Dr. Cook describes the clinical manifestations of endocarditis and how to treat medically and surgically for best outcomes.
We'll talk about in endocarditis today. Um So just a couple of editorial comments about endocarditis. We've really seen an explosion in the number of cases uh in the last decade really. And there's, there's a few reasons for that. Um for any of you who've watched the Hulu series Dope Sick. And you can see exactly what happened uh throughout Appalachia, there was a few things that happened that were key in, in driving the Ivy drug epidemic, which is largely what has driven the, the huge uptick in the number of endocarditis cases in 1995. Uh Big Pharma introduced OxyContin and that drug was touted as a uh something initially for cancer, but then also for chronic pain. And I can remember, uh two years after that, I started as a trauma resident in 1997 and that drug was being uh touted even to us as residents as something that you could give people twice a day, gave them good pain control for noncancer pain. So we had tons of patients who were, you know, broken limbs and trauma, uh uh whatever it might be that we put on that drug. And uh the addiction rate was, was touted as next to zero. And we, we had no evidence of that at the time. That's just what we were told, but there were not good studies on that. So we, we believe that at the same time for those of you who practiced in the decade after that, you will remember the the fifth vital sign pain is the fifth vital sign. So vital signs, the four classic vital signs are objective measurements. But for the first time, we introduced the fifth vital sign as something that was totally subjective. And you had these pain scales with, you know, the, the happy face versus the sad face or one through 10. And I can remember being called at three o'clock in the morning with a, a pain, a patient who had eight out of 10 pain. And this was the first time I'd been called. And uh the nurse said that, you know, the patient had eight out of 10 pain and I was like, wow, I just saw them not long ago right after I made post browns after midnight and she was sleeping and she said, no, she was still sleeping, but I woke her up and asked her what her pain level was. Most people with an eight out of 10 pain, you know, don't not sleeping. So she demanded that we give some kind of pain medicine. And I said, yeah, I really don't think we should and documented in the medical record was, you know, doctor Cook refused to give pain and pain medicine and there was a physician successfully sued for inadequately treating pain. So this became something that was touted by every medical society and by even J CO and then the heroin back in those days was still fairly expensive. But then people figured out how to make it cheaper and cheaper and cheaper and it became widely available. So that was the second really big hit that started the opioid epidemic. And then the third big hit was that uh even as recent as 2014 IMF or illicitly manufactured fentaNYL came on the scene and that has uh been manufactured here but is, has largely been shipped in um and smuggled into the US. So that has been our third wave and now we're seeing lots of deaths. Uh And that, and I just say that because this is what's really driven endocarditis, but we'll go through some of the reasons. So when you look at endocarditis, I got this slide here that says is this lasagna or endocarditis? The the two in the middle are lasagna. And if you see everything around it, this is really how these valves look, they are absolutely destroyed. Uh The vegetations uh on there do look like these uh beefy red collections of, of garbage and, and this is all real endocarditis. You see that there's an unfortunate pathologic specimen here uh of someone who's uh died from endocarditis, that's a uh an infected valve. Um And there's a uh perforation of the uh uh anti leaflet of the uh micro valve. Uh So, uh and then this is uh aortic valve cusps and you can see that this is completely eaten away. So we'll go through some of the considerations, clinical manifestations, how we make this diagnosis? What are the complications? How do we treat it medically and surgically and what are those outcomes? So, uh first described microbial vegetations in a 39 year old male that was 18 of six. And then that term was coined endocarditis in 18 41 by Boul Yard. Uh William Osler then described the clinical features uh at the Royal College of Physicians lecture in 18 85. And he turned the term uh termed it malignant endocarditis because as you know, this was the pre antibiotic era uh by 40 years and dated modern heart surgery as we know it by 70 years. So there was no treatment for this and endocarditis was almost uniformly lethal. Uh Taro and the cell first described it uh uh in treating endo cardia surgically by ligating a P P D A. That was odd to me the first time I read this because I thought, how do you, how do you treat by ligating something? And, and they had a local infection and obviously, a P D A is an area of turbulence, there was a local infection and simply by shutting off that uh turbulent area era and area and giving them antibiotics, he was able to treat that. Uh I thought it would have torn through. Apparently that patient survived. And then as you know, uh Alexander Fleming discovered antibiotics in 1928. But then slowly, over the next decade, different antibiotics were discovered their use uh became popular in the 19 forties. Antibiotic use just exploded and was used for everything under the sun before we really knew about uh antibiotic resistance. Um And then in 1965 Wallace performed the first uh aortic valve replacement uh for endocarditis. So how do we define it? It's a microbial infection uh in the endothelial lining and its characteristic lesion that we see both pathologically. It was how it was described. But we, we describe grossly and certainly on uh what we know on echocardiogram is the vegetation uh which is just a collection of bacteria you see here that there's uh endothelium, there's collection and a large infiltration of uh lymphocytes uh into that area. So how does someone get endocarditis? And then you know how virulent is it for that person? Well, this is true for almost any disease but uh the hemodynamics, uh the turbulent flow denuded endothelium are sort of the set up for this. So vagar lesions that exist uh how virulent are the bacteria. Uh And then what are the host defenses? And you can say that is, you know, for almost anything. So, um, many things can happen when you have, uh, endocarditis. So there can be local destruction of the tissues. The valve might leak, uh, prosthetic valves can be so, uh, encumbered by large vegetations that they actually become stenotic. Um, so I, I have some, uh, pictures of, uh, ST stenotic or nearly obstructed tricuspid valves, uh, or the person can go into heart failure. Uh, meaning that the leak is so bad, they, they come in and, and uh almost shot from congestive heart failure or abscess formation. If you have uh one of the aortic root, uh that's eating its way through the heart, then they can come in and heart block, visualize into any chamber. And we've seen it go from, you know, aorta into the dumb, the left atrium into the right atrium, uh uh and freely rupture even or distal embolization. So, uh they can come with a stroke or uh an acute limo from an emus or uh develop all of these um septic emboli. And commonly, we see them in, you know, the large blood filters in the body and the kidneys and the and the spleen less so in the liver. Uh but also in some of the large muscle groups, uh soas and paraspinal abscesses are very common. So, traditionally, native al endocarditis was, you know, just a few per 100,000 persons and uh predisposing factors or poor dental hygiene. Obviously, we all get bacter remic every day, every one of us, every time you brush your teeth, you get some amount of bacteria in your bloodstream, not a problem, you're healthy, your body just takes care of it and it's not a big deal. Uh However, if you have an overwhelming amount of bacteria getting into your bloodstream, uh from really poor dentition, your body can't overcome that. Um long-term venous access, obviously, any foreign body uh diabetics prone to any infection for whatever reason I V drug use, of course. And if there is some preexisting bi or abnormality, uh for prosthetic uh endocarditis, uh it can be as high as, uh, you know, 25% throughout a lifetime is reported. Uh I would say it's 7% in developed countries as high as 25% in some undeveloped countries. And largely that's because of, of hygiene and the cumulative risk that we tell people it's about 1% per year, which for valve surgery, that's about true for stroke or major bleed if they're on cumin as well. So the definition of early and late endocarditis is really arbitrarily made at about one year. Um But if you look at the bacteriology of, of uh early endocarditis versus late, they really are different. And we assume that most early endocarditis occurs at some point during that hospitalization, either there was a contamination at the time of surgery or the patient got a postoperative pneumonia or U T I or whatever it had something to do with contamination in the per operative period. And usually uh the the peak incidence of that is 60 days, the bacteria staph epi staph aureus, um and gram negatives and fungus mortality has been reported as 76%. Again, these are, this was uh sort of in the, um I would say pre ivy drug use era. Um because these were a lot of the uh all comers at that time that tended to be older, sicker diabetics and, and renal failure, chronic dialysis patients. Um but even still the mortality, I think this, I keep this number in here because I think it points to uh the fact that when you operate on somebody, if they become infected soon thereafter, the 12 hit of an operation plus a reoperation and the difficulty of that and the fact that their host defenses have not been able to overcome this uh early on really speaks to the operative mortality of these reoperations late is a year afterwards and bacteria can be from uh various sources. Um And organisms tend to more closely resemble that of native valve endocarditis. But um mortality is reported as high as 44% uh in the uh non I V drug abuse era. And so this slide just demonstrates that there is still uh some uh difference uh in native and prosthetic valve uh endocarditis. Um staph uh epi you see uh more and uh prosthetic uh endocarditis, most of these are relatively similar but uh similar but, you know, beans, uh group strep, a relatively benign, uh, comes more often from the mouth and you'll see that uh often in native. So how do they present? Sometimes it's just fever, they'll have this malaise flu, like uh type symptoms, anorexia, myalgia. Um All these things and on physical examination, you were taught all these uh things in medical school, oar nodes, which are really an immunologic phenomenon. Um They're not uh not uh truly an imbo phenomenon. Janeway lesions and splinter hemorrhages are uh are uh embolic as well as Roth spots and sub uh conducive hemorrhage. And then, uh obviously someone can present with a stroke. We recently had someone who um had gotten a ver a couple of years ago and he presented uh with a uh a lower extremity imbalance, an acute leg and then that got taken care of. And then a couple of days later, he had a stroke and he did, OK, recovered from that and was still in the hospital and uh was very, and eventually had to go to surgery, but it was uh proved to be uh quite an undertaking for him and uh unfortunately, didn't survive um, splenomegaly. Uh splenomegaly tends to occur when the infection has happened slowly and insidious, insidiously more with uh native Almen carditis. And then obviously on the cardiac exam, you'll see uh uh new or changing murders and they present in C H f if you look in the upper left, uh here you see, uh these are uh ross uh raw spots on the um on the uh eye and the sub conducive hemorrhage, uh Jane Wade lesions, Osler's nodes and, and splinter hemorrhages under the uh fingertips. So, uh they can present acute uh staph aureus, uh or other uh organisms that tend to be more virulent. Uh Usually it's a more fein course, you will see signs of peripheral M B I uh most often and they can have uh uh perv or abscess. So, if they come in really sick, it's been acute. Uh generally they have the more uh virulent organisms and the SIA and, and complications that are gonna be more severe. Sub acute can be sort of indolent. You might see someone who was, you know, you know, uh elderly or, you know, sixties or seventies and they had their teeth cleaned a few weeks ago. Then, you know, a month later they just started feeling sick, they went to their doctor, they got put on a short course of antibiotics for bronchitis. And then now they've come into the hospital and, and obvious fever. You get an echo and find that lo and behold now they have uh endocarditis of one of their valves. So it can be a bit more protracted. And as I mentioned to you, uh spin mega is more common, uh they will have some cutaneous signs. Antibiotics can cure a lot of those. So some of the trans male and to female, uh there's tend to be more males than females. But this is with the exception of I V drug use. And I'll show you some slides on that um uh acquired uh heart disease uh that obviously we see people living older and longer. And so, uh they tend to have more problems with, with whatever the sequel of valve dysfunction might be. But endocarditis is one of those. Uh There's, we see more acute cases now than we did before, more staphylococcus. And one of the things that I had noticed and uh we had not yet published on uh but I was embarking on that project before I left W B V was that we saw a huge number of CIA uh for the and, and it really has not been reported on significantly in the literature and these were not people that had been in the hospital and on ventilators, but people who were coming in for the first time and we were starting to see that people were injecting the tap water. And um and uh so then we started and suspecting that in some of the, you know, surrounding uh counties uh that we're seeing this from that. It was actually in some of the uh water systems. Uh when you see that pink uh film that would grow in the shower when you were in college and you never clean the shower you know, that's CIA, so it's very common. It's ubiquitous. But for whatever reason, we started seeing quite a bit of it. Um, the, so the diversity of the organisms that we saw historically, uh, obviously I V drug use. And since there are so many people now that we're putting valves in even tar, uh we're starting to see more because lots of people are getting val therapy. They didn't give val therapy before. Uh We don't see rheumatic heart disease that often uh streptococcus is less. We don't always see these classic signs and uh the median age has fallen substantially largely because of the opioid epidemic. Uh This was uh a slide I put together uh for S T S presentation in 2018 and this was just at W V U. And if you look at the number of tricuspid valve operations that were done um from 2012, 2014, it's less than 10. And then 2017, we saw a huge uptick and then 2018, uh we, we ended up doing 88 isolated Tricuspid valve operations that year. Nothing or nothing else for endocarditis. Um And almost all of them uh were due to uh I V drug use. I think only one or two was like Pacer lead or something like that. So, uh you can just see that it exploded. And if you look at the, uh you know, repair and replace, it's roughly 50 50 2017 and 2018. Uh, and you can see that our operative mortality, um, over that time was, you know, relatively flat, but it was low, single digits. So for the track husbands, it's, it's actually very low and that's largely because it's, you know, a lot of these could be done on pump, but, um, you know, beating heart and most of them were in their twenties and thirties and, and a significant number of, of teenagers as well. So my slide just froze up so I can go on and talk a little bit about, you know, the diagnosis. So there's, I have a lot of slidess in here uh that I've kept uh because I've given this talk of various forms uh before about Duke's criteria modified by Duke's criteria. What's the real, how do we make this diagnosis? You suspect it, you get a blood culture and you get an echo. I mean, that's really what happens in the modern era. Uh So if you look at TT E and T E E, uh T E is more sensitive, um when you do have something on att E, it can be very specific and particularly true for right sided lesions. T E uh some would say is certainly more cost effective just because of its uh sensitivity. Uh certainly it's better at seeing left sided lesions if you have someone you know who's larger or obese and you're looking at the micro valve. Um uh or if they have an intervening aortic valve, it may be incredibly difficult to see it on a transthoracic echo. So, um if there's pavin or extension and root abscesses, things of that nature, it's certainly a little easier to see on T E E. So this is a very busy slide, but it basically says if you think that it's fairly high risk on your suspicion, uh They've had uh a prosthetic valve, they've got numb congenital heart disease, they've got complications. They come in with a fever and heart lock then uh and you suspect that there's some type of aortic root involvement, uh just go for the T E E otherwise, you know, screen them with a transthoracic echo almost. We almost never go straight to T E E though. We almost always just get a transthoracic echo because it's non invasive. Some of these people are quite sick and you don't wanna sedate them for that. So if you look at these criteria and how do we make the diagnosis? Well, pathologically, uh if it's demonstrated on culture or if you get actually a piece of it and send it to path either from heart surgery or a an embolized uh uh piece of vegetation, obviously, you've got the diagnosis. Um So, you know, I remember memorizing these in medical school. So, and I went through this big, you know, list and I was like, OK, it's gonna be definitive if we've got two major criteria or if it's one major and three minor or if it's five minor and there was a list of 12 minor which I don't even have anymore because I don't, I don't even remember them. Um, so if it was possible though, if you had one major, one minor or if you had three minor, then you thought it was possible. I literally memorized that whole list of all those things in medical school because you memorized everything in medical school. But it's so unimportant clinically as to what we do today. I mean, I don't know if anybody remembers, oh, I can't remember seeing over the last several years having exposed all these patients where anybody even the most uh um ardent of internists who were rounding or infectious disease, writing anything in the chart about the number of dukes criteria that they saw. But I keep it in here for that reason because it is of, you know, historical uh significance. Um So they reject it really if uh you know, symptoms resolve with antibiotic therapy and you really don't have any other evidence of it. So the major criteria were really uh you know, blood cultures and then the echo or these high risk organisms. What are the hay organisms? And this was a favorite question that we always asked uh the medical students rounding with us. It's Hoopy or uh aggregated Bater, which I always memorized it as uh a bacillus. So I still use that as the pimping question on rounds because I can never remember Agri Aggregator Bater and doesn't even sound right. Uh cardio bacterium, I canella combo and, and these are all uh normal flora. So, you know, um I saw a couple of cases when I was in the military um of this. And so what happened was, you know, um guys got in a fight, he punched another guy in the mouth, had a horrible hand infection. So obviously, the the hand infection came from the other guy's teeth. Um And he got into carditis from that and uh he grew out I can. So um so the, the major criteria for the for dukes is get an echo and the blood cri and, and uh and a blood culture and that will give you the uh diagnosis. So there's all kinds of minor criteria that I won't go through. Uh obviously, medical therapy. The goal is to uh sterilize the bloodstream. If it's a small vegetation on echo. And even with the prosthetic valve, we can do that. A lot of prosthetic valves, we see it can find to just the leaflets. And if it's a small vegetation, particularly if it's late after a year, there's no annular involvement and we can clear the blood cultures and the vegetation is less than a centimeter. Many of times we can treat those people with antibiotics alone, even if it's prosthetic and endocarditis arbitrarily, we've set this length of time at six weeks. Uh we uh tend to use bacteria cyle as opposed to bacteria, static uh antibiotics. Uh But really we uh tailor it towards whatever we find uh broad spectrum uh early. But then uh move on to uh a more targeted therapy. Uh Just like you would with any other drug uh for people to come in with uh with these large vegetations. I'm often asked, should we put them on heparin? There's no evidence that putting them on an anti platelet agent or, or something is going to prevent this. The vegetation is the real risk. You know, getting platelets to then stick on the vegetation and hoping to put them on heparin prevents that happening, doesn't really work. So this was a very interesting study in 2019 that came out and they talked about po partial oral versus uh uh I V treatment. So that traditionally we've been treating these people for, with I V uh for up to six weeks. Now, in the drug abuse population, you typically would have to hospitalize them for the entire time. If you take somebody and you operate on them and you let them out of the hospital a week later with a pick line. You have now given them the absolute best access to shoot up drugs that they've ever had in their life and guaranteed that they will. The recidivism for I V drug users is 85%. So you give them a pick line it's almost 100 so, lots of hospitals. And what we had developed was that these people had to stay in the hospital for a total of six weeks, as you can imagine, especially when we hit COVID. And we had as many as 15 people in the hospital who were hobby drug users on antibiotics. It took up a lot of beds. It's, it's not just the 15 beds, it's the 15 beds for six weeks. So, uh, it's, it's very costly. It's intensive. Um, and fortunately those people get, you know, drug rehab and psych and counseling. They get every kind of therapy, possible group therapy, uh, music therapy, whatever we could do to get, you know, people reengaged in life. Um, but, uh, what this study did was it randomized, uh, patients about 100 each in a group two, uh, to get, uh, sorry, 200 each to get, um, I V antibiotics for up to two weeks. Everybody got I V for a couple of weeks and then the last four weeks, some continued, uh, half the group continued with I V and then half were switched to oral and the primary outcome of mortality, uh, a surgery that you didn't plan on doing, uh, some type of embolism, uh, relapse of bacteria with the organism that they, that you'd already cultured, um, from the time of, uh, randomization and what they found that, um, there was no inferiority to oral antibiotics. So, this has not been widespread yet. Uh There is going to be a trial coming through C T S net. And for those of you who are familiar with C T S net trials, um that this is gonna be embarked upon very soon that hopefully will have an answer to this question for uh endocarditis um soon. So uh certainly was non inferior. So the complications, Vaulter function, as I mentioned, uh the valve can be totally destroyed or can be perforated or a single cord rupture, which can cause severe uh leak, uh peral or extension. It can cause abscess as heart block. As I mentioned, they can develop any kind of fistula uh or, or heart block. Uh as I mentioned before or uh embolic meaning stroke, uh aneurysms and mycotic aneurysms uh can happen because you can actually infect the wall of a blood vessel. And this was typically what you would see um in the pre antibiotic era when people would get uh mycotic aneurysms of the ascending aorta with secondary to syphilis, um systemic emboli and then splenic infarct. So obviously, if they come in in heart failure, uh their valves are leaking so bad or stenotic, that is an indication if their uh blood cultures do not clear if they have any type of abscess or per or extension, they have an embolic event once is not necessarily a mandate for surgery. But if it's recurring, you have the suspicion that you're not gonna get away without an operation or fungus, we simply cannot cure fungus unless it, unless it is uh extirpated surgically. Um Other indications if it's a difficult to treat organism, I already mentioned fungus, but also staph aureus and pseudomonas. When we see those, we're less likely to be able to treat those patients with antibiotics. Um If there's a prosthetic valve, the his, if there's a per viar leak, we see that valve moving or rocking or we see uh any type of flow around the valve, you're not gonna get away with that an operation. Uh The vast majority of the time, if it's early, you're more likely to need to operate on them. Uh And if they just are septic or if the veg vegetations are large, now that definition and years past used to be two centimeters, but we now uh have shifted that down to one because we know that the embolic uh potential for them over one is uh pretty significant. Um And it is a risk factor for uh hospital death. Um Also other uh high risk uh vegetations are on the anti leaf of the micro valve if it is highly mobile and I'll show you some echoes of that. Uh And uh my uh tends to embolize more, more so than aortic. So the vegetation length and the mobility, as I mentioned, the P values for those uh comparative to other vegetations makes them uh extremely likely to embolize. So, stroke ischemia, renal spleen, hepatic and FARC, we saw lots of joint abscesses. People had to get uh joints either openly drained or aspirated. Uh lots of paraspinal abscesses that had to be drained with C T Guidance. This was a gentleman that uh probably eight years ago or so, um I took and, and uh fixed his um micro valve and then we were seeing him a couple of days after words and this is what he looked like. He's intubated, he's sick and he's extremely febrile. And so why is the guy so sick? We've already fixed him and we see t his belly and he had a massive spinach abscess that we didn't know about. And so we took him urgently to the operating room. I actually helped the general surgeon that night. And uh the guy was so sick and you can see this massive uh cavity in the center of the spleen here and the whole spleen is uh practically destroyed. And this was a couple of hours after surgery soon. He's got a spleen out it, uh dried up. So, the principles are, we always get an interp T E. We try not to manipulate the heart before we put the aortic cross clamp on many of times with Vaulter surgery. Uh almost always with aortic and mitral surgery. We will put a left ventricular vent in, it gives us a bloodless field. However, we're not gonna put that vent in, um, and put something across the microvalve and risk. Um, uh knocking one of those emboli off before the air to cross clamp is in place. And generally, we don't put any vents in the heart until the, uh, vegetations are removed. Um, careful attention to myocardial protection. You never know how extensive the operation is gonna be until you get there. So, uh, if they've got severe aortic insufficiency, uh, you suspect that you might be there for a while doing a root replacement. We'll arrest those hearts with retrograde cardio plegia. We always try to send inter operative cultures. Sometimes it may differ from the blood cultures that you've gotten up to that point. Uh And in a couple of cases, you'll find echo evidence that you have to take some someone to surgery, but they've had good antibiotic therapy and you don't know what the bug is. You just, uh you've got culture negative endocarditis at that point and you have to suspect that it's fungus at that point. And you really should be very vigilant about sending interoperate cultures and then careful attention to aseptic technique. Generally. What I'll do is with the surgical principle is you have to do a radical ex extirpation of everything. Sometimes you hate to do that because you just keep cutting and cutting and cutting and there goes the mitr root, there goes the mitral curtain, there goes the interior leaflet of the, of the uh mit and you're staring at this ma and the dome of the left atrium and you're staring at this massive hole and how are you gonna put all this back together? And the temptation is to start cutting less and less and trying to save things because if you do that, cut everything out, you're gonna have to put all that back together. Well, that never works out because if trying to sew through tissue that is not healthy, first of all, the stitches don't hold, you're gonna have bleeding, patients gonna have substantial problem and you can guarantee that they're gonna get infected. So uh absolute uh Debre of everything that is, that is grossly infected. And then we, we will typically get rid of all of the contaminated instruments. Every pickup that has been used to grab vegetations. You're not now going to use to sew on the normal valve when you put it in or the prosthetic valve, right? So we get rid of all those instruments. Surgical team changes gloves and I will often use a pal irrigation. You see that we do this on uh big open wounds uh for extremities, uh you know, uh abscesses and things like that, but I'll actually do it inside the heart. Uh Some people will use beta dime um whatever we can. And there's, there's even cavities where I've patched that I've stuffed antibiotic beads in uh that we've used for orthopedic uh procedures. So we have to eradicate the infection and then obviously you need to correct any hemodynamic defect. If you can repair the valve, that's great. Uh If you can't obviously replace it and close any fisa, we avoid as much prosthetic material as you can. But, you know, that is not the most important thing because we can even put mechanical valves in these people and, and lots of, you know, prosthetic material with an entire, you know, artificial root. The most important thing is uh is radical surgical extirpation as you would for a cancer operation. Um We can use Altos or bovine pericardium. Uh Many times I'll use homographs for infected roots. Um I just did a homographs on a guy that's getting ready to leave the hospital. Fortunately, he was very sick. We don't do them as often because homographs are not great. They really are not a good solution long term, uh particularly for young patients because they don't last. And you can guarantee if the patient survives within 10 years, they're gonna need something done to that again. But the problem is is that when you have somebody that um has got such a large amount of tissue missing, the added uh amount of tissue that comes with a homograph, the crest of the ventricle is also harvested um and also the entire anterior leaflet of the mitral valve all the way down to the cords. And you can use all of that tissue to stuff into the big abscess cavity. And, and uh and also to reconstruct the interior leap to the micro valve, which was what we uh just did in the, the, the gentleman that's in the hospital. So, um, you can select mechanical or bioprosthetic valves. Uh It doesn't really matter that much. We used to think that you should never use mechanical valves. But again, the real uh problem is surgical extra patient. If you got a young patient who's gonna reliably take Kinin, you can do a mechanical valve, I would say probably never do it in a drug user. Um, if they survive, you know, um, you put mechanical valves and I've done it, I've put mechanical valves and, you know, you have a conversation with a 35 year old drug user. I swear to God, I'm never gonna do it again. I'm never gonna do it again. Uh I did this a couple of years ago and I put, uh I put a mechanical aortic valve in a guy and he came back infected from reusing. So I won't say never. Um I've also done it in a couple of patients that, you know, were reliable. They turn their life around and they never use drugs again. But uh you have to give those considerations to the IY drug population. So, mechanical versus bioprosthetic. If you look at the literature, uh, one says that uh prosthetic uh endocarditis um is higher if you use mechanical. Another one said it's higher if you use bio prosthetics and some guy noticed uh no difference. So it, you know, we do know that homographs are less likely than the others to become infected. But I mentioned there's some real problems with that. Um, risk factors for occurrence. If you did it for acute endocarditis versus healed, sometimes we'll have people that actually heal their endocarditis, but they come in with a valvular dysfunction that you have to go fix. That's easy because the tissue is healed. There's no active infection there. It holds stitches well, and that's a, that's a great operation. Uh And they're very likely uh very unlikely to get reinfected if it's non strep etiology. So, staph aureus and fungus, uh you're likely to have problems with infection again or you can much more so than you would with uh with strep. If there was major destruction of, of things, if it was a long, difficult uh reoperation to fix something, they're more likely to be reinfected. And then uh aortic valve versus, versus microvalve. Uh there's less annual destruction with the microvalve. And generally, we don't see uh significant involvement with the analyst of the Nitrol that we can't take that out and patch it rather easily with the aortic root. It's, it's a little more difficult. So, um I think there's a tendency of surgeons to not be as aggressive and that probably could account for some of that. Uh cerebral imparts are common for left sided lesions. Uh Most are embolic. Uh There's minimal risk of hemorrhage of those. But certainly we do see them, uh, bleed, uh, and embolic infarct is not necessarily a contraindication for surgery. However, if they do have a hemorrhagic infarct, um, you really have to think about when you're going to operate on them, you take somebody and give them 35,000 units of heparin for bypass run. If they've got a bleed, it can get worse. So, what I would say about that is we used to get MRI S and never operate on someone with a hemorrhage for at least 2 to 4 weeks. Um, however, we've sort of changed our management with that. We look at it if it's a low risk, um, emus as far as bleed and usually we'll have neurosurgery and neurology sort of intervention or neurology weigh in what they think that risk is, uh, we might take them to surgery sooner than later. Here was why we really had this, uh, this is from 1995 while we thought, you know, historically, we should wait after, uh, any type of embolic stroke. Is that, uh, that, you know, they would do better if we wait a couple of weeks. And so really, we just said, oh, they had a stroke. We have to wait two weeks even if it was nonhemorrhagic. That's really not true anymore. Recent data says that, uh, really you should operate on those people if they don't have, uh, a hemorrhagic bleed. And even if the, if the hemorrhage is uh not severe, you can consider operating on them most of the time we will get a repeat MRI the day before surgery just to make sure that any known hemorrhage has not worsened, uh, and then take them to the operation. And this just confirms that for um uh mortality and exacerbation after surgery was highest around that two week mark. And that's traditionally why we waited. So usually for cerebral andar, we waited two weeks. If it was hemorrhagic, we wait four weeks, we really don't do that anymore. So we operate when it's otherwise uh clinically indicated. And the MRI has shown that it's um uh relatively stable and small bleed. And I can't really define stable and small for you. Uh Other than say that, you know, small punctate infarct versus a large hemispheric infarct, those are obvious. But in between there, it's, it's, it's a judgment call. Um So mortality uh you know, is reported anywhere from 10 to 30%. It really depends on the activity of the infection. I think 30% in this era is, is high. But obviously all comers. Uh if you look at these operations, it's not, it's not the uh all people are not the same risk factors for death. If they have an abscess, if it's a staph infection, if they present it in heart failure, if they already have preoperative renal failure, if it's a prosthetic valve or if they're old um when we take these patients to the operating room and they have heart failure, it's really a bad problem, particularly if they've got fever. It is a, it's an incredible challenge to operate on someone who is both in cardiogenic and septic shock at the same time. Um We do it. Um uh but you see what, you know, I've, I've had a gentleman in the IC U now for over a month and, and that's what you end up with someone who's in hemorrhagic, uh or who's in a heart failure and, and also in septic shock. So, abscess and uh and high creatine are, are independent risk factors for this. I will burn through some of these because in one form or fashion, I've already mentioned this. But uh long term uh survival. If you look at these people who've had endocarditis, you see that, uh you know, to 10 to 15 years, a lot of people who've had endocarditis, they don't live very long largely because that is the substrate of patients that get uh endocarditis, um tend to have lots of other comorbidities. If you look at uh long term survival and tissue versus mechanical uh valves, it's really not significantly different. Uh Long term. Uh Mark Moon did this study uh quite a long time ago. Uh And uh looked at the difference in mechanical bioprosthetic and homograph. You see, with the homograph, that's the triangle lower line. There's a huge early mortality largely because those patients are extremely sick. Um And it tends to level off after a number of years. However, at 10 years, homographs are failing and those people are getting reoperations for severe aortic insufficiency and calcified roots. And for any surgeon that's ever done that, a calcified homograph route is one of the most daunting operations that you can embark upon. Uh, staff much worse than non staff organisms for uh long term mortality, abscess. Uh as you can see, and then the risk of reoperation is much higher for abscess. Um long term survival and 30 hos 30 day hospital survivors if they're uh culture positive, uh If you look at uh native versus prosthetic, prosthetic is worse long term. And uh the risk of reoperation uh really doesn't go away. They still have as long as they've got uh a valve in place. They can, they can uh have a need for an operation, uh risk of reoperation and uh uh for cultural positive. Uh not, not that different for mechanical and um tissue valves. Um So, reoperations typically, as I told you for a paravalvular leak, uh that's almost always uh when you're not gonna treat with antibiotics. If they've got severe valve dysfunction, um recurrent uh positive blood cultures and hemolysis, uh or emus. Uh Absolutely. No, no. You see this is a uh large vegetation. You see that is highly mobile, this is more than two centimeters. Uh This is extremely high risk. I I said my, this is a tricuspid vege vegetation. Uh You can see that this is extremely high risk for emus. These patients will present with uh multiple abscesses in the lung. Here's a valve repair, uh huge vegetation in the anterior leaflet and this is uh an extensive uh parac cardial uh patch that's placed and then the analysis stabilized with the ring. Sometimes we don't put rings in, it's probably not necessary all the time uh in, in these valves or you can do some other type of um either a pericardial strip uh or sutures to, to stabilize the analyst. Um We can do any uh number of, you know, classic valve operations uh for these um this shows uh uh replacement uh of the valve which we, which we do. Sometimes I'll do those with interrupted stitches. Uh I liken endo carditis to replace the valve to, to use Prolene. There's no interstices in a prolene stitch as opposed to a um a braided suture, but that's, that's merely anecdote. Um You can see this is a huge microvalve vegetation, uh blotting down into the, to the left ventricle. Um Here's a large vegetation on the anterior leaflet of the micro valve uh and severe uh turbulent flow. Um We can repair these by uh um you know, taking out sections and putting the valve together just like we would for a uh P two prolapse and uh techniques that we learned for mixin disease or we can patch them uh with autologous per cardial patches. You can see that uh here is a uh hole um in this uh anti leaflet of the mit valve. Uh And then you can see here uh I'm taking a uh little ruler and measuring the defect, the defect is under here uh afterwards. And then you can see this patch that I've uh put in for this anterior leaflet, the microvalve and then here's the repaired valve that's being hydros statically tested with Saline. Uh The patch is kind of under here. This is not the best picture, but you can see that this valve is now uh competent. That's an easy and fun fix. Um We can do sliding plasty just like we did for Xom disease and any, any number of creative ways that you can uh put these valves back together. Sometimes if there's large abscesses, you'll have to de breed those and then try to reinforce them. However, you can, this is uh an unfortunate 33 year old girl who gave birth came in a few weeks later and uh heart failure. Uh she had uh uh peripartum uh endocarditis and you can see she has severe uh aortic valve uh regurgitation. Uh This is uh a looking through the aortic valve and you can see down into the left ventricle. This is a uh aortomitral curtain that was completely eaten away and then uh subsequently patched. Uh This is uh a uh hole in the cusp of the aortic valve. And we can patch that with alto Picard. Sometimes when prosthetic endocarditis, as I mentioned, the root abscess will eat its way not only through the root, sometimes it can friendly rupture uh or eat its way into the dumb of the left atrium or into the right atrium. And so one of the ways that they can present in heart failure is with a left to right fistula. You can see this thickness here between the aortic root. This is the dome of the left atrium. This is the aortic root. And you can see that this is a large root abscess. Uh Here's another uh aortic root abscess, an interior leaf of the microvalve left atrium, left ventricle. You can see that this is the aortic root and here's a as a large root abscess. Um So this is a redo operation. And uh I've just put these videos in here just to kind of show you, you know, some of the technical challenges that we face when we operate on these people. Uh You can see that everything's stuck. We're having to take a, a lot of time to dig away millimeter by millimeter. Uh We're on cardio pulmonary bypass at this point. This is the venus canal and the right atrium, the heart's decompressed, but the heart is still beating. Um And you can see we're starting to dig down through all of this inflammation and you get the sense that now the tissues are starting to separate a little bit easier largely because they're infected. Um, but it's still, you know, quite stuck from the previous operation. We're now applying the order to cross clamp here and the heart's starting to arrest and now the, um, the heart is arrested, the heart is no longer beating. You can see that we have this decompressed root and, uh, we're digging out, uh, all of this uh tissue and then um somewhere in one of these, it's this picture or the next one. Yeah, it's this one. I believe we're just digging around and you see, pour out just a huge amount of puss that's, that's coming and pouring out there. So we'll literally see collections of, of puss like that. We culture it, make sure that we're getting the appropriate cultures, dig all this mess out and then um we go and open the aortic valve. This patient had had a prior uh aortic valve and now had a uh root abscess. And you can see that this here is the, we, we have to re replace the root. So this is the um left Maine and we're mobilizing the uh coronary buttons. Here. At this point, we use these little cardio plegia catheters to put them directly uh into the osa and deliver cardio plegia. And uh this one is in the left and this one here is going into the right uh coronary artery. So for these long operations. My cardio protection is very important. We're just digging out the rest of the valve and mobilizing those buttons. And then a lot of times with all this tissue here, I will actually do a pulse la uh Irrigator. Uh This was something that was developed for large trauma wounds and orthopedic surgery. But I've used it many times uh in the heart and actually we put antibiotics in there. Um And then we put these traction sutures in here. This is the homograph. So this is a cryo preserved uh donated human aorta. When people donate organs, we can, they can also donate tissue. And this is one of the um uh important things about organ donation. Some people who are not, organ donors can actually donate tissue. That's helpful. I'm cutting away part of the anterior of the microvalve where the cords are. And then we just prepare this by getting rid of some of the uh excess tissue. This is the crest of the left ventricle that's very thick. Many of times we can use that to put in these abcess cavities, you're seeing the underside of the cusps. And typically, what I'll do is just take a pen and I'll mark uh where these are. Um So for proper orientation, but also make a circumferential mark about three or four millimeters below uh all the way around so that I uh know that if I'm constantly putting stitches through the blue line, uh I can't, I can't be hitting the valve because if you put a, a stitch in the valve, this is the, the whole ascending aorta, you can see that uh all of the head vessels are still attached there. And uh we'll typically just sew this in with a running stitch and then we'll, you can use interrupted stitches as well. But there we are parachuting this down here, it is in place and then here it is implanting. We've already implanted the left mane and this is implantation of the right uh main coronary and then putting the homograph back to the patient's name, native aorta. And you can see the a cross clamps removed, the heart's starting to beat and, and here is what it looks like. And these are just some still photos showing that the roots implanted and we're still giving cardio plegia uh into the uh to the root. And this is a way to deliver cardio plegia into there. We partially plant this to deliver, pressurize the root and check these buttons to make sure that they're hemostatic. So, what's the problem with that operation? Um Well, this is a report of 33 homographs done for that indication. The 30 day mortality is almost 10%. You can see that's quite high. And in some centers, you know, it's even much higher than that. Uh the one and five year survival rates 80% and 60% respectively. So these patients don't do Well, long term, uh, the 15 and 10 year freedom from reoperation, uh is, is pretty abysmal. So 50% of these people are gonna need reoperated on at some point, some of them for infection, but a lot of them are for homographs. So I don't like using homographs and it's usually only, I'll use it when it looks like a bomb has gone off. And, and, uh, you really, uh, or in the case of the, the one that I did here, I knew that guy was gonna have an open chest. And so I debated, should I put all this back together with Bovi and pear? Um And uh or should I just use, use a homograph? The guy was sick and I really suspected he was going to have an open chest. There was a large void. And so I somewhat reluctantly used a homograph knowing this data, but I thought it was the best thing to save his life and his chest was open for several days. Uh So, conclusions um indications are usually uh heart failure and, or sepsis uh for some reason, uh Also M B I uh obvious uh from all of the, that we, that we say about the recurrence of endocarditis. But the, you know, the, the point that I try to drive home is that the, the real problem with the recurrence is uh inadequate uh surgical ex ex patient, uh operative mortality can be high in acute infections. But, uh, if you get them through the operation, as long as they don't reuse drugs, uh, the, it's pretty good outcomes overall. Um, subsequent reoperations for the non IBI drug use population are not that common. Uh, the usual indication is a per prosthetic leak. Um, and like I said, it's not high outside of, uh, recidivism. Uh, if you look at these, you know, people, um, and you look at what we have to do, there's no really good way to treat them other than surgery for, for some of these people that I mentioned. So, if nothing else transplant, uh, and endocarditis, uh, they're gonna give us some, uh, job security. So, uh, any questions about that?
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