Infective Endocarditis

what's up ninja nerds in this video today we're gonna be talking about infective endocarditis a lot of talk about we're gonna have some fun if you guys like this video you benefit from it it makes sense please support us and the best way you can do that is by hitting that like button counting down the comment section most importantly you gotta subscribe also if you guys want some awesome notes some amazing illustrations to follow along with during this video go down the description box below we'll have a link to our website where you guys can check out all that stuff and follow along all right let's get into it let's talk about infective endocarditis all right infective endocarditis when we talk about this disease we have to have a basic definition talk about the causes and well then we'll go into more pathophys and clinical features etc all right basic definition of endocarditis very simple it's inflammation of the endocardium usually due to some type of microbial pathogen that's it it's a simple concept right so what i want us to do is actually take a look here at the different components and structures of the heart that are relevant in this disease so here we have a view of the heart here we're going to have the left side of the heart so we'll have left atrium we'll have left ventricle right ventricle right atrium obviously here you have your pulmonary trunk and then here you have your aorta if you look here inside the chambers of the atria the ventricles and even the outflow tracks into the pulmonary artery and aorta they all have this green lining on the inner component of it what is that that's the endocardium that green stuff right there right there is the endocardium so in someone who has endocarditis there's inflammation of that layer what does that layer cover it lines the chambers of the heart but you know what we really care about it's this we care about the heart valves the heart valves have a layer of endocardium what is endocardium really what is that it's a simple squamous epithelial tissue with a little bit of areolar connective tissue that's all it is we have that layering the heart valves and someone who has endocarditis they develop inflammation damage or destruction of that endocardium and then they form these nasty microbial vegetations and there's so many different complications of these dang little goombox on those heart valves and we'll talk about what those complications are later but here's what we have to discuss what are the things that lead to this what caused these microbial vegetations the erosive damage by the vegetations the septic emboli the immune complexes and even the septic appearance in these patients we have to talk about that before we do that we have to have one more little advanced definition of infective endocarditis there's actually two types all right we have something called acute infective endocarditis acute infective endocarditis is one of the ways that we can define this condition meaning that these patients look really sick they look septic appearing so they can have very tenuous hemodynamics they may be hypotensive they may have significantly high fevers they may have like new heart failure or worsening heart failure symptoms they can have septic amylase that are popping all over the place these are really really sick individuals and the big thing i need you to remember about acute infective endocarditis is the inflammation of the endocardium of the heart and heart valves due to a really highly virulent pathogen so this is due to a very highly virulent pathogen and there is a bunch of these but there's only one that i really think is worth you guys actually remembering you know what that is it is good old staphylococcus aureus don't forget that bad boy okay so acute infective endocrine is the first thing that i want you to understand within the definition of infective endocarditis septic appearing patients high fevers heart failure that's new or worsening a lot of murmurs now septic emboli immune phenomenon and these are due to highly variant pathogens such as staphylococcus aureus there's another definition of this a sub definition that we call subacute infective endocarditis in this condition here these patients don't look as sick okay they're not as sick they may be relatively well let's just actually put not super sick i know that's really basic and we'll go into what that looks like but these patients honestly they have may have very like non-specific symptoms they may have very low grade fevers they may have some types of like dyspnea shortness of breath some fatigue ability but nothing truly that points out that an obvious infective endocarditis it's a little bit more difficult to diagnose one of the big things with this one is that this indolent course is usually due to low virulent pathogens and so these are not really damaging types of pathogens and the best example that i can think of for this one out of all that we'll talk about is streptococcus viridance okay so what i really want you to obtain about the definition of infection endocarditis is yes it is the inflammation of the endocardium particularly the endocardium that lines the heart valves is the most susceptible and is due to pathogens we can further classify that into acute subacute acute really sick subacute not as sick appearing acute due to highly virulent pathogens subacute less virulent pathogens acute staphylococcus aureus is that nasty pathogen and subacute streptococcus veridians is the more common pathogen now we have the basic definition here okay what we need to do is now talk about how does these nasty vegetations form and the downstream effects of it well the first thing that you have to remember is there's some type of abnormal valve that there's a predisposition to this condition what do i mean let's say here i have an abnormal heart valve and for some reason there is damage to that endocardium okay i damage the endocard you know the endocardium is really cool because one of the cool things about the endocardium is that the endocardial cells release particular types of molecules like prostacyclin so you know what they usually release they release things like pg i2 they release things like nitric oxide and what these do is they inhibit platelets from sticking but if you have damage to the endocardium can you release nitric oxide can you release prostacyclin now no this process is inhibited and you can't inhibit the platelets from sticking now and now the platelets just go ahead and say hey baby i see some underlying collagen i'm going to stick stick sticky to it and then these platelets come and they bind and form this nice little platelet plug on that area where there's damage to the heart valve and the underlying endocardium is now ripped or sheared off and we have underlying collagen exposed and then platelets come and stick to that and they form a little platelet plug and then after that platelet plug is formed you have other types of proteins that come and stick to this to anchor this platelet plug down and that's your fiber mesh so we have to ask ourselves the question what led to me tearing or ripping off the endocardium obviously it was something that damaged the heart valves what are those things that damage the heart valves or make them more predisposed to injury that's a great question right and i know you guys are smart enough to figure this out so let's talk about those things those particular things that increase this risk of ripping off the endocardium could be rheumatic heart disease you know in rheumatic heart disease there's excessive amounts of antibodies and these antibodies will destroy the actual endocardial lining ripping that endocardial lining away right the other thing could be some type of history of infective endocarditis so if you had a previous history of infective endocarditis that pathogen would have damaged or torn away parts of the endocardium and now there's lots of fibrosis and areas of rip to peace pair endocardium and exposed underlying collagen other things is particular conditions such as a bicuspid so a bicuspid aortic valve for some reason these patients they form lots of calcifications and they're very susceptible to infective endocarditis for some time reason the other one is damage to the mitral valve leaflets mixomatus degeneration of the mitral valve leaflets you know what this condition is called mitral valve prolapse there's one more that's actually interesting here that's all native problems and these native problems here what i mean is this problem with your own original heart valve it's no underlying prosthetic valve that's present the other thing is having some type of congenital heart defect this could be things like vsds there could be a bunch of other ones you know cyanotic lesions of certain types like truncus arteriosus and tetralogy of fellow et cetera vsds is one example though but if you have any of these native valve conditions there is underlying damage injury to these valves which predisposes uniformly these platelet fibrin clots you know there's a name for these dang things right and again we're just zooming into one structure we're just zooming into the left atrium here just as an example but this could be on any of the heart valves we're talking about here if that is the case then these little platelets and fibrins that are sticking to the heart valves are called n b t e's non-bacterial thromboemboli and all these sons of guns are is platelets and fibrin that's all they are and they're sticking to areas of injured heart valve tissue what's another particular thing it might not have to be any of these native valve problems it could actually be some type of prosthetic valve so if someone has some type of prosthetic valve these valves are at very high risk for particular types of binding of pathogens and binding of platelets and thrombin okay so very very important thing here so having an abnormal valve creates an opportunity for these npe tes to stick to the actual abnormal valve damage valve tissue or prostatic valve tissue and again to recap what are these nbtes the mbtes are two components here they're components of platelets and fibrin remember there is no pathogen or bacteria that are associated with them okay we got our abnormal valves now once we have the abnormal valves when we actually form these nasty little mbtes what is the next thing that we need we need bacteremia so if someone develops bacteremia this has an opportunity for bacteria to get into the bloodstream once the bacteria get into the bloodstream they can stick to these mbtes they can multiply they can colonize they can actually form a lot of nasty microbial vegetations that we see up here that can start eating away at the valve and the perivalvular tissue and may cause a bunch of downstream complications let's talk about these all right so we have the abnormal valves that have been damaged now we got to get the bacteria into the bloodstream to bind to those mbtes that are on those abnormal valves so again remember what are the different things that can cause abnormal bowels rheumatic heart disease infective endocarditis previous history of infective endocarditis again some type of mitral valve prolapse a bicuspid aortic valve a congenital heart disease like a vsd as an example and then again a prosthetic valve once we get the bacteria into the bloodstream they can bind to those nbtes and form microbial vegetations that cause nasty problems okay how do we get the bacteria into the bloodstream and what are those bacteria or other types of pathogens besides bacteria like fungi that how what are they and then how do they get into the bloodstream is the question okay so the first one that we have to talk about is staphylococcus aureus and again what did i say i want you to remember this one as acute infective endocarditis super virulent super nasty pathogen another thing i have to have you guys remember right here is staphylococcus aureus is actually one of the only types of pathogens one of the few that actually doesn't need an abnormal valve they can actually damage a healthy valve it is so pathogenic and so highly variant that it can actually damage a normal valve it doesn't need a actual abnormal valve to cause these nasty microbial vegetation so that's a big thing to remember it still can do this to abnormal valves and form nasty microbial vegetations but remember it can also do it to healthy office and it's one of the only ones here that we're going to talk about that can do that don't forget that okay how do we get the staph aureus into the bloodstream remember it's a part of our our skin flora so anytime you have an opportunity we have a break in the skin an opportunity for that pathogen to infiltrate boom you got bacteremia that staphylococcus aureus so if someone has a nasty abscess what if they have like a nasty skin abscess that's just filled with miser mrsa and you cut into that or the infection disseminates into the small nearby blood vessels and then gets into the bloodstream and then now you have this pathogen in the bloodstream you have bacteremia these are going to stick to those mbtes and make the microbial vegetations boom here's the big one you can i'm serious you can't forget this guys high high yield here is any time someone has iv drug abuse and they're using dirty needles they're sharing needles with somebody else so somebody had a needle they put it into their skin got staphylococcus aureus on that needle gave it to another person that person took that and injected into themselves they just injected that bacteria into their bloodstream so iv drug abuse with you know not utilizing clean sterile needles is an opportunity for that pathogen to get right into the bloodstream and cause bacteremia stick to the mbts and cause these nasty vegetations next thing anytime we introduce catheters or any type of prosthetic hardware and we're putting it into the body we're cutting them open we're pushing catheters through the skin we're opening up the chest wall allowing for the bacteria on the skin to evade in that's an opportunity to get staphylococcus aureus into the bloodstream or directly into the heart you know one of those ways you're doing a procedure called a central venous catheter where you put it into a subclavian or an ij or ephemeral and you have to go through the skin you have to push that catheter through the skin that bacteria can get right into the central circulation and move right to the heart boom you've got a pathogen that can cause this staphylococcus aureus is one of them so any kind of like central venous catheter that's been in dwelling and sitting in for a long period of time is an opportunity for that to cause a staphylococcus aureus bacteremia and the subsequent infective endocarditis all right and then again all these prosthetic hardwares so having a prosthetic valve that's being placed in or having like a pacemaker like an aicd or a paster that's being put in those wires those prosthetic valves they can just bind have a high affinity for the staphylococcus aureus that they can stick to these actual structures the aicds the pacemakers and prosthetic valves okay so that's the big thing these are the ways that the bacteria can get into the bloodstream once it gets into the bloodstream it sticks to the mbts makes the microbial vegetations and leads to the negative consequences we'll talk about later okay streptococcus varidance what did i say for this one okay here's another thing all the ones that we just talked about here for staphylococcus aureus that covers all the acute the superseptic appearing ones the new heart failure the really high fevers the ones that look really really sick the subacute ones are the ones that don't look as sick they're more indolent not you know specific symptoms that are super obvious and the big one that i wanted you guys to remember is streptococcus viridan so again what i want you to remember for this one most common cause of sub acute infective energy don't forget that but all the rest that we're going to talk about are subacute but this is the most common out of those subacute categories so streptococcus veritas how does this bad boy get into the bloodstream you know it's a part of our teeth it's actually part of a oral flora i should say and so because it's a part of the oral flora anytime you have an opportunity or break within the normal barriers of the skin the oral flora boom bacteria can get in the bloodstream so if you have you know poor dentition in other words you have like 32 teeth but like 30 of them are in your pocket you have a bunch of areas where the bacteria can just pour right into the actual bloodstream or you're getting some type of like dental procedure so it's some type of dental procedure where you're actually going in and cleaning or moving or causing some type of erosion of tissue or introducing an opportunity for bacteria to get right into the bloodstream what are those dental procedures if you must know i'm not even kidding it could be something as simple as like a cleaning or like a root canal something of that nature puts you at high risk for this bacteria to get into the bloodstream there's so many different types of streptococcus varidance i don't know if it's really worth the squeeze to remember them but they're subtypes of this and so sometimes in the example or in the question they may say what's the underlying pathogen for this type of subacute infective endocarditis and it may not present with streptococcus variants it may present with the subtypes which is streptococcus midas streptococcus mutans streptococcus milleri streptococcus sanguinis streptococcus sopranos or streptococcus or alice so if you see any of those it is the same type of group under that category of strep viridance so don't forget that okay the next thing is these hasic organisms now here's the big thing i think is also worth mentioning staphylococcus aureus is gram positive this is gram positive streptococcus varidance this is gram positive you're going to notice a trend here gram-positive tend to be the most common pathogen that causes infective endocarditis that's kind of a good thing in a way these bacteria just love to stick to the actual heart valve tissue haysic which is actually there's a bunch of bacteria within this group is a gram negative rod so this is a gram-negative bacteria it's one of the few really one of the big ones that you is worthy to remember so the gram-negative hasic organisms used to be thought as the most common cause of subacute infection endocrineitis but not anymore now we know it's streptococcus viridance but what does these hasic molecules what does it stand for and there's a bunch of names for these one is there's called haemophilus okay so homophilus the other one is called aggregator so aggregator c is for cardio bacterium e is for ekinella and k is for kingella so if they ever kind of present a question stem where they say hey this patient has you know subacute effective endocrinitis we did a blood culture and the blood culture came back as one of the hasic organisms and they said which one of the following would you pick here it would be one of these so haemophilus agricobacter cardiobacterium achinella and kangela and again you know what's really interesting is these bacteria streptococcus varidance and hasic organisms the way that they both get into the bloodstream is the same concept this is the part of the oral flora the hasic strap viridans are part of the oral flora so if someone has poor dentition they're getting a dental procedure something as simple as a root canal or a cleaning that has an opportunity for the haysic or strap varidance to get right into the bloodstream and these poor things will cause bacteremia and stick to the abnormal valves particularly where those mbtes are and cause microbial vegetations okay next one here enterococcus enterococcus is another type of gram-positive bacteria and again please don't forget that this is again all sub-acute that we're talking about here enterococcus is a part of our urogenitary tract so any type of uti very specifically though i would focus more on pyelonephritis because then what happens is that bacteria can empty into the bloodstream so now we can just have this empty right into the actual renal circulation and boom you have bacteremia but it doesn't have to just be a uti sometimes if you're going and you're putting like a catheter up here or uh doing some type of procedure like a you know a ureter stent or something any anything like that so you're doing some type of eurogenitary procedure that is an opportunity for the bacteria to maybe get into the bloodstream through some break in the part of the actual integrity of the wall of the ureter the wall of the renal pelvis or anything like that for the bacteria to invade right into the bloodstream okay so any type of urogenitary procedure any type of uti particularly pyelonephritis is an opportunity for the anterococcus to get into the bloodstream again bacteria may stick to the mbtes and cause a microbial vegetation the next one here is called staphylococ uh so this i'm sorry sorry streptococcus galaliticus so again it's in a kind of a it's not a cluster it's in kind of like a nice little straight line here this is streptococcus gallolyticus streptococcus galliticus used to be also known as aka streptococcus bovis it changed though recently that the streptococcus galliticus this one here in someone who has like a nasty tumor of their colon so they have some type of colorectal cancer and then less commonly if they have some type of inflammatory bowel disease like uc or crohn's disease there's a break within that barrier an opportunity for the bacteria that are in our gi tract to just move right into the bloodstream and then cause bacteremia and then stick to the actual nbtes and cause microbial vegetation so if someone has a blood culture coming positive for this better think about getting a colonoscopy to look for a colorectal carcinoma okay almost there guys the next one here is called staphylococcus epidermidis so it's in a cluster and again this is a gram positive still part of that subacute category this one what i really want you to know here if there was like a couple different terminologies or different like you know buzzword terms pathonomonic terms staphylococcus epidermidis loves prosthetic valves i would not forget that it loves any kind of prosthetic hardware really an aicd any type of pacemaker if you're putting in again a prosthetic valve these are very specific things that they love they love prosthetic hardware but i would focus more on that prosthetic valve they can bind to the prosthetic valves and definitely cause infective endocarditis okay so they can bind to any kind of mbte that's present on these prosthetic valves but we have to ask the question how do they get into the bloodstream to be able to bind to these prosthetic valves or aicds or pacemakers that's the question so it's a prominent bacteria on our skin so really what's interesting is any type of opportunity for the bacteria to travel along like a catheter that's inter that's actually on our skin and get into the bloodstream is an opportunity to cause an infection right so if this bacteria travels along the length of like a catheter so they haven't i'm not even kidding like something as simple as like a peripheral iv something like a picc line something like a central venous catheter anything that's on the skin and the bacteria can travel on the track of that catheter into the bloodstream that is an opportunity for that bacteria to get into the bloodstream and when it gets into the bloodstream you have bacteremia it binds to the prostatic valves or prostate hardware and boom you get microbial vegetations on that and infective endocarditis man we're good guys we're moving along here the next one here is candida big thing here all of the things that we've talked about are all bacteria except for candida candida is a fungi and so with fungi they're not very super common bacteria they're not super common types of pathogens that you'll see causing infective endocarditis except in a certain population which are very susceptible or have opportunistic types of infections that can arise so you know in patients who have some type of decrease in their immune system function so that for example they have hiv aids or their status post transplant or they're on some type of chemo radiation whatever they have immunosuppression these bacteria are usually i'm sorry these immune system cells are usually able to clear any type of pathogen that may be present within the bloodstream but if you have a decrease in your lymphocytes a decrease in your neutrophils or macrophages and now they aren't able to clear the actual pathogen from the bloodstream they build up enough that they can start to cause the pathogenic infections and this is type of opportunistic pathogenic infections and so with candida be thinking about patients who have hiv aids status balance transplant chemo radiation and you're putting in any kind of prosthetic hardware so i would add in here that these candida love to bind to prosthetic hardware and again i mean valves aicds anything like that they love to stick to but the way that they can do that is if you have an immunosuppressive condition such as hiv aids or again your status post transplant okay we went through all the different types of causes we went through the definition acute subacute we then talked about again the abnormal valves and how those things lead to nptes then we talked about the bacteremia component how the bacteria get into the bloodstream and when they do they bind to the mbtes and make these microbial vegetations that cause a bunch of problems but we talked about the very specific risk factors for bacteremia how they get into the bloodstream and i think now that we've gone through that let's talk about the pathophysiology and how that ties into the clinical features and their physical exam findings all right guys so let's recap everything we talked about just in a quick fashion here so we have again somehow it has infective endocrinitis again inflammation of the endocardium what do we need we need an abnormal valve and we need bacteremia so how do we get the abnormal valve you guys remember we strip away the endocardial lining through rheumatic heart disease bicuspid aortic valve history of infective endocarditis mitral valve prolapse congenital heart disease or you have a prosthetic valve once that happens you expose the underlying collagen because you break away the endocardium and cause platelets to stick to this area once the platelets stick to this area they form a platelet plug what binds to the platelet plug to kind of anchor it down guys you guys remember the fibrin so then the fibrin sticks to this anchors these bad boys down what are these things here called nbtes non-bacterial thromboemboli then you have someone who develops bacteremia whether that be through again whatever kind of bacteria staphylococcus aureus that gets into iv drug abuse through peripheral catheters through central venous catheters through some type of abscess through prosthetic hardware streptococcus viridans and haysic organisms gets in through the poor dentition dental procedures enterococcus utis streptococcus galilicus colorectal cancer or you have staph epidermidis that gets in through the skin loves prosthetic hardware or candida and immunosuppressed patients who are getting also some type of prosthetic hardware or iv drug abuse gets into the bloodstream once that gets in and that pathogen is there what does it do it sticks to these mbtes on their surface then when it does that it infiltrates into these nbtes and sticks in there and now what we have is we started off with first and nbte second we get a microbial vegetation the downstream negativity from this is that this microbial vegetation can start to stimulate our immune system like it'll activate our immune system will come to the area bring lots of white blood cells like neutrophils and macrophages to the area so what's going to come to the area now you're going to have macrophages coming to the area you're going to have neutrophils coming to the area that are going to try to fight a mountain immune response against these microbial vegetations and there's going to be a lot of immune system activity going on here you know what happens when our immune system gets super activated it increases the production of cytokines such as interleukin 1 such as interleukin 6 such as tnf alpha and there's a lot of downstream effects from these things and we'll talk about what those things are but that's one particular type of thing that i need you guys to remember here is that our immune system is going to come to this area and try to fight with these microbial vegetations which will mount a inflammatory type of response okay once that happens and you get this inflammatory response here what's the next thing that can happen here okay so let's again as a nice little recap here we have our ripping away from the valvular diseases or the abnormal valves we get our nbtes that form here after we get our mbtes that form here we get the bacteria that gets into the bloodstream or the pathogen that gets into the bloodstream they form microbial vegetations on the surface they infiltrate into the mbte and they activate our immune system which causes cytokine release now the other thing that can start to happen here which is unfortunate here you know these immune system cells that get called to the area here so again you got your macrophages here we have our neutrophils they're really trying to fight against these pathogens and they're releasing very specific types of cytokines you know these vegetations particularly the microbes in these they release a lot of proteases a lot of destructive enzymes these actual white blood cells will release very specific types of cytokines as well what will they release they'll release things like reactive oxygen species and they'll also release proteases you know what the downstream effect of this is having a lot of reactive oxygen species lots of proteases that are being released and again proteases by the white blood cells reactive oxygen species by the white blood cells and proteases by the bacteria these proteases and reactive oxygen species start chewing away at the valve tissue and they start eroding the perivalvular tissue and this can become a problematic issue so look they're just chewing away these valves so what's the downstream effect of chewing away the valves so if we chew the valves away there's going to be valve destruction and there's going to be peri-valvular destruction there are so many downstream effects that come from this and this is one of the worst case scenarios with this because if you chew the valve off or true the perivalvular tissue now these valves can't function and so you end up with acute heart failure you end up with really nasty murmurs and so these are big things to think about also it creates this nasty opportunity for an abscess or if there was a prosthetic valve now that thing doesn't work and you've got a prosthetic valve that's dehist and dysfunctional now big big complications to think about with this one okay so we got the increase in cytokines from the immune system fighting with the vegetations we've got the vegetations and the immune system releasing proteases reactive oxygen species which are chewing away of the valve and the perivalvular tissue last but not least again to recap you guys will never forget this abnormal valve creates an opportunity for platelets to stick platelets stick fibrin comes attaches to this area makes a nbte bacteria gets into the bloodstream bacteremia stick to the mbtes infiltrate into the mbtes once they've infiltrated again we get the immune system response so increase cytokine release we get the immune system and the bacteria in the vegetation trying to undergo destruction of the valve and the perivalvular tissue and the last thing that can happen here is sometimes whenever blood is like flowing through this area it actually may flick off a piece of these vegetations and when you flick off pieces of these vegetations which have the bacteria in them and all that fiber and platelets and stuff like that what are these things here called so we just break off a piece of the vegetation this is called a septic emboli so what are these called septic emboli and you have to think about all the downstream effects of this septic emboli it's like having a clot like if someone has atrial fibrillation you break off a piece of that clot that's in the atria and it goes ahead and circulates throughout the bloodstream if it's on the right side obviously we have to talk about right-sided ambilight but more commonly it's left-sided in black so we'll talk about that as well but these are big things to understand guys not to forget okay that's one particular complication here's another thing our immune system remember those like white blood cells so you're going to have those plasma cells and these plasma cells are going to be kind of pumping out antibodies against these microbes that's what our immune system does it tries to make antibodies against the microbes and when it makes these antibodies it'll try to stick to the antigens on certain types of bacteria and then what will happen is parts of that antigen and antibody will break off and so now i have this freely circulating so maybe here's a little bit of the fibrin and platelets and then here is the pathogens here and on some of these pathogens they have antigens on their surface and some of these antibodies are sticking to them and what happens is these little things here these little antibody antigen complexes they can go and deposit into various tissues of the body and we'll talk about what that does but these are called immune complexes so man we got all of these things that we have to talk about now individually and what these patients would look like we know the pathophysiology of how there's increased cytokines valve destruction perivalvular destruction septic and blind immune complexes what does this look like on the patient that's the question so what about these increased cytokines so again the example we're using here is we're just looking at the left atrium so remember everything that we're looking at here is the left atrium but it can occur on any valve i just thought it was the best diagram here for this component which again we're talking about the left atrium in this situation here so again what is this tissue that lines this here again guys this is the endocardium endocardium here and again there's a breaking away of the endocardium and so all this is going to be a nbte that are sticking here and again they'll have the fibrin on it and you'll have your pathogens your bacteria here and then again just to be for completeness sake here we'll have our fiber mesh either way though we know that these are going to cause our immune system to come to the area here and our immune system is going to increase the release of interleukin-1 interleukin-6 and tnf alpha what do these things do that we can actually see or measure in a patient first thing it does is it works on our hypothalamus so it loves the hypothalamus and what it does at the hypothalamus it tells the hypothalamus to increase the production of prostaglandin e2 and what that does is that increases our body temperature so it resets our body's thermostat and makes the body temperature higher so it's more difficult for bacteria to survive and that looks like a fever so they may have fever they may have chills they may have rigors things of that nature okay but this is a big big factor here is looking for a fever in these patients the other thing is it tells the bone marrow hey guys we're overwhelmed by these microbial vegetations and they're really hard to beat i can't do it i need you guys to actually pump out more white blood cells to help me make more white blood cells like neutrophils more macrophages more lymphocytes because i need more help and when we stimulate our red bone marrow to do this to increase the production of white blood cells what is that called this is called leukocytosis and so sometimes what you may see is that you get a cbc on these patients and they have an increase in their white blood cell count the next thing is these cytokines love to alert our entire body and say there's a lot of inflammation going on and so it'll act on the liver and when it tells the liver hey lots of inflammation going on the liver will increase the production of two types of acute phase reactive proteins that are important to measure and this is esr erythrocyte sedimentation rate which tends to be elevated and c-reactive peptides crp which tend to be elevated again what are these things here called these are called your acute phase reactants they're very non-specific they're not going to help they're not going to establish the diagnosis but they may tell you that there's a lot of inflammation and possibly some type of infection going on here and that's something else that you can add on to your studies so look for a patient with fevers rigers chills a bump in their white count and maybe a super increase in their uh what's called acute phase reactive proteins it'd be awesome if you could actually have prior measurements so that you can see how much of a difference there is if they have an acute illness okay the next thing which is the valve destruction and the perivacular destruction there's a lot of that going on what does that look like on the patient well here's the thing i need you to know we've got to talk about the valves and the peripheral tissue that's most commonly affected because there's four valves here how do i know which one is actually going to be the most likely affected well there's a nice way to remember this left-sided is more common than right-sided first off so let's actually write that off here so the left side is going to be more commonly affected than the right side that's pretty easy i think right away but then we should go okay we got left-sided is the mitral and aortic which one's more common the affected here it would go first so you have first left is definitely more common on the right but it goes in order here first is mitral second is aortic then we go to the right side okay which one's more common here on the right side is it the tricuspid of the pulmonary tricuspid now here is one particular exception which we have to mention they love to mention this in the textbooks in patients who have iv drug abuse with staphylococcus aureus this is preferred so you can remember try to stop doing drugs to try to not do drugs okay so again iv drug abuse staphylococcus aureus they prefer the tricuspid valve and so you definitely want to think about this in a patient in the clinical vignette they have iv drug abuse they have some type of right-sided heart failure they have a regurgitation murmur of their tricuspid valve think about that okay this is a big one that could be more affected and then last but not least is going to be the pulmonic as the least commonly affected valve in infective endocarditis okay so we got now that this is the valves that are more like commonly affected definitely left side more common than right side mitral first aortic second tricuspid third except in situations of iv drug abuse okay particularly with staphylococcus aureus it tends to be the more preferred one and then last but not least is the pulmonic okay we covered this what would these patients look like if they tend to affect more likely these two valves okay mitral and aortic since those tend to be the more commonly affected ones that's a great question so if i had these pathogens these microbial vegetations that were on the mitral valve and they were chewing away they chewed and chewed and chewed and now i got just this little nub of a mitral valve leaflet left over what are the leaflets supposed to do whenever our ventricles contract they're supposed to slap together and prevent backflow am i going to be able to prevent backflow into the left atria now no and so in these patients what am i going to see one of the first things that i may see is if the mitral valve is affected so if the mitral valve is affected i may see a new mitral regurgitation murmur that may be one particular thing that i see the second thing that i may see is if there is actually a mitral there may also be particular issues here so you know whenever somebody has a mitral regurgitation they push blood back into the left atrium right during systole all that blood just floods right back down during diastole and so what happens is the ventricles get over filled with blood and what can happen is this can cause a patient when they overfill with blood in their actual left ventricle so now imagine all this blood is just accumulating in the left ventricle accumulating accumulating accumulating it'll back up into the lungs and these patients can develop pulmonary edema the other thing that can happen here is that if you have all this blood that's accumulating in your left ventricle every time you kind of contract blood to push out into the aorta you keep pushing some of it into the atria so imagine here like for example stroke volume is like 70 milliliters right so out of the volume of blood that you're trying to push out of the ventricle into the order you want it to be 70 mls let's say that in this patient as my to regurge 50 of it is going out of the aorta and 20 of it is going into the atria that's a reduction in true stroke volume then i'm not getting as much blood out into the aorta because some of it's going back into the atria if that's the case a lower stroke volume leads to a lower cardiac output a lower cardiac output can cause hypotension and so something else you may see in these patients is hypotension to the point of cardiogenic shock so don't forget this as well okay so mitral what would that kind of look like there you get a numerator regurgitation murmur again other one to think about is the aortic it's the same kind of concept you can get a new aortic regurgitation murmur and in these patients the same kind of concept here blood is going to be back flowing from the aorta into the ventricle you're going to get more filling of blood within these ventricles it's going to back up into the lungs and again the things that you'll see in this patient is pulmonary edema and you'll see hypotension with that classic cardiogenic shock and these patients the big thing to take away from this is what you notice they can develop acute the overarching theme here is they can develop acute left-sided heart failure that is the big big thing here for these patients that have this chewing away of their valves and since the mitral and the aortic valve tend to be the more commonly affected valves you'll see patients with acute left sided heart failure shortness of breath due to pulmonary edema disney on exertion proximal nocturnal dyspnea orthopedic hypoxemia they'll also have hypotension they'll have cold extremities well not well perfused extremities these are big things to be thinking about as well as a new mitral regurgitation murmur or a new aortic regurgitation murmur boom shakalaka we've uncovered that okay the next thing here that we have to talk about so we talked about if they chew away the valves right so again they chew away the mitral valve leaflets you get mitre reguards if they chew away the aortic leaflets boom you get an aortic regurg what if they chew away the tissue around the cusp or the leaflets what happens then why is that a problem okay you know if somebody has uh for example let's say here's our mitral valve and here is the aortic valve so again this is our left atrium this is our left ventricle and then here is the aorta okay we have here the mitral valve we're just looking at it in kind of a a cut here where we can see the two cusps the anterior and posterior leaflet in this situation what happens is what if somebody has a nasty infection particularly of their mitral valve and it starts to so here's that nasty vegetation there on the valve and what it starts doing is it starts eating some of the tissue around the valve what is that tissue here called the perivalvular tissue and then when it erodes away that tissue it starts causing a nasty type of abscess to form here that's one particular thing the same kind of concept here what if it's again you have an infection a big old vegetation or goombak on the aortic valve and it starts to eat away some of the perivalvular tissue and extends out into that tissue and then you get this big infectious bacterial accumulation outside of that annulus or in the perivalvular tissue called a abscess these are the nasty complications you can get with the perivalvular destruction and so one of the big things to remember in this situation here is when you have perivalvular destruction this can lead to nasty abscesses so like ring abscesses or perianular perivalvular abscesses what's the issue with these well think about it if it was on the aorta so if it was on the aorta you're obviously going to get a murmur because what can happen here is you can actually start potentially causing inflammation and then dilating the aorta and if you dilate the aorta you pull the valve plus farther away from one another that's easy regurgitation murmur that's one thing but the worst case scenario is look what is right next to the the annulus of the aortic valve the av node and the bundle system this abscess can just infiltrate right into the av node or the conduction system and guess what this can cause conduction blocks so these patients could develop av blocks or bundle branch blocks and that's one big thing to think about here the other thing is what if we had an abscess that was kind of close to the mitral valve or there was a mitral valve abscess look what is literally right next to this thing is this pink tissue here that's the pericardium what if this infiltrates into the pericardial tissue and causes inflammation of the pericardium and a nasty purulent pericardial effusion that's what you can see potentially with the mitral sometimes it can happen with the order but look how close that is with the mitral so i could see here again eating away this area could cause a murmur that's also another potential but it also could lead to what else pericarditis plus or minus a nasty purulent diffusion so these are definitely things to think about that can happen with effective endocrinities they can cause perivalvular destruction leading to these nasty abscesses so peri-valvular aortic abscesses peri-valvular mitric mitral valve abscesses spreading to the conduction system with aorta causing aortitis inflammation leading to a regurgitation murmur abscesses around the mitral valve again if that happens and it eats away at the tissue around that it can form a mitral peri-valvular mitral abscess and then again eat its way towards the pericardial tissue or spread to the pericardial tissue causing pericarditis and a nasty purulent pericardial effusion okay what else could we see here because we're not done we got to keep going man so the other thing that i want you guys to think about here is with something else that's interesting so what if we this is all native valves these are all our own valves that are being destroyed and chewed away so our own normal valvular tissue our own normal perivalcular tissue that's being eaten and destroyed away what if it's actually not our own normal valve what if this is the actual prosthetic valve so what if there's a situation where this valve is a prosthetic valve so we don't have a native valve this is a prosthetic valve and the tissue around that all right so there is destruction of that perivalvular tissue where what happens is you're supposed to sew the prosthetic valve in so you see how there's like this areas here that what happened is you had the vegetation here here's the vegetation it was on that valve causing an infectious you know destruction but then it spread and started destroying some of the tissue that was kind of anchoring the prosthetic valve to the wall of the aorta right so now it's torn away what i did is i separated this prosthetic valve you know what they call that when you separate the annulus of the prosthetic valve from the wall of the aorta in this situation the aortic prosthetic valve that's called a dehiscence and so now what happens is i destroy the perivavular tissue and i lead to prosthetic valve dehiscence the problem with this is that now i have a little leak where blood let's say whenever we have diastole it's supposed to shut these semilunar valves to prevent backflow but now i got this little space here where the prosthetic valve dehist away from the wall now blood can just leak right back into the left ventricle through that little area called a perivalvular leak and so this could cause a para valvular leak and this would be problematic because this can lead to a prosthetic valve dysfunction so big things to be thinking about here that we've talked about so far lots of cytokines causing the constitutional symptoms lots of destruction of the valve right leading to chewing of the valve away if it chews the mitral valve or the aortic valve since they're the most commonly affected it can lead to acute left-sided heart failure with pulmonary edema hypotension and new murmurs please don't forget that if they destroy the perivovler tissue they can invade that perivaler tissue that's been eroded away and form nasty abscesses ring abscesses around the aortic valve or the mitral valve if they spread from the aorta they can go to the conduction system causing conduction blocks if they spread from the mitral valve into the pericardium they can cause pericarditis infusions if this isn't a native valve it's a prosthetic valve that's been adhered or sewed into the wall and the infection is actually spread and de-hissed or torn away the actual sewings that are anchoring the annulus of this prosthetic valve to the wall and you chew that away now it's not functioning anymore blood can leak back around that called a perivacular leak and now your prosthetic valve that's dehist is dysfunctional it's not working and we're probably gonna have to repair that dang thing let's move on to the next part here which is talking about septic emboli all right so let's move on to the next part which is the septic emboli remember we said that this is what happens whenever you have for example some we're going to talk about two different types remember i said there's right sided and left side let's actually talk about right side at first because it's the easy one so right sided emboli so you guys remember here we said that we have some type of vegetation right so we have that microbial vegetation that's formed on top of the valves particularly where the endocardium was damaged you form the mbtes and then you get the microbes that bind onto it boom we're caught up they're on the valves what happens is you flick off pieces of that vegetation and they move along the circulation this this is like scary makes you pucker up your stink hole a little bit but in this situation you flick off a piece of these emboli and they go moving through the pulmonary circulation oh my gosh what happens if one of these embly gets stuck and occludes the blood flow through the pulmonary circulation can you drop off the co2 and pick up the oxygen no and so this can lead to a pulmonary embolism that's one particular thing so pulmonary embolism you know what else is really nasty about these things man sometimes they're small enough that they can leak they can actually eat away or leak out of the pulmonary capillary tissue into the lung tissue more likely they eat through so because sometimes they get stuck in here and then they actually start digesting away the actual tissue and then infiltrate into the lung tissue when they infiltrate into the lung tissue they can cavitate and literally cause abscesses and so another particular thing that you can see here is you might see lung abscesses where they can cavitate really nasty stuff man so that's the big thing with the right sided emboli now what if i had some emboli that were stuck on the mitral valve or again it could be the aortic valve but again mitral valve tends to be the more common one but we're just going to use this one so we got these actual vegetation stuck on the mitral valve you flick off a piece of these actual emboli they move through your systemic circulation they go up to your brain they go to your spine they go to your hands and your feet and they go to your your kidneys in your spleen and all over the dang place these are your left-sided emboli and these are the scary ones my gosh they are so fearful of things that can happen with these so again what can happen here we pop off one of these emboli they move through your systemic circulation let's say that they go up through the carotid system and they block the blood flow to your carotid system or one of the branches of the carotid system boom you have a patient that develops a acute ischemic stroke oh my gosh that's so terrible right the other thing is they can get stuck in the vessels in the actual brain chew away at them eat away at them and i'm not even kidding can cause bleeds they can cause bleeds in the brains so ich is subarachnoid hemorrhages these can cause ich they can cause subarachnoid hemorrhage they can even eat away and chew at the vessels and infiltrate the brain tissue when they infiltrate the brain tissue they can actually cause nasty abscesses and so you can even get cerebral abscesses so you're seeing the point here that these things are really really nasty okay so we have brain infiltration strokes bleeds abscess it can also form these little emboli that gets stuck in the vessels that are on the nail beds you know those tiny little vessels here in our nail bed and what happens is if the blood son of a gun if the blood flowing through them you get the little emboli stuck in them and then they actually start eating away and hemorrhaging on the actual nail bed they can produce splinter hemorrhages so that's one thing so you may see these hemorrhages in the nail bed the other thing is they can cause hemorrhages on the actual palms of the hand and the soles of the feet but they're not very painful so what are these two things here called so the first one here so let's actually number this so we know the first one on the nail beds are called splinter hemorrhages okay that's the one and then the second one here which is on the palms of the hand and soles of the feet these little hemorrhaged areas of vessels on the palms and hand soles of the feet that are painless these are called chain ways lesions okay what happens if some of these like little emboli that are floating down they get stuck in some of the vessels that are going to the discs are going to the vertebrae and they start chewing away and eating away and causing destruction of the disc and the vertebrae this can lead to what type of situation here so one this would be you may have something called disguise or spondylitis or you may even see the worst case scenario osteomyelitis it could even deposit into the joint tissue cause inflammation of the joint tissue causing a hot septic joint and so the second thing that you may see is septic arthritis oh my gosh the other thing that you can see here is that some of these emboli can actually get stuck in the vessels of the spleen they can get stuck in the vessels of the kidney or they can form abscesses in the spleen what can happen here so first thing that can happen is it gets stuck in the spleen or stuck in the kidney so you can see a splenic infarct significant amounts of abdominal pain or they could cavitate into the spleen and cause a splenic abscess so you can see a splenic infarct is one or you could see a splenic abscess and the last thing is you could see a renal infarct and this may cause a decrease in urine output this may cause an increase in their bu in their creatinine these are all particular things that you can see in these patients so to summate here if a patient has concerns of infective energy maybe it's a right-sided septic emboli they had developed shortness of breath hypoxemia tachypnea all of these things or they develop shortness of breath with increased sputum secretions and purulence uh types of cough and productive cough and secretions nasty things like that hypoxemia be thinking about septic emboli like a pe or an abscess if they develop neurodeficits they become weak on one side they develop dysphagia they develop particularly like this r3r they have sensory losses things like that gaze preferences think about maybe some type of stroke bleed or abscess if you see that they have lesions on their hands palms on the hand soles of the feet are on their nails think about splinter hemorrhages or janeway's lesions if you see back pain from disciples or osteomyelitis of the vertebrae or they have a hot painful tender joint like in septic arthritis if they have abdominal pain in their left upper quadrant or if they're having maybe some type of flank pain but more likely they're having a decreased urine output and you check their bmp and they have a bump in their bu and their creatinine think about a renal infarct let's move over here to the next component and the last part here for the the pathophys and the clinical features and physical exam findings which is the immune complexes all right so the next thing is these immune complexes that we said right so that was the basic concept where again you have like these vegetations the microbial vegetations and then again what happens is there's pieces there's antigens on the microbes so let's say here's an antigen there that was from the microbes and again your immune system your plasma cells were making antibodies that were against these particular antigens and now you have an immune complex what happens is these immune complexes can get distributed through your circulation most commonly systemic circulation and when these antigen antibody complexes get deposited into different areas what are the clinical features that we could see from these immune complexes well one is they could deposit onto the pulp of the digits and if they deposit here into the pulp of the digits they produce these painful lesions right here you know what these are called usually on the tips of the fingers here these are called osler's nodes and i remember that these are painful by osler ouch so osler's nodes that's so cheesy right but it works okay osler's nodes ouch so these are painful immune complex lesions that are on the pulp of the digits the next thing is that these immune complexes can also deposit where else they can deposit into the retina and so they can get actually into the vasculature and when they get into the vascular they deposit into the areas of the retina and cause these hemorrhagic lesions that occur here in the retina you know what these things are called these are called roth spots these are called roth spots and last but not least these immune complexes which i think was probably the most commonly known ones is they can get into the circulation here of your glomerular circulation your renal circulation and here they can deposit into the glomerulus near the basement membrane and the glomerular capillaries and what happens is there's an immune reaction that occurs here and this starts to erode and destroy some of the glomerular tissue and when you destroy some of the glomerular tissue now you alter the permeability of the glomerulus you know what's normally not supposed to be able to filter out of your glomerulus guess what it's red blood cells and protein these things are not supposed to be filtered out into your urine but in these patients who develop these immune complex lesions that destroy away the glomerular base membrane they get red blood cells in their urine because red blood cells are not supposed to be able to filter across here but they do and the other thing is proteins proteins big big plasma proteins are supposed to be repelled by your glomerular base membrane but if it's damaged you don't have that thing to be able to prevent that and that leaks into the bloodstream as well so then you get lots of protein urea so what are the two things that you'll see here you see lots of protein called protein urea and you get lots of red blood cells in the urine which is called hematuria the combination of this due to the destruction of the glomerulus produces a very specific type of condition where there's the inflammation of the glomerulus and components of the nephron we call this glomerulo nephritis okay the last thing that i want you guys to understand here is there's one more thing that can happen here it's very non-specific i'm not going to really go into it because there's not a lot of data to really kind of give me any answers to why these things happen but some of the very specific types of antibodies that when we measure them in the bloodstream this very specific type of antibody tends to be very elevated in these patients so you can see osler's nose you can see raw spots you can see glomerulonephritis but one of these particular antibodies that we can actually measure that seems to be involved in this inflammatory process and this immune antigen anti this antigen antibody deposition process is a very specific type of antibody called rheumatoid factor and so sometimes you can check this particular antibody and it seems to be positive in these patients a rheumatoid factor is positive within their serum so immune complexes don't forget painful lesions on the the actual pulp of the digits osler's nodes visual changes so if they're having difficulty with their vision and you look under fundoscopy and you see lesions on the retina roth spots and then lastly they have blood in their urine protein their urine this could be glomerulonephritis and then again you can also check the serum rheumatoid factor and that tends to be positive through an unknown pathophysiological mechanism okay we covered all of this let's head to the next step here which is how do we diagnose how do we clinch the diagnosis of infective endocrineitis with confidence let's get into it all right so let's talk about the diagnosis of infected fingerprinting believe it or not it's actually somewhat kind of challenging because not all the patients will present perfectly in your clinical vignettes it'll be relatively simple though so when we talk about this actual diagnosis the first thing that we need is we need to get an echocardiogram on these patients but that begs the question okay an echocardiogram definitely is going to give me a good look at the heart when in doubt whenever there's a question of like what's the best cardiac test it's more likely echocardiogram but when we get an echocardiogram the question is which one should we get generally when someone walks through the door of the hospital they're getting admitted it's most likely that they're going to start off your first kind of initial test will be a transthoracic echocardiogram basically you're taking the probe you're putting it on the chest you're looking in different views the sub xiphoid view a pair of stone long axis short axis apico all these different types of views and you're trying to get a global look at the heart that the best of your ability however for some of these particular types of infective endocarditis especially the ones like the aortic valve and getting a good look at some of these particularly like near the uh the mitral valve it's difficult to actually see them sometimes and so really the sensitivity and specificity is the absolute best with the trans esophageal echocardiogram so really we start off with the transthoracic echo but we the best test and the confirmatory is really going to be the trans esophageal echocardiogram highest sensitivity and specificities like greater than 90 and so the difference between a t-e-e and a transthoracic t-e-t-t-e is a trans-esophageal echo as you basically swallow the probe it goes down the esophagus and look at the heart from the posterior aspect from the esophageal view and so that's the difference there so again trans-esophageal echo is going to be the best test it's the confirmatory test so for example you look at a tte and you see a big old goombach on the valve you're likely going to still need to get a te to confirm and really get a global look at that vegetation or goombak on that valve okay so i'd start off with the tte but definitely get the tee the next other thing that's important about the tee is the t e e can pick up other complications that you cannot see with the tte and that is very specifically those abscesses so those ring abscesses it's going to be really really tough to pick those out with the tte so i would definitely for the tee definitely get that so it's going to pick up those actual perivalvular ring apps this is much better than you would with a tte okay good deal next thing what are we looking for on the echo so we get the echo we know that the tte is the first but t-e-e is the best confirmatory and definitely could pick up complications that you can't see with the tte that being the peripheral abscesses what am i looking for obviously the first thing is this big old goon box sitting on the valve right so if i see first thing a vegetation boom i have one of the positive echocardiographic findings i could stop there but let's say i don't see the vegetation because it's so small but when i throw on color doppler i can see that the actual vegetation chewed away the valve that it creates a regurgitation murmur so i see a new or let's say they have previously you had a previous echo and it showed that they had a little regurgitation there across the mitral valve but now it's severe so it's worse so a new or worse murmur particularly again a regurgitation membrane let's actually write that down newer or worse regurgitation murmur this is it's going to be way more common for it to be a regurgitation murmur than it would be some type of sonatic murmur because you're chewing away the valve so you're not good forming a good seal okay that's one thing the other thing that you could be looking for here is a certain type of prosthetic valve dehiscence remember i told you that in patients who have prosthetic valves if they have an infectious vegetation that you can't see but what you do see is you see the prosthetic valve like rocking back and forth rocking back and forth and paravalvular leaks so you see color doppler and you see a new murmur there that could be indicative of a prosthetic valve dehiscence and again that's way best seen with a te in this sense but if we were looking here and we see someone who has a prosthetic valve dehiscence that would be a positive echo finding and i would be boom i have one of the particular findings that i need here off the echo so if i see a vegetation done if i see a new or worse worsening type of regurgitation without a vegetation done if i see a prosthetic valve dehiscence with or without a vegetation done last thing is if i get that te and i see this nasty abscess that's forming around a valve so i see some type of peri valvular abscess and believe it or not these are more common with the aorta than the mitral so these would be the things that i'm looking for all right so a couple different findings vegetation big ol goombak don't see it but you see a new worsening regurgitation murmur prosthetic valve dehiscence where you see the valve rocking back and forth and then lastly you see that abscess the ring abscess that's actually formed around the actual valve annulus particularly aortic valve more commonly affected than mitral valve that's the echo findings now the other thing i need so this tells me that i have a cardiac lesion or i see the downstream effects of that cardiac lesion what i need is i need the bacteria that are basically causing this lesion and the reason why is first off i need to prove that there's bacteremia that's the cause of this lesion these nasty vegetations that are causing these problems but the second thing is i need to narrow my antibiotics against these types of pathogens that are in the bloodstream so when i put people on antibiotics i start with empiric and we'll talk about what that is but i've got to narrow it down to the specific type of pathogen and that's where i use these blood cultures now when i obtain blood cultures the purpose is to basically find bacteremia okay it's to find bacteremia and in this situation we need to go back and remember all the different types of bacteria because when we say we find bacteremia we want it to be for the typical pathogens that we discussed prior i'm not going to write all of these down but i am going to quickly rattle them off for you again staph aureus strap viridans gram-negative hasic enterococcus strep galalyticus staph epidermidis and candida remember these were those pathogens that are the typical ones there is another one called coxiella bernetei but i think it's kind of like beyond the scope of this lecture but don't forget that one as well okay so we find the bacteremia that's the purpose of the blood cultures when we do these we actually want to get three sets of cultures okay and we want to get the three sets of cultures on these patients now when we do that and we draw these cultures we want to try to draw them from different sites and technically at different times i think one of the biggest things to remember here is you want to try to get a lot of blood because in a patient who has infective endocarditis it's an endovascular type of infection and so that's a continuous infection so whenever you get these blood cultures i think the goal more should be trying to get a lot of blood in these blood culture containers so that you can actually get a good number of potential bacteria in that actual container when you test it you find the bacteria that's causing this issue but again they ask you to get three sets of particular types of blood cultures you're looking for anaerobic aerobic and then you also have your fungal cultures as well but when you do that and you obtain these cultures what you're looking for is if you have let's say that you drew three cultures when you drew three sets of cultures if out of those you have a positive blood culture for one a positive blood culture for another boom you have established the diagnosis of particularly the bacteremia and so all we need technically for this is at least two positive blood cultures from the three cultures that were obtained three sets of cultures there is other ways that we could say the patient has bacteremia it doesn't just have to be two positive blood cultures that are spaced out it also could be persistently positive blood cultures so another way that we could say this is not just two positive blood cultures but we can say that the patient is persistently positive blood cultures and we're not going to go down the rabbit hole of this because there's all these different types like okay you got to get two positive blood cultures from you know different sites greater than 12 hours apart or if you draw more than three cultures and majority of them are positive but the first and last one are in our part i think that's beyond what we really need to know we just need at least two positive blood cultures from these patients when they get three sets of cultures if at least two of them are positive for the actual pathogens that are typical to cause infective endocarditis we've established bacteremia and in the presence of this potential echocardiographic findings we may have enough to say that this is infective endocarditis okay so we get our echo we get our blood cultures that's not it though because there's other things that we can do to evaluate this patient so obviously get the echo get the blood cultures you can order a bunch of other lab tests and other imaging tests but what those are really looking for is that these things called minor criteria which we'll talk about down here when we talk about the duke's criteria but really the test that i want to look for is the septic emboli i want to look for all the tests for septic emboli and all the tests for immune complexes because these are other things i can use in aiding in my diagnosis of infective endocrine so let's talk about these all right so when we test for all these septic emboli that we can throw okay first thing to think about is more commonly the left side of septic implied but we can add in here the last thing is the right side of step to give a lie but what are the tests that we can look for for left-sided emboli what did i tell you strokes bleeds abscesses so get a look at the brain my friends get an mri of the brain so an mri of the brain may tell me if i see some type of infarct if i see some type of abscess if i see some type of bleed and these are big things to consider in patients who maybe have an altered mental status they have some non-specific neurodeficits and you want to go and see if they have some type of septic envelope to the brain the other thing is look for any types of septic emboli that they spread to the vertebrae maybe they have some type of disciples maybe they have some type of spondylitis and so you're looking for evidence of osteomyelitis or spondylodiscitis you can get an mri of the spine looking for any evidence of the abscesses to have actually spread or emboli to spread to the spine so now you're looking for some type of spinal cord abscess the other thing that you can look for is some of the abscesses that form within the spleen or infarcts that you develop within the spleen and so sometimes looking for these may just be good to look for a splenic ultrasound so i think a splenic ultrasound is not a bad thing sometimes you can get a ct of the abdomen as well so if you've got a splenic ultrasound or you've got a ct of the abdomen and pelvis this may actually give you a little bit of a look there to see if you can see any kinds of hypodensities or abscesses that are present in the spleen it also could be a good thing to get a renal ultrasound so renal ultrasound may show that you have like an emboli that's stuck within one of the renal vessels that might be a particular thing but the other thing is look we had an injury to their kidney right if we we blocked for example let's say here you have the artery that has a little emboli in it okay so here's my septic emboli it's blocking the blood flow we're gonna have some injury to the kidneys so you can see signs of an acute kidney injury with an increase in their bu in an increase in their creatinine a low urine output these are things that i can obtain from a bmp okay so look for evidence of potentially an aki look for decreased blood flow via renal doppler ultrasound simple stuff right the other thing is use my dang eyes and my physical exam put your hands on the patient look at the patient and look for any evidence of splinter hemorrhages on their physical exam i think this would be a good thing to do right the other thing is look for any types of lesions that are present on the palms of the hand soles of the feet and these are usually painless so look for splinter hemorrhages or janeway's lesions the last thing to consider is what if it was that right-sided septic emboli that just blew their way to the pulmonary circulation so if it was that i think it might be beneficial to get a ct pa or some type of ct of the chest maybe even start off with like a chest x-ray look to see if you see any types of opacities or any types of abnormal nodular lesions on their chest x-ray get a ct of the chest and particularly with the pulmonary angiogram look for any pulmonary emboli and look for any cavitory lesions or abscesses in the lung tissue these may help you with the right-sided pulmonary emboli but you see all these tests that i could use if i did any of these in any of them i found an abnormal one of these findings boom i get a point for a septic emboli finding and that helps with my diagnosis okay what about the test for immune complexes so in this situation here a big thing to be thinking about for these patients is again we had the glomerulonephritis the raw spots the osler's nodes and that positive rheumatoid factor what can i test for this one so in these patients for glomerulonephritis i want to look at the urine i want to see what's going on in that urine so i might just do like a urinalysis and with with microscopy some mirror analysis with microscopy and look for red blood cells in the urine particularly cass red blood cell cass and i'll look for lots of protein in the urine and the other thing is i may have an acute kidney injury with these patients right so if they have some type of acute kidney injury i may also get a bmp to look for an increase in their bu in and an increase in their creatinine and so what may help me with this a b m p okay so i can get a bmp in a urinalysis with microscopy look for hematuria look for proteinuria maybe a bump in their renal markers and this may boom i get a point for an immune complex phenomenon that helps me my diagnosis maybe i don't have that though and maybe what i do is i look for these roth spots and i look for them via what's called fundoscopy so i do a flundoscopy study and when i do that i'm able to visualize the particular lesions on the retina when i dilate their pupil and i see the lesions there that may be a point the other thing is if i find these types of lesions on the digits of their fingers right so i see on the pulp of their digits and i have they have these painful osler's nodes and again what helps me with these they are painful osler ouch that's going to be from my physical exam and if i see that boom i get a point the last thing is i could check that rheumatoid factor so if i order a rheumatoid factor and that's positive boom i get a point for an immune complex phenomenon so you guys get how from all of this i can establish a pretty good like base for an understanding the diagnosis of infective endocarditis okay now that i've done my test for septic emboli i've done my test for the immune complexes the last thing that i have to talk to you guys about is what is the modified duke's criteria how do i use that criteria and being able to see did i make the diagnosis of infective endocarditis or have i not all right so how do we use the modified dukes we're basically taking everything that we talked about up here and even some of the stuff that we've already previously recap we'll have to recap a little bit and putting it all together to make the diagnosis of a patient with infective endocarditis you need a couple particular things here so we have things called the major criteria and the minor criteria to really establish the diagnosis to say okay i've diagnosed this condition i either need one of the particular three things i need two major criteria if i have two major boom i've diagnosed infective endocarditis the second part for the modified duke says okay you only have one major but on top of that you also have three minor you've established the diagnosis of infected endocarditis the last scenario says you have no major criteria but you have five minor criteria boom you've established the diagnosis of infective endocarditis so we have to understand now what the heck is the major criteria and what the heck is the minor criteria and how do i kind of utilize all the things that we've talked about up to this point which seems like forever to make this diagnosis well the major criteria to really boil it down you need a positive echo finding what were those positive echo findings my friends a vegetation a newer worsening murmur a prosthetic valve dehiscence or a perioval abscess you have one of those you have a major criteria the other thing that you also need here is you need positive blood cultures and they have to be at least two positive blood cultures or they have to be persistently positive oh and they also have to be for the typical pathogens that is super important so in order to actually fit this definition of positive blood cultures you have to have two positive or persistently positive blood cultures and they have to be for the typical pathogens that we discussed okay the only one that i said they can add on there is that doesn't have to have two positive blood cultures or persistently positive blood cultures is coccielo bernadii that's the only one okay that's your major criteria so if we have both of these that's two major boom i've diagnosed it i'm done that's why finding a vegetation having two positive blood cultures for the typical organisms or persistently positive you're done but let's say you only have one of maybe you have an echo finding of particular vegetations and you don't have the maybe the blood cultures that are fitting the actual criteria that we want here so in that case we move on to the minor criteria because now i need three minor plus the echo finding let's say i have a vegetation what are the three minor criteria that i could have to establish this one let's actually talk about all five and then we can actually say okay i got three of these as an example the first one here that i need is i have to have a fever and a fever is defined as greater than 38 degrees centigrade or greater than 1.4 degrees fahrenheit remember i told you that was a huge symptom that was from that cytokine release the second thing i need is i need some predisposing factors and please tell me that you guys did not forget all of the predisposing factors that i talked about with the abnormal valves prosthetic valve history of infective endocarditis rheumatic heart disease bicuspid aortic valve congenital heart diseases we talked about those or mitral valve prolapse if you have one of those you have a predisposing factor for an abnormal valve what about the bacteremia iv drug abuse skin abscesses you have an indwelling central line a dialysis line a chemo port you have some type of iv drug abuse your immunocompromise you have dental procedures or some type of poor dentition you have hematologist dissemination from the git from the urinary system all of those things that we discussed if you have any of those things that put you at risk for bacteria or abnormal valves boom you fit the definition the next thing is i need positive septic emboli phenomenon so in other words if i get an mri and i see a patient there's a bunch of strokes all over the place i get a splenic ultrasound it shows an abscess or an infarct i get a renal ultrasound it shows a renal infarct i get splinter hemorrhages or jane waves lesions or i have a ct that shows a pulmonary emboli or an abscess in the lung boom i have positive septic implied finding i have to have a positive immune phenomenon so if i get a bnp in a ua and it shows that i have protein area hematuria and increase in b unicronian i've established an immune complex if i did flundoscopy and i found the raw spots boom positive or if i checked for a rheumatoid factor boom positive or i found painful lesions on the pulp of the digits boom positive roswell's notes that's an immune complex and that's a positive point and last but not least is you have blood cultures not meeting major criteria what is what the heck does that mean meaning you don't have two positive blood cultures they're not persistently positive blood cultures or they're not positive for the typical types of pathogens that cause infective endocarditis that means that it's a minor criteria so for example if i had a patient who had a vegetation that's a major and they had a fever predisposing factor and a positive mri boom we've established the diagnosis or they have no major findings and they have all of these they have a fever they're having they have iv drug abuse they get an mri that shows a multiple emboli in the brain they have immune complexes with a positive maybe glomerulonephritis and they have blood cultures that some of them are positive but not two they are persistently positive but they don't meet that true definition of the complicated thing we talked about or they're not positive for the typical pathogens boom i've established the diagnosis i've gotten all five so that is how we diagnose this actual condition the last thing that i have to discuss here we just have to talk about it is there's actually patients who can have something called non-infective endocarditis and we have to be thinking about this when we're going through our differential so we have to ask the question could this patient have endocarditis but it is not due to a pathogen and so there's two types of conditions that you have to think about one is any advanced malignancy so any type of advanced malignancy and i have one particular organ here to think about here and that is the pancreas if someone has a pancreatic tumor like a carcinoma these bad boys are super super annoying because they actually increase a lot of cytokines that increase clots they form little micro thrombi and these micro thrombi love to stick to the valves and form these micro clot vegetations they're literally vegetations but they're sterile vegetations they're not containing infectious pathogens that's one particular thing okay so we can develop non-effective endocarditis so you can have a dysfunction of the valve they could potentially have murmurs they could have particular types of issues where they can throw off little emboli but they're not septic emboli so these are things that they can have but they're not due to a pathogen so they don't typically have like super high fevers they typically don't have the immune complexes but they could have valve dysfunction and again they could pop off some of the emboli but they're not septic emboli okay the other thing here is that we have an increase in inflammation due to lots of antibodies that are being produced and this condition we consist we think about something called sle systemic lupus erythromytosis in this condition your body produces lots of antibodies these antibodies increase inflammation and with increased inflammation this increases the activity of small microthromby that form onto the heart valves and again you get these vegetations what's really important to remember here is these have two particular types of names so for advanced malignancy that causes these micro clots we call this marantic endocarditis which is a non-effective type and for sle we call this libman sax endocarditis well okay i have these microthrombi so i have a patient maybe they have some low-grade fevers maybe they have little vegetations on their valves maybe they have some type of emboli maybe they have valve dysfunction so they have heart murmurs and some type of situation like that and i get an echo the echo is positive for vegetation they don't have positive blood cultures though right so that's one particular thing i can use to check off here so if i were to say for my diagnosis for these patients their blood cultures would be negative that's one particular thing the next thing here is if i were to treat these patients the treatment for these patients tends to be antibiotics that won't work for them now that doesn't mean that it's definitely non-infective endocrine eyes if you give someone antibiotics and they don't actually improve that could still be an infective endocarditis that just needs surgery but for these patients they typically will not improve with any type of antibiotic regimen what absolutely probably needs to be done for these patients is they have blood cultures that are negative they don't improve in antibiotics that's one way but oftentimes you need a biopsy to really confirm but really it's looking for the underlying conditions if you go ahead and do a ct of the abdomen you find a big pancreatic tumor or you do an mrcp and you find a big pancreatic tumor or you test them for sle and they're positive for sle it is something to think about doesn't mean that they can't have sle and a true infective endocrinitis doesn't mean that they can't have a pancreatic tumor and effective endocarditis but it helps you to kind of think through your clinical reasoning and try to have an idea is this some type of non-infective or infective if my blood cultures are negative i could consider a biopsy to definitely confirm this if my antibiotics aren't working that could also help my diagnosis and if i have this underlying condition here present that could also help my diagnosis so again now that we've talked about the diagnosis and the differential let's talk about the next step which is how do we treat infective endocarditis and how we prevent it from actually developing in patients who are at higher risk of developing in the future all right indigenous let's now move on to the last part here treatment and prevention so when we're talking about the treatment of infective endocarditis it really comes down to antibiotics all right so we're trying to clear that infection that's causing this damage to the valve and the septic emboli and the immune complexes the nasty fevers so it's a really kind of complicated condition but really when it comes down to the treatment you clear the actual infection that's causing this problem and you start to see some improvement now in these patients they sometimes can be relatively hemodynamically unstable especially in the acute types where they truly chew away that mitral valve the aortic valve they cause an acute left sided heart failure with sometimes going into complete cardiogenic shock these patients can be super sick so in these patients you can try to immediately start them on antibiotics after you obtain their blood cultures start them on empiric antibiotics for the patients who are less sick the subacute types of infected endocarditis you could actually get their blood cultures and hold off on empiric antibiotics right away unless they really look somewhat sick they have some of the symptoms they have some concerns or they're not as hemodynamically as stable as you'd like them to be you could potentially start an empiric antibiotic regimen but for the most part in acute infective endocarditis we're starting impaired antibiotics for the subacute types it kind of depends sometimes you can wait until the blood cultures come back in this case though we're going to talk about empiric antibiotic regimens for acute and subacute whether you have a native valve or a prosthetic valve just right off the get-go starting the empiric antibiotics we're not going to go down the rabbit hole of talking about every single type of pathogen and the antibiotic that goes along with it i don't think it's truly worth that because it's just an extensive memorization i think we're going to get a good idea of the empirics the surgical procedures that we need to do for these patients and what are the indications for that and then we'll talk about prevention so let's go through the antibiotics empiric antibiotics okay so again it comes down to two different categories i think is the best way to remember this so first thing again antibiotics get your blood cultures first then after you get your blood cultures start your empiric antibiotic regimen okay what is that empiric antibiotic regimen now the empirical antibiotic regimen depends upon the valve that's affected so let's say that you have a native valve infective endocarditis in other words you have a nasty microbial vegetation of your mitral valve you have a nasty microbial vegetation of your aortic valve or of your pulmonary valve or of your tricuspid valve regardless one of these valves has a nasty microbial vegetation and causing an infection when this comes down to it you want to establish is this acute so in other words do they look really septic appearing do they have very high fevers do they have an intense leukocytosis do they have a bump in their crp and esr do they have an acute onset left heart failure with a nasty regurgitation murmur do they have a perivalvular abscess do they have a prostatic valve dehiscence do they have nasty septic emboli do they have immune complex phenomena in any of those kinds of situations you should definitely buy on high alert for acute infective endocarditis in that situation if it is acute the most common pathogen and this is why i stressed it is staphylococcus aureus and there's two different types for this son of a gun there's misa and there is mrsa in this situation here we can actually use two antibiotics to cover for this the two antibiotics that we'll give for these patients is vancomycin so vancomycin will cover your mrsa species and then what we can do is is we can add on another type of antibiotic so the other one that we can add on here is something called cefazolin or naphthalene so these are the two types that we can add on a beta-lactam really is what we kind of categorize this as but the beta-lactams of choice is cefazolin because this is going to cover your gram positive more or what is the other one the other one that we can utilize besides cefazolin in these patients is nafilin so you can also utilize naphthalene and this just gives good augmentation sometimes vancomycin monotherapy is not enough for your gram positives so it might not cover all the gram positive and sometimes it might not be good enough against the mrsa species so you can give vancomycin which will cover a good chunk of your gram positives especially the staph aureus and you can get augmentation of the vancomycin making it work a little bit better with cefazolin and naphthalene that's what the guidelines say for native valve acute infective endocarditis most likely due to staphylococcus aureus what if it is that patient population that it is sub-acute this is more likely to be a huge just a massive types of you know bacteria that we have to be thinking about but we want to be thinking about strep viridance we want to be thinking about your hasic organisms we want to be thinking about your enterococci okay so with these types of situations and we want to cover these let's actually bring this over here so we're not you know intruding on this here but we have hasic or we have entero caucus in these situations we have to be able to have a good range so again vancomycin will cover most of your gram positive bacterias because strep variance is positive and pterococcus is positive but to give a little bit more coverage against enterococci and against the gram negatives you're going to need something a little bit more than vancomycin and so sometimes what we'll consider in these patients is something called ampicillin but particularly we add on a little bit so we add ampicillin plus something called sulbactum it's a combo so sometimes we call this unison but it's ampicillin sulbactum and that'll cover your hasic and your enterococcus a little bit more the other thing that you can do sometimes is you can add on especially if someone has a penicillin allergy you can actually do something instead of ampicillin sulbactum and you could do something called ceftriaxone ceftriaxone because that'll cover your hasic and your enterococcus a little bit better but this is what you'll do for a patient who has a sub-acute native valve infective endocarditis likely due to strep virus dance hasick and enterococcus it's still vanq covering your staff your grand positives and then adding on more coverage with ampicillin soul bacterium to cover your gram negs pasics and the enterococcus if they have a penicillin algae that they can't take ampicillin then you give them ceftriaxone boom we're good we covered the native valve endocarditis and we covered the two components here and again it's important to remember that this is empiric because what happens is after you get your blood cultures you start them on empiric antibiotics your blood cultures come back positive then what you do is you narrow you remove certain types of antibiotics so maybe it comes back just as misa well i don't need vanco i can just do nafcylin maybe i come back and it only is enterococcus or hasic well then i can just do like ampicillin so you get the point or i can do rocephants i have triaxone i can remove certain types of antibiotics and narrow it down to the specific type of pathogen i don't want to go down that rabbit hole because it'll take the rest of the you guys will be won't get this video done okay so we're just going to talk about the basic empirics and then we're going to move on now to the next component here the next category that we have to talk about is something called prosthetic valve so prosthetic valve infective endocarditis so in this category we have a patient who has a prosthetic valve so maybe they have a prosthetic valve like an aortic prosthetic valve and with this there's now a nasty goombach on it a nasty microbial vegetation that's starting to cause destruction of this valve decrease the function of this valve what do i need to know okay well i got to clear that dang infection so i have to know again with these prosthetic valves i can have acute remember which type of pathogen loves prosthetic valves that is an acute category staphylococcus aureus but if you remember the one for the subacute it was staphylococcus epidermidis but you also have the strap viridans you have all these other ones but again acute don't think don't forget about staphylococcus aureus and again you're covering mrsa and misa so it's the same dang thing you're giving these patients vancomycin you also need to consider something here in these patients who are getting the vancomycin for the staphylococcus aureus sometimes we add on another antibiotic and this is a betalactum but it's not the one that you would think you would think oh this is a relatively simple one i think i got this one i'll do cefazolin and nafsillum you would think that but it's actually not that sometimes what we like to use instead of these tends to be more cephepine for some reason cefazolin doesn't work as well in these patients with prosthetic valve acute prosthetic valve infection carditis as compared to a patient's with getting cefepime so sometimes cepipine tends to be tends to be much more superior in these patients okay here's the where it's a big difference though so we have vancomycin and we have a beta-lactam we add on one more so the next thing that we have to add on here is gentamicin and gentamicin is the big thing here for the prosthetic valves so don't forget that one that's going to cover again a bunch of your staphylococcus species your mrsa and then the last thing here sometimes we'll add on rifampin but we don't add this up front because sometimes it can cause resistance to other types of antibiotics and make it actually not as good for these patients so you don't want to add this up front you may add this a little bit later like maybe a week later in these patients okay so again a cube prosthetic valve infective endocarditis likely due to staph aureus vancomycin add on a betalactum you would think it would make sense to give you cefazoline or naphthalene but instead we find that cefepime sends to be better in these patients with prosthetic valves and then the big difference here is gentamicin to give you your more staph aureus coverage plus or minus rifampin but at least wait about a week before starting it up because it can cause resistance to other types of antibiotics okay the next thing is what if it is sub-acute so subacute again you're thinking about all these ones that we just talked about guys so again staph epidermidis is the one that loves prosthetic valves epidermidis you're talking about strep viridans you're still talking about the gram-negative hasic you're still talking about the enterococcus so all of those are still the exact same the only one i think i added on here that just to you know jog your memory and good space repetition here is the staphylococcus epidermidis just remember loves prosthetic hardware but with these again what are we doing we're covering our staff species so with the staff species we want vancomycin we're also going to cover our strap viridians are hasic or enterococcus so we have to do ampicillin sulbactum so we'll do ampicillin sulbactum and then the same concept here if the patient has some type of penicillin allergy you can switch it with ceftriaxone the only thing that's different here is that we are adding on gentamicin and that is one of the big things to cover more of our staff species here and then again plus or minus rifampin in some of these patients that is going to give us the big bulk of stuff that we need to know for this so it's actually relatively simple so when you think about it to really sum this up in patients who have native valve infected mineralities they're getting vancomycin and a beta-lactam for the acute type that is particularly cephasyl and naphthalene for the subacute they're still getting vank but instead of giving a beta lactim we're giving some like specifically the uh cefazolin and naphthalene we're giving a very specific type called ampicillin sulbacthum but if they have a penicillin algae we're giving ceftriaxone but really in the grand scheme of things for native valve you're getting vanco and a beta-lactam vanco and these are still beta-lactams okay you're just getting specific types within the prosthetic valve you're just having to give a little bit more staph coverage so you're still giving vanc and a lactam just a specific type being cephepine and then adding on gentamicin plus or minus rifampin and then for the sub-acute prosthetic valve endocrineitis you're still giving vanco for the staff you're giving the ampicillin sulbactum for the strep varidance and enterococcus and you're adding on the gentamicin to cover more staph plus or minus the rifampin it's actually relatively simple when you think about it right that is our empiric antibiotics once our blood cultures come back positive for the specific type then you can narrow your antibiotic regimen as we discussed which we're not going to go into the depths of because i think that'll literally be the rest of the day and we will never finish this video so let's move on to the next component here which is okay what are the patients that i can try the antibiotics get it all started but i should probably give cardiothoracic surgery a call and say hey i think this patient needs the valve replacement or they need their valve to be repaired at this point in time what are those scenarios let's talk about that so for surgery again the basic concept with this one is whether you're doing surgery it's going to be replacing the valve or repairing it so it's either a valve repair or it's a valve replacement and that kind of depends on the cardiothoracic surgery's opinion so once you get them consulted they'll have more of an opinion in that situation but what are the indications that i should you know bring them up and say hey got to consider this and this it would be considering heart failure so a patient has acute left-sided heart failure so they have i'm not even kidding acute mitral regurge so acute mitral regard or acute aortic regurg where they're literally i'm not even kidding they have significant pulmonary edema so cr you know shock you know just this nasty pulmonary edema and they're in full blown like cardiogenic shock on multiple pressers with left ventricular dysfunction in these situations you need to get these patients immediately to surgery to repair that sometimes for these patients with mitral regurgitation you're putting them on pressers on inotropes you're filling them up with fluids you're trying to potentially um maybe even use like an intro aortic balloon pump you're putting them on bypass you're doing a bunch of things and then getting them the surgery to get it repaired periodic regular just same thing you're putting them on ionotropes you're putting them on pressers potentially being careful a little bit with the pressers and you're also supporting them with bipap don't do an introverted balloon pump you'll kill them and then get them to surgery so that you can get that valve repaired or completely replaced but that's a big one here the next one is at any time any time a prosthetic valve has any dehiscence that's not something that you're going to just magically heal there may be some fibrosis that occurs over time but that valve is going to continue to cause problems and likely put some into an acute heart failure because you're going to have that perivovular leak you're going to be at risk for abscesses to form around that prosthetic valve that's dehist away so again i would say in these patients who their prosthetic valve is now dysfunctional because it's to hist away from the actual wall not being connected analyst to wall anymore they need to go to surgery and get that repaired the other situation is if they have a peri-valvular abscess these are just not going to get better with antibiotics it is super unlikely so if they have a perivacular abscess the antibiotics not be it might not be enough to penetrate into that or clear that infection enough you actually might have to go in and clear that remove all the stack from that abscess and then potentially repair the valve or significantly replace the valve in these situations boom you have to go to surgery so acute heart failure prosthetic valve dehiscence or a peri-valvular abscess that's not going to clear well with antibiotics the other thing is if you have a patient who you're putting them on this bug juice so you're giving them these iv antibiotics or you're giving them the bug juice and they're just not getting better they are not improving so there's no improvement in these situations i would say that's a consideration to say okay they're not getting any better i'm likely going to have to go in there remove the valve remove the vegetation repair the valve whatever it may be the other thing is you have to think about the particular types of pathogens there's some pathogens that are so nasty that you can put them on iv antibiotics and they're not going to get better or you put them on iv antifungals and they don't get better we didn't talk about that and patients who have potential candida we sometimes actually have to put them on iv antifungals like amphotericism caspar fungin a lot of nasty things and so sometimes these patients who have staph aureus or they have candida in these patients they're likely going to need surgery because they're just so nasty and so pathogenic at certain times that they're just hard to clear with iv antibiotics or iv antifungals like amphotericin b and caspal fungi and things of that nature so i think that kind of covers the basic components here that again if you have an acute left side heart failure cardiogenic shock parasitic valve dehiscence a perivacular abscess no improvement on iv antibiotics or you have the really nasty pathogens that are unlikely to clear in patients who have candida infections like iv i'm sorry such in patients who have immunosuppressive conditions or nasty staphylococcus aureus you may have to go in there and actually repair or replace that valve last but not least the patient has a recurrent septic emboli so if they have recurrent septic emboli this is something that you got to get a hold of and maybe you have them on antibiotics and they're not getting in better and they're still infarcting part of their brain or maybe they're having nasty abscesses that haven't actually been able to be controlled because you're not penetrating the blood-brain barrier enough or maybe you have some type of bleed that's occurring here like an ich or a subarachnoid hemorrhage from a mycotic aneurysm or maybe you have some type of splenic abscess or maybe you have a renal infarct or maybe you have spondylodisciitis or a septic joint or all these other complications that can result from constantly popping off the septic envelope off these vegetations on the heart valves that would warrant a patient to actually go in and repair that valve or replace that valve because without getting that actual disease valve off you're going to continue to keep developing strokes or bleeds or abscesses all over the dang place and you have to clear that actual valve away and try to get rid of all these other infections that are occurring throughout the body so when you put in the fresh valve that actual pathogens don't lick back on to that actual new valve so again with recurrent septic emboli that you keep flicking these things off all over the place you need to consider replacing replacing and repairing that valve and then clearing the infection before you put that fresh valve back in okay that covers the antibiotics that we need to know empirically that covers the surgery and knowing the indications as to when i got to go to surgery last but not least let's talk about the prevention with endocarditis prophylaxis people are at high risk and are getting certain procedures that they need to maybe take an antibiotic before they do these procedures let's talk about the endocarditis prophylaxis so the last thing we have to talk about is patients who are high risk of getting infective endocarditis if they get some type of special procedure what are those patients we got to talk about some certain cardiac conditions if these patients have these specific cardiac conditions that we'll talk about they're getting one of these specific procedures they're at high risk now of getting bacteremia latching on to one of their actual diseased heart tissue and causing infective endocarditis so we should give them a particular antibiotic maybe 30 to 60 minutes prior to that procedure that reduces the risk of bacteremia causing infective endocarditis what are those cardiac conditions there's four don't forget i'm ready here we go the first one is if you have a history of infective endocarditis you have a prosthetic valve that definitely puts you at high risk the third thing is you have a congenital heart defect particularly a cyanotic lesion but it could be a cyanotic and last but not least if you're status post heart transplant and now with that heart transplant you poor thing you have a valvulopathy associated with that all of these things there's some type of increased risk of the bacteria that you introduce into the bloodstream latching on to one of these actual issues here the damaged valve a prosthetic fresh valve a valve that may be having some underlying issues because of a congenital heart disease or a valvulopathy with a patient who has a heart transplant if that happens and you get one of the following procedures you're at high risk now for bacteremia to damage these valves so what are those particular procedures first thing is anytime you're getting a simple dental procedure so you're going to the dentist and when you go there you're getting a cleaning i'm not even kidding you're going to get a cleaning you should probably get some antibiotics beforehand if you're going to get a root canal or you're ripping out all 32 teeth out of the you know out of the mouth i'd say that's something that you're getting dentures something like that you definitely need to be getting some antibiotics beforehand because you're having an opportunity for bacteria to get into the blood and bind onto these damaged heart valve tissues the other thing is if you're getting some type of ind so you're getting an ind an incision and drainage of an abscess and this could be like a skin abscess so you have a nasty like skin abscess or you have like a musculoskeletal abscess that you're about to cut into and there's an opportunity for the bacteria to enter into the bloodstream through that way that's another thing to be thinking about or you're going to be doing some type of respiratory tract incision or biopsy anything like that is an opportunity to break the barrier of the respiratory tract and allow for some of the flora in that area to enter in the bloodstream and bind onto these actual damaged heart tissue and cause infective endocarditis again don't forget another thing that actually there's in the literature that actually says that anytime somebody actually gets a um they're inserting a cardiac type of structure a prosthetic hardware like for example you're putting in an aicd you're putting in a pacemaker or some type of wire into the heart anything like that you might actually require especially if you have any of these cardiac conditions you may also require some type of antibiotic prophylaxis prior to that so what is the antibiotics that we give so the first one that we start off with is can you take po so can you take medications oral if you can amoxicillin is the one to go with okay can you not take po so if you can't take po and now you have to get iv or im then we do what's called ampicillin okay now if you have a penicillin allergy that you can't take amoxicillin if that's the case then we consider something like azithromycin and if that isn't the option for you another one is clindamycin okay in these situations here when you give this antibiotic again i would say the most important one to remember here because it's going to be the most common one is amoxicillin when you give this medication you want to give it at least 30 to 60 minutes prior to whatever the procedure is that you're getting if the patient has one of the following four conditions a prosthetic valve and a history of infection endocarditis a congenital heart defect and a heart transplant with a valvulopathy engineers in this video we covered a behemoth amount of information i'm so tired and i hope that you guys made sense i hope this stuff made sense i hope that you guys understood it i really hope that you enjoyed it and engineers as always thank you love you and until next time [Music] you

Channel: Ninja Nerd

Views: 81,901

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: iaO8110iSzI

Length: 108min 46sec (6526 seconds)

Published: Mon Mar 14 2022