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What's up ninja nerds? In this video today, we are going to be talking about pneumonia. There's a lot to discuss. We'll go over the pathofizz. We'll go over the different types of ways that we can kind of classify pneumonia based upon the microbes, based upon how you acquire it, based upon the location, and we'll talk a lot about that stuff.
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Then we'll go over some of the features and complications, really tying things together. We'll talk about diagnostics and finish up with some treatment. All right. All right. So when we talk about first things first the kind of the pathofizz behind pneumonia. Whenever patients develop pneumonia you have to think about the different mechanisms by which they can develop pneumonia.
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Obviously pneumonia is an inflammation infection of the lung tissue itself due to a particular pathogen. This could be bacterial, this could be viral, this could be fungal, could be a lot of different entities, right? Most common it's going to be bacterial though. But the ways that the bacteria get into the respiratory tract is important.
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Now one of the ways that this can happen is usually aspiration right and so when I mean aspiration this usually means that some type of secretion whether this be like secretions within our oral ferings so some of the salivary secretions and things from our oral cavity nasal cavity all of those things kind of draining down unfortunately into the airway.
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So oral fingial aspiration is actually tends to be one of the most common ones. I'm going to represent that with this orange arrow here where some of the secretions within this oral fangial portion here. Instead of it going down into the esophagus, which is this green tube, it unfortunately goes right down into the blue tube, right into the airway.
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Right? And whenever these pathogens that are within these secretions get sucked up down here into like a little bronchial or alvoli, they have the ability to cause damage to the lung tissue, inflammation of the lung tissue, infect it, and then lead to pneumonia. Now another mechanism besides oral feringial secretion.
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So let's actually put like a little one here. So one is to represent the oral feringial type of aspiration. The second aspiration which is really nasty really scary is gastric. Right? So someone has some type of situation here where some of their gastric secretions go right into their air tube.
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This would be the second one. So some type of gastric type of aspiration. So if someone has gastric aspiration, there could be a lot of different reasons for this particular problem. But either way, that's a way for the bacteria to be able to move from parts of our esophagus, from our stomach, some of the natural flora within this area naturally to get into the lung tissue cause injury, inflammation, infection, and then you got pneumonia.
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So my question for you is how would these particular pathogens that are coming from our oral fingial secretions or from a gastric secretions even get into the actual lung tissue? How does it get into the airway? That's the question, right? because we should naturally have protective reflexes there to prevent us, right? You try to go and stab like the back of the tonsils or the throat, you're going to have a gag reflex or something kind of gets in the proximal airway, agitates the tissue there, cough reflex. Or instead of oral fangial secretions or things coming from our GI tract, uh going upwards into the airway, they should naturally go down into the GI tract. So the normal swallowing process, those should also all be intact. But what if a patient doesn't have those intact? So what if for some particular reason you have right for example here we have our central nervous system here's going to be like the the parts that control a lot of these particular reflexes. So let's say here's a lot of the different cranial nerves that are involved in some of the particular gag reflex particularly within the cough reflex or particularly within the swallowing
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reflex. So now you have a disease process for whatever particular reason it may be. And what it's going to do is there's going to be some type of disease process or depression, whatever it may be, that's shutting down this cough, gag, and swallowing reflex. So in these patients, the primary reason by which they aspirate is the loss of the gag reflex or a decrease in the gag reflex, a decrease in the cough reflex or a decrecrease within the swallowing reflex.
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And that basically prevents us from being able to prevent things from going into the airway and also prevent us from naturally allowing things to go into the GI tract and then undesiraably go right into the airway and create an opportunity for pneumonia. Now my question to you is what kind of things would actually cause this disease process where you inhibit this central nervous system diseases baby.
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Nothing crazy to think about it right. So one would be if you have any kind of CNS disease think about this it's not too complicated. You have a stroke you damage part of the brain. seizures, Parkinson's disease, multiple sclerosis, lots of different diseases which are going to lead to this inhibition of this pathway ALS, right? The other one is any kind of CNS depression.
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And I think this is important also to be able to remember. So it may not be a disease process, but if you have patients who are on some type of opioids or they're also uh taking particularly maybe some type of benzoazipene or they're being sedated or they're being paralyzed for because of the ventilator or they're having to be intubated, whatever, you're taking away that natural type of reflex from the central nervous system.
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So any type of CNS depression would also be a big one. The really big ones that I really want you to remember here especially is alcohol use as well. So alcohol use is a big one here as well as any kind of sedation. So, I would remember sedation or neuromuscular blockade, things of that nature.
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But either way, you're shutting down the cough, gag, swallowing, reflex, allowing for aspirated material. Now, here's the thing. This kind of things happen and then the microbe gets in. What are some of the microbes that we should really be concerned with whenever patients aspirate? There's a lot of different bugs, but the ones that I really, really want you to be thinking about, especially in patients with some type of underlying aspiration.
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The particular bugs that I would actually be somewhat concerned with, the microbes, if you will, that I would think about in this particular scenario is Klebsella. So, one would be klebsella. This is a really, really nasty bug. Okay? This is very common in patients who are an alcohol user, have some type of aspiration from a CNS disease.
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Other ones would be anobes. So, anobes are really, really nasty one. You want to know why anorobes? Because this will come from the GI tract. GI tract naturally is going to have a lot of anorobic bacteria. And the other one that I would also consider here is going to be staflacus arius.
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So the ones that I would actually be really really potentially considering and patients who have some type of aspiration would think about klepsiella anorobic bacteria and potentially staflacus ararius due to aspiration loss of or decrease in gag cough swallowing reflex due to CNS disease or CNS depression of some particular eeology.
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All right boom roasted next particular thing what would be another reason why someone actually has a pathogen get into the actual airways cause inflammation infection and lead to pneumonia. One is you inhale a really nasty kind of hardy pathogen and what would that potential pathogens have to be? What would be some of the risk factors that would be associated with it? So let's say that you're in a population particular in a particular environment where there's a high kind of volume population, lots of close contact in situations where there's lots of this close contact, lots of a highly populated individuals, you're at risk for some particular types of pathogens that I think are worthy of remembering. And the ones that I would really want you guys to potentially think about here in situations where there's lots of close contact, a lot of people hoarded together within a very tight population is really be thinking about myopplasma, pneumonia. This is a really big one. Myopplasma. I would also think about chlamyia and I would also think about influenza.
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Think about influenza as well. Okay. So these are really really big things to be able to consider in these particular patient populations is again whenever you have a lot of close contact there's an opportunity for a lot of these particular pathogens to be passed on via respiratory droplets inhaled boom right into the airway and have the ability to cause a particular infection.
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So think about influenza, myopplasma, chlamyia, sometimes leanella as well, but I would put a plus minus with legionnella because the real particular thing that you really want to remember here with legionnella is think about I'm just going to put here. Think about water sources. I would really want you to think about contaminated water sources, but this could still be in highly populated types of areas, hot tubs, pools, showers, you know, AC units within a lot of different hotels and things like that. All right, but we got aspiration. We got inhalation, particularly within close contact, airborne pathogens. But here's another one. Maybe it's not like a persontoperson transmission via myopplasma, chlamydia, influenza, or leanella. Maybe it's some type of like soil or dust exposure or like nasty droppings from particular animals that put these patients at high risk. And it's dependent upon the geographic location, which is very high yield. So sometimes you can have a lot of fungal infections, really really nasty fungal infections. And the ones that I want you
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to remember that they may test you on the exam is they may say there was a patient who had potentially has pneumonia and he was just hiking in southwestern United States near California. Whenever you hear southwestern portion of the actual United States, you want to think about something called coxidio micosis, but I'm going to put coxidio here.
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So think about coxidio micosis. Whenever some people say they were, you know, doing a lot of spelunking, they were looking at different birds and bats and stuff like that near the Mississippi or Ohio River Valley areas. You want to think about hystoppplasmosis. So look for that on the clinical vignette.
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So hystopplasmosis particularly think about that that kind of buzzword terms bird bat droppings Ohio Mississippi River Valley area or spelunking. And the next one is if you think about broad-based yeast in the east, right? This is going to be particularly more on the western side, I'm sorry, the eastern side of the United States.
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So if you see kind of like the southeastern northeastern part of the United States, think about the broad-based yeast in the east. This is going to be blasto micosis. So think about blasto. Okay. So these are the particular types of fungal infections that I would want you guys to be aware of and potentially airborne inhalation.
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So this would again be the particular microbes. But again when we talk about these particular microbes, we're really talking about a fungal type of infection. So this would be a fungal type of population that I would want you guys to think about. All right. So these are the big big big things that I really want you guys to be aware of for the potential eeologies.
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First one aspiration. Second one inhalation. Now what if a patient let's say for whatever reason they don't have any particular problem with maybe an aspiration or an inhalation but they have a something other kind of problem down here that has to do with their normal respiratory function because they have underlying types of diseases that are altering their natural immune system defenses such as mucostiliary clearance.
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Let's talk about how that potentially could be another problem for patients that developing pneumonia. If a patient does have no problem where they didn't aspirate something, right? They didn't have any situation where they inhaled like a hearty pathogen like a fungal infection or a mopplasma, chlamyia, leionella or viruses, then you want to be thinking about is there something wrong with the actual anatomy of the respiratory tract.
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Is there a defense system a little bit altered in a particular way and so one of the big kind of defense mechanisms that our actual respiratory tract has is what's called mucosilary clearance. It's a really interesting concept. So you have psyia right there beating beating beating. They're usually beating things upwards.
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So if you have something kind of stuck within the bronchi or the trachea, generally these guys, little guys will beep beep beep beep beep beep the bacteria mucus upward so we can spit it out or swallow so it doesn't stay within our respiratory tract and sometimes we'll have little mucous globules that will trap the pathogen and again make it easy to be able to beat that bacteria up via the psyia.
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Let's say that there's disease processes that either really chalk up the mucus where the cyia now they can't handle all this mucus. They're trying to beat against this thick thick mucus wall or there's damage to the psyia. Now you don't have the ability to move that mucosilary clearance or escalator.
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What are disease processes that would alter this and then lead to an opportunity for pathogens to kind of like get locked up in the lower airways cause inflammation and infection leading to pneumonia? One disease process that would really kind of increase this mucus production. Think about it guys, it's not really hard.
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What about cystic fibrosis? So think about potentially someone who has what's called cystic fibrosis or they have the other disease. Maybe it's not due to cystic fibrosis, but it's due to other particular things such as malignancies or such as primary celery disynesia, a lot of other inflammation of the airways.
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And this could be something like what's called bronchiactis. Bronchiactis. And so in these particular situations, you know that this is going to increase a lot of the mucus. If you increase the mucus, are the silia going to be able to beat the bacteria and all that mucus upwards? No. Because now the mucus is going to get so thick.
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Imagine that these like psyia, they're trying to be able to push like 2,000 lbs versus like 10 pounds. Now they got this big thing that they got to try to move. That's not going to allow for the bacteria to be easily cleared. Plus, it's going to create an opportunity for bacteria to not get moved.
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And so then what happens is some of these like nasty little pathogens, they're supposed to get in cleared. Guess what? They kind of just stay in these areas and then they move down into like the smaller bronchios and alvoli and create an infection. Other situations is maybe it's not an increase in the mucus.
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Maybe the problem is that their psyia is all jacked up. Maybe we inhibit the potential pilia. What if I damage the cyia? You know what kind of diseases would actually damage the psyia? What about COPD, right? Or maybe they don't have underlying COPD, but they are a smoker. So sometimes patients who are like big big smokers, we know that the tobacco also will cause destructive damage to the psyia and elderly individuals.
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So as you get older, you kind of lose some of that natural function of the psyia. So elderly individuals will also have this high risk potentially here. Now we have an understanding of like these are the patient populations. Now what I want you to think about is what kind of microbes would potentially be present here because if our psyia isn't beating or the mucus is getting too thick it creates an opportunity for the bacteria to not get mobilized.
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They stick down here and they cause pus toform and then they lead to infection pneumonia. The potential pathogens that I would want you guys to really be aware of potentially within this situation here is there's a lot of them. Okay. One is I want you to be thinking about this very very specifically with your COPD patients.
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So in these COPD patients and with patients who have COPD, they're at very high risk for something called hmophilus influenza and something called moracella cataralis. These are really really nasty types of bugs that actually can accumulate here and cause nasty nasty infection. The other thing is that patients who were actually going to have cystic fibrosis and bronchiacttois, you know what's really really bad with this one with cystic fibrosis and bronchiacttois.
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These are at really high risk for a really nasty bug called pseudamonus. So it's called sudamonus origigosa. So I really really want you guys to be able to remember that one as well. The next particular thing that I also want you guys to be thinking about is that patients who are elderly and who smoke, so smokers and elderly individuals are at very high risk for another type of pathogen, particularly this one that I would want you guys to be thinking about is Legionella.
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Remember we talked about that one with the contaminated water sources. So contaminated water source, but also be thinking about this as an atypical pathogen in patients who are smokers and elderly. So these are the big things that I really want you guys to be thinking about in this situation here. All right. So let's say that there's a problem where again patient aspirated they aspirated some of these particular pathogens into their airway because of an alteration in their natural central nervous system function or they inhaled a really hearty nasty pathogen because of close contact or they were in a particular geographic location that put them at high risk for a fungus or they have some type of alteration within the normal normal defense system of the respiratory tract like impaired mucosil clearance. What if by some terrible situation, we get a pathogen that gets into the bloodstream. When it gets into the bloodstream, it then spreads to the lungs. Oh, that'd be a terrible situation. But guess what? Patients who are IV drug abusers are very high risk
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from whenever they're using dirty needles. You know, in the skin you have a potential pathogen called staflacccusarius. So in patients who are IV drug abusers, they have this risk of taking this pathogen from dirty needles getting into the bloodstream and spreading to the lung tissue where it can then cause inflammation and infection.
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Obviously they can get endocarditis and things like that as well. But this is a big one. So because of that I really want you guys to be thinking about staflacccus arius and patients who are IV drug abusers. The only other thing that I would potentially want you guys to think about with staflacccusarius is not just from IV drug abuse but sometimes add this into your memory don't forget this one is that sometimes in a patient population where they just had the influenza so they just got influenza after they have influenza their immune system is a little bit kind of like not as protective they're at high risk for staflacccus ararius so postinfluenza infections uh infections these patients are at high risk for staflacccusarius remember two things ivy drug abuse and post-influenza for stafllo caucusarius. All right, but that's another route. That's another way that patients can develop pneumonia. They can aspirate, they can inhale, they lose their mucosil clearance or they get it in the blood and it spreads to the lungs. Here's the other thing. What if the patient gets it spread from the blood, right? So, it
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comes from the blood hematogenously gets into the lungs or it's inhaled, it's aspirated or there's an impaired mucosilary clearance and it gets into the lung. Either way, the same result is the the same kind of thing here. We develop inflammation, infection, and then we develop pneumonia. What if naturally our immune system is there's another altered there's another defense. We have macrofasages.
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We have our immune system that will come and try to be able to clear and get rid of the pathogen and get rid of all that kind of infected material. That's our natural kind of immune response. But what if a patient doesn't have a good immune system? What if for whatever reason whenever they come in exposure to that actual pathogen, their macroofasages aren't doing very well.
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They try to recruit a lot of lymphosytes and neutrfils, but all of this is particularly depressed. And so their ability, all of these immune system cells to be able to work and clear this infection is inhibited because their immune system is depressed. They have a decreased function of their macrofasages.
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Particularly decreased number of lymphocytes would be the big big one that I want to want you guys to think about. And again, just decreased activity of the immune system in general. What kind of patients would be really really high risk? HIV. So I want you guys to be thinking about patients who particularly are immuno compromised such as HIV or what else? Maybe they have diabetes.
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Maybe they have CKD, maybe they're alcoholics, maybe they're status postransplant, right? Or maybe they're on some type of amunosuppressant medication. What are some types of amunosuppressants that you guys would really want to be aware of that they may present on the actual exam? Think about TNF alpha inhibitors. Think about um your demarss.
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Any kind of things like that. Steroids would be a really big one. So any of those demarss, any of the actual types of steroids would be really really big things to think about. So these are the things I really want you guys to be able to be aware of. But now here's the thing. Microbes that patients are really high risk of when they're imunocmpromised is also really really important.
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So if a patient is imuno compromised, they are really really at high risk for a lot of different microbes and I think it's worthy of mentioning some of these. One of them especially in these imunocmpromised patients you want to be thinking about is sudamonus. Sudamonus is very high risk in these patients with underlying disease process as an immunosuppression.
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The other one that I would really want you guys to think about here especially in this patient population is leanella. Legionnella is another really big one. It's that atypical type of pathogen that we talked about with the contaminated water sources elderly and smokers. The other big thing here is something called PJP, pumocystic gerraishi pneumonia.
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This is a fungus. And the big big population that you need to be aware of when they present this on the exam is patients with HIV. And I can't stress how important this is a CD4 count less than 200. If they present that on the exam, they're trying to point you to this. It's a PJP that's causing the pneumonia.
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So a patient who's imunosuppressed with HIV, CD4 count less than 200. Think about that particular pathogen. The next thing that I want you guys to be thinking about besides this one is also think about, you know, sometimes some of the viruses like CMV would also be another particular one to be thinking about and any type of really other underlying kind of nasty fungal infection would be a big one.
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But the big ones I really think about is Sudamonus, Legionella, PJP, CMV, and there could be a lot of other like nasty ones as well, potentially other fungal infections. But for right now, I'd say that these are the primary ones that I really want you guys to be able to remember.
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Let's let's stick with these ones as the primary ones here. Okay. All right. So, we have, I think, a pretty good understanding now of how patients can develop pneumonia. It could be from an aspiration problem. It could be from an inhalation problem. It could be from an impaired mucosil clearance problem. It could be because it spread via the blood to get to the lung tissue, IV drug abusers.
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Or it could be because they got it in from the blood or they got it inhaled, aspirated, impaired mucus clearance. any one of these mechanism but their immune system wasn't competent enough to clear the infection. Okay. The last thing that I want to talk about here is whenever patients we talk about pneumonia we talked about it with respect to pathophysiology mechanisms.
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We talked about it with respect to microbes but we didn't talk about the acquisition of pneumonia. So what what do I mean by this? I want to briefly talk about because we'll talk about later in the diagnostics or something called community acquired pneumonia and hospitalacquired pneumonia.
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It's really straightforward. It's not hard. Community acquired pneumonia, you acquire the infection, the pathogen from the community, which it means it's a special type of bug. Streptocous pneumonia is a really, really important one that I can't let you guys forget. So, whenever you have a patient who has what's called communityacquired pneumonia, think about streptocus pneumonia.
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That's going to be one of the most common types. Usually, you'll see that with the elderly patients as well. So if you really wanted to add it into the list here for the elderly, I would also add in here streptocous pneumonia and this is going to be the most common cause of community acquired pneumonia in most patients.
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Okay, but they acquired it within the community or they got admitted into the hospital and with less than two days in the hospital has to be key. Less than two days in the hospital or out in the community they acquired the infection from strep numo. If it's hospitalacquired there's a usually a very specific definition.
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So hospital acquired pneumonia is they've been in the hospital for more than 48 hours more than two days and now the bug changes from strep numo to a very very nasty resistant bugs that you can encounter in the hospital and usually the most common type of hap or hospital acquired pneumonia is a subtype called VAP ventilator associated pneumonia.
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These are patients who have an endotracheial tube within their airway or some type of tra like they have a tra or they have an endotrachial tube and what happens is once they're in the hospital for greater than two days they now have nasty bugs that they can actually form and the two bugs that I really want you guys to remember here is going to be MRSA so methasylan resistant staflacccusarius and the other one is going to be pseudo mononus.
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Now in patients who develop ventilator associated pneumonia due to they have an endotracchial tube you obviously need that and more than 2 days to have the actual diagnosis. So they haven't have an endotrachial tube in for greater than 2 days or 48 hours. What are potential things that put these patients at risk? I think that this is one that I would actually consider remembering for the exam.
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Okay, they may ask this because it's relatively high yield. oftentimes when patients are in the ICU, we give them particular drugs to suppress their gastric acid production to prevent them from getting like stress ulcers. And so we may give them things like proton pump inhibitors. We may give them things like H2AS, like famotadine.
00:23:38 - 00:24:03
And what that does is that suppresses their gastric acid production so they don't get ulcers. But you know what else it does? It increases the gastric pH. Do you think bacteria survive better in a high pH or a low pH? They survive better in a high pH. And if that's the case and for whatever reason they reflux some of this around the edges of the endotrachial tube and it gets into the lungs, this can really cause a little nasty pneumonia.
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So I really want you guys to remember that gastric acid suppression tends to be a very very big potential cause for ventilator associated pneumonia. The other one here is when patients are being sedated. Normally if you have pathogens there you cough and cough and cough and you'll clear those secretions or you'll get suctioned.
00:24:15 - 00:24:36
If patients aren't getting actively suctioned, so there's decreased suctioning, decreased suctioning of potential secretions that can build up, form a film, and then lead to an infection. Or if you're having a lot of increased sedation. So when patients are on lots of sedation, they don't have a lot of that cough reflex to clear a lot of their secretions.
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Or you know what else is really bad? If they're paralyzed. If you're paralyzed, can you cough? No. And so whenever you're either not suctioning out the secretions and getting them to cough or you're taking away their cough and their natural kind of like mechanisms to clear secretions such as an increased sedation or increased paralysis for whatever potential reason.
00:24:52 - 00:25:11
These potential things really increase the risk of ventilator associated pneumonia. But you need an endotrachial tube for two days and then think about these particular bugs for CAP. What I say less than two days in the community or in the hospital and strep numo. All right, let's move on to features and complications.
00:25:09 - 00:25:23
All right, my friend. So, a patient develops pneumonia, right? They have an infection of their lung tissue. Whenever they start having an infection of their lung tissue, what are some of the features, the complications when they present this on the vignette, right? They're going to say, "Oh, this patient has pneumonia.
00:25:20 - 00:25:40
" No, they're going to say, "Okay, the patient's coming in and they're presenting with blah blah blah blah blah blah blah." And then they may present some of their underlying lung disease that maybe puts them at risk for aspiration. They were in very tight controlled crowds. They were like hiking in southwestern parts of the United States.
00:25:36 - 00:25:55
They have an imunosuppressive condition. They are an IV drug abuser. You get the point. So it's important to be able to understand what are those features and complications that really point you towards pneumonia. Now remember I told you that I used the terms a little bit loosely. I didn't really mention them and discuss them in detail. But there's a typical pneumonia.
00:25:54 - 00:26:13
And what I really mean by typical pneumonia is this is the pneumonia that most people think about that are like a very specific bacteria like subset. So this is like your streptoccus pneumonia, your klepsella, your homophus influenza, your staff orius etc. All of those nasty bugs sudamonus and so on and so forth.
00:26:11 - 00:26:33
When we talk about atypical pneumonia, we're talking about a very specific subset. Okay. So, what I want to do is I want to write down here because I didn't mention them a ton, but you talk about something called atypical pneumonia. And when I talk about atypical pneumonia, really what I'm saying is this is a very specific subset.
00:26:28 - 00:26:50
And I like to just break it down a little easy. Myopplasma, chamophilia, and legionella are the three atypical pathogens that I really want you to remember. And so, I'm not going to write all this down. I'm going to abbreviate it to help you guys remember it as well. I always remember atypical.
00:26:44 - 00:27:47
MCL, moppopplasma, chlamyia, leionella. And then the other one to remember is your viruses. Remember I told you influenza, parinfluenza, CMV, SARS KV2, and COVID 19. So there's a lot of different viruses out there that could also fit within that atypical umbrella. The key thing that you have to remember is that with atypical pneumonia due to myopplasma, due to chlamydia, due to leionella or due to viruses, they won't present with a lot of the classic features that we're going to see with typical pneumonia. Often times the key ways to differentiate this subset is they present with upper respiratory tract infection-like symptoms. So that's really what I want you guys to remember for the atypical types of pneumonas due to these pathogens. Think about upper respiratory tract infection type symptoms. What does that include? Well, it can cause headache. So, think about headaches. Think about some type of like
00:27:44 - 00:28:04
nasal congestion or rhinora. You know what else is a really big one? How about a sore throat? So, some type of sore throat sometimes. Here's the other big one that I would want you guys to remember. Earachches. So I want to show you guys a potential picture here. Especially with myopplasma pneumonia.
00:28:02 - 00:28:21
You know with myopplasma it can cause a really nasty infection of the tempanic membrane and cause bullis maringitis. They may present this on the actual exam. So think about this when they say ear pain atypical features like upper respiratory tract infection symptoms. Go looking in that ear.
00:28:17 - 00:28:46
This is what it would look like. All right. So that's some of the big things. Now sometimes upper respiratory tract infections they may have very lowgrade fevers and myalgas and arthralgas. So you can also add those features in there as well. So think about a lowgrade fever. Okay. But these would be the big things to think about.
00:28:43 - 00:29:03
Upper respiratory tract infections are really going to be the key things. So headaches, sore throat, nasal congestion, earachches with the bulis maringitis and then again some low-grade fevers, myalgasalgis, arthis things like that. Here's the big big stuff with the typical. Now, everything else that we're going to talk about now is is typical pneumonia.
00:28:58 - 00:29:24
For the typical pneumonia, you see a lot of classic features. Whenever you have, let's say here's this area of infection. So, you have all of this part of the lung is all locked up with bacteria. When it's all locked up with bacteria, it's going to cause a massive inflammatory type of process which release a lot of cytoines, interlucan one, interlucan 6, all these things that you probably don't really care about.
00:29:21 - 00:29:40
But what they do is they really kind of work on your central nervous system and particularly at the level of the hypothalamus and your hypothalamus says oo got to increase the body temperature so that the bacteria can't survive baby. Oh I may have to make these patients shake a little bit due to this type of problem.
00:29:36 - 00:29:57
So they may develop fever and riyers very common features in patients with a typical pneumonia. And I'd be really important to remember here that it would be more of a highgrade fever rather than a lowgrade fever. The other thing is as you lock up this kind of like alvoli, now look at this. Look at this.
00:29:54 - 00:30:19
I'm going to lock up these poor little alvoli with pus and I'm going to even maybe hit some of the bronchioles. Normally whenever we have a good measurement of oxygenation, it's dependent upon the ventilation of the alvoli and the perfusion to the alvoli. Let's say in this situation the perfusion is normal. So the ability to move blood through the pulmonary vessels and pick up oxygen is good.
00:30:14 - 00:30:36
But the ventilation in this situation is decreased because now I got to try to send oxygen into this locked up alvoli. It's going to stop right there and I got to try to send oxygen down here. And now the oxygen has to try to move across these all sucked up and pusfilled alvoli.
00:30:30 - 00:31:03
Imagine how little oxygen is going to move into these alvoli. So what's the end result here? Because I have something called a low ventilation and a normal perfusion. I get something a combined effect of these called a VQ mismatch. Do you guys remember this from our hypoxmic respiratory failure lecture that whenever VQ mismatch this can lead to hypoxmia due to this alvoli being filled with pus.
00:31:00 - 00:31:23
Here's the next thing. When a patient gets hypoxmic, what are the potential reflexive reactions that they may present on the vital signs? Let's come down and talk briefly about that. Now, here's another really interesting thing that they may present. So, they may say, okay, the patient's coming in, they have high-grade fevers, they got rigers, they have low O2 saturation on their pole socks.
00:31:20 - 00:31:40
And then when they look at the vitals, also maybe in the vignette, they may also say something else. And I want to just kind of explain why this usually happens because it's a pretty concept uh dependent type of thing. So whenever you have this locked up area that causes that VQ mismatch, right? So decrease ventilation to this portion of the lung.
00:31:37 - 00:31:59
So whenever you mismatch that portion, decreased ventilation, good perfusion, it leads to hypoxmia. So low levels of oxygen within the blood. So there's going to be poor oxygenation at this point here. Now we know that when that gets into the pulmonary circulation, that'll go back to the left side of the heart, right? We know pulmonary veins return to the left heart.
00:31:55 - 00:32:25
And whenever they return to the left heart, you'll empty all that blood into the left ventricle. From the left ventricle, you'll take this blood and then send it outwards into your aorta and into the corateed system. Now, what you guys probably remember is that there's all these different chemo receptors within the aorta and the corateed uh bifurcation there that pick up the sensation of oxygen or pick up the concentration of oxygen.
00:32:21 - 00:32:48
And whenever the concentration of oxygen is low, it really activates these chemo receptors and they send su these impulses into the central nervous system. And then your medulla goes like haywire and it says, "Oh geez, the oxygen's low. I got to increase the blood flow out of my heart to the lungs to increase profusion and I need to increase the respiratory rate to increase my ventilation.
00:32:43 - 00:33:17
" And so subsequently what happens is you'll notice that the patient may have an increase in their heart rate and they also may have an increase in their respiratory rate and depth. So they may present to kipnic or disnic and tacocardic hypoxmic fevers and riyers. Okay. What else? If you think about this locked up area here and let's say that some of this pneumonia is involving some of the actual bronchi and bronchios and you got some of this pus that's kind of filling into the lungs here.
00:33:14 - 00:33:35
Here it's filling into the alvoli. It's involving some of the bronchi bronchioles. Whenever you inflame the bronchi and bronchios they're really really heavily innervated by a lot of different types of noisyceptors and kind of like uh cough receptors. And so when you stimulate this because of a lot of inflammation they're going to go haywire.
00:33:31 - 00:33:59
send that information into your central nervous system and your central nervous system will say, "Oh, okay. There's a lot of secretions and mucus within the airways. If I cough, I may be able to clear some of those secretions up." And so it produces this intense cough reflex. But the cough should be what? Productive. All right? So that is going to be a big thing to think about here with these patients.
00:33:54 - 00:34:24
So look for a productive cough filled with a lot of mucopirulent sputum high fevers riygers hypoxmia reflexive tacic cardia tacipnia which may look like they're breathing hard and working hard to breathe. The other thing here key types of basic foundation stuff is whenever you have let's say inflammation of the lung parinma here and it gets close to involving the nearby plura.
00:34:17 - 00:34:40
If you agitate or inflame the plura, guess what else there is near that plura? Pain receptors, agitation receptors that are going to be able to pick up that sensation of inflammation and send that to the central nervous system. And these are sematic motor fibers that present with referred type of pain.
00:34:36 - 00:35:02
And so they'll have pain in their chest whenever they take a breath. What is that called? Pleuritic chest pain. very common in any type of pulmonary pathology to present with a pleuritic chest pain. So look for puritic chest pain, productive cough, hypoxmia, reflexive typia, tacocardia, high-grade fevers and riyers.
00:34:58 - 00:35:59
With atypical, you don't really get a lot of that stuff. You know what I'm saying? MCL viruses. The other thing that I really want you guys to think about here is these [clears throat] are really high yield concept is your physical exam findings. So you know when a patient gets a locked up portion of the lung let's say here's a big old consolidation in their lung when they have this consolidation you go and you try to do your physical exam there's big big things that they may ask you they may even ask you these questions they may present it in the clinical vignette where you have this area of consolidation so that's filled with fluid that's filled with pus that's filled with cells all of those things is a really kind of fluid consolidation here that's a big term I actually want you guys to get away so consolidative findings so consolidation is a big big thing that they sometimes will ask you on the exams. So if you have a consolidation there is this concept that air right whenever sound is moving through particular substances if it moves through air and it moves through fluid. So between the two which one would it actually move faster through and better through it moves better and faster through the fluid than it does
00:35:57 - 00:36:17
the air and so it increases the intensity of a lot of physical exam findings. So one of the things that I would actually be very very important to consider here is you go to the chest and you percuss. If you really do that, you'll hear something called dullness to percussion.
00:36:10 - 00:36:37
So, you'll have a lot of dullness to their percussion. If you listen and you take the stethoscope and you put it over their chest and you have them perform some specialized types of activities where first thing you do is you have them say uh 99 and you're listening to their lungs or where the area of consolidation is.
00:36:33 - 00:36:56
when that sound is moving through the consolidation when they say 99 it's going to sound so dang clear and it shouldn't sound clear. So because of the air usually that's filling that space. So if they have what's called a able to hear the 99 clearly during oscultation that's called a positive broncophony. That's a really big one.
00:36:53 - 00:37:21
The other one is that sometimes you'll have the patient say e. And when you say e, whenever the sound moves through that consolidation, it really kind of amplifies it and changes to where it gonna sound like a. So if it goes from e to a, that's a consistent with a consolidative finding. So we call that positive ego. Remember e and egophony.
00:37:12 - 00:37:36
E going to a egopo. [sighs] Okay. The next thing here is that sometimes we can have them whisper. And so when you normally you have whisper be like one two three one two three. What that will do is is you shouldn't be able to hear that really at all and a patient who has all air filled lungs.
00:37:32 - 00:37:50
But if you have a consolidation that sound's going to move really really easily and you're going to be able to hear it relatively well. So if you can hear one two three when they whisper very very easily it's consistent with the consolidation. So it's called whispered peckery. I'm not going to spell that out because I'll probably butcher it.
00:37:49 - 00:38:16
The next thing that I also want you guys to consider here is if you do something called tactile femitus, you take the hypoththenar eminences and you put it on the area of where the consolidation is. Normally vibration that's moving from the sound waves moving through their airway through the plura through the chest wall onto your hypoththenar eminence is kind of dependent upon air, right? But also what the fluid that it actually is moving through or the substance that it's moving through.
00:38:12 - 00:38:38
When that sound waves move through a a fluid consolidation, the actual vibrations are intensified. And so you'll feel that way more intensely in in a patient who has a consolidation than those with normal lungs. And we call that increased tactile framitus. So they will have increased tactile framitus. All right, my friends.
00:38:34 - 00:38:57
These are big big findings that I would really don't forget for your exam because they will probably ask you this as consolidative findings. Okay, so we have these as the features of typical pneumonia. And here's what's the scary thing with with pneumonia. When patients develop pneumonia, they can develop a couple associated complications.
00:38:52 - 00:39:12
So let's say here we have a pneumonia in this left lower lobe. Left lower lobe is all locked up with bacteria and pus. Well, that's going to cause a localized inflammation. So the capillaries are going to become leaky. They're going to be invasive dilated and fluid's going to start leaking out into the plural space.
00:39:06 - 00:39:37
If the fluid leaks into the plural space around that area of a pneumonia, what is this called? It's called a paranneemonic eusion. Sometimes though it can really get locked up and actually some of the bacteria. So sometimes you know what can happen is you can have some of the fluid here but some of the bacteria actually kind of spreads contiguously into the space and makes it really loated type of appearance.
00:39:33 - 00:39:55
And so you can get two potential complications. One is you have a sterile inflammation around the pneumonia and one is you have a lot of inflammation with a lot of laculated bacteria and pus within the plural cavity. What are these called my friends? This is called first one a paranmonic eusion. A parneonic ausion.
00:39:52 - 00:40:18
We talked about this in the plural disease lecture. You guys remember that right? And then the other one this one here where there's a laculated type of a pus infection within the plural cavity spreading from a localized area of pneumonia. This is called a impaema. Impaema these are scary complications from this disease. Okay.
00:40:13 - 00:41:13
So impaema here paranommonic eusion here. All right. What else can happen here? The other really big thing here is that sometimes if you get like a lot of anorobes in stafloccasarius or klepsella remember I told you that anorobes klepsella stafloccasar aspiration. In those situations, what can happen is you can have like an infection here, right? But then the bacteria get really smart, especially anorobes and those anorobes start kind of walling off the bacteria and then you can have this infection here where you have this big big cavity filled with let's just kind of make it all nasty here. All this pus and bacteria here. What is this called? When you have this cavitation in the lungs where there's actually the ability for the anorobes or klepsial or stafloccasar to wall themsel off. This is a lung abscess. This is another potential complication here that you would want to remember with patients who have pneumonia. The other thing obviously is that as you start causing inflammation and infection of multiple alvoli and
00:41:12 - 00:41:32
bronchios, let's say that you just continue to keep spreading. This is very very common with like bronco pneumonia, but you start causing multiple alvoli, diffuse alvolar damage to occur and you can lead to ARDS. So acute respiratory distress syndrome is another one. Remember, we talked about that before as well.
00:41:28 - 00:41:44
This is a pretty common ethiology, right? Here's the big one, though, and I think this is really important to remember this one because it leads into how we kind of like risk stratify, diagnose these patients, and determine which one needs hospitalization, which they'll probably test you on, and which ones don't.
00:41:40 - 00:42:04
So, sometimes, let's say that you have a really, really nasty pneumonia in this patient, right? Here's their pneumonia. And then what happens is some of the bacteria from this pneumonia seed into the circulation. That's not good. And if they seed into the circulation, now you have bacteria. Bacteria doesn't necessarily mean sepsis.
00:41:59 - 00:43:00
But if it seeds into the circulation and it starts causing potential organ failure, ooh, then we might be getting into that kind of sepsis criteria. Especially if the patient is having like hypoxmia, low blood pressure, tacocardia, tacipnia, fevers, you're getting into that range of sepsis. Now if you have a patient who has pneumonia that starts seeping into the actual circulatory system what happens is it causes vasoddilation increased capillary permeability when these pathogens get out here and uhoh what do we get? We get a low blood pressure low mean arterial pressure. We stop profusing organs my friends. And as we stop profusing organs such as the kidneys, the liver, the brain, multiple other organs, you can lead to multi-system organ failure. And on top of that, you start altering the normal coagulation system and decreasing the number of platelets that are important to form clots. And then you start consuming them to make a bunch of different clots. But then you have the chance of bleeding. What is this called?
00:42:58 - 00:43:22
DIC. So it's really really important to remember that patients who develop pneumonia have a very very high risk of sepsis. Okay? Especially going down the road of septic shock. All right, my friends. Let's now go into the diagnostics of pneumonia. All right, my friends. So, we've already talked a little bit about this already with the kind of diagnostics.
00:43:19 - 00:43:33
We talked about CAP versus HAP, but I just want to kind of take a little quick second here because there was a couple things that I said and I didn't write down, but I just want to kind of like again keep testing your knowledge, right? So, a patient comes into the emergency department. They come into your clinic, whatever it may be.
00:43:32 - 00:43:48
They're presenting with cough, shortness of breath, fever, they have low O2 stats, they're a little tipnic, they're working a little bit hard to breathe, they're short of breath, they're complaining of that, right? Their rest, their heart rate's a little bit up. You hear evidence of consolidation on their physical exam.
00:43:44 - 00:44:01
They got a productive cough. They have pleuritic chest pain or maybe they just have the atypical. So they have low-grade fevers, upper respiratory tract infections like headaches, sore throat, you know, nasal congestion, runny nose, maybe they have a little bit of myalgia, arthralgas, etc.
00:43:58 - 00:44:18
Whenever a patient comes like that and you think about the risk of them having pneumonia such as the ethologies and pathophys, the next thing is to determine is this a community acquired or a hospitalacquired. Right? So community acquired pneumonia, there's a couple different things I want you to know. So obviously it was acquired within the community.
00:44:12 - 00:44:43
So we can say it was acquired within the community up to less than two days in hospital. And the reason why this is important because this determines the risk of what types of bugs, bacteria, pathogens that the patient is most likely going to have. And you can use that degree of suspicion to say it's likely that it's cap and so I therefore can use this particular antibiotic regimen.
00:44:39 - 00:44:58
But if it's greater than 2 days in the hospital, you can't say with confidence that this is the same bug. It might be a different one. So you have to change your antibiotic regimen. That's why it's important. So community to less than two days in the hospital, they develop this pneumonia, if you will.
00:44:54 - 00:45:55
Now when patients develop pneumonia within the community oftent times it tends to be kind of this lowbar pneumonia and there's a very specific pathogen I already told you that you see in patients greater than 65 years of age elderly most common in nursing home facilities it's the most common one streptocous pneumonia so it's going to be most commonly streptococcus pneumonia second line would be homophus influenza marxelicaris in your copd patients okay the next thing that I want you guys to understand is hospital acquirement. So this would be cap. All right, community acquired pneumonia. HAP on the other hand is you have them greater than two days in the hospital and this could be in the hospital they got a tube down their airway intubated like like a VAP which is the most common subset of HAP. In this situation often times this type of pneumonia is usually bronco. So it involves the bronchi, the bronchioles and a little bit of the alvoli and it's
00:45:53 - 00:46:55
a little bit more scattered in that sense. We'll talk about this a little bit later when we get into the imaging. But oftent times for these patients for HAP the very specific types of pathogens that I want you guys to remember about for this one is oftent times going to be uh generally when we think about HAP what did I tell you before MRSA and we said pseudomonus these are the two bugs that's why it's really important to understand because when you're in the hospital you have multi-drugresistant pathogens nasty pathogens that you'll have in the hospital that you won't have in the community. That's why it's important to know this definition. Now, when you establish whether it's a HAP or a CAP based upon this type of discussion that can help you to determine your antibiotic regimen, then you kind of say, okay, I think this patient I have a certain degree of confidence that they have pneumonia. Let me get some labs. Let me get some imaging. Maybe they ask you on the clinical vignette. What's some of the labs that you would order for this patient? Or maybe they present
00:46:53 - 00:47:13
you with the labs. And you have to kind of use the clinical context, the clinical features, and based upon it being CAP or HAP, which types of labs are more suggestive or better for you. Often times, it's not really that many. There's a lot of extra labs, and I don't think they're super critical.
00:47:09 - 00:47:36
So, one of the things that I would do consider right away is what if they are presenting with features of upper respiratory tract infections. So if they have any features of upper respiratory tract infections, I would just go right away and get a respiratory viral panel because this is going to be helpful to look for maybe um influenza.
00:47:35 - 00:48:00
Maybe it'll help me to rule out some type of SARS KV2 like in um you know COVID 19, RSV, etc. So there there there's so many that I can I can pick here, but that's the first thing that I would do. Do they have any of these features? Do they have the atypical presentation? Send that off first. I would do that first.
00:47:53 - 00:48:12
The other thing here is often times just get some basic blood work for the patient. Often times if they have this pneumonia, what did I tell you? That it's going to activate their immune system, right? And if they activate their immune system, it's going to cause an immune response. It's going to release all those cytoines.
00:48:09 - 00:48:34
It'll activate their bone marrow, have them amp up their white blood cell production. So if I expect to see an increase in their white blood cells, whether this be lymphosytes more in viral or neutrfils more in bacterial, I would order a CBC. Not too bad, right? The other thing here is so if I think that that could be one potential thing.
00:48:30 - 00:49:04
The other thing here is that sometimes with these infections, they can cause that multi-systemm organ failure, right? And if I'm concerned about multi-systemm organ failure, I'm concerned about sepsis. So sometimes what can happen is I'll actually check maybe a BMP. Okay. And so if I check their BMP, what I'm looking for is is there any evidence of an acute kidney injury, increase in their BU? Is there any increase in their creatinine? Because this is telling me a little bit more about concern for organ failure.
00:48:58 - 00:49:26
So is the pneumonia causing sepsis? It's not helpful in the diagnosis. You see what I'm saying? I'd say that anything CBC would be better than the BMP in this situation. What could be potentially helpful is that whenever you are really doing this for the exam, the BMP may also show you low sodium.
00:49:19 - 00:49:57
If a patient presents with low sodium who is elderly, smoker, immuno compromised, and has some type of exposure to contaminated water sources, which one should you think about, guys? Legionella. So, think about Legionella. All right. The other thing here, sometimes some of these pathogens, okay, they can get into the bloodstream and then they can get filtered across the kidney and can get filtered into the urine.
00:49:52 - 00:50:19
Specifically, some of their antigens can be tested. And so we can test the urinary antigens. And so what I'll do is I'll test the urinary antigens specifically for strep numo and leanella. All right baby. So these are some of the things that I would start off with. A CBC to look for a luccoytosis. That's probably the easiest one.
00:50:15 - 00:50:43
A BMP to look for any acute kidney injury or hyponetreia. Acute kidney injury would be more concerning for early sepsis. Hyponetriia suggestive of leionella. and then consider the urinary antigens to look for strep pneumonia or leionella. The other thing here is that sometimes this inflammation can actually work on the liver and when it works on the liver you may have the liver increase the production of something called CRP.
00:50:39 - 00:51:14
I don't think that this is super helpful. So I wouldn't really worry about this one. The other thing is that sometimes some of these ant some of these actual pathogens may get into the bloodstream and cause kind of injury to the liver and cause a bump in the LFTs. And one of the things I would consider here is in a patient who is hyponetriia, nausea, vomiting, diarrhea, elderly, smoker, imunompromised, and some type of contaminated water source.
00:51:08 - 00:51:35
You bet it leanella. Look for this. Hyponetriia, increased LFTs. think about Legionella. All right. The last thing that I would also consider here is if you're concerned that the patient is developing sepsis, I would get blood cultures. So consider also testing the blood to make sure that the pathogen hasn't seeded into the circulatory system.
00:51:29 - 00:51:48
So checking blood cultures may also be a good thing. And then if you really want to figure out what's the specific type of pathogen because often times you'll start antibiotics empirically in really sick patients. When you get the sputum cultures back, it'll tell you, "Oh, this is the pathogen. Oh, okay.
00:51:44 - 00:52:07
It's strep numo. I don't need to have all these intense antibiotics. I can get rid of these and then use the specific antibiotic for that pathogen." So, sputum cultures may also be helpful to take and really kind of run like a suction down there. And what you can do is if you can get the suction down there and pull some of the sputum out or what usually it's in the proximal airways, you suck some of that sputum out.
00:52:04 - 00:52:26
You can suck some of that sputum out and then put it into a tube and then send that off to be tested for culture. So you can do what's called a sputum culture. And that's really just to help you kind of like narrow down the antibiotics once you get the bacteria back. Okay. All right. I hope that made sense with the labs.
00:52:22 - 00:52:47
The big ones that I would really be worthy of considering here is your CBC, your blood cultures, your sputum cultures, and your respiratory viral panel. And then potentially a BMP to be looking for and again hyponetriia with increased LTS thinking about leion. They like to ask that on the exam. Okay, let's go through imaging, which is actually way more superior and way more important.
00:52:43 - 00:53:05
I think the really really important thing to be able to elucidate here is the imaging. So, not only knowing a couple two different things, what the actual image would suggest off the chest X-ray if they present it to you, is it a low bar? Is it an interstitial? Is it a bronco? So, we'll talk about that briefly here in a second and then we'll take a look at some images.
00:53:00 - 00:54:01
But also, there's also other ways that we can define pneumonia, right? So, microbe acquisition and also location. So when we think about the actual type of pneumonia based upon location we can define them again here we have lowbar and it's not too hard uh bronco pneumonia because you know the nice thing about this is that the they were very very generous when they came up with these names and had them actually like make sense and then last one is interstitial and I think there's two particular um things that I want you guys to take away from from this kind of like location description of pneumonia. So lowbar pneumonia, it's straightforward. It's a pneumonia that's occupying one of the loes of the lung. So if I had a pneumonia here, I could have a bunch of different types. I could have a right upper lobe, a right middle lobe, right lower lobe, left lower lobe, left upper lobe pneumonia. In this situation, I'm just going to pick a right lower lobe pneumonia. Right? That's that's all it is. But the big pathogen that I want you guys to be thinking about because they
00:53:59 - 00:54:23
may ask you this is already talked about up there. Strep numo. Strep pneumonia. I'm going to put strep pneumonia right there. Okay, the next one is if you have a bronco pneumonia. It's not hard. It's involving the bronchi and the bronchioles, maybe some of the alvoli as well. So, it's going to have like patchy, it's going to be very patchy and it's going to be extending kind of scattered throughout the lungs.
00:54:22 - 00:54:52
So, it'll be kind of like very very patchy opacities that you'll see bilaterally. This is bronco pneumonia. And usually the microbes for this one if it's hospitalacquired yes it's MRSA it's sudamonus but if it's community acquired that's a different situation. So what I want you to remember is if it's communityacquired pneumonia I just do it like this because it helps me to remember it.
00:54:44 - 00:55:13
Staflacus arius streptoccus pneumonia hopus influenza and klepsiella for the community acquired bronco pneumonia. For the hospitalacquired pneumonia, we already know MRSA and sudamonus origin. So I'm going to put PSA there. Okay, so that's really what I want you guys to be thinking about. Okay, so if we have a low bar pneumonia, it's situating to one of the loes.
00:55:10 - 00:55:36
If it's bronco, it's involving the bronchi bronchios. It's scattered bilaterally like these kind of like patches. Interstitial, it's involving the interstitial spaces. So the pathogen is kind of infecting not the lung parankma itself. It's causing infection here in the interstitial spaces. And this, my friends, is very common with your atypical pneumonia.
00:55:33 - 00:56:34
What did I tell you was atypical pneumonia? The way that I wanted you guys to remember it, MCL and viruses. So MCL, myopplasma, chlamyia, leionella. Which one would these be the most common out of those three? Myopplasma. young children in college dorm like college or dorm rooms very close contact occupied spaces they're young healthy and usually that's going to be one of the most common types of atypical don't don't forget that one if it's like um young kids in very close contacts like generally like dorms are the best examples that they'll present this in or or like you know uh boot camps and things like that but the other one will be viruses all right I think that gives us a pretty good idea of the types of pneumonia that we have on imaging Now, let's take a look at a bunch of imaging. All right, my friends. So, I think one of the big things to think about is, okay, we get imaging. Well, what kind of imaging do we get? Do we get a chest X-ray? Do we get a CT? Often times, a chest X-ray should be the initial test. Whenever patients coming in with like shortness of breath, this neopluritic chest pain, they got perin
00:56:32 - 00:56:50
cough, any kind of thing like that. It's not a bad idea to just start off with a quick initial chest X-ray. It's ease of access and it's going to be a quick one that you can get done. So, I would do that one first. The only time I would really do a CT is if you don't really know what's going on off their chest X-ray.
00:56:46 - 00:57:01
their chest X-ray is inconclusive. Um, you are treating them for pneumonia and they're not getting better. Um, and then the only third reason I would say is if they're immuno compromised. So, I'd say three reasons why you get a CT. Chest X-ray is inconclusive, but you still have a high degree of suspicion that it's pneumonia.
00:57:00 - 00:57:19
You're treating them for pneumonia. They're not getting better. Um, and then third is they're they're imuno compromised and you think that they may have some type of weird pneumonia um that was worthy of taking a better look at. Okay, so first one here is bronco pneumonia. How can I tell? It's not situated to like a particular lobe.
00:57:15 - 00:57:38
I can see that there's like patchy. You see how there's like patchy consolidation here, patchy here. It's kind of uh patchy over here. So, it's this patchy kind of bilateral consolidations in both lungs. That's bronco pneumonia. Think about this in outpatients with that stafloccus, streptocus, hmophilus, and klepsiella.
00:57:37 - 00:57:57
If it's hospitalacquired, think about MRSA and then sudamonus. Okay, let's take a look at another chest X-ray. All right, my friends. Here's another chest X-ray for a patient who came in. They had headaches. They had uh kind of like some nasal congestion, rhinora, sore throat, earachches with bullis maringitis.
00:57:52 - 00:58:53
Um they had some low-grade fevers, myalgis, arthralgis, they're young, they're they're living um in a dormatory and boom, you think about myopplasma, right? Or chlamyia. That'd be another one. And if I said contaminated water sources in an elderly young individual who smokes or amunosuppressed and etc. you think about Legionella or viruses, but this right here, when you see this kind of like fine like threading, like it almost looks like a ground glass type of appearance, it just looks really really odd. Um kind of like someone who's like out in the winter and you're blowing on like the the glass when it's really cold and it kind of looks like that. It has that kind of ground glass opacities, but it's very very fine reticular markings that are moving from the hilum outwards towards the plura. This is very very classic of your interstatial pneumonia. Okay. So this would be on your differential for myopplasma, chlamyia, leionella, and viruses. All right, my friends. So we're taking a look here at what's called a PA and lateral chest X-ray. That's deser that deserves
00:58:50 - 00:59:09
another question. Which type of X-ray do I put into the thing? Like if they ask me like what kind of X-rays are the best if they asked me. The best would be a PA and lateral chest X-ray. APs can kind sometimes distort the anatomy and kind of not provide the best clinical picture.
00:59:05 - 00:59:25
PAS are going to be really really good pictures um that will really kind of enhance the you know the chest wall and show pathology and lateral X-rays are really good because sometimes you can't see those lower loes on a PA view and so if you put them in a lateral X-ray you can get that lower lobe view which is really nice. Okay.
00:59:22 - 00:59:42
So, I'd say PA and lateral chest X-ray are going to be the best test that you can do if you had to pick between the chest X-rays. PA lateral because PA will give you the upper lobes and like maybe a little bit of like the right middle lobe, but the lower lobe sometimes can be hidden and then you can get that better on that lower that lateral chest X-ray.
00:59:38 - 01:00:02
So here we can see right upper lobes look good. Left upper lobe looks good. Right middle lobe looks good. Can't really see the right lower lobe. Left lower lobe I'm seeing some opacity here because it's kind of like obscuring the edge of the heart like that left heart border, but I might be missing some of the lower parts going down into the behind this diaphragm portion.
00:59:58 - 01:00:16
So I put a lateral in there. And look at that. I can see here in this like left lower lobe really consolidated area here. They got a left lower lobe pneumonia. So, that's what you'd be looking for and thinking about strep numo is a big one here. Okay, let's take a look at another X-ray. All right, my friends.
01:00:13 - 01:00:34
Here's another X-ray X-ray. Look at that. Right upper lobe. Looks clean. Right lower lobe looks clean. I'm able to kind of pick out my right heart border. Left heart border here. I can kind of make it out. So, I definitely don't see any opacity of the left lower lobe, but I'm kind of obscuring over here near the left kind of portion of the medastinum near the aorta and the pulmonary knob.
01:00:29 - 01:00:49
I'm kind of obscuring my left upper lobe. It looks hazy. It looks opacified. That's a left upper lobe pneumonia. Okay, that's a low bar pneumonia. Let's take a look at another one. All right, my friends. So, here I can see here my right upper lobe looks clean. My left upper lobe looks clean.
01:00:44 - 01:01:05
I can see pretty well my left heart border. So, left lower lobe looks relatively good. But look at that. My right heart border I can't actually make out completely. And there's a little opacity or hazy consolidation here on that right middle lobe portion. That's a right middle lobe pneumonia, my friends.
01:01:02 - 01:01:22
All right, let's do a look at another X-ray. All right, so here's another one. I look at my left upper lobe, it's clean. Look at my left lower lobe, it's clean. I can see the nice left heart border. Right heart border is nice and clear. So, I don't have a right middle lobe pneumonia. If I had a lateral view, I'd be get I'd be able to get a better view of my right lower lobe and my left lower lobe a little bit better. But I don't have that here.
01:01:19 - 01:01:35
But what I do see that pops out like a sore thumb is this kind of right upper lobe opacity. And I can even kind of see because see know here's the fissure. So you have your horizontal and your oblique fissure that would come down here. I can already see my horizontal fissure here.
01:01:33 - 01:01:54
So there's kind of like that little fissure that's bulging there. And then again, I know that I have like this opacity that's involving my right upper lobe. So think about that one as well. Okay. All right. Let's take a look at another type of image. All right, my friends. So this is a CT. So again, in this patient, we ended up getting a chest X-ray.
01:01:50 - 01:02:09
They had an interesting type of kind of consolidation involving like their right upper lobe, even getting in to a little bit of their middle lobe, but primarily kind of like their right upper lobe was really getting hit. And what we are concerned about is kind of like the way it looks.
01:02:06 - 01:02:23
So, what I wanted to do is I wanted to show you something really interesting on the CT, why it's so good. It really is like the best for pneumonia. Um, but we try to just reserve it if we're kind of unclear. We don't have enough from our chest X-ray, they're not getting better with antibiotics or they're imuno compromised.
01:02:19 - 01:02:39
When I look at the CT here, look at the right lung. You can already kind of see here in this right hemithorax here. You can see kind of this hazy opacities in comparison to the left one. Looks nice and airrated. And as I go down, it's getting worse. More opacities, more opacities, more opacities, more opacities. And boom. You see something really interesting.
01:02:35 - 01:02:54
You see how here's like a bronchus that's kind of coming off here and it's moving into this consolidation and it's open. There's a lot of air moving into it and then it stops. It's like a cut off here. [snorts] These are called air bronco. This is very characteristic of pneumonia.
01:02:50 - 01:03:17
So if you see a consolidation and you see these opened up air kind of filled cavities moving into the consolidation that is called a air bronco. Pretty consistent with a patient having pneumonia. Okay. So that would be a right kind of lobe pneumonia. Generally it's kind of if you kind of look here you can see it's actually hitting more of in this patient's case it's definitely involving more of their upper lobe.
01:03:14 - 01:03:36
All right my friends let's now talk about the treatment of pneumonia. So we're going to talk about this in particularly focusing on the antibiotics that we're going to use to treat the infection. It's an infection of the actual lung tissue, right? So the primary focus should be treating the actual infection. There's a lot of supportive measures that come into it as well.
01:03:31 - 01:04:31
Obviously treating potentially the hypoxmia that they may have the work of breathing. We're not going to go into that. We talked about that with the acute respiratory failure lecture. But what I really want us to focus on is here the antibiotics. But the antibiotics are really really kind of dependent upon what kind of pneumonia we have and that's really dependent upon how we stratify these patients and determine their need for outpatient care in hospital care but not in the ICU and then ICU level care or they've been in the hospital for a couple days more than two days more than 48 hours and they've developed pneumonia so they have a HAP right so let's talk about this really quickly so you have a patient come in and this is really only applying to what's called the community acquired pneumonia. So, this is really trying to determine is this a community acquired pneumonia that can go home, to the floor, or to the ICU. The way that we do this that they will likely ask you on the exam is something called the curb 65 score. And so really what this consists of is confusion. So you're probably like, wait, Zach, where did confusion
01:04:29 - 01:04:46
come into play? Remember I told you that if a patient gets pneumonia, one of the complications is the bacteria can seed into the bloodstream cause in a decrease in their minor arterial profusion. They don't peruse the brain as well. They don't peruse the kidney. They don't peruse the liver, they develop multi- systemm organ failure.
01:04:43 - 01:05:04
One of the first things for elderly individuals is that they develop confusion or altered mental status. And this is due to kind of the septic feature. So if they're already presenting with sepsis, isn't that a concerning sign? Absolut stinking lutely it is. So confusion is a very concerning sign. The next thing here is uremia.
01:04:57 - 01:05:24
Now uremia, wait, Zach, uremia, wasn't that with the you know the increase in the ura off of the patients uh uh particularly their BMP? And whenever we say the uremia is present, we say greater than like 20. So we're saying like greater than like 20 in this situation. That would be concerning. What that would tell me that they have an acute kidney injury telling me that they're decreasing the profusion to their kidneys potentially.
01:05:21 - 01:05:40
So they have an acute kidney injury. Yeah, that's a concerning sign. That means that they need to be hospitalized. Zach, what if their respiratory rate is like really high? It's like greater than 30 breaths per minute. They're like breathing super super fast. They're super tic. Their work of breathing is very scary.
01:05:37 - 01:05:54
Would I feel comfortable sending that patient home? No, that's a very concerning sign and that is another big one. The next thing is blood pressure. Blood pressure. Blood pressure. That was the thing with the map, right? The mean arterial pressure that's dropping. If they're hypotensive, is that the problem? Absolutely.
01:05:50 - 01:06:14
So, if their blood pressure is low, and what I mean by low is we're talking about two particular parameters. If their systolic blood pressure is less than 90 millimeters of mercury or if their diastolic blood pressure is less than 60 millimeters of mercury, this is a concerning sign. And the last thing is patients who are greater than 65 years of age, they're obviously at higher risk of worse outcomes.
01:06:10 - 01:06:33
And so because of that, that's we're assuming that as you get older, your immune system is becoming compromised. You have an impaired mucous clearance. And also, you likely have other co-orbidities that put you at higher risk and we don't feel comfortable sending those patients home sometimes. And so if you are 65 years of age or greater, you are at high risk.
01:06:31 - 01:06:54
And what we do is we sum up all the points. So if you have one of these, you obviously get a point. And what we do is we kind of risk stratify based upon their score. If their score is between zero or one, that's a patient that I feel relatively confident that does not have sepsis multi- systemm organ failure and can decompensate.
01:06:48 - 01:07:14
I can send these patients home. So this would be a cap outpatient. Okay. If their score is two, okay, then I'm a little bit more concerned for this patient. This is a patient that could potentially decompensate and they need just a little bit more observation. Maybe not an ICU level care, but they need some observation.
01:07:09 - 01:07:32
So, this is a CAP, but this is going to be a nonICU admission. Okay. And the last one is they have three plus. This is a patient that you're very concerned with. They have a very high mortality rate and we should not send them to a a home. We should not send them to a nonCU. They need a very close observation and very aggressive care.
01:07:28 - 01:08:28
These are patients that have a community acquired pneumonia and require ICU level care. So that's how we should risk stratify these patients. Okay. But I want you to understand why we use the curb 65 and what's the purpose of looking at these parameters not just memorizing it. Okay. Now we've risk strratified, we've determined those with high mortality, low mortality, intermediate mortality and then we say okay now that I have kind of a sequence I can treat these patients accordingly to CAP outpatient, CAP 9 ICU, CAP ICU and then what else? HAP hospital acquired. Let's talk about that. All right. So when we talk about these patients, we now can kind of group them into the CAP outpatient CAP inpatient CAP ICU and then we'll talk about the HAPS, right? Greater than the two days in the hospital and then we'll briefly briefly talk about aspiration. We won't spend a lot of time on it. Now with CAP outpatient, what I want you to remember is in these particular populations, you're really kind of thinking about the atypicals. That's the big big one. Possibly even strep pneumonia as well. So for that what really covers the shrep
01:08:27 - 01:08:48
pneumonia covers the atypicals pretty well the first option that I would consider in these patients would be your macrolytes. So a zithroyc um would be kind of the one or doxycyc which is one of those particular I'm going to put doxy which is one of the actual tetracycans that we can consider as well.
01:08:44 - 01:09:11
So doxycycline would be a pretty good one as well as um a macroy is the other alternative option there. Okay either one. The second option here would really be a respiratory floricquinolone. And the reason we would consider this, don't do this one first just because of high resistance. I would really only do this if a patient has an underlying comorbidity that puts them at high risk or they've gotten antibiotics in less than the past 90 days.
01:09:07 - 01:09:30
If they have, then you can consider that they may have a little bit higher resistance. And so because of that I would then say okay a respiratory floricquinolone may work well if they had antibiotics in the last 90 days or a co-orbidity they're present. Okay. All right. So that would be that situation there.
01:09:29 - 01:09:57
Next one. If a patient has community acquired pneumonia and they're actually in the hospital but they're on observation not in an ICU setting. You can do somewhat of the same thing here. We could still do a respiratory floricquinolone. That's definitely an option here as a monotherapy. The other option here is I would consider doing same thing up here a macrolyide or doxy plus a betalactam.
01:09:54 - 01:10:19
And the preferred betalactam is obviously dependent upon where you are in the world in the hospital but oftent times the most preferred agent is sept trioxone. Okay. Seph trioxone is one that I would definitely consider. All right. For a patient who is in the ICU, they have community acquired pneumonia.
01:10:14 - 01:10:47
They're in the ICU. In that situation, you could do somewhat of the same thing. But unfortunately, we kind of get rid of the doxycycline. And so, all that changes here is we can do two options here. One is we can do a macrolyide, so a zithramycin, or we could do a respiratory floricquinolone. The only thing that's different is I add a betalactim to one of these particular regimens.
01:10:41 - 01:11:10
It doesn't matter which one you pick. Okay? So you can pick either one of these as an option. So this would be how we would start cap outpatient, macrolyte or doxy just by itself or a floricquinone only if you meet this criteria. Cap in the hospital it's a little bit different. You can do respiratory floricquinone by itself or you could do macrolyide or doxy plus betalactum.
01:11:05 - 01:11:33
When you get into the ICU, you don't use doxy. It's usually macroly plus a betalactum or respiratory floricquinolone plus a betalactum. That's it. Preferred sept trioxone is a betalactum of choice. Sometimes you can do augmentin which is a moxicylan clavulanate is another option as well or aecylan sactin which is also known as unison but this is usually the easy one to remember.
01:11:26 - 01:12:26
pap this is generally greater than two days in the hospital right so whether this is with a tube down your airway or not you're in the hospital for two days or more and you have pneumonia it is now a hap you're covering a different type of bug what is the bugs that I told you to not forget the first one is don't forget about MRSA so generally you treat with venkcomy another option is called lenazolid Okay, sudamonus originosa in this situation what are we covering with there's so many of these so I'm going to abbreviate but we call this piperylin tasobactum sometimes pipaso or zosin the other one is called sephop and the other one that I would also potentially consider here is your amoglycosides so to me genttoycin amicin I would really avoid these though
01:12:24 - 01:12:56
they're really harsh on the kidneys So, I'm going to put amino glycosides, but I would really try to avoid these as an option in the the test question as well as in real life. Okay. The other thing that I would also consider here is if a patient is HIV positive, let's see if you guys remember this, HIV positive and their CD4 count is less than 200.
01:12:49 - 01:13:18
I suspect PJP. what should I treat them with because PJP is a really really nasty one and this one I treat them with what's called Bactrum trimethopre sulfomthoxisol. The only other thing I would add on is is that sometimes you can add on um a fluoricquinolone a respiratory floricquin like levofluxin or amoxifyin if you think that the patient has leionella.
01:13:14 - 01:13:36
If they do have leionella you can add on a respiratory floricquinolone but let's not get too far down that rabbit hole. These are the big things that I really want you to remember that you may get on the exam. The last one is aspiration. I don't want you to get too locked up on this just because I don't think that it's actually super correct to be honest with you according to what you'll need to know for the boards um in comparison to true life aspiration pneumonia. Think about it.
01:13:32 - 01:13:55
What kind of pathogens? Anorobes is the big one. What is the lung? Is it airrated very very aerobic or is it anorobic? The lung is filled with oxygen. So it's going to be hard for an anorob to be able to survive in the lungs, right? So therefore unless the patient has a lung abscess or unless they have an empa, we don't really treat for anorobic infections with these particular bugs.
01:13:51 - 01:14:23
on the exam you do but in real life you don't. So what are these? Think about clintomy. Clintomy would be one potential option here. Um another one may be what's called um augmentin. So augmentin. So we call that amoxicylin clavilonate. It's called augmentin. And the third option that you may consider, again, I really don't think that this is worth mentioning, but metroniditool plus a betalactin, but these are things that you may see on the exam.
01:14:19 - 01:14:38
If you had to pick between one, I pick clinomy if they really ask you. But often times, because the lung is so airrated, we don't treat aspiration pneumonia with these types of pathogens. We just treat it as though it's a hap or a cap. Same treatment unless they have a lung abscess or an empathema.
01:14:34 - 01:14:58
Then we treat with the clintomy or the augmentin or the betalactam and then the uh metroniditool. All right my friends the only thing I would actually tell you guys to remember potentially for the treatment of pneumonia is just remember prevention. How do we prevent this? We'll talk about it more in the vaccinations lecture but you're going to be talking about your numacco vaccination.
01:14:52 - 01:15:12
So PCV13 generally at 2 416 uh 2 4 6 and 12 to 15 months of age and then the PPSV23 vaccination that you get at 65 years of age or older or if you have a lot of underlying conditions that make you at risk in patients 2 to 64 years of age. But that'd be a good prevention that they could ask you. All right, that covers pneumonia.
01:15:09 - 01:15:35
All right, my friends, let's do another case study here. So here we have a 72-year-old male presented to the Niner Clinic with perilin cough, dysnia, riyers, and progressive confusion. past medical history for COPD, diabetes, and HIV. So, we know this patient is going to have pneumonia, but some of the features here that are s suggestive of pneumonia and are concerning is because she has a perllin cough.
01:15:31 - 01:15:52
So, she's got a perllin sputum production. She has dysia. So, dysnia could be indicative of a lot of the consolidation causing hypoxmia to some degree. She's got riyers, which could be due to the fevers from a bacterial type of source here. If she's got progressive confusion, maybe kind of s suggesting to some degree that she has some type of organ dysfunction.
01:15:48 - 01:16:10
She may not be kind of allowing for proper profusion of the brain. And so, especially in elderly individuals, we can see that. So, concerning finding there, but her past medical issues also kind of supportive of worsening kind of lung problems. COPD can cause a lot of nasty bugs there. Diabetes makes her a little bit more of imunocmpromised.
01:16:08 - 01:16:30
Plus, she's HIV positive. That also makes her super imuno compromised. So she's got a lot of risk factors here for increasing the risk of her having some type of pneumonia. COPD again a lot of thickening secretions a lot of bronco spasm and again because of the not being able to beat the mucosil apparatus that's a problem.
01:16:26 - 01:16:49
Diabetic she's also kind of imuno compromised HIV imuno compromised may not be able to have the immune system response that she needs to fight off any kind of normal pathogens in her airway. So very concerning findings here. So, and she's 72, which makes her a little bit more elderly and again reduces the amount of psyia, reduces that kind of fight process there.
01:16:45 - 01:17:08
So, concerning findings here, oh, vitals are not very good at all. She's in big trouble. So, vitals BP is 80 over 50, so she is hypotensive. She's slightly tacocartic, so heart rate's 110. Respiratory rate is 32, so she's slightly typnic as well. Um, and then her temp is elevated, so she's got a temperature of 101 degree Fahrenheit.
01:17:02 - 01:17:28
So she's febal typnic tacocartic and mildly hypotensive. And on top of that her SPO2 is dookie. Um so she's on 84% and she's already on FiO2 of 60%. So she must be on some type of supplemental oxygen source that's giving her 60% FiO2. So maybe some type of like highal canula or you know etc.
01:17:24 - 01:17:55
So in general this is a concerning finding for this patient. So she's hypoxmic on oxygen supplementation, febra, tekypnic, tacocardic and hypotensive. So very concerning signings. Now when we go to the chest and we go to examine this patient, we want to think about signs of consolidation. So things that are going to actually alter the kind of like process of oscultating, altering the process of tactile primitus, oscultating the process of like the sounds or whispers um and percussion.
01:17:51 - 01:18:13
So how do we find concerning findings of consolidation? So if we hear bronchial breath sounds that means that there's a consolidation as the bronchus is actually trying to run into the smaller bronchios it's running into a consolidative area. So we're going to hear the breath sounds proximal to that consolidation such as bronchial breath sounds when we're percussing.
01:18:08 - 01:18:32
Generally anything that's more fluid fil or pusfilled in this kind of case is going to give a more dull type of percussion and it's going to be louder on tactile feminis too. So they'll have an increased tactile feminis. They'll also have a positive broncophony, egoffany, and whisper pectiloquy on their specialized tests.
01:18:27 - 01:18:45
Okay, so that's important as well. So these are all findings that are supportive of consolidation here for this patient. So how do we go about diagnosing pneumonia? Well, there's a lot of different things that we can do. We can get a bunch of different labs. We can get a bunch of different imaging.
01:18:41 - 01:19:02
I mean, obviously starting off with like a CBC wouldn't be a bad idea and a CMP. Um, so what we would see with the CBC in this patient is that she has a luccoytosis. So she has an elevated white count, maybe supportive of an infectious eeteology. Her CMP shows a BUN of 30. So she's got an elevated BUN.
01:18:57 - 01:19:19
Um her creatinine was also elevated slightly. Her LFTs are normal. Her sodium is normal. Again, this is important when it comes to Legionella. Her blood cultures when we actually tested her and then she ended up going into the floor. Um well actually we'll see where she'll where she'll be able to go, but she goes somewhere in the hospital.
01:19:15 - 01:19:39
Um her blood cultures actually came back positive for homophilus influenza and streptococcus pneumonia and then her sputum cultures were positive for PJP Hlflu and streptococcus pneumonia. Um her CD4 count because she is HIV positive we wanted to check is less than 200 and her imaging on chest X-ray shows bilateral patchy consolidations.
01:19:35 - 01:20:02
So this woman has got a lot of different problems here. So what we're seeing is she has a bacterial infection, right? Both bacteric and pneumonic. She has HIV with a very very low CD4 count and she's definitely got bilateral patchy consolidation supporting more of like a bronco pneumonia type of finding. So she's got a luccoytosis.
01:19:57 - 01:20:20
She has potential uh signs of acute kidney dysfunction, bacteria, positive sputum cultures, and the source of her bacteria is probably from her lungs. And she's got a low CD4 count putting her at high risk of PJP, which she's positive for. And her lungs are supportive of consolidated findings here.
01:20:16 - 01:20:37
So, she's definitely got a really, really bad pneumonia, secondary to strep numo and H flu. And then she's also got a little bit of PJP due to her CD4 HIV less than 200. Okay. So what are the three types of radiographic pneumonia? I talked about bronco pneumonia but what are the different types? So there's lowbar, bronco and interstitial pneumonia.
01:20:33 - 01:20:55
So lowbar pneumonia is when it's usually like a socked pneumonia. It's consolidated to potentially usually one lobe or two loes. So generally it' be like a right middle lowbar pneumonia right low lower lobe uh kind of like lowbar pneumonia. So it's usually kind of socked up. Usually we very commonly see this in numaccoal pneumonia.
01:20:52 - 01:21:53
Broncoon is more scattered, bilateral, patchy, and usually we see that kind of involving like the smaller bronchios and alvolar tissue as well. Usually you can see a lot of different bugs that cause this one. Um, and then the last one here is interstatial pneumonia. So you see a lot of kind of like interstatial infiltrates um and usually like this reticular reticular nodular kind of opacification and we usually see this with like the myopplasma, the chlamydia leionella. Um, so that's important to remember here. Whereas the bronco you see things with like staff and strep and hmophilus and klepsiella a lot of different bacteria. All right. So we have a patient who we're definitely concerned has pneumonia. I think the question that we have to ask ourel is is this a a community acquired pneumonia or a hospitalacquired pneumonia? Well, she just got into the hospital. She just arrived. She's not even been in the hospital for more than 48 hours. So because of that I would say that this is a community acquired pneumonia. She acquired this in the community. She hasn't even been in the hospital for very long at all. So what level of care is another great question to ask that
01:21:51 - 01:22:10
this patient may require and how does actually one go about determining what level of care. So remember I told you about the curb 65 score. So what out of these does she have and then based upon that what puts her at high risk. So you see here her curb 65 score she has confusion.
01:22:05 - 01:22:29
We actually see that in her HPI. She does have uremia. Her ura was greater than 20. It was actually 30. Her respiratory rate was 34 I believe. So she's got typia. that kind of supports that her BPs are soft, so she had an 80 over like 50, so she kind of fulfills that. And she's 72. She's greater than 65 years of age.
01:22:24 - 01:22:50
She has all of those findings. And so, generally, when someone has like findings that potentially high, like three or more, um, that's very concerning and they require ICU level care. So, this patient needs to go to the ICU. Now, when we send her to the ICU, we're going to start her on antibiotics because obviously the c the source of this is a bacterial pneumonia.
01:22:45 - 01:23:09
There's so many different types of bacteria that can cause pneumonia, but likely hers is again because she's 72 and the most common cause of community acquired pneumonia in elderly individuals is streptoccus pneumonia. And on top of that, she has COPD and diabetes puts her at high risk for hemophilus influenza.
01:23:07 - 01:24:10
and she's got HIV which puts her at risk for PJP. She's got a multi- bacterial type of polyicrobial pneumonia here and with evidence of sepsis too, my friends. So, she's also septic. So, with that being said, if we were to kind of treat, let's say that we didn't we excluded sepsis at this point in time and we were only treating the pneumonia, we were not treating the sepsis, what kind of antibiotics would we put her on based upon her curb 65 score putting her in the ICU level care? Well, we would do a betalactim and a macrolyte generally is going to be the first thing that we'll do here. Or we can do a floricquinolone and a betalactim of some type, right? But these these would generally be what you would start a patient on. So you would do this and get them started on this and then when their cultures come back as we already have them now, we would narrow down according to what we think is best. But again, I think a betalactto and a macroyte or a betalactam and a fluoricquinolone would put her in this kind of ICU level
01:24:06 - 01:24:38
category. Now, if we had her becoming septic, we could potentially change the antibiotics up a little bit. Often times patients just get put on something like venkcomy and piperasobactum. But I think the best thing here is that she would be appropriate with a betalactam antibiotic um such as sept trioxone um and a macrolyte such as something uh as we've talked about before like a zithroyc um in in this particular situation.
01:24:34 - 01:25:02
If that wasn't appropriate you could do a betalactone like sept trioxone and a fuoricquinolone. If there was concerns that she had MRSA, which she does not have MRSA because our cultures came back with no MRSA, we would treat her with venkcomy. If her cultures came back positive for sudamonus originosa or we had concerns for that, then we put her on something like piperentesact or sephopene, but she doesn't have that.
01:25:00 - 01:25:17
So, we're going to treat her for what we would suspect based upon what the guidelines are that we talked about in the whiteboard and what her sputum cultures and blood cultures came back positive for. Betalactam and a macrolyte or betalactam and a floricquinolone would be appropriate here.
01:25:14 - 01:25:44
There's one other thing that she did test positive for which is PJP and PJP generally we should treat these patients with backrum. So I would also add on backumrum in this particular situation which is the trimethopram sulf with oxazol. The next question that I actually did kind of lead into this is that when you have pneumonia, one of the complications of pneumonia, obviously you can get things like ARDS, you can get paranormmonic eusions that can lead to empathemas.
01:25:40 - 01:26:07
There's a lot of different things that can happen with this potential disease. But one of the worst case scenarios that we can see here is that the patient can actually kind of seed some of the bacteria into their circulation, their systemic circulation, which can cause worsening features of hypotension, tacocardia, severe fevers and then sometimes becoming refractory to fluids and vasopresses.
01:26:03 - 01:27:04
We can see the patient becoming septic and going into septic shock. So right now the patient does have features of sepsis and some degree of septic shock because they are lower on the blood pressures and we're seeing organ dysfunction now. So I would say that this patient is in the point of septic shock which is concerning and again we would treat the patient accordingly for septic shock such as putting them on vasopressors uh fluids you know with a minimal kind of fluid approach and then on top of that considering things such as um you know antibiotics obviously that we would already have this patient on for their pneumonia. So treating their pneumonia, vasop pressors to support their blood pressure, plus or minus a little bit of fluids, just being careful not to fluid overload them. But anyway, that's how we would go about this patient. Now, getting back to the actual concepts here that I need you guys to remember for the exam is remembering these buzzword terms. And so thinking about the microbe can really come ac across on the
01:27:02 - 01:28:03
clinical vignette. So if they kind of use the term strep pneumonia um or you think that it's strep pneumonia which one of these would be more of a support of strep pneumonia and I want you to think that it's the most common cause of community acquired pneumonia and elderly individuals that's streptoccus pneumonia all right staff I want you to think about postinfluenza and IV drug abuse and again think about MRSA as a hospitalacquired pneumonia type of pathogen that's very very dangerous [cough and clears throat] Pardon me. The next one is Hfluxella. So [clears throat] for Hlflu Maracella, I want you to think about COPD years and even some degree bronchiacttois. The next one here is klepsiala. Think about alcoholics and CNS disease and depression. Anything that increases the risk of aspiration would be klepsiella. And then sudamonus definitely think about imuno compromised or imunosuppressed and cystic fibrosis is a
01:27:59 - 01:28:22
harbinger for sudamonus as well. Myopplasma think about young healthy and close quarter living especially dormitories. [clears throat] Legionelli you want to think about contaminated water sources. They're smoker. They're elderly. They're imuno compromised. That's the big one there. [snorts] U PJP think about HIV AIDS.
01:28:17 - 01:28:46
CD4 count less than 200. Coxidomicosis is the fungus in the southwestern United States. So California. And then you have the next one here which is hystopplasmosis. This is the bird or bat droppings that you see during the spelunking kind of events uh in the Ohio and Mississippi River Valley. And then blasto micosis.
01:28:41 - 01:29:06
Think about the yeast from the east. All right. So eastern uh United States think about blasto micosis. And then lastly anorobic bacteria think about in situations of aspiration events. All right my friends that covers pneumonia. I hope that it made sense. I hope that you guys enjoyed it. As always love you. Thank you.
01:29:00 - 01:29:09
And until next time, [music]
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