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Pneumonia Basics: A Clinical Perspective

Jul 23 | 3:30 PM

Understand the basic investigation & line of management of pneumonia from one of the best pulmonologist in the country. Let's brush up all the required basics starting from types of pneumonia, clinical features, diagnosis, X-ray picture & the management protocol we need to follow.

uh today we are going to discuss about the basics and the clinical perspective of pneumonia so it's going to be really really going to the real uh understanding of what pneumonia means how it starts and how do we really interpret these different aspects of pneumonia so as clinicians i mean all of you are doctors and you are done lot of practice you have finished 10 years of practice who are some are on the verge of practice some are dreaming of practice so at some point of time each one of you will be holding a x-ray in your hand and explaining what is happening to that particular person who is sitting in front of you and this is where instead of that person with the specs i suppose each of us should imagine yourself in that position so try to understand try to first imbibe the thought that you are seeing x-ray and you are trying to interpret and tell a person what you could see from the x-ray now x-rays are something like an image a mirror image of what is happening inside the lungs so i'm showing you a couple of x-rays at the beginning so that you start actually feeling yourself that you are seeing a patient you're understanding what is happening to that patient so this is a typical x-ray of a patch i'm using a very layman term patch and where is the patch if you try to distribute the lung when you when i mean what i mean by the lungs is the area of the lungs on either side of the heart then we need to distribute into the upper zone the mid zone and the lower zone so please each and every aspect of what i am trying to tell you will be somewhere or the sometime or the other useful to you when you interpret x-rays not necessarily always of pneumonia but any lung disease now another trick i can say a trick to interpreting x-rays is always compare the right with the left so you compare the right upper zone the left upper zone the right mid zone the left mid zone the right lower zone and the left lower zone okay so in this particular x-ray if each one of you are able to appreciate then there is a patch what we call as opacity opacity means it's more white on the right lower zone as compared to the left lower zone so there is a patch which means it's a opacity what do we mean by opacity opacity implies that the air in that part of the lung is lesser and that part of the lung which had air is now actually replaced by tissues by solids and solid give rise to a opaque picture or opaque image on the x-ray so x-rays are going to be just a guidance about where is the opacity we do not know whether it's a mass we do not know whether it is tb whether it is bacteria whether it is fungus we do not know that so this is going to be very very simple understanding of what we mean when we say that we tell a patient see i feel your x-rays suggest you of a pneumonia or you read a report on the radiologist's comments saying x-ray suggest your right lower zone pneumonia so a haziness or opacity which is not shifting the structures near to that opacity is usually a consolidation or a pneumonia okay so you see a opacity but the structures which are close to the opacity are not getting pulled neither getting pushed then that opacity is most likely going to be a pneumonia or a consolidation now let's see one more x-ray now i'm going to pause here for or maybe 15 seconds for all of you to see this x-ray and if you have seen the x-ray then compare first of all the upper zones on either side the mid zones on either side and the lower zones on either side if you have done that then by now what you should have seen is that there is a opacity in the right upper zone and the mid zone as compared to the left side of the lung if you have done the that effect then i will say you are at least 30 percent of your job of understanding pneumonia is done okay so there is a opacity in the right zone and the lower zone as compared to the left side the trachea is in the center you can see a black or a blackish line right in the center that's a trachea so it is not pulled neither it is pushed the heart is in place the diaphragms are in place so that is what we can say it's a in homogeneous opacity in the right upper zone at the mid zone we can say which is not shifting the mediastinum so if i know the history then i can call it a consolidation x-rays are a part of the patient's story you have not read the entire story unless you have known the history of the patient unless you know the symptoms of the patient so this is one of the x-rays now let's see this x-ray again i pause for maybe 5 to 10 seconds try to understand try to first of all imagine that you are holding this x-ray and you are trying to interpret this x-ray the patient is waiting to hear from you the patient is anxious because by now he has read the report and the report says possibility of tb or query tuberculosis etiology so x-ray now this x-ray is showing again let's compare don't don't we don't have to start thinking of tb and malignancy and so on and so forth so what we can see is there is an opacity in the right upper zone and compared to the left upper zone there is an opacity also there is opacity in the left mid zone and the lower zone as compared to the right lower zone so there are two opacities in the right upper zone and the left lower zone all right so if you are getting this then we proceed dr ruchar is is this going okay is am i audible it's going perfect so so if you if you want to stop anytime if there is a query from anyone please tell me to stop i will stop and i will sort that out yeah yeah yeah so if you have any queries just put it in comment box i'll take it out yeah yeah so moving on now let's go directly to what actually happens when we talk of a pneumonia see there are very many things a patient will come to you with a patient patient says i feel exhausted i feel tired now all these symptoms arise because of this particular anatomical diagram in front of you now we are going to try to assimilate anatomy physiology pathology microbiology biochemistry symptomatology radiology and come to a clinical diagnosis let's see uh how much time it takes maybe if we finish it an hour or so or maybe a little extra or if people are sleepy and dr rucha tell me that's enough then we will move on to some other day sometime but till the time you people are not bored we will try to continue this so anatomically we can see there is a trachea there is a bifurcation of the bronchus then there are the lobar bronchi then the segmental bronchi the bronchioles and the alveoli now our focus today is purely going to be the bronchioles and the alveoli that is going to be our focus why our focus is going to be that because when i say today that we are talking of pneumonia the disease is in the alveoli in the smaller airways and that particular anatomical aspect of the respiratory tract is termed as parenchyma it is termed as parenchyma lung parenchyma so it is the alveolar duct alveolar sacs and you can see the saccular arrangement now to be more precise you should know this diagram this diagram is actually given in physiology books where you can see the rb is the respiratory bronchioles and they keep on dividing the rb to rb3 then the alveolar ducts and then the alveolar sac this is the parenchyma and whenever you have seen a patient whose x-ray shows a haziness or a patch or opacity the ones which we saw and you have told the patient your x-ray pneumonia you're actually trying to tell the patient dear friend your respiratory bronchioles your alveolar ducts and your alveoli are undergoing some pathological change some anatomical change all right so try to put each and everything into perspective x-ray shows opacity it's an inhomogeneous opacity no shift of the mediastinum you need to compare it with either side and what is happening actually internally the parenchyma what is the parenchyma the respiratory bronchioles the alveolar ducts cellular sac of that person are getting affected now let's be a little magnified image of the same same position same area where we can see that there is an airway that is the air goes into the alveolus that is called as ventilation okay the fact that air passes through the lumen of the trachea the bronchus the bronchi and then they reach the alveoli is the ventilation the oxygen it crosses across the alveolar basement membrane into the blood vessels into the pulmonary circulation that is called as diffusion and the oxygenated rbcs flowing through the pulmonary vessels is the perfusion so there are three things which are happening so try to imagine these things happening as we move on with today's topic which is pneumonia again i'm again emphasizing that pneumonia means alveoli you can see that the normal alveoli or sac and the filled up alveoli with secretions that is the simplest way you can understand what happens in a patient of pneumonia many times i have heard students say sir on auscultation there are vesicular breath sounds and when i ask them why do you call them vesicular there is a silence so the explanation is very simple because alveoli are sacks and sacs are vesicles so any air which is entering the alveoli causes vibration of these sacs and that sound is called as vesicular because there are the vesicles so the same change happens in this particular alveoli as you can see from the diagram that there are secretions which get collected in that particular area of the bronchi or the respiratory bronchioles the alveolar ducts and the parenchyma okay so this is what is called a pneumonia now if you read up the books any book you take hutcheson greys anything what is the pneumonia it's an acute inflammation of the lung parenchyma all right so one let's dissect each word acute so the history has to be usually from eight to ten days it may go from two to three weeks also so acute history inflammation what is inflammation it's a change which happens in that particular anatomical location because of a pathology so there is something abnormal which happens and there is inflammation and we very well know the changes which happen in inflammation the most common and the most important change which happens is lot of cytokines lot of mediators they start getting collected in the area of inflammation and they are causing more swelling okay so gradually we are now understanding what is happening in this patient to cause solidification of the lung remember in the x-ray what did we say that x-ray becomes opaque that part of the lung becomes opaque means the lung is replaced by secretions and solid tissue so let's see what exactly happens again to make it very basic a normal alveoli and the alveoli the parent gamma filled up with secretions when i say secretions it actually implies mucus and pus and the alveolar become congested okay it becomes congested too much of crowding in the alveoli which was empty so it's like a train compartment which was empty and suddenly at 8 30 a.m the office time starts and the entire compartment becomes congested with people similarly this alveolar gets congested with mucus with pus with neutrophils with bacteria with macrophages so there is a congestion happening in this alveoli and that stage of inflammation is called as stage of congestion it's it's absolutely very logical why it's called a stage of congestion now if this is the stage of congestion the one which you are seeing right now then what will this person tell you so he's going to tell you you are going to ask him he sits in front of you let's say you started your clinic today and you get the first patient in front of you okay he comes and says you're happy because the first patient has come to your clinic obviously the patient is not very happy because he is a patient and he sits in front of you ask him what do you have what problem do you have and the patient says this particular patient i am showing talking of the patient in the slide which this patient has he says okay so three things he has told you cough expectoration fever remember fever is the most important sign of inflammation the fact that he is saying secretions expectoration means the mucous glands are secreting excessive mucus now if i hear this i am going to surely start this patient on a mucolitic because he is talking of mucus and he is talking of mucus which is causing him irritation and discomfort [Music] foreign which means that his oxygen demand and supply are not going synchronized okay so the oxygen requirement is more when he exerts what we call as the work of breathing but the supply of oxygen is not what what is required is not is not as much as is required so there is a exertional breathlessness there is a cough with expectoration and there is fever this is stage of congestion x-ray will show a patch in homogeneous no shift of the mediastinum history will be patched and the alveoli actually will be something like this as you are seeing on the x-ray so we talk of the first now this is pure theory and sometimes i really don't like theory but we need to complete the the understanding based on the stages of what we call as consolidation so stage of congestion so stage of congestion is the cells now you imagine that there is a bacilli which has come into the alveoli and this alveoli which was empty contains the bacilli contains mucus plugs contains neutrophils because they are the cells of acute defense so neutrophils these neutrophils are releasing cytokines so more inflammation is happening and this alveoli which was empty is getting congested patient says book khasi breathlessness what happens next now two things happen at every juncture one first point is if the patient's immunity is improper okay see now the point comes as the host immunity that's why when you're talking of pneumonia you should always do a blood sugar of the patient even if he says diabetes even if he says mera diabetes problem sending blood test please do a blood sugar whatever the age of the patient because immunity is very important and today diabetes is the most important factor which causes immunity to come down so we are trying to put investigation also into the picture we are trying to put the symptomatology also into the picture and putting anatomy and pathology also into the picture so patient says now you're going to also tell him to do a sugar when you're planning his investigation he also says exertional breathlessness now mark my words here you ask the patient here and he says it is yellowish or greenish so it means past cells more than neutrophils more yellow the sputum more yellow the expectorate so he if he says example that means there is severe inflammation more number of neutrophils all right so mucoid less neutrophils purulent more neutrophils six days have passed he comes to you the next stage what happens at that point of time the lungs become so sensitized with the inflammation and the cytokines that the vessels in the periphery of the alveoli they become more permeable they become dilated so there is vasodilation and increased permeability so the wbc start getting entry into the alveolar area of disease along with the wbc obviously now this means the stage of inflammation has reached red hypnotization okay that is red hypothesization where rbc's also come into picture now at this point obviously the patient comes to a doctor because blood in the sputum is something which is like a shock wave runs through the patient cough for five days patient doesn't come but one one five ml spit and blood patient will run to the doctor so he comes to the doctor doctor does the x-ray each one of you imagine you are seeing this patient imagine you are advising this patient to do a x-ray and x-ray shows a patch there is a haziness you are going to investigate further and that's what we will decide because you need to know what happens next that's very very very important okay so now we have i will not go into the next stage because it is all about gray hypnotization and resolution but i will come back some time to this great appetization first let's stick around and understand what happens in red hypothesization so this is a little bit of a smaller slide because obviously histopathology and we are talking of histology not one of the most loud subjects amongst the clinicians because it's usually studied only for the exam sake and the pathologist is the one who tells us what's happening and we have read of histology more so because we want to finish the journals with the eosinophils staining and the reddish staining and all those things but please remember you will have to go through this particular diagram which talks about the stage of congestion stage of red hypothesization this is very very very important because if i just start talking about streptococcus pneumonia classic lepsi and ammonia and microplasma pneumonia trust me you will actually not remember what i spoke because all this has been told to you sometime you have read it also but we need to really understand what happens in these lungs to to know when we treat a patient with augmenting or pipracine or cephalozone or so on and so forth so stage of congestion as you can see there is only and only inflammatory cells and neutrophils stage of red hypnotization rbc's come into picture and that's why the lung appears red in color and since it is getting filled up with tissue there is solidification and this solid content or this solid texture is compared to the texture of the liver and so it's called as red hepatization now i assume everyone has understood till here stage of congestion to stage of red hypothesization dr aman raja is saying i also don't like histology so i am your i think our interests match in that respect but we need to learn this part of histology because i am trying to explain to you as much as possible so the red hypothesization stage is where you are going to intervene you are going to treat now let's come to a very simple parameter called as c reactive protein at this point only i am telling you because we are talking of inflammation and c reactive protein is a protein naturally its c reactive and protein so it is synthesized in the liver and any inflammation anywhere in the body it increases this increases okay c reactive protein increases so at this point when the patient has come to you with cough fever and hypoxia or maybe exertional breathlessness you tell him blood tests you were going to tell him a cbc i'm going to come to leukocytosis and leukopenia later but one of the markers which is doing the rounds now is about crp so crp is going to be high okay it is obviously going to be high so one of you should remember that in blood test cbc we are going to do we are going to do a c reactive protein now one more marker comes into picture which is called as the pro calcitonin this is all part of stage of congestion and red hypothesization that's why i put it here that is pro calcitonin now what is procalcitonin it is a marker it is a biomarker means whenever there is a bacterial inflammation just mark my words whenever there is a bacterial inflammation it up regulates the synthesis of procalcitonin it up regulates and procalcitonin is pushed in the blood all right so there are two inflammatory markers one was crp second is procalcitonin what is the difference crp increases in any inflammation any place there is inflammation crp will be high you talk of cardiomyocarditis rheumatoid arthritis pneumonia any place what is procalcitonin it is a marker which actually tells you more clearly about a bacterial inflammation so now it's left to you which marker you want to do i'm not going to tell you which one you should do i'm leaving at that point so these are the two important markers you decide which one to do and then according to that you will have to tell the patient suppose you have done a good marker you have found that the treatment is perfect you treated the patient okay you treated the patient and patient starts getting better now comes the problem at this point the patient is treated very well by you you talk of dr eman you talk to dr raja you talk of any person who has been in our list of attendees today and each of you have treated the doctor the patient correctly now two ways happen one is a stage of fibrosis means the macrophages they induce and fibroblasts leave their fibrous tissue which is gray in color and it is solid so it is called as stage of gray hypnotization that is the stage of fibrosis what is the stage of resolution stage of resolution is that there is no fibrous tissue left at all the treatment was given but the disease completely cleared without leaving any scarring that is the stage of resolution now why this is able to why this is so important is because you will see many patients of tb many patients of pneumonia who come to you even after six years saying sir x-ray patch it is not going at all now that is actually the stage of fibrosis or scarring whereas you will see other tb patients whose x-ray is normal and you ask did you have tb in the past and that person says yeah five years back i took treatment for tb and now i'm fine but his x-ray is normal so there is a difference in what happens beyond the stage of red hypnotization few go in the stage of fibrosis few go in the stage of resolution remember there is no disease left fibrosis is scarring and it is going to be permanent the problem is it's going to be permanent on the x-ray x-ray if the patch is not going to go away whereas in resolution the x-ray becomes normal now why this is important i'll let's go back to the patient i mean all these things which we learn you know i mean at this point of time after seeing patients and patients and patients now actually i realize when my pathology teacher used to say tell me okay read the robbins properly read the chota robbies read the bada obvious you should mug it up you should remember it my physiology teacher used to tell draw diagrams of histology do this do that it is all actually coming back when we see patients when we see x-rays and the x-rays have not cleared up so that is the stage of fibrosis or gray hepatization okay now this fibrosis or grey hypothesization is never going to go now the question which i suppose each one of you should have in your mind or if not you the patient definitely has in mind now see the answer is in the particular history taking okay what is history taking patient had a disease say on monday okay on monday and he took the treatment or he started the treatment from say friday in five days he started the treatment so the duration of onset of disease and onset of treatment was not much but you imagine a patient who is got the disease today say 23rd of june of july and he actually neglects himself takes wrong treatment doesn't go take the medicines properly and start the correct treatment after almost four weeks or three weeks so what is happening the onset of disease and the onset of the correct treatment is much wider more wider this time more chances that the person will develop fibrosis or gray hepatization all right so it's not in the doctor's hand no doctor can decide what will happen but why this is important is that if this patient which we were talking about he comes to you you treat the pneumonia please tell him that x-ray may not become completely normal if you do not tell him the patient may still feel reported treatment is completed so please this is very very important that you should be understanding while telling the patient counseling the patient okay so stage of grade hypothesization stage of resolution now this is the gross anatomy so you remember your first mbbs days or the first year medical school days where we were pushed into the anatomy hall it was formal in stinking and you were dissecting and you could see the grass appearance of the lung so this is how it looked like it was a red hypothesization i'm sure no one really paid attention that time because everyone was so much angry anxious apprehensive excited to be in an anatomical anatomy dissection room but this is how the red lung looks like it is red in color and solid as well so so yeah so that's that's definitely a very very important marker again i can say where ferritin talks about inflammation and it can tell you the prognosis okay it's a very good question very good point to be noted about ferritin so ferritin is one more blood test which we can actually do to know about sepsis severity and prognosis so crp procalcitonin and ferritin now going through the basic again we come to this patient now remember there were three symptoms which he had one was fever second was cough with expectoration and third was breathlessness on exertion okay exertional breathlessness so we are going to tackle the exertional breathlessness aspect now fever is because of pyrogens so cytokines mediators they release pyrogens pyrogenesis that particular molecule which causes genesis of pyrexia so pyrogen so the fever comes into picture inflammatory exudate neutrophils macrophage debris mucus everything is the expectoration so cough with expectoration fever and we come to hypoxia now you need to understand this particular diagram or maybe a diagram after that but try to just remember that when we breathe in you me and all of us who are sitting in our our comfort and we are breathing in oxygen and we are exhaling the amount of air which all of us are breathing right now is 21 of oxygen okay so we are breathing in oxygen which is 21 which contains air which contains 21 percent of oxygen that's why it's called as fio2 fraction of oxygen in the inspired air okay fraction of oxygen in the inspired air so we breathe in that it goes into the alveoli it disperses across the basement membrane into the capillaries and we are maintaining our saturation that's the perfect balance so there's ventilation diffusion is happening in the interstitium that is a space outside the alveoli and perfusion is happening in the blood vessels so there is a matching between the ventilation and the perfusion so v is equal to perfusion that is ventilation is equal to perfusion now perfusion is denoted by a constant q so ventilation equal to perfusion means no hypoxia all right ventilation equal to perfusion means no hypoxia what happens in consolidation what happens in pneumonia is that this alveoli contains lot of debris so the oxygen molecule is reaching into the alveoli but there is so much of secretions in the alveoli that it is unable to reach into the capillaries this causes a mismatch between the ventilation and the perfusion means ventilation slows down perfusion is happening at its normal space the pace is going on the rbcs are moving but the amount of oxygen molecule reaching into the rbcs is lesser all right so there is a mismatch between ventilation and perfusion and this leads to hypoxia so what is the cause of breathlessness in pneumonia it is hypoxia what is the mechanism of hypoxia vq mismatch so there is vq mismatch there is hypoxia the oxygen saturation the amount of hemoglobin which is saturated with oxygen reduces and the heart pumps the lesser oxygenated oxygen it goes through the aorta and it reaches the carotids and the carotid body that is the carotid chemoreceptor senses that there is less oxygen in the blood and it sends signals to the apneustic center and the pneumotaxic center and that sends different signals to the intercostal muscles and the diaphragm and the person starts breathing faster which we call as tachypnea and he becomes aware that he is actually exerting to breathe he has to do some effort to breathe which is called as subjective awareness of one's own breathing this definition is of dyspnea so dyspnea is subjective awareness of one's own breathing that happens in a patient of pneumonia which is exertional exertional because the work of breathing is more but the oxygen supply is not adequate and all this is happening because there is vq mismatch and vq mismatch is happening because the parenchyma is getting inflamed okay so we are trying to combine everything in this patient we understood why there was cough with expectoration we understood the color of the sputum also we understood about the fever also and we understood about the hypoxia also so as the patient becomes more breathless what is happening the ventilation is becoming lesser and lesser and the perfusion is remaining normal so the vq mismatch is worsening so if you are treating a patient let's assume that you all are treating a patient he's a 60 year old man who says sir i checked my saturation today and it was around 91 my fever is still continuing i'm still getting cough and i'm taking your treatment i'll come back after four days he comes back after four days you check the saturation in front of you it has become 85 so from 91 it has dropped to 85 the same patient sitting in front of you after four days of treatment why it is happening it is happening because the vq mismatch is worsening means the ventilation is reducing and the perfusion is remaining normal okay so the saturation is decreasing and the vq mismatch is worsening now let's see what is this diagram yeah so you can try to understand from this diagram something more we are going towards evolution of a pneumonia i can say try to focus on this diagram you can see right in the center normal vq okay that is normal ventilation and perfusion normal vq so the person maintains his blood oxygen levels now you see the left side there's a completely blackened alveoli where the in this case the alveoli is so much filled up with secretions and pus and bacteria and macrophages that it's almost completely there is no space in the alveoli to actually the oxygen to go inside so there is no ventilation but normal perfusion that is the extreme of a vq mismatch no ventilation normal perfusion that is called a shunt okay that is called a shunt now i will try to put it in the form of a patient because this becomes too bookish or too theoretical now this same person who had saturation had dropped to 85 say he was somewhere between the normal vq mismatch and the shunt that is the low vq you can see that there that was a patient of consolidation where the ventilation was less and the perfusion was normal now he comes back to you after 10 days of treatment and by the time he comes back to you his saturation is 78 and you tell him please get admitted you need to get admitted you tell the relatives rush him to the icu we can't have a patient with a saturation of 78 and you rush him to the hospital he's in the icu you give him oxygen but the saturation only comes to 85 it doesn't go to 98 that is because there is a shunt which is happening now means the alveoli are so flooded with secretions with fuss with macrophages that even if you are giving oxygen though the saturation is not improving this scenario is called ards acute respiratory distress syndrome ards okay so it's an extreme of the vq mismatch and it is called a shunt and the characteristic is you give oxygen but the saturation doesn't improve and why i'm putting it in this slide though we are talking of pneumonia because ards is the most dreaded complication of pneumonia okay this is a very very important aspect you should remember so a patient comes to you let's go back to the patient again he comes to you with an x-ray i think we are a little wiser now wiser by the last 40 minutes of my talk so he comes to you now he says i'm getting cough i'm getting fever i'm getting some amount of breathlessness but only when i walk it's been there since a week you say get an x-ray done you do an x-ray it shows a haziness or a patch which is inhomogeneous and you now understand means this is a consolidation you ask him do you smoke because the way we thought of diabetes we should also know smokers have a poor immune system and can progress to more disease so are you do you smoke then we ask do you have alcohol because alcohol is another factor which causes lot of aspiration it also reduces the immunity so you need to ask of alcohol then you ask him do you have any other comorbidities like a kidney disease because that again causes a problem because we are going to use antibiotics and we need to be having kidney creatinine good because many antibiotics are passing through the kidneys then we ask him do you have any liver problem so we are going to evaluate in short a cbc possibly a crp and a pro calcitonin and ferritin i'm not going into the debate of why not crp only why not only ferritin why not procalcitonin i think we can reserve one of the talks just on biomarkers of inflammation but cbc is a must we are going to do sugars that is at most important you are going to do a creatinine and a bun remember it is very very very medicine very very very important okay creatinine and bun if you find that the creatine is more than 1.5 or the bun is more than 30 it means you need to be very careful with this patient okay so cbc sugars bun creatinine very important four parameters now one more aspect i am going to add to it which is going to decide his prognosis because these diseases which cause hypoxia and cause so much of inflammation they have an impact on our metabolism even our electrolytes are very important when you are treating a patient of pneumonia if the sodium is less than 128 or i would say less than 129 it is a very very important parameter as a prognostic sign because this patient can develop fatigue he may develop drowsiness he may develop altered sensorium so i'm trying to explain to you all together because we cannot have everything as a separate talk but since you are treating a patient of pneumonia now understanding pathology you are understanding hypoxia you need to know that when you are advising blood tests there has to be a reason it's not going to be a fever panel just do a fever panel and do everything i don't know what it is for it's not that you need to know each of those parameters why you're advising hemoglobin leukocytosis and leukopenia both are important parameters to decide about the severity counts more than 12 000 counts less than three thousand are important prognostic markers okay leukopenia is not good leukocytosis is not good so both are important we are going to talk about the b1 creatinine we are going to do a liver function test we are going to do more importantly electrolytes okay so these are prognostic markers liver enzymes may not be done at the first shot unless there is a patient with a liver disease so just proceeding because i think we are 15 minutes short of 10 p.m i hope people who have had dinner are not falling asleep because this is a very important topic and i i'm sure everyone will come across pneumonia patients very often so there is this particular uh shunt normal and a dead space i am not today talking of dead space because that's a completely different entity but try to remember that vq mismatch is the reason behind hypoxia and pneumonia and the severe pneumonias actually have a rds or they go into ards now this is breaking into absolutely the microbiological aspect or we can say the physiological aspect about pneumonia in each and smallest though the slides and the headings are very small i will explain to you in simple words is that it only implies that neutrophils come into picture neutrophils macrophages fibroblasts lymphocytes and fibrin and all these release extensive number of markers especially the neutrophils which are the i i think il-6 is something which is very common now because of co with every i think forget the doctors even the patients are knowing about il-6 though half-hearted but they still know it when we uh go for rounds i suppose each of you who have worked with covet patients they themselves are one of the important factors of inflammation or markers so we should be all these things come into picture so the things which we perhaps perhaps ignored in our first mbbs and second mbbs are coming back to haunt you when you become a medical doctor okay they will haunt you in terms of the histology and the pathology and in the terms of the microbiology we have not yet touched upon that part the gram positive and the gram negative and the other things but this is what a grape hypnotization looks like okay gray hypothesization so the area which was red becomes gray it is solidified and it looks grayish in color now having explained to you about symptoms about the pathology anatomy we will come a little more towards the microbiology okay microbiology it is very important because we are going to tell the patient to do a sputum test we are going to choose our antibiotics everything depends on the microbiology so before you start reading this slide let me tell you one thing that there are two basic types of pneumonia simple way to understand is a community acquired pneumonia and a hospital acquired pneumonia we are sticking only to a pneumonia as a broad base because if we understand this we can sometimes go into detail of hospital acquired and many many things more but let's first understand that the commonest reasons why a patient develops pneumonia in the community is because of streptococcus pneumoniae then there is a organism called as moraxella catarrhalis then there is an organism called as hemophilus influenzae and there are atypical bacteria like chlamydia legionella mycoplasma so remember again we put it one together a patient comes to you with a community acquired pneumonia let's go back to the same patient he says hemophilus influenzae moraxella catarrhalis or atypical bacteria like chlamydia legionella mycoplasma six of them the most common organisms all right these three are going to be very very very common now symptoms will overlap amongst each other we really can't sit and say oh this pneumonia is only step two or this pneumonia is only moraxial or cataract it's not possible there are certain clues which can help us but no one can really see an x-ray and start commenting that this is only and only this pneumonia it would not be a good thing to do that first of all let's confirm that it's a pneumonia so now when we say that there is an alveoli with lot of secretions okay there are a lot of secretions x-rays showing a patch you put your stethoscope on that area because now you've seen the x-ray or maybe before the x-ray you try to put the stethoscope and he say he takes a breath so what happens is that the secretions in the alveolar and air goes in he takes a breath air reaches the alveoli and the parent carbine causes bubbling of the secretions so in which phase of respiration it's in the inspiratory phase of respiration so inspiratory phase of respiration causes bubbling of these secretions and inspiratory foreign sounds are called as rals ras are also the same as repetitions okay repetitions and roles are the same there is there is no such specific explanation or description for people who say crackles and different different versions of that but for all practical purposes remember repetitions and ras all right so secretions air goes in bubbling of secretions which face inspiration inspiratory foreign sounds are called as repetitions so in pneumonia what will be here repetitions all right now imagine this i don't know how much see the problem with this kind of talks i'm not saying a problem shortcoming is that we can't have an eye to eye contact you know otherwise i would have actually gone through each and every frame and i would have asked a question are you understanding what do you feel it is but any which ways thanks to this app at least we are able to meet together in some way or the other so secretions in the alveoli air going into the alveoli bubbling of the secretions and we hear the sound it's like you have a bottle of water and there is a straw and you blow in the straw and we hear the gurgling sounds so those are similar to repetitions all right so that's how it is that repetitions are heard due to secretions at the same time if if at all now everyone should understand that air is a bad conductor of sound you know we talk i mean i was a very poor student of physics and maths but somehow i remember this this only and only this statement of physics that air is a bad conductor of sound so this helped me in understanding pneumonia so imagine an alveoli which is normal and containing air and imagine an area of consolidation which is solidified air is a bad conductor of sound solid is a good conductor of sound so when you auscultate over a normal lung and you tell the person say one two three you hear one two three when you auscultate over this lung which is having consolidation and he says the same words one two three we hear it more louder okay that is called as vocal resonance so the louder sounds are called as vocal resonance happens due to solidification of the lungs it means that the lungs is changing and the air is becoming less and it is replaced by tissues so i hope you are getting this about the atypical bacteria now why they are called atypical bacteria i need to spend at least a minute on this that is chlamydia mycoplasma legionella uh when we talk about bacteria and i explained to you that streptococcus pneumonia is one of the commonest bacillus it's a gram positive cocaine streptococcus okay it's a gram positive bacteria whereas hemophilia is influenzae and moroxellar gram negative bacilli what is gram positive and gram negative i'm trying to just take you into that because i'm sure you have not brushed up your you know microbiology since ages you've been busy with other patients and asthma copd tb and kovid and so many things but bacilli have a peptidoglycan wall okay it's a wall which is made of peptidoglycan peptides and glycan it's a thick wall if the wall is thick and you put the color which is the the violet crystal violet color which is the shading or the stain which is there in the gram stain then the peptidoglycan which is thick it retains the violet color okay they are called as gram positive organisms in some bacilli the peptidoglycan wall is very very thin so you put the the stay in the violet it doesn't pick up and then you put the saffron in stain but it picks up so these become gram negative bacilli so gram positive bacilli are those with a thick peptidoglycan layer and gram negative is the one with the thin peptidoglycan layer okay but they have the coloration which can differentiate between gram positive and gram negative in some bacilli there is no peptidoglycan layer so they can't be stained and those are the atypical bacilli okay they are the atypical bacilli so they can be stained so that they are neither gram positive they are not negative that's why they are called as atypical bacilli legionella mycoplasma and chlamydia so that is the difference in their microbiology but not only that there is also a difference in their clinical presentation so i'll give you two examples to make it a little simple one is uh doctor sushila is seeing a patient okay i'm taking on him because i can see she has written something on the chat box but dr sushila is seeing a patient and the patient comes and says madam i am feeling a lot of i'm feeling a lot of discomfort my right side chest is congested i'm feeling lot of cough expectoration difficulty in breathing and high fever if you were touches one not two one not three since last two three days that's the problem and you and she does an x-ray which shows a localized patch localized in homogeneous opacity which is a consolidation now she treats this patient fine some other patient comes to her that patient says adam i am getting cough but it is more or less dry i mean since five six days i am getting a cough not getting much of expectoration but my body exceeds your body my i can't bear the body it means i have to take protein even my joints are aching body is aching i had some loose motions also two three days back getting a track off fever is there headache is there now madame takes x-ray and x-ray shows look different different patches a little haziness on the right upper side little haziness on the left middle side so both the patients have a pneumonia okay both of them have pneumonia but look at the difference systemic symptoms are more in atypical pneumonia okay systemic symptoms lose motions headache body ache joint pains weakness diarrheas dry cough think in terms of atypical pneumonia cough with yellow sputum high grade fever localized patch on an x-ray think of a gram positive or a gram negative pneumonia of course we are going to investigate and do so further and then come to our diagnosis but this is just try to explain why we have to choose different antibiotics so again i'm perhaps offshooting from things but doctor sushila is treating both of them one patient had high fever cough with sputum x-ray was localized patch so i would like to use an antibiotic which covers gram positive and the gram negative bacilli because it could be streptococcus it could be h influence it could be more acceleralis so i may perhaps you use a combination of amoxicillin with clavillionic acid the second patient dry cough body ache those motions weakness headache i am suspecting atypical bacteria my drug of choice would be a macrolide like clarithromycin or azithromycin so your line of treatment would change if you think about in terms of the microbiological aspect okay so before we proceed i am just trying to put it all in one go is that patient comes with a short history cough fever weakness and breathlessness on exertion you have understood why the patient gets caught with expectoration you understood about the fever and you understood about the vq mismatch if the pneumonia progresses it's going to be leading to a rds which is actually a shunt and we have also discussed about the dyspnea now just next 5 10 minutes we will discuss because i know our listening span is maybe different but our understanding span is not more than 60 to 80 minutes so now this x-ray i'm sure everyone has understood because there's an arrow pointing towards it there is now no nothing to be really you know yeah i think why one question is very important dr dinesh kumar is asking what is the atypical viral viral pneumonia treatment so we will discuss the treatment aspects but in viruses there is unfortunately no treatment you know there are many viruses and millions of viruses but we really don't have a very good treatment for each and every virus the way we have for bacteria but maybe one of the times we will discuss the treatment aspect of each different type of pneumonia at this moment let's try to finish the understanding of the perspective so this is a patch that's inhomogeneous opacity right upper zone we can see it he comes with symptoms of cough fever breathlessness and so on and so forth and we would uh treat it with antibiotics so uh dr samya acyclovir for viral pneumonias we are talking of respiratory viral pneumonias usually acyclovir is a drug of choice for herpes so we really don't start off with an acyclophile the commonest respiratory virus is a respiratory syncytial virus and we really don't treat it with acyclovir but as i said you know we will discuss it sometime because it's a very interesting topic of treatment of pneumonias as well now you can see this style put back the earlier x-rays try to focus on this x-ray the one with the arrow try to understand the opacity when i mean what i mean by saying try to understand the opacity read the x-ray knowing the anatomy pathology physiology which is happening in this person's lung parenchyma i want each of you to imagine it that there are neutrophils coming there there are fibroblasts coming there there are cytokines being released and this area is getting inflamed now this gentleman comes back to you after five days of treatment let's see what happens what do you see in this x-ray in this x-ray for those who have not been able to appreciate i can say that the density has become more opaque it has become more opaque means more white compared to the earlier x-ray right it's become more white compared to earlier x-ray so this is how the consolidation progresses this is a low bar pneumonia so anatomically we can say low bar pneumonia when only one lobe is affected multi-lobar pneumonia or third is the bronchon ammonia where there is diffuse infiltrates throughout the lungs all right but this is a low bar pneumonia now the pneumonia further progresses and it affects both the sides of the lungs bilaterally and here the patient presents with severe hypoxia patient is admitted put on oxygen not improving and we call it ards so this is the progression of a pneumonia happening because of one either the virulence of the organism is very high means they are very strong they are resistant so we are using an antibiotic but the bacteria or the organisms are resistant second host immunity is very poor that's why i said when you investigate for blood tests please do do see do a cbc why cbc because hemoglobin hemoglobin is very very important aspect you are treating an ammonia like this and is hemoglobin is six you are treating it correctly with good antibiotics but if the oxygen carrying capacity of that patient's blood is not correct is not good then he is going to develop problems so you need to interpret the hemoglobin you need to interpret the wbc counts even for that matter platelet counts because any kind of severe infection suppresses the bone marrow okay and that may lead to thrombocytopenia so this is one more complication pneumonia more dense ards now what is happening in this x-ray try to see the x-ray properly is that you can see a dr rucha how much time more should we take 15 minutes uh yeah so we can go up to 10 minutes and maybe after that we can do a second pass yeah i think so because because yeah so i'll just finish off these five x-rays so this x-ray shows a white patch and in the white patch you can see a blackish area try to localize that there is a small black area within the white patch now this is how the pneumonia progresses this progresses means there is gradually a breakdown when there are lactic enzymes lies the alveolar walls the sac walls the alveolar ducts are broken down by the chemicals which are released by these bacteria and multiple alveoli coalesce together to form a large area containing air which is actually called a cavity so there is slowly a cavity formation i am just going to the next x-ray i think this will be a better quick x-ray to show you can see that there is a roundish area which is a white line which is rounded inside that there is a black area which is the cavity so this is the progression of a pneumonia so we started from a pneumonia continued to progress the disease this happened because he did not go into the stage of fibrosis and resolution it in fact became a complication of a pneumonia so cavity formation is a complication of an ammonia the way ards is a complication of a pneumonia all right so this patient who has a cavitation is actually a pneumonia either untreated wrongly treated resistant bacilli host immunity poor or some comorbidity so one of them is leading the patient to develop an ammonia to break down and form a cavity now i am coming back to this x-ray now what is this x-ray showing you can see in the right lower zone there is opacity and there is a obliteration of the right costophonic angle okay obliteration of the right costophonic angle so what's happening in this patient so you will get such patient that's why i'm trying to tell you this that there's an x-ray which shows a pneumonia this pneumonia starts progressing and it touches the periphery means this is the pleura so it touches the periphery that is a visceral pleura the visceral plural starts rubbing against the parietal pura and the fluid starts getting collected into the pleural cavity so there is inflammation of the pleura and pleural effusion which is called as as dr talath has said syn pneumonic effusion so there is a paraneumonic or a syn pneumonic effusion so this is one more complication of an ammonia so we have gradually now entered into the realm of complications of pneumonia so one was a rds second was cavitation third is a sin mnemonic diffusion so there is a pneumonia and it has progress now this is the patient who might also say the fourth symptom of respiratory disease chest pain so till there was pneumonia there was no chest pain because lungs are painless lungs don't cause pain but the moment the parietal pleura is touched or inflamed patient says now this is meaning that his pleura is also getting entangled into the process and he's developing pleura c or pluritis and he's going to develop a sin pneumonic neural effusion so that is the evolution or progression or complication of a pneumonia now so we have talked about ards cinematic effusion cavitation now in this cavity you can actually see if anyone can guess let's see i'll wait for at least five seconds if anyone can guess what's there in this x-ray if you may not answer but at least mentally you can guess i can reach your minds as well through this app so there is a cavity definitely yes so dr nith is correct so there is a cavitation as but dr manmohan rathor is saying we can see a air fluid level in the cavity there is a horizontal air fluid level in the cavity means that there is a lung abscess okay so cavitation was there no doubt but now that cavity is getting filled up with pus and that pus is settling down and forming a layer which is called as a air fluid level so many of you have got it that yes there is a cavity but please remember that there is a difference in an empty cavity maybe you can see it here this cavity and then this particular cavity having a layer of fluid at the base so that at the base of the cavity that's the air fluid level now this patient so so we have come towards the end of understanding the complications of uh pneumonia and now we come to the sequelae of an ammonia okay secretly sequelae means the permanent outcome of an ammonia complications are treatable you can treat a cavity you can treat a lung abscess but this is a sequel no doctor abhishek this is not fibrosis there is a difference to it so this is the sequel now what happens is remember let's not go into x-ray i'm going to go back the x-ray because you're going to start thinking about fibrosis now what happens you try to understand the anatomy go back to the anatomy the good old days of grey's anatomy book which you first bought in your medical school go back to that okay so when you are seeing a patient with a consolidation multiple areas being affected fibrous tissue being deposited peri bronchial fibrosis also happens peri-bronchial means along the walls there is fibrous tissue and it pulls the bronchi and distorts the bronchi so there is distortion of the bronchi and at places they get dilated they get pulled dilated distorted torches so it becomes like a paper which is crumpled and forms multiple small small small small cysts not cavities but multiple small cysts now this is a sequelae of a pneumonia and this equally takes almost months to years to happen okay months to years and this equally is called as bronchiectasis okay there are multiple cysts we can see throughout the right lung the trachea is pulled to the right side the heart is pulled to the right side the diaphragm is pulled and there are multiple inhomogeneous opacity or cysts so these are this is bronchiactasis remember we will for some time discuss bronchitis but bronchiactasis happens after a fulminant infection of the lung parenchyma and that's the reason why you see bronchitis in patients with tb many of our patients of tb have post tuberculosis bronchitis many patients of pneumonia land up with wrong cactuses so tractional bronchitis as dr bina says cystic bronchitis so all these are anatomical description of the bronchial distortion dilatation and destruction but this is permanent so this person is never going to be asymptomatic this is a sequel a doctor zombie not a complication complications are treatable bronchitis is permanent so it's an outcome it's a sequel it's a end point or which cannot be reversed once of symmetry arterial blood gas leukocyte count blood urea electrolytes c reactive protein csf analysis is not done in everyone of course but we are going to think about that because bacterial meningitis is a very very important complication of streptococcal pneumonia especially in the pediatric age so we need to think of patients who are having altered sensorium persistent fever persistent vomiting don't forget to do a csf i mean you may focus so much on the lungs that you are treating only a pneumonia but the problem could be that it has progressed and it has led to bacterial meningitis also so i think with that i've tried to put you know all the aspects right from basic to understanding and diagnosing pneumonia one important aspect which is left yet is of course the management part there are many things to discuss about it but anyways we will meet sometime again so dr rucha over to you thank you thank you for giving me an opportunity and i'm sure i'm happy that people were actively involved in this

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