for before we move any further does anybody have any questions they wanted to ask I’ll give you 10 20 seconds to put in any questions in the chat make sure you understand what we’ve done so far before we move on to um HP cental lobular nodule and Trin bud how to differentiate so Central lular lobular nodule is a DOT Tre in bud is literally a tree so you want to see a branching opacity so you want to see a bunch of grapes um when it’s Rel fine but Central orbit n are essentially just just dots very subtle can be ground glass very fluffy looking or they can be very discrete and more dense looking uh but they are essentially just a DOT with nothing around them uh nothing touching them m perfusion how to know which is abnormal uh if the black is too black or the white is too black uh White is too white I’m guessing the question uh the answer is experience white is ground gloss is more easier to appreciate sometimes the the hypo attenuating or the the the darker part of the lung can be more subtle and it comes with experience um obviously when the dark part hypoa part of the lung is air trapping you can see it be more prominent if you do an expiratory scan uh but but that’s a that’s a question for experience name of the sign in s that pulls the bronos posteriorly there is no sign um it’s just a description okay moving on let’s go on to HP um mindful of the time so HP or hyper sensitivity in neumonitis um unfortunately gets very um ignored in the more uh populated or the um you know areas in the subcontinent or India or Africa is where you have so much um air pollution that can go undiagnosed for a long time it’s more a diagnosis um in in the western setting but it doesn’t mean that it doesn’t happen elsewhere it just goes undiagnosed more much longer um point of time it was previously described as acute Subacute and chronic but over time the trend is changing and the trend is now to call it non-fibrotic versus fibrotic in terms of exam and F frcr specifically I would ask that you still stick to the acute Subacute and chronic terminology because that is how unfortunately we are a bit behind you know things take time to filter into the the general Radiology population from subgroup Sub sub speciality so for now if you’re describing it for a scan for a referral as a general theologist stick to the the more basic or the the the PO the classification that is more common which is acute Subacute and chronic acute and Subacute by definition are non-fibrotic by definition they are reversible chronic HP um isn’t really reversible but you can have fibrosis in it that is stable chronic is synonymous with fibrotic acute and Subacute is basically the same thing what is different is the is the onset so the time of onset from the symptoms or the time of onset from the insult that gave them that HP uh is the major differentiation so it’s arbitary differenciation because when you have a scan in front of you of the patients said they became breathless a week ago or a month ago uh it can be inaccurate is because that’s when they first noticed the symptom that doesn’t mean the symptom hadn’t started 8 weeks before that it’s more um easy when you have a clear enticing pathogen so you know it was a bird they bought it was a pet they had um it was occupation they started so they started working in a certain Factory or a certain occupation a certain chemical a certain Budgy or a parrot so then it’s it’s more um easy to identify the exact time that the HP would have started so just reiterating stick to the acute Subacute and chronic acute and Subacute are by definition reversible whether they are or not is depends on the patient actually listening to the doctor and stopping that exposure if you have a bird that’s giving you HP and you don’t get rid of the bird you’re never going to come out of that Subacute phase are you and then will inevitably um end up with chronic HP my mouse is stuck for some reason give me one second let’s try again no yeah okay so like I said acute HP will ultimately turn into this Legacy term that we won’t use anymore we use more non fibrotic HP terminology but for now acute HP um is a term we use to define um abnormalities in the lung that are pre-dominantly ground glass this ground glass is typically nodular but it can be diffused if very severe of the patient had a very severe reaction to whatever caused them to have HP you can even have consolidations that patient is usually pretty unwell if somebody presented with acute HP and had consolidations on their scan because of HP the chances of them getting diagnosed with HP are very negligible because the minute you have an unwell patient presenting to you and you have consolidation you are going to call it infection if nothing you may put in a differential of um organizing pneumonia or metastatic disease or something like that HP is usually pretty low down on a differential for somebody reporting acutely unwell patient with raised inflammatory markers and consolidation on a CP scan so acute HP that has consolidation often goes undiagnosed it’s often in retrospect that we realize that that consolidation was actually all HP it is more easy to differentiate um HP from infective causes when you have the typical ground glass capacities that are nodular the nodular opacities are very clearly Central lular in distribution they are soft as in they look a bit fluffy fluffy meaning you can’t clearly outline their margins but you can see that they are Central OB they’re usually small small enough for you to see them but small enough they’re usually under 5 mm in size they can occasionally have well defined borders and even be slightly more dense um but if the history fits and the Imaging fits you can still be pretty confident that is P so this is what scan will typically look like they will have diffused bilateral Central lular nodules and how you know they are Central opular is because you will magnify it you will go right up to the Fisher and you will see that none of the these nodules actually touch the Fisher when you go right up to the plural surface you will see that none of these ground glass nodules ever touch the plural surface ever touch the media stal surface so you know this is sitting in a space that is incapable of touching the plura so that’s only the central glob space and they are more commonly ground glass and fluffy uh subcentimeter but they can on occasion be more dense the only difference in acute and Subacute when the abnormality is cental L nodules is the time from onset the time from the insult and over time this will be an arbitrary differentiation so Subacute when it acute phase continues and the um the the the very thing that is giving them hypersensitive neumonitis continues to be in that patient’s life they go on to develop more sub acute HP what happens if somebody has a very severe acute HP they come into hospital and this is seen pretty commonly as they come into Hospital inevitably that thing that was giving them HP was left behind at home or at workplace because they happen to be in the hospital they got well and the doctors thought they got well because they were given antibiotics so that starts the cycle of being diagnosed then they go back home and they become unwell again they come in again again in the acute phase because they’re in the hospital they’re away from that pet or that chemical they get better uh and they get uh labeled wrongly as resolved infection recurrent infection it’s only when the acute phase was um mild enough for the patient to be at home do they go on to be develop the Subacute phase or more commonly when the patient is a healthy young person or a healthy um adult they cope with the symptoms and they have this smoldering HP that becomes Subacute HP Subacute HP is the most common presentation out of all three phases of HP um it is indistinguishable from the acute phase purely based on Imaging it is based the diagnosis will be based on the onset of symptoms and the history the acute and the Subacute and The Chronic they lie on a Continuum and depending on the time uh it is called Subacute and even in the Subacute phases you can see early fibrotic changes or early Distortion and then if untreated or un by untreated I mean they don’t get rid of the the the substance or the the pet or whatever is giving them HP they go on to develop fibrotic changes sometimes very rarely they can even get rid of that um antigen and still go on to develop fibrotic changes this is um technically not supposed to happen and some people say that this happens is because you actually labeled them wrong you didn’t never actually found out what was giving them HP so they could have HP because of multiple things so technically if they they get rid of the um the the chemical or the pet they shouldn’t go on to develop fibrosis if they do we do see it happen and the theory is this happens is because there was still something else in their home or their work space that was um giving that irritation or that information to the airspaces or the lungs um Subacute is usually bilateral B symmetrical both loaves all loaves no clear zonal predominant if it is slightly milder you can see that it tries to favor the upper and the mid zones anything that we inhale and it irritates our air spaces tends to go in the upper to Mid zones if it’s um uh if you inhale something that is heavy and aspis being one of the very common things then they settle into the bases of the lower lobes of the lungs and those changes happen in the lower lobes so if somebody says why is asbestosis in the bases whereas other inhalational or occupational lung diseases are in the upper and mid zones is because of the the substance they inhale the weight and the size of it so HP is usually uh caused by substances that are very small Airborne or inhalational um so fumes or pet hair or something like that and they usually tend to um favor the upper and mid zones when they do develop fibrosis the fibrosis is also very clearly mid Zone predominant it actually likes the mid Zone more than the upper lobe and the aps it can track into the bases but being PR purely basil fibrosis makes it very unlikely to be HP just going to pause for a second have a drink of water so this one when you can see that this patient does have ground glass or Central OB nodules but you can also see that they started to get that architectural Distortion the broni has started to dilate they turned this squiggly irregular beaded appearance so that means the lung around it is getting a bit fibrosed a bit distorted a bit abnormal technically at this phase this could still be reversible if they if they heal completely that could go back to a normal diameter of the broncus or this can be the first signs of the patient developing chronic HP so this is first mentioning on the scan that there there is clear evidence that this is St a Subacute disease because why is that because you see Subacute uh HP you want to see sub uh CR glass Central lular nodules presence of central lular nodules implies active disease and by active I mean acute and Subacute so because somebody can have chronic HP that doesn’t mean the patient needs treatment especially if they asymptomatic of the imaging has been stable for The Last 5 Years so they don’t really need treatment they shouldn’t it might be an incidental finding on a scan but when you see that cental L nodularity you you know that this is active disease that’s qu that’s a question you will frequently get asked by the respiratory physician when you report that Scan they will make might pick up the phone and call you and say actually I was wondering does the patient have active disease and what they mean what they’re implying is is there Central opular nodularity a chronic HP being the last phase or the last bit in the continue or the end stage of the HP being chronic means fibrosis fibrosis by definition implies irreversible but you can have fibrotic features in Subacute that may be reversible chronic HP favors the upper and mid zones that favor um favoring means the reticulation or the architectural Distortion favors mid zones but the the main sign that you want to see in HP is air trapping and that air trapping is usually more clearly seen at the lung bases so the lung bases can be abnormal in the sense that they show very clearly Mosaic attenuation and if you do an expiratory scan it becomes more prominent so you know it’s air trapping that can be more prominent at the basis but the fibrosis itself has to be more prominent in the mid zones uh honeycombing you can also see honeycombing is a sign I’ll come to later uh it’s also seen um it can be seen in HP so it doesn’t mean that if everything else looks like HP but you have honeycombing you think to yourself no and now I can’t possibly call it as HP that’s not true you can see honeycombing in end stage HP as well um this is what I meant by the air trapping so air trapping is usually more prominent at the lung basis and that’s usually because of the breadth of inspiration or the amount of lung parena you can see is more at the lung bases for example you see this uh different texture different attenuation of the lung next to each other that same patient on the expiratory scan you can see that this is versen so the dark part has gotten significantly darker the lung around it has gotten significantly whiter so that is clearly air trapping air trapping in a very small area of the lung you can find in any any expiratory scan if you look hard enough what you mean by air trapping in the context of diagnosing somebody with HP is you want want to see that air trapping bilaterally at least one area in all the lobes of the lung to confidently say that this is actually air trapping the question you most commonly think to yourself or somebody will ask you is isn’t it possible that the air trapping was air ra disease as in the patient has asthma and they still have a bit of I for some other cause and they both happen on the same time in the same patient the answer is yes that happens quite commonly that’s where the distribution of fibrosis will come into play that’s where the history will come into play that you have to put it all together and come up with a reasonable differen but yes you can have air trapping because of underlying mild Airways disease asthma and the patient has I so you can have both at the same time this is what I mean by the distribution of fibrosis so the traction is a sign of fibrosis meaning there’s some something around it it is pulling that broncus so when I mean fibrosis I mean traction the traction and the distortion in HP will be predominantly in the mid zones predominantly upper and mid zones so that’s what you see in these slices so mid Zone Upper upper lobe um arit Distortion Traction in the context of the bilaterally um the lungs look Mosaic it looks like there’s air trapping so that looks pretty good to call somebody as chronic HP and the reason I’m calling it as chronic is because I don’t see any nodules I don’t see crown glass Central ular nodularity so I know this is only chronic you can have Subacute on chronic so the patient had chronic HP um they went on and got something else a new pet a new occupation that gave them HP or something else or the same exposure the same unknown antigen they had last time they can have the same thing over and over again and that’s quite common to see subut chronic HP before we come on to um idiopathic or the IPS I’ll pause for a second and see if you guys have any questions so far about HP so 30 seconds can asthma patients develop HP they can can HP patients develop asthma they can will you be able to tell them apart on the scan no on Imaging alone any difference between acute versus Subacute if it’s uh if this the patient is well enough to be ambulatory as in the patient isn’t on the itu isn’t really really unwell no there is no way of differentiating acute versus Subacute the only way you can differentiate acute versus Subacute is when the patient had consolidation as well so they were so Advanced or so severe a disease they had nod nodularity as well as consolidation so you don’t really get consolidation in Subacute when you see consolidation you you tend to call it acute HP but that is a very rare presentation is exper Phase needed to diagnose air traing absolutely if you’re going to label somebody’s chronic HP uh uh expiratory scan uh is absolutely necessary so this sometimes that happens at the time of initial depends on your protocol so if the patient was being worked up for I and they had a scan requested as specifically for hrcp the initial um broad assessment for underlying I will include an inspiratory spiral it will include an um inter spaced expiratory some countries for example the American guidelines even recommend a spiral expiratory in the UK don’t do that you and you can have even have prone so that’s your initial assessment for I sometimes you can have a suspicion of um HP come up from some other source so the patient had a staging scan for some other reason the patient ended up with the I MDT saying is this HP so the patient never had an expiratory stand so the first step would be to um uh get a small limited study a limited interspace expiratory scan and when you can definitively call that as air trapping on the background of lungs that look like HP you are pretty sure that that patient has chronic HP effect of smoking on HP fact of smoking on anything isn’t good and HP isn’t any different uh the one rule of thumb was used to be true was the P if patient has we were told I’m sure all of you were that if the patient has asthma they can’t smoke which isn’t really true because nowadays when you have vaping and all these um so by smoking you mean tobacco and then there’s vaping then there’s marijuana smoking there there’s all sorts of um substances that are mixed in marijuana to smoke so smoking in itself can give someone HP especially if that smoking is not tobacco if that smoking is um vaping so there’s an entity that’s quite interesting if you guys Google it is called vaping Vape lung so vaping related lung injury is quite uh significant when it presents it’s very severe we’ve had three or four in the last one year and they look very bad so vaping is would is it’s kind of um HP as well isn’t it so yeah smoking isn’t good for anyone smoking alone depending on what you smoke can give you HP as well can I be unilateral it can be I can have all sorts of we presentations and it it can be asymmetrical quite commonly it can very rarely be um unilateral as well then the question comes in is that I primary I or that was did that patient just have an infection on that side of the lung or that patient had a hemorrhage on that side of the lung that they ended up with a scarred lung that looked like I so that’s a discussion what’s happening but um but that technically yes they can so moving on to idiopathic pneumonias interational pneumonias so the term that is used very interchangeably is uip and ipf and that is something I would really hope you guys get um very clear in your mind um by the end of today’s session is that ipf does not mean uip and uip does not mean ipf ipf is um diagnosis it is a disease uip is not a disease it is a description of a pattern so saying uip doesn’t mean anything IPS are just terms to describe Imaging they are not diseases so interstial pneumonias and idiopathic P fibrosis are two different things they’re used interchangeably and a lot of people who um not clear on the concept use the word interchangeably so when you call somebody as idiopathic pulmonary fibrosis you’re giving them a death sentence there is no cure idopathic per fibrosis there are antifibrotic drugs those are very expensive depending on which Healthcare System you work in they are hard to get your hands on depending on where you are in the world and the end stage treatment for any ipf is lung transplant so pulm fibrosis is a very serious diagnosis no is it is a irreversible disease that is a de sentence so ipf is a disease that is a diagnosis of exclusion once you have excluded every other reason the patient can have bad lungs you are left with a diagnosis of exclusion there is no test that will tell you that you have ipf there is no symptom that will tell you you have ipf definitively lung biopsy can but that is not route you want to take commonly because somebody with disease lungs is also at a higher risk for complication from lung biopsy so it’s it’s a um it’s reserved for very specific questions so um just to repeat ipf and U IP doesn’t mean the same thing the IPS the uip the the lip the dip nsip all the IPS are descriptive terms of what you see on Imaging those patterns can be seen in many diseases and that pattern when you describe it implies a certain differential diagnosis it doesn’t mean a specific disease so um that’s the point that I hope should be really clear in your mind the diagnostic process in somebody who has suspected I or diffused pulm lung disease is you want to know whether that patient is has ipf that’s the end point of any I discussion when the patient has a scan and that scan is abnormal the radiologist just will describe the scan come up with a um a pattern that they think fix that scan appearance and that pattern will then open up a few differential diagnosis for example if I say this patient has uh this patient has D on the scan and I think this is nsip so NSP is not a disease the respiratory physician and I will discuss the scan in I MDT they will say are you are you fairly confident that you think NSP is the best fit and now will say yes then we look at a few abnormalities or the few diseases that can give an nsip pattern of O and those have specific tests that the physician will do based on what the patient is presented as and and that’s how it it will go the diagnostic process the the scan alone will never give you a bond or clear diagnosis even if you have very clear traction mular itation honeycombing all the the tick points and you say def definite U pattern of lung diagnosis is consistent with ipf you shouldn’t be saying that on a scan you should be saying consistent with the uip pattern of fioptic lung disease why that patient had that pattern you cannot possibly know so don’t give very serious diagnosis based on Imaging op so focus on the on the pattern and not the underlying cause the pattern will guide you down a certain route and that route is hardly ever explored by the general ideologies it comes out of a multidisiplinary team meeting so the the pattern differentiation the pattern classification uh is done by various societies there are two large main classifications that have followed in the world there’s American or the ATS guidelines and there is the flesh Society guidelines depending on where you are in the world you can follow either of them there is a lot of overlap between them the main difference between the American and the fleshner is the is the push for biopsy in the American one and uh the American guide and the difference other difference being that the American guidelines actually endorse expiratory scan that is spiral that’s a higher do scan and the flesh Society does not whereas other difference being that the biopsy Trend so the American guidelines will uh suggest a biopsy on almost all the elds whereas in the UK or where we follow the fleshner guideline uh the biopsies are reserved when you don’t have clear answers on the scan if you you can make a fairly clear fairly confident diagnosis of ipf based on the scan we don’t go down the biopsy route so the uip patterns the definite uip patterns and the proper uip patterns don’t really end up having biopsies because there are limitations there are costs there are waiting times and all that to consider and this is unnecessary risk that should be avoided if it can be most places in the UK uh we practice a hybrid sort of guidelines so some in some classif some aspects we follow the ATS in some aspects we follow the fresh guidelines this is not meant to confuse you this is just meant to put things into perspective the only thing that would be important for you at your stage is to U understand the the main four um categories that you want to put a scan into so once you made the diagnosis there’s definitely I you want to then go down these four roots can I put it into any of these four boxes and how you can put into any of these four boxes is how is we’ll go through that in in the next few minutes the definite and probable uip patterns are almost identical there’s only one difference between the two patterns and that is honeycombing we’ll come to that in a bit um but these four categories are present in ATS and they’re present in the flesh n so they’re fairly similar in that sense uh definite uip probable uip both basil predominant both sub plural the main thing to consider for these two definite and probable is that you don’t see any other predominant abnormality other than reticulation so too many lines in the lung is the main problem there is or they can be a bit of ground glass but that ground glass change will always be considerably less than the degree of reticulation so the main predominant abnormality is too many lines articulation that happens to be peripheral and it absolutely needs to be basil predominant it can be anywhere in the lung but it has to be worse at the base of the lungs and by base I mean lower half of the lung not not back steer part of the lungs if there is any feature on the CT in addition to this that is inconsistent with uip that means if there is too much air trapping there are too many consolidations there is too many there is neemo thoric there’s too many cystic changes there is there is significant empa uh any of that feature in addition to those features that we want to see in uip would prevent that scan to be put in these two boxes the distribution can be a bit abnormal it can be heterogenous it can be asymmetrical very rarely it can be uh unilateral very rarely and I mean once in 5 years rarely um and the main difference between definite and probable uip is presence or absence of honeycom you can have have everything that looks like probable uip but they still um round glass but there slightly more than you would want to see so you want to call it probable uip but you’re not really um 100% sure there’s some ground glass that makes you a bit uneasy there’s some features that you can’t rep put here or there anything that that eventually will probably will end up being probably uip but today right now on the scan is indeterminate for uip gets called indeterminate for uip and why that is important is you don’t want to label somebody is probable uip because when when you put down somebody that route down that route you close down other avenues so keeping them in the in determinant for uip pattern box makes the referrer or the clinician think outside the box they will still look for other um diagnosis that may be reversible for example like Sid dois or Loma or um scma sad connective tissue diseases drug indu anything that makes you slightly uneasy um you should uh towards indeterminate for uip rather than push it down probable uip when there is clearly abnormalities on it that can think that make you think of alternative diagnosis alternative diagnosis will come to after this for example organizing pneumonia for example hypersensitivity neumonitis for example t ified plal plaques that make you think of asbestosis for examples a patient that is known to have con disease patient has ra they have a dialated esophagus they have joint erosions you can see on the scan so that’s when you think of alternative diagnosis so you was Will describe the features and you will describe the additional features and put in some additional um possible differential diagnosis rather than calling it uip your probable uip so how would you approach a scan that shows um abnormalities so first you will see whether there is interstitial abnormality or whether there is interstitial lung disease lung disease means a disease process that needs a work up abnormality can be a transient change it can be insignificant change it can be incidental finding postam focal area of change so Ila and I are not the same thing Ila gives you a bit more luxury describing an abnormality and dismissing it I triggers the whole Cascade of refer to respiratory refer to I MBT and all that so once you are sure there is reticulation significant enough for me not to be able to dismiss it you then want to look for fibrosis and how you look for fibrosis is you look for traction broni dilation once you have convinced yourself that you can see areas of the lung where the broni are being pulled there is traction you know there is I and you also know there is established fibrosis once you have those then you need to look at the distribution is it basil is it sub plural is it honeycom all three check uip check is there anything that is in addition to these findings that make me think of alternative diagnosis is the plura okay are the lymph no okay uh is the patient known to be a connective tissue disease patient none of that uip check all of that present but honeycombing absent you need to uh call it probable uip and if there is anything anything slightly uneasy about it there’s gr GL that is a bit too much uh there is slightly architectural Distortion more in the upper zones you can’t really call it basil any of these feel free to call it indeterminate for uip so I’ll put this slide up and then ask you guys do you think there is I and if so in which three of these do you think there is I so 30 seconds starting now for for okay okay let’s go through what you guys have said so Shima has said a has fusions absolutely right so she the patient in a has bilateral plural fusions then they have this sepal thiing at the long bases so what do you think that is that would be fluid overload so that wouldn’t be I B has consolidation absolutely right uh and some of you have said um Shima kin a an and Donna that none of them Max have I and you guys are absolutely right all of this is just sepal thickening for another cause this is smooth sepal thickening the sub plural lung looks very smooth and very normal um sepal thickening being more Central so this is sepal because of fluid overload heart failure this one is just consolidation and causing a bit of architectural Distortion around it so this is this linear at this is confusing you because the other lobe looks pretty okay the sub plural part will looks okay and this in the context of plal diffusion um should not be thought of as I so none none of these is actually I uh traction bonal dilation so traction bonal dilation by definition you want to see something around that broncus pulling it whether that is reticulation or whether that is ground glass it will be reticulation pulling that broncus in uip patterns of fibrosis it will be ground glass enovation around that bronos and that Broncos getting dilated so you will then think is this ground glass fine fibrosis or is this ground glass um nsip so nsip historically was used to be classified as um cellular nsip and fibrotic nsip but nowadays we just focus on calling it NSP rather than trying to focus too much on which type of NSP it is so I dilated bronchus the lung around it is completely normal is primary bronchiectasis a dilated bronchus the lung around it is abnormal is traction bronchial dilation if that abnormality is traction that is a uip pattern when that uh area around it is ground gloss you start thinking of nsip when that consolidation when there is clear consolidation around it you have to think whether that is reversible that is just normal infection finding um and I’m sure all of you will appreciate that in C you have this consolidation and you can see bronchite through it so this is just air bronchogram this is not traction bonitation you see broni more clearly when they’re in the middle um of a white area like consolidation so they’re more striking or moreable but it doesn’t mean that they are dilated in B uh the brona the typical squiggly irregular worm like and the lung around it is very coarsely um reticular so this Co reticulation sub plural predominantly um with dilated brona reaching up the plural surface that struction mon dilation the first one is very subtle that’s why put it in uh but you if you focus closely there is traction bronation the thin bronos going all the way up it is irregular it is non- tapering and the lung around it is coely reticular so all three uh all the first two is traction mulation and third is this common consolidation with the bit of air bronchograms the other thing to to think about I is not to overall it uh if the patient is a 92y old with no other symptoms presented with the KCT KU and you can see the base of the lungs the base of the lungs don’t look perfect don’t go ahead and call it I there is something called age related change or age related I with age our lungs get stiffer um less elastic so they can look a bit abnormal on Imaging it is forgivable up to a certain stage and Beyond a certain age you have to think pragmatically whether is there any benefit in overcalling or pushing this patient down a diagnostic route for very mild early changes or can I just miss this as age related changes for example in this one if you look if if this was your first scan uh and you saw this sub plural change this patient happened to be a 95y old um I would urge you to her on the side of under calling it and just describing it and say maybe um attributed to Patient age if this was a 60y old and you had these lungs you shouldn’t be calling it as gauge related change because that would then in the context of age and especially symptoms make you think of is this early I uh and the only test in reality is followup so when you see these patients followed up if they actually had no symptom at that point it would be not unreasonable to recommend a one year followup so if they came back in one year and they ended up with a scan like that you know they clearly have I and it is progressing at this if this was the initial scan you would be way more confident calling this I but on the first one uh depending on age patient presentation um that your report would be tailored according to that but if you do look closely you do see a bit of traction there as well this a very medial part of the lung especially near the lung bases is where we have degenerative changes in the spine so you can have dense prominent osteophytes sitting there so you can have focal fibrosis next to degenerative changes of the spine and that’s not I that is just the lung reacting to a foreign body so the osteop is passing into the lung and the lung around it kind of reacts to it so that’s not I you can describe it if it’s very prominent but you can say that’s focal fibrosis related to degenerative changes of the spine does not need any further work up because that will almost certainly be asymptomatic the other thing I can U mimic as is dependent change so if you look especially in the acute inpatient setting unwell patient a heavy patient patient who’s been lying in bed for a long time because they’re unwell for some other CA because if you if you CT them it’s not it’s very common to see dependent chain so dependent Chain by definition should be dependent and with time and the number of scans you report and the number of uh years of experience you have you get pretty confident calling it is dependent change and most of the time we don’t even notice it anymore when that dependent change shows up on a scan that was done to look for I then you look a bit more closely then you start noticing everything more closely then you start confusing yourself so that was you uh scan for I um investigation and you saw this change if you can see convin yourself that this change is only in the dependent parts of the lung whether that is uh fine reticulation or whether that is um subtle ground glass it will be dependent chains when that chain starts creeping up laterally around the lung in more interior areas is when you uh should start getting uncomfortable by dismissing it and especially when you can see the broni get dilated in it or around it you then start to think whether this is a bit more than I would dismiss it the first step would be to recommend a prone scan because on a prone scan this should improve or resolve and that would um tell you whether this is a dependent change or R but this certainly worth asking yourself that question when you see the changes if you see changes look for them interiorly and naturally if you can’t find anything to yourself is this all just dependent change and my over calling I uh so what is honeycombing honeycombing is a sign that is associated end stange lung fibrosis it is end fibrosis the end of the airspaces architectural Distortion progresses and progresses and then the normal tissue dra through Distortion ends up with end stage cyst formation uh this cyst doesn’t need to be stacking they don’t need to be on top of each other even one cyst can be honeycombing but your confidence in being able to diagnose it as honeycombing should be very low um when it’s just one cyst you see so that’s why we ID recommend that when you see a cyst sitting right up to the plal surface can you convince yourself this is just a cyst or are you sure this isn’t a broncus that is um seen out of pain so the lower half of the broncus is in another slice and you can see the top end of the end of the broncus sitting on the plural surface and it looks like a cyst but just an end on broncus when you see them stacking up to each other two three then you can be sure this this can’t be a bronchus and that’s why traditionally we want to see two or three C stacking up before we call it honeycombing the honeycombing doesn’t need to be on the lateral part of the lung and it can be paramediastinal can be next to the feral uh Lura it can also be right in the middle of the lung because it will look like in the middle of the lung but it’s actually the base of the lung um so on the basil slices you can see honeycombing right in the middle but if you look at sagittal this is actually the the lower surface of the subal surface honeycombing means end stage fibrotic lung disease it does not mean ipf it means definite uip you can have definite uip pattern with uh ipf and many other diseases as well not it’s not really helpful but it’s certainly worth pointing out that you can see honeycombing in non uip pattern as well for example nsip and uh HP can also show honeycombing but it should be certainly not be the predominant Factor so uh I’ll pause here and make sure you guys understand so far if you have any questions put them in the chat give 20 30 seconds what is bronchiolectasis bronchiolectasis is that end Airway dilating all the way up to the plural surface and how can we broncus versus bronchia acuses bronchus is a primary abnormality of the bronchus bronchiolectasis is only seen when it’s fibrotic lung disease because the end Airway doesn’t really have that much muscle in it that will have primary bronches so when the end Airway dilates all the way it’s it’s almost always because of fibrosis um one small s with articulation can be called uip absolutely not no you want to be really confident and you want to ear on the side of caution before you label somebody as definite uip uh if you have one cyst with reticulation that’s not indeterminate for uip that’s probable uip is it mandatory for honeycombing to be layers it is not it depends on your experience if you are a very experienced cardiy radiologist you one layer of honeycombing you can call is honeycombing but my question to you with would be are you sure this is not parpal empa and this is honeycombing you don’t really know do you so it’s um better to see it stacking up there is not a technical requirement for it to stack up um one of you asked me in the question high can we use empis matus cyst or just cyst you cannot use empatis cyst because EMP empa means destruction of the lung cysts mean a space occupying Legion that is a cyst a cyst can be a tumor a cyst can be a bronos a cyst can be anuma a cyst can be um congenital uh so yeah don’t call it empat cyst call empa empa and C CST and I hope you would attempt to differentiate between the two like I said before cysts have Wall andas do not um if there is a thin wall parima cyst how to differentiate between MMA versus Neato seal Neato seal is usually caused with an insult to the lung so either infection and most commonly trauma you might see the seen uh as a result of acute injury to the lung it is like a pop of the lung it happens with blunt trauma it can have happen with infection especially PCP pneumonia um that’s neum neum seals can have a wall or they can look like they have a wall empa should not have a wall empa is not a lesion emphysema is just empty space where lung used to exist so how to differentiate empa is you want to look for that Central DOT sign you want to see a strand of tissue going through that cystic area you want to see a DOT hanging in the middle of that that is a vessel that used to feed that part of the lung you want to see a strand of SEPTA that will likely be uh containing that vessel in it so that’s how you differentiate empa from cyst emphas do not have walls and they have usually have something hanging in the middle uh this is how typically you would be very happy calling it as honeycombing you can see Stacks and stacks of cysts and you can see dilated bronos going into it if you saw that you will be very uh comfortable calling that as honey forming the problem happens when they’re not so obvious so for somebody who have asked before what is bronchus this is bronchiectasis so this is that bronchus this bronchus you can see going and then disappearing this is a cyst sitting next up to the plural surface this cyst is likely another broncus that is seen on another slice either above or Beyond it so that’s broncy and because this is one cyst you want you shouldn’t be happy calling this honeycombing when you see these this is cyst on cyst so 1 2 3 four cyst this on on um a is definite honeycomb uh definite uip and B is probable uip other than the honeycombing bit there isn’t any difference between them in terms of distribution or um other morphological features uh nsip is the second most popular IP um nsip by default is assumed to be caused or associated with another Disorder so nsip is usually seen in connective tissue diseases or associated with some other diseases so the patient can have um underlying connect to tisue disease they can have an autoimmune disease they can have drug induced tox toxicity um something else going on with them so if if you have a scan and you labeled it as NSP that referrer will inevitably order 100 other tests to look for what is going on they will do all sorts of antibodies um ana SLE scma ra all sorts of things they will look at the drug history they will look at the patient history um to look for other underlying disorders that are associated with NSP in most commonly um connect to tisue disease so it’s it’s uh a rare diagnosis much rare than probable or definite uip and when you do diagnose somebody with NSP they have to have other disorders excluded uh and once they are excluded uh and you’re left with purely nsip it is rare but it can happen and what happens with nsip is it can evolve uh a and like I said before these intertial pneumonia aitis is just a pattern of I somebody has nsip today doesn’t mean next year they’re not going to have uip so the pattern can isol evolve the only pattern that does not evolve is definite uip that’s why the word definite in it and that is why the reluctance to not overall it uh if you have called somebody as definite uip the understanding is this pattern will never change the severity can progress but they will always be definite uip and nsip by definition probable uip by definition can evolve nsip can turn into probable uip probable uip one day can have superimposed viral pneumonia or infection or acute exacerbation they can look like NSP uh or they can both progress into definite uip but once in definite uip they’re not going to progress in any other way other than uh progression of severity for for for for for e for for for uh this can give it a go I would like you guys is to Define what the abnormality is and give it a pattern and we’ll go from there 30 seconds starting now for okay let’s look at the scan again and look at the predominant abnormality the predominant abnormality on the scan is ground glass not articulation so you can see ground glass on both sides is clearly more on the right side the ground glass has a bit of texture to it um so I think some of you may be confused by the texture and calling that articulation but if you look at the periphery um those lines are actually just dilated broni and the predominant abnormality more centrally and interiorly is ground glass that ground glass is clearly causing traction because the broni are very significantly dilated within that ground glass compared to outside it so bilateral abnormality the predominant abnormality being ground glass that ground glass is clearly causing traction Bon dilation why you know this is tractional not primary bronches is because outside that ground glass there is no dilation so uh can this be an acute finding that is reversible yes but if I told you this look like this um a little uh similar to this but this is progressed over the last 6 months um then you would certainly think is this I this is predominat ground loss with traction the best fit would be nsip uh can this progress into probable uip or change into probable uip and and ultimately end up with the probable UI definite uip pattern of course it can but right now um on this scan this is the nsip pattern of disease the other pattern uh you guys need to think about when you see bilateral abnormalities in multiple loes is organizing pneumonia so organizing pneumonia uh can be an entity in itself when it is called cryptogenic organizing pneumonia or it can be organizing pneumonia due to another cause organizing pneumonia is also so a pattern of distribution of abnormality on the CP it is not a disease the disease is cpage UN recognizing pneumonia and that means it is organizing pneumonia without any cause and that is a diagnosis of exclusion most most recently the disease we all reported plenty of unfortunately was covid and organizing pneumonia was one of the patterns very clearly seen and associated with given covid so a lot of infections a lot of drug reactions a lot of of um drugs um pharmaceutical drugs recreational drugs can look like organizing pneumonia uh that organizing pneumonia is not cryptogenic organizing pneumonia it is organizing pneumonia appearance of an infection or an inflammation when you have no other cause for that organizing pneumonia you end up excluding them you end up with cryptogenic organizing pneumonia this used to be called Bop now it’s called cop or organizing pneumonia the the feature you want to see um to in a especially in an exam scenario is you want to see fluctuating consolidation today they presented like this um they would improve uh they won’t improve in antibiotics they would improve in steroids uh 6 months from now they presented the same way but this time the right the areas we saw previously had gotten better they had new areas in new locations so fluctuating consolidation or fluctuating ground gloss bilateral can be any lobe any distribution um distribution as in within the lungs top to bottom can be organizing pneumonia the pattern of organizing pneumonia is bronchocentric or subal and when you see it bilaterally and extensive it becomes more easy to diagnose it when you see it subtle for example hair uh you might not think of organizing pneumonia the thing about organizing pneumonia cryptogenic organizing pneumonia is an I so when you have diagnosed or excluded um other causes when you left with a scan that looks like this at the top uh you have no choice to call it cryptogenic organizing pneumonia that patient these patient respond very well to steroids but they can’t be on steroids forever so they get uh medium to long-term steroids then they are tapered off they can recur or relapse it’s a constant struggle to find that balance some do really well never have another flare again um that’s not to say they’re not going to have another flare in 10 years time complete cryptogenic nobody knows why it happens but that’s what it looks like it looks like sub plural consolidation it looks like Bronco Centric consolidation it can be consolidation or it can be ground glass or it can be boths Um this can resolve completely or it can resolve with a bit of scarring and by scarring I mean a bit of architectural Distortion in the areas that consolidation used to be or they can end up with a progressive fibr fibrotic I so that’s in could keep progressing keep pulling the lung around it keep distorting the lung around it and they will end up with chronic op or chronic organizing pneumonia and that’s a ftic lung disease unfortunately has no cure uh that’s the evolution of it that’s the cute presentation of it you can have plural infusions but there usually a reactive plural diffusion it can Infuse you a bit because you start thinking down the infection line when you see plural diffusion but you see bilateral sub plural bonr Centric cons consolidation with airb programs that over time weeks to months will Evol start evolving into Distortion so you start seeing that irregular um pulling of the Bron ey you see The Irregular Squigly margins that can be reversible uh but weeks to months when that consolidation completely goes away and he left with that Distortion alone that would be um scarring if that keeps evolving or the patient is symptomatic and it keeps progressing that is fibrotic op rarely you can see a purely bronchogenic pattern of for this is very rare and it’s usually seen in drug induced or chemotherapy induced diseases or opportunistic infections can sometimes mimic this but it’s purely bronchocentric so the along the bronchi the inflammation sits it looks very pretty on a scan it’s a very striking appearance it’s also very rare to see this appearance because when you realiz more commonly when you have this you have sub plural consolidation as well this is a very specific pattern of op rare but obviously becomes more easier to diagnose because you can’t really call this infection or anything else can you so Dad or dad depending on where you are in the world is diffused alol damage it just means that the lungs or type two nytes in the elial cells undergo necrosis it’s usually uh driven by a cause so the cause can be ards cause can be an es schic insult a pancreatitis even or it could be idiopathic Without a Cause so when it’s idiopathic diffuse severe pneumonitis that’s called AIP or incute intertial pneumonia diffuse LV damage is a term used to describe severe bilateral abnormalities you can’t really tell whether this is inum or the lung space the Airways or it’s also sever you can’t really different anything at all is um it’s can be described as diffuse alular damage it is a term I would discourage you using um and it’s usually uh reserved for itu sort of patients and when the changes are so Advanced that you’re it’s like a spectrum of when you don’t know whether this is ards or this is diffuse Al damage whether there’s a bit of hemorrhage in the middle when they had vasculitis or that c caused a Cascade of events it’s a descriptive term um it can have it has a acute exudative phase if the patient survives it it’s hard to survive it but in modern medicine the ventilator supports young patients healthy fit patients can recover from it and if they do recover from it sometimes inj um the recovery can be very remarkable then the reparative phase starts the repairing phase of it are actually more damaging to the lung because it’s causing Distortion and fibrosis and um pulling and almost permanent damage during that repair so that repair will the kind of repair the lung goes through will determine what day will end up as an end stage deficit in terms of lung function um so it’s the most common presentation of diffused alv damage is uh drug induced and by drug induced I don’t mean recreational drugs I mean chemotherapy drugs immunotherapy drugs can cause that um when you stop the drug the patient improves what happens is sometimes these chemotherapy drugs are used in connective tissue diseases and patients with connective tissue diseases can have abnormal lungs and the drugs they give them for those connective tissue diseases can give you that those lungs so it gets really hard to differentiate it usually it’s it’s a it’s a um mechanism of looking at when they started a drug and trying to hold the drug for a few weeks or months and see how the patient did but it can be confusing uh again diffus AL damage can look like diffus ground glass patchy tending towards consolidation can be basil or it can be everywhere uh just to point out that when you see diffused ground glass and you see Traction in the middle of it that looks so uniform you can’t really call that diffuse Al damage so the word you should be thinking of if you saw that scan is nsip because you don’t you don’t really see Distortion you see uh almost um radiating dilated broni sitting in diffused ground glass n so this is actually fibrotic NSP um this pattern I put in there because this is a pattern of diffus alol hemorrhage and not F alveol damage um both happen usually at the same time but when it’s purely Hemorrhage um the patient obviously is coughing up Buckets of Blood uh and that pattern is um very typical for diff I’ll be hambridge rather than damage coming to CT I’ll pause here because I know this is getting confusing so I’ll pause here make sure you guys don’t have any questions before I move on 30 seconds for questions please when I say bronos Centric I mean uh it’s tracking along the broncus and in the end air space so the the bunch of grapes around it so it’s when you see a nodular focus of consolidation you can see an airway coming into it and that’s bronos Centric or you can say per Bron bronal when it’s going along linear with the bronchus so interchangeable peribronchial when you want to say linear when you say Blobs of nodular consolidation when you can see a bronos going into it is bronos Centric and op be diagnosed on the first scan or do we need follow-up scan you can diagnose it on the first scan when it’s when it’s op and it’s clearly op it’s very nice to look at um and when you’ve seen it you can if you’re confident go ahead and call it like I said it’s a you’re describing the lung appearance you’re not really calling it cop you I think your question is can you can cop be diagnosed on the first scan so the cough cannot be diagnosed on the first SC organizing pneumonia can be whether that organizing pneumonia is cryptogenic organizing pneumonia or that organizing pneumonia is covid or nitrofur lung or chemotherapy induced lung you can’t how to differentiate fibrotic and Sip and Dad so the F dad patient or diffus damaged patient is very very unwell that patient is in the itu that patient is not sitting up and talking to you nsip patients are ambulat patients um walking around being worked up of file because something that develops slowly over months two years the patients po really well and the patient over months has reduced exercise tolerance they’re not really that unwell looking uh moving on to connective tissue I so connective tissue or ctd I is a term reserved for interstitial abnormalities in patients that have known connective tissue diseases the most connective tissue diseases you get asked about in the exam are these five so SLE ra Scleroderma yogin and there is a lot of overlap the one that is slightly different from the other four is ra ra is the only one that presents more commonly with uip rather than nsip so when you call somebody as nsip they will get worked up antibodies against cmma and as and all that whereas a rheumatoid is more U tending uh the nsip pattern can be seen in all four of the all five of these actually but when they are seen in floroda they’re almost you can’t distinguish them apart that’s why the patients are worked up for all of them together so all of the antibodies are done together IG and all that and whatever lights up or whatever has um positive results they go down that road and obviously then you have to examine the patient and look for the clinical symptoms with Florida you’re going to look for the esophageal dation and you know the skin changes and all that El is um very heavily plura based so patients when you think remember fusions pericardial infusion plural fusions pericardial thickening plural thickening SLE is the one that that goes towards the plura ra also gives plural fusions sometimes pericardial fusions these are the ones that you need to think of especially for exam point of view um the connected tissue diseases that like membranes pericardial plural um they can be thickened but very mildly barely perceivable thickening on Scan they can be slightly enhancing but fluid is what you’re looking for chlorid is not so much uh ra I’ll focus on more because ra is the one that is most confusing because the ra patients can have not only I but they can also have Airway diseases so ra is um special in this sense that sometimes the I comes before joint manifestations of RA so the patient not may not know they have ra um or the joint comes first and the I comes later or the I never comes what can almost never happen is that they get the I but never The Joint um and the I is almost never clean I it’s I as well as Airways disease the airway disease they get is bronchitis so the broni uh the large Airways mediumsized Airways have inflammation around them so the Airways can get thickened so it looks like a bit like bronchia acuses with thick broni inflamed broni and when you have inflamed Airways you get infection so super added mild infection atypical infection infection comes three in butd nodules so fluffy looking nodules dirty looking lungs dilated broni thicken broni is the airway problem of RA so ra related Airways disease Airway diseases is further divided into obstructive and non-obstructive I’m not going to go into that um today the I can happen concurrently with the Airways sometimes they can have only Airways but the I is usually ever never just I it has I and a um the I favors and if you look at the pie chart favors uip more than other patterns so it will start like probable uip and by the end it can be definite uip pattern um and the patient has known AR so they will label it if even if you report it as um a definite pattern definite uip pattern of long fosis and the history says r a patient the diagnosis the patient will get out of the MDT is ctd uh very rarely they can um present as diffus alv damage it’s very rare and the patients don’t really tend to do very well when that happens um ra like I said when they are predominantly or only everyway related problems with ra or ra related brontis you have the stream Bud um nodules being the main problem thicken Airways being a main problem and when you have I predominant problem you have the probable or the definite uip in this coronal coronal case when you have the honeycombing or you can have a mixture of both a bit of ground glass bronchia acasis then you have I so a bit of everything put in together um I know it’s that’s not already helpful in terms of you want a clear you know I will look for this this this to call it ra but the point to remember about ra is the patient will present um may present as joint problems they may present with Airway problems the scan may be messy looking there will be a bit of Airway issues a bit of I issues um so there’s no easy answer I’m afraid uh I won’t go into SLE and chlorida because the thing to remember about them is they will present as NSP and obviously for exam purposes you look for dilated esophagus and all that um moving on to drug induced lung disease drug induced includes uh pharmaceutical drugs and it includes recreational drugs um different drugs favor different patterns there is a lot of overlap um there are some exam favorites in terms of these drugs nobody expects anybody to remember all the drugs that cause different patterns so nobody’s going to ask you which drugs you know give you a fibrotic pattern uh of I or which drug gives you isolated ground glass or abnormality on um drug induced lung disease has a bit unreasonable and because there is so much overlap what does happen is uh the exam history or the patient history in real life will say the patient is on this this drug um and you will look at a scan that looks abnormal and with abnormal you will go through the the pattern is there I is this an acute pattern is this uh you will look for the pattern is this uip pattern is this op pattern is this a fib brosis as an nsip pattern is there just Mosaic inovation there’s a bit of ground glass there’s a bit of darking I can’t really tell what’s going on any of those uh is worth describing and any of those could represent a drug induced lung disease the only way of definitively diagnosing drug induced lung disease is to stop the drug and followup most of these they cover with those squally the lung heeds very well when the insult is extern extrinsic um when you stop the drug the lungs come back comes back within months um to how it was the symptoms um recover much quicker than that Imaging recovery is delayed uh organizing pneumonia is the number one uh um presentation you see of drug induced L disease it’s because it’s so striking on a scan it’s easy to differentiate from other for example low bar consolidation or um uip ipf the op pattern makes people think more down the drug induced line than any other pattern uh nitrofur unfortunately still very commonly over subscribed by GPS for prophylactic of UTI it’s um it’s seen and shouldn’t be it’s it comes in the exam as well um and it gives an OP pattern it can give a mosaic pattern the very specific exam related questions you will get is around certain drugs that are exam favorites uh chemotherapy drugs there are so many of them so don’t bother learning around the names of the chemotherapy drugs that are imun drugs any of those you can Google when you have a patient presenting with a certain abnormality and see whether that drug is actually neot toxic is a directory International directory of drugs that are because it is mandated by drug agencies to um put your drug on that list if that drug is known to cause or has caused significant patients uh neot toxicity so that directory is free and accessible to everyone so you can look up a drug that you’ve never heard of before and the patient happens to be on it you can look it up whether that drug is actually more toxin um the common ones you will hear RAB Nitro toin um cyclophosphomide mexit methra is very uh commonly seen because methot trit happens to be a treatment for ra ra can give you I and mexit can give you I so you can have an RA patient on mexit and the question is does the patient have me exit induced lung injury and that’s a really really hard question and the thing to look for then would be acute looking changes and by acute looking changes I mean diffuse ground glass more consolidation um dirty looking abnormality that has come on within weeks uh or months even so the last scan was three months ago and the scan looked very different now they have new ground glass and the patient was put on mexit so the acute looking changes should make you think of drug induced rather than purely fibrosis um in terms of uh the pattern itself unknown drug that’s your presentation uh that’s that’s bilateral architectural Distortion ground glass standing towards consolidation can you think of any infection that would look like that can you think of ards that would look like that pulmonary edema look like that you can’t really fit into anything else and bizarre looking interesting looking patterns that are bilateral quite significant uh involving all the loes should make you think of drug induced um lung disease Methotrexate like I said before um seen quite commonly and it also recovers pretty well when you stop the drug so that’s the patient’s recovery over um weeks to months and the patient improved with no squally cyclide a chemotoxic um chemotherapy drug can give pneumonitis can give you I can give you drug induced lung disease all these terms you can use interchangeably because you’re describing an acute or Subacute abnormality you can describe uh the scan as there are bilateral changes with architectural Distortion ground glass uh areas tending towards consolidation in the right lower lobe um that should make you think of either atypical infection so whether that patient has maybe covid or any viral pneumonia that was really bad and the patient wasn’t to compromised it look like that it should make you look think of drug induced pneumonitis over time they will the lung as it’s getting put through that insult will constantly be trying to heal itself so it will start developing architectural Distortion within days so you can have acute inflammation and you can have distortion on the same scan and over time the acute inflammation if the drug is stopped will go away an architectural Distortion will take a bit longer to resolve and may never resolve completely odone um exam favorite because they want you to look at the liver uh density and notice that it’s a heart medication that can give you I uh there’s no specific pattern that you see of it for the lung the the feature that makes you cleanse the diagnosis the deliberate Innovation and believe it or not it’s pretty fairly commonly seen in real life as well cocaine is an uh is also hemotoxic the abnormalities seen are seen in acutely unwell patient those patients are presented with a heart AIA or cardia arrest or itu setting and the lungs can look abnormal the problem that happens with cocaine long is because the patient lost Consciousness and they had to partic rest because they were you know on cocaine that’s how they came to the hospital if the question is while that patient was collapsed did he aspirate yeah he might have but is that um ground glass neot toxic neosite inflammation because of cocaine either so this patient happened to be well and conscious no aspiration uh and that was um uh called as cocaine lung but cocaine lung can look like aspiration pneumonia it’s predominantly ground glass it’s predominantly Airway centered uh it’s usually bilateral there is no clear zonal distribution it’s interesting scan to look at when you see it uh just at the end I will talk about couple of rare ields just out of interest and because they happen to be exam favorites but I will pause here and see if you guys have any questions for me because we ahead of schedule we’re going to finish in 10 minutes or so if you have any questions uh feel free to put them in the chat for the thing I would say to Shima is a lot of people find it confusing and it’s completely reasonable to find it confusing uh the one thing you can look at for organized pneumonia like I said before a lot of organized pneumonia patients do get um diagnosed incorrectly as Bron pneumonia they get if they’re unwell to be enough to be admitted in the hospital they inevitably get put on antibiotics and then the patient doesn’t improve and then somebody thinks of giving them a sh of steroids or a for of steroids and they do really bad um and that’s how it the timeline happens uh fairly commonly the organizing pneumonia if you see the distinct pattern of bronos centric and clear sub plural patches of consolidation Bronco pneumonia shouldn’t really give you that Bron pneumonia can have patches that are more Central and the batches that are more peripheral there can be a bit of ground glass around it where is organizing pneumonia is more uh artistic looking is one way of explaining it um is hypers sensity pneumonitis the same as external allergic alitis yes it’s the same disease to different names is there any time Gap to diagnose op rather than effective pneumonia no no you don’t need you can have organizing pneumonia today and be diagnosed with it um there is no time frame you need to wait uh what is that entity with Central DOT sign with thick wall Central DOT sign Central dot of air with equ equ don’t really understand the question what is the entity with Central dot of air with equal don’t understand the question sorry you can explain it a bit better I may be able to answer that question from a complete new starter how do you tell the difference between atelectases and reticulation reticulation are smaller smaller lines multiple lines sitting around the plural space atelectasis is a band a thin band a long line that will cross multiple pulmonary lobules whereas reticulation is a small very small line different and they should be multiple you can’t have one little strand of reticulation it will be a diffused abnormality multiple lines sub plural thin straight can you can ground glass Haze be superimposed on honeycombing no and I would like you to be able to tell me me why that is because honeycombing is dead lung is non-existent lung so there is nothing there there is nothing to get infused with ground gloss abnormality there’s nothing to fill uh if there is a cyst that is filled with anything it will be an osmus cyst or it will be a cavity in the lung that has got an infective and air fluid level maybe that’s what you mean but honeycombing shouldn’t have anything imposed on it uh if Ma profusion where exper scans shows air trapping can be give differential of pulmonary versus smaller disease if you have expiratory scan that shows you air trapping that give you a definitive diagnosis of air trapping in a ra disease you can then kick pulmonary vascular abnormalities out of the window and give only air based disease because vascular abnormality will not give you air trapping whereas Airway abnormality will okay moving on last bit is the unusuals these are the ILS you will see um or commonly larger tertiary Care Centers and they you will see them in transplant centers you will see them exam setting very commonly uh lamb lch and there’s a new entry new K in the block called GL uh lamb is lymph angul myosis is actually a tumor that is a proliferation of the Lamb cells in the lung kidney and the lymphatics U people think it is only genetic but it is actually more sporadic than it is inherited uh there are guidelines to diagnose somebody lyang mosis there are guidelines called from the Japanese society and the American society from 2017 um because if you see features of lamb on CT you ideally want two other featur from the ones listed below so you want to see the tuberculosis complex or you want to see Ral Ang my lipoma or kylo thorx um before you can label some lamb lamb is a progressive disease it is a disease with no cure the only cure being a transplant it is not an indolent disease so when these patients um you can’t really call somebody lamb and then expect them to do okay they will inevitably progress if they were actually lamb and they will end up with end stage disease when all of the lung parenchima will get replaced with cysts um and there will be nothing to aate the lung and the transplant will be the only thing left patients usually young females uh nonsmokers uh the abnormality is diffused as in there is no zonal predominance in terms of next to plura away from plura which lobe which position it can be anywhere in the lung they are are cysts so as as an entity of a cyst they require to have a wall these walls can be thin enough that you can’t see them for example if this was the scan you had um and you were doing busy on call with at scans during the night and this was a scan you would dismiss it in less than 5 seconds and call it empa and not look back and that is how these patients do get um go undiagnosed only when it is so Advanced and prominent and bilateral and the underlying lungs happen to be very healthy that you can see the cyst wall do they get picked up um and um when they have cysts the cysts are the only abnormality in the lung so lamb patients don’t have anything else it’s a normal lung with cysts no reticulation no I nothing uh in otherwise a young healthy adult the when it’s pretty Advanced they can present with complications so the complication they will have is one of those cysts will pop they will have an nemox or can present with the kylo thorx because those lamb cells can also proliferate in the lymphatic channels in the chest so um they can present with recurrent Kyo thoris uh the other disease to think of is lch uh langran cell histiocytosis um the understanding now this has evolved over the last few years is that lch is just within the spectrum of smoking related lung disease so smoking related lung disease can have anything um from just empa to just a bit of central lular upper Zone nodules to both to diffuse bilateral ground glass so a dip sort of pattern and over time they can have um cysts so these cysts that these um smokers develop are inflammatory cysts so because of that they are IL defined like almost star speculate looking small cyst bilaterally and over time these cysts cavitate and turn into sorry these nodules cavitate and turn into cysts uh to clinch the diagnosis of LC you want followup scans and you want to be able to find the cyst that on the previous scan was a nodule so you can be sure that this is the nodule that cavitated and became a cyst and you if you see multiple nodules turning into cyst you are very confident and labeling it lch uh for exam point of view they they will be in a smoker the extreme lung bases will be preserved uh they have thin walles they can be slightly thicken but they can be um because they’re in a smoker’s lung it’s a messy looking lung they can look thickened they they are they can have a Confluence of C or they can be bizarre shapes um but rarely do they exceed more than five to 10 mm so this is what I mean by the IL defined nodules the nodules can look almost speculated but because this the speculation is Fluffy looking it doesn’t really make you think of metastatic deposits uh you know as a first instinct because some of them are more dense some of them are more fluffy and none of them are more than a centimeter they’re irregular looking speculate looking but not like the nodules you see in metastatic disease and over time these nodules cavitate and turn into cysts and that’s your uh lch uh that’s I think my last slide I will pause here and ask you guys if you have any questions before we finish call me noes coalescing to form a patchy area of consolidation it indicates benign iology it indicates granus inflammation so sosis can look like that PB can look like that rarely even um unfortunately metastatic disease can look like that but the word coalescing nodules is used for TB and sosis is reticulation same as interlobular lobular sep sing the process is the same articulation just means lines perpendicular along the plural surface but yeah it’s the same um pathology that that is that looks like that g is uh is a new group of I that that’s seen in patients who have combined immun deficiency syndrome so patients um I don’t know if you guys it was a very famous movie I forgotten the name you know kids who have very skid so severe immuno compromised immuno deficiency that almost called Bubble baby so they have to stay inside and always be protected and they have um all sorts of imun deficiencies you know I G cells and all that lymphoid lympo neutropenic all that so they this is I that is with those patients um it is very very rare it looks like a bronos Centric nodular looking basil predominant um it looks like atypical infection so these patient keep getting walked up from microbacterium infection um the airway is inflamed and that is actually anld that is GLD there’s no smoke history of smoking exclude lch no history of smoking excludes lch in male or female okay feedback link please
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