TPES 2024: Dr Raffael Zamper "Select cases in liver transplantation"

hi everyone thank you for joining the meeting today it's a pleasure to be part of this event not only as a speaker but as a member of the planning committee as well uh in this presentation I'll discuss some selective cases in liver transplantation focusing on how interop played a crucial role in managing unexpected hemodynamic complications uh before I begin I declare that I have no e e e recording in progress and this steel frame shows the flow convergence in the uh Vina contractor and we classified this TR as at least moderate Med of AIO RV flow outflow showing normal circumferential shortening of the RV you can see the PA catheter cles to the rvot down there and here we appreciate the same TR jet that we saw before four and the four chambers with a minimo I say Trace Pi in the rvot continu wave doler of the TR jet gave us an [Music] estimated recording in progress e heavy inflow outflow reinforc a significant drop in the preload to the heart two Chambers view showing empty LV as well and the long axis shows the same also showing absence of Sam systolic interior motion of the mitro valve and all this find is they are quite common during clamping they're compatible with severe hypo hypovolemia which is usually managed with some fluid administration and vas oppressors however in this patient specifically I'd say that a larger than usual amount of fluids was necessary to achieve a tolerable hemodynamic situation um and um that was possibly due to some lack of collateral circulation or insufficient collateral circulation so the patient received approximately four liters of fluids and that included crystalloids 5% alumin and one unit of red cells and that was all during the anhepatic phase then as we proceed to the reperfusion the situation became very complicated so the EOC cardiogram initially showed right ventricular distension as you can see and that was different from the initial exam RV inflow outflow showed good reperfusion of the graph with this uh artifacts that resemble air bubbles but actually are U Cod fluid mixed with blood coming from the raft and the LV now was uh last empty than during the anhepatic phase but we were expecting a larger chamber uh with a you know as a surrogate of a higher cardiac output due to the uh significant increase in preload to the RV and we had the same impression when we look at the long access View and then the right ventricle begin to show signs of failure with the lateral wall displaying reduced contra ility now directly correlating with the left ventricles difficulty in maintain adequate card output due to under feeling so you can see septo deviation to the left side and this patient eventually progress to right ventricular ballooning with almost no feeling on the left side of the heart and that culminated with a cardiac arrest in PA so initiate did resusitation with adrenaline and chest compressions and we managed to restore spontaneous circulation after couple rounds of CPR still the EOC cardiogram revealed signs of stasis possible small clot in the right atan indicating potentially a trombos formation due to low float State during the cardiac arrest and we use dyotropic support and Pulmonary viso dilation with nitric oxide to stabilize the patients and that allowed the surgery to be completed good cardiac output was restored and at the end of the procedure we basically had a hyperdynamic normal functioning heart RV showing basically a normal systolic function the four chambers and kind of an RV flow out flow but you can see good fractional RF shortening good circumferential shortening here and same for the LV on the four chambers in two Chambers View and here's a long axis uh although this patient had an extended ICU length of stay he eventually was discharged home with a good function of the liver graft no neurological deficits which was a positive outcome given the extremely critical intraoperative scenario moving on to our second case today we have a 50 years old patient with curosis from metabolic disease M score 25 Child Bug C12 patient had a history of hepatic compensation with enop and atis and a recent GI scope showed large esophagi overis with no signs of active bleeding he also had a history of insulin dependent diabetes hypertension obstructive liap apnea asthma gird and psoriasis uh this patient's preoperative Echo also seem quite favorable showing a hyperdynamic left ventricle with an EF between 65 and 70% normal right heart and coronary angiogram that showed no coronary artery disease so this is the interop echo that initially showed normal B ventricular systolic function looking at the RV specifically this again little enlarged due to fluid overload overload from curosis that I mentioned before we even had this 3D of the RV confirming normal systolic function you can have a good you know sense of RV function using the 3D image at the top of your screen however after reperfusion you know patient had a hemodynamic collapse which we quickly identified through a te to be caused by this massive trombosis extending from the IVC into the right atrian ventricle but was practically blocking the blood flow through the heart you can note the U complete deviation of the interal septum to the left and the left ventricle completely empty unable to be filled adequately RV in flow outlow shows the massive clot crossing the RV the situation required an emergency intervention we end up administering out of plays in incremental doses while perform in CPR and te was crucial in monitoring the response to autop plays uh and that gradually show the clots decrease in sign in size and uh normalization of blood flows you can see here size of a clot smaller there's systolic activity in the RV still dysfunctional but with contractility present here 30 minutes after the TPA there's almost resolution of the clot with what I would call a normal RV systolic function at least in this view close to the end of the procedure we couldn't see clot in the heart anymore and at that point patient had minimal hemodynamic support however the process as you could imagine was not without any bleeding complications the trombolisis with alpl in the surgical setting led to a bleeding of very difficult control the patient required massive blood transfusions to achieve a reasonable hemostasia and eventually was taken to the ICU with the abdomen still open requiring a take back to the a few days later for hemostasis and procedure completion this patient also did well with the liver graft functioning properly and no neurological deficits being discharged home after a few weeks and to wrap up the third case this involves a 64 years old with a complex history of decompensated curosis this patient had a previous uh TPS procedure due to refractory atis had also an alcoholization of hepatic Nole and additionally he presented with the partial nonocclusive portal vein thrombosis that was an incidental finding at the time of the diagnosis of HCC patients preop tte like in the other cases did not show any significant abnormalities left ventricle with normal size hyperdynamic EF 7075 right ventrical completely normal in both size and function and the intop at the beginning of the procedure showed a normal lvot without any signs of flow acceleration um or lvot obstruction as you can see this patient had a normal mitro valve with a normal mitro valve lifl size as well however patient develop systolic anterior motion of the mitro valve which we call Sam after the clamping of the IVC that's a phenomenon where the anterior LIF flat of the mitro valve moves towards the lvot during syy and this displacement can cause lvot obstruction and significant MIT regurge we usually use the four chambers in the long view to identify it that's a steel frame the M of A4 Chambers and it shows the the kink in the interior mitro valve leflet towards the lvot in a gap in the coaptation of the mitro valve and that's the cause of a significant posterior mitro regurg jet with a prematur close closure of the AR valve and low cardiac output I understand this is a very busy and clutter uh color flow Doppler and so I have slowed down the loop to let you appreciate DMR being generated during late CST and here's a steel frame demonstrating the uh severe jet posteriorly directed with acceleration in the lvot here's another loop now in Long axis to show the deviation of the citation point in the interior Mally flat towards the lot and this slow image so Loop shows the generation of the mrr jet that you can see now and in this case hypovolemia contributed to the development of sand after clamping and so to treat it we gave fluids phrine and also beta blocker to control heart rate in this case we used asmol um and as you can see te confirmed the complete resolution of Sam after these interventions with the anterior mitro leaflet returning uh completely to its normal position the mitro regurge almost completely disappeared now with a very small uh Central jet that was probably there before and normal flows in the LT as well in this Zoom the long axis view shows normal mitro valve citation complete resolution of Sam we still with the clamp on however U after the clamp was removed and during reperfusion s reappeared but now exacerbated by a significant drop in the svr and peripheral Vis dilation despite adequate Venus's return once again Echo was crucial in guiding our treatment which involved strict heart rate control and peripheral V constriction to avoid and we avoided in this case volume overload because we knew there was a lot of preload and with these interventions we managed to stabilize the patient who was transferred to the ICU stable without any uh need for beta blockers and with minimal visal pressure support this Loops shows U normal outflow tracks colorflow dupler minimal Central Mr and that's in the end of the procedure and this patient had an uneventful post-operative course and was discharged from hosital within the expected time frame in conclusion three cases presented today they demonstrate the importance of uh intop te uh in patients undergoing lever transplants in all cases despite a normal extens preop investigation the patients developed an expected hemodynamic collapses during surgery the first case right ventricular failure poster perfusion um second case massive trombosis identified by echo echo also used to guide trombolisis and resuscitation U third case the development of Sam during surgery was quickly diagnosed and treated demonstrating how te can be vital for early detection of complications and for guiding realtime therapeutic interventions this case they reinforce the message that te is an indispensable tool in the inop management of patients undergoing liver transplants not only allows rapid and accurate identification of hemodynamic complications but also effective guides therapeutic interventions and that significantly contributes to procedur of success and improved patient outcomes um i' would like to thank the organizing committee for the invitation and the opportunity to participate in this highlevel event available for questions during the QA session thank you very much perfect Rafael thanks so much for that and uh so I'm happy to move over to the Q&A session where we have our speakers uh Dr Cosman G join us this afternoon but uh all the other speakers are here to answer questions so I'll just start rolling out by uh one of the questions I have actually for Jake something that we see at our Center sometimes which is um in patients that have uh secondary ponary hyper tension due to LV failure um when you do preoperative swans and you see that they have elevated PA pressures uh what's the Approach at your Center for normalizing those before transplant in order to try to minimize RV failure um so I mean what usually I've had experience with is if they're not optimized beforehand either with diuretics or pulmonary Vasa dilators like selenop um they're not even heart transplant candidates so uh if they've been optimized on medical management and they've had an improvement or response to the um medications um then they'll obviously be listed so then in the operating room well usually I'll even start them on Nitric as soon as we induce and then uh if it's uh still severe depending on RV dysfunction and things like that uh I might even have the surgeons put in uh wires into the groin before inducing um so that's usually what I've done in the past um I'm sure people have many different opinions but um that's usually the kind of stepwise i' I've gone through with it I think the situation that happens here sometimes is that we have a patient that is not necessarily known to have supremely elevated pulmonary pressures but then they're managed as an outpatient they may or may not be on a cardiomem system and when they come in for their actual transplant the pre-operative um PA line shows that they do have elevated pressure so then the question is you know we can aggressively try to get those down with medical management mown diuretics and the acute period within like eight hours transplant but then you know when you go to sleep and you induce anesthesia and you initiate positive pressure ventilation is very different strategy and I don't think we have a consistent cut off where which we say okay we're not going to go ahead with this transplant versus the ones where we try to get through um do you have a number or like I know it's there's no like kind of right answer but you have a number in your head that that uh you usually try to Target before proceeding um I mean I I don't know of any data behind the specific number um but usually what I've dealt with is U making sure that they're well sedated have a lot of like opioids on board they're paralyzed um uh make sure the volume status is good and then measure make sure the number is real and then um if they need dialysis I I have seen um us do a inoperative CRT to try and get some uh volume off uh quickly and see how the uh uh pulmonary pressure change with it um and then also with adding the Nitric and seeing how they respond um and then kind of just discussing with the surgeon like is this a good patient do they have other comorbidities involved is this strictly just a a type two pulmonary hypertention um is there renal failure things like that um and then it's kind of like a a multidisiplinary decision um but it it's not an easy answer I I think generally speaking um like 2third systemic is probably where I would kind of start thinking like hey I don't know if this is a great choice but um definitely the conversation with the surgeon would be at least with half systemic I think one of the things that maybe differs between Canada and the US is that the well we hear anyway is that the US surgeons are much more aggressive in terms of putting them on lvads as they wait for versus Canada but it's just something that's going to be sent are specific as well okay we have a question from the chat which is has anybody demonstrated improved outcomes with the use of te for lung transplant I'll open this up for yuliam and Jen I think Jane already was um addressing the question Jan you want to go ahead and um yeah sure uh we have I don't think there's anything that out there that has demonstrated specifically that te uh for lung transplant has improved outcomes and I think that comes that ties together with um a that's question and Marchant who was texting me about this as well um it's just the decision-making process for addressing stenosis compression a kinking of an an asmosis it's not just we see it fix it first of all you have all kinds of things that affect your measurements uh and two um you know just because you fix something doesn't mean that can make it better and so I think it's just it's so specific to each patient and the surgeon uh and you know the donor lungs the recipient lungs I don't I think it'd be very hard to prove that this is going to affect your outcome I I mean I agree I think that uh with the accent of uh randomized you know control trial it's very hard to say this is a standard of care you know uh the te will you know uh definitely you know improve Alon and whoever is not using te you know is uh you under standard of care we never can do that I think that it's just a risk benefit decision uh that you will you know uh discuss with the patient the surgeons the team um as Jane I think address in the in the qia section if you have a patient that is coming for a single long transplant no RV dysfunction you know uh I mean sick but not that sick probably a te will not make a difference now when you're talking uh you know about a patient that has severe you know RB failure coming for a double Lo transplant patient that is in a uh Eggo or will needo or cpv and you're going to be doing canulation and you know a very complex case so probably you know the risk benefit you know will you know tell you that te will be a good idea that it's not definite and just as a Paul just for context would you say that like what percentage of liver and lung transplants at your Center get routine trans esophagi eloc cardiography I'll say 100% 100% all of our L transplants yes 100% 100% of livers as well the surgeons actually loved it sometime they want the answer of the complications you know be given by all and by the te which sometimes is impossible I mean I have to be honest with you sometime we're doing a a te in a long transplant and the patient is so hyper dnamic and the heart is so compressed that you can really see anything and the answer is not there but somehow they feel like okay if you can give me own answers you know I know what to do so it's sort of like you know choice uh and do we we use it for every case honestly justify probably not but we do rapael how about at London experience how many liver transplants get te there routinely yeah it's close to 100% Marcus yeah that's a routine um standard of care here only if there's any contraindication I don't remember having one recently maybe active bleeding uh from the GI tract but uh other than that all all patients get we we one caveat to that is that we don't do transgastric views here okay we sit in the esophagus and we believe that that's enough to guide us with the um you know most uh complex scenarios U as you saw my U slides many of our patients not many but some of our patients the secret once they still get a PA catheter uh which also guides us with some uh you know management for svr PVR um but the te is a standard of care here 100% that's and Jen um just go to go back to your slides about pulmonary vein uh like flow velocities and evidence of turbulence um that we often see that here and we report it often I I say I can't always convince the surgeon that it's going to be hemo dynamically or clinically significant though and and what percent like you do they often accept higher flows given the clinical context or is it do you have a high degree of revisions where they no no I I I don't I can't even recall off the top of my head anytime I've reported higher flows that the surgeon has gone back and fixed it I'm even trying to think back in Toronto if they've gone back they're like no it's gonna be fine yeah I just I just want like so makes me wonder whether we're using kind of uh outdated values whether higher flow velocities are acceptable in lung transplant because it doesn't seem to necessarily correlate with worse outcomes despite some of the papers from maybe 10 years ago would suggest but I I don't know the answer to no I I agree well first of all I think you are gonna see higher flows regardless even if there is no problem uh you know they're hyper dnamic you're on eemo maybe on bypass like those are just going to affect your flows so so I think you are going to see that and um you know those structures are obviously very delicate to just say go fix it I don't know there's a risk there I think there's a big risk there also but but you know I do rely on it for someone personally I'm very stingy with fluid Management in lung transplants it's really nice for me to like okay we can do another 500 cc's and and you know I'm Not Gon to blow up the RV yeah that's think that I remember um one of our transplant surgeons uh when we hir him uh and you know we did interview and he was upset with assessment of the pulmonary veins you know during the transplant and the only question that he asked about an doing the te is that do they know how to do it and he was so upset that's all he cares he didn't care about any other you know thing and it's funny because we do it in every case so in one case I actually told him like Hey listen you you know the Velo are very very high and he looked at me and say like okay what do you want me to do about it and I was like okay oh it was like you have been obsessed you know and now we finally are telling you okay they are super high and you are asking me what to do about it so yeah usually they don't do anything they just sort of like watch it and sometime we get called to the uh unit later when the patient is not doing well and there is no other answer like why the patient is not doing so well so we get called to the ICU to could you please interrogate the pulmonary veins uh again and see if that is the answer so maybe we can extent it or maybe we can do something about it we had the issue and I don't know if this is a happening any other institution but we have an issue that some of our cardiologists um intervention of CI they are not really used to make sure pumonary vein flows so when they get called to the uh bedside to do it they usually ask for the card anesthesiology can you do it this is not something that I do every day so that's why we get involved you know later in the ICU unless the ICU person is a card you know an or someone that is you t35 and just to appreciate difference differences in practice um here an noen will be able to to test to um in lung transplant they're a little bit resistant to use inotropy only because they feel that uh it may uh contribute to worsening of pulmonary pressures in the post uh you know transplant period um do you use Echo to guide your inotropic decisions or do you tend to use more vasil constrictors in the acute peroperative period in then transition later B was similar to what you guys do we start with Nori um and but the the difference is that we hook up inhal nitric oxide for everybody everyone yeah yeah yeah yeah but if there's a question it's more of a question later if there's ARB dysfunction no one's going to complain about noon or Epi I know that was a thing where you had to have a just discussion with the surgeons and tono but here they're way more relaxed about it but again we do start off in Hil Nitric from the beginning with everybody everybody routine Administration yeah yeah okay I think Marin has a question we'll go uh Marchin do you wanna um thank you guys for your excellent presentations uh well it's uh you partially answer my question it looks like that practicing solid organ transplantation mandates Echo um that's true that in our Center we we don't do it routinely for lungs or livers but uh maybe we just become lazy or or it's just believing in our own practice but uh the examples Rafael examples which shown we saw it many times with our liers some M yeah liver transplants we know that 20% of candidates developed coron artery disease um thrombosis uh we have also paradoxical emboli in patients with portopulmonary syndrome where amount of air going through collaterals was so big that patients were going to RV failure we could see it very clearly uh the question is uh especially in States uh what about certification if you are lung transplant anesthesiologist or liver transplant anesthesiologist do you need to be certified echo cardiographer or this is just basic exams and findings are so obvious that that maybe basic training is enough what what is your opinion uh I you know I in my residency the liver team was not cardiac trained and they put to ease for their liver transplants and it was just there was they were just expected to be able to manage you know it was treated like a rescue Echo but throughout the entire case and they didn't have any major issues if there was something some crazy finding you know there's always a cardiac anesthesiologist around to ask but I don't there was no issue and they were expected to do it from basic training I think from the survey that they showed in my slides from 2024 most of the people were not certified actually for liver transplant so and that was one of the downsides I can share my experience here in London um we are as small group of Consultants that do lever uh there is as Dr gut showed in his presentation there is a significant overlap between cardiac and uh Li transplants at a point that right now five out of the eight are cardia Consultants as well but the requirements have been for the next highes U have been it has been decided that they have to be te certified the for the ones right now that are not certified they were grandfathered but are still training te on a daily basis with us and we always do the transplant in two Consultants uh with one of them being a te certified person so we're moving towards uh a direction where te is a requirement for T certifications a requirement for Li transplant anesthesia that's interesting to hear Marin any follow-up question no I think it's uh it's Rafael this is a very good point Point um on one hand as Jen mentioned this is rescue which is and I know that in us most of residents now I get a basic training but because sometimes these decisions are so difficult and we need to to make them quickly probably having certification uh it puts extra weight on on what comes from our end because consequences from surgical re intervention are sometimes very significant for palman veins I agree with you I mean we know that outcome is worse the lung is congested but the options what to do with them is is very limited if they try to redo it surgically it usually makes it even worse and even if you do stenting it's also not the most straightforward and it's very tricky um so uh but but I liver you are right Rafa liver is so complex with with lung or heart we can always crash back on pump or NE more regroup I think with liver we can just shoot ourselves yeah there's no rescue so that's that's and decision must be made very quickly so it's a very good point you're correct we had a five for the past I going to say three four years we had five interoperative massive trombosis after release of the clamp uh all of them were treated right away with TPA of course we had to deal with the bleeding afterwards but uh um none of the patients died in the O and four of them were were discharged from hospital eventually which is way different from what you see if you search a literature in terms of mortality for interoperative uh trombosis I think the administration of out the plays in a very fresh clots basically dissolves the clot um for and and helps U you know restablish hemodynamics at some point it's very sobering to think about um from our from our side only because I would say we were still we're still at the place where we use uh te in the minority of liver transplants i' probably say in the realm of kind of like maybe 25% or less and only if there's a really strong indication in terms of uh you know cardiac dysfunction preoperatively so it's uh it's you know the it was absolutely life- saving in these case scenarios that you showed and it just uh you know gives us pause to think about whether or not we're missing opportunities to intervene more despite the fact that you know as an S suggests there's probably no widespread studies that show significant clinical impact but the numbers are probably going to have to be huge in order for you to catch a signal right so so it's just interesting to to see we have another question in the chat here from victtor Nera from Halifax and he asks what dose of TPA do you use in these cases so hi hi Victor okay can you okay can anyone do does anyone go first it's fine I can so in in my place I usually use I start with 2 milligrams and I go to four if the clut is big and it doesn't go away uh some of my colleagues here actually prefer to start heparine first they give 5,000 hearin they wait for the clut to dissolve they say uh it usually goes away I've noticed that in their cases but if it doesn't work they have to go to TPA also so that's the first dose two milligrams and then four I think that's what's in the literature too and reports Le that is exactly what we do here in London and uh TPA is not in the O it takes a couple minutes to arrive so uh we uh we also give 5,000 uniters of Heering if we see a clot and this became such a an interesting topic here multidisciplinary discussed uh that we end up deciding to administer um heing 3 to 5,000 units before the clamp for the high M patients so we do that in our place too we give 2,000 of Heine on every case and we we are monitoring the acts just to see what happens and it's varable it doesn't help Act is not a good indicator it's all over the place you know so it's it depends on the fibrinogen it's very complicated but one thing one interesting thing is that these patients usually they have the worst coagulation Arrangements because they're so sick and although we give Hein we didn't notice an increase in the bleeding at a point that we we haven't given protamine after reperfusion to any of these patients that I can recall so we never gave for me so this leads to our next question actually from the chat which are uh which and what dose of antithrombotics are using initially let's start by answering this question for liver transplant but I actually want to hear what people's uh opinions and and um experiences are with antithrombotics and lung transplant especially those on ECMO um just because we're starting to move in that direction at our Center I would love to hear what other people are doing so first off we'll say what are the dose of antithrombotics uh that we're using in liver transplant these days at the very two to four milligrams we start with two we go to four I think we have the same practice so as boluses and fusion or Bolis bis and is that informed At All by uh what you see on the them or is it just empiric is what we no just based on a te and in Miami is there any resistance to administering some U coagulation products such as octaplex which are a little bit controversial in liver transplant uh we do but only after uh the artery is done I see I see but if if it was indicated you would have no problem giving that if we have to yeah okay and uh Raphael yeah same doses here to to for milligrams we we try to avoid um coagulation treatment as much as possible before reperfusion uh we don't have any cont indications for we we still give preference to [Music] ffb clot reposition and we do use a lot of fibrinogen concentrate um but there's no Contra there's no push back for octaplex or other PCC use here which is you know Center preference so we still use ffp sure sure I understand and then Jenny iiam um do you routinely use antithrombotics in lung transplant sorry you might be muted no we don't we don't we don't use that just out of curiosity so the discussion that was happening here is that we analyzed what the transfusion rate was was within the first one or two days of transplant and our transfusion right here despite the fact that you know um experientially we would think that not many of our lung transplants get blood products in the O it seems that within the first you know 24 to 48 hours of transplant about 80% 70 80% were getting transfused which kind of initiated a quality assurance product of whether we were missing an opport project to determine whether we were missing an opportunity to give antithrombotics in in an attempt to try to minimize some blood products Administration in these patients um do you have do you have any uh any similar experience at Miami in terms of your rate of transfusion I think uh I mean this is anecdotal from what I've done here versus in Toronto um I think that you know if I see a hemoglobin of you know 7.8 then I'm going to transfuse I think it was here but I think in Toronto they like just wait till it drift down a little bit but I think that's what's causing the PO that's my that was my first thought that that's what's causing the post transplant transfusion that they got a little bit of fluid and then they drop down right right I understand and so also I noticed that it's very much uh surgeon driven so surgeons will tolerate a very low you know hemat during the cases and they will be okay to you just hold on on any products uh some Ser will be asking you to you know give you know blood get products so that is you know it's a thing that I I I have noted through the years that vares the most who is doing the case you know and what the preference are and is there any resistance to use of ffp in lung transplant given that it has a high antigenic potential and and potentially highest risk of developing uh respiratory complications after or is that not really a concern not not between us and the surgeon I think the limiting factors Pharmacy that when you ask for it it takes so long for it to arrive unless it's prediscussion it's just just call for the ffp if you need it okay I understand okay I'm just checking the chats here doesn't look like there's any additional questions any any additional questions or comments from our panelists at all okay thank so much for having us marus you for this opportunity no no thank you guys for all your hard work participation in our Symposium thank you so much okay so I think we'll wrap up the session there and we'll move on to the lunch break uh we have a a a little bit of extended time I think we can probably take about 50 minutes and we'll come back for uh our next session at 2:00 okay see you all then you