Pneumothorax | Etiology, Pathophysiology, Clinical Features, Diagnosis, Treatment

what's up ninja nerds in this video today we're going to be talking about pneumothorax but if you guys really want to follow along truly understand this topic go down in the description box below it'll take you to our website on our website we have some amazing notes that are done by our medical writers our medical illustrators also make some very beautiful diagrams of the board before it's actually filled out after it's filled out so it just helps you in really understanding this topic and following along and just effectively learning this topic so please check that out also if you like this video you benefit from it it helps you please support us by hitting that like button commenting down in the comment section and please subscribe all right let's get into it all right ninja nurse let's talk about pneumoforax well what is a pneumothorax it's basically air within the pleural cavity right that's all it is a pneumo thorax is air within the pleural cavity that usually causes the pressure in the pleural cavity to go up to the point where that pressure is greater than the actual intrapulmonary or alveolar pressure and then leads to the collapsing of the lungs and there's a ton of different complications that can arise from that really briefly to kind of make a little bit more sense about why pneumothorax is developed based upon the physiology real quick you have two different layers of plural right you have a plural layer here that i'm drawing that's kind of connected to the chest wall kind of like clings to the chest wall and pleura is basically it's kind of a mesothelium it's like a simple squamous epithelial tissue with a little loose connective tissue but this one here that's clinging to the chest wall this one is called the parietal pleura okay there's another one this one that's actually clinging to the lung tissue so it's actually sticking to the lung parenchyma that one is called the visceral pleura and then there's a space a potential space that contains a little bit of fluid a little bit of serous fluid that space that exists between the visceral plural right here and the parietal pleura this is called the plural cavity and again a couple big things that i want you guys to remember about the pleural cavity first thing is it contains a little bit of serous fluid and that serous fluid the goal of it is to allow for a little bit of lubrication between the visceral plure and the parietal pleura okay it allows for them to stick a little bit but it also allows for them to rub up against one another whenever we breathe and so there's not a lot of like dryness and friction between the layers because that can cause inflammation but here's a big thing i want you to remember the pleural cavity normally doesn't have any air in it and here's the biggest part okay please don't forget this the pleural cavity has a pressure we call this the intra plural pressure the intrapleural pressure which is the pressure in the pleural cavity is usually what we call a negative pressure to be exact like if you guys want to go back and watch our biomechanics video on the mechanics of respiration it'll make more sense we can explain it there i don't want to go too crazy in detail because we have too much stuff to talk about but the basic concept is intrapleural pressure is about negative four millimeters of mercury less than the intrapulmonary pressure or the pressure in the alveoli okay we usually use the terms like zero millimeters of mercury which means that we say that the pressure in the alveoli is zero in a sense that means it's equal to the atmospheric pressure which is like 760 millimeters of mercury right the pressure in the pleural cavity is usually negative now think about this think about it really simply pressure things like to move from areas of high pressure to areas of low pressure so if the intrapulmonary pressure so the pressure in the actual alveoli the lungs this is your intra pulmonary pressure this is usually zero millimeters of mercury so it's usually a zero pressure but it changes with inspiration and expiration it may become positive one positive two positive negative one negative two millimeters of mercury change during inspiration expiration but usually the pressure is always greater than the intraplur pressure and that's a good thing because think about this if you want the lungs to expand if the pressure in this cavity is higher than the pressure within the lungs would the lungs be able to expand outwards no but if the pressure inside of this pleural space is very low it's negative in comparison to the pressure in the alveoli or the lungs it's going to be easy for the lungs to be able to move against that low pressure system because it'll be able to go from high pressure to low pressure but here's the problem [Applause] what if you get a little leak somewhere we'll talk about how but you start getting air that's accumulating in the intrapleural cavity or the pleural space okay so now you got air that's accumulating here oxygen nitrogen those can generate kinetic energy can increase pressure inside of the pleural space so now the pressure which was supposed to be a negative pressure let's say that that intrapleural pressure now that it has air in it is positive pressure in comparison to the intrapulmonary pressure it's a positive pressure let's just say give it plus one plus two millimeters of mercury right so it's plus one plus two in comparison to the intrapulmonary pressure now if the pressure in the pleural space is greater than the pressure in the lungs is the lungs going to be able to inflate against a high pressure no because now it has to go from low pressure to high pressure it doesn't usually work that way it takes a lot of effort it takes a lot of work and so because of that the pressure in the pleural cavity will actually start pushing on the lungs causing them to collapse that is a pneumothorax beautiful so what i wanted to take away from this the basic concept of physiology visceral pleura parietal pleura exists space between it is the intra is called the pleural cavity the pleural cavity contains fluid shouldn't usually contain any oxygen the pressure should be negative the negative pressure in the pleural space is what allows for the lungs to be able to expand during inspiration okay if the intrapleural pressure goes up it becomes positive greater than the intrapulmonary pressure because you get air into that area then the pressure in the pleural cavity becomes greater than the intrapulmonary pressure and the pressure gradient is lost now the pressure is kind of going to start smashing on the lungs causing them to collapse the question is how in the heck did air get into the pleural space my friend this is how think about it like this you get a break within the chest wall for some reason you get a break within the chest wall and air leaks in to the pleural space that way that could be one potential reason so there could be a break within the chest while allow for air to slice and dice into the actual pleural space or there could be something wrong with the actual lung tissue where an issue with the lung causes air to leak into the pleural space as well so we have two potential causes that we can think about here there could be an opening up of the chest wall and air leaking in or there could be an opening up of the lung and air leaking into the pleural space either way that pressure in the and the actual pleural space can become pressurized if it becomes either positive or near pi you know equal to the pressure in the actual alveoli or in the lungs it can start pushing on it causing collapse so now that we have a basic understanding of that let's talk about the causes there's two particular ones that i want to talk about there's spontaneous and then there's traumatic pneumothorax now there's another subtype called attention pneumo we'll talk about that in a little bit but spontaneous pneumothorax there's two types a primary spontaneous neurothorax and a secondary spontaneous dynamo with rice all i want you to focus on please primary spontaneous pneumothorax is there is no lung disease present the patient does not have any lung disease secondary spontaneous is the patient does have an underlying lung disease okay so they have a pneumothorax likely secondary to their lung disease no lung disease it's a primary spontaneous neumothorax and there's other factors that are related to this that you need to remember what are some of those factors okay big thing to remember for primary spontaneous is this happens in tall thin males generally who smoke smokers okay so tall thin males usually young as well young so tall thin young males who are smokers these are potential like triggers now why this is we'll talk about in just a second there's a thought about shearing forces but what i want you to think about is smoking is a very big risk factor being tall thin young male but what do you think is a potential condition that can predispose a person to being tall thin and tall and thin particularly in these kind of cases what do you think there's a very interesting condition where you can see this in what's called marfan syndrome okay so marfan syndrome marfan syndrome is kind of a genetic condition where there is a defect within the fibrilline gene right and these individuals can be very tall they can be they're very thin they can have very long fingers so this is a condition that you want to think about so if a person has marfan syndrome they're at higher risk for a primary spontaneous domethorax because of the secondary features of their condition which is them being very tall and thin okay so we got tall thin young males who are smokers or patients who have marfan syndrome how does this happen okay you see here you have the lung parenchyma and then there's this little like little like blebby thing that's existing there this is actually called it's underneath the plural you see the blue line goes right above it it's just beneath the pleura so we call this what's called a sub plural and it's usually near the apex that this happens in these people subplural apical blebs and it's basically just like this little sh like what happens is whenever people are tall and thin they're males and again they're young is it creates a shearing force between kind of this area here that creates these little like blebs that can develop and what happens is these blebs are very susceptible to any kind of increase in high pressure so for example if one of these tall thin young males who smokes or has morphine syndrome decides to go ahead and valsava or hold their breath or do something like that the pressure inside of the actual thoracic cavity increases enough it could rupture that bleb and then air can then leak from the actual lung straight into the pleural cavity and what do they have as a pneumothorax okay beautiful so we understand the primary spontaneous pneumothorax what about secondary spontaneous neutronics let's talk about that all right secondary spontaneous pneumothorax okay this is a very interesting one so you want to think about this there's something wrong with the lungs that are predisposing the individual to being at high risk for developing a pneumo and i like to make it easy on myself right what's a condition that would cause the lung to just have more air and it would like you know you have more air and so because of that the lungs are just a little maybe a little bit more puffy they can kind of like bulge out like a little like bullet and because of that those bullet can potentially rupture and then leak air into the pleural space what's a condition where you can have hyperinflation or just big baggy lungs or you can't get air out because there's some kind of narrowing of the airways obstructive lung diseases right obstructive lung diseases so in a patient who has what's called obstructive lung disorders right and we'll we'll list them in a second but think about this if you have obstructive lung disorders so these are let's say these are your normal lungs right and then because of some condition maybe it's hyperinflation right and this hyperinflation there's many different mechanisms behind this but the lungs get bigger and puffier right maybe but think about this what could be causes of this you know in someone who has emphysema they actually have their they kind of destroy some of the actual connective tissue around the bronchioles okay so what happens is imagine here you have like an alveolar sac okay and then here you have like a bronchial okay that's supposed to be draining air out right so generally you want co2 to exit well what happens is because they lose let's imagine here in pink is some of this connective tissue they get so much destruction of some of the connective tissue that they lose that ability to have this connective tissue that kind of keeps these bronchials open so whenever they exhale these bronchioles actually collapse and so now you can't get air out and so now there's kind of some air trapping as a result and these alveolar are going to kind of plump up a little bit all right take another situation maybe it's not just the bronchioles collapsing or them having destruction of the alveolar septal membranes as well and then having these big plumpy alveoli another thing to think about is what if they have a lot of like here's their airway so let's say here's their airway and they have a lot of mucus secretions right so they have a lot of mucus secretions and these mucous secretions that they have is really narrowing the airway and so you want to be able to get co2 out but there's so much mucous secretions that it's plugging up and blocking the co2 from getting out and because of that you're just puffing up those airways or maybe the there's a lot of like swelling or edema or inflammation of some of the actual bronchial walls and that's also causing the inflammation is kind of narrowing the airway as well so there's a lot of these conditions that can do that right and as a result because these airways kind of become a little bit more puffy and hyperinflated you know what happens as a result they can develop these little things that develop near the actual pleura and these little things these little baubles are called bole and these bole are very very susceptible to rupture and if they do rupture look what can happen if they pop boop you're going to put air right into the pleural cavity okay so that is the big thing so let's talk about some particular obstructive lung disorders that can cause this hyperinflation that can cause this air trapping effect via the bronchiolar collapse via the mucous secretions via the edema within the bronchial walls what are some conditions that you guys can think about well what about something where emphysema we already talked about that right so emphysema or there's another condition where you have a lot of chronic inflammation and mucous secretions within the airway chronic bronchitis what is those two collectively called copd so in a patient who has what's called copd which consists of chronic bronchitis we'll just put c b and then emphysema right another one is whenever you have a lot of inflammation and also just a lot of edema within side of the potential bronchial walls because of a lot of allergic reactions in situations like asthma or there's another condition called cystic fibrosis you know when a patient has cystic fibrosis they get a lot of mucus secretions and you know what happens is because of those mucous secretions they cause dilation and plugging up of the airways and then the bronchials start actually going under this dilation and the walls get kind of very thin and it can lead to what's called bronchiectasis so what can happen is a patient with cystic fibrosis can develop a condition called bronchiectasis and that bronchiectasis also cause a lot of mucous plugging thickening of the actual bronchial airways and then as a result they can develop this dilatation and thinning of the membrane because of a lot of inflammation these are potential conditions that i want you guys to think about they can develop bole the bullet can then rupture okay because of this hyperinflation or another term that we use is like air trapping okay beautiful okay another way i like to think about this is maybe it's not just they're trapping air maybe there's actually something that's destroying the lung tissue it's destroying the lung tissue and the lung tissue is destroyed maybe close to somewhere near that plural are near an area where it actually can leak into the actual pleural space so the next one i want to be thinking about is is there any kind of destructive lesions so that's another big one to think about is there any kind of destructive lesions or diseases that can actually cause destructive or cavitary lesions so destructive lesions or what's called cavitary lesions this is a big one and the first one that i want you guys to think about is infections infections are probably going to be one of the biggest ones so you know there's a condition there's a very nasty disease that can actually cause very nasty cases necrosis it can cause cases necrosis of the actual lung tissue it can cause cavitary lesions and as it destroys some of the lung tissue it then allows for that lung tissue to uh be destroyed and open up into the actual pleural space that is tuberculosis so if someone has tuberculosis another big one that they love to ask on your exam you know there's a condition whenever a person has hiv aids their cd4 counts getting low they have an opportunistic infection called pneumocystic uh pneumonia pneumocystic pneumonia pcp they actually now they call it pjp actually so pneumocystic geravicius pneumonia but this is actually something that can happen in patients who have hiv aids with low cd4 count it's opportunistic infection this can cause inflammation of the alveoli alveolitis and then that alveoli as it becomes inflamed inflamed inflamed it actually can lead to rupture of the alveoli and then air leaking right into the pleural space so you have conditions like tb you have conditions like pjp what else you know someone who has like some type of malignancy they have cancer you know in lung cancer there's a very specific type though of lung cancer which has high rates of pneumothorax squamous cell carcinoma so what is this called squamous cell carcinoma swami cell carcinomas they're cancers they have the ability to outgrow their blood supply they can evade and contiguously spread through the lung tissue and if they spread enough that they start involving parts of the pleura and near that kind of apical near the parenchyma plural interface eventually that could wear away and create a destructive lesion that could allow for a pneumothorax okay so effectively what i want you guys to remember here is this can be due to infections like tb pjp one other one to remember is if someone gets a lung abscess this is another one so don't forget that one as well is lung abscess lung abscess is another one to not forget as well so destructive cavitary lesions like infections like tb pjp lung abscesses or lung cancer especially squamous cell carcinoma this describes our secondary spontaneous pneumothorax causes let's now talk about traumatic pneumothorax causes all right so let's talk about traumatic pneumothorax obviously the etiologies of these are relatively like they're not too bad they make sense it's some kind of trauma but while we're here i want to talk about there's two types of traumatic pneumothoraxes that you could potentially see well one of the big things here is let's say that somebody had some type of traumatic injury where there was a break through the chest wall right so here's the break through the chest wall and air is able to leak into the pleural space right and also able to leak out of the pleural space so whenever you take a breath in the air can leak in through the pleurals like leaking through the actual opening in the chest wall into the pleural space and whenever you exhale the air can exit out from the pleural space out into the atmosphere this is a special type of traumatic pneumothorax and they call this an open and open pneumothorax sometimes it's even referred to as a sucking chest wound right because whenever you take a breath in you suck air through the actual defect within the chest wall into the pleural space and whenever you exhale you actually exhale air out through that defect within the chest wall okay so this is an open pneumothorax what would be different is if you had again a traumatic pneumothorax where there's a break within the chest wall and air can leak in but let's say like it's weird like you have like a rib fracture or something but it's like a valvey kind of thing whenever you take a breath in this kind of like opens up a little bit and air can leak into the pleural space but whenever you exhale this kind of flap comes down and air isn't able to be exhaled out through the defect in the chest wall during expiration this is called a closed pneumothorax so it's a very simple concept it's not too bad it's a simple thing open pneumothorax which can happen in traumatic pneumothorax is a defect within the chest wall if air can come in during expiration and out during expiration that's an open pneumothorax if the air only comes in and it does not leave the defect during expiration it's a closed pneumothorax it's almost kind of like similar to what we just talked about over here with spontaneous north rocks it's just the air is leaking into the pleural space from the lung tissues from a defect within it whether it's a hole in it whatever it might be okay now let's talk about this next aspect of traumatic pneumothorax believe it or not we always kind of think oh there was you know a car accident they got hit with a baseball bat they got stabbed in the the chest with a knife or something like that sometimes it's actually inadvertent from medical therapies what is that called whenever there's unfortunate kind of like things that can happen as a result of medical therapies it's called an iatrogenic type of effect right so sometimes you can have iatrogenic atrogenic pneumothorax that can be sometimes a result of trauma what are examples of iatrogenic traumatic pneumonia sorry guys i had to take a break rob made me laugh the reason why is with iatrogenic i i frequently when i work in the icu i do a lot of central line procedures and one of them is called a subclavian central line when you do subclavian central lines there's always a chance it's it's a risk that you can potentially cause a pneumothorax so it's something that can potentially happen so nitrogenic harm that could actually be as a result of trauma here could be some type of subclavian central line placement we call that a central venous catheter placement you know what else it could be due to sometimes if you actually have a big whopping pleural effusion and you have to go in and tap it and drain that pleural effusion what is that called a thoracentesis sometimes you may hit that lung too so a thoracentesis another thing is if you're doing like a biopsy sometimes if you're doing what's called like a pleural biopsy that could also be a potential risk too you're doing like a pleural biopsy for some reason so those are simple things another one that's really interesting is when you're doing mechanical ventilation so sometimes one of the big things is if a person has like very let's say you know the copd lungs kind of like they have hyperinflation of their lungs and you're pushing them with high pressures or they have acute respiratory distress syndrome and you're pushing high peeps so high peep on what's called the mechanical ventilation like whenever you're mechanically ventilating it's called positive and expiratory pressure it's the pressure that you try to exert into the alveoli during the expiratory process so that you stent them open keep them open sometimes that high peep can cause barotrauma it can injure the alveoli and then that can also cause a pneumothorax you know what else is unfortunately inadvertent cpr you can potentially break a rib during cpr and that rib fractured segment can potentially cause a puncture in the lungs so cpr is another potential therapy that you have to be aware of i think that you guys get the point out of all of these but atrogenic potential causes of traumatic pneumothorax is also something to think about okay what else is another potential thing that i want you guys to think about it's non-iatrogenic so what are things that are non-iatrogenic it's not like an inadvertent uh thing that happened from medical therapy so this is where you get into like motor vehicle accidents so some type of blunt trauma maybe it was a massive fall okay you fell you cracked a rib and that rib fractured segment caused a traumatic pneumothorax other causes that you got to be thinking about is you know bullets if those penetrate through the chest wall hit the lung you can get kind of a double whammy there for a traumatic doom with ice or a stab wound right so these potential things are uh things to think about for traumatic pneumothorax so we have an idea now pneumothorax air within the actual pleural cavity how did it get there these primary spontaneous pneumothorax the secondary spontaneous pneumothorax or the traumatic okay now that we under we know that the problem with that air being in the pleural cavity is that the pressure can rise it can push on the lungs it can cause it to collapse what are the negative things that we can think about what are the potential very very dangerous complications that can arise from pneumothorax and what are some of the clinical manifestations that we can make sense of through the pathophysiology all right so let's talk about the pathophysis of pneumothorax now it is not that bad to actually make sense of this right so let's say here we have a patient they had a normal lung right from one of the causes right they're tall thin young males smokers marfans they got copd they got asthma they got cystic fibrosis bronchiectasis they got destructive lesions tb pjp lung abscess they had lung cancer they were gonna have traumatic pneumothorax whether it was a hydrogenic non-nitrogenic and they get air that leaks into this fluorocavity pressure rises it's no longer negative intrapolar pressure it's now becoming zero to positive pressure in the pleural cavity is going to be greater than the inter-pulmonary pressure i know you said it if the pressure in the pleural cavity is greater than the intrapulmonary pressure it's going to start pushing things like to go from areas of high pressure to low pressure so to go from the pleural cavity the pressure will start pushing onto the intrapulmonary area so it'll push towards the intrapulmonary pressure and start collapsing the lungs what is the lung made up of lung parenchyma's having like a simple squamous epithelial tissue right particularly the alveoli right so what happens is as this pressure starts rising and starts pressing and pressing and squeezing on the lung and as you start squeezing on the lung you start collapsing some of the microscopic structures of the lung let's take a look at what happens here if we zoom in on that portion of the lung we get an alveoli this is a normal alveoli right this is a normal we'll put normal alveoli so oxygen will be coming into this bad boy there's no particular issues of being able to get oxygen to the alveoli it's not collapsed in any way shape or form oxygen can easily diffuse from the alveoli into the blood there's a good gradient and then co2 will be able to move from the blood to the alveoli and be exhaled with no issue right and this normal kind of alveolar type of appearance here and a person who develops a significant pneumothorax to where the lung is being compressed and now the alveoli which are the microscopic components of that lung boom that bad boy starts getting collapsed if it starts collapsing can you feel as much oxygen through that little sucker as compared to this one no so now i'm gonna be struggling to be able to bring oxygen into that little baby alveoli and so because of that less oxygen will end up in the actual alveoli and so that's going to affect the gradient because normally oxygen is usually going to be very high within the alveoli and oxygen is usually lower within the pulmonary capillary blood and so that creates a pressure gradient where oxygen easily moves from areas of high pressure to areas of low pressure if this alveoli super collapsed now the oxygen concentration in the alveoli is lower the pressure is going to be lower and so now if you compare that there's not going to be as much of a pressure gradient and so less oxygen will diffuse from the alveoli into the lungs and if there's less oxygen diffusing into the out from the alveoli into the lungs what does that cause what does that cause whenever there's less oxygen that's actually diffusing into the pulmonary blood and eventually into the systemic arterial blood hypoxemia so as a result the patient may develop hypoxemia so this is a potential that can occur now if we go back to this thinking about vq mismatching and so on and so forth what's happening is there a problem with the profusion here no there's no problem with perfusion right so the actual blood flow to the alveoli should be fine it's intact you're perfusing the alveoli the problem is the ventilation so if you were to look at the vq ratio here would it be low or would it be high well the ventilation is decreased and you have normal perfusion so the vq ratio is decreased there's a decrease in the vq ratio and again hypoxemia due to alveolar collapse due to pressure in the pleural cavity being high squeezing down on the lungs squeezing down in the alveoli making it difficult to actually inflate them that leads to the next question what are some of the symptoms besides hypoxemia so not only they could actually be completely asymptomatic right so they can have no symptoms depending upon how small the pneumo is if the pneumo is really small it's not having a lot of that compressive symptoms they might not have any real market or significant hypoxemia sometimes they can be completely asymptomatic but you know what else if there is all that air here's our pneumothorax here one of the big things to think about is that sometimes these patients most common symptom is sometimes like dyspnea so they can present with a shortness of breath right and generally that may be related to the hypoxemia that may be related to because if you're having to inflate if you're having to drive air into this lung that's maybe a little bit deflated you're going to have to work harder than you usually would have to to inflate that lung against this higher pressure within the pleural cavity that takes work and that can lead to shortness of breath the other thing is because you're separating the pleura there is actual nerve endings that actually supply these areas and so it can cause a referred pain to the chest especially when you're breathing because of the separation within these actual pleural linings and so this can cause what's called a pleuritic chest pain so that's another big thing to think about so not only can they have dyspnea not only can have they have pleuritic chest pain you know what else is a big thing to think about another thing to do is just take your stethoscope listen to their lungs if they're taking breaths in it should sound equal bilaterally right assuming that they have no difficulty being able to inflate both of those lungs if they have a decent pneumothorax you may hear absent breath sounds or decrease breath sounds on the affected side so listen take that stethoscope out take that litmen out and see if you hear any decreased breath sounds or worst case scenario maybe it's even absent the other thing that you can do is if you really want to we don't don't always do it but it's a good practice to do it is you percuss you percuss the chest wall and generally what you should have is a natural kind of resonance of the actual percussion if it starts to sound drum like or tympanic like we call that hyper resonant that could be potentially indicative of a pneumothorax so hyper resonance on percussion could be indicative of a pneumothorax the next thing if you really want to do it is you can take the hypothenar imminences and put it on their chest and have them say 99 99 and you're testing tactile premise the vibrations to hit the actual hypothenar eminence in a patient with a pneumothorax because of all that air it's affecting the vibrations that are actually being transmitted through the actual bronchi and so you'll have a decreased tactile formatives so there may be a decreased tactile framethis you know what else is interesting about this condition sometimes what happens is let's say that here you have like a little we have like a little bronchial airway here so here's like a little bronchial airway let's say here you get like a little bronchial airway so sometimes let's say that here the cause of the pneumothorax was like a leakage right here right so you pop this kind of like alveoli for some reason that we talked about over here sometimes what happens is not only can it dissect into the pleura it can actually travel along the mediastinum up the mediastinum and into the subcutaneous tissue when it does that it dissects through the mediastinum and up into the subcutaneous tissue what is that called subcutaneous emphysema so you can actually develop like these air pockets with inside the axle usually near the neck or near the actual chest wall and so that might be another potential sign of a pneumothorax is sub cutaneous emphysema you know one more thing hypoxemia what's a reflexive reaction to hypoxemia what does our body try to do whenever we are hypoxemic it'll send information to what structure it'll activate those chemoreceptors that we've talked about before if it stimulates the chemoreceptors that'll activate our central nervous system and then our central nervous system will try to do what increase our respiratory rate what does that call when you have an increase in respiratory rate tachypnea so they may develop tachypnea as a potential reaction as well so they may have a person with hypoxemia their hypoxemic type of reaction may be tachypnea they may have shortness of breath because of having to work harder to inflate those lungs they may have crunching of their chest or near their neck because of subcutaneous emphysema the air leaking and slicing through the mediastinal airway they may have pleuritic chest pain pain with every breath they may have decreased breast sounds or absent breath sounds on the affected side where the pneumo is hyper resonance upon percussion and potential decreased tactile parameters another thing that you should be looking for is do they have any open chest wound is there any opening so another thing to be looking for just being observant is is there was any kind of like let's say here was the the point here where there was an opening in the chest wound so that's another thing to look for is to look for any signs of open chest wounds or any signs of rib fractures so maybe you you know they have tenderness to palpation they have some echomosis around some area you want to feel for any step-offs any kind of tenderness to palpation any echosis around that area may be a sign of rib fracture so again looking for any opening of the chest wounds looking for any rib fractures there's also other potential things to be looking for okay the next thing that we have to talk about which is probably the biggest topic here is going to be the topic of tension pneumothorax so this is a type of pneumothorax that can develop and this can develop from any of them it can develop from a primary spontaneous pneumothorax it can develop from a secondary spontaneous normal thorax or it can develop from a traumatic pneumothorax okay usually more common of the traumatic variety but it can develop with any of the types of pneumothorax this is a very serious medical complication that can develop from this condition a really high yield topic let's talk about it okay so if we have someone who has a tension pneumothorax what happens in this condition okay so here let's say that this person has a pneumo whatever the cause was whether it was a primary was a secondary weather was a traumatic there's air here in the pleural space pressure in the plural space is increasing it's compressing on the lung as it's compressing on the lung the pressure starts becoming very very positive so the intrapleural pressure continues to rise if the intrapleural pressure starts to continue to rise and it presses on the lungs you know what it starts to do it starts to shift everything from this affected side to the opposite or contralateral side it starts shifting everything from the affected side to the contralateral side so imagine this lung just completely collapsing and then imagine on top of that you're trying to squish the contralateral lung you're just compressing alveoli left and right what would be the result of that go back to what we talked about just a second ago if we were to really zoom in and look at what that could potentially look like here here's your normal alveoli after you had some normal ventilation so we had that ventilation process that was normal the profusion which was your q component that was normal but then you started to have this tension pneumo and that tension pneumo as a result caused collapsing of the alveoli so now as a result your ventilation is decreased but your perfusion may still be normal and so what happens as a result of this because this alveoli is so collapsed you're going to have less oxygen diffusing from the alveolar into the blood because less oxygen is able to get into the alveoli because of it being so significantly collapsed okay so less oxygen is getting in less oxygen is diffusing and as a result the patient develops severe hypoxemia as a result okay and what's the reflex of reaction to hypoxemia the reflexive reaction is an increase in respiratory rate so they may become tachypnic and they also develop an increase in heart rate a reflexive kind of tachycardia to try to increase blood pressure to perfuse more areas of alveoli in attempts to increase the oxygenation process so there may be a reflexive tachypnea and a reflexive tachycardia as a result okay but a significant hypoxemia can result from attention pneumothorax okay it has a very very scary effect on the heart so imagine this think about all the different components of the heart first thing i like to want i want you guys to think about is the svc so think about the super vena cava imagine that you're pushing you're smashing this heart on the side and you're squeezing at this point you're squeezing the superior vena cava so this is the superior vena cava if you're squeezing the superior vena cava what's going to happen to the venous return well generally the venous blood is coming from the upper extremities down into the right atrium right if the superior vena cava is compressed from this tension pneumo you're going to get a decrease in venous return but even worse than that it obviously can do two things a decrease in venus turn could potentially drop your stroke volume and effectively drop your cardiac output and effectively drop your blood pressure but you know what else it can do if the svc is compressed and there's less venous return it starts backing up and it backs up into the veins that are just kind of proximal to it so you have svc brachiocephalics and then ijs and ejs and they start getting puffy and you can develop what's called a jugular venous distention so they may develop less venous return which can drop their pressure but they can also develop jugular venous distension because of the compression of it and causing venous congestion proximal to the compression okay what if you compress the ivc so you're starting to again smush things and angulate the ivc the same thing happens here if the ivc is compressed ivc is compressed you get a decrease in venous return if you get a decrease in venous return you get a decrease in stroke volume a decrease in cardiac output and a decrease in their blood pressure man that's not good okay what else what if i'm smashing and i'm pushing the right heart like i'm squeezing i'm really squeezing and pushing on that right heart and now the right ventricle is being compressed so now the right ventricle is being compressed what is the problem with that well if the right ventricle is being compressed that does two things again it's going to decrease the preload it's going to make it harder for you to be able to get blood into the right side of the heart and if that's the case that'll drop your stroke volume and that'll drop your cardiac output and that'll drop your blood pressure okay what else though here's another thing whenever you have such a it's a significant kind of tension pneumo what happens is the right ventricle doesn't get a lot of room okay it's getting really smashed up against this other lung so it doesn't have a lot of room and so what it starts doing is it actually starts causing the interventricular septum to bow in to the left ventricle it bows into the left ventricle but you know when it's the worst imagine you take a deep breath in and when you take a deep breath in most of the air is going into this this lung right here and so it smashes up against the right ventricle more significantly during inspiration which bows the ventricular septum towards the left ventricle worse during inspiration and so because of that the left ventricle has a very narrow left ventricular outlet and so because of that because you bow the interventricular septum that increases the afterload on the left ventricle as a response to that the blood pressure is going to the actual stroke volume will decrease and the cardiac output will decrease and the blood pressure will decrease but it's very very very specific this is only during inspiration you know what this is called whenever you have a drop in blood pressure of like 10 to 20 millimeters of mercury during inspiration this is called pulses paradoxes pulses paradoxes so again think about that right so again we have ivcs compressed or angulated decreased venous return svc is compressed jvd decreased venous return right ventricular is compressed decreased preload decreased drug volume decreased cardiac output decreased blood pressure if the during inspiration you're bowing the interventricular septum towards the left ventricle you increase their afterload you cause them to have less stroke volume less cardiac output less blood pressure during inspiration which is called pulses paradoxes and then the only other thing i want you to remember is if the right ventricular cardiac output drops the responsiveness to this is that again the same thing you know blood generally will go from the right ventricle it'll go through the pulmonary artery it'll go from the pulmonary arteries back to the pulmonary veins and from the pulmonary veins into the left atrium left ventricle and out through the systemic circulation so we say that if the right ventricular blood pressure drops that will cause effectively the left ventricular blood pressure to also drop and what is the reflexive reaction to a person having a decreased systolic blood pressure a reaction to that decreased systolic blood pressure is they develop a reflexive tachycardia so we have a pretty good idea here of what could be the potential complications of someone developing attention pneumothorax is that uh lung-wise they can have hypoxemia due to a collapsing of the alveoli creating a hypoxemic effect and a reflex of tachycardia tachypnea they could have compression of ivc svc affecting venous return and causing jvd for svc the right ventricular compression decreasing their blood pressure also causing the interventricular septum to bow causing pulses paradoxes and because the right ventricular outflow because the right ventricular blood pressure is dropping effectively that's going to drop the left ventricular blood pressure which again will create a reflex tachycardia the only other thing that i want you to remember is if this tension pneumo again is developing here and it's pushing everything from this side towards the other side it's shifting the entire kind of mediastinum it can also cause the trachea to shift so it can cause tracheal shift or deviation particularly to contralateral side of the actual pneumothorax and so that is another big thing to remember all right so effectively we've covered the clinical features of pneumothorax and then the scary clinical features that being attention pneumothorax okay now that we've covered that let's talk about the diagnostics all right so when we're diagnosing a pneumothorax right there's a couple tests that we can do we'll take a look we'll take a look at some images we'll take a look at a chest x-ray we'll take a look at a lung ultrasound and chest ct all of these can be utilized to diagnose a pneumothorax but really quickly the most important thing to remember and this will show up in your exam and it's most important to think about in clinical world attention pneumothorax should not wait for a chest x-ray attention pneumothorax should be diagnosed clinically based upon what we just talked about decreased breath sounds hypotension tracheal deviation tachycardia jvd so on and so forth and based upon that immediate needle decompression followed by a chest tube should be the actual correct course of action for attention pneumo so just remember that we utilize these tests for pneuma but we clinically diagnose attention pneumothorax let's take a look at these images real quick all right engineers let's take a look here to chest x-ray remember what i told you guys again for when you're diagnosing a patient with a pneumothorax if they have a tension pneumothorax you do not wait for a chest x-ray you treat immediately based upon their clinical features and things that are hemodynamically unstable for them so if we had a patient that we did get a chest x-ray and we suspected animal thorax what are we looking for we'll take a look here we have a chest x right here this is the right hemi thorax it's the left hemithorax you can see the heart here you can see your right hemidiaphragm left hemidiaphragm now what we're looking for is we want to look to see the lung markings you see the lung markings how it's going all the way out to the periphery on this right side and always look at those apexes always take a look at those apexes okay don't forget those that's where you'll miss pneumos so on the right side i see lung markings all the way out and if i look here on the left side whoa here's the lung and i don't see any lung marking it's really really like hyperlucent right here this is a pneumothorax and a pretty big left partial pneumothorax on this person okay so again what do we have here on this patient we have a massive kind of left pneumothorax on this patient with the collapsed lung and we're already starting to see signs it's not a tension pneumo yet but we're already starting to see some signs of this actual mediastinum getting pushed a little bit to the actual contralateral side so if this doesn't get actually decompressed there is a potential for this to become a tension pneumothorax all right so this is a super obvious pneumothorax let's see if you guys can pick out this next one all right ninjas let's take a look here at a little bit more of a subtle pneumothorax let's see if you guys can find it so again let's kind of a b c to e right airway following the trachea it's staying midline it's branching out into our primary bronchi we're looking here at the breathing are they taking deep breaths is there a little like any hyperinflation is there any atelectasis good you know inspiratory effort here we can see that the lung markings are going all the way out to the periphery on that right side we see nice and crisp costophrenic angles here at the diaphragm this costophrenic angle here on the left is way wider and deeper in comparison to the right hemi side hemithorax that's a little interesting so i got a deepening of that left costophrenic angle looking at the mediastinum the heart it looks to appear to be kind of midline here a little bit kind of you know pointing apex towards the left so that looks good i don't see any widening of the mediastinum let me come over to my left lung it looks like it's inflated properly we are following our lung markings all the way out it looks like it's going all the way out here but what i tell you guys always to look at look at those apexes right lung markings look like they're going all the way out here but if i follow here lung marking lung marking lung marking and it looks like it stops like right here let's zoom in let's take a look here because we don't want to miss any kind of pneumothorax oh ninjas what do we see here you see this right here that's our plural line the plural line the visceral pleura is separated from the parietal pleura on the chest wall and then look how the lung markings stop going because they stop at that pleural line there right in this vicinity is the pneumothorax this is a left apical pneumoforax so it's a real subtle one but you will miss it and if we come over let's actually compare this to the other side go over here and look we can see that when we're following this the lung markings are going all the way out i don't see any evidence of a plural line don't get confused again with the the ribs and the clavicle but i see complete pleural markings all the way out here pulmonary markings and i don't see any evidence of a pleural line or any pneumothorax so this patient definitely has a left apical pneumothorax really really subtle but it's there so again what do we have here we have a patient with a left apical pneumothorax all right let's take a look here at an ultrasound of a patient with a pneumo all right ninjas let's take a look here at an ultrasound i love to do ultrasound again it's a quick thing that you can do bedside and look for any signs of absence of lung sliding that is the big key word to remember for a pneumothorax is any absence of lung sliding let's go ahead and play this video here of an ultrasound you see how the lung is actually sliding with each breath that's actually going to be the pleura okay but we're looking here at this point of the lung underneath the ribs so here's the rib you have like the muscle and the ribs on the sides here you can see here that there's no sliding of the lungs on this point here this is evidence of a pneumothorax so again when we're looking at the lung what are we actually looking at we're looking for this pleural line here this is the pleural line we're looking for this to slide if there is an absence of sliding at this point right here it could be indicative of a pneumothorax all right let's go ahead now and take a look at a ct of a pneumothorax all right engineers let's go ahead and take a look here at the ct now so again ct is really good for being able to look for pneumothorax that are maybe really difficult to be able to see on a chest x-ray or maybe you're trying to determine if you want to actually intervene and just get a little bit of a better idea of how to size the pneumothorax a little bit more effectively so if we take a look here we're going to look at our lung window and we're scrolling again a little bit of orientation this is the right hemothorax left hemothorax this is the heart here pointing towards the left you're already starting to see something really interesting here as we start to scroll up we see no lung markings no pulmonary vasculature filling into this area here as we continue still nothing as we go up we go up we can already see the lung part here this is actually going to be that visceral pleura pulling away from the parietal pleura and we see all air in this component of that left aspect of the hemithorax and again you can see again all of that pneumo there this is actually the axial view if you wanted to get a little view of it on a coronal view this is the right lung this is the left lung we have the heart here in the center and you can kind of see all of that pneumo there if we kind of scroll back up you'll start to see some of the lung tissue come into place all of that is air that is our pneumo we can still see a little piece of it there so this person definitely has a left kind of partial pneumothorax on them so again what we see here shablam a left kind of partial pneumothorax most likely this person will need a chest tube all right that covers all of our images let's get back into talking about some of the labs that we can look at for a patient with a pneumothorax all right so we took a look at those images right now the other thing that you can do in a patient especially if they're hypoxemic it's not a bad idea is you can get an arterial blood gas and arterial blood gas is an isn't a bad idea um and so what we would do this is to see you know what kind of hypoxemia do they do they have hypoxemia so this can help us to actually establish you know is there truly hypoxemia but you can generally kind of go off of your o2 set you don't have to stick a person into the artery causing pain to determine if they have hypoxemia but also can determine kind of the respiratory status so generally if someone's to kipnick and they're breathing off their co2 really quickly trying to be able to ventilate the alveoli the best they can they may show signs of a respiratory alkalosis and again this could be the result of their tachypnea then breathing really fast blowing off their co2 you lower the co2 the ph goes up and they can develop a respiratory alkalosis so this is another thing that you could do but again the best thing to do in this kind of scenario is to follow with the above images clinical diagnosis for tension pneumothorax and you can also assess with an abg if you see that they have signs of hypoxemia and you want to evaluate that further all right let's talk about the treatment of pneumothorax all right so let's talk about the treatment of pneumothorax so first things first is supportive therapies when we're treating a person with pneumothorax actually believe it or not all patients should get supplemental high flow oxygen there's actually a a good reason behind this so all of these patients should get some type of supplemental oxygen and generally this can come in different ways you can give it through high flow like you can do what's called like a non-rebreather or you can do something called high flow nasal cannula but you just want to try to be able to give oxygen and generally the higher concentrations higher fio2s you know fraction of inspired oxygen you're not really focusing on pressure or flow rates you're just focusing on the percentage of oxygen there's a reason why it's actually really interesting because when you have a pneumothorax right okay most of the air and we're going to talk about this in a second we'll zoom in on a diagram over there believe it or not most of the air that we actually breathe in is nitrogen 78 of what we have within the alveoli of air is nitrogen and only 21 of it is oxygen so whenever you give a person a supplemental oxygen you're actually pushing higher amounts of oxygen into the alveoli we'll talk about why that's important all right let's come over here and see what it actually does so what actually happens with this is let's say that you put them on supplemental oxygen inside of this actual let's say here this is the pneumo okay so we're kind of zooming in on this area here here's the alveoli and here's the pneumothorax inside of the pneumothorax you're going to have lots of nitrogen okay lots of nitrogen okay because again what's generally within the alveoli is what nitrogen and then there was a hole within the alveoli it leaked out into that actual pleural space you give the person what tons and tons of oxygen if you flood this alveoli with tons of oxygen it actually starts kind of pushing some of the nitrogen concentration down so now look at the concentration now there's very little oxygen there's not usually a lot of oxygen in this area here but look what happens if the nitrogen concentration 78 percent there 78 is nitrogen in this actual pneumo the nitrogen pressure inside of the actual pneumo is higher than the pressure within the alveoli and there's more nitrogen concentration where will the nitrogen want to go from areas of high pressure to areas of low pressure and this nitrogen that's in the pneuma will start getting absorbed and sucked into the alveoli and as you do that what starts happening to the pneumothorax the air starts getting resorbed from the pneumoforax and that's what's really cool about this so giving them supplemental high flow oxygen allows for the resorption of the pneumothorax over time and so that's a really cool thing that you should do for all pneumothorax so all patients with a pneumothorax should get supplemental oxygen via the form of non-rebreather high flow nasal cannula and it helps to be able to enable the resorption of the astral pneumothorax okay now that we talked about that let's talk about the next thing which is patient who is unstable how do i mean unstable technically they're hypotensive they're hypoxemic they're tachycardic in those kinds of scenarios a patient should probably receive some immediate therapy so the things i want you to remember for unstable individuals do they have a tension pneumothorax do they have a bilateral pneumothorax or do they have a pneumothorax and are requiring mechanical ventilation these are the classic three scenarios where a person is generally going to be unstable attention pneumo is definitely going to cause an instability it's going to cause hemodynamic instability hypoxemia bilateral numerals are just very problematic and then if a person has a pneumo and they're under mechanical ventilation why is that bad think about that if a person is on mechanical ventilation we're increasing the pressure okay that we're running through the lungs and into this actual damaged lung and now what was maybe a smaller pneumothorax your positive pressure ventilation is pushing more air into the pneumo making the pneuma potentially even bigger which can quickly tran convert it into a tension pneumothorax so you understand that so it's a big thing to remember that if a person has a tension pneumothorax a bilateral neurothorax or pneumonia that they're going to need mechanical ventilation being under positive pressure ventilation they should get what kind of treatment and that scenario the first thing that you want to do is what's called a needle uh decompression or thoracostomy sometimes they call so needle decompression and so what a needle decompression is it's kind of a temporary thing you take and you find the second rib so here's the first rib here's the second rib okay you're going to go in between in that intercostal space and you're going to find the midpoint of the clavicle so here's the first rib here's the second rib i'm going to go into this second intercostal space so i'm going to insert a needle kind of a larger bore kind of needle into the actual intercostal space and the hopeful goal is that whenever i get it into that space i get it into the pleural cavity and if i tap into the pleural cavity and i have that opening now i can allow for air to leak out of that actual large bore needle and into the atmosphere allowing for an equilibriation of pressure hopefully however this is not something that will last long you'll eventually have to bridge them over to what's called a chest tube okay in a chest tube generally what we do for these is you actually go around the fourth or fifth intercostal space so one two three four five so i could go like let's say fourth intercostal space and you go in between the anterior and mid axillary line so a chest tube is generally going to go in the fourth or fifth intercostal space so if i were to give an example here one two three four we could go right here fourth intercostal space okay in between the anterior and mid axillary line you throw the chest tube in there okay and again that'll be usually connected to some type of vacutainer and allow for the ability to drain that pneumothorax okay so we have an idea now patient who needs supportive therapy all patients who are unstable meaning they have a tension pneumo bilateral pneumo or they have a pneumo and they're actually under mechanical ventilation with a risk of potentially becoming attention they may need needle decompression and eventually a chest tube sometimes we just forego the needle decompression it just goes straight to the chest tube okay which is common but again remember these things okay the next thing that we have to talk about here is what's called a open pneumoforax and open pneumothorax is obviously going to be in a patient who's had some type of trauma so what happens with an open doom orthorex we already kind of know here whenever a person takes a breath in the air leaks into the pleural space and whenever they breathe out the air leaks out of the pleural space right and they call this kind of like a got a sucking chest wound right now what we do is eventually they're going to need a chest tube they'll eventually need a chest tube but what we do to help out in this scenario is it's very interesting you use like a partially occlusive dressing so partial occlusive dressing so you take like this little like kind of like adhesive like kind of like sticky padding like a little adhesive kind of like sticky loose padding there and you put some gauze tape on three out of the four sides and you leave one of them with no gauze tape the reason why is imagine this when you take a breath in the problem with this sucking chest when this air is getting in every time you take take a breath out and then it's exiting whenever you exhale what we want to do is we want the air to get out when we exhale but we don't want any more air to come in when we inhale how do i do that if i have like this like loose like imagine like saran wrap almost okay so imagine like saran wrap imagine i had a hole like here on my lungs right or my chest wall a little bit of saran wrap okay when i take a deep breath in the saran wrap is gonna it's gonna try to stick and suck in towards that actual chest wall defect so no air is going to be able to go in through that area but then when i exhale the saran wrap kind of relaxes a little bit and air will be able to leak underneath that little area where we don't have that third gauze tape there so air will be able to leak out during expiration which will help to be able to kind of prevent any more air from continuously accumulating but it'll be blocked because whenever we inhale imagine that adhesive dressing kind of getting sucked in really preventing any air from getting to go in through that chest wound so this is something that we do is we use a partially occlusive dressing and eventually they're going to need a chest tube but don't put the chest tube in where they have the defect put it in another intact skin site okay okay open pneumothorax baboom we did it now what's next the next thing that i want to talk about is a stable high risk treatment so what the heck does this mean so usually stable and high risk is generally going to be those that are what's called those who have secondary spontaneous pneumothorax so those with lung diseases okay so patients who are stable but they're a little bit more up on the high risk category meaning what do i mean by stable they're not hypotensive they're not tachycardic they're not super um hypoxemic in this way and so in those kinds of scenarios if they're not super tachycardic they're not super hypoxemic they're not super hypotensive they have the ability to even speak in like full sentences they're considered to be stable in that sense so in those patients who have underlying lung disease we go based upon the size of the pneumo so let's say here we measured here's the apex of the lung you can do two measurements you can either measure from the apex of the lung to the cupula or you can take at the level of the hilum you can measure from the pneumo outwards like this if it's less than two centimeters from the hilum area that's considered to be like a smaller type of pneumothorax and if it's less than three centimeters from the apex to the actual top of the coupe leather that is actually considered to be a small stable pneumothorax in these scenarios generally what you can do is you can consider observation what most time may happen is you can just observe them get a repeat chest x-ray maybe get a repeat chest x-ray see if it's getting any worse and if it is getting any worse you can just go ahead and do a chest tube okay now for someone who has an a little bit different we measure from the apex to the cupula and it's greater than or equal to three centimeters or we measure the level of the hilum from this pneumoforax here and it's greater than two centimeters this is considered to be a large but stable pneumoforax for this we go straight to a chest tube and then icu monitoring okay so i think we got a good understanding of that generally whenever it's someone who's stable high risk meaning that they're secondary spontaneous pneumothorax they have underlying lung disease it's less than three from the apex or less than two at the level of the hilum you can observe get some repeat chest x-rays if it gets any worse it gets bigger they start to become unstable chest tube if it's large in these sizes that we have here they get a chest tube all right the next one is stable and low risk so stable and low risk this is going to be patients who have primary spontaneous pneumothorax so this is usually either their first pneumothorax they don't have any underlying lung disease in these kinds of scenarios again we still measure we measure from the apex to the cupula or we measure out the level of the hilum and again if it's less than two centimeters greater than i'm sorry less than two centimeters at the level of the hilum and then less than three centimeters at the level of the apex in this condition we say it's small and this is just observation and you can get some repeat chest x-rays in a couple hours you can go with the supportive therapy and generally this will kind of resorb on its own if it doesn't then you may need to put in a chest tube for those that are actually greater than or equal to three centimeters from the apex of the cupula or at the level of the hilum it's greater than or equal to two centimeters then in this patient they still say that you can observe but generally what may happen is you can observe but it may lead to you trying what's called a needle aspiration and if the needle aspiration fails then they may need to get a chest tube okay so that's kind of how we go about this so again stable low risk for primary spontaneous stimuthorax if it's less than three centimeters from the apex of the cupula or less than two centimeters the level of the hilum you observe repeat the chest x-ray for those that are usually a little bit greater so we consider them larger but they're still lower risk we usually can observe but if at any point in time it becomes bigger with repeat chest x-rays or they become a little bit more symptomatic or unstable we can consider a needle aspiration and if it fails you can put in a chest tube last but not least if a patient has recurrent so this is usually surgical pleurodesis or pleurosis is usually good for patients who develop what's called recurrent pneumothorax and a patient who is recurrent pneumoforax and they continuously require maybe chest tubes or interventions in some way shape or form you can actually cause a parotis or pleurodesis and you can do this two ways what you can do is you can do this chemically so there's what's called a chemical pleurodesis and there's what's called a mechanical fluoredesis okay chemical polarities actually utilize a chest tube and you through the chest tube you push into the pleural space some really nasty harmful chemicals you can push in things like talc you can push in things like silver nitrate and you can push in things like doxycycline and what these do is all of these three particular things can induce a fibrotic reaction and that fibrotic reaction will start to actually stick the visceral pleura and the parietal pleura together pretty much obliterating the actual pleural space and so therefore you won't be able to actually even put air into that space because you've obliterated that space another way that we can do that is we can actually use what's called a vats procedure so a video assisted thracostomy and what they do is they actually go in through there and use some type of like a probe and just rub and apply friction to the pleura and the hopeful goal is that after applying friction and rubbing against the pleural visceral parietal pleura it'll cause a fibrotic reaction eventually hopefully obliterate the pleural space so that is the eventual goal with a surgical pleurosis for patients who develop recurrent pneumothorax iron engineers that covers pneumothorax all right ninjas in this video we talk about pneumothorax i hope it made sense i hope that you guys enjoyed it as always ninja nerds until next time [Music] you

Channel: Ninja Nerd

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Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: 3sayOPbXyGw

Length: 71min 21sec (4281 seconds)

Published: Tue Nov 02 2021