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Pneumonia Basics: A Clinical Perspective (Part - 2)

Aug 06 | 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.

[Music] hi everyone uh i'm dr rucha i welcome you all to second part of uh clinical prospective basics of pneumonia so it has kindly agreed us agreed to this and he is taking our second session on this uh the very first session we did last week last week and the recording is available uh you can go and watch that in the replay section uh so i'll not take much time today i have just few instructions and i'll introduce uh sir to those who have uh newly joined for this particular session sar is a renowned pulmonologist uh in india and he's currently practicing at a nanopt super specialty hospital and uh today he will be taking the part two so uh good evening everyone and thanks dr rucha and netflix for giving me this opportunity to again connect with all of the doctors whom we did last time also so uh for those who have attended and for those who have not attended also last time we are going to be today discussing a little more advanced about management of pneumonia because the last time we had discussed about the basics of pneumonia and the absolute outline about what exactly we mean by pneumonia and what is uh the different pathological stages of pneumonia right so we started with this slide i'm going to take five minutes just to go through each each of them or maybe quickly just go through all the earlier times presentation so this was the first slide which i had shown and i wanted each of you to remember and to imagine that you are the doctor who is seeing this x-ray so that you get the seriousness of the matter the interest of the matter as to you are actually going to see at some point of time or you have seen at some point of time a patient who has shown you the x-ray and the x-rays suggest you of a pneumonia so all of you who are today with me have to now go into that particular frame where you are going to be the doctor who is treating this patient who had a patch of pneumonia and this is how we had started so the x-ray which showed haziness which is inhomogeneous and obesity is there no shift of the mediastinum and so on and so forth this is how we had gone through uh we had talked about pneumonia being involvement of the lung parenchyma which is the alveoli the alveolar sac alveolar ducts and of course the smaller airways then we had discussed about the respiratory bronchioles and also related to the microscopic structure about what we mean by pneumonia now again i'm not going to wait at this because we have gone through this for almost one and a half hours last time even discussed in detail about the stage of congestion and red hypothesization what is gray hypothesization what is fibrosis what is resolution okay so try to remember these names try to remember these terminologies because as we go further and further and into delve into what exactly do we do when we see a patient of pneumonia you will come back to these particular slides every time because to be a good clinician you need to be a good anatomy pathology physiology doctor so you have to remember these different places different sites different changes okay so though i i understand dr uh just saying who like dislikes histology and so on and so forth but remember that we are supposed to be knowing this and we are also supposed to be knowing the gross anatomy about how the lung looks like subsequent to that we are discussed about this particular diagram which was very very crucial in our understanding about what is vq mismatch the ventilation perfusion mismatch so for those who have not been able to uh you know go through the basic of pneumonia please go to the recorded version sometime because as we go on further talking about sepsis ards you will have to refer to this particular diagram where the ventilation and the perfusion are equal that's a normal vq and at one extreme you can see a black circle which is the shunt and that's where our patient of ards is right so there's a normal vq as you can see in the center on the left you can see a black circle which is the shunt where there the alveolar filled up with inflammatory fluid inflammatory secretions neutrophils and in between that there is a vq mismatch so that's where the patient of pneumonia and the shunt will be a patient of ards so this also we had discussed we had talked about the inflammatory changes which happened and subsequently we had talked about the complications of pneumonia okay so try to remember these these are different different presentations which each of you you will see patients remember now when a patient comes to you he is not going to come always and always with a pneumonia he may come to you with a pneumonia and its complication or he may come to you with a pneumonia and it's equally even those we have discussed as to what are complications and what are sequelae so these are the different complications where the pressure presents with an ardha's bilateral diffuse shadows there are patients who present with effusion which we termed as a sin pneumonic effusion so that's the right cp angle blunted which is a complication of pneumonia we discussed what is the difference in the symptom of pneumonia and pleurisy there is a marginal difference in the symptoms which is the pleuritic chest pain a cavity formation lung abscess formation bronchiectasis which is the sequelae and then we had stopped at this particular slide which talked about the investigations in a patient of pneumonia now this is just to give you a broad outline about what are we going to do next how do we interpret the next and today we are going to discuss a few things about the inflammatory markers we are going to also talk talk a little bit about the il-6 and the crp and different small bits of knowledge which we read at some point of time they are called as phagocytosis opsonization apoptosis okay though they may sound how do i clinically feel it relevant please remember that when you are treating pneumonia you are treating a diagnosis of pneumonia but what you are actually treating is the pathological change you are actually treating is the molecular change what you are actually treating is the inflammatory markers so we are going to boil down to the simplest bit of the pneumonia change and pneumonia pathogenesis because you are going to treat it and you are going to treat it with antibiotics so we had also discussed about the gram-positive gram negative bacteria and this is a classical x-ray of a inhomogeneous opacity in the right upper zone and here the arrow is pointing out to a patch or a to a haziness which is called a pneumonia all right so let's take the story from here so this patient comes to you he says you ask since how many days he says since about five to six days so it's a short history he's got cough there is expectoration last time we have discussed why the expectoration is yellowish in color why there is purulence and we very well know it is because of the neutrophils now remember these small small words which are very important neutrophils bacterial inflammation as you go through the next few slides you will realize how do we differentiate between atypical bacteria the gram-positive bacteria and the viral pneumonia so yes we are going to talk about crp also it is crp that is the c reactive protein and it is a purer form there are different metabolites or what we call as the chemical bits of crp but we need to do a complete crp that is c reactive protein so dr sarthak the answer is that we need to do a c reactive protein now we will go to the crp in the next few slides but before that before investigating what are we going to do we are going to examine the patient right we are going to examine the patient now in today's era somewhere we are probably neglecting clinical examination because we have got access to x-rays we have got access to doing a ct scan but we cannot forget the bedside findings the clinical findings so i will just try to explain to you for especially for the students or the interns or those who are pg students who are yet to appear for an exam is that when you auscultate a patient we hear breath sounds and those breath sounds are called as vestibular breath sound they are the normal breath sounds now why are they called vesicular breath sounds is because the sac the alveolar sacs are vesicles and so the sound which is generated when the oxygen when the air enters this alveoli enters these vesicles and they vibrate they inflate deflate this particular movements makes a sound which is a sound generated from air entering the vesicles that's why it's called as a vesicular breath sound which means that if these vesicles what are we talking the vesicles the parenchyma is not normal it is anatomically the structure is distorted okay mark the words structural distortion of the vesicles gives rise to an abnormal sound and that sound is called a bronchial breath sound so which diseases cause distortion is all the diseases which we just now discussed it would be pneumonia there is distortion there is inflammation there is cavitation there is distortion lung abscess there is distortion bronchitis is there is distortion so there is an abnormal structural change which happens in these lungs and that's why the sounds are different and they are called as bronchial breath sounds okay so first please remember vesicular breath sound because of vesicles that's normal and bronchial because the structure is being distorted the vesicles are not no more vesicles they are either fused together stuck together or distorted or destroyed so cavity bronchitis lung abscess consolidation all will present with the abnormal sound which is not vesicular and it is called as a bronchial breath sound the next factor which each one of us should know that air is a good conductor of sound right so when a person b auscultates over a normal lung and we hear a sound we tell the person to say one two three we can hear the syllables one two three but now imagine that this particular vesicle this particular alveoli filled with lot of pus lot of secretions that means the air is replaced by secretions it is solidifying and solid is a good conductor of sound so now the breath sounds or the syllables become more louder okay they become more louder so we call it as there is a increase in the resonance of these words which are said which are talked which are vocal so it is called as vocal resonance so vocal resonance is increased in patients in whom the parenchyma is solidifying all right so vesicular breath sounds one bronchial is another vesicular is normal now just to make a few things clear remember the characteristic of the bronchial breath sound is that air goes into the parenchyma now there is lot of secretions in the parenchyma so it has to actually go through the secretions then the exhalation starts which means that there is a gap between the inspiration and expiration so there is a gap in the inspiration and expiration which is also heard when we auscultate the trachea there is a gap in inspiration and expiration so the sounds are similar over the trachea and a distorted vesicle the characteristics of the sound are similar but but for all practical purposes we never auscultate over the trachea unless we want to hear a tracheal narrowing or a sound because of the tracheal obstruction right so we usually put a stethoscope on the chest wall and try to understand whether it is vesicle or it is vesicular or it is bronchial there is a difficulty at times because we are not used to auscultating very much so there may be a difficulty in understanding whether the sounds are vesicular or bronchial but remember that whenever there is a bronchial breath sound because of the solidification the vocal resonance will be increased okay the vocal resonance will be loud so increase in the vocal resonance means that there is solidification of the parenchyma means that the sounds over there are not vesicular and bronchial so it is like equal to equal to equal to so bronchial breath sounds there would be increased vocal resonance the reasons are the same because there is alteration of the anatomy and there is replacement of air with secretions with solid material so there is bronchial breath sound and secretions one more sign we had explained last time that whenever there are secretions in the vesicles and air enters the vesicles it will cause bubbling of these secretions which is called as an inspiratory foreign sound so this inspiratory foreign sound is called as repetition or rals now putting it all together we will go back to this x-ray there is a haziness in the right upper zone or an opacity when we say opacity it means the air is getting replaced by tissue that's why it looks more white that's the principle on x-ray lungs look black solid or liquid will look white so if there is opacity and suppose you are auscultating on this exactly over this opacity on the right side of the chest wall what will you hear one you will hear bronchial breath sounds now you know why you are calling them bronchial because the characteristic is different from vesicular all right so they have bronchial you know why they are bronchial bronchial because the structure is altered the anatomy is altered so it is no more vesicles it is altered secondly when you tell him to say eight nothing or you tell him to say one two three you will hear the sounds more loudly you hear the syllables more loudly that means vocal resonance is increased third when he takes a breath you will hear inspiratory foreign sounds which are indicative of secretions so there are repetitions so there are three findings which come up in a consolidation one bronchial breath sound second increased vocal resonance and third is repetitions please try to remember these or understand this i don't say you should remember you should understand why it happens if i ask you a question at this moment of time for those who have understood what we just now discussed that this patient develops a lung abscess on the same area on the right upper zone or the upper part of the lung or there is a cyst or a cavity the pneumonia cavitates then what will you be able to hear try to think about it for i'll wait for five seconds there is a cavitation in the same area where the arrow is pointing you have put the stethoscope and you are trying to listen to the sounds so first is the sounds will not be vesicular that is the first finding there will be bronchial breath sounds second you tell him to say one two three you will hear loud sounds so vocal resonance will be increased third you will hear secretions so there will be repetitions all right so three findings came up now let's assume one more case this patient had a pneumonia say five years ago he's come to you now with right sided bronchiactasis we last time discussed one of the x-rays which showed bronchiactasis so he has now multiple cis multiple honeycombing areas in the same part of the lung now you imagine that try to listen to what the lungs are trying to tell you don't think that these are just sounds which i have read in a book called as vakil golwala or pj mehta or hutchinson think that these lungs are trying to explain to you what is happening to them because you can't see them so they are making sounds so that you can understand what's happening to them so there's a right upper zone bronchiac testes or honeycombing you have put the stethoscope and you're trying to listen now you hear that these are not vesicular sounds they are something different okay let's assume we never know what sounds there but they are not dif they are different from the normal vesicular sounds so you tell him on the same place you keep the stethoscope and you say tell him one two three bully and he says that and you compare it with the other side and you find that they are much louder why they are loud because now the air is getting replaced by tissue this tissue there is a lot of fibrous tissue there is a lot of secretions thick secretions so there would be lot of fibrous tissue there and we can hear them more loudly because the solid conducts sound better so the vocal resonance is increased and thirdly we also hear secretions because the bronchitic cysts are filled up with lot of secretions so you can hear repetitions all right so these are things which are to be remembered to be understood now it is purely your examination of patients which will make you remember these things okay it's just repeatedly examining them listening the audio clips by putting a youtube video you will hear some sounds but you will have to see listen on patience you will have to compare it with the other side it just listening to one sound will not be enough but i am trying to tell you the reason why you hear these particular findings vesicular sounds bronchial breath sounds repetitions and increased vocal resonance all right so there are three these fine three findings we are there sometime we will take a probably some maybe whenever we can actually have a clinical examination uh you know session because it has in inspection palpation percussion and auscultation i'll just tell tell you a little bit of percussion because someone had put up a question can would there be an important finding on percussion now when you percuss over the chest wall say that you are percussing over the chest wall you hear sounds those sounds are because of the sounds because of the lung tissue there is ribcage there is pectoral muscles there are lymphatics there are capillaries so you are percussing over tissue as well as air so you are hearing a sound which is called as resonant but that does not mean it is only air it is also the skin the muscle the rib cage everything so you are hearing sounds through that and you are calling them as resonant now what will happen if you are percussing over this area on the x-ray means this right upper zone the disease is there and you are percussing over that area will it be the same like a resonant note it will be different why it will be different because now the air is becoming less and the tissue is increasing okay it is getting replaced the alveolar as we had discussed in the earlier slides that there is a lot of tissue getting deposited the inflammatory tissue so the sound which is generated or which is heard on percussion is not resonant but it is also not completely solid okay remember now try to understand this because dr akshay is saying it will be a dull note on percussion dr akshi you yourself will tell me the answer uh so imagine that this part of the lung the right upper part of the lung it is containing 70 tissue and 30 air now you can see some areas of black white some black white so you are percussing over a area which has 70 percent issue 30 air if i give you an example that's the same area which is pointed by the right arrow has a mass completely solid mass okay solid mass no air only solid you percuss over solid you will hear a dull note but is this a solid mass it is not a solid mass it is still having air but the tissue is much more but air is still there it is not completely solid so the note over this particular part will be called a impaired note it is called a impaired note in this particular x-ray i am saying now for those who have answered it could be a dull note let me tell you as the consolidation becomes more and more dense okay we had discussed in fact we had seen an x-ray earlier i would like to try to show you that x-ray if we can it's perhaps going a little bit too behind but i have to show you that x-ray now you see this particular is what you are talk we are talking about you can see it is patchy inhomogeneous you will get a impaired note on this but you see this x-ray you can see that it is more white more dense okay it is more dense means the component of air is still going down and solid is increasing so as the solid increases you will find that the impaired node now actually becomes a dull note okay it becomes a dull note so we are getting a dull note now at this point of time so in short every consolidation need not have always an always impaired node as the consolidation becomes dense it will become a dull node okay it will become a dull node so i hope we have been at least able to go through a few aspects about examination one is about the vesicular to bronchial breath sounds then about vocal resonance about repetitions and about a impaired note or a dull note okay so these are a few things which we can actually try to understand when we do a clinical examination now x-ray is with you you know the history of the patient you have examined also and you are now certain that there is a parenchymal disease going on in the lungs so we turn to investigations like a blood test so now let's go a little bit deeper into the blood test so i think last time again we had a little little bit we had discussed about what is c reactive protein about a pro calcitonin about wbc counts okay so there are a few things like this which are very simple and very applicable so bacterial pneumonia viral pneumonia and atypical pneumonia why i have taken these three reasons is because we have we know that when a patient comes to us from a community we call it a community acquired pneumonia and the common reason is streptococcus pneumonia moraxella catarrhalis or it can be atypical bacteria or viral pneumonia so there are different different uh biomarkers which are present one is the c reactive protein the procalcitonin and the wbc count now please go through each of these properly because crp is something which is very commonly done and i think with every respiratory infection it is done so crp increases in bacterial pneumonia is no doubt okay so if crp is significantly high suspect bacterial pneumonia but if the patient is having fever and cough x-rays showing pneumonia but the crp is on the lesser side try to think first in terms of a viral pneumonia of course in feminine infections it will increase but it's a it's not a very specific biomarker this is just a small small tip towards how to interpret this amongst all this a very important parameter is pro calcitonin and if you see this then procalcitonin is something which increases in terms of a bacterial pneumonia okay it increases in bacterial pneumonia so if you suspect a bacterial pneumonia duo pro calcitonin procalcitonin is a is a is a protein or it's a it's a molecule which is generated in inflammatory tissues and it can be induced actually by interleukins okay we'll come to that how each one of his entangled we will see so pro calcitonin wbc count and crp all these are very very very important markers try to remember this we'll try to take up the question on on on the next few slides which are going to come because the next is one another parameter which was asked last time about ferritin okay because this is one more marker which is done as a blood test we have to take ferritin and take crp and try to put them into a box which is something like this it's only a guiding parameter now if a patient comes to you and he says i am having cough and fever always i try to tell each one of you don't think this as a slide this is just for putting it on this on your presentation so that you know it try to think that you are treating this patient patients are today well read they have google at their feet and they can easily google it out and ask you can i do a ferreting can i do a crp and you should be able to at least answer to them or explain to them what is the importance of ferritin and what is the importance of crp okay so ferritin more than 1000 and crp remember now try to put these boxes so if you have a patient whose crp is less than 40 okay it is less than 40 and ferreting is less than thousand you can tell okay the less risk of infection is less and very less risk of deterioration so it's a prognostic marker okay it's a prognostic marker that's how you will have to utilize these small bits of information from the blood test okay crp and ferritin now we come to a very very basic diagram the next five to six slides are actually going to take you to the the simplest basic of a blood test it's not so easy for us to you know just advise a crp and a pro calcitonin if you have if you do that remember as a doctor you should also know the cost of the test which you are advising okay you should also know the cost of the test which you are advising so if you advise a pro calculator please find out how much does it cost if you are advising a crp please find out how much does it cost because if you are advising it repeatedly you should also know how much is it important for you to decide the treatment or change the treatment every investigation you do for a pneumonia then you should be trying to apply it to your knowledge yes dr anirudh is saying this pic reminds me of robin's yeah it does remind you of robin's and that was one book which i always dreaded every time there are my friends used to like it but i used to always dread it okay so now we go to again a simple breakdown of this now why i put these slides is because this slide is actually tells you about what antibiotics do we choose and what is the pathogenesis of each different type of pneumonia you may be using pepra saline tazobacting you may be using amoxicillin clavolinic acid you get a patient of pneumonia you start clarithromycin but why are we using them what is the mechanism what is the reason so all these things are actually answered by these slides which we used to look in the microscope and try to identify them so there is a lymphocyte and there are monocytes and mass cells now pay attention to only two cells the t lymphocytes and the neutrophils okay t lymphocytes and the neutrophils now you should also be seeing the monocytes in it what does the monocyte do it induces or it helps in formation of the macrophages so macrophages neutrophils lymphocytes okay three important cells arising from the stem cell the lymphocytes the neutrophils and the monocytes all right so if you have understood this place try to remember it for the next 40 minutes because we need to you know put it everything into perspective of a pneumonia now i i'm trying to make it as simple as possible but i don't want it to be a conventional talk on pneumonia and hospital acquired pneumonias and use cholesterol and use piptas and this and that because at the root of what we treat we should know what we know okay we should exactly know what we are understanding so remember any inflammation in the lungs there are a lot of cells in our alveoli in our parenchyma neuroendocrine cells which the inflammation or the instigating agent which is an organism now this organism has a cell wall or it may not have a cell wall those organisms which have a cell wall are the ones which are gram positive and gram negative this we had discussed last time and those which do not have a cell wall are the atypical organisms or for that matter certain other organisms like viruses so there are atypical organisms which do not have a cell wall and bacteria like gram and gram-negative have a cell wall which is made up of peptidoglycan now these cell walls in some people and some organisms have endotoxins or these bacteria emit endotoxins that's the simplest way i can tell you which causes induction or instigation or excessive expression of two important chemicals one is the interleukins which is very popular now with kovid and tumor necrosis factor okay i i don't know how many of you are really trying to understand this but if you are using clarithromycin and augmenting and monosave or whichever antibiotic please remember you are actually treating all these different markers you may be happy to see that the patch has resolved you may be happy to know that okay the patient is better but what you are actually targeting what you are treating is the interleukin 6 and the tumor necrosis factor alpha okay tnf alpha so these are those these markers get induced by inflammation and then they cause the crp to be profusely generated or increase or induction of c reactive protein got it so putting it backwards which is the commonest test which is done crp which is the cheapest test which is done amongst all this crp so we do a crp if it is high it indicates the il6 levels also could be high the tnf alpha levels could be high and it indicates that the inflammation could be high so we are actually going the other way round when we say that crp is high understood so if the crp is high then it induces further different changes okay try to please remember this i may i may be sounding a little too offshoot and boring but but you need to know this i mean treating x-ray is not not the best thing to happen you need to treat the changes which happen in that patient's lung in that gentleman's or lady's lung okay you need to know this so those the antibody production as you can see there is antibody and the endotoxin and they unite and there is opsonization opsonization is a word which i never used to understand till i started understanding about antibiotics and why we use it so optionalization means there is coating of the bacteria so that they can be easily phagocytized so this is a very important step now please understand suppose you have a patient who is a diabetic suppose you have a patient who's on steroids suppose you have a patient who is immunocompromised you have a patient who is malnourished what is going to happen opsonization does not happen adequately coating or making the organism ready to be phagocytized does not happen adequately and the patient may worsen because now there is no phagocytosis okay so if we put it in simple words it becomes like either the healthy cell will go into a necrosis so i can understand we have different types of like necrosis which again was a very very difficult thing to be answered in an exam casiation necrosis liquefaction necrosis and so on and so forth but either the tissue gets necrosed that it swells up there is leakage of the cellular contents and it dies or it can be apoptosized apoptosized means the macrophage goes there it engulfs the organism okay so there are two ways it can happen it purely based on our understanding of immunopathogenesis and this is also the reason why some patients of pneumonia worsen and why some don't okay so now this is a very important slide i can say is you start from one two three four five i'll just take five more minutes on this particular aspect of molecular understanding is that the organism actually gets fragmented and the macrophage engulfs these organisms okay macrophage and engulfs is that is by phagocytosis if our immunity is good as we said the opsonization is good let's assume that stage is good that there is a coating of the antibodies but now the macrophage activity is not adequate it may happen that the macrophage activity is not have not adequate then also the infection will worsen the disease will worsen the third thing which can happen is that we can this is a little too much of a crowded diagram but see the second one the one in the pink one is that the organism has been eaten up by the phagocyte or the macrophage but the macrophage is weak or the organism is more virulent strong so the organism breaks the organism breaks open the macrophage and it comes out so it is called as suicidal death where the organism the microphone is destroyed and it comes out and there is more severe inflammation this induces the secretion of more inflammatory markers and this is the place where many patients develop either a inflammatory syndrome where we have seen with cowed also there is an inflammatory syndrome and subsequently there is lot of fibrosis also means severe the inflammation more is the fibrosis so for those patients whose x-rays have shown post infective fibrous tissue deposition which i am sure you have seen x-rays where patient has been treated for pneumonia one year ago but their x-ray still shows a patch what has happened is that the antibodies were there was a good optionalization there was good phagocytosis but the macrophage were not adequate enough or the whole or the agent was so toxic so virulent that it broke open and it came out again inducing a very severe inflammatory change and that led to the severe inflammation once that happens i hope i hope i'm not going too fast so that each one of you you know assimilates what is happening we started off from a patient who had pneumonia who had cough fever breathlessness and patient was examined he had bronchial breath sounds increased vocal resonance and there were repetitions x-rays showed a inhomogeneous you did the blood test blood test showed that the ferritin levels were high the crp was high procalcitonin was high in a bacterial pneumonia calcitonin was low in a viral pneumonia you understood that the prognosis is not good you also did the blood sugar you also did the bun creatinine because you wanted to know if other systems were involved when i say you did this you are supposed to do this that's why i'm saying you did this i understand that we are all good clinicians in spite of giving the best of treatment the local infection it ended up into the bloodstream through the pulmonary circulation it ended up into the bloodstream it is by again a small word but we never paid attention to it it is called diabetes diabetes means there is a secret the leakage of the cells the bacteria into the blood circulation and it leads to what is called as sepsis so this is the most dreaded complication of an ammonia so the patient starts with a localized lung infection cough fever crp is high is immunosuppressed either the macrophage function is not good or the neutrophil function is not good or the lymphocyte function is not good or the monocyte function is not good because of all this the il-6 levels are high tnf alpha levels are high subsequently the crps are increasing but the organism was very strong very virulent it broke through the macrophages and led to sepsis this is where we may have a patient who is having infection in his bloodstream and we come to one more test which is called as blood culture because now the organism is shared into the blood and we get it positive in the blood culture now for all those who are going to treat in the hospital these are all going to be in the hospital okay we are going to treat in the hospital we have got different steps now these steps are towards poor mortality okay more and more prognosis becomes poor and poor and poor that's the increasing mortality chances mortality index so there is a severe inflammatory response there is a sir then there is a stage of sepsis then there is a stage of severe sepsis and then there is a stage of septic shock we of course cannot manage to cover how do we treat sepsis and how do we uh you know start using these different different medications uh for this yes diapidasis is is is a is a process where there is a leakage and the capillary permeability is more but along with that even the septic foci or the bacteria organisms also get shed and the blood supply through the bloodstream happens okay so so this is where you land up and when we talk of sepsis perhaps this is the last slide before we move on to actually coming back to knowing different types of pneumonia and managing them when we say sepsis it indicates involvement of multiple organs okay because of endothelium affection because of coagulabity hypercoagulable states cellular dysfunction and cardiovascular dysfunction now this you need to remember why you need to remember we don't want our patient to reach to this level let's be sure of that i am trying to make it an entire gamut of what pneumonia is but we as a doctor and for that matter the patient also does not want to go to this level of sepsis so that's why we need to know what to do so that we can prevent them from going on to sepsis right and for that we should know when it is called a bacterial pneumonia when is it an atypical pneumonia all right so let's let's go to the simple basics of atypical pneumonia why they are called atypical because they don't have the peptidoglycan layer and that's the precise reason why they don't get stained with the gram stain not only that even their presentation is atypical so if a patient of bacterial pneumonia has acute presentation of 24 to 48 hours of cough purulent secretion and fever a patient of atypical pneumonia will be having possibly body ache headache loose motions dry cough running nose coreisa so these would be in favor of atypical pneumonia so more systemic symptoms okay so that is something which can be of help to really understand one more is one more thing point you should remember suppose you see a patient's x-ray which shows a localized patch like the one we saw there's a haziness in one particular lobe most often it's a bacterial pneumonia but if you see patches of pneumonia either upper lobe then mid zone then somewhere in the lower zone distributed throughout the lungs most probably it is a viral pneumonia or a atypical pneumonia okay so that is the rough idea it doesn't confirm anything but it's just a rough idea and where do these atypical organisms come from they can come from anything it's basically an environmental infection so from the air conditions from the hospital water supply even patient to patient so this is how usually a patient of atypical pneumonia usually a younger patient so even if you have treated community acquired pneumonias you will find them middle-aged to elderly diabetics patient with copd patient with asthma patients with bronchitises they come up with a localized bacterial pneumonia most of the time okay so that is one of the ways that we can you know perhaps try to understand about what exactly is a bacterial pneumonia and we have already discussed this so not going into too much of details that uh there is a chlamydia microplasma lesion one more point of interest you should know that commonly we use beta-lactam antibiotics for those who have started treating or who are being in the clinical practice you use very often a combination containing beta-lactam antibiotics now beta-lactam antibiotics work very well on the peptidoglycan layer of the bacteria but the atypical organisms do not have a peptidoglycan layer so there is not much use by using a beta electrum antibiotic if you are suspecting a atypical bacterial infection okay so that is one reason where the choice of antibiotics may differ so try to put everything into one after the other so that you try to prevent these particular things from happening the severe types for that you should take help of this particular slide and i think each of us may be from the basic medicine to the post graduate to a surgeon or any kind of you know practice these few things are very very very important aspects when you see a patient of pneumonia because prognosis is what matters i mean a patient comes to you for what he has three four questions in his mind he has to know he sits in front of you he tells you his symptoms you examine you go and sit in front of him and what does he ask you he asks you doctors what problem do i have that is his question so you should have an answer for that next question he has is how long will it take for me to get well so that answer you should have which is the prognosis the third question he asks is is it a very serious problem for that you need to have few prognostic markers few few indicators whether this disease is progressive whether the outcome is going to be bad so try to have these three answers with you when you sit in front of a patient you know the examiner asks you exactly the same questions before you become a doctor and the patient asks you the same questions after you become a doctor so the examiner sits in front of you and he asks so what do you think on the x-ray what's the diagnosis the patient says doctors what do you feel it is the examiner asks so tell me few things which will tell you whether this disease is severe or mild or moderate so the patient asks you doctors and the third is the examiner is going to ask you okay tell me the management of this disease and the patient asks you doctors so it's the same question it's just a partition between before being a doctor and after being a doctor so this slide will actually help you to understand the respiratory rate is important the blood pressure is important the age is important and his sensorium is very important okay so you need to know what is the status the neurological status of this patient tachypnea hypotension and age which is called as a curve index and you can see that there is curve one curve two curve three cop four and five that is whether he should be in the icu whether it should be admitted or it should be treated at home so this is a very important parameter and then we can actually think in terms of treatment to make it a little more easy for us because every day you will come across some new antibiotic put up in front of you right from quinolones to newer cephalosporins and so on and so forth so we need to know what are the antibiotics which we have now again don't go on this too much of details in this slide i will tell you a simple understanding of antibiotics the most earliest of antibiotics which has been used is penicillin okay that's the earliest of antibiotic and it used to be used as a broad spectrum antibiotic means gram positive gram negative atypical everything it is covering anaerobes but injectable it was plus reactions it used to cause so there was there was a different formulation of penicillin group which is the amoxicillin amoxicillin was given almost six to eight hourly means three to four times a day ten days but causes loose motions in few people and of course those who are allergic to penicillin group may have a reaction that's why and with research came up another group of drugs which was of course the toxicity claim which came up the tetracycline group of drugs and then came the cephalosporins and the quinolones so there has been an evolution of drugs to cover a gram-positive gram-negative atypical bacteria now of these the commonest ones and the recommended ones is amoxicillin because it is cheap available everywhere and it covers most of the gram positive and gram negative organism but the problem is that these organisms are becoming now resistant to amoxicillin and to try to overcome that resistance we need to add a clavolonic acid to it which is amoxicillin with clavolinic acid so the best option to prevent or to avoid resistant organism to kill resistant organisms is give a combination of amoxicillin with clavelinic acid which as you know everyone is using most of them are using it but it is not wrong to use only amoxicillin okay so if someone is using amoxicillin it is not a wrong prescription you don't have to criticize it how can he not use a clevelandic acid it is absolutely a prescription of choice and it's a good prescription and patients do get better with it but since the resistance is increasing specially to step two in streptococcus pneumoniae we give it with a combination of clavillionic acid not to forget that atypical organisms like legionella microplasma chlamydia they don't get treated with glycolinic acid and amoxicillin so we have to resort to a macrolide group of drugs that is clarifying so we have our option of platform icin there is also cephalosporin like cepheroxine so there are different groups of drugs fortunately they are all available very easily and very tolerable also you have to pick and choose according to your choice of patience and requirement there is no hard and fast rule use only this or use only that but try to monitor the patient in terms of the clinical improvement all right so this is again a very simple chart which tells us about with comorbidities without comorbidities so not going into the details of that as to which antibiotics and which one not to give and so on and so forth i'm very clear with that amoxiclav is a good combination clarithromycin for atypical is a good combination you can always go in for use of a quinolone as well okay even levofloxacin is a good mono drug single drug which covers gram positive and gram negative organisms one point each of us should remember that quinolones also cover tuberculosis okay it treats tb also so there could be a problem if you are by mistake or inadvertently treating tuberculosis without conforming so we generally try to avoid levofloxacin while treating a case of pneumonia because it may give rise to a resistant form or it may be inadvertently or treating a tuberculosis pneumonia because even tuberculosis can present as a pneumonia you don't need to really think that tb means it has to be a long-term symptoms and long-term disease and so on and so forth all right so with that i think we have tried to put each and everything about a consolidation or a pneumonia right from its complications to the sequelae to clinical manifestation and to going to the very very basics of what is crp what is procalcitonin what is ferritin and how to apply each of them so that we can be wiser and better in preventing the complication of sepsis so this just lists out the different organisms which can create a problem and give rise to an infection now how do we confirm these organisms so i'm just trying to explain to you one if the patient is getting a sputum please send a sputum for bacterial culture which will tell you bacteria because naturally bacterial culture so it's going to tell you about the bacteria then secondly if the patient is having uh say there is a test called as a bio fire bio fire is a pcr based test a polymerase chain reaction based test where a swab is taken like a swab is taken for kovit test similarly a swab is taken and that is sent for a panel of pneumonia so it has got different types of influenza which are investigated different types of bacteria which are investigated and we can actually get a report in almost two to three hours so it's a swap test it is called as bio fire not all labs do it so it is not as popular but it's a definitely a test to reckon with you will get the viral ideology also faster so there is different groups of organisms which can lead to a particular infection all right now coming to the last few slides about what is the bacterial in ammonia and viral pneumonia please remember now as they put up on the slide the cell which is more involved you know viral pneumonia is the lymphocyte the cells more involved in the bacterial pneumonia are the neutrophils and the macrophages so that's the cellular difference which happens in a patient with bacterial pneumonia and viral pneumonia but we need to remember that pneumonias when they are bilateral think more in terms of a viral pneumonia with the present kobe times obviously any patient comes to us with high grade fever or with cough and x-ray or ct scan shows bilateral patches we will be first wanting to rule out a viral pneumonia but at the same time do not forget that there can be coexistent bacterial pneumonia as well especially if the patient is an elderly individual a diabetic okay not to forget the different mechanisms which we actually treat through the endotoxins that is the optimization and the apoptosis which we talked about so macrophage activities is very important and that's the place where we have to think in terms of boosting up the immunity immuno modulators come into picture so this is just a chart to really you know try to consider everything which we discussed x-rays the wbc count the biomarkers the lower respiratory tract and the fewer so there are different pointers which can tell you but as a clinician as a treating doctor you will nearly really need to get to the root of it okay so we have to get this clearly etched in our mind that don't keep on doing crps every day i mean there is no point unless you find a clinical deterioration so you may have a crp but you may repeat it after 48 to 72 hours however one bottom line which i need to tell each and everyone do not treat the biomarkers treat the patient crp may take a longer time to return to normal crm may take a longer time to return to normal so if the patient's symptoms are regressing patients x-ray is better saturations are improving please do not have to go on repeating the c reactive protein okay we need to see the clinical aspect of the patient as well now certain very important aspects about the high risk cases someone was asking about the fungal pneumonias so fungal pneumonias are very common in these particular group of patients as much as even viral pneumonias and one of the commonest reason which we see today as everyone will agree is the high usage of steroids especially during the covet times so we need to be very careful when you are using high dose steroids because there is a chance of a fungal pneumonia it would take perhaps an entire hour or one and a half hours to cover different types of fungal pneumonias how to diagnose them right from their galactomanian levels and antifungals but i leave it at this point that we need to identify the cases because a healthy person would not be a host for developing a fungal pneumonia a healthy immunocompetent person is not a host to develop a feminine viral pneumonia okay we can get viral infections off and on we obviously know the influence influenza virus is the commonest virus and we everyone gets it even healthy individuals but it's a self-limiting disorder so putting them into boxes which are the fungal pneumonia candida aspergillus atypical pneumonia we have discussed viral pneumonias the adenovirus the rsv the respiratory syncytial virus influenza virus cytomegalovirus herpes simplex virus and parasites and protozoa so all of them can lead to a pneumonia so keep your eyes open keep your ears open remember to what the patient is saying suppose the patient says to you doctors he's probably trying to tell you or the lungs are trying to say that there is an anaerobic infection so we are talking of an anaerobic infection viral pneumonias do not present with a foul smelling odor atypical bacterial infections do not present with a foul smelling odor so you need to step up your antibiotics to cover anaerobes okay so you need to cover that as well so the person may say that i am getting lot of cough but it's spout smelling the sputum is fall smelling so you need to remember that these are anaerobic and the commonest ones which develop lung abscesses are those who are alcoholics or aspiration unconscious patient patient on steroids patients who are diabetic so those are the patients who develop power smelling expectoration and they may develop a lung abscess now fungal pneumonias i'm i'm winding up now because we're already reaching our time is that there is histoplasma blast uh there is there are different fungi if you see but the commonest ones which we are seeing is aspergillus and candida okay these are the two common ones and sputum examination is the best way to conform a fungal pneumonia there is a test called as a galactomannan acid galactomanin acid which is done by a blood test also which can raise the suspicion of it being a fungal pneumonia so if you have a hiv patient a diabetic patient anemic patient patient on steroids bilateral pneumonia think in terms of a fungal pneumonia don't stick to your idea that it has to be only covered and covered and covered okay so you need to remember these things there are not much to do or much treatment options left with us when it's a viral pneumonia one which we have treated during the swine flu times is the osceltamavir that is being used even today because influenza virus continues to be a commonest infection and the other medications like amantadine and other ones are not available except one of the ones which is available is gan cyclovir when we give a specific organism like cytomegalovirus again cytomegalovirus antibodies are positive or igm or cytomegalovirus positive bilateral diffuse shadows patient worsening deteriorating will all point towards a cytomegalovirus infection yes in antifungals we have got different antifungals i don't think we can really distribute each of them because there are pros and cons for everyone like fluconazole hydroconazole or economy and the different groups of fungi need different antifungals which is a exhaustive topic but keep your eyes open for the aspects of pneumonia which we have discussed do not ignore the smaller things like the crp values the blood sugars the creatinine always insist if a middle aged or elderly person comes to you with a pneumonia insist on getting his glycosylated hemoglobin insist on getting his creatinine levels okay you should be asking for this a patient who is not responding to your conventional line of treatment think of resistant organisms so your culture sensitivity would be of health to know which antibiotics should we choose always and always do not forget tuberculosis tuberculosis still remains the commonest cause of death amongst respiratory infections and tuberculosis can present as a pneumonia so if you see a patient with a pneumonia even if it is an acute presentation do not overlook that it can still be tuberculous pneumonia okay so from the last four last time we met all of you met me and this time we have started off seeing an x-ray sitting in front of the patient understanding the stages of pneumonia based on the anatomy and the pathology then we talked about the physiology of vq mismatch and the shunt then we talked about the symptomatology of what the symptoms of this patient would be subsequently we went through the different radiological presentations complications of pneumonia cavity lung abscess cinnamonic effusion bronchitis ards what ards means and then today we discussed about that is about the smaller changes which happen at the level of the inflammation like optionalization phagocytosis macrophages apoptosis and how interleukin-6 crp ferritin all these markers become important and then the prognostic markers like the curve index curve 65 and how to differentiate between each different type on a rough basis on an outline basis and how to prevent our patients from worsening and going into the different stages of sepsis so i suppose we have tried to assimilate everything in as much uh as possible on a zoom on a lot of the zoom on your matte flips each one of us to treat our patients in a better way in a better manner and helps us all

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Dr. Salil Bendre

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dr. Salil Bendre

Dr. Salil Bendre

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