Latest / European Society for Vascular Surgery / ESVS 2025 Mesenteric Ischaemia Guidelines Q&A - Pt 2 - with Guidelines Writing Committee

Transcript

ESVS 2025 Mesenteric Ischaemia Guidelines Q&A - Pt 2 - with Guidelines Writing Committee · European Society for Vascular Surgery

0:12
to the ESVS podcast. This is Suzanne Stokmans
0:15
and you are listening to part two of the Q &A
0:17
series of the 2025 ESVS clinical practice guidelines
0:21
on the management of diseases of the mesenteric
0:24
and renal arteries and veins. In this podcast,
0:26
we will highlight the new, complex, and most
0:29
controversial recommendations in this guideline.
0:31
On today's episodes, we will dive deeper into
0:33
median arcuate ligament syndrome, acute mesenteric
0:36
ischemia, and non -occlusive mesenteric ischemia.
0:39
I would like to warmly welcome back Dr. Koelemay,
0:41
Professor Geelkerker and Dr. Leone. Thank you
0:44
all for joining us again for this second episode.
0:46
And a special welcome as well to Dr. Kärkkäinen,
0:49
vascular surgeon at Turku University Hospital
0:51
in Finland and final co -chair of the guideline,
0:54
who is joining us for this episode. Hi, hello
0:56
everybody. Thank you and hi everybody. Good afternoon.
0:59
We're starting this episode with a rather controversial
1:01
topic, median arcuate ligament syndrome or MALS.
1:05
It's thought to be the second most common cause
1:07
of single vessel mesenteric arterial occlusive
1:09
disease and results from external compression
1:11
of the celiac artery by the median arcuate ligament,
1:14
which passes over the aorta at about the level
1:16
of the first lumbar vertebra above the celiac
1:19
artery origin. The anatomy is clarified in figure
1:21
2 in the guideline. This anatomical configuration
1:24
is often asymptomatic, but in some patients,
1:27
particularly those with low diaphragmatic insertion
1:30
or high celiac origin, the muscular or fibrous
1:33
diaphragmatic band can compress the celiac artery,
1:35
most pronounced during expiration, and cause
1:37
postprandial abdominal pain. Because symptoms
1:40
overlap with many other disorders, most remain
1:42
a diagnosis of exclusion. Recommendation 26,
1:45
Class IIa, Level C, states that MALS should be
1:48
considered in highly selected patients with otherwise
1:50
unexplained chronic abdominal symptoms and celiac
1:53
artery stenosis or occlusion due to external
1:55
compression. Highly selected is defined as 1.
1:58
Post -perineal pain associated with at least
2:00
one of the following. Dietary modification, unexplained
2:03
weight loss, unexplained diarrhea. 2. External
2:05
compression of the celiac artery causing a 70
2:08
% stenosis demonstrated by two imaging techniques,
2:10
which includes at least an inspiration and expiration
2:13
sequence. CTA with 1mm sections, and three, abdominal
2:16
ultrasound and esophageal gastroduodenoscopy
2:19
with no abnormalities. Could you tell us more
2:22
about the typical MALS patients you would consider
2:24
for intervention and share your thoughts on their
2:26
ongoing CAROSA trial, the randomized study comparing
2:29
video -assisted retoperitoneal median arc with
2:31
ligament release to a sham procedure? MALS is
2:34
still a controversial diagnosis. The pathophysiology
2:37
is poorly understood, and there is, in my opinion,
2:40
supporting evidence that ischemia is the cause,
2:43
and there is only anecdotal evidence that plexus
2:45
compression has caused the pain of these patients.
2:48
Since 1972, there's a discussion started by Shilachi,
2:51
a famous American surgeon, who said there is
2:54
no real scientific ground. The benefit of treatment
2:56
of this disease is more than a placebo effect.
2:59
There is still a lot of arguments to underline
3:03
to support that statement. We decided in the
3:05
Netherlands to really give the answer, does MALS
3:08
exist, yes or no? And we started the Schlierk
3:10
-Arter Release or SHAM operation. Completely
3:12
blinded study, the patient does not know what
3:15
kind of operation was performed at all. Also,
3:18
the doctors who see the patients after the operation
3:20
does not know what is done. It is a superiority
3:23
study with an expected success rate for the celiac
3:25
artery release group of 70%. That's based on
3:28
two scoping reviews from Jimenez in 2012 and
3:32
more recently from Juliette Blau of Laura Metz,
3:34
which expected a success between the 69 % and
3:38
78%. And for the SAM operation, we expected a
3:41
success rate of 30 % that is based on five previous
3:45
RCTs, including... sham operation arm. At this
3:48
moment, 45 out of 70 patients are included and
3:51
we expected the final inclusion in Q4 this year,
3:56
at least in six months blinded follow -up that
3:59
we can report early 2028. So the Tsilatsi doctrine
4:02
will be settled somewhere in 2028. And then the
4:06
next discussion is what kind of operation you
4:09
perform. In my personal opinion, open release
4:12
is obsolete. It should not be done. The most
4:15
logical way is a keto -resistant left -sided
4:17
endoscopic approach. Then you cleavage the left
4:20
side of the ligament, and that's enough. The
4:22
operation is also done by gastrointestinal surgeons
4:24
in a laparoscopic way. They are very experienced
4:27
to do that. It's more difficult to have a complete
4:31
release of the cardiac artery by an anterior
4:34
laparoscopic approach than by a retipineal left
4:37
-sided approach. Maybe that's the next trial.
4:39
Thank you, Bob. We are eagerly waiting for the
4:42
results of the CAROSO study as well. I would
4:45
like to go back to the diagnosis and signs of
4:48
median arcuate ligament syndrome. The celiac
4:51
artery compression by the median arcuate ligament
4:55
is actually quite a common finding, and you cannot
4:59
have a syndrome unless you have symptoms. We
5:02
actually did a study of 500 patients that were
5:05
more than 65 years old who underwent CT scan
5:09
for acute abdominal pain in the emergency department.
5:13
And we saw that 10 % of patients had external
5:16
compressing of the celiac artery. Now, the symptoms
5:19
are characterized by postprandial abdominal pain
5:23
and food aversion, quite like in the... chronic
5:26
mesenteric ischemia. And if you have these symptoms
5:29
and the finding, then you may have or you may
5:32
not have median arcuate ligament syndrome. I
5:35
would also highlight that The typical median
5:37
arcuate ligament syndrome patient is between
5:40
20 to 40 years old. So if the patient is 70 years
5:44
old, look for other causes of abdominal pain.
5:47
It has been shown in a couple of recent studies
5:50
that two -thirds of patients undergoing median
5:53
arcuate ligament release will benefit from the
5:55
procedure, whereas one -third will not have long
5:59
-term resolution of symptoms. Most recent study
6:03
was from the Dutch group that was just accepted
6:05
to the European Journal. Another multicenter
6:08
study was published in Journal of Vascular Surgery
6:12
in 2023 and a Mayo Clinic study in Journal of
6:16
Vascular Surgery in 2021. This is what I think
6:20
the patients need to understand. Surgery for
6:23
median arcuate ligament syndrome is still experimental
6:26
and it is difficult or impossible to tell which
6:30
patients are going to benefit. I hope the upcoming
6:33
study will share some light into these issues.
6:36
Thank you. I think we are all eagerly waiting
6:38
for the results of the CAROSA studies in the
6:40
next two years. Recommendation 27, class 1, level
6:44
C, states that duplex ultrasound of the mesenteric
6:46
arteries during inspiration and expiration is
6:49
recommended as the first -line examination in
6:51
patients suspected of median arcuate ligament
6:53
syndrome. What are the typical duplex ultrasound
6:55
findings you would expect to see in a patient
6:57
with MALS? Increasing pyxoskeletal and endoskeletal
7:00
velocity during expiration reflects the dynamic
7:03
compression of celiac artery by the arcuate ligament
7:06
during expiration. And this is not abnormal.
7:10
You see in nearby every person during deep expiration
7:13
that the pyxostolic and endostolic velocity is
7:16
a little bit increasing. So it's more than normal.
7:19
That's also difficult for this discussion about
7:22
this syndrome. So you can see on the duplex what
7:24
happens with your celiac artery flow during expiration.
7:27
You can't see any symptom on the duplex. Symptoms
7:31
and anatomy are two separate things, and you
7:33
have to have them both before you can say these
7:36
patients maybe have median artery ligament syndrome.
7:39
for my own ultrasound examination. Sometimes
7:43
it happens that I'm not able to visualize and
7:47
to examine these vessels. In your opinion, how
7:50
many patients move from ultrasound to CTA to
7:54
better understand this disease? Before we started
7:57
the COSR study, we performed duplex in all patients
8:01
as first and only diagnostic tool. It was accurate
8:04
in 90 % of the patients. So in 9 out of 10, we
8:07
can visualize the esophageal artery properly,
8:10
good, without any doubt in an exploration. And
8:13
then it's a very sensitive, accurate technique.
8:17
So in one out of 10 patients, we can't see it.
8:19
And then the next step is CTA or MRA in inspiration
8:22
and expiration. The difficulty of MRA in expiration
8:25
is that they really need to expirate during a
8:28
third of 45 seconds. And that's not easy. So
8:31
I always ask the patients, if there is a discrepancy
8:34
between the MRA and the duplex, do you really
8:36
keep your expiration during the MRA? And they
8:39
all say, no, that was not possible. That's the
8:41
reason I prefer a duplex. It makes sense to do
8:43
a duplex ultrasound since median arcuate. Ligament
8:46
compression is a dynamic stenosis, so why would
8:49
you not do a dynamic examination? Recommendation
8:53
28, class 1, level C, states that multidisciplinary
8:56
management at specialized centers is recommended
8:59
for patients suspected of having median arcuate
9:01
ligament syndrome. In your opinion, which specialists
9:03
should be part of that multidisciplinary team,
9:06
and what roles do they each play in the diagnostic
9:08
and treatment pathway? I am a real believer of
9:12
this recommendation just because I do not work
9:15
in an ultra -specialized center for this disease.
9:20
I think that it is mandatory that into the multidisciplinary
9:24
team it is included at least one gastroenterologist
9:27
that conducts the initial evaluation and rules
9:31
out other common causes of gastroenterology symptoms.
9:36
Radiologists, sonographers, they are really important.
9:39
and to perform a very good ultrasound examination,
9:43
also second and third level imaging if needed.
9:46
Pain management specialist may be included in
9:50
the team just because there is some evidence
9:52
that sometimes celiac plexus block may play a
9:56
role in this disease. I think that the definitive
10:00
treatment team, it is composed by vascular and
10:04
or general surgeon. It depends on the skills
10:08
of the team. And finally, I think that a supportive
10:11
care team, it is needed. Psychologist, psychiatric.
10:16
Even these specialists are required to rule out
10:19
other diseases. And finally, a nutritional physician
10:24
might be helpful to increase the nutritional
10:28
aspect of the patients. In the diagnosis part,
10:31
I do not need a pain management specialist. The
10:35
metaphor to the leg. If you have critical lipid
10:37
ischemia and you have a local block, you don't
10:39
have any pain anymore. But I don't need that
10:41
block to diagnose critical lipid ischemia. You
10:44
don't need a psoriasis block to diagnose MALS.
10:46
There is no evidence in literature at all that
10:49
you increase the accuracy of the diagnostic workup.
10:53
At this moment, we are successful in 8 out of
10:55
10 patients, durable relief of symptoms after
10:58
psoriatic artery release, and the plexus block
11:00
does not increase that number. There is no evidence
11:03
at all for that. All these patients should be
11:05
discussed, sometimes more than once, and you
11:08
need consensus. I have a comment on the surgery
11:11
part of the treatment pathway. These procedures
11:14
are performed in many centers that will never
11:17
achieve such a high caseload as the Dutch CMA
11:21
referral center in NGAD. Learning techniques
11:24
such as the retroperitoneal endoscopic approach
11:28
or robotic median arcuate ligament release can
11:31
be challenging. The anterior laparoscopic approach
11:35
to the celiac artery may not be optimal due to
11:38
the angle of the instruments to the celiac artery,
11:41
but it is a familiar approach to upper gastrointestinal
11:46
and pancreatic surgeons. I think it is vital
11:48
to have a vascular surgeon in the team, especially
11:52
in case major vascular injury occurs. Thank you
11:56
for this great discussion on MALS. More information
11:58
on MALS and a detailed description of the video
12:00
-assisted retroperitoneal median arc with ligament
12:03
release could be found in the previous ESVS podcast
12:06
with Professor Geelkerk and Dr. Metz on this
12:08
platform, published in March 2023. I will be
12:11
sure to put a link in the show notes so you can
12:12
all listen to it as well. Now I would like to
12:15
switch to another subject, acute arterial mesenteric
12:18
ischemia, or AMI. AMI has a high mortality of
12:21
50 % and the diagnosis is based on one clinical
12:24
presentation. two, vascular stenosis or occlusion
12:27
on CTA, and three, signs of intestinal injury
12:29
on CTA. The diagnosis is ultimately confirmed
12:32
by resolution of symptoms after revascularization.
12:36
Arterial fibrillation is present in one -third
12:38
of AMI patients, so every patient with atrial
12:41
fibrillation and acute abdominal pain should
12:43
be suspected of having an acute SMA embolism.
12:46
The typical clinical triad for acute embolic
12:49
SMA occlusion is severe abdominal pain with minimal
12:52
findings on examination, so disproportionate
12:54
pain, bowel emptying, so vomiting, diarrhea,
12:57
and the presence of a source of embolism, most
12:59
often atrial fibrillation. Could you describe
13:02
the three phases of AMI caused by an embolism?
13:05
We have a very painful patient with a discrepancy
13:08
between the severe pain and an unremarkable abdominal
13:12
examination. Then the bowel gives up its resistance,
13:16
known as the silent period. Due to transmural
13:19
necrosis, signs of peritonitis develop, and because
13:22
of metabolic disturbances and bacterial translocation,
13:26
the patient's condition rapidly deteriorates.
13:29
The end of the villus is the end of the bowel,
13:32
which is the end of the patient. It should be
13:35
remembered that this classic triad is not uniform
13:38
to acute mesenteric ischemia and applies only
13:41
to patients with sudden occlusion of previously
13:44
patent superior mesenteric artery, such as acute
13:48
embolic occlusion. However, even in embolic occlusion,
13:51
symptoms vary based on the location of the occlusion.
13:55
When the occlusion is very proximal, the symptoms
13:58
are often most severe. However, the symptoms
14:01
can be more obscure in distal occlusions owing
14:04
to the collateral blood flow. So I think the
14:06
classic triad is actually quite rare in the spectrum
14:10
of acute mesenteric ischemia. The important thing
14:13
to remember is to always suspect embolic acute
14:16
mesenteric ischemia in patients with acute abdominal
14:19
pain and atrial fibrillation. You have to think
14:23
about the spectrum of acute abdomen in a patient
14:26
that is, let's say, 40 years old. It's completely
14:29
different than a patient who is 80 years old.
14:32
In a 40 -year -old, I would say that acute embolic
14:36
occlusion of the superior mesenteric artery is
14:39
a possibility, but it's very rare. So it's mostly
14:42
a disease of the elderly. The mean age of the
14:45
patients with occlusive acute mesenteric ischemia
14:48
in a non -selective cohort is 80 years. And the
14:53
issue with that is that, especially the youngest,
14:55
in the 35 -45 -year -old, they are not suffering
14:59
of really acute mesenteric ischemia, but they're
15:01
suffering of acute ongoing mesenteric ischemia.
15:04
If you really ask the patient, did you have postprandial
15:08
pain the last three months? What is your weight
15:11
for the last three months? Can you eat a normal
15:13
portion for the last three months? The answer
15:15
is never all the times. No, I can't. And that's
15:19
a sign that it's acute on chronic mastitis ischemia
15:21
in the youngest. I agree that acute embolism
15:24
is very rare for the years of age, but it's not
15:28
impossible. Nobody dies of an unnecessary acute
15:31
CTA in the middle of the night. If you miss an
15:34
acute mastitis ischemia in the middle of the
15:36
night, the patient's prognosis becomes very,
15:38
very poor. If you demonstrate in a very nice
15:41
Finnish study, an 80 % three -month mortality
15:44
of acute mastitis ischemia, that's very, very
15:47
high, much higher than cerebral infarction or
15:49
heart infarction of other well -known diseases.
15:52
Yes, 80 % mortality if not revascularized and
15:56
then... If you can do the revascularization,
15:59
you can reduce the mortality by half. It's still
16:03
40 -50%. And that's still much higher than if
16:06
you have an acute cardiac infarction with a successful
16:09
PCI. So still, we recognize these patients too
16:13
late. This is very true. So we briefly touched
16:16
upon the difference in acute embolic versus acute
16:19
thrombotic SMA occlusion, but what exactly is
16:22
the difference in presentation and what are the
16:24
major contributing factors to the acute thrombotic
16:27
SMA occlusion? We talked about acute symptoms
16:30
in embolic mesenteric ischemia, but the clinical
16:33
presentation of thrombotic acute mesenteric ischemia
16:36
is often obscure and the symptoms can develop
16:39
either suddenly or over several days depending
16:43
on the extent and the acuteness of the arterial
16:46
occlusion. A sudden onset of acute abdominal
16:49
pain may develop when a previously patent superior
16:53
mesenteric artery occludes suddenly due to acute
16:56
thrombosis of an underlying atherosclerotic lesion.
17:00
However, if the superior mesenteric artery was
17:03
already chronically severely obstructed with
17:06
sufficiently developed collaterals, an acute
17:09
thrombosis of the SMA may not essentially change
17:12
the blood flow to the mesenteric. Moreover, quite
17:14
often acute mesenteric ischemia develops upon
17:17
severely obstructed or chronically occluded mesenteric
17:21
arteries. typically involving both the superior
17:25
mesenteric artery and the celiac artery, without
17:27
any evidence of acute thrombosis in the CT scan.
17:31
This is the classic presentation of acute on
17:34
chronic mesenteric ischemia. The atherosclerotic
17:37
superior mesenteric artery obstruction in acute
17:40
mesenteric ischemia can be therefore either acute
17:43
or chronic, thrombotic or calcified. These are
17:46
all the manifestations of the atherosclerotic
17:49
vascular disease. As mentioned previously, prior
17:52
symptoms of chronic mesenteric ischemia are common
17:55
in the acute and chronic patients. Some patients
17:58
may have even undergone exploratory laparotomy
18:01
or, for example, for gastrointestinal issues
18:06
without relief of symptoms before the disease
18:09
fully escalates in acute mesenteric ischemia.
18:12
Also, there are often other factors besides the
18:15
obstruction of mesenteric arteries that may contribute
18:18
to the development of acute bowel ischemia. These
18:21
include anemia, dehydration, low cardiac output,
18:25
or basically any major previous surgery. Sometimes
18:28
mere fluid resuscitations, correction of anemia,
18:33
Administration of antibiotics may reverse the
18:36
acute intestinal ischemia. However, the patient
18:39
will remain at risk of recurrent acute on chronic
18:42
episode unless treated with revascularization.
18:45
I completely agree with your comment, but I also
18:48
have one important remark. In the metaphor to
18:51
cardiac ischemia, if I'm suffering of ongoing
18:55
cardiac aversion, you don't start with a thoracotomy
18:58
and resect the ischemic part. of my left centricle.
19:02
And thereafter, you are thinking, what can I
19:04
do with my coronary arteries? Nobody will survive
19:07
that. Why do we do it in another way in acute
19:10
mastitis ischemia? First, revascularize, and
19:14
thereafter, resect. And not in other way around.
19:17
If you have a patient with an acute abdomen,
19:20
these patients have the right on an appropriate
19:24
diagnostic imaging. That means CTA. arterial
19:28
venous phase with an experienced radiologist
19:31
or vascular surgeon or gastroenterologist who
19:33
assess this imaging appropriately you can diagnose
19:36
it on time. Diagnosing acute mesoteric ischemia
19:39
in the operation room is in my opinion a mistake.
19:43
Recommendation 31 class 3b level c states that
19:46
a single measurement of biomarkers such as lactate
19:49
or diademir to confirm or rule out the diagnosis
19:52
in patients with a clinical suspicion of acute
19:54
mesoteric ischemia is not recommended. This is
19:56
a notable change from the 2017 ESVS guidelines,
20:00
where Didemir was recommended to exclude AMI
20:03
due to its reported 100 % sensitivity and negative
20:07
predictive value. Could you explain the reasoning
20:09
behind this change and what new evidence influenced
20:12
the updated recommendation? Of course, this shift
20:15
was influenced by evidences, mainly systematic
20:19
reviews and meta -analyses. These studies have
20:21
examined the diagnostic accuracy of various biomarkers.
20:26
The overall conclusion from this new evidence
20:29
is that a reliable single biomarker or even a
20:33
combination of biomarkers that can thoroughly
20:36
solve the diagnostic dilemma and reduce the time
20:40
to diagnosis of AMI has yet to be found. This
20:44
is why we issued several recommendations regarding
20:47
diagnosis that suggest to use different tools,
20:51
both radiology, biomarkers and clinical examination.
20:57
Surely it would be nice to have a blood test
21:00
for screening acute mesenteric ischemia in such
21:03
a way that we use troponin T to screen for acute
21:06
myocardial infarction, but we do not screen D
21:09
-dimer in patients with acute abdominal pain.
21:12
This is because there is no data how D -dimer
21:16
behaves in especially early acute mesenteric
21:19
ischemia. For example, in patients with acute
21:22
and chronic type of presentation, and we do not
21:26
want clinicians to start ruling out acute mesenteric
21:30
ischemia based on D -dimer. I don't think that
21:32
D -dimer has been investigated extensively and
21:36
exclusively in patients with embolic acute mesenteric
21:40
ischemia or to rule out transmural bowel necrosis.
21:44
Maybe these are some ideas for future studies.
21:47
but i don't know you guys but i still struggle
21:52
to explain to some general surgeons colleagues
21:56
or some er colleagues that even lactate is not
22:02
a specific biomarker of AMI and also that we
22:07
have not to wait to rush the patient under the
22:12
CT machine to take scans because the patient
22:15
has negative lactate. So I think that the important
22:19
message here is that we have to think. about
22:23
AMI. And it doesn't matter if we have to fight
22:28
during the ER night shift and we are young. If
22:32
we have any suspect, we need to rush the patient
22:35
and take some scans. Systemic lactate is too
22:38
late. The capacity of the liver to clear your
22:41
lactate is very, very high. So if you have liver
22:44
failure or clearance of your lactate, entry the
22:47
liver by the portal V, then you have two possibilities.
22:50
Ischemic liver failure. end stage, or such an
22:54
enormous amount of lactate that it has the liver.
22:58
In both cases, you have end stage disease. And
23:02
it means it's not the end of the villus, it's
23:04
the end of the bowel, and the end of the bowel
23:06
is the end of the patient. Thank you for this
23:09
clarification. Recommendation 33, class 1, level
23:13
B, states that urgent CT with contrast enhanced
23:16
in arterial and venous faces with 1 mm or less
23:19
slices is recommended in patients suspected of
23:21
acute mesenteric ischemia, regardless of renal
23:24
function. Could you walk us through the typical
23:25
CTA findings in AMI and comment on the diagnostic
23:29
accuracy of CTA in this setting? When we started
23:33
doing research on mesenteric ischemia, that was
23:36
more than 15 years ago. We actually began by
23:40
teaching our emergency department radiologists
23:43
how to suspect acute mesenteric ischemia in the
23:47
CT scan for acute abdomen. This quite soon led
23:51
to increasing number of early diagnosis and revascularizations,
23:55
mostly endovascular. First, you take a look at
23:59
the vascular findings in the CT scan. The patency
24:02
of the mesenteric vessels should be reported.
24:06
consistently in all patients and not sporadically.
24:10
Then, especially when the mesenteric vessels
24:13
are diseased, you need to look very carefully
24:16
at the intestinal findings. The intestinal findings
24:20
in mesenteric ischemia can be what I like to
24:23
call definitive or unspecific. The definitive
24:26
findings often seen in advanced bowel ischemia
24:31
are lack of bowel wall enhancement or pneumatosis.
24:36
both of which are not definitive signs of transmural
24:40
bowel necrosis, by the way. However, in early
24:43
ischemia, for example, acute and chronic situation,
24:47
the intestinal findings can be very subtle and
24:50
unspecific and easily overlooked. You need to
24:53
be careful. This can be, for example, bowel wall
24:57
thickening, bowel lumen dilatation as a sign
25:00
of bowel paralysis. mesenteric edema or peritoneal
25:05
fluid. Then you need to rule out other causes
25:08
of acute abdominal pain such as pancreatitis,
25:11
strangulation, etc. When the vascular findings,
25:15
intestinal findings, and an appropriate clinical
25:19
presentation overlap, you have acute mesenteric
25:23
ischemia. We have tried to illustrate this in
25:26
figure number three in the guidelines. The rheologist
25:30
has a very difficult task, but at the end, we
25:34
all know the answers. If you look back, you can
25:36
see near all the signs on the CT scan. But what
25:40
is very liable is the assessment of the three
25:44
mysteic arteries, celiac superior mysteic artery
25:47
and inferior mysteic artery. Is it occluded?
25:49
Yes or no? Is it stenosis? Yes or no? Is it atherosclerotic?
25:52
Yes or no? That is very liable with a positive
25:56
and negative predictive value nearby 100%. But
26:00
the other signs, like wall sickening of the bowel,
26:03
dilatation of the bowel, mesoteric strengthening,
26:05
arthritis, pneumatosis, are very subjective and
26:08
not very reliable. If you have a wall thinning,
26:11
then the odds ratio of transmural necrosis is
26:14
13, very high, but not proven. I agree with what
26:17
you said. First, start with the description of
26:20
your three main vessels. Are they open? Yes or
26:23
no. If they are stenosed, what is the reason
26:26
of the stenosis? Also important for your treatment.
26:29
And never rely on the subjective parameters.
26:33
They're only guiding you a little bit. Don't
26:35
rely on them. It may be worth to mention that
26:38
recommendation 32 highlights the importance of
26:41
the clinician to mention the suspicion of acute
26:43
mesenteric ischemia when you refer the patient
26:46
for a CT. There was evidence to suggest that
26:48
that improves the diagnostic accuracy of the
26:51
radiologist. After the diagnosis of AMI, it's
26:54
now time for the treatment. The new recommendation
26:57
34, class 1, level C, states that it is recommended
27:00
to treat patients with acute mesenteric ischemia
27:03
in centers with 24 -7 multidisciplinary service.
27:06
and experience with both open and endovascular
27:08
mesenteric artery revascularization. Recommendation
27:11
35 plus 2A level C states that revascularization
27:14
first before bowel resection should be considered
27:17
in patients with acute mensteric ischemia. This
27:19
is also summarized in figure 4 of the guideline.
27:22
In your centers, what is the typical workflow
27:24
after AMI is diagnosed, from immediate revascularization
27:27
to assessment of bowel viability and postoperative
27:30
care in the ICU? How do you coordinate these
27:32
steps to optimize outcomes? In my hospital, we
27:35
are the Dutch Juveuro Center for Acute Mensteric
27:37
Ischemia. All patients suspected of having hematopoietic
27:40
ischemia, receive an urgent contrast enhancement
27:43
in both the arterial and venous phase. And if
27:46
misdiagnostic occlusive disease is confirmed,
27:48
patients are immediately transferred to the end
27:50
-choice suite, where pec -genus misdiagnostic
27:52
stenting is attempted. And it is successful also
27:55
in completely occluded SMAs above the 90 % of
27:59
the patients if you have the right equipment
28:01
and experience. And at the same time, so not
28:04
afterwards, but at the same time, The patients
28:07
are resuscitated by the endosodialist or the
28:09
intensivist in this anterior suite. If the pectin
28:12
is unsuccessful, then the patient is transferred
28:15
to the hybrid operation room, where we can perform
28:18
retrograde open minsterextenting. A laparotomy
28:20
is not performed immediately, because when you
28:24
open the abdomen, it's very difficult to distinguish
28:27
reversible and irreversible sphere. ischemic
28:31
bowel. Maybe I can talk about my experience in
28:34
my previous hospital in Kuopio University, which
28:37
is in Eastern Finland. And now I have been working
28:40
a year and a half in Turku, which is in Southwest
28:42
Finland. That's completely different. But in
28:45
Kuopio, we documented results for treating acute
28:49
mesenteric ischemia for the past 15 years. During
28:52
that time, we did some 50 endovascular revascularization
28:56
for embolic acute mesenteric ischemia and 130.
29:01
endovascular revascularizations for thrombotic
29:03
acute mesenteric ischemia. So we were very much
29:06
endovascular first. And we had a 24 -7 on -call
29:10
interventional radiologist service. And they
29:13
did majority of the cases in an NGO suite, actually,
29:17
rather than hybrid OR, with, I must say, very
29:20
good technical success rate in percutaneous and
29:24
a great approach. We did not routinely assess
29:27
bowel viability, only on demand. If the suspicion
29:30
of bowel necrosis was high or the symptoms did
29:34
not subside soon after revascularization. So
29:37
actually, less than 50 % underwent laparotomy.
29:40
About one -third required bowel resection. Overall,
29:44
I think the treatment workflow may be adjusted.
29:48
according to local resources and expertise, but
29:51
you should have a planned treatment algorithm.
29:54
It is quite interesting that we have an algorithm
29:56
for ruptured aneurysms, but not so much for acute
30:00
mesenteric ischemia. The incidence rates of these
30:03
acute II emergencies are actually the same, at
30:06
least in Finland. So I might ask you, do you
30:09
have like a written algorithm on how to treat
30:12
patients with acute mesenteric ischemia? I am
30:15
working on it, but it is a massive administrative
30:18
issue. But I hope in one, two years to have it
30:22
written and to start at the same time a research
30:25
project on it. And hopefully in the next years
30:28
to spread the protocol to the entire region.
30:32
We have the algorithm, the workflow as I described
30:34
in our hospital. discussed and accepted by all
30:38
relevant specialties in the hospital. So the
30:40
emergency department, the IC unit, anesthesiologist,
30:44
radiology, vascular surgeon, GE surgeon, they
30:46
all work in line with the same algorithm. That's
30:50
for every disease, very important. New in the
30:52
guideline is recommendation 39, class 2B, level
30:55
C, quantitative endocyanine green, fluorescent
30:58
imaging, ICGFI, may be considered as an aid in
31:01
the assessment of bowel viability in patients
31:03
undergoing laparotomy or laparoscopy. acute mesoteric
31:06
ischemia, how can ICG -FI assist the surgeon
31:09
intraoperatively and what added value does it
31:11
provide over traditional visual assessment of
31:13
the bowel? It works quite simply. We inject the
31:16
fluorescence dye in the endosynion green into
31:18
the bloodstream intravenously and then visualize
31:21
its flow using a specialized near infrared camera
31:24
system. Specialized software can even perform
31:27
a quantitative assessment by analyzing the fluorescence
31:30
intensity over time to create time intensity
31:33
curve. And from this curve, you can derive many
31:36
parameters, like time to peak. And the great
31:38
value of this method is it is objective and highly
31:41
accurate for detecting microcirculatory perfusion.
31:44
This allows for precise demarcation, this minimizes
31:47
the length of the bowel resection, and crucially,
31:49
also reduces in microcirculation nowadays the
31:52
need for costly and risky second -look operations.
31:55
It really works, and it's not very difficult.
31:57
Thank you for your explanation. It's well known
32:00
that patients with acute mesoteric ischemia sometimes
32:02
require extensive bowel resection. Is there any
32:05
evidence or guideline guidance on how much small
32:07
intestine and colon should ideally be preserved
32:10
to minimize the risk of short bowel syndrome?
32:12
And after extensive resections, how do you typically
32:14
approach nutritional support and feeding in these
32:17
patients? There is no literature. There's only,
32:20
I think, personal experience. We have patients
32:22
with less than 70 centimeter small bowel in situ
32:26
and only the descending colon. We understand
32:29
most of this and after a year or more than a
32:31
year thereafter, they have all... only oral diet,
32:34
so no peritoneal nutrition anymore. It takes
32:37
time and it's unpredictable, in my opinion. A
32:40
bowel of less than one meter is not a reason
32:43
to stop treatment of these patients. But Mark,
32:46
your hospital is the Dutch expert center on sure
32:49
bowel disease. Yeah, there is a team on intestinal
32:52
failure, but I have to admit I'm not part of
32:54
that team. I'm not sure what the minimum required
32:56
length of bowel is to survive. It's about a meter.
32:59
It might be less because there's anecdotal reports
33:02
of patients who survive with just 30 centimeters
33:05
of small bowel. But I'm not the expert in this.
33:07
With regard to feeding, that might be interesting.
33:09
We had a scheme that was adopted from your institution
33:13
that we wanted to add in the guidelines. how
33:15
to refeed patients after colon resection, after
33:18
revascularization. But the reviewers didn't want
33:21
us to put it into the guidelines. So there's
33:22
no one -size -fits -all protocol to treat these
33:25
patients and also parental or enteral nutrition.
33:28
So that's as much as I know, which is very little
33:31
actually. And we're good to say here that there
33:33
is consensus. Don't start parental nutrition
33:36
before revascularization. In acute mystic ischemia,
33:39
that's clear. And thereafter, it's trial and
33:42
error. In some patients, function came back.
33:44
four or five or six days and in some patients
33:46
it takes six months. Take your time. I guess
33:49
the length of viable bowel in order to survive
33:53
depends on a number of things. The patients are
33:56
often old and fragile, and the classic 70 to
33:59
100 centimeters may not apply unless you have
34:03
the entire colon and the terminal ileum. I as
34:06
well do not have any data to offer, but these
34:08
things need to be considered individually. One
34:11
thing I try to remind from time to time to our
34:14
GI surgery colleagues is that when bowel resection
34:18
is required in mesenteric ischemia, the principles
34:21
of cancer surgery do not apply. meaning that
34:25
there is no need to cut out the mesentery. On
34:27
the contrary, the mesentery with all the important
34:30
marginal collaterals should be spared and the
34:33
resection line should be kept close to the bowel.
34:37
Now let's move to the final topic of today's
34:39
episode, non -occlusive mesenteric ischemia or
34:42
NOMI. Could you start by explaining how NOMI
34:44
is defined and diagnosed? NOMI is... characterized
34:48
by vasospasm of the gut circulation, usually
34:53
caused by systemic conditions like shock rather
34:57
than a clot. This means, basically, in my personal
35:01
experience, the picture of the Nomi patient,
35:04
it is a very sick patient with several comorbidities.
35:08
Most often they are hospitalized, probably in
35:13
ICU, suffering from a cardiac shock or other
35:17
severe diseases? We had a discussion with the
35:21
reviewers because the classical definition uses
35:23
angiography to establish a diagnosis. And we
35:27
decided to do away with that because currently
35:29
no one takes the patient to the angiosuite or
35:32
the hybrid OR to do an angiography to confirm
35:34
the diagnosis. So we had some discussions as
35:37
to how to establish a diagnosis, but I think
35:40
you mentioned it completely. You will need some
35:42
kind of imaging. Currently, this will be CT scanning
35:45
to make sure that there's vasoconstriction. because
35:47
of severe infection or another condition that
35:50
causes the patient to be in shock. I agree. Even
35:52
in my experience, moving a little bit away from
35:55
the recommendations, we usually don't perform
35:58
DSA. on these very sick patients, and usually
36:02
what we see on the CTAs, it is most of the time
36:07
enough. However, we do have a recommendation
36:10
stating that can be considered to use vasodilators,
36:16
prostaglandins, and of course, we have to consider
36:20
heparinizations in these patients. But I do really
36:25
think that most of the time, CTA, it is enough.
36:29
for the diagnosis and if really needed probably
36:32
it is much more important the surgical laparotomy
36:37
to decompress the abdomen and if needed to reset
36:42
necrotic tissue. Yeah, and you have to be aware
36:44
that risk of dying because of this NOMI is very
36:47
high. In -hospital mortality is about 70 -75
36:50
% patients in this condition. Yeah, and the reason
36:53
is that the acute mystic ischemia, the non -occlusive
36:56
acute mystic ischemia, reflects an underlying
36:59
severe disease. So it's a combination of both.
37:02
So it does not make sense only to treat the non
37:05
-occlusive mystic ischemia. You have to repair,
37:08
you have to resolve the underlying disease in
37:10
combination with supporting. the bowels circulation.
37:14
The last question on this topic we already discussed
37:17
a little bit. The guidelines provide several
37:20
specific recommendations on NOMI. Recommendation
37:22
43, class 2A, level C, states that NOMI should
37:25
be suspected in patients in shock if the CTA
37:28
shows signs of lack of bowel enhancement, small
37:31
bowel thickening, intestinal pneumatosis, in
37:33
the absence of a significant stenosis of the
37:35
superior mesenteric artery. And recommendation
37:37
44, class 1, level C, states that urgent decompression
37:40
laparotomy is recommended for patients with suspected
37:43
NOMI and... concurrent abdominal compartment
37:45
syndrome. Finally, recommendation 45, class 2B,
37:48
level C, states that intra -arterial administration
37:51
of vasodilators such as papavarin or prostaglandin
37:55
in the SMA under protective heparinization may
37:57
be considered for patients with NOMI. What are
37:59
the typical and geographic signs of NOMI on DSA
38:02
and are there any additional strategies or recommendations
38:05
you would consider for managing these patients?
38:07
As we said before, the classic signs on DSA,
38:12
signs of mesenteric vasospasm. This is a diffuse
38:16
narrowing and irregularity of the peripheral
38:20
mesenteric branches. You can see narrowing of
38:24
the SMA main trunk or impaired or poor feeling
38:29
from the organs and delayed venous return. reflux
38:35
into the aorta but as i said before I think that
38:39
it is important to prevent shock, to treat shock
38:44
or the underlying causes, and to improve the
38:49
overall hemodynamic of the patient. And also,
38:53
it is relevant to administer broad -spectrum
38:56
antibiotics and protective heparinization. We
39:01
do not have a huge experience with vasodilator
39:04
in these patients. I think if you have a young
39:07
patient, then you are kind of allowed to try
39:10
anything to save the patient. There is some evidence
39:13
that intra -arterial infusion of vasodilator
39:17
agents such as papaverin or iloprost could be
39:20
helpful, but the data is very limited. I think
39:23
primarily the treatment of NOMI should be targeted
39:27
to treat the underlying condition and trying
39:30
to optimize intestinal blood flow by conservative
39:33
means in the ICU. And laparotomy is done only
39:36
when irreversible bowel necrosis is suspected.
39:40
The signs of this could be, for example, increasing
39:43
lactate and metabolic acidosis in arterial blood
39:46
gas analysis, increasing need of vasoactive agents,
39:50
dilated colon with a paper with thin bowel wall.
39:53
An exploratory laparotomy only to see that the
39:57
bowel is still viable in a patient with NOMI
40:00
does not help but may worsen the overall condition.
40:03
Of course, this does not apply to CASE with abdominal
40:06
compartment syndrome. That wraps up our second
40:08
Q &A on the 2025 ESVS Clinical Practice Guidelines
40:12
for the Management of Diseases of the Mesenteric
40:14
and Renal Arteries and Veins. Today, we focused
40:17
on acute mes... Steric Ischemia, Mals and Nomi,
40:20
but there's much more left in the guidelines
40:21
that we will cover in part three next week. Thank
40:24
you to our guests for sharing their expertise
40:26
and thank you to our listeners for tuning in.
40:29
Be sure to join us next week for part three of
40:31
this series. Until then, take care and goodbye.
40:35
Bye -bye. Bye.