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So, um it's my absolute pleasure to introduce Doctor Steve Holmes. He is a GP and a committee member of the British Thoracic Society. He has lots of involvement with the International Primary Care Respiratory Group. He is a renowned educator and, and led to believe has over 300 publications to your name. Is that right? Steve? I'm afraid so. Yes, that is, that is, that is absolutely incredible. So, folks, it's my pleasure to hand over to Steve and to introduce him to you for tonight's talk CO PD making a good diagnosis. Absolutely. Thanks so much, Tim. Um Lovely to be here. I'm, I'm just wondering whether I can get away with uh first two years with the M MPS. But uh I don't think I'll do that. I've, I've actually been a member for a long time. So it's something different. But let's move on. This is gonna be a good clinical update about CO PD and it's primarily about making the diagnosis. I'm gonna go into the treatment at another time, but this is gonna be really about getting that diagnosis right. The sort of things we all want to do. A few of my Bits and Bobs that I'm doing at the moment. So you get an idea. It is primarily linked in with um UK practice, but I've got a reasonable amount of international experience, ongoing involvements in that as well. Um Equally so there's a few of the bits of work that I do both academically and with other providers that should be declared, including some of the pharmaceutical companies. This have not been funded whatsoever by any of the pharmaceutical companies. And I don't have any involvement with um the tobacco industry. So let's crack straight on. What I'm gonna try and do is talk about how, what it is that makes a good diagnosis. How can we identify people with suspected CO PD and what are the common catches that will catch the, the clinician who wants to do a good job out? I'm gonna talk about a couple of new areas coming through at the moment and then some of the common problems that you'll see in people with CO PD or who haven't got CO PD but have been misdiagnosed just to help us through as we, we think through that clinical aspect cos sometimes it's really straightforward, but it's not always that easy. So there's been quite a lot of guidelines and strategies about, there's a gold strategy that comes out every year that's designed for a global market. Um It gets partially updated. Um It has some of the features of a guideline but it, but it does it call itself a report and strategy because it doesn't have the balance or the literature review technique to use a guideline. And we have nice now, which is coming up for five years out of date, um last published in 2019 are very relevant to the United Kingdom. But again, there's a lot of other guidance out there and it's what we're thinking about. What is the sort of evidence I use to inform my practice. Important to think that guidelines are guidance to inform good practice, not tram lines that we must adhere to. And that's something that's been said very clearly by those very high up in, in the um guidelines system within the. So let's quickly base it on somebody who a lot of us will be able to relate to Joan. 60 years old, started smoking in the old days when she was at school. 15 isn't the youngest. I've seen people starting out quite a few people starting before that smoked for 45 years or so. Um works as a company secretary. And one of the key things about people with CO PD that Hillary Pinnock described really nicely professor up in Edinburgh was around that history of getting breathless. When you walk quickly with your family, you go out with your family or your friends and they're just that little bit faster than you. They can get round on the up a hill a little bit quicker they'll walk to a football ground more quickly than you, you seem to get there. And one of the nice things that some of my patients have said is I've developed an interest in taking photographs on a walk in the country and I look in shops, I wouldn't normally do to catch my breath again when I'm in the city. Um, because that allows me and others to stay with me without me being exposed as being a bit more breathless. So it's a subtle way. It's a way of life. It doesn't suddenly come on like chest pain from a heart attack or if you suddenly notice a lump in your breast. Similarly, quite a few of these people will get increasingly prolonged infections often during the winter. This sort of old fashioned classic Bron bronchitis. So worthwhile. Just thinking through what am I looking for and case finding people with CO PD, trying to find those people has been well established for more than 20 years. The nice guide hasn't changed for 20 years and the gold advice remains very much the same in line with this people over 35 with a history of smoking or previous smoking and exertional breathlessness, a chronic cough, certainly with regular sputum production, sometimes that frequent uh winter bronchitis. And also thinking about people who say they've got a wheeze or definitely they have had a wheeze heard by a healthcare professional. So when I first started the medicine in some parts of the country you'll occasionally hear somebody say, well, the only effective treatment for CO PD is to tell them to stop. But that's not been true for the last 25 years. There's been plenty of evidence from Cochrane reviews and national guidance around the value of um, immunization around smoking cessation. Yes, we know about that. But also about the medications we use really importantly about pulmonary rehabilitation and considerable evidence around steroids and antibiotics and their use in people who have flare ups of co PD exacerbations. So let's talk through the diagnosis. It is really straightforward. It's a good history and examination, not just a history. Most of the people certainly in the UK will have a consistent smoking history. Some may have an occupational history as well, but it's very important to exclude things like atrial fibrillation, aortic stenosis, pleural effusions and things like asthma in as part of that differential. So think about what the patients telling you persistent breathlessness rather than the variable breathness you get with asthma. Um is, is one of the key things but do listen to the chest as well in basic investigations. Certainly worthwhile doing a chest X ray within 3 to 4 months. If you haven't had one done recently, it doesn't look good if you think you've got a diagnosis of C A pe and a few weeks later, the diagnosis of cast name where the lung is made or they've got a large pleural infusion that you've missed listening in. Similarly, a full blood count has been in the v as a basic test for uh 20 plus years now to exclude anemia. And another cause of breathless, saw somebody presenting like that the other day and nice as put in body mass index that won't really alter your management. But it may help uh in terms of diagnosis, but it may help in terms of management for those patients who have cons uh considerable amount of obesity trying to help them there. The diagnosis is not made by spirometry. It is confirmed by good quality spirometry in the current climate and all all groups that sort of agree with that. So confirmed on the basis of history and examination and basic tests with supportive spirometry. In some situations, you might want to think about an alpha one antitrypsin level. That is the patient around 3545 younger people who, who are smoking and who you are thinking about making that diagnosis. Also, people who are, you're thinking about making the diagnosis, the picture fits in, but they've never smoked because it would be unusual to develop um CO PD without that smoking history in in the world. Similarly, think about high resolution CT scans, uh increasingly being used to pick up things like bronchiectasis. And very importantly, the average age of diagnosis. CO PD is 64. The average age at diagnosis of heart failure is 74 that hasn't changed in 20 years. We're still diagnosing roughly at the same time, but do consider a cardiovascular evaluation as well. So hopefully that's given you it history examination, straightforward tests, confirmed spirometry. Let's think of the common catches. Now, let's think about the younger person and the older person who's never smoked. So younger person say 35 year old diagnosed, having had a nasty infection, um, having had spirometry performed, I think the first thing that I'd be thinking in that sort of situation is, is it something else? Is the spirometry right? Is the history right? Is there something else behind this? And the three common things to think about one I mentioned now from one my anti tripp earlier, but I'll touch that again, but do think about asthma and I'll talk you through that a little bit. Um Spirometry. Basically, we do a straightforward biggest breath than you possibly can breathe out as quickly as you possibly can measure that. We repeat it with 500 mcg of salbutamol single actuations through a a space I uh pressure meter dose inhaler and look for what is termed significant reversibility. If there is no reversibility or things don't go back to normal, there can be a temptation to say, well, that must be CO PD then or I've, I've made the diagnosis. It's straightforward, but please think about the acute patient you might have seen in the emergency department who has had an acute exacerbation of asthma if you gave them five individual puffs of salbutamol, their respiratory function might improve a bit, but it probably won't go completely back to normal. And the patient who's been treated for CO PD, who is now back to really having no symptoms whatsoever or very rarely, especially if they've had an inhaled corticosteroid think was the diagnosis actually asthma, not CO PD. So first thing to think through mentioned Alpha one antitrypsin and that is worthwhile screening for gold, recommends screening every patient for this. The nice guidance is more. So looking at the younger age group. Um but for those, there is a family history, it's certainly worthwhile being very conscious of Alpha one an trypsin and getting one of our specialist colleagues involved. The other big catch, which is probably something that most of us are much more familiar with than the alpha one antitrypsin deficiency is drugs that are illegal. So people who are smoking heroin, a very high percentage of being detected in the UK with CO PD fixed ratio disease. Um cannabis increasingly we're getting the same sort of findings um linked in probably with um some of the additions to the cannabis that are going into the product that people are smoking. The same is true of crack cocaine. Um And so those unfortunate people who appear to get hooked on to some of the the the tougher controlled drugs, please think about CO PD in that group and see if you can help them because often they will benefit from our interventions. The final one is to just talk about shoe, shirt and water pipes. The Hubble bubble pipes that used to be quite trendy on the streets in London. Um You can often see in different cultures for a while they were thought to be safe, but a single pipe is worth roughly 100 to 200 cigarettes, a single pipe. And when I did a little bit of work out in, um, the Middle East, interestingly mentioning this, a few of the clinicians there were saying that explains why I'm seeing quite young women who've been smoking in the home environment cos they wouldn't normally smoke the cigarettes, the sticks. Um, when they're at home coming in with very severe CO PD at a young age. So watch out for the shisha pipes. They're not safe, right? Let's just think a little bit more now about the older people when we thought about drugs, Alpha one and asthma as potential causes. Um, in an older person, especially if they haven't smoked. Sometimes they often get their symptoms diagnosed linked to, uh, an infection occasionally that can be made because, well, it must be, mustn't wheeze and they're quite old. It must be CO PD, but that often isn't the case. And really, please make sure you do tests to establish whether it is, it is or it isn't the commonest cause of CO PD in people without a smoking history is under treated asthma. Two big studies in Europe looking at those group of patients and establishing quite a lot of factors that fit in with um under treated asthma. So nonsmoker think uh have they had asthma for a long time that we haven't been treating the two studies I'm quoting there were done retrospectively when people were admitted or referred into a specialist unit. The what's happened more recently is we've been able to do some retrospective studies looking at patients with confirmed asthma and how well they do with treatment. And that is showing very similar results to what we found earlier. So that's now that undertreated asthma will leave people more prone to see CO PD. Um study here, 8000 people with a with asthma followed up over about 20 to 30 years. Um often with uh looking at how long it takes before they develop CO PD and showing that people with optimal adherence compared to those with intermed intermediate have a much lower risk of developing CO PD people with untreated asthma at risk. That's important, especially when we're thinking about treating Children in their younger years. It's also important when we're thinking about um encouraging our our patient in their twenties, thirties, forties. So that's one group to watch out for is the is this asthma that has now got a fixed component linked in with under treatment over time. The other common area that we see as a cause of um potential CO PD but probably a misdiagnosis is in the old population where they have a ratio of less than 70%. Now go globally to make it easier. Um Gold said 70% or less in anybody of any age. That's the F EV on to F EC ratio force expiratory volume at one second. How much you blow it in one second compared to the forced vital capacity, the biggest breathing you can and how the amount of air you can blow out with that. Normally, we expect to get most of the air out quickly. That would be 80 90% as time goes on lung function deteriorates a little bit. We're not quite as fit when we're 60 as we were when we were 20. And so does that ratio change over time? And that's been shown in quite a few studies and that's why a lot of people and certainly a lot, if you look into the nice guidance with more detail and it's mentioned in gold as well, people sort of talk about the patient without symptoms with a slightly low F EV one F EC ratio. So that's in the blue shades that you can see on there being misdiagnosed with CO PD, they don't have the symptoms, they have a probably a lower limit of normal response. It's not that fixed ratio that goes throughout all of life. They don't need treatment. So one of the areas to watch out for equally. So if you remember what we talked about early on a patient who's got an F EV one F EC ratio of 71% aged 21. That's gonna, that's right on the margins. I would most people of that age group to have a significantly higher um ratio when we look to them often K. So that's hopefully given us a bit of a view of the basics. Let's just think about some of the other complications coming through in different environments. The first one to think through on that is imaging it for the last 25 years. We shouldn't make the diagnosis of co on a chest X ray or on a um CT scan alone. The evaluation of hyperinflation suggesting CO PD is one of those hazardous things that is not particularly, it's a bit like guessing. You can't be sure that it is CO PD. So please, if you see a report saying hyperinflation is suggesting CO PD that requires us to do proper spirometry. The second area with that is quite often and sometimes in some of the studies between 30 50% of people who have a high resolution CT scan undertaken depending on the reporting will have evidence of emphysema and not all of that warrants a, a proper diagnosis of CO PD for those that are interested there. And you're getting caught with the um report suggesting emphysema on a CT or a A chest X ray. This nice guidance in nice that sort of talks us through it and effectively people who do have emphysema are more prone to go on to develop CO PD in time if they are current smokers and you do the spirometry and it shows evidence that fits in with CAD and all the history and examination fits in, treat them with CO PD. The, the report is fine. That's about 25 to 30% if they're a current smoker, but their spirometry is normal. Um then certainly smoking cessation advice sensible. They are technically at more risk of lung disease including lung cancer. And at the moment, we're trying to work out when should those people be re monitored? But they s at that point, there's not a definite need to make that diagnosis, a non smoker with normal spirometry and no symptoms. Again, it's worthwhile just checking up on family histories of lung cancers. It's worthwhile thinking about passive smoking in Alpha one and it's worthwhile asking them to come back for reevaluation if symptoms start to develop. So that's quite neat from, from nice and quite useful if you're getting caught with some of these imaging coming through. And that's where some of the gray area is starting to make quite a bit of impact in the way that guidance is thinking. So back in 2016, people talked about smokers who didn't fit the criteria for CO PD on their spirometry, but appeared to have a lot of the symptoms of exacerbations, activity limitation, et cetera, et cetera. Um, a lot of those were given medications but they didn't have that firm evidence for CO PD. So that was one thing where people were saying well, should we just treat people symptomatically rather than worrying about the spirometry? And in a way, that's what has pragmatically happened. What people have just done because it seems Sentinel for quite a long time. But now what gold has started to look at and people have started to describe is what could be considered pre CO PD. Like we pre diabetes. That is somebody who doesn't have an obstructive ratio, but they have emphysema and they have respiratory symptoms. And again, that's allowing groups of people now to be researched to see, is there something there that might make a difference? The other group that's causing quite a lot of interest amongst the respiratory community at the moment is a preserved ratio, impaired spirometry. That means their F ev one F EC ratio is still normal. They're not reversing like you would expect with um asthma, but their overall efficiency of getting air out is less than 80%. So they've got some, I they've got some impaired spirometry, but it's not classic. And if you, we look at those, that's roughly about 10% of the population and we know that group does have a risk of progressing to CO PD. So for both of those groups what gold is currently recommending is that we keep a watchful eye on those. We certainly make sure they have smoking cessation and they're suggesting that it's really time that we did more research. Why is that? Well, there was a bit of research that came out two years ago that looked at the group of people who were smokers but had preserved lung function and they tried the normal treat drug treatments that we would give these patients. That's your inhaled dual bronchodilators. And they didn't find any change in symptoms. So, slightly disappointing that trial. But that, but in a way, thinking it through if somebody is smoking is certainly worthwhile, helping them to stop smoking with people more at risk. It's worthwhile thinking about um their immunization status and it's worthwhile encouraging increased activity, get the best out of the lungs they can. So there are simple things we can do for this group of patients. A few other things to put into our mind as we talk about the CO PD is not every patient who smokes or has smoked. 25 years will get CPD. In fact, many don't get it at all of those with a normal lung function, not all rapidly decline, decline at the same rate. And some people will have a fairly normal rate of decline if we can monitor them and treat them well. So we don't quite know why. Probably 80% of people who smoke don't develop co PD, they might develop cancer, they might develop heart disease or other problems. But about 20% do go on to develop CO PD if they uh have a 20 pack year smoking history. But even if they do that, the rate of decline can vary quite a lot. And that's one of the reasons why people are now starting to look at. Are there other things on top of the smoking that leave people more predisposed? And Dina Stolz from Switzerland and Alva Auguste from Barcelona and colleagues have produced a couple of really important lancet based papers. Um Talking about thinking about the genetics of CPD that actually are from one antitrypsin. The damage that can occur in early life is potentially leaving people more prone um along with recurrent infections and then that smoking vaping exposure along with environmental exposures, the biomass fuels and other things like that as part of the big system that goes along. And if we think about that as a context of everybody going through their life, what I'd like to do, first of all, on this image is look at the yellow line that is normal lungs and that's a child whose lung function increases in size as they get taller and taller until they get to about the age of 25. And then it very slowly declines over time normal person. What can happen is that if we go for the blue line, the line is somebody who perhaps wasn't as well nourished at birth, perhaps had infections during birth and never gets to the same level of lung function as the normal person. But then if they're lucky and things that are maintained after that and they get adequate nutrition and they don't get more infections, their lung function holds its own. However, if you look at that blue line and there's a, the black part can be underneath that says premature death. That is the person who's getting increased infections or is having problems because of smoking. And that's the very yo, that's the younger people we see who sadly have much worse outcomes and premature death, potentially linked to smoking or other environmental issues. So that, that's our young ones. If you go up to the yellow line, the normal group, again, people smoking, there can result in an early decline. And that again would be a typical feature of CO PD. And finally, the people who've had lots of uh a good upbringing, they've been lucky, no infections, lots of good food, they get their maximum lung function. They also probably get an added value of what's in their family history and end up with super normal lung function. And again, we would expect those to deteriorate very slowly over time. The odd thing to think about in that group is if they have been smoking or been exposed to environmental hazards, it might take quite a long time before we pick up that person as having significant lung damage from what they after that because we don't know what their lung function is to begin with. So, around into the boundaries of currently where people are starting to think about perhaps how we become more subtle and how we make that diagnosis of CO PD. So we've done the basics, we've done a little bit of what's coming in the future. What I want to do now is just go back through um some cases, I think it, some cases not six, but um um I can't remember might be sticking to six of common problems. We see, but don't always spot in people with CO PD or a label of CO PD. So the first one is John. He has an exacerbation, CO PD. He gets seven days of treatment and he says I'm not better yet. I need another course of antibiotics and steroids. Uh because I'm, I'm just not quite better yet common story in a lot of primary cares scenarios. Um Sometimes, um it's interesting how we should reflect on what's going on. So let me talk you through some things for this. Virtually all the trials of exacerbations of CO PD suggest for the 1st 48 to 72 hours. We use an increased amount of short acting be after that time, we can start an oral corticosteroid or antibiotics or both. But virtually all the research is based on antibiotics and steroids being initiated at 48 hours if somebody is dramatically poorly and their onset is a matter of hours. Probably at that point, we should be reviewing them and assessing them for things like, uh, pneumothorax, sudden onset. This is much too quick for an exacerbation. Think about things like, um, pneumonia would all that sort of feature. Um, some people who've just been tipped into heart failure might deteriorate much more rapidly than did they expect with an exacerbation of CO PD? Or as is quite commonly the case, people having transient variations, feeling panicky and feeling 1015 minutes in, I need to start my steroids now. So first thing is make sure they start at the right time if they need the steroids. Second thing to bear in mind is the median time for most people exacerbations to last is 11 to 13 days. So most people, if they think they need treatment until they feel better will be phoning you back cos most are gonna last between 11 and 13 days and quite a few will last a considerable amount of time longer. So, a useful to know that's the sort of average time it takes before people are feeling significantly better. If they're not feeling better, perhaps we need to be doing something differently. Third thing along with that is virtually all the guidance globally and in the UK is around a five day course of antibiotics. Um Antibiotics might depend on your locality in association with a five day course of prednisoLONE, 30 mg and nice gold and the cockle reviews. All fitting with that this. Now what's worthwhile remembering is if that person is not improving, it's worthwhile examining them. They need seeing because people who have exacerbations in the literature, we know if it's not an exacerbation, it can be. And I've written them down at the side, you can read those but things like poly carcino of the lung, bronchiectasis, effusions, heart failure, af none of those will get better with a second or third course of steroids and antibiotics. They need different treatments. So that needs clinical review and assessment. The patient phones up and says, um I'm just phoning you up for another course of antibiotics. I usually do, but I'm quite a lot better. Perhaps just a few more days will be fine. We need to reassure them strongly. It's ok. The five day course is fine. That's like five or seven day courses. They've been in the hospital for pneumonia. They don't need longer courses. Indeed, there's quite a lot of evidence literature that people er, sorry, the literature for the steroid use is primarily in hospital in patients, but more protracted courses where in randomized trials have worse outcomes than shorter courses for people with CO PD at hospital. And we know the implications of antibiotics and um multidrug resistance in people who have frequent courses of antibiotics. Um I don't need anybody to, to explain that to you. So do they need another course or should I evaluate them? It may be a different diagnosis. It certainly, most people of CPD don't need to five day course of antibiotics or three or four. They need one out if they're getting better reassessment. So, let's go on to case two. I'm not sure the inhalers are working. I'm always coughing. Um, I'm producing lots and lots of phlegm. It's often discolored. I might have CO PD but I've never been sure really and can have some more antibiotics. Again. Let's think that one through again, that should make us be really thinking about bronchiectasis. Most of these people have a lot of phlegm. Considerable numbers will be breathless as well. Hemoptysis equals rapid referral, suspected lung cancer, first, new presentation. But this group of patients can be quite a bit younger, they can have symptoms ongoing for years. And if you culture pneumonia, usually because they've had lots of course of antibiotics, that's another high risk feature that suggestive of bronchiectasis. What, who, who should we be suspecting it in? Well, it's common in people with CO PD. So they might coexist. It's common in people with reflux and asthma too, inflammatory bowel disease and rheumatoid arthritis. And some of the there are cystic fibrosis PCD and other areas. So again, just think if you're seeing somebody coming in, have they got any other conditions that might suggest bronchitis the diagnosis clinically in primary care? And that's where I'm primarily working is a straightforward x-ray to begin with. And then if that is normal, I will then ask for a um high resolution CT scan. Most of my c well, sorry, a third of my colleagues in the UK now have this available to them. Two thirds at the current time in primary care, don't um the government have put through the recommendations to the NHS to say this should be happening. If you're one of the two thirds that don't get access, it's worthwhile asking why you're not getting access, cos the evidence and the arguments have been made it and I suspect the answer you'll get back is there's not enough resource there. A lot of the indications are that we would use that test much more sensitively and sensibly uh rather than just doing it as a routine test on anybody who walked through the door. Um So really important to, to think about imaging or referral. If you don't have access to imaging, if we're making that diagnosis, it is worthwhile for a number of reasons. One is respiratory physio and pulmonary rehab are very useful. The second is if they, if the diagnosis of asthma or CO PD was incorrect, you can stop the inhaled cortico steroids, they don't benefit things. And thirdly, this group of patients benefits from a slightly more protracted course of antibiotics often um 10 to 14 days rather than the CO PD or pneumonia, five or pneumonia maximum. Seven. So hopefully, that gives some ideas. And anybody who's had three exacerbations in a year, I believe, and the guidance recommends should be going back under specialist review. A few quick things to remember about bronchiectasis. Um The prevalence figures vary. It's probably more common than we think. Um, did a quick survey in our practice and um only about two of the 16 were under specialist care of those with a diagnosis of CO PD of my, of bronchiectasis and my and they weren't the right two, a lot of people with bronchi cysts that we have in primary care appear to have quiet disease. They've had flare ups, they've had act, it's shown evidence of bronchi. And then for some reason, the disease has become quiet and they may not have had any problems for 4567, 1015 years. Those that are having persistent problems, warrant specialist input. Those that aren't having any problems at all aren't turning up for requiring any about antibiotics that that doesn't require any more specific intervention at the moment. Um Other quick things to think about with bronchiectasis is when you give the antibiotic 10 to 14 days, send a sputum sample preferably just before and when the sputum sample returns, if the patient is better, don't treat if the patient is not better change the antibody brand. If that is warranted. If you culture pseudomonas, specialist referral is the key tips on that. So I realized I'm going at quite a pace. Um And that's still, I can listen to this again and, and scribble down other bits you've got, but the slides are there to act as made prompt as well. Do think about if you're doing a quick review of these patients, make sure you review their other diseases properly, make sure they've had more than three exacerbations as they get back under specialist care, make sure they, that you encourage influenza pneumococcal And nowadays COVID um immunizations as recommended and think about that steroid discussion. So let's keep going on. We've got about minutes left. We'll try and get through these last three cases in that time. Um Breathing, getting worse. I'm often um having problems with my oxygen levels. I'm m measuring those at home. Are you sure this is just CO PD? And probably the key thing to think about with that is patients who are coming in who are very hypoxic, often on minimal exertion. The people who come in looking really breathless when they come into the room, put a sax machine on straight away, often 70% and then it creeps up over the next 5, 10 minutes can be young people with CO PD or lung disease. Do think about interstitial lung disease. These patient people don't all smoke. There can be a smoking history. It often takes a long time before they're diagnosed. They often have a persistent cough and breathlessness and as the disease progresses increasingly low sats and one of the classic things you can hear in men is bilateral inspiratory, like velcro under a bit of water. If you can imagine hearing that, it's a quite a fine noise that's worthwhile. Listening in for bilateral, both, both bases. I PF until proven otherwise, fairly similar, slightly rougher than expect with the fine creps you see in someone with heart failure, um clubbing of the fingers again, think lung cancer. We see that early on and don't worry about spirometry. Leave that to a special colleague. Our job with this is if we think about it, get a chest X ray and refer them in for more specialist um imaging CT scans would be one of the key things that people would go for. The problem with spirometry for suspected bronchiectasis and suspected interstitial lung disease is in both of those conditions. The spirometry can be normal or it can be restrictive or it can be obstructive. So it doesn't actually help at all when we're making that initial diagnosis. Quick thing there to say that there's a lot of variation in the CT scans. It really is a specialist um problem to be managing. There are lots of subgroups of people with interstitial lung disease. More than 203 100 described um split down into things like the rheumatoid diseases, hypersensitivity, pneumonitis in many parts of the world. Sarcoid would be very common. Um And actually part of the reason in our busy primary care setting to get one of our specialist colleagues involved is it can be due to quite a lot of jobs they've been involved in or leisure activities, hot tub lung, coffee workers, lung, all sorts of things described as potential um to, to causing this. A lot of us will have heard of Bird Fancy his Lung and Farmers Lung. Um, but it's, there are a lot of others as well. It needs a bit of um detective work to work it out from our side. Do think about occupations, cotton, coal mining, working with asbestos. So our plumbers and people like that can be more prone to an interstitial pulmonary fibrosis drugs, methotrexate, cyclophosphamide c still a bit controversial. Is it the rheumatoid that's doing that or is it the drug? But be please be aware, those sort of patients have got linked in with interstitial lung disease. Amiodarone. Definitely nitro is becoming increasingly used. And from what I'm understanding is getting increasing numbers of patients who are being detected as having interstitial lung disease quite late on because of the drug that they've been taking. It hasn't been happening before. So again, please start thinking about antibiotics and make sure you warn people if you're even thinking about initiating nitrofuran towing yourself and ask what the review mechanism is. If one of your colleagues from specialist care is doing that, connective tissue diseases. Yes, that's fine. Um A variety of those that we should be aware of the rheumatoid sl e systemic sclerosis, well associated with um interstitial lung disease infections, the atypical pneumonias and PCP in people with HIV infections. Not seeing as much of that nowadays, which is good news, tuberculosis and chlamydia can equally cause this interstitial scarring that you get as part of the the fibrotic process, other quick areas to think through on that. Um I PF is probably the commonest. It is primarily because we haven't found a cause. Um But it's worthwhile looking for causes. There are a couple of treatments available for interstitial fibrosis and some of the other variants of interstitial lung disease. Now, so there's a change in emphasis in trying to make this a more of a an area to make sure we give patients a fair chance. The prognosis often is as poor as someone with lung cancer um in in interstitial lung disease and also past history of cancer. Think about a recurrence and if they've had radiotherapy linked to breast cancer or other cancers that can cause a fibrotic process in the lung as well, what I've my summary from that is it's complex. My, some of my colleagues really love this topic. They get really complex diagnoses made working in the multidisciplinary teams and getting people onto the right treatments and with that right level of expertise. So again, I think this rightly should be moving on to our specialist colleagues. I PF common um prevalence rates are um going up from what we're diagnosed, we're picking out more people with this. Although the progress progress can vary. I think the important thing about this is there are treatments available in secondary care that have a few side effects, but they, they can be really good for our patients. Other thing to bear in mind is this is the group of patients who might end up with very high oxygen concentrations, the fibrosis going into the airways, preventing oxygen absorption, meaning they might end up on 810 L of, of oxygen a minute rather than the normal 2 L. So another one to think through, let's keep moving on those. Um My CO PD is slowly getting worse. My wife told me to come in cos I'm not sleeping very well and I'm also waking up at night. Um and my ankles are swelling sort of give away that I think. But remember CO PD doesn't usually occur on its own. This work from Stuart Mercer and colleagues showing that the people with most long term conditions have other long term conditions. CO PD is no different in that group and heart failure again is not an uncommon uh finding in patients with CO PD when you start looking for it. Don't forget other comorbidities like osteoporosis and ischemic heart disease. And remember, erectile dysfunction is often the first sign of cardiovascular disease. If we, we're looking for other things going on stiff, I'm just gonna jump in and interrupt you. Er, the slides have moved on there now. No, no problem. I think the slides were lagging behind a little bit for folks. But, um, I think they've caught up now, they've caught up. Ok. That's fine. So, cardio, very quickly, cardiovascular disease, um, can occur in the same patient. We know that we're in primary care. We see this a lot of the time. Do think about that in our patients who are, who've had COPD for a number of years. And again, just thinking through the, the basis, this is um straightforward stuff, think about a loop dy attic if they're really mean, admit otherwise, get a pro B MP, arrange an E TG and bloods and depending on your area that would move you into the echo zone. So into the last um this one I put down is more senior people. Again, walking, it touched on something I spoke about at the beginning about keeping fit. Um One of the most vital things we can do is encourage our population to keep that fitness going per rehab is fundamental for that. But a lot of patients have problems after they've been in hospital. And deconditioning often results in breathlessness without change in lung function, often without a wheeze, sometimes associated with obesity, but many of our patients become less fit and that is one of the reasons why they're more breathless. Sadly, in the UK, we are pretty unfit. This is a work from health Education England, but showing that a third aren't taking enough activity and 45% of women, um, a nice study looking at us, France, Netherlands, Germany, Australia and Finland and the UK. You can guess where we go, we're gonna come because I'm putting this up. But I think most of you wouldn't have thought would be 20% worse than the USA, most of us would have said. Well, in America they, they really aren't involved in a lot of exercise that we see as a total population. But actually, they're much better than we are. Something that we've really got to think about changing because, and this is the dramatic thing about patients with CO PD being admitted is in activity for a week. You lose about 10% 12% of muscle strength in hospital for 3 to 5 weeks. You've lost 50% of that muscle strength. Lots of evidence that if you can keep people more active in hospital, they do better. But g regaining 50% of your muscle strength if you're determined is gonna take months and many of our patients seem to give up. And one of the problems with giving up is that when you give up, you end up with a lot more uh problems of breathlessness of tiredness. You're also more like to fall because you become more frail and the whole spiral of deconditioning takes its toll. So probably as important as the medications keep our patients active. Finally, one of the great mimics of um respiratory condition. Uh is just worthwhile thinking through patients will often end up with CT scans. Um But one of the things nice B MJ article a couple of months ago, thinking about exacerbations, thinking about people who are increasingly breathless. A lot of those 25% of unexplained severe CO PD exacerbations linked to pulmonary emb eight times higher in older people than in younger people just think through is this potentially pulmonary emb? Um These are the risk factors that have been established at a er European respiratory level. Um Interestingly, they don't put down um CO PD, but they do mention respiratory failure, they don't talk, but probably what they're thinking more about is bed rest associated with being ill. Um Key things about that is if you don't think about it, it's easy to miss. Not all patients who have a pulmonary embolus will have a DVT as well. So I don't think you're, you've escaped into the quite a lot will have quite localized pleuritic chest pain and it is worthwhile getting them in to get treatment early if we detect that most of us now are familiar with the well score. Um and most of us have access to D DIMER and if we need to C TPA S, there are some trials coming out if you think about 1015 years ago when we started man PT S in the community, some trials looking at managing P emboli now in the community. Um and certainly something we should be thinking through. So I've gone through whistlestop tour of a considerable number of the common cases coming through six cases. I've also been through the pre CO PD and prism and try to run through the basics of how we make that good diagnosis. Hopefully that's been useful. Hopefully, that will have given you some clinical tips and reminders the next time you see a patient coming um into the surgery and hopefully it'll make life easy for you. Thank you very much. Indeed. Are you on min? Are you muting? I'm not sure Tim, we can't hear you unfortunately, but uh, hopefully you can hear me, Steve. Um I on my back online at all. Um, I can see a couple of the questions so I try and answer a couple of questions every two or three minutes. Let's have a, let's have a go at that. The, so in the question and answers, what I can see is, um, well, what have you got here in? What patients with high resolution CT be requested when I was doing that, I would be saying get the right diagnosis. Think about it. One of the ways with bronchiectasis is even with a normal chest x-ray, you can't exclude it. But if the symptoms are all there, good, a good sensible comment to the radiologist will normally mean they'll say actually they know what they're talking about. Increasing episodes of acute respiratory infections, phlegm most of the time discolored. Um Yeah, they're gonna need that if they have to wait six months to see a specialist and then get sent for it. We're just delaying that diagnosis. So, um that would be a sensible group to think about. I wouldn't be doing it just as a screening tool. Um And there isn't any great evidence for screening with H RCT at the moment. Um Those who, who Vape vaping is interesting. Um The evidence hasn't been accumulated yet, but there is certainly concern in the lancet documents about the potential for vaping causing damage in the long run. Um in terms of development of C APD that hasn't been established at the current time. Um And so that, so that's quite a tricky one. Next one on the list is how does undertreated asthma lead to CO PDI think people are considering that the untreated inflammatory ain inflammation if it isn't treated over time on top of recurring infections. And um the mucociliary increase that you get with that will cause small amounts of scarring and cause a fixed airways disease as time goes on. Um, for people with PRE CO PD, do we treat them as CO PD in primary care? The answer to that is we don't really know yet. Certainly it's worthwhile with PRE CO PD being really positive about support to stop smoking, really positive about pulmonary rehabilitation and exercise, really positive about um their immunizations with COVID pneumococcal and influenza vaccination. The medications are often used by our specialist colleagues and I suspect by us, but the evidence base for that isn't particularly there. Let's get the basics. So I can get that triple smoking exercise and immunizations right to begin with. We know that's cost effective, but I'm drifting into the treatment level at the moment. Um, what is the sort of follow up on monitoring needed care? And again, that, that will come into some of the, the um discussions when we talk about management, can adults viral induce? Wheeze in the same way that young Children do. Yes, adults can get AAA wheeze linked to a, an acute viral infection or an occasionally acute bacteria, but often it's a viral infection. Um, and we can hear that wheeze, I certainly, I've seen a few people who I've treated as um 5560 year old. Oh, this, this probably is gonna be CO PD, isn't it? They're wheezing. They've had a cough for a couple of weeks. They've had long smoking history, treat them and within 10 days their, their peak flow has gone back from 250 to a stunning 600 or something like that. Yes, adults can get a viral induced wheeze as well. It's not quite the same as that in Children and that's um, a separate talking itself are nicotine pouch is safe. I think most people at the moment are being concerned about any form of nicotine as it's addictive, leading people into the track of going if they can't get hold of a pouch safely, perhaps going back to vaping or making their own vapes or getting back to it. So most of my colleagues would prefer patients not to be taking any form of nicotine and certainly not the smoking. There's a damage limitation argument in people with established lung disease who smoke sticks and trying to get them on to what might be safer. And that may be the role there but not well proven at the moment. Um Quite a long question here about the, the meet and duration of exacerbation is longer than five days. Yeah, I think if the patient says they're improving most of my patients. Now we've been doing this in the, as a team in the practice for about 56 years. Most patients don't phone up, they're getting better. They phone up at saying I'm not getting better. Um, I phoned out my house who've tried to give me some more treatment, but can I be checked please? This, this isn't right. Um That five day course is fits in with virtually all the guidance. Um So yeah, it's about excluding the other differentials that should come into our mind if things are persisting. Would you do ABM P at diagnosis? I would be using that when I'm suspecting heart failure. I wouldn't do it at diagnosis of unless I was thinking out that differential and I wouldn't do it handly at the moment because there isn't a great deal of evidence for it. How can we suspect and diagnose pulmonary sarcoidosis again, that fits into some of that pul pulmonary fibrosis, interstitial lung disease, chronic cough, persisting something unusual. Get a chest X ray. It also fits into the basic diagnosis. Um Can we get a chest X ray early on before we make the diagnosis, which may show um evidence upon the sarcoid. One of the reasons for that basic investigation, how many courses of nitrofuran to would increase the risk? I don't think that's well established. I haven't seen evidence about the exact number. There seems to be people who are more susceptible than others and it seems to be not a single short course but put on to more of the um prophylactic antibiotics in patients with um persisting lower urine retract symptoms where I've heard about this most. I think probably we've come to the end of our time. Um Let's just see if I can see if anybody else is about. Excellent. My apologies. I had a little bit of a technical hitch up there, but I've been clicking through the Q and A with you there. So just to add an absolutely massive thanks to Steve and thank you for taking on some of our colleagues questions there. Everyone is getting lots of thanks, great chats, lots of nice comments coming through in the chat. There. Um which is absolutely great. A couple of takeaways I certainly had um those effects of the non cette tobacco, um choices like illicit drugs. Um, the hospital deconditioning. Wow. I currently work on wards. See so much of that. Um And some of those reasons to refer to specialist care, you know, greater than three exacerbations or the fight of pseudomonas and stuff. Very key points to take away for me. Anyway. Um Folks, I am going to very quickly just pop up one slide that I want to, I want to share with you. Um It is the QR codes to the Apple and Android Metal app. And if I can very quickly show you just on my own camera here, I was looking up the metal app uh about chronic Obstructive Pulmonary disease, a lovely little link in there in the reference section that takes you straight to the NHS patient information leaflet, which should be really helpful for people to use in their day to day practice. Uh Steve, we have reached the end of the session, really want to say another massive thank you for another great session. We look forward to hearing from you again, hopefully with, with, with another, with another element on, on this absolutely huge topic. Um And thank you very much everyone. Um We hope to see you at our upcoming events. Um We have cancer and lifestyle medicine with doctor she kissam, I'm just going to pop that into the chat and the next upcoming one after that management of commonly abnormal blood tests in primary care with, um, a familiar face, Kevin Fernando as well. So, um, we look forward to seeing you then Steve. Thank you so much once again and have a great evening, everyone. Thank you so much. Right.