Podcast Episode 9: Septic Vascular Surgery: When Infections become a Surgical Challenge

In this episode of “Focus on Vessels”, Dr Barbara Rantner speaks with Professor Thomas Betz and Dr Thomas Karl about the challenges of septic vascular surgery. The focus is on infections of native vessels and prosthetic infections, their diagnosis, and current treatment strategies: from open surgery to endovascular procedures. The experts explain why these rare but highly complex clinical conditions often require interdisciplinary treatment and specialist expertise.

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Rantner: Welcome to a new episode of “Focus on Vascular Surgery”!
My name is Barbara Rantner; I am a vascular surgeon and now a senior consultant at the TUM Hospital on the Right Bank of the Isar, though I’m still based in Munich.
This podcast is designed to offer you, our listeners, a platform to delve deeply into the topics that shape and advance our field.
Together with our guests, we’ll explore the latest developments in surgical, endovascular and preventive vascular medicine and discuss current issues from science, teaching, clinical practice and the real world. True to our motto: “We take vascular thinking further.”
After a short break, we’re finally back today – I hope you’ve missed us too – with a new episode. Today’s topic is septic vascular surgery. It’s an area where, as a vascular surgeon, you’re very quickly forced to step outside your comfort zone. At least, that’s how I often find it in my daily clinical practice. Today we’ll be looking at key aspects of native vessel infection and also the treatment of prosthetic infections. And I’m delighted that the three of us are back together again today to tackle this highly complex topic. I’ve managed to persuade two renowned experts to join me for today’s discussion. First of all, I’d like to introduce Thomas Betz, who is the Head of Vascular Surgery in Straubing and published a book on today’s topic just a few weeks ago. Joining him is Thomas Karl, Head of Vascular Surgery in Bad Friedrichshall and Chair of the DGG Commission on Hygiene, Wound Care and Septic Vascular Surgery. I am truly delighted to welcome you both here today and would like to thank you in advance for your time.

Betz: Hello everyone.

Karl: Yes, hello from me too, and dear Barbara, thank you very much for the lovely introduction; I am also looking forward to our discussion today. It’s an exciting and very complex topic.

Rantner: Thomas, we can get straight into it: as I’ve already mentioned, you’ve been serving as Chair of the DGG Commission on Septic Vascular Surgery for several years now, and the very fact that there is a commission dedicated to this field underscores its importance.

Septic vascular surgery can be divided into two areas: native vessel infection and prosthetic infection. Would you be so kind as to give our listeners a brief overview of the distribution and different clinical presentations of native vessel infections to start with? And could you perhaps elaborate a little more on the difficulty of differentiating between inflammatory and fungal diseases – something that usually concerns us most in the context of aneurysms?

Karl: I’ll do my best. As you mentioned at the start, vascular infections and prosthetic vascular infections are a very complex field, and when it comes to prosthetic infections – Thomas Betz will of course have more to say on this – the focus is primarily on differentiated and individualised treatment planning. With native vascular infections, diagnosis is often a particular challenge, specifically the differential diagnosis, and that can be complicated.
So let’s start by trying to sort out native infections a little. Basically, there are: bacterial, less commonly viral – for example, virus-associated endotheliitis in the context of the COVID-19 pandemic – and even less commonly, almost exclusively in immunocompromised patients, pin infections. In principle, all vascular regions can be affected, both arterial and venous. The route of infection can be haematogenous or involve direct invasion from neighbouring organs or from the periarterial tissue, for example in the case of septic erosive haemorrhage, intravenous drug abuse, or septic embolisation, as was originally described in the first account of septic endocarditis, a so-called mycotic aneurysm.
Pathogens, frequently staphylococci, Salmonella species or streptococci, but also rare other organisms: Pseudomonas, Coxiella burnetti, the causative agent of cow fever, or Clostridia, which can be ingested as spores via food, can trigger a native vascular infection.
Clinically, the classic signs of inflammation are common: fever, pain – though this may not always be present – and frequently, in cases of rupture, an emergency situation; indeed, the majority of native aortic infections are observed at the stage of rupture, presenting with the classic signs of shock, tachycardia and hypotension.
Infectious aortic aneurysms are, in turn, a subgroup of native aortic infections. However, these should no longer be referred to as mycotic aortic aneurysms; for several years now, the nomenclature ‘infected native aortic aneurysms’, abbreviated to INAA, has actually become established.
It is important to note that vascular infections are potentially life-threatening; aortic aneurysms in particular carry a very high risk of rupture, often within a few hours or days, regardless of their size. This means they require rapid treatment – usually surgical. Antibiotic therapy: this is, so to speak, the foundation and the cornerstone.
Diagnostics, as I mentioned: we need material to confirm the presence of the pathogen, microbiological tests, laboratory tests, and CT scans. There are the so-called DELFI criteria, which have been described in the consensus paper, consisting of clinical signs: fever above 38 degrees, sepsis, concomitant infection; CT morphological criteria, which are: the rapidly progressive, sacciform aneurysm, periaortic fluid or gas, periaortic soft tissue loss; and the laboratory criteria. Evidence of pus or abscesses, and positive microbiological results, thus allow us to confirm the diagnosis.
It is important – and this is truly crucial – that as much material as possible is obtained for microbiological diagnosis before initiating empirical broad-spectrum therapy. Ideally, three blood cultures – aerobic and anaerobic – from different venipunctures, not from a central venous catheter or an indwelling venous cannula, but freshly drawn, and if necessary, repeated every 24 to 48 hours, ideally during a rise in fever. And if there are corresponding symptoms, such as a urinary tract infection or pneumonia, then urine and tracheal secretions are also required. It is important to distinguish native infections from vascular graft or endograft infections and aortoenteric and bronchial fistulas, as well as from non-infectious vascular involvement, which may appear clinically similar, but these must be distinguished separately.

Rantner: I’ve learnt a lot already, Thomas. So it’s become established that you mentioned the abbreviation INAA – I’d never heard of it before. Well, it’s always… one is always in need of learning. Very good.
What, as you’ve already hinted at, repeatedly leads to confusion in clinical practice – not just among our own junior doctors, but across disciplines too – is precisely the distinction from inflammatory vascular diseases, which, as you said, can present with similar clinical pictures. Perhaps you could say a few words on this again so we can gain some clarity?

Karl: Well, traditionally, of course, one immediately thinks of Ormond’s disease. However, this term is historical and should actually no longer be used; nowadays, we refer to it as idiopathic retroperitoneal fibrosis in the form of chronic periarthritis. Ultimately, it is a collective term for inflammatory processes around the aorta, mostly infrarenal, but it can also affect the thoracic aorta. And ‘inflammatory aortitis’ is ultimately just a descriptive term, typically seen on ultrasound or CT scans, referring to the thickened aortic wall and this so-called ‘mantle’ structure.
And now we can differentiate this further: idiopathic retroperitoneal fibrosis is an autoimmune disease, and there is an IgG4-associated form. In this case, aortitis is merely a manifestation of a systemic disease. And there is non-IgG4-associated idiopathic retroperitoneal fibrosis, which is seronegative and lacks typical histology.
Then there are further secondary forms of periaortitis: malignancy-associated, including primary vascular malignancies and angiosarcomas, as well as drug-induced forms, which are not at all uncommon. There are many drugs that can trigger such conditions. Just last week, we operated on a patient with a checkpoint inhibitor-associated aortic aneurysm, i.e. monoclonal antibody therapy for malignant melanoma. But there are also many other drugs that can trigger this, as well as radiation-induced periaortitis.
And then, last but not least, the large-vessel vasculitides, namely Takayasu arteritis and giant cell arteritis. And that makes it difficult to distinguish initially between this chronic periaortitis and a primary infection. But that is crucial, because the treatment is completely different. In cases of infectious causes, we must of course not initiate any immunosuppressive therapy. And that is why we must distinguish between them. Ultimately, it is important to consider an infectious cause as highly probable—until proven otherwise—based on clinical signs of infection and these Delphi criteria. And in cases of other beta-symptoms, such as weight loss and fatigue, one must consider periaortitis. And then the diagnostic approach is different, alongside the CT scan and laboratory tests. Contrary to what one might think, it is not the serological elevation of IgG4 that is decisive, but the histological findings from a tissue biopsy. This is where one finds classic IgG4-positive plasma cell infiltration. Serologically, this is not decisive.
These are, so to speak, the factors one must consider: malignant periaortitis in the context of an autoimmune disease, drug- or radiation-induced causes, or infectious causes.

Rantner: Yes, that alone is incredibly complex. The patients are generally seriously ill and are usually already severely affected. To be honest, the same applies to those with
prosthetic infections. Thomas Betz, I’m going to try to differentiate a little here: Thomas Karl, Thomas Betz, yes, we’ve already discussed this a bit beforehand. But now, Thomas Betz, you’ve been looking into the topic of prosthetic infections very intensively recently. You’ve published a book on it. The first question is: why did you engage with the topic so intensively in the first place? Why do you think this deserves a bit more attention? And are the figures for those affected significant enough that even the average vascular surgeon should expect to encounter a patient with a prosthetic infection and should also be able to manage a prosthetic infection, which is, after all, often an emergency? What’s your view on this?

Betz: Well, to be honest, in my case I had to deal with the treatment of prosthetic infections quite early on during my training. I trained under Markus Steinbauer in Regensburg, and at the time, my senior consultant was looking quite intensively at prosthetic materials as part of his postdoctoral research. It’s also the case – and this is a pity to say – that there isn’t much good evidence on this topic. And up until 2020, there weren’t really any standardised guidelines either. Everyone basically treated patients as they saw fit, and then in 2020 the European guideline from Conti was published. That was a really good first attempt at addressing the issue, though it must be said that the level of evidence was very low. And in the German-speaking world, there is actually relatively little literature on this topic. There is a book by Zühlke from Wittenberg on septic vascular surgery, but it is quite old. So we got together with Markus Steinbauer and Ingolf Töppel and thought we’d write something up in German for the German-speaking world and publish a book on it.
To be honest, it must also be said that the number of vascular prosthesis infections is relatively rare; in the peripheral area, the rate is around 1.5 to 2 per cent, and in the central area 0.6 to 3 per cent, and the vascular surgeon is actually rarely confronted with this.
What we do encounter relatively frequently, however, are wound healing disorders that arise in the context of post-operative care; these occur in around 10 per cent of cases, and they can indeed lead to a vascular prosthesis infection. I think it is absolutely vital to have a basic understanding of what to look out for when seeing such a patient in A&E. It starts, as Thomas Karl has already mentioned, with ensuring that microbiology samples are taken and not immediately starting broad-spectrum antibiotics if clinically justifiable. And it’s personally important to me that colleagues – who will undoubtedly treat these cases well – can take away a few basic points to guide them when a patient with such a problem turns up at their department.

Rantner: That’s the perfect segue into the treatment strategy, given that we’re now in a situation where we need to consider options for those affected. Thomas Karl, you’ve already outlined the complexity of these patients. The mere fact that infection of the native vessel occurs via different routes often means that we have to keep comprehensive treatment in mind – not just comprehensive diagnostics, but comprehensive treatment as well. Personally, I see – perhaps far too often by now – patients who, following spondylodiscitis, suddenly develop, as I always say, mycotic aortic aneurysms, where we then have to coordinate an interdisciplinary approach to determine what the ideal management should look like. In your opinion
, what should the focus be now? What advice can you give our listeners on what the strategy should be? Is the primary concern now bacterial reduction? Which organ should be addressed first? We’ve already discussed the significant bleeding risk associated with aortic infection; what are your thoughts on that?

Karl: We’re actually now only talking about true vascular infections and no longer about the differential diagnoses mentioned earlier. Ultimately, the question is, of course always, what kind of situation am I treating the patient for? Is it an emergency? And when you know that—I’ll say it again—mycotic aortic aneurysms, i.e. infection-related aortic aneurysms, frequently present at the rupture stage—up to 50 per cent become clinically apparent at the rupture stage and end up with us—and the same applies to septic aortic bleeding in intravenous drug users—then the question is naturally always: Do I still have time for a differentiated plan? Is this a palliative situation – ‘life or limb’? And ultimately, the time available for appropriate diagnostics and surgical planning is very limited. And if we just consider the topic of aortic aneurysms – specifically infectious aortic aneurysms – and bear in mind that, as I said, they are frequently treated at the rupture stage. I believe that the decision to treat them endovascularly is often entirely legitimate. And then, if necessary, one must subsequently consider: do I leave it at that? There is also quite good evidence that, in selected cases, endovascular therapy can indeed be used to treat the condition with acceptable results, and it is not merely a bridging procedure; I do, in fact, consider open late conversion during the course of treatment. So ultimately, provided there are no consequences of a rupture and there is time to plan the procedure, then in my view – provided the patient’s circumstances, general condition, comorbidities and operability allow it – one should always aim for surgical debridement. And as a rule – this is, so to speak, the gold standard in my department – for central infections, we aim to implant in situ using autologous tissue via the femoral vein (NICE), even though these are complicated, major and lengthy procedures; the advantage is that in situ is always better and carries the lowest risk of reinfection.
It is clear that we need antibiotic therapy, ideally tailored to the resistance profile. And if one does not wish to perform autologous reconstruction, there are also various other replacement materials available: homologous, senological, alloplastic, endovascular – the entire spectrum. And endovascular is certainly becoming an increasingly viable option. We have 20 years’ experience in this area, in the treatment of infected aortic aneurysms with EVAR implants, and the survival rates are not bad at all: 70 per cent after one year, 50 per cent after five years. However, these patients generally always require lifelong, continuous antibiotic therapy. If they stop taking them, this usually leads to a recurrent infection. You need to be aware of that; but when you consider, on the other hand, how high the perioperative mortality rate is with open surgical treatment, I believe endovascular therapy offers a perfectly legitimate approach, even as a long-term treatment and not just as a curative option. Basically, if the patient is operable, stable, has no malignancy, open surgical treatment, resection into healthy tissue, in situ debridement, autologous graft – that would be my preferred approach, so to speak. And as regards organ preservation, that is again a highly individualised approach. If, for instance, one first performs an EVAR implantation in the case of an aortoduodenal fistula, then one naturally gains time and can consider the options. However, if one wishes to resolve the issue permanently, I believe there is certainly no way around a combined vascular-visceral surgical procedure, even on a unilateral basis.

Rantner: Exactly, these are precisely the complex situations – whether you’re thinking of spondylodiscitis or, say, an aorto-bronchial or aorto-duodenal fistula – where, as you’ve already said, you really find yourself in a situation where you can even consider cure rather than just palliative care. That’s not actually all that different, Thomas Betz – you’ve already briefly raised your hand. So the strategy of autologous reconstruction, bacterial reduction and soft tissue conditioning is also something that’s now favoured for prosthetic infections. Or what else did you want to add on that point?

Betz: I wanted to agree with Thomas Karl. Well, of course, we must keep things in perspective; if I now have an infected bEVAR or fEVAR, it naturally has to be assessed differently than if I have an infected Y-prosthesis that I can easily clamp infrarenally. And of course I have to consider: what can the patient tolerate? What are the patient’s wishes and intentions? And it is entirely legitimate to say – and this must be discussed with the patient – that palliative therapy is an option if the prospects of success are very low.

Karl: Yes, perhaps just to add to that: Well, I know of at least two patients, in my own experience, who have stabilised very well following endovascular therapy, who feel very well, who subjectively have no symptoms, and who simply couldn’t bring themselves to opt for open late conversion and said: ‘No, the mortality rate is a relevant factor after all, and I’m doing well clinically; I accept that and would rather undergo long-term antibiotic therapy.’ So you have to make it clear that this is always a very, very individual decision.

Rantner: Thomas Betz, whilst preparing for this, I thought to myself that if I had to choose now, I might actually prefer a prosthetic infection, because in my everyday clinical practice that often affects the leg, the limb. I mean, of course, we also have open aortic prostheses that somehow become infected over the long term; we’ve already discussed EVARs, but frequently, as you’ve already said, you see inguinal infections following wound healing complications, bypass infections, perhaps due to secondary bacterial spread in patients with stage 4 PAD.
So what is the strategy here, how should one proceed? You said you’d like to provide a guideline on how to proceed. Is it about reducing bacterial load, is it actually always about vascular replacement, or where can one find guidance on this?

Betz: Well, in principle, I would always look at it this way: if I have a patient with a suspected prosthetic vascular infection – let’s say they come to A&E following a femoropopliteal synthetic bypass and then present with the clinical signs and indications, such as redness, overheating, a fever, fluid around the bypass visible on ultrasound, and a fluid collection around the bypass on a contrast-enhanced CT scan – where there is a high suspicion of an acute prosthetic infection in the bypass. If the patient is operable – which, to be honest, they almost always will be in peripheral cases – then I would first take serial blood cultures. It is also perfectly legitimate, provided the patient is not bleeding and has no problems with the anastomoses, to drain the fluid first and attempt to isolate bacteria from the aspirate; then, once I have preserved the relevant material, I would start broad-spectrum antibiotic therapy. This would be a broad-spectrum penicillin, because the most common pathogen affecting prostheses is Staphylococcus aureus in two-thirds of cases, and then I would plan the replacement using an autologous vein for the peripheral access; that is actually what the guidelines state, and if we are completely honest, one will probably always find an autologous vein in some way, you can also use a composite vein made from two arm veins; that will always work, I think, or in most cases, or you can use paired veins and suture them together. And then you would carry out the appropriate prosthetic replacement, remove the prosthesis, debride the bypass site; if there is a massive infection present, I would reroute it, that is, reroute the bypass into a new bypass site, and what is absolutely crucial is that you provide adequate plastic coverage for the bypasses in the groin; this is relatively straightforward using a sartorius flap, and if a sartorius flap isn’t available, you can use a rectus femoris flap, and if you can’t do that, as a vascular surgeon, you can do quite a lot, but your plastic surgery skills are limited, then you can of course bring in a plastic surgeon to help with the plastic coverage in the end.

Rantner: Yes, but there’s no getting round the need to remove it…

Betz: If I had a fluoride prosthesis infection, I would always remove it.

Rantner: Because there are already reports that it’s been screwed and vacuum-sealed and then nicely conditioned, and then, goodness me, if it’s only in the bypass course and the anastomoses aren’t affected: what are the chances of success if you now refuse, so to speak, to actually remove all the synthetic material?

Betz: In my experience, it will always depend a bit on – as you’ve already said – whether the anastomoses are affected or not. I come from a school of thought where, in cases of prosthetic infection, we consistently remove the material. I’ve always had relatively good results with that approach. Of course, there are also data and studies that have investigated whether these prosthetic infections can be cured using NPWT, i.e. VAC therapy. Our colleagues in Zurich have published quite a lot on this in the VASGRA cohort. The results aren’t actually bad at all, it has to be said; but based on gut feeling or my own experience – and this is a bit of an opinion – do they all come back later with bleeding or a recurrence of the problem? That’s the experience I’ve had. I don’t know, Thomas, you’re already in the starting blocks.

Karl: Yes, well, thank you very much for passing the ball to me. I must of course say something about this, because I started working on the topic of VAC therapy for vascular prosthesis infections relatively early on and, in the early years – I still remember it – in 2005, at the Vascular Studies Congress in Stuttgart at the time, I really got a beating. And then Professor Kasperczak stood up and said, ‘Dr Karl, we couldn’t possibly disagree more.’ And our data wasn’t actually that bad. And then, of course, the Zurich group came along and there was a publication titled ‘Paradigm Shift in Vascular Infections, Prosthesis Infections’, along the lines of: ‘We can now treat everything with NPWT therapy.’ I now take a more nuanced view.
Firstly, when anastomoses are affected, there’s always the question of whether it’s an early infection, a late infection, a low-grade or high-grade infection. If the anastomoses are affected, you really need to be certain that the anastomosis is intact. And there are two pathogens where, in my experience, you can be 100% certain that septic erosive bleeding will occur. These are MRSA and Pseudomonas. With Pseudomonas, it’s always the case. This is because the virulence factors attack the native vessel. In other words, it’s not the bypass that fails, nor is it the suture, but the native vessel. Vacuum therapy in cases where Pseudomonas aeruginosa is detected in a prosthetic infection is a sure-fire recipe for septic erosive bleeding. Naturally, as the doctor on duty, one might hope that it catches the other colleagues during the night, but these cases need to be debrided.
And the same applies if a complete prosthesis is infected and is, so to speak, floating. But in the case of early infections, where the transition from impaired wound healing to prosthetic infection is often not entirely clear-cut, I believe there is a realistic chance of achieving healing through a constellative, prosthesis-preserving therapy. Central prosthesis infections need to be removed. But in the periphery, with minor wound healing complications at the P3 bypass, P3 segment or, more commonly, in the inguinal region, I believe there is a chance and it is legitimate to try.

Rantner: That’s actually the perfect segue into the topic of potential replacement materials. Because why are people often reluctant to replace the prosthesis, given that, as you said, it’s a bit of a faff to have to piece it together a few times or perhaps switch to the arm vein? Is homograft still an option? Personally, I’m a big fan of pericardial tubes, unless I want to introduce a third pathogen into the mix, or unless it’s somehow infected with Candida, because then it just dissolves into thin air, in my experience. Silver prostheses – are we still discussing these? Biological materials, bio-coated prostheses – where do you currently see the best options if there’s actually no vein available anymore, or if the calibre simply doesn’t fit?

Betz: Well, I think you have to differentiate between central and peripheral prosthetic infections. For peripheral prosthetic infections, autologous grafts are the first choice; that’s what the guidelines say too. That makes sense, really. Homograft is recommended as the second option, but to be honest, I’m not so keen on that because it’s labour-intensive, it’s expensive, and it’s not off-the-shelf – you don’t have it sitting in the cupboard; you have to order it. That means you can’t use it in an emergency, and you need a certain amount of experience with the material, which is quite fragile. And in the periphery, it has relatively poor patency rates. There is little data on it, and the reinfection rate in the periphery isn’t nearly as good as everyone always thinks. There is just one study on it, and the reinfection rate goes up to 19 per cent – that’s for the homograft. It will always be a bit of a matter of faith as to what I use if I don’t have an autologous vein. If, for example, I only have a prosthetic infection in the groin and say I want to replace a patch graft, then I’ll always find a vein, I think. If I don’t have a vein, I can also use a superficial femoral artery that has undergone endarterectomy, because in most cases the superficial femoral artery is occluded in these patients. Or, of course, what I can also do is remove the bypass and manage the anastomoses accordingly. And often the patient then has claudication or severe claudication, and I can leave it at that. If I don’t have a vein, I would use an Omniflow prosthesis, but that’s because it’s my personal preference and I have the most experience with it. Although it must be said that, regarding the data on this, there aren’t actually any good data and there isn’t much data either, but that’s the case with all publications dealing with peripheral vascular prosthesis infections. I wouldn’t use silver at all, because I’ve had bad experiences with it and because the reinfection rate is relatively high, to be honest. And everything that’s been published on silver in the periphery – Zegelmann published quite a lot on this in the 2010s. The situation was that he essentially conducted large-scale studies in which he implanted silver prostheses in patients who were at a certain risk of prosthetic infection. The results aren’t actually that bad – that is, if you use silver prophylactically – but in the case of an active infection, I wouldn’t actually use the silver prosthesis, to be honest.

Rantner: Thomas Karl, pericardial tubes as aortic replacements – so you do that from time to time?

Karl: Yes, we’ve done that too, but as I said, I did it once because I needed an additional tube, so to speak, as the femoral vein wasn’t quite long enough for the replacement. I think pericardium—that is, xenograft—is a good concept. I’d tend to see it as, let’s say, a second option. I don’t think homologous is the best option either, for the reasons mentioned; Thomas Betz has already summarised it wonderfully. For the same reasons, I don’t think homologous is ideal either. In the case of a central low-grade infection, I believe one could consider using a triclosan-silver-impregnated prosthesis. I’ve done that once, in a truly low-grade case as part of spondylodiscitis, with a good result. So I think you really need to cover the full spectrum, but clearly: in situ autologous, xenograft, pericardium and then everything else. That’s actually how I’d see it.

Betz: Ideally, we don’t actually know what leads to the resolution of this infection. Is it the prosthesis material, is it the biological reinforcement—centrally, for example, with omentoplasty—or is it simply our antibiotic therapy? There are also case reports where prosthetic infections are centralised in fluid collections, which are punctured, and then antibiotic therapy is administered based on culture results. And it stabilises to the extent that they do not start bleeding and that they have a certain survival time. So the crux of the matter in septic vascular surgery is always that the data situation is, understandably, simply poor.

Karl: And of course, the studies are difficult to compare because there is no standardised classification and so many factors play a role. And naturally, most centres don’t have large case numbers at present. And in that respect, it naturally always makes it difficult to make a truly good evidence-based statement.

Rantner: Yes, that’s actually a wonderful summary of what I mentioned at the start. Septic vascular surgery, whether it involves deep-seated vascular infection or prosthetic infection, as it’s now come to be understood, is not just in my view—but I think you’ll agree with me—one of the most complex areas in vascular surgery. It’s multidisciplinary, requires a great deal of experience, a great deal of equipment, a great deal of skill, and a great deal of interdisciplinary collaboration when it comes to the patient’s overall care. And once again, in these podcasts we keep coming back to the point where I bring up this hospital structural reform, because, after all, politicians continue to strive for increasing centralisation. And if you look at a patient like this, a classic case with a fungal aortic aneurysm, which can actually occur anywhere. It’s not a given that they’ll only present at a tertiary care hospital. What do you think, how will this play out? Will centralisation have a positive effect? Can this still happen on a nationwide scale? Is it even necessary? Thomas Betz, you said that prosthetic infections are rare anyway. So in terms of necessity, or what is your opinion on this?

Betz: Well, I simply believe that many colleagues are very capable of treating this effectively – that’s one thing. The other is that, in order to treat it effectively, you simply need a certain infrastructure, which the hospital must provide. You need appropriate CT diagnostics, MRI, and possibly nuclear medicine if you want to perform a PET-CT. You need a microbiologist you can consult when it comes to antibiotic therapy. And not every hospital has that. In that respect, I think this is something that should really be treated at specialist centres. What I think is really important is that when people see a patient with a prosthetic infection, they develop a sense of: What can I do in my own hospital? What can’t I do in my own hospital? And that they treat the patient correctly. In other words, that they develop a sense of when they need to transfer the patient and when they don’t. If I now have a patient with a fungal aneurysm, where I say I can manage it well endovascularly, it would be a good solution for me, for example, if in an emergency I treat it endovascularly in the periphery – provided the colleague is competent and has a prosthesis in stock – and then transfer the patient to a centre for conversion. That’s how I imagine it. Unfortunately, there are currently only three service groups. So I don’t know how things will develop. But I simply think that vascular prosthesis infections are a matter for specialist centres.

Rantner: Thomas Karl, what do you say?

Karl: Well, I think I see it similarly, because it is very complex. But we also have the problem – and we discuss this at every opportunity – of dwindling expertise in open aortic surgery. And that will, of course, lead to the formation of centres, which is also what is desired. And then the question is, who will actually still be able to handle it in an emergency and in such a complex situation involving such highly demanding procedures? And I believe it will be the normative force of the factual in the case of a rupture. If the patient is lucky and ends up in a hospital where it can be treated endovascularly, then that’s probably what they’ll do and say, ‘OK, then a centre can take care of it afterwards, if a late open conversion is needed.’ And in other situations, if he’s lucky and ends up in centres that have the full range of options available, he might have a better chance. But, it must be said, centres or, rather, vascular surgery clinics that treat, on average, some 17 aortic aneurysms per year and manage 80 per cent of these endovascularly will not have the expertise in open aortic surgery required to treat a complex, infected aortic aneurysm via open surgery. However, for such procedures – which, of course, require an immense investment of resources – the question ultimately becomes a very different one: who is going to pay for this in Germany’s healthcare system in future? And I believe this will cause considerable problems over the next 20 years, and then we will see how things turn out for these patients. I believe that, given the hospital structure and service groups, we will hardly be able to maintain comprehensive care for such complex cases. And when you know that they arrive in an emergency with a rupture, then things will probably not end well for some of them.

Rantner: Yes, well, this concerns us all; it’s relevant to us all. A lot is shifting in healthcare and in training, just as you said. Who on earth is supposed to be able to treat these difficult patients so efficiently from start to finish?
A wonderful topic, a wonderful conversation. I’d like to thank you all once again very much for the time we’ve spent together and for the excellent presentation. I’ve learnt my lesson – luckily I’ve written it down – I’ll never use ‘Morbus Ormond’ again, even though I’m always quite proud to have used it.
I’d also like to thank you, dear listeners, for dedicating your time to us once again, and for taking an interest in us. Please feel free to send us your feedback. Please feel free to write to us at podcasts@medizinkommunikation.org. And we’ll be in touch again at regular intervals. I look forward to welcoming you back soon and wish you a wonderful spring until then. Stay healthy and stay curious!