So I guess we'll go ahead and get started. I don't think all of our speakers are here, but because we have such a limited time for the presenters, hopefully they'll show up. Are you one of the speakers? You're, you're, which one are you? Okay, all right. Perfect. So maybe most of them are here. So the other person that's going last, hopefully they'll show up. You're here? Okay. So everyone's here. So it is time to get started. So I'm Audra Schwack. I'm an interventional pulmonologist at UT Southwestern, and I'll just be moderating the session. So I'm going to introduce all the speakers, then y'all can come up, and I'll try to have your presentation open. The only instructions we were given in terms of presentations is when you get to the end. Just don't leave it on the slideshow as overslide. Just go back one slide if you stay up here for any questions or anything like that. I'm not sure what happens, but maybe it'll stop working. There were some issues in one of the other sessions. So I do have to read some things here before we get started. This is the oral presentation session for interventions in cardiothoracic abnormalities. We have some really good cases planned for you here. So a reminder that all sessions can be evaluated through the mobile app or online on the program. So don't forget to evaluate this session and the speakers when it's done. All of the presenters are required to verbally disclose any financial relationships or any that they do not have. So that should be included in the presentation, so expect that. All rights are reserved. The visual and audio content presented during the meeting is the exclusive property of CHESS, so no personal recordings of the content in the meeting are allowed. And please assist CHESS staff by keeping the aisles and the exits clear. Silence all cell phones and pagers during the presentation. I hope no one brought their pager to Hawaii. But please make room for attendees to have a seat by moving to the center of the rows, you know, if we get short on room here and leaving empty seats at the aisle. And CME Claiming will open on Wednesday, October 11th at noon. So I don't know that anyone has any questions, audience response questions in the presentation, but if they do, you know, just keep your phones handy just in case. So I'd like to go ahead and introduce our first speaker. Each speaker has about eight minutes to present and then a couple minutes for questions. Certainly if there's no questions right after the presentation, we can open it up at the end if we have extra time. So I'll introduce Amanda Caccini, who will be talking about cardiac tamponade, a rare presentation of profound hypothyroidism. Hi, thank you so much. All right, so I am Amy Cicchini and I'm from Eastern Virginia Medical Center. I'm a second year fellow and I'll be discussing a rare presentation of profound hypothyroidism presenting as cardiac tamponade. I have no financial disclosures. So my objectives today are essentially to discuss and inform everyone of an exceptionally rare complication of a very common disease, discussing the management and of this rare complication as well as further complications of the treatment that she received, and then a brief overview of the pathophysiology of her disease process. So our patient was a 45-year-old female who presented with a two-week history of progressive shortness of breath with exertion, dull chest pain, and progressive generalized swelling. Her past medical history was significant for hypothyroidism, which was diagnosed in 2007 with a TSH level at that time of 160. However, she did have severe depression and had very poor outpatient follow-up, so she was non-compliant with any sort of thyroid replacement therapy and actually with any other medications whatsoever. So whenever she presented to the emergency room with those symptoms, her pertinent exam findings were a very flat affect, distant heart sounds, diffuse body edema, and very dry flaky skin. She was hemodynamically stable. However, she did have bradycardia with a heart rate in the 50s. Her relevant lab data on admission was a TSH level of 93, so pretty elevated, not quite as much as in 2007, but very elevated. And then she did end up getting T3 and T4 levels, which were undetectably low. She also had an NT-proBNP level that was elevated at 1797 and a slight elevated troponin level of 22. Her EKG showed sinus rhythm with low voltage, and then this is her chest x-ray, and it showed an enlarged cardiac silhouette. So at this time, with her enlarged cardiac silhouette, the symptoms she was presenting with, she did get an echo that day, and it showed a large pericardial effusion with pre-tamponade physiology. So as you can see, there's quite a significant pericardial effusion here. However, as she was hemodynamically stable, it was late in the evening, it was decided for her to undergo pericardiostentasis the following day. So the next day, that was done, and 720 milliliters of serous anguinous fluid was drained. And so afterwards, she had another echo that showed a small to moderate circumferential pericardial effusion without any evidence of hemodynamic compromise. So it was effective at that point, and all her fluid was sent for cultures and cytology, but everything was negative. So at this point, the effusion was attributed to her profound untreated hypothyroidism. Endocrinology was consulted, and they diagnosed her again with profound hypothyroidism with myxedema features, and they started her on 200 milligrams or micrograms of levothyroxine IV, five micrograms of liothyronine IV, and then streptosteroids. However, a couple of days later, she did have increasing shortness of breath and then mild hypoxia requiring two to four liters of supplemental oxygen. So another chest x-ray was obtained, and it showed a large left-sided pleural effusion. So pulmonology was consulted. We did a thoracentesis. This is actually the picture of the bag because we were pretty surprised to see how sanguinous this fluid was. We drained 800 cc's out and then sent that for cultures, cytology, and a hematocrit level. So afterwards, after she had the thoracentesis, this was within an hour after, she actually had even worsening shortness of breath, and she was requiring four liters consistently of supplemental oxygen. And then stat labs were obtained at that point, and her hemoglobin level had dropped down to six from 8.2, I believe, and a hematocrit was 20.9 percent. We quickly got the pleural fluid hematocrit level back, and it was 10 percent. So a hemothorax would be if the pleural fluid was 50 percent of the serum hematocrit level. And so she just, with 10 over 20.9, she just missed the cutoff for hemothorax. So at this point, we were very concerned that she had a complication of her pericardiocentesis and that she was leaking blood, essentially out of her heart, into her mediastinum, into her thoracic cavity. So we ordered a stat echocardiogram, and it showed early tamponade physiology. And while this was, as the stat echo was coming, she again became hemodynamically unstable, more hypoxic, and was moved to the ICU. So because we did see the tamponade physiology, at this point she was taken by cardiothoracic surgery for a pericardial window and for a VAS procedure. And during this, another 750 cc's of sanguinous fluid was drained from the pericardial space, along with 150 cc's only of serous fluid from the pleural space, and they did perform top pleurodesis. So at this point, her complications were attributed to a leakage from the site of her pericardiocentesis. So as we all know, hypothyroidism, pericardial effusion is a common complication of that. However, it is pretty rare for someone to have such untreated hypothyroidism that they actually accumulate enough fluid to form tamponade. The mechanism behind this is essentially increased vascular permeability, which allows influx of albumin into the pericardial space. So over time, the albumin is sitting there, the fluid leaks and leaks and leaks into the pericardial sac, and patients become very slowly progressive because- progressively symptomatic because the pericardium just very gradually stretches and the pericardial sac fills with fluid. So as a result of the very slow accumulation, the patients who are symptomatic just present with progressive shortness of breath. But many patients are asymptomatic, and I've actually had another patient who had a similar presentation, and she actually came in just with constipation, and it was incidentally found that she had a large pericardial effusion. So this is something that we just may incidentally find as well. The treatment for hypothyroidism-induced pericardial effusion is just thyroid replacement therapy. However, if they have features like this patient of myxedema, you would also want to do T3 supplementation and stress to steroids as well. And obviously, if they become hemodynamically unstable, then you should perform pericardiosynthesis. So in conclusion, hypothyroidism is a very readily treatable condition, and it's a preventable cause of cardiac effusion and tamponade. It's really rare to see this, as most patients are compliant with their thyroid hormone replacement therapy. So it's exceptionally rare for patients to accumulate this much fluid to cause tamponade. But this is something that we should all be aware of, because I know in our hospital, we have a heart hospital, we see a lot, and we get a lot of transfers for pericardial effusions. And so hypothyroidism is something that we should always evaluate for in patients with this presentation. Here are my references and my co-authors. Thank you all so much. So the title of my talk is Management of Bronchocutaneous Fistula Using Endobronchial Valves, a Hybrid Approach. I'm Audrey Pendleton. I'm a cardiothoracic surgeon and a recent graduate from Rush University Medical Center in the Department of CT Surgery, and I have nothing to disclose. The objectives of this discussion are to discuss the various etiologies of bronchocutaneous fistula, as well as traditional treatment, which can be very invasive and morbid, as well as novel and newer treatment options. Additionally, we'll be talking about pitfalls and strategies on how to manage complications. Bronchocutaneous fistula are abnormal connections between the tracheobronchial tree and the chest wall. They are very rare, and they're most commonly associated with infections such as aspergillosis and actinomycosis. They are a very unusual complication after cardiac surgery. Management can include extensive surgery in which the fistulae are taken down, which can be very morbid. Endobronchial valves are devices that are placed via bronchoscopy and have a well-established role in treating bronchopleural fistula, emphysema, and prolonged air leaks. In this talk, I'll discuss the role of endobronchial valves in a hybrid approach to managing bronchocutaneous fistulae. The patient is a 71-year-old woman who underwent a coronary artery bypass grafting at an outside institution. She developed a sternal wound, which ultimately required a sternectomy and flap coverage with plastic surgery. Bronchocutaneous fistulae formed, which compromised the flap. The patient had recurrent chest wall infections, respiratory infections, and the flap failed as a result, despite prolonged antibiotic use and vac therapy. She was referred to our institution for further management. Her exam was significant for a sternal wound bed with two blowing bronchocutaneous fistulae. So here's one of the fistulae and here's the second fistula. And then in her CAT scan, you can see here from the anterior segment of the right upper lobe, fistula tract forming. There's some air there in the chest wall, and this is its exposure to the atmosphere. Given her history of multiple chest surgeries, we elected to manage these bronchocutaneous fistulae using a hybrid and less invasive approach. With bronchoscopy, we were able to manage With bronchoscopy, we occluded the right middle lobe orifice, which resulted in cessation of the leak from one of the fistula. We deployed a 7-millimeter endobronchial valve to exclude the entire right middle lobe. Similarly, occlusion of the anterior segment of the right upper lobe with a 6-millimeter EBV resolved the second fistula. The patient returned to the operating room one week later for primary closure of the cutaneous fistulae with a redo flap and reconstruction by plastic surgery. The fistulae were each closed with 3-ovigral suture pledged with an acellular dermal matrix. Her post-op course in the hospital was uneventful. She completed her antibiotic course and she was discharged home. However, as an outpatient, when she returned to the office, she had developed persistent cough fevers and had expanding anterior chest wall subcutaneous emphysema, which was concerning for a recurrent fistula. So this here is a picture from the original procedure. This is the Olympus umbrella shaped valve. The way it works is that it blocks entry distal to this device, but it allows expired air to come out around the peripheral distal to it. So it's a one-way valve mechanism. This is the, after her initial procedure and redo flap reconstruction, this is the flap with the drains that the plastic surgeons placed, and then deep to this is our repair, primary repair of the fistulae. So we returned to the operating room for incision and drainage with debridement and packing of the sternal wound. Under bronchoscopic guidance, the EBVs that we originally placed were removed and debris and purulent fluid were aspirated distal in the distal airways. Next, we use a different type of valve. These are EBVs with Heimlich-like mechanism that were deployed to exclude again the entire right metal lobe orifice. And this time, instead of just doing the anterior segment of the right upper lobe, we put three separate endobronchial valves in each of the segments. So it essentially occluded the entire right upper lobe. The patient did well postoperatively with antibiotics and wound care. A follow-up CT scan showed resolution of the fistulae. We'd elected to wait three months, repeat her scan, and ultimately brought her back to the operating room to remove the EBVs, and she's been doing well since then. So this is a somewhat blurry picture of the Zephyr valves that we used. It has a Heimlich-like mechanism where the valve remains in a closed position at baseline, and when air or any debris distal to this needs to be expelled, it comes out through that valve and then returns, but doesn't allow air or anything to go in the opposite direction to the distal airways. So bronchocutaneous fistulae are rare and they are complex to manage. Patients present in various ways, most commonly with persistent productive cough and recurrent chest wall infections. When presented with this problem, it is imperative that a multimodal approach be implemented, including treatment of any underlying and persistent infections and definitive management of the fistula. It is also important to involve multiple specialists, including infectious disease specialists, sometimes plastic surgeons as we did in this case, as well as interventional pulmonologists and or thoracic surgeons. In our case, we had both an interventional pulmonologist and our department. Options for management include operative takedown and repair of the fistula as well as endoscopic techniques. Since these patients tend to have underlying comorbidities and complex chest surgical histories, an operative approach may be prohibitively risky. Endobronchial valves are one-way valve systems that occlude the airway and they prevent air from traveling distantly to the vise. There are multiple reports describing their use for bronchopril fistula as well as emphysema, but to our knowledge, there are no other reports describing their use as the primary management in bronchocutaneous fistulae. When considering this approach, identifying the location of the fistula radiographically and via direct visualization, i.e. through a bronchoscopy, is important. During the procedure, once the culprit bronchus is identified in size, the EBV is deployed and seated in the orifice. In our patient, we had a recurrence after the initial procedure, but managed this complication by both changing the type of EBV to the one with the Heimlich-like mechanism, which may lead to better drainage from the distal airways and occluding the entire right upper lobe instead of one segment. We can't really comment on which valve is better based on one case, but in this patient, our second attempt was successful with a different type of valve and the additional valves placed. Aspects of management with these valves that must be kept in mind are that when planning this procedure, it's imperative to have an understanding and assess the underlying lung function and reserve of the patient because you're essentially eliminating either segments or lobes, depending on how many valves you place. In our patient, she had a functional bilobectomy. Her right middle and right upper lobe were excluded. So even though it's temporary, it's important to discern if they can tolerate this from an oxygenation ventilation standpoint. There's also reported incidence of 27% for pneumothorax with the majority of them occurring the first three days post-procedure. These data was from the LIBERATE trial, which examined the use of Zephyr valves in managing emphysema. It may be an overestimate in other patient populations who don't have such compromised lungs and friable tissue as patients with emphysema do. However, it is important to keep in mind the proposed mechanism of a post-procedure pneumothorax is that when the treated lobe has a sudden decrease in volume, the remaining lung expands and then results in small parenchymal tears. We've had several patients in which we've used these valves and we haven't had any pneumothoraces, but we always get a chest x-ray and keep them for at least a day or two post-procedure with daily chest x-rays. The recommended length of treatment for these valves is at least six weeks. We kept them in for three months due to her complex history as well as our initial failure of treatment and the need for further interventions. If the patient is doing well clinically, has no evidence of recurrence on CT scans or infectious sequelae based on your clinical exam and labs and everything else, then the bronchoscopy should be performed. And if there's no evidence of recurrence, then the EBVs can be removed. In conclusion, these fistulae are rare and complex problems and they are very challenging to manage and the treatment can be incredibly morbid. The role of EBVs in managing these fistulae is evolving but is less invasive and less morbid than open surgical repair and can be effective when used in combination with other treatment modalities. And that's it. Thank you. I'd like to thank the Chest Conference for allowing me to give this oral presentation and bring this case to all of you guys. Does anyone have any questions? Well, it was done in an outside institution, so in reviewing her records there wasn't anything that jumped out other than the fact that she had underlying diabetes, some underlying comorbidities that increase the chance of infection, but just having a reduced sternotomy and a reoperative field is an increased risk for specifically sternal infections. So that alone put her at a higher risk. There wasn't anything in the operative reports that, you know, they didn't have to reopen her, there was no specific complications, it just developed. Is there any way to choose it at first? Yes. You know, the interventional pulmonologist that we collaborate with, I asked him that exact question and he said, to be honest, since there isn't really established better treatment, he went with one he was more familiar with and he had used in the past and hadn't had an issue with. In this particular patient, when this happened, he started to look for alternative valves and we did a little bit of kind of review and talk to different reps and everything. So we decided to go with this to try something different. We also used additional valves. So it's hard to know, yeah, because in the initial treatment, the other segments of the upper lobe did not seem to be contributing to the fistulae, although who knows if there's collateral, you know, it's hard to know. So we, for an extra measure of protection, we just take, she was able to tolerate from a pulmonary reserve standpoint, not all patients could, but we wanted to give her the best chance of resolution. So we took out, we occluded all the segments. And I think that also had an impact on, you know, on her being healed from this because probably originally there was some collateral communication. The spiration valves are usually the ones we use for prolonged air leak, just in bronchoplural fistulas. Those are the ones that are kind of on yet off label for use. And so that's probably one reason why the interventional pulmonologist was more familiar with that, I would guess. Yeah, yeah. It just seemed that's one, yeah, exactly. In this particular case, you know, she had had such a complex history with recurrent infections. I mean, cultures were growing, multiple things. She, ID was very involved. And so it's possible that even though we thought we'd given her enough time to heal from the infection, a tenant of fistula management is that underlying infection needs to be controlled. And so it's possible that we did it a little too early, even though there was no clinical evidence of an active infection. Probably it was, like many of these things, multifactorial. Maybe it was the valve choice, again, the number of valves and taking out all the segments, as well as maybe some persistent underlying subclinical infectious issue that just needed a little more time to resolve that contributed to the initial failure. Okay, thank you. Thank you. Okay, I'll introduce our next speaker, Nathaniel Robinson, who's talking about combined angioembolization and surgical approach to complex pulmonary arteriovenous malformations in a young male. Thank you. Good morning, my name is Nathaniel Robinson. I'll be presenting a case of a hybrid approach to complex pulmonary arteriovenous malformations, and we're located in Rochester, Minnesota, at the Mayo Clinic. I'm one of the general, I'm sorry, one of the cardiothoracic surgery fellows. We have no disclosures, nothing to talk about. We present a 19-year-old male who was symptomatic since the age of six years old, and his mother had noticed some nonspecific findings with some red spots on his nose and arms. He had recurrent nosebleeds and recurrent upper respiratory tract infections, and was also having some, like, flat purple fingernails, odd signs, and more significantly, he was affected by dyspnea, fatigue, especially when compared to his peers, and even some syncopal episodes with hypoxia. His father had been diagnosed in the past with pulmonary arteriovenous malformations, and primarily was just managed medically and almost with nothing, but with that on the table and something to consider, a chest x-ray was performed to evaluate for his symptoms, and they identified the image you can see here, a left lower lobe opacity. With that being a finding, we further went to chest CT, which diagnosed and further characterized the pulmonary arteriovenous malformations, and an echocardiogram confirmed that there was a right-to-left shunt. And even further, to get more, you know, percentage data, we did a nucleotide, a radionucleotide evaluation of this shunt and found his index to be eight percent. So over the course of really about, you know, 10 years, from 2009 to 2021, he had embolizations over and over, and every time he'd get an embolization of this area, he would have resolution of the symptoms with improvement, and then, you know, months to years later, he would have, once again, recurrent symptoms, and then another shunt index that showed he had a repeat increase in his shunt. After the fourth embolization and recurrent symptoms, we did a repeat shunt index, which showed a 15.8 percent. It was at this point that they looked for surgical evaluation, and our team was consulted to provide that. Here you can see a preoperative CT angiogram. It was obtained, which raised some concerns. If you look here on the left lower lobe bronchus, you can see, actually, from the left main stem bronchus on, these large hypertrophied bronchial arteries that kind of track centrally and move along the left lower lobe bronchus, and then end in that pulmonary arterial venous malformation. It was all surrounding the area right where we were intending to do surgery, and we were concerned that these hypertrophied vessels would be a significant risk for hemorrhage, both intraoperatively while we were doing the case, and then even post-operatively. As a result of that concern, we decided to refer this patient to our colleagues in interventional radiology and ask about embolizing these feeding vessels. They agreed, and he underwent coil embolization of these feeding bronchial arteries, which were going down to the left lower lobe, and you can see here on left to right, the before and after, with a pretty satisfactory result. And even though that was a great, you know, step towards safety, we still felt like this case was a pretty good amount of risk. We initiated with a thoracoscopic approach, knowing that we may need to go to open very quickly, but started thoracoscopically, and were able to perform a left lower lobectomy. Despite the preoperative embolization, the risk of these bronchial arteries was still in our mind, and we felt it was pretty high risk. It proved difficult as we began to develop the plane over the pulmonary artery through the fissure. It was not a straightforward plane, and we felt like these recurrent embolizations that had occurred had induced a lot of inflammation, and so these periarterial planes were fibrosed, and they were obliterated, and we couldn't find it very easily. But we ended up going from the bottom up and started with the pulmonary vein, and were able to successfully stay thoracoscopic. In this picture, you can see even an embolization coil partly extruding from one of these basal arterial trunks. And so as we were going over this with a stapler, we were a little worried that the stapling device wouldn't be able to fire successfully and create seal, and so that was also something we were concerned about. But again, fortunately, all went well, and there were no issues with bleeding. In fact, the blood loss was only like 200 cc's, so that was a success. Post-operatively, his only issue was a small volume air leak, and that resolved on day six when we were able to then take out his chest tubes and discharge him. We repeated a radionuclide shunt study one month later, and his shunt index had substantially decreased from 15.8% down to 1%, as you can see here. More importantly, though, the patient's symptoms were resolved. His dyspnea and hypoxia were gone, and he felt like he could be more active. And fortunately, at year one and year two, when we called to follow up, he had no recurrent symptoms and hadn't even come back to see a physician because he was doing so well. Coil embolization is the mainstream intervention for these pulmonary arterial venous malformations. However, there can be these difficult cases where recanalization can occur, and the literature would say up to 25%. When encountering a patient who has these persistent pulmonary arterial venous malformations, despite coil embolization, it's important to consider a systemic pulmonary reperfusion as the etiology and cause of that recurrence. Like in our case, where the systemic hypertrophied bronchial arteries had developed, we believe those were the etiology of recurrence to these AVMs. It's also too important the risks associated with repeat embolization, which can be stroke from the particulate that you use to embolize. You can also develop many enlarged fragile collaterals from embolizing and shunting blood from one space to another. From a surgical perspective, pulmonary arterial venous malformations, the embolization itself may increase the bleeding risk because that shunting of blood elsewhere can cause hypertrophy of vessels that were normally not so big. Interoperatively, it's also important to consider that periarterial scarring from previous embolization attempts may make your dissection quite difficult and more dangerous. It's also important to consider that the actual embolization technique used in these vessels may become something you have to consider when discussing how you're going to ligate it. Are you going to use a stapler or other methods? And so planning for that and planning for failure of your primary method is important to have success. That's it. Thank you. Does anyone have any questions? Yeah. Yeah, we were literally going to clamp and tie. And depending on how disastrous it turned, we were very prepared to open and do a thoracotomy. So that was all talked to, both the patient and his family beforehand, that we expected the preoperative embolization to have significantly reduced that risk, but the vessels were still there and we were still going to have to go through them. And so if that failed, it would have been clamp and tie. right yeah no I feel like the failure was in what I read when I was preparing this it was mostly failure to successfully get the patient to resolution of their their shunts and their symptoms that led people to be brought to us in the thoracic surgery realm so I think if people can be successfully embolized and it resolves the AVM and that goes down and they're able to keep their lung lobe or whatever it is perfused and still use it then people don't need to go to surgery but it's when you have recurrence and failure that you just got to take it out I know we were felt fortunate it was good thank you okay so I'll introduce our next speaker Eugene almost on we'll be speaking about by atrial thrombus of percutaneous PFO closure device complicated by infective endocarditis thank you for the intro dr. schwach good morning everyone great to be here happy to talk to you guys today about a by atrial thrombus that formed in the setting of a percutaneous PFO closure device this case was also complicated by a suspected case of infected endocarditis this was done on their collaboration with our gill heart and vascular Institute with dr. Peter Haig and dr. son retta on the division of cardiothoracic surgery you guys can call me Matt Eugene's my mild-mannered alter ego from the University of Kentucky I'm a categorical resident pgy-3 I have no disclosures basic outline of events talk about the case presentation our patients echocardiographic and cardiac imaging findings management and her case resolution and further discussion a little bit about PFO closure device placement usually performed in the setting paradoxical embolus once we've ruled out all other primary etiologies for acute ischemic stroke TI a's usually with visualization of an atrial septic defect or PFO on bubble study typically a lot of these folks are on antiplatelet regimens following placement device and we're hoping to highlight a very rare but often serious complication is thrombus formation and in this case serving as a nidus for inflammation and suspected infection our patient is a 39 year old female she initially presented to us with crushing mid-sternal chest pain to the cardiac critical care team essentially five months prior interestingly enough she had a cryptogenic stroke workup involved finding an actual PFO with subsequent closure with a 25 millimeter gore cardioform septal occluder with her presentation on our initial she did reveal she was not compliant with her post-procedure antiplatelet therapy also has social determinants involving previous substance use and current use at the moment her initial workup on the slide litany of labs but the big highlights are leukocytosis at 12-8 electrolytes for otherwise with inappropriate limits and then her actual biomarkers were negative EKG with sinus tachycardia and a BNP at 200 we did draw blood cultures on admission and then later on in the admission I included it here she did have CT head and a CT head and neck that were performed giving concerns for either underlying residual neurodefects or any new neurodefects the meat and potatoes comes from this slide here and see if I could play it so her echocardiographic findings as you guys see from above shows a large mobile thrombi it's adhering to the interatrial septum as well as a PFO closure device on this preliminary measures about 3.4 by 2.4 on the right 3.2 by 1.6 on the left and you could see that there's oscillation across the tricuspid annulus we had a formal TEE that was done again showing that device is present thrombus is present but again a large organizing mass attached to both atrial surfaces on right and left there's a pedunculated shape on the right moving in and out of the tricuspid valve orifice no significant stenosis or regurgitation a separate image on the TEE there we also got a pedun cardiac CT with mild focal uptake surrounding the PFO closure again suggesting more thrombus trapping was during the course of her admission that her initial blood culture is actually positive from MSSA and recurrent bacteremia thereafter she also started to develop fevers and it was at this point we kind of had a multidisciplinary approach involving our cardiac thoracic cardiothoracic surgeons as well as our infectious disease essentially the discussion surrounded PFO closure device removal versus long-term antibiotic suppression and need for antiplatelet therapy in the long term in the interim she was placed on IV nafsilin and eventually the decision was made for open PFO device closure section removal of the biatrial thrombus and then analogous pericardial patching of the result in ASD and those are the images as above with thrombus itself interestingly enough we were able to send it off mostly inflammatory debris no micro growth she tolerated the post-op for a period pretty well actually got discharged to acute rehab with a four-week course of antibiotics thereafter and again a lot of talk about the surgical treatment being favored over just general conservative medical therapy again discussing a little bit about the risk for thromboembolization her history of non-compliance and any suspected device infection as a result from the bacteremia she kind of highlights for the conclusion this is a bit of challenge in regards to actually trying to elucidate is this most device thrombosis or are we concerned now for an infective endocarditis picture and the serious complications of PFO highlights again in this case again usually antiplatelet therapy is favored at least in a six-month period following percutaneous PFO closure and then lastly critical care mindedness involved a lot of multidisciplinary approach again with our surgeons with our infectious disease colleagues driving ultimately indications for removal of the actual PFO device and thrombus removal given the setting of bacteremia those are my references thank you very much everyone any questions it actually shortened it they were looking at either six to eight weeks further so we actually cut it in half and was able to go in oral suppression thereafter made it a lot better for her compliance as well too thank you very much everyone okay so I'd like to introduce our last speaker Jacob McAuliffe I'm sure I did not say that properly so feel free to expand upon that we'll be talking about conquering the giant successful surgical resection of a massive coronary artery aneurysm with intraluminal thrombus okay good morning everyone so my name is Jacob McAuliffe chief resident at Eastern Virginia Medical School you got pretty close I have nothing to disclose and I apologize this slide comes from one of my other presentations this week I'm going to be talking about a pretty interesting case of coronary artery coronary artery aneurysms that's a mouthful CAA for short and some management discussion so case presentation so we have a seven-year-old coming in with a one-week history of progressive dis exertional dyspnea and right shoulder pain his initial ED workup was pretty unremarkable except he had a significant D timer which prompted a CTA which was remarkable for this absolutely massive peripherally calcified mass that was seen to be compressing pretty much everything in the chest the in particular the right heart the sending a word and SVC I will also say like anecdotally it's not up on the slide but he had been more chronically complaining of dyspepsia he had EGD that was unremarkable so this thing was obstructing the esophagus as well so he was transferred to tertiary center for cardiothoracic evaluation up on this slide we have basically all the modalities the highlights being you know he had preserved EF 50% he did have abnormal septal wall motion and then multiple studies demonstrated that there was flow through the through this mass so it was better characterized as a thrombus within the posterior to sender the right posterior descending artery he had preserved cardiac index and but did have multi-vessel coronary disease and so here we have a TEE image of the mass that you see the right atrium and the right ventricle are significantly compressed and then on the your right side of the screen we have a CCTA image with the dimensions and like I said it's absolutely massive thrombus in the chest so after weighing interventional options the patient was consented for a section under bypass support and via interior astronomy the aneurysm was successfully mobilized off of the right ventricle but this did require bovine patch repair while you know perioperatively they did a simultaneous cabbage of the posterior descending artery and the ramus intermedius the patient tolerated the procedure very well was transferred to a dedicated CT ICU he was on mechanical ventilation and did have some ionotropic and vasopressor support but he was extubated within 24 hours and he was off all infusion support within five days so here we have just an image of the the bovine patch repair of the right ventricle and then this is the the thrombus that was excised and you can see it's absolutely huge so leading into some discussion so coronary artery aneurysms are routes are pretty uncommon and they're often clinically silent so we call any dilation any focal dilation of a coronary artery greater than 1.5 times the reference vessel an aneurysm so they they garner the the term giant when they're over 2 centimeters so this one being you know depending on which access you measured it 12 to 17 centimeters so this was an absolutely massive coronary artery aneurysm they are like I said pretty uncommon with more advanced imaging modalities the prevalence of just regular coronary aneurysms are as high as 5% but massive giant coronary aneurysms coronary CAAs are still exceedingly rare with the estimated prevalence being as high as 0.2% of the general population so the pathology the pathophysiology of coronary artery aneurysms aren't well understood there's they are highly associated with atherosclerotic disease and other conditions such as Kawasaki Takayasu other connective tissue diseases and vasculitides and traumatic and iatrogenic vessel wall damage have also been described in the literature as far as management go there there really isn't consensus guidelines most of the literature out there is just case series and expert consensus so for smaller CAAs the there have been some retrospective cohort studies that really haven't demonstrated any difference any significant difference across medical PCI or surgical management approaches so this is largely a field for future study there and when we talk about medical you know so there's not great evidence for dual antiplatelet therapy or anti coagulation either you know primary or secondary prophylaxis in this patient population moving on to you know surgical consideration so giant artery giant CAAs and those in affecting the left main artery and those affecting bypass grafts are there is evidence that surgical resection is the you know the first line therapy and I this the bottom bullet point is I think the most interesting thing to talk about in this case so one of the feared complications of coronary artery aneurysms is in situ thrombosis prompting or leading to ACS so the fact that this this job to the seven-year-old gentleman had a thrombus of just under 13,000 cubic cubic centimeters just kind of hanging out in his right coronary artery is pretty astounding that he he was presenting with you know exertional dyspnea obviously having some demand in his coronary circulatory you know sorry losing my words there for a second but the fact that he you know didn't have ACS I think is quite remarkable so just in summary exceedingly rare case presentation of a massive coronary aneurysm it was a technically challenging operation but the patient successfully tolerated resection with cabbage and we mitigated a very high risk for future adverse events.

coronary artery aneurysm

intraluminal thrombus

exertional dyspnea

right shoulder pain

surgical resection

bypass support

bovine patch repair

Cabbage procedure