Latest / European Society for Vascular Surgery / ESVS 2025 Mesenteric Ischaemia Guidelines Q&A - Pt 3 - with Guidelines Writing Committee

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ESVS 2025 Mesenteric Ischaemia Guidelines Q&A - Pt 3 - with Guidelines Writing Committee · European Society for Vascular Surgery

• 0:13
  and welcome to the ESVS podcast. This is Suzanne
• 0:16
  Stockmans and you are listening to part three
• 0:18
  of the Q &A series of the 2025 ESVS clinical
• 0:21
  practice guidelines on the management of diseases
• 0:23
  of the mesenteric and renal arteries and veins.
• 0:26
  In this podcast, we will highlight the new complex
• 0:29
  and most controversial recommendations in this
• 0:31
  guideline. On today's episode, we will dive deeper
• 0:34
  into mesenteric venous thrombosis, renal vascular
• 0:37
  diseases, and visceral artery dissections. Welcome
• 0:40
  again, Dr. Koelemay, Professor Geelkerken, and Dr.
• 0:43
  Leone, and thank you for joining us on this second
• 0:45
  episode. Hi, hello, everybody. Acute mesenteric
• 0:49
  venous thrombosis is the least common cause of
• 0:51
  acute mesenteric ischemia. It's typically defined
• 0:54
  as thrombosis of the superior mesenteric vein,
• 0:57
  with or without extension into the portal or
• 0:59
  splenic veins. This can lead to venous mesenteric
• 1:02
  ischemia, which is rare and often triggered by
• 1:05
  either transient or permanent risk factors, similar
• 1:08
  to other forms of venous thrombosis, such as
• 1:10
  malignancy, trauma or hormonal therapy. Interestingly,
• 1:14
  in 20 to 30 % of patients, no underlying cause
• 1:17
  can be identified. As with arterial mesenteric
• 1:20
  ischemia, mesenteric venous thrombosis can present
• 1:23
  in both acute and chronic forms. Could you elaborate
• 1:26
  on the main differences between acute and chronic
• 1:28
  mesenteric venous thrombosis and how these patients
• 1:31
  typically present in clinical practice? Well,
• 1:34
  when we discussed venous mesenteric thrombosis,
• 1:36
  we actually realized that patients will not be
• 1:40
  suspected of venous thrombosis. when they come
• 1:43
  to the emergency department. They will typically
• 1:45
  present with pain, anorexia, probably diarrhea.
• 1:50
  When the physician wants to have a more accurate
• 1:52
  diagnosis, they will make either an autoabdominal
• 1:55
  sonography or a CT scan. And then on the CT scan,
• 1:59
  it will be obvious that there's a venous mesenteric
• 2:02
  thrombosis. So in fact, in the acute phase, it
• 2:06
  is characterized by pain, malaise. anorexia,
• 2:10
  not feeling well, and then you have a diagnosis.
• 2:12
  And in the chronic form, which is arbitrarily
• 2:16
  after four weeks, symptoms will probably reside
• 2:19
  and the patient will develop collaterals because
• 2:22
  of a portal hypertension. And in this way, the
• 2:25
  chronic mesenteric thrombosis can be recognized.
• 2:29
  Do you think that really acute mesenteric venous
• 2:31
  thrombosis really exists? We know in the natural
• 2:34
  form, an acute embolism in the SMA at that moment.
• 2:38
  the ischemia is starting and the symptoms are
• 2:40
  starting. But in my experience in mystic venous
• 2:43
  thrombosis, the symptoms are developing in days
• 2:47
  or mostly weeks. So really acute, normal penis
• 2:51
  outflow. And at that moment, it will be thrombosed.
• 2:54
  I think it does not exist. What is your comment
• 2:56
  on this hypothesis? Well, you're trying to get
• 2:59
  philosophical already. And I must admit that
• 3:02
  I haven't given it this deep thought. I think,
• 3:05
  though, there is some kind of acute penis mass
• 3:07
  attack thrombosis because the patient may come
• 3:10
  with acute symptoms. These are the patients in
• 3:12
  whom it is considered to do thrombolysis. It's
• 3:15
  relatively rare. So nobody has a huge experience.
• 3:18
  acute mesenteric venous thrombosis patients.
• 3:20
  But in my experience, if we talk to these patients,
• 3:23
  nearby all have gradually developing symptoms
• 3:26
  and not this afternoon at three o 'clock, it's
• 3:29
  starting. That's not the case in venous thrombosis.
• 3:32
  It's an interesting thought, actually, because
• 3:34
  development of mesenteric thrombosis, it's not
• 3:37
  acute. Patient will be admitted. will be observed
• 3:39
  and then symptoms will subside or the patient
• 3:43
  will deteriorate. So there's not an acute moment
• 3:45
  of acute ischemia with a dead bowel that you
• 3:48
  have to take out or have to revascularize. It's
• 3:50
  interesting why in one person this will lead
• 3:53
  to congestion and then in the end the need for
• 3:56
  bowel resection. Whilst in the other patient,
• 3:58
  there's a really mild development, a mild course
• 4:01
  of the disease actually. In arterial forms of
• 4:04
  mystic ischemia, there is not much evidence and
• 4:07
  there's a lot of... In the most rare cause of
• 4:11
  acute myceliac ischemia, the venous form, there's
• 4:13
  even no evidence at all. So it's all personal
• 4:17
  opinion and personal thoughts. Maybe the clinical
• 4:20
  presentation can be acute, but I can't imagine
• 4:23
  there is an acute thrombosis. So the thrombosis
• 4:26
  developed gradually. And one moment you get symptoms.
• 4:29
  There is a moment the patient come to the doctor.
• 4:32
  Some patients came to the doctor. with a completely
• 4:35
  developed mesoteric venous thrombosis. And in
• 4:38
  that moment, the ball could be at risk. But also,
• 4:40
  in my experience, it has the best prognosis of
• 4:43
  all kinds of mesoteric ischemia. So it's good
• 4:45
  to realize that there is a thrombosis present,
• 4:48
  which not necessarily leads to ischemia. of the
• 4:51
  bowel, whereas most often when it's on the arterial
• 4:54
  side, a thrombosis or embolism will lead to mesenteric
• 4:57
  ischemia. Recommendation 49, class 1, level C
• 5:00
  advices using contrast -enhanced CT, including
• 5:03
  arterial and portal venous phases for patients
• 5:05
  suspected of mesenteric venous thrombosis. What
• 5:08
  are the characteristics, CT features you assess
• 5:10
  in these patients, and how reliable is CT in
• 5:13
  distinguishing acute from chronic mesenteric
• 5:15
  venous ischemia? I think duplex is not. accurate
• 5:20
  to diagnose venous thrombosis. Two reasons. It
• 5:25
  can be in the small vessels, and you can't imagine
• 5:27
  then the duplex. And the second reason, in most
• 5:30
  of these cases, the bowel is distended. There's
• 5:32
  a lot of air inside the bowel. And in that moment,
• 5:35
  duplex is not the appropriate technique. First,
• 5:37
  second, and third choice is CT scanning. And
• 5:40
  then... You must assess the venous part itself.
• 5:43
  It means the superior mysderic vein, the spleenic
• 5:46
  vein, and in the end, the portal vein, the drain
• 5:48
  of the bowel. Everything that's happened in the
• 5:50
  bowel is transported to the portal vein. You
• 5:53
  have to assess them accurately. That's the most
• 5:55
  easy part. But you also have to assess more non
• 5:58
  -vascular findings, like bowel wall thickening,
• 6:01
  bowel wall dilatation, bowel wall thinning, mysderic
• 6:04
  fat stranding, pneumatosis, portal venous gas.
• 6:07
  These are all criteria for... severe ischemia,
• 6:11
  but none of them is proven transmural necrosis.
• 6:15
  That's the difficulty of CT scanning and performing
• 6:18
  CT scanning is like in the arterial phase. It
• 6:21
  should be a contrast -enhanced CT with arterial
• 6:24
  and venous phase. And then if you expected a
• 6:27
  venous thrombosis, please also perform the venous
• 6:30
  phase in one millimeter slices. Due to the rarity
• 6:34
  of mesenteric venous thrombosis and the limited
• 6:36
  high -quality evidence, there is no universally
• 6:38
  agreed -upon treatment strategy. The main objective
• 6:41
  in acute mesenteric venous thrombosis are to
• 6:43
  prevent thrombus propagation, restore venous
• 6:46
  patency, and avoid bowel infarction, portal hypertension,
• 6:49
  and recurrent thrombosis. In chronic cases, treatment
• 6:52
  also focuses on preventing and managing complications,
• 6:55
  such as gastrointestinal bleeding and portal
• 6:58
  cholangiopathy. First -line therapy systemic
• 7:00
  anticoagulation, which achieves venous recanalization
• 7:04
  in approximately 40 % to 80 % of patients. Supportive
• 7:08
  care, including pain management, fluid and electrolyte
• 7:11
  replacement, and bowel rest, should be initiated
• 7:14
  promptly. The new recommendation 51, class 2B,
• 7:17
  level C, suggests that endovascular venous thrombolysis
• 7:20
  or mechanical thrombectomy can be considered
• 7:22
  in patients with acute venous mesenteric ischemia
• 7:25
  who deteriorate despite anticoagulation. you
• 7:28
  elaborate on the different endovascular treatment
• 7:30
  options available and whether there's still a
• 7:33
  role for surgical treatments in these cases?
• 7:35
  We are talking about the most rare cause of mesenteric
• 7:40
  ischemia and here we are talking about a small
• 7:43
  portion of patients not responding to anticoagulants.
• 7:47
  The new recommendation for endovascular therapy
• 7:51
  focuses on directly treating the massive clot
• 7:54
  burden and rapidly restoring blood flow. However,
• 7:59
  these are used in a very small percentage of
• 8:03
  people and the available endovascular options
• 8:06
  are catheter directed thrombolysis, mechanical
• 8:10
  thrombectomy and a combination pharmacomechanical
• 8:14
  thrombectomy. These procedures are minimally
• 8:18
  invasive and are performed via percutaneous access,
• 8:22
  most commonly through transhepatic or transjugular
• 8:27
  approach into the portal system. The essential
• 8:30
  role of surgery is to manage the life -threatening
• 8:34
  complication of NVT, namely the bowel infarction.
• 8:41
  Personally, I don't see a modern role for open
• 8:46
  vascular surgery to remove clots in these districts.
• 8:51
  And I do think that procedures should be performed
• 8:54
  in selected centers that have the numbers to
• 8:58
  reach the learning curve in these procedures.
• 9:01
  I do think that in these cases, centralization
• 9:04
  is mandatory. The evidence for catheter -based
• 9:08
  interventions for this is very... poor. We used
• 9:11
  a systematic review, including nearly 500 patients,
• 9:14
  and these were uncontrolled series. So in fact,
• 9:17
  there's no control with anticoagulation, no head
• 9:20
  -to -head comparison at least, and we cannot
• 9:22
  be sure whether this is actually more beneficial
• 9:25
  than anticoagulation. The flowchart shows that
• 9:28
  if a patient does not improve on anticoagulation,
• 9:31
  you may consider doing an endovascular treatment.
• 9:33
  I agree that experience with this is very limited.
• 9:36
  also in our academic hospital and probably also
• 9:38
  in your institution. And you might have a say
• 9:41
  to centralize interventions for this because
• 9:44
  of the rarity. Well, thank you for this clarification.
• 9:47
  We already talked a little bit about heparinization
• 9:49
  after the initial phase of systemic anticoagulation.
• 9:53
  Oral anticoagulation is typically started within
• 9:55
  two to three weeks. Traditional vitamin K antagonists
• 9:59
  were the drugs of choice, but small retrospective
• 10:01
  studies now suggest that direct oral anticoagulations,
• 10:05
  or DOACs, are also safe, reflected in a new recommendation,
• 10:08
  53, class 2b, level C. Patients are generally
• 10:12
  treated for three to six months, although the
• 10:15
  optimal duration of anticoagulation remains uncertain.
• 10:18
  Recommendation 54, class 2A level C, and 55,
• 10:22
  class 2B level C, state that extended anticoagulation
• 10:26
  with either vitamin K antagonist or DOACs should
• 10:29
  or may be considered for patients with acute
• 10:32
  mesenteric vein thrombosis who have transient
• 10:34
  risk factors for venous thrombosis. Giving the
• 10:37
  limited evidence, how do you decide on the duration
• 10:39
  and type of anticoagulation? coagulation in your
• 10:41
  clinical practice? And do you see DOEX becoming
• 10:44
  the preferred option over vitamin K antagonists
• 10:47
  in these patients? Well, in fact, this is a touchy
• 10:49
  area for surgeons because venous mesenteric thrombosis
• 10:52
  is mainly the domain of internal medicine, also
• 10:55
  because of the underlying causes for venous mesenteric
• 10:59
  thrombosis. In fact, surgeons, at least in our
• 11:02
  hospital, are not in charge for the definitive
• 11:05
  treatment of these patients. And the experience
• 11:07
  with DOEX is limited. So in fact, We decided
• 11:11
  to make a disclaimer in this guideline to recommend
• 11:14
  DOACs as a 2A but as a 2B. You might consider
• 11:18
  this as off -label because it has not been investigated
• 11:21
  for venous mesenteric thrombosis. And the internist
• 11:23
  cannot give you the definitive answer either.
• 11:26
  I think that in the future, when there's more
• 11:28
  experience with DOACs, it seems logical that
• 11:31
  these will take over because it's easier to dose.
• 11:34
  There's no need for checks. But this is why it's
• 11:37
  quite a safe recommendation. for DOACs to use.
• 11:41
  And then your question about extensive use, this
• 11:43
  is interesting because from the internal medicine
• 11:46
  systematic reviews and meta -analyses, it became
• 11:50
  obvious that continued anticoagulation was in
• 11:53
  fact beneficial. So when patients discontinued
• 11:56
  treatment, they had a higher risk of recurrent
• 11:58
  thrombosis instead of when anticoagulation was
• 12:00
  continued. But this should be balanced, of course,
• 12:03
  against the risk of bleeding, which was higher
• 12:05
  in patients who continued anticoagulation. to
• 12:08
  say but i think that we won't never ever have
• 12:12
  reliable evidences on on this specific topic
• 12:17
  so i think that what proposed is a wise decision
• 12:21
  And also here in Italy, in my practice, it is
• 12:25
  an internal medicine job, this one. So now it's
• 12:29
  time to switch topics again. We are now moving
• 12:32
  into vascular kidney disease, starting with renal
• 12:35
  artery stenosis. This is a completely new section
• 12:38
  in the 2025 guideline. So all the recommendations
• 12:41
  are new. We could easily dedicate an entire episode
• 12:44
  to this topic and we just might in the future.
• 12:46
  But for now, I've selected the most relevant
• 12:48
  recommendations for clinical practice to discuss.
• 12:51
  today's podcast recommendation 63 class 3a level
• 12:55
  a states that percutaneous transluminal renal
• 12:58
  artery angioplasty with or without stenting is
• 13:01
  not indicated in patients with any degree of
• 13:04
  renal artery stenosis and controlled hypertension
• 13:06
  and renal function In clinical practice, how
• 13:09
  do you decide when a patient moves from conservative
• 13:12
  management to being a true candidate for revascularization?
• 13:15
  And who usually takes the lead in managing these
• 13:18
  patients conservatively? Is that typically within
• 13:20
  the vascular surgeon's domain, or are there more
• 13:23
  often referred and followed by a nephrologist
• 13:25
  or other specialists? It was interesting to learn
• 13:28
  that actually since the 90s, where the trials
• 13:32
  were performed comparing medical therapy against
• 13:34
  renal artery stenting, there's no new information.
• 13:38
  part of these guidelines is new as part of these
• 13:40
  guidelines, but they used to be in the peripheral
• 13:43
  artery guidelines and the guideline steering
• 13:46
  committee decided to include it in the mesenteric
• 13:49
  and renal artery and venous guidelines. It was
• 13:52
  interesting to read that there is no new evidence
• 13:54
  since the 90s and all the trials comparing stenting
• 13:58
  versus medical therapy were negative. So they
• 14:00
  did not confer. any benefit of intervention over
• 14:05
  medical therapy. With us, it's the vascular internist,
• 14:08
  the vascular medicine department, who takes care
• 14:10
  of patients with hypertension. It's a matter
• 14:13
  of taste whether you should proceed to renal
• 14:16
  artery angioplasty. And you may consider this
• 14:19
  when a patient is on three, four antihypertensive
• 14:22
  drugs, which can be very invalidating, incapacitating.
• 14:25
  And then you can consider doing an angioplasty
• 14:28
  in order to reduce the number of antihypertensives
• 14:32
  in order to improve your quality of life. It's
• 14:35
  not a strong recommendation to do this, but you
• 14:37
  can consider treating patients with angioplasty.
• 14:40
  And the same actually applies to renal function.
• 14:44
  And with us, that's more in the field of the
• 14:46
  nephrologist. indeed, in the vascular medicine
• 14:48
  as well. Let's now turn to patients who do have
• 14:51
  an indication for revascularization, starting
• 14:53
  with fibromuscular dysplasia, or FMD. FMD is
• 14:57
  an idiopathic, segmental, non -eterosclerotic,
• 15:00
  and non -inflammatory disease affecting the muscular
• 15:02
  layer of arterial walls. It leads to stenosis
• 15:06
  of small and medium -sized arteries and accounts
• 15:08
  for roughly 10 % of renal artery stenosis cases
• 15:11
  with a clear female predominance. Recommendation
• 15:14
  64, class 2A, level C. states that percutaneous
• 15:18
  transluminal renal artery angioplasty with bill
• 15:21
  outstanding should be considered for patients
• 15:23
  with resistant hypertension despite taking three
• 15:25
  or more antihypertensive drugs and a renal artery
• 15:29
  stenosis of more than 70 % due to fibromuscular
• 15:33
  dysplasia. Why is stenting not routinely performed
• 15:36
  in FMD and in which situations would you consider
• 15:39
  placing a stent? Again, we are moving for a quite
• 15:44
  rare disease, FMD is, I think, a different beast
• 15:49
  compared to atherosclerotic stenosis. If we rely
• 15:54
  on evidence, we can see that a simple PTA, it
• 15:58
  is quite effective in these patients and yields
• 16:02
  excellent long -term results. So stenting is
• 16:06
  not routinely performed. and it is reserved to
• 16:10
  has a bailout strategy and this is driven by
• 16:14
  two main pillars high success rate with simple
• 16:18
  pta and the risk of complications coming from
• 16:23
  stenting because of course every time we put
• 16:27
  metallic stents in these specific arteries that
• 16:32
  are not atherosclerotic vessels this is associated
• 16:36
  with higher risk of complication in the long
• 16:39
  term. What kind of complications do you foresee,
• 16:42
  Nikola? I think that these patients are at a
• 16:45
  higher risk of dissection. And of course, when
• 16:48
  you start putting a stance and then you have
• 16:51
  a dissection and then you need probably a second
• 16:54
  stance. And of course, all the time we do additional
• 16:58
  maneuver, we can face additional complications.
• 17:03
  This is the main complication that I foresee.
• 17:06
  Recommendation 66, class 2A, level C, states
• 17:10
  that percutaneous transluminal renal artery angioplasty
• 17:13
  with stenting should be considered for selected
• 17:16
  patients with resistant hypertension despite
• 17:18
  taking three or more antihypertensive drugs and
• 17:21
  an atherosclerotic renal artery stenosis of more
• 17:24
  than 70%. What is the success rate of renal artery
• 17:27
  stenting in controlling resistant hypertension
• 17:29
  and what is your approach to post -procedural
• 17:32
  antithrombotic therapy and follow -up in these
• 17:35
  patients? I would cite the one registry, which
• 17:37
  is the Hercules study. And there were about 200
• 17:40
  patients who had more than three antihypertensive
• 17:44
  drugs and a renal artery stenosis. And they were
• 17:47
  treated with renal artery stenting. And it was
• 17:50
  interesting to learn that there was a reduction
• 17:52
  indeed in systolic blood pressure, which was
• 17:55
  about 10 mils of mercury. So this might be significant.
• 17:58
  But they still had the same number of... antihypertensive
• 18:02
  drugs as before the interventions. It's not sure
• 18:05
  whether this would help you to get rid of some
• 18:08
  of the drugs that you need to take. And it's
• 18:11
  also interesting to know that there was no effect
• 18:13
  on renal function. So there's not very hard evidence
• 18:16
  that it's useful, but you may consider this.
• 18:19
  There are two large randomized control trials,
• 18:21
  the ASTRAL and the CORAL trial, both including
• 18:24
  above the 800 patients. They were randomly allocated
• 18:27
  to PTA plus optimal medical treatment or optimal
• 18:31
  medical treatment alone. Again, there were no
• 18:33
  significant difference in the primary and secondary
• 18:35
  endpoints. including blood pressure, progressive
• 18:37
  renal insufficiency, cardiovascular events, and
• 18:39
  deaths. And this was also substantiated by a
• 18:42
  systematic review published in 2021, summarizing
• 18:45
  that the only occasion for invasive treatment
• 18:47
  of renal artery stenosis is a rapid deterioration
• 18:51
  in kidney function in patients with a clear and
• 18:53
  limited bilateral stenosis at the origin of the
• 18:56
  renal arteries and with remaining kidney parenchyma.
• 18:59
  Another new section in this guideline covers
• 19:01
  Nutcracker syndrome, a rare condition caused
• 19:03
  by external compression of the left... This compression
• 19:15
  results in dilatation of the left renal vein
• 19:18
  and increased venous pressure, leading to venous
• 19:21
  hypertension. Patients may present with microscopic
• 19:24
  or macroscopic hematuria, flank abdominal or
• 19:28
  pelvic pain, proteinuria, as well as dyspareunia,
• 19:31
  dysmenorrhea, orthostatic hypertension and fatigue.
• 19:33
  How is the diagnosis of Nutcracker syndrome established
• 19:36
  in clinical practice? I think you just mentioned
• 19:39
  all the signs and symptoms, so I'm not going
• 19:41
  to repeat them. You may add some imaging, and
• 19:44
  for this you can use a duplex ultrasonography,
• 19:47
  which shows compression of the renal vein, or
• 19:50
  make a CTA. confirm the dense compression of
• 19:53
  the renal vein. I think that the challenging
• 19:56
  part of diagnosis and eventually treating these
• 19:59
  patients is that if you have macroscopic hematuria
• 20:03
  and other symptoms, it is quite clear that the
• 20:07
  patient is symptomatic. But when you have some
• 20:09
  mild blank pain, mild discomfort, it is very
• 20:14
  difficult to... establish the diagnosis because
• 20:18
  we have on one hand the radiological diagnosis
• 20:22
  and on the other hand the clinical diagnosis.
• 20:26
  I think that sometimes it is very difficult to
• 20:28
  match these two diagnoses. Basically what we
• 20:32
  do here is that unless we have macroscopic hematuria
• 20:37
  or proteinuria or at least we have some lab results
• 20:43
  Usually we treat this patient conservatively.
• 20:47
  When we are talking about treatment, there are
• 20:49
  three new recommendations on this topic. Recommendation
• 20:52
  69 to 71. For patients with mild symptoms, conservative
• 20:55
  management is recommended. As you just said,
• 20:58
  this is class 1 level C evidence. An open surgical
• 21:01
  treatment, typically by left renal vein transposition,
• 21:04
  should be considered for those with a confirmed
• 21:06
  diagnosis who experience severe symptoms. Class
• 21:09
  2A, level C. And finally, endovascular stenting
• 21:12
  may be considered for selected patients with
• 21:14
  severe symptoms. Class 2B, level C. In your clinical
• 21:17
  practice, how do you decide when a patient's
• 21:20
  symptoms are severe enough to warrant intervention
• 21:22
  rather than conservative management? And once
• 21:24
  that decision is made, how do you choose between
• 21:27
  an open surgical approach and an endovascular
• 21:29
  one? What are the key factors that guide that
• 21:31
  choice? I think the audience should be aware
• 21:34
  that the only class one recommendation in this
• 21:38
  domain is that conservative management is recommended
• 21:41
  for patients that establish diagnosis of nutcracker
• 21:44
  syndrome who have mild symptoms. So that means
• 21:46
  doing nothing and talk to your patients and explain
• 21:50
  their symptoms is in most cases enough. And that
• 21:53
  is in line with the other three compression syndromes
• 21:57
  in the abdomen, the MALS, the Wilkie and the
• 21:59
  May -Turner. If they have mild symptoms, only
• 22:02
  talk to them, sometimes every year, but it helps.
• 22:05
  Paraphrasing Cilacci, his 1972 statement about
• 22:08
  MALS, it's also valid, in my opinion, for a nutcracker.
• 22:12
  No patient had ever been proven on scientific
• 22:14
  grounds to have an abnormality of visceral structures
• 22:17
  or function which was caused by exoluminal compression
• 22:21
  of the left renal vein between the SMA and the
• 22:23
  aorta, or supposed relief from the intervention
• 22:26
  could be anything else than a placebo effect.
• 22:29
  There is really no support. However... Personally,
• 22:33
  I believe in the diagnosis in very, very selected
• 22:37
  cases. And in these cases, we prefer left renal
• 22:41
  vein reimplantation downstream in the inferior
• 22:44
  caval vein. We do not perform in my institute
• 22:48
  stenting of the left renal vein. We observed
• 22:50
  a few displacements, and we also observed in
• 22:53
  one case that the stent was in the pulmonary
• 22:56
  artery. If you have severe symptoms, then it's
• 23:01
  a really easy intervention for an experienced
• 23:04
  vascular surgeon to re -implant lesion of vein
• 23:07
  downstream in the inferior cable vein. Maybe
• 23:09
  if you do something, in my opinion, that should
• 23:12
  be a class three B recommendation. Don't harm
• 23:16
  your patient. But that's my personal experience.
• 23:19
  As we discussed in the second chapter, the diagnosis
• 23:22
  and treatment of MALS. provoked many emotions
• 23:25
  among the members of the writing committee, the
• 23:28
  reviewers, and also the guideline steering committee.
• 23:31
  We had extensive discussions as to whether we
• 23:33
  should include MALS and also about the grading
• 23:36
  of the recommendations. The interesting thing
• 23:38
  is the number of publications on nutcracker syndrome
• 23:41
  are even less than on MALS. And the reviewers
• 23:44
  and the steering committee were much more easygoing
• 23:47
  with the recommendations for nutcracker syndrome.
• 23:50
  That was really striking. Their opinion was as...
• 23:53
  hours to treat patients conservatively conservatively
• 23:56
  and conservatively and only do anything in case
• 23:59
  of severe symptoms. And then it was quite easy
• 24:02
  to issue recommendations about surgery, although
• 24:05
  the results of surgery are, well, not as good
• 24:08
  as patients who had been treated for MALS. And
• 24:10
  also there is some evidence about stenting, uncontrolled
• 24:13
  studies, so not head -to -head comparisons with
• 24:16
  surgery, which, as opposed to Bob's experience,
• 24:19
  report good results for stenting. But it is quite
• 24:21
  obvious for everyone that surgery should be the
• 24:24
  treatment of choice. So we followed this after
• 24:27
  extensive... discussions but the thing that i
• 24:29
  remember is this are the extensive discussions
• 24:32
  about mouse and then for nutcracker syndrome
• 24:34
  we would be easygoing about recommendations when
• 24:37
  you create such a guideline there are a lot of
• 24:40
  topics to discuss and if you place nutcracker
• 24:43
  as one of the first topics you discuss i think
• 24:45
  the recommendation will change if you discuss
• 24:48
  this after two days of really deep discussions
• 24:51
  everybody say okay there is no evidence what
• 24:54
  do you think I agree. And that's also how it
• 24:57
  works. And if you really change the guideline
• 25:00
  and committee, I think in MALS, but also in Nutcracker,
• 25:04
  the recommendation can also be changed. Yeah,
• 25:07
  but the good thing is that there are external
• 25:08
  reviewers and also the steering committee. So
• 25:11
  we're not the only ones to decide what's coming
• 25:13
  into the guideline, but the grading as well.
• 25:16
  And then it really struck me how easy all our
• 25:18
  colleagues were about the recommendations about
• 25:20
  Nutcracker, for which there's even less evidence
• 25:23
  than for MALS. Let's continue. Chapter 9 is solely
• 25:26
  focused on visceral artery aneurysms, rare vascular
• 25:29
  abnormalities, often discovered incidentally
• 25:32
  thanks to modern imaging. Although most remain
• 25:34
  stable, their rupture can be catastrophic. Diagnosis
• 25:37
  is best made with CT angiography and treatment
• 25:40
  decisions depend on symptoms, aneurysm size and
• 25:43
  location. Urgent repair is indicated for symptomatic
• 25:46
  or mycotic aneurysms, while endovascular repair
• 25:49
  is now preferred over open surgery when anatomy
• 25:51
  allows. For small asymptomatic aneurysms, typically
• 25:55
  below 30 mm or 50 mm for pancreatic or duodenal
• 25:59
  arteries, regular imaging follow -up is recommended.
• 26:02
  In women who are pregnant or of childbearing
• 26:04
  age, even small splenic or renal artery aneurysms
• 26:07
  should be treated due to the high risk of rupture.
• 26:10
  So the key question is, how do we find I think
• 26:22
  it's a key point of discussion, this one. Of
• 26:24
  course, we need to find a balance. We need to
• 26:27
  avoid unnecessary intervention. And I think that
• 26:31
  this is mainly made on size threshold. But when
• 26:35
  you look at these guidelines and you compare
• 26:38
  these guidelines with the American one, you can
• 26:41
  see that there's a huge heterogeneity in the
• 26:45
  threshold for elective repair. And unfortunately,
• 26:48
  this comes by the lack of true reliable evidence.
• 26:53
  And also, as we said before, it is a matter of
• 26:57
  committee discussion. But when we discussed this
• 27:01
  threshold within the committee, we looked at
• 27:04
  the largest publications on the topic. When you
• 27:08
  look at this publication, you can see that most
• 27:11
  aneurysms are greater than 3 cm at selective
• 27:15
  treatment and this is the threshold for basically
• 27:19
  all the visceral vessels with one exception that
• 27:23
  is pancreatic and gastrointestinal arteries.
• 27:27
  For these arteries, we choose the 1 .5 centimeter
• 27:31
  threshold and also this comes from one publication
• 27:36
  the largest one from the US that showed that
• 27:40
  the diameter at repair of these lesions was greater
• 27:45
  than two centimeters and this means that ruptured
• 27:49
  aneurysms usually are greater than two centimeters
• 27:53
  and that's why we choose one and a half threshold
• 27:56
  so this is true for elective repair when we come
• 28:00
  to urgent repair i think that the undisputable
• 28:03
  indication it is ruptured aneurysm we can talk
• 28:07
  about symptomatic one and even in this case when
• 28:11
  you ruled out all other possible causes explanations
• 28:15
  we need to think that it is the aneurysm and
• 28:20
  so this is an indication for urgent repair one
• 28:24
  of the most debated topic it is regarding pregnant
• 28:28
  and childbearing age patients here my personal
• 28:33
  point of view it is that in this patient at least
• 28:37
  you have to discuss the topic with the patient,
• 28:41
  explain risks and benefits, and I think it is
• 28:44
  a shared decision. I personally won't go for
• 28:48
  trait indication to repair to all size childbearing
• 28:54
  female or all size pregnant patients, but I think
• 28:58
  it is important to discuss risk and benefit with
• 29:01
  them. In figure 8 of the guideline, you will
• 29:04
  find a clear overview summarizing the recommended
• 29:07
  treatment thresholds for visceral artery aneurysms.
• 29:10
  Now moving on to chapter 10, which focuses on
• 29:13
  the diagnosis and management of spontaneous isolated
• 29:15
  dissections of the celiac artery, superior mesenteric
• 29:19
  artery and renal arteries. How do these patients
• 29:22
  usually present and what is the best way to classify
• 29:25
  these dissections? These patients can present
• 29:27
  in different ways. There can be asymptomatic
• 29:29
  patients because of a CT scan. It's made for
• 29:32
  a different reason, and then a dissection of
• 29:35
  the celiac artery or SMA is detected. There may
• 29:38
  be symptomatic patients, and they mostly present
• 29:40
  with pain, abdominal pain. A CT scan is made,
• 29:44
  and then the diagnosis is made. There have been
• 29:46
  several clinical classifications, but in the
• 29:49
  end, there's not so much clinical relevance as
• 29:52
  to the classification. In the end, it will not
• 29:54
  predict the outcomes, which is usually benign,
• 29:57
  because for most patients, it can be treated
• 29:59
  conservatively and only treated. them when complications
• 30:02
  occur, such as bioschemia or suspicion of bioschemia
• 30:06
  or rupture or aneurysm formation. So you may
• 30:09
  question whether clinical use of this classification
• 30:12
  is really relevant. When we talk about treatment,
• 30:15
  that is also discussed in recommendation 95 to
• 30:18
  98. This addresses the management of isolated
• 30:20
  dissection of the visceral arteries. This guideline
• 30:23
  advises that conservative treatment, including
• 30:26
  blood pressure control, pain management, and
• 30:29
  bowel rest, should be the first -line approach
• 30:30
  for patients with asymptomatic or uncomplicated
• 30:33
  symptomatic dissections, class 1, level C, just
• 30:36
  like you just mentioned. In addition, antiplatelet
• 30:39
  therapy may be considered, class 2a, level C.
• 30:41
  For patients who do not respond to medical management
• 30:44
  and in whom bowel ischemia is suspected, endovascular
• 30:48
  revascularization is recommended, class 1, level
• 30:50
  C. In clinical practice, what criteria are used
• 30:54
  to decide when a patient with an isolated visceral
• 30:57
  artery dissection should transition from conservative
• 30:59
  management to endovascular intervention? This
• 31:03
  is really difficult, but on the other side, also
• 31:05
  a very easy question. I will explain why. The
• 31:08
  evidence, as Mark explained, is only anecdotal.
• 31:11
  And neither the Sakamoto nor the Jun anatomical
• 31:15
  classification can predict the clinical course.
• 31:18
  of mystical artery dissections. So whether or
• 31:21
  not to intervene is a typical team consensus
• 31:24
  decision. Discuss it with your colleagues and
• 31:28
  observe the patient. And if you get a bad feeling
• 31:31
  in your belly, a sense of unease during observation
• 31:34
  or optimal medical therapy, then maybe there's
• 31:38
  a place for an intervention. And it's important
• 31:40
  to realize that more than 80 % of the patients
• 31:42
  who received optimal medical treatment didn't
• 31:44
  require any further intervention during their
• 31:48
  stay on Earth. Thereafter, I don't know. So I
• 31:50
  understand that this answer offers little concrete
• 31:54
  guidance, but maybe that is simple, is it more?
• 31:58
  Let me challenge you, Bob. What is the optimal
• 32:01
  medical therapy for these patients? I think we
• 32:04
  do the same as in line with orthodissections.
• 32:07
  lower the blood pressure. If the blood pressure
• 32:09
  is low enough that the patient has not any symptoms
• 32:12
  anymore and still has good functioning other
• 32:15
  organs, we are happy. The second treatment is
• 32:18
  that we start thrombocyte activation inhibitors.
• 32:21
  We believe that makes sense. We don't know. And
• 32:24
  how about follow -up of these dissections? Do
• 32:26
  you need lifelong follow -up? That's also unclear.
• 32:29
  Most of the studies who do follow -up have a
• 32:32
  horizon of, say, two years. And after that, the
• 32:35
  patients are probably discharged, lost their
• 32:37
  follow -up. So we don't know beyond this point.
• 32:40
  But there doesn't seem to be many changes in
• 32:42
  the diameter or aneurysm formation after a dissection
• 32:47
  of the mesenteric artery. So it might be good
• 32:50
  to study this for a longer period. And maybe
• 32:52
  we can do this in the prospective arm of the
• 32:55
  eVisor project to gather more evidence on that.
• 32:58
  But probably the same as with visual aneurysms,
• 33:01
  the cause seems to be really benign. So with
• 33:04
  this last statement, I would like to close part
• 33:06
  three of this podcast. Bob, you wanted to say
• 33:09
  something. something. I would like to take this
• 33:11
  opportunity to thank all the members of the writing
• 33:13
  committee, the review committee, and also the
• 33:16
  senior editorial board of the journal for our
• 33:19
  inspiring oral and written discussion. And in
• 33:21
  particular, I want to emphasize the not to be
• 33:24
  underestimated role of Mark Kulamai, our chair.
• 33:27
  Mark, your dedication and the work you put in
• 33:30
  to realize this guideline was indispensable and
• 33:33
  cannot be valued enough. Thanks for that on behalf
• 33:36
  of the whole festival community. Thank you so
• 33:38
  much. for these compliments, Bob. And it was
• 33:40
  a pleasure doing this in the end, not always.
• 33:43
  And it was a pleasure to do this podcast because
• 33:46
  we did the discussions all over again and it
• 33:48
  brought back good memories of the discussions
• 33:51
  we had. Thank you so much for this comprehensive
• 33:53
  overview of the 2025 ESVS clinical practice guidelines
• 33:56
  on the management of diseases of the mesenteric
• 33:59
  and renal arteries and veins. We went through
• 34:01
  the whole guideline in these three episodes.
• 34:03
  Of course, much more information and literature
• 34:06
  can be found in the guidelines. So I would encourage
• 34:08
  everyone listening to this podcast to go through
• 34:11
  the entire document in detail. Also, there will
• 34:13
  be an international multidisciplinary symposium
• 34:16
  on June 5, 2026, titled New Perspectives on Mesenteric
• 34:21
  Ischemia in Rotterdam in the Netherlands. I will
• 34:24
  put a link to this symposium in the show notes.
• 34:26
  Thank you, Dr. Koulemai, Dr. Geelkerken and Dr.
• 34:28
  Leone so much for sharing your time and expertise
• 34:31
  with us. It has been a pleasure. And thank you
• 34:33
  again. And this goes to the whole writing committee
• 34:35
  for tremendous work, which will help all vascular
• 34:38
  surgeons and their patients. Thank you all out
• 34:41
  there for listening. sure to follow our socials
• 34:43
  to be in the loop of next releases have a great
• 34:45
  day bye