foreign what's up Ninja nerds in this video today we're going to be talking about pleural diseases that includes pleural effusions and pneumothorax before we get started if you guys like this video it makes sense to you please support us and you can do that by hitting that like button comment down the comment section and if you can subscribe also really suggest go down the description box below there's a link to our website on our website we have a lot of other cool things that we offer great notes great illustrations we're making exam prep courses for those of you taking your exams like the step one the step two the pants Etc so check that out also we've got some great merchandise if you guys are interested as well but let's start talking about plural diseases so plural diseases there is two that you guys have to be able to recognize that's plural effusions and pneumothorax with a pleural fusion the problem is fluid so there's some type of fluid and there's an increased amount of it that's actually present with inside of the pleural space so that's the space that's usually between the parietal and the visceral pleura so again lots of fluid we'll talk about the types of fluid and get into a little bit more in the depths of that in a second but this is the first concept to understand now when a patient comes in with a pleural effusion they can present with a lot of different findings sometimes the most common one is they have like the sense of pain whenever they're taking a breath in and out and that's sometimes what we refer to as pleuritic chest pain so listen for that somewhere in the clinical vignette that should tip you off to think about a pleural disease in general so pleuritic chest pain can be pretty common the other thing is if it gets pretty large and it compresses the lungs it definitely can affect the patient being able to take a deep breath in so watch out for Disney as well that's another common feature sure so those would be two big ones but this is the one that I really want you to remember second thing is that if a patient comes in and they have all this fluid that's actually present within their pleural space it can affect different types of physical exam findings one of those is tactile framitus so that's one thing when you kind of put your hands over the back and you say okay say 99 and your ability to be able to feel that on your hypothene or eminences is usually going to be reduced and that's because there's this fluid that's altering that transmission so you want to watch out for a reduction in their tactile fremitus the other thing is that if you go ahead and you percuss so you take and you percuss over the different parts of the lungs where the pleural effusion is it's going to be really really dull because of that fluid there so listen for dullness to percussion that's another potential sign that there may be fluid present with inside of that area okay or some type of consolidation to the lung tissue so dullness on percussion the last thing here is that if you take an auscultate over the lungs especially where that pleural effusion is the lung sounds are going to be really decreased so listen for any kind of decreased breath sounds these are usually some of the findings that are super suggestive of a pleural effusion is again decreasing tactile fremitus increasing dullness on percussion and decreasing breath sounds in combination with pleuritic chest pain now we've gotten to the point of how these patients will present now the question is what's causing this fluid well it depends on the type of effusion they have is it transitative or exudative so transitative effusions are usually going to be effusions that contain lots of fluid minimal amounts of protein very little concepts of cells as well so let's understand why that would happen one of the etiology is super super common probably going to be one of the most common you'll see is a patient who has congestive heart failure when you have congestive heart failure cardiac output whether it's systolic or diastolic your cardiac output stinks so you aren't able to get blood flow out of the heart and if blood isn't getting out of the heart where will it go it'll back up into the left atrium and then what happens is it backs up into the pulmonary veins what happens to these patients what's called pulmonary capillary wedge pressure it increases so if they're pulmonary capillary wedge pressure which is a surrogate of their left atrial pressure if it's high that means the pressure inside of these capillaries is high so the hydrostatic pressure the pressure that pushes things out of these capillaries is higher and so things like water other electrolytes certain types of filtrates very little amounts of proteins will leak into this area so there's going to be lots of plasma molecules here now with that being said you're going to have some proteins but it's going to be very little and you may have another specific type of protein called LDH but it's going to be very very little so I want you to remember that it's not going to have a lot of proteins it's not going to have a lot of LDH these are going to be some of these components that are present inside of this plural space so this is the plural space this is the capillary and this is part of that lung tissue so we're just really zooming in to this area right here now that's one problem is the pulmonary capillary wedge pressure is high the ability or the pressure inside of these cap layers are High they'll push things out into that pleural space lots of fluid all right so you're gonna have tons and tons of fluid and that's usually going to be things like water and electrolytes but the fluid is going to be very small in proteins and small in LDH these are usually markers of lung injury inflammation increased capillary permeability another reason this happens is patients have destruction or injury to the synthetic function of albumin whether that's because of cirrhosis or they're losing albumin in their urine and this could be in situations of nephrotic syndrome so I want you to remember two particular diseases one is cirrhosis where you lose the synthetic function you lose the ability to make albumin so albumin is reduced inside of your bloodstream the other disease is called nephrotic syndrome and this is where they have injury to their podocytes and they just PPP out a ton of this albumin into their urine so either way the amount of albumin that's present within the bloodstream is reduced what does albumin do in your bloodstream it helps to keep water in certain things inside of the bloodstream if you have less of it what will happen they won't stay in the bloodstream and so unfortunately the oncotic pressure reduces and it causes fluid to not remain into the bloodstream and instead go out here into this pleural space increasing the amount of fluid but again this fluid is going to be very poor in proteins and poor in LDH the reason why is this should signify that there's truly no lung injury that's actually taking place here there is no lung injury that's taking place here and that's what these two things are kind of telling me that there is a lot of fluid but that fluid is not rich in proteins and LDH if I come over to this next son of a gun here this is excitative effusions and exudative effusions there's some type of lung injury or inflammation and when I talk about this I'm talking about the lung parenchyma and even some of the tiny little blood vessels in those area they're injured or inflamed so that's the problem here is there is a massive amount of lung injury so we'll put lung injury or we can even say not just lung injury but lung inflammation or lung inflammation for whatever reason now because of that lung injury or inflammation this is usually going to trigger a cytokine pathway so cytokines will be released when that lung becomes injured and inflamed you'll have lots of inflammatory cytokines and what these inflammatory cytokines do is they cause your blood vessels to become dilated and really leaky and if they're leaky they're not going to be very good at controlling what leaves the blood and enters into this Pleural fluid and so unfortunately as a result you have increased capillary leakage and this will have no real good control of what leaves the blood and enters into that plural space and so as a result you have things like proteins fluid LDH molecules and even potentially if there's lots of inflammation you can even have lots of white blood cells coming to the area so what would I see here I see lots of fluid I see lots of proteins lots of LDH and potentially I might even see some immune system cells so what am I going to want to watch out for I'll see tons of proteins tons of LDH and maybe even some white blood cells potentially will kind of put a plus minus because it depends upon the etiology but usually it's increased so we'll actually put that usually for the most part most diseases is increased increased amounts of LDH increased amounts of proteins and a massive massive amount of fluid now with all of that being said since this stuff is leaking out into these spaces and now I notice a difference here between the fluid consistency if there is a lot of proteins LDH and particularly white blood cells that tells me that this is a surrogate for lung injury lung injury is actually occurring and that is how I can use this as a diagnostic tool to tell me oh this could be an executive effusion versus a transitative fusion question that I have to ask myself is what's causing the lung injury or parinkable inflammation there's so many things and that's what makes it difficult it could be things like pneumonia which is extremely common you know pneumonia you develop what's called a paranormic effusion that's so common so here let's actually write that because I'd say that's probably out of all of them the most common cause is what's called a Para mnemonic effusion that's a very common cause another one could be things like tuberculosis which is that's a really big one as well another one could be malignancy so any kind of like lung cancer other particular scenarios could be autoimmune diseases autoimmune diseases are really big ones that I would want you guys to remember trauma is another one so what we can call like a hemothorax sometimes you may hear that term a hemothorax let's actually write that down chemothorax and there could be some other random ones so other random ones that come in there is sometimes I think this is actually how I yield to remember sometimes there's this lymphatic structure that actually runs right here it's called the they call it thoracic duct sometimes in certain scenarios you can hit that and it can cause that to accumulate some lymphatic fluid into the area and we call that a kylothorax so sometimes remember that this could actually be due to thoracic duct injury and just remember this term called a kylo thorax there is Rich and chylomicrons which is rich in triglycerides that are present within that plural fluid but these are the big reasons why the patient has lung injury or lung inflammation causing capillary leakage that covers the effusions now what I need to do is let's take it to the next step and say okay we got a new move thorax we get air we got lots of air that is present within the pleural cavity now the question then comes up similar to what we did with pleural effusions what's the presentation again there's injury in some way shape or form to the plural so pleuritic chest pain is a very very common one and again if these get big enough they can't alter the they can cause compression of the lung tissue lead to atelectasis and make it hard to breathe so Disney is another common finding on physical exam you're going to see a lot of the same stuff tactile fremitus is going to be reduced so like wow these kind of sound the same Zach how am I supposed to be able to difference differentiate it well here's one big thing dullness to percussion is significant for pleural effusions and consolidation of the lung tissue timpani is very specific in some ways a shape or form for pneumothorax so look for timpani on percussion that's a little bit more suggestive of a pneuma4x and the other thing is that they will have again decreased breath sounds so a lot of these things kind of look the same decrease tactile fremitus increase temperature on percussion and decreased breath sounds plural to chest pain disna common findings question to ask is why is this air in the pleural cavity same way why was the fluid in the pleural cavity the reasons why is three particular processes primary spontaneous pneumothorax secondary spontaneous simple thorax or trauma what do I mean by primary spontaneous pneumothorax I want you to remember this in primary there is no lung injury or disease in secondary spontaneous pneumothorax there is lung injury or disease and that is super super critical to understand the differences between these two now we've gotten that out of the way lung injury is not present or disease is not present in primary spontaneous what's the cause usually this is seen in patients who are very tall thin young and are males all right so tall thin on what that would be like young again what would that be like that'd be nice and males and another thing to add on is sometimes in the clinical vignettes they love to mess with you and say oh what if the patient has a history of ehlers download syndrome or marfon syndrome that can be somewhat helpful so I'll put a plus or minus if they have ehlers download syndrome or marfons that does add some utility for the question to say oh that also makes it very interesting and precarious for a primary spontaneous pneumothorax now what happens with these patients is these tall thin young males with potential conditions like this connective tissue diseases is they form these like tiny little blabs at the Apex so we call these sub plural apical blebs and it's just an unfortunate process that happens in these people these like little blebs here and sometimes for whatever reason these things can rupture and if they do they pop air can immediately leak from the lung tissue right here into the actual pleural space and there we go air is now leaking in there that's the reason that the patient can develop that there should be air and the lung tissue there should not be air present within the actual plural space and now air has the opportunity to enter so there's one reason tall thin young males potential history of these sub Pro apical blebs that is the primary process that can occur here with secondary spontaneous pneumothorax it's patients with an underlying lung disease and what I mean by this is you have to have somebody who has two one of two things one is their hyperinflated lungs so with hyperinflation comes increased risk of boolay and other types of weird structures so with hyperinflation you increase the risk of these things called boulay or other things like blebs as well and because of that if you think about this now the lungs are super super kind of like stretched to the max there's a very very high risk chance that they could actually pop and cause air to leak in this is especially common in COPD more particularly in the emphysemidis patients you can see it in the chronic bronchitis patients but I would say it's extremely common in the emphysema patient and another one would be the asthmatic patient a severe asthmatic patient so think about COPD more particularly the emphysema type and then think about asthma particularly your obstructive lung diseases where they have a hard time getting air out so they obstruct pump up their airways increase the risk of these processes the other one is infections or some type actually let's actually rewrite this necrosis there's some type of lung necrosis this could be from infections and this could actually be from malignancies as well but either way there is something that is causing necrosis of lung tissue and if it necrosis that's an easy opportunity for this to rupture through into the pleural cavity air enters boom there you go you got a you got a pneumothorax so it's one of these two particular scenarios that I think is important for you guys to remember it's either increased hyperinflation or its increased lung necrosis and that's the primary cause of their lung injury or disease all right we come to the last one which is probably the easiest one for trauma it's super straightforward you've injured you've caused some type of you lost the Integrity there was a plural puncture is usually one particular thing so you punctured through the parietal pleura through the visceral pleura into the actual lung and then cause an opportunity from right there that puncture for air to leak right in super straightforward right nothing crazy the things I would want you guys to remember from this from external sources would be any kind of needle or any sharp object so I think trauma would obviously be a super common one um a thoracentesis which is when they try to go in and remove fluid from patients who have pleural effusions and another one is Central lines this is extremely common in patients who get things like ijs or subclavian lines and then they just are placed by inexperienced providers or for whatever reason it occurs they hit that pleura and cause a plural puncture that's enough right there another reason is you're driving so much air um into the patient's lungs so we call this like barotrauma this is very common with mechanical ventilation where you're pushing just these insanely large volumes of air into a patient and or patients are taking have what's called Auto peep where they're they're air trapping and they're getting their lungs a little bit bigger so either way it's very common to happen in patients who are on mechanical ventilation but it doesn't matter if they have lung disease or if they don't have lung disease the primary process here is that there's some traumatic event it had nothing to do with their structure nothing to do with their lungs it's a process of trauma whether it's external or whether it's coming from very high Airway pressures so again this is usually seen in high Airway pressures all right where you're just mashing air into the lungs usually like high peeps or high tidal volume strategies these are the things that I want you guys to remember now we've talked about plural diseases in a pretty good amount of detail what I need you guys to understand is okay I can identify the causes the pathophys the clinical features what happens if that Pleural fluid is so big what are the complications that can arise and the next thing is what if that pneumothorax is so big and it starts pushing on things what are the complications that can arise all right my friend so now we're going to talk about the complications that can arise in patients who develop plural diseases so we'll start with plural effusions and this patient they have a massive pleural effusion right and so what happens is their plural fluid really is pretty high and that actually starts increasing the pleural pressure and when the pleural pressure Rises that will then start leading to some potential problems so here's all this Pleural fluid that increase in Pleural fluid will then increase the pleural pressure and when the pleural pressure increases guess what it's going to start doing to the lung tissue it's going to start squeezing and compressing the lung tissue so and as a result you get lung compression and whenever you compress the lungs you can make those alveoli collapse all right and what do we call that whenever the alveoli collapse this is called atelectasis and so the result here is these patients can develop some pretty decent atelectasis and sometimes we call this compression attaelectasis but we're just going to call this atelectasis now here's two alveoli right so we're just kind of zooming in on this particular area here and seeing what's affected whenever this complete low of the lung is being compressed when that lung of the low when that lobe of the lung is being compressed these alveoli start getting smaller when they get smaller now what you do is you alter the ventilation you lead to the patient not getting an adequate amount of ventilation to this alveoli into this alveoli so there is a reduction in the ventilation process even though the perfusion process blood flowing through these pulmonary capillaries is completely normal but whenever the ventilation is thrown off you develop something called a VQ mismatch so as a result you get something called a VQ mismatch where there is a reduction and the ventilation we call this a low VQ mismatch there's a reduction in the ventilation but a normal perfusion now if there's decreased ventilation that means that decreased oxygen is moving here across the alveoli now if decreased oxygen is moving across the alveoli in response to this then the patient will develop things like hypoxemia that's a potential complication if there is a massive atelectasis so the more the atelectasis the more the VQ mismatch will be stimulated and the more hypoxemia will ensue now if this happens where the patient develops something like hypoxemia this is an example of a type 1 respiratory failure this is what can potentially result here where the O2 is relatively reduced and then the CO2 is somewhat normal or maybe even decreased now when these patients become hypoxemic it's because the lungs are being collapsed and compressed but imagine how that's going to actually cause problems you're going to want to try to take in these deeper breaths to hopefully properly ventilate that alveoli and so other features that may become super prominent in these patients is that in response to this hypoxemia they may increase the respiratory rate they may increase their work of breathing as a response to this and so you really want to watch out for this this could be signs of respiratory failure or respiratory distress so again big things to understand is a potential complication of pleural effusions very large political fusions can increase pleural pressure compress the lungs cause atelectasis cause VQ mismatch cause this hypoventilation of the alveoli now now less oxygen comes across hypoxemia can then precipitate an increase in respiratory rate and an increase in the work of breathing if these patients are breathing really fast and working really hard to breathe sometimes they'll blow their CO2 off and so you may see signs of respiratory alkalosis this is the big thing to consider here the other concept that is really big and you need to remember this for pleural effusions is they can develop these things called empyemas This is extremely extremely common in patients who develop pneumonia so let's say here a patient develops a left low bar pneumonia when they develop that left lower lobe pneumonia that infection of the lung parenchyma will cause increased capillary leakage fluid will then start leaking into this pleural space so then we develop what do we call that before what was this called a paranormic effusion but let's be a little bit more specific we're going to call this a uncomplicated paranamotic Fusion so this is a uncomplicated this is pretty much a normal exudative effusion uncomplicated para mnemonic effusion but then what happens is the infection continues and it spreads so now the infection that's right here some of the bacteria begin to leak out of those capillaries as well and some of the white blood cells and so now you have the opportunity for some bacteria to be combined with that fluid and again just to remind yourselves what is that fluid going to be really really rich in rich in proteins and rich in ldls but it's also going to have some white blood cells in the area so now at this point we have a patient with what we call a complicated paranormic Fusion because now there's some bacteria in there there's lots of white cells in the area sometimes the ph and the glucose can drop here as well but then we get to the worst case scenario we get to the point where this infection that's actually within this left lower lobe it's spread over caused that uncomplicated apparent amount of confusion which then progressed to a complicated paranormalic Fusion but now some of the bacteria they spread out here and they start to organize and when they organize they cause lots of white blood cells to come to the area lots of inflammation to come to the area and then what they begin to do let's actually use let's do this black color here they begin to cause a fibrotic shell to form around it and become super loculated so now you have this loculated effusion here which is just literally filled with pus it's bacteria dead cells white blood cells this is now what we call a empyema this is now a empyema empyemas are potentially dangerous and the reason why is one is you want to look for a patient who maybe had a pneumonia and they continue to have persistent fever so look for patients with very high fevers maybe a continuously increased white blood cell count or a patient who appears to be septic right so they appear to be septic in these scenarios and empyema definitely can precipitate these types of features is high fevers high white blood cell count and they can stimulate sepsis because what happens is this bacteria can spread into the bloodstream and cause systemic bacterial infections but what you're going to notice is this is the progression where a patient can start off with pneumonia that begins with an uncomplicated paranamotic effusion the difference here is the bacteria begin to kind of jump in right the bacteria begin to jump into the fluid and so do white blood cells and then you go from a complicated perineumonic effusion to a empyema and this is where you begin to form Frank pus and loculations and that's usually the key terminology that you guys want to be able to understand between these guys but this is the complications that can arise in these patients is you can start off with just a little bit of fluid there that's rich in protein having some cells but then bacteria can spread into the area cause it to become an infected fluid and then that fluid can become very purulent and frankly pus containing with loculations and fibrotic material around it and that can cause these persistently high fevers persistently high white counts and potentially precipitate sepsis usually a patient has pneumonia they get treated for the pneumonia maybe the pneumonia continues though to cause these effusions and those effusions grow into an empyema they'll have again a recurrence of their symptoms and that's usually going to make you queue in to think about an empyema all right now that we've talked about pleural effusion so let's now come down and start talking about the next complication which is pneumothorax when a patient develops a pneumothorax the problem is is that they got a lot of air inside of that pleural cavity we already talked about the reasons for it when you have a bunch of air so there's an increase in the air in the plural space right now naturally let's actually be very very specific here there shouldn't be air in the pleural space there shouldn't be so any presence of air in the pleural space is considered to be a pneumothorax so should just be a little bit of fluid but if for whatever reason you decide to build up some air I'm just going to put an increased arrow in front of it because again it's you have air present within the plural space the more air present in the pleural space the more the pressure inside of that plural space will increase so now this patient can have an increase in their plural pressure if you have an increase in their pleural pressure this should start to look very familiar as compared to above what would that do to parts of the lung right here air is rising in the air the pressure here is rising it's pushing pushing on this lung area it's pushing on the lobe it's compressing it what's it going to do it's going to cause lung compression that lung compression if it's on a particular area in this example the right lower lobe what's it going to do to the alveoli making up that right lower lobe collapse them what's that collapse called atelectasis what does atelectasis do it leads to V Q mismatch and that can lead to hypoxemia so the more air in the pleural space the more the pleural pressure Rises the more lung compression you'll experience the more atelectasis and you will stimulate this VQ mismatch to ensue now when this happens think about this these should normally be normal healthy alveoli I'm taking this section here of where this compression is and I'm zooming in on it this is being super compressed all of this is now air up here it was Pleural fluid so these are being smashed down if these are being smashed down now they're tiny little alveoli and I can't bring air in to these alveoli properly so there is a reduction in the ventilation and therefore normal perfusion so that's the vacuum mismatch if I reduce this now what's going to happen to the oxygen or gas exchange across this area it's going to be reduced if I don't exchange gases properly especially oxygen what will be the precipitating result here the patient will have low blood oxygen levels which is called hypoxemia and if the patient has hypoxemia so their spo2 drops or their pao2 drops what can that lead to that'll cause the patient to feel like they're short of breath so they'll have to work a little bit harder to breathe and they will breathe harder and faster and so this can look one of two ways the respiratory rate can go up if it allows and their work of breathing the use of accessory muscles like nasal flaring intercostal retractions belly breathing all of those things will occur if the patient breathes fast and deep enough they will expel tons of CO2 and precipitate a respiratory alkalosis which is also common in these scenarios but again respiratory failure is common in both of these pleural diseases what's a big differentiating factor here is what's called a tension pneumothorax and this is the scary thing that you can't miss on the step two it'll be blaring to you it'll literally be super obvious patient has air in their pleural cavity right so the pleural pressure is through the roof because of this right so there's tons and tons of plural pressure in here and because of that the lung is being significantly compressed what really is the big thing here is attention pneumothorax can occur because of a primary spontaneous pneumothorax a secondary spontaneous pneumothorax but it's very common with a traumatic pneumothorax let me explain how this happens let's take this piece of lung right here this area here and zoom in on it I'm just zooming in on this portion right here what happens is during inspiration regardless of the cause of the pneumothorax it doesn't matter air will enter into the lungs and then what happens is you have this break and the parenchyma and the visceral pleura there's the break that creates an opportunity for air to enter right into the pleural cavity boom air is in there during expiration for some weird reason you create this thing called a one-way valve where air can enter so this could open up but during expiration somehow these this break within the pleura and the lung parenchyma re-comes back together it collapse together so now air won't be able to enter back into the lung and it'll stay in the lung so air can enter can't exit that is a recipe for disaster because you know what it's going to do it's going to keep all this air which I'm representing here in blue a lot can come in and none can go out that is going to massively massively massively increase the plural pressure if the pleural pressure Rises it'll start squeezing in the lungs which you'll see the respiratory failure but you know what else you'll see you'll see compression of other things inside of the mediacinum so what it'll start doing is Imagine here I have all this air and it's pressing on the lungs as it presses there's only so much lung you can compress that it actually starts shifting everything in the mediastinum to the opposite side so now I'm going to shift the trachea to the opposite side I'm going to start squeezing on the right heart now what's that going to look like you're going to get a couple effects out of this one is if I shift the trachea they also have tracheal deviation examine that look to see if the trachea appears to be deviated on exam or chest x-ray so tracheal deviation is really big okay and that's because of this crazy high intrapleural pressure all right so that's one thing that can happen here so we're going to bring this down to stimulate this whole pathway that we're going to talk about here this is high enough that it's boom pushing the trache to the opposite side the other thing is it's going to compress the right heart if you compress the right heart what's the right heart supposed to do bring blood into it it's good for venous return but now if it's being compressed are you going to have good venous return no so venous return is impaired so they have what's called a reduction and their diastolic filling so whenever the heart's supposed to relax you're supposed to get a lot of blood coming into it but it's not going to if you reduce diastolic filling blood is going to back up from the right atrium remember your Anatomy to the superior vena cava up to the brachiocephalics up to the jugular veins and the blood is going to pump these suckers up and what's a common finding that you will see you will see something called jugular venous distension that's one potential finding right so you'll see a finding of jugular venous distension the other thing is if you can't fill the ventricles that reduces your preload if you reduce your preload what do you do to your stroke volume you drop it what do you do your cardiac output you drop it what do you do to your cardiac what if your cardiac output drops what happens to your blood pressure that drops so they'll have a drop in cardiac output which will lead to a drop in there blood pressure what's that called when your blood pressure is low hypotension so one finding here that we're already seeing is the patient can have hypotension jugular venous distension tracheal deviation all because of the pleural pressure being so high that it's causing what's called a mass effect or mediastinal shift all of these things are occurring because of that high intrapleural pressure the other thing is take a second listen to the lungs what would you not hear very well on that side breath sounds so if I have a patient with absent or decreased breath sounds tracheal deviation hypotension and jugular venous distension what could it be attention you don't get a chest x-ray you put a chest tube in right away or at least decompress them all right we've now identified the plural diseases now we have to diagnose these which is how do we diagnose just a plural Fusion I want to find it I can easily find it by getting a chest x-ray look at that meniscus sign we call here which is usually pretty indicative of what we call a pleural effusion here and that right hemithorax I could also do a chess CT this is a really good one you can see here they have a left pleural effusion maybe even like some Associated like air bronchograms they might have an ammonia so that gets really good at being able to identify complications like empyemas potentially so that's one of the great things I like about that but the best test I'd say to start off with really differentiating a transitative or oxidative is a thoracentesis so you find the actual pleural effusion you tap into the pleural effusion with a needle and if you tap into this pleural fusion it's going to suck some of that fluid off and they're going to go test it once you're testing it for as you're testing it for color so does it look clear pleural protein is there are very little of it is there very little plural Ada LDH this usually tells me that the pulmonary capillary wedge pressure is low this usually tells me that there's low oncotic pressure and that this is more transitative in appearance and the other scenario let's say that it looks cloudy let's say that the protein is really high and let's say that the LDH is high this is more suggestive of lung injury and this would be more suggestive of an exudative effusion so then what do I do okay well if I think it's a transitive infusion I got to think about the causes most likely at CHF from an elevated pulmonary capillary wedge pressure or it's cirrhosis and nephrotic syndrome from low albumin levels causing low oncotic pressure from the exit date of a fusion I want to obtain a pleural glucose this may seem odd but when you obtain the pleural glucose it really helps you to delineate the types of things that can cause this we talked about pneumonia particularly perimetic effusions and one of the nastiest ones is in pyema we talked about tuberculosis we talked about malignancy and autoimmune diseases and pancreatitis and all those things if I get a pleural glucose this is really helpful the reason why is if it's normal it tells me three things it's either a kylothorax because of high triglycerides if I tested that it's usually indicative of a hemothorax by lots of red blood cells in history of trauma or it's usually a pancreatitis or esophageal rupture if there's lots of amylase and again a normal plural glucose if the plural glucose is low there's only a couple different causes and I remember the mnemonic of this by Meat and now I'm going to go through this one is if the acid phase bacillus stain is positive it's more suggestive of tuberculosis if they have an Ana or a rheumatoid Factor that's positive it's more suggestive of an autoimmune disease if the cultures are positive and they have a really low pleural pH that's more suggestive of an empyema or a complicated paranormal confusion and lastly if there's abnormal cytology and maybe lots of blood or red blood cells that could be suggestive of malignancy usually grade four at that point but you can remember this mnemonic of low pleural glucoses by Meat malignancy and pyema autoimmune and tuberculosis and that's actually kind of helpful but again I think the biggest thing to take away from this for your boards is what's the light's criteria this is the criteria that we use to determine if it's likely transitive and exudative and then we can go down the chain that we just discussed if there's lots of pleural protein and we say that by if you compare the serum a protein to the plural protein If the ratio is greater than 0.5 that's suggestive of an exudative if the amount of LDH in the pleural fluid in comparison to the serum LDH is greater than 0.6 that's suggestive of an oxidative effusion and if the pleural LDH is greater than two-thirds the upper limit of normal of the serum LDH it's suggestive of an exited refusion if none of these are present it's likely transitative and the most common transitative one is CHF so with that being said if I have a patient who I go through I finally have an exudative effusion I go through and it has a low pleural glucose maybe there's lots of white blood cells and I'm trying to determine if this is this uncomplicated complicated or empyema how would I go about that when I analyze that Pleural fluid if it looks slightly cloudy that could be uncomplicated but if it looks really cloudy that's probably complicated and if it looks purulent or Puffs containing it's likely an empyema that's one way the next one is look at all those things we just talked about what's the plural pH if it's high or at least greater than 7.2 it's more uncomplicated but if it's less than 7.2 it could be complicated or an in-payema what's the glucose if it's relatively normal that's uncomplicated but if it's low it's complicated or an empyema and then lastly look at the pleural white blood cell is it less than 50k all right that's uncomplicated but it's greater than 50k it's likely complicated in paima so I'm still having difficulty I'm only being able to differentiate these by appearance right now okay is there any other ways all right well I could get cultures if the cultures come back negative that means bacteria haven't invaded into the rural space yet if cultures are positive it primates that bacteria have invaded into the space again not super helpful here or is there another way what if I get Imaging I get a chest CT and off that I see no loculations now I see that this is more likely uncomplicated or complicated and if it comes back loculated it's more likely an empyema with that being said if it's uncomplicated it's usually just antibiotics if it's complicated or npyema it's usually antibiotics and giving them a chest tube all right that leads us right into the next step how do we treat pleural effusions well it's really treating the underlying cause but if a patient's in respiratory distress because of their pleural effusion it's probably best to do with thoracentesis and actually to pull that fluid off because it won't be causing as much atelectasis and unfortunately respiratory failure so if we can do that and then treat the underlying cause that would be the best thing the other concept is when do I put in an indwelling plural catheter it stays in there it's not just a one-time tap and done usually this is happening if I'm performing multiple forests and TC's particularly if the patient has malignant related pleural effusions and you can just let that and dwell in there and continue to drain so that's a nice thing for that the other one is I do a chest tube in what circumstances would I do a tube thoracostomy where I would actually insert in the chest tube in the fourth intercostal space usually antioxillary line it's usually if they have an empyema like a loculated nice nasty like thing that's going to be one reason or they have a big fluid accumulation of blood like a hemophorax all right any other reasons would not be necessary for a pleural effusion if they have failed to respond to antibiotics and they have failed to respond to a chest tube and usually even TPA that gets put into the chest tube drain to really break up the empyema then sometimes they may require surgery where they get what's called a video assisted thoracoscopic surgery and that would be for like a refractory in my email the last thing here is what's called a pleurodesis or chemical or mechanical paralysis you can either go in surgically and rub against the pleural layers and cause it to obliterate and lose the space or you can put in drugs like doxycycline or talc and what that does is that kind of creates a little fibrotic reaction and then this will obliterate the actual pleural space so you can't form any effusions anymore and that's for patients who have a refractory malignant infusions usually a malignant again that's the big thing all right so that's how we would treat plural effusions but again I think it's the most important thing to remember is that you have to treat the underlying cause because if you don't the effusion will just reaccumulate so again I think it's a big example here is that patients who have transitive effusions secondary to CHF you can do a thoracentesis if they're an overt respiratory failure but if you don't continue to decrease them and treat their underlying disease it'll reaccumulate so that's oftentimes a really important thing to remember because now we move into the diagnostic approach so you have to ask yourself the question always what's the scariest pneumothorax tension do they have one okay they do you better grab that needle decompress them shove a chest tube in because this patient can die if you don't if they don't have that then you want to go looking for other things again it's not attention to what they're actually it could be any type of pneumophorex as long as it's not tension so get a chest x-ray you'll be able to see right away oh there's no lung markings here and there's the you can actually see the plural line right there in this scenario here same thing you can see there's absence of lung markings here and that the lung is like there it is right there there's your plural line right there so you can definitely see and identify that this patient has a pneumothorax by the absence of lung markings if you really wanted to go the next step and say what's the cause you really could evaluate if they have underlying lung disease but oftentimes the history is usually the key if a patient just was in a traumatic incident they just had a central line placed they just said a thoracentesis done they were on the mechanical ventilator they have no underlying history of lung disease or they have a history of COPD or something to that effect you can do that but if you want to look you can get a chest CT and this may be able to show you some boolay or some emphyseminist findings which could suggest like a secondary spontaneous pneumothorax but again it's just another way of finding the pneumothorax once you've found the pneumothorax you have to treat these patients and one of the best things to do is say okay is it big enough that they're not going to resolve on their own and the patient could progress and get worse if it's not it's less than two centimeters from the chest wall to the actual plural line you can just observe watch them see if it goes away on its own oftentimes giving them oxygen to pull nitrogen from that space can help and getting serial chest x-rays to see if it gets bigger or watching them to see if they develop any worsening symptoms like respiratory failure if it gets bigger greater than two centimeters or they exhibit any signs of respiratory failure you need to put a chest tube in fourth intercostal space anti-axillary line and then if they develop attention it's automatic needle decompression and then chest tube alright my friends so now let's move on to the next step here which is discussing a little bit more information about chest tubes so you may experience a question or two but you may experience this more in your clinical clerkships so let's talk a little bit about this so we have this chest tube in right and there's many different reasons we've already talked about a couple one is a patient has particularly a type of a fusion that is exudative in nature like an empyema or a hemothorax that would be one indication for a chest tube the second one is they have a pneumothorax and you're trying to drain either fluid or air of some sort out of the actual pleural cavity now what you do is you have the tube going into the actual pleural cavity now if it comes from the patient the first thing it does is it empties into this type of component here called the chest tube like this is usually what we use called pleuravax or Oasis and these are different types of chest tube kind of setups now this is going to be the tube coming from the patient delivering blood or delivering pus or delivering air and then there's going to be another thing that we'll talk about a little bit later which is a tube it can go towards the suction on the wall now this is the suction control the suction control is basically what you set for the actual degree of suction for the chest tube so for example you could set the wall suction to like I don't know 22 000 centimeters you know per of water it won't matter the suction control on the chest tube is what you usually generate and that's usually set to negative 20. here's just the manometer which kind of just give you an idea of that this is called the suction control chamber we'll talk about the Three Bottle system again this is the chamber that is usually filled with a little bit of water and wet vacs and that degree in the amount of water that you have determines the amount of suction that you're going to be able to generate you also have what's called a water seal chamber it's exactly what it sounds like it seals off air so that it prevents air from kind of leaking back into the collection chamber and then back into the actual patient's pleural cavity so it seals off the actual air and prevents it from going backwards so thus the name water seal and then we have this thing called The Collection chamber and it's literally what it says it collects things like for example blood if it's a hemothorax Kyle if it's a kylothorax pus if it's an empyema and again that's the whole point of that now when we talk about this we talked about three particular Chambers The Collection chamber the water seal and then the suction control chamber now when we take these and look at them individually we use this three bottle system if you will but this three bottle system is built into one specific thing called a pleuravac or an oasis so this is going to be the tube coming from the patient and what it'll do is it'll deliver everything it'll deliver fluid if there is any fluid in the actual pleural cavity This Could Be Blood this could be pus this could be Eric's Etc and it'll deliver it into the collection bottle there's going to be a tube that comes out of the collection bottle and moves things over into the water seal chamber so this part is where blood and fluids and all that stuff stay they don't move over into the next chamber if there's any air that's present inside of the patient's chest it'll move via the collection bottle over in to the water seal chamber when it moves into the water seal chamber the air will then actually move into the water and bubble and basically the whole point of this is that this air that actually gets into this water seal chamber it kind of dissolves and it kind of moves out into this kind of chamber and prevents it from being able to move backwards towards the collection bottle and that's what's really cool about this one now generally whenever a patient has a chest tube we can use this concept called a two bottle system in other words if a patient has a pneumothorax or they have a little bit of an effusion you can actually set this thing to water seal and essentially what that means is fluid will drain out of the chest into the collection bottle if there is any air it'll move into this actual Water Seal chamber and that's it it won't move any further there's not going to be any suction that's generated against the actual pleural cavity to suck more air out so sometimes this is what we call setting the chest tube to water seal we'll talk a little bit more about that but there's specific things that you should be monitoring for in the actual Water Seal chamber but let's say that the patient does have a really big pneumothorax and it's not going to be able to completely kind of resolve what by putting them to Water Seal you need to generate suction to really cause those two layers of the pleura to come together and kind of become opposed again and so sometimes in order to do that you need to generate enough kind of suction or pressure to really kind of suck the actual two layers back together so what we'll do is sometimes we'll actually have again air moving via this third tube into this third bottle called the suction bottle and again this is usually filled with water there's two tubes that are actually coming into this suction bottle one is a tube that kind of comes from the atmosphere and what this does is this allows air to come into the actual suction bottle and again help with being able to regulate the pressure that can be generated from the suction control chamber it's kind of like the regulator if you will the third one is the actual tube that will come out of the suction bottle and go to the wall suction so that's the concept here is that you can set a degree of suction or pressure that you want to pull air out of the actual chest but it's regulated by this vent and the degree or the amount of water that's present in this suction bottle all right which is very important to prevent injury to the lungs again usually the suction control is set to 20 centimeters and again let's talk now about this three bottle systems and things that you should be monitoring for again the collection chamber is collecting fluid so you really want to look and see if they had an empyema and it's not putting out enough enough output you need to consider okay maybe I have to instill some TPA maybe they need a Vats so that's important to be watching out for if they have a hemotharaxin they're putting out a ton of blood this is very concerning and this may mean that you have some vascular bleeding that you have to take them back to the or and figure out same thing I told you the water seal chamber which is this one which is where air should bubble if there's lots of bubbles that means that there's a potential two things one is that the patient still has a pneumothorax and air is leaking from their chest into the collection Bottle Into the Water Seal chamber or if they don't have a pneumothorax there's air that's leaking into the tubing somewhere along the process of the chest tube and you have to evaluate for that all right usually a chest x-ray to rule at pneumothorax good position of the actual chest tube and then kind of evaluating the tubing system along the way the thing that you should be watching out for and sometimes we'll hear is that the patient exhibits in their water cell chamber titling which shows that the fluid is moving up and down and that's usually just the changes in intrapleural pressure whenever a patient breathes they generate a pressure that can help to pull that fluid up the actual Water Seal chamber tubing and then whenever they exhale it comes back down but that's normal with breathing what you want to watch out for is if it's not titling that could mean a couple different things if it's not titling it could mean that there's like a potentially a kink within the tubing or the tubing is occluded of some sort so that's something to be able to watch out for the last one is the suction chamber so the suction chamber again you set a particular pressure off the suction control you can generate wall suction but that's not the important thing it's the degree of pressure that you set the actual suction control chamber to that's important so if you get a little bit of bubbles that's normally you want to have bubbles that's indicating that you're having appropriate amount of suction that's generated from the suction control chamber but if you're having excessive amounts of bubbles that means that the suction is too excessive and you need to turn that down because what can happen is it can actually cause kind of the chest tube to suck on the lung if you already kind of obliterated that space and you resolve the pneumothorax now it's just going to suck on lung and kind of cause more injury so that's something to watch out for all right my friends I hope that made sense I hope that you guys enjoyed it and as always until next time [Music] thank you