

23:06like COPD or bronchiectasis, it's good

23:08to get a chest x-ray to just get a look.

23:10So, in COPD you see that chronic classic

23:13hyperinflation, increased lucency, AP

23:15diameter, all that stuff.

23:17Uh flat diaphragm. In bronchiectasis you

23:19see something very specific. You see

23:21kind of like these like bronchial

23:23cuffing and tram track signs. But that's

23:26not always the best off your chest

23:27x-ray. So, one of the things I like to

23:28do is get the PFTs to say, "Okay,

23:31I still think it could be an obstructive

23:32lung disease. I don't know if it's

23:33chronic bronchitis or if it is

23:35bronchiectasis." Get the PFTs cuz that

23:37can be helpful. If it shows a low FEV1,

23:40a low FEC, and an FEV1 over FEC ratio

23:42that's less than 70%, that's definitely

23:45supportive of obstructive lung disease,

23:46even if they have this increased total

23:48lung capacity, residual volume,

23:49functional residual capacity. We

23:51definitely know it's obstructive lung

23:52disease.

23:53Particularly maybe in this case

23:54bronchiectasis if they have chest x-ray

23:56findings that are supportive of it. What

23:58would be the real good test though to

24:00really help me if I'm confused between

24:02COPD and this particular case of

24:05bronchiectasis? A high resolution CT is

24:07really good. The reason why is

24:10radiographically bronchiectasis is often

24:12times diagnosed. And what you look for

24:14is you look for this massive bronchial

24:16dilation. Look how dilated and cystic

24:19appearing these airways look. On top of

24:22that, there's also another one which we

24:23use like the ratio between the bronchial

24:25wall. Here's your bronchial kind of like

24:26wall here. And here's an associated like

24:28vessel. Usually when the wall bronchial

24:31wall diameter in comparison to the

24:32vascular diameter is like greater than

24:34one or 1.5, it's super suggestive of

24:37bronchiectasis. So, if I have chest

24:40x-ray findings that may be supportive of

24:41bronchiectasis, obstructive lung disease

24:44findings, and a high resolution CT that

24:46shows these findings, I can pretty much

24:48with confidence say I have

24:49bronchiectasis. So, then you got to

24:50figure out the cause.

24:51So,

24:52often times that kind of means going

24:54back and looking. Okay, do they have any

24:55things that would suggest what? Cystic

24:58fibrosis, test the, you know, sweat

25:00chloride test or the CFTR test.

25:03Uh check for immune immune deficiencies,

25:05check the IG levels, check for HIV.

25:08Look to see, do they have any kind of

25:09like massive like tumor or foreign body

25:12that's present within the airways on

25:14their CT scan or their bronch shows

25:15that? Okay, maybe it's an airway

25:16obstruction.

25:18Do they have autoimmune factors? Maybe

25:20it's RA or SLE. Do they have a sputum

25:22culture that suggests that they have H

25:24flu or pseudomonas

25:28maybe it's recurrent infections. And so

25:30those are the ways that we can kind of

25:31go about looking at bronchiectasis.

25:33And how do we treat these patients?

25:35Well, one of the biggest things is

25:36finding the cause and treating the

25:37underlying cause cuz that'll reduce the

25:38chronic inflammation, whether it's

25:40reducing the mucus production, reducing

25:42the

25:43um kind of like bacteria accumulation,

25:45reducing the chronic inflammation,

25:46autoimmune diseases, you got to treat

25:48that.

25:49But one of the things that you can kind

25:50of do while you're treating the

25:51underlying cause is really clear that

25:53mucus, man, cuz that stuff can really

25:55kind of cause problems as you saw the

25:56downward cascade of it. So usually this

25:58is via chest physiotherapy. You can do

26:00this like with this this little child

26:01probably has cystic fibrosis. So they

26:03have on this like vest and it kind of

26:05like per hits and kind of percusses the

26:06chest and helps them to kind of cough

26:08and clear their secretions. You can also

26:10kind of lay them in certain postural

26:12positions where you can help to drain

26:13some of the secretions and clap and hit

26:15on their back. Sometimes you can do

26:17nebulizing therapies that are kind of

26:19like thin up the mucus like hypertonic

26:21saline or muco

26:23N-acetylcysteine therapies and that kind

26:24of thins out the mucus making it easier

26:26to cough. But anything to kind of clear

26:28that mucus is really important so that

26:30you don't trap bacteria and cause

26:32chronic inflammation.

26:34The other thing is in these patients,

26:36you're doing mucus clearance, but you're

26:37also going to have a lot of bacteria

26:39that are colonizing. So I think it's

26:41important to reduce bacterial growth to

26:43knock down the risk of recurrent

26:44exacerbations and infections. And so you

26:46have to ask yourself the question, has

26:48the patient had three plus exacerbations

26:50where they've had to be treated with

26:51antibiotics per year, then they probably

26:53need to be on antibiotic therapy until

26:55determined otherwise. And you should

26:57probably try to tailor it towards the

26:59pathogen from their sputum culture. Cuz

27:01if it's pseudomonas, fluoroquinolones

27:03are going to be preferable outpatient.

27:04And if it's not pseudomonas,

27:06azithromycin may be the preferred

27:08measurement there.

27:10The last thing I think is really

27:11important for bronchiectasis is reducing

27:13the risk of hemoptysis. These patients

27:16may require bronchial artery

27:17embolization at some point in time in

27:18their life. And if they have recurrent

27:20events of hemoptysis, it may even

27:22require surgical resection of the

27:23diseased lung segments.

27:25Well, my friends, that covers

27:26bronchiectasis. I hope it made sense. I

27:28hope that you guys enjoyed it. And as

27:29always, until next time.

27:34[music]