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Is there a predilection for emboli to occlude the SMA?
Yes, there is a predilection for emboli to occlude the SMA, which relates to the
anatomy of the SMA [2, 3].Many, if not most of these cases of AMI, are embolic in
etiology. The SMA, being a large caliber vessel, allows emboli to more easily pass
into it. Also, compared to the 90-degree takeoff of the celiac artery, the takeoff of the
SMA is a less acute angle. Emboli, therefore, generally bypass the celiac artery
takeoff and pass into the SMA much more readily. So, for those reasons there is a
predilection for emboli to occlude the SMA.
How long do you have in AMI before you need to intervene?
Several studies indicate that if there’s 100% occlusion of the SMA, you have
approximately 6h before bowel infarction will occur. If you have a 75% occlusion,
you have about 12h before you would need to intervene before infarction occurs
[3]. While this may seem like time is on your side when attempting to make a diag-
nosis of AMI, it’s not and any delays increase mortality and can complicate surgery.
Bottom line: “AMI is a medical emergency.”
How would you manage this?
Any patient that has acute mesenteric ischemia, whether it’s embolic or throm-
botic, should receive systemic heparinization [1]. Therefore, the initial approach,
when there is a concern for AMI, should be to immediately start full anticoagulation
with IV heparin. They should be NPO and placed on broad-spectrum antibiotics to
cover bacteremia secondary to bacterial translocation and the potential for sepsis.
Denitive treatment is ultimately going to require revascularization, either radio-
logic or surgical.
When do you decide to use surgery as opposed to interventional radiology?
Decisions regarding revascularization require consultation with both vascular
surgery along with interventional radiology [4]. If a patient is showing signs of
peritonitis or advanced ischemic changes/infarction such as worsening abdominal
pain, fever, or leukocytosis, surgical intervention is indicated. Otherwise, radiologic
intervention, specically embolectomy or angioplasty/stenting, is the preferred ini-
tial approach.
Do you know how useful the nding of thumbprinting on KUB is? Is it sensi-
tive, specic?
It’s not very sensitive and you don’t see it very often, but when you do it usually
indicates severe ischemia or infarction. Therefore, plain X-rays of the abdomen are
generally not very helpful in the diagnosis or management of AMI.
The patient has a mesenteric angiogram and thrombectomy but afterward devel-
ops hypotension with a BP 90/60.
Is there any role for pressors in a hypotensive patient with mesenteric
ischemia?
Yes, but with care. If you do decide that a patient needs pressor support, you
should, in general, avoid alpha-adrenergic pressors, such as vasopressin, as they can
cause vasoconstriction of the splanchnic arteries and worsen the ischemia. While
low-dose vasopressin might be safe to use, more often dobutamine or dopamine are
used since they don’t cause vasoconstriction of the splanchnic arteries [2].
A follow-up X-ray shows jejunal distension with wall thickening, pneumatosis,
and air in the portal vein.
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How would you manage this?
These are worrisome signs of bowel infarction. The patient needs surgical inter-
vention for possible resection of the infarcted bowel. A second look operation is
many times done during the same hospitalization to evaluate and remove any
remaining, non-viable bowel. Short bowel syndrome is an unfortunate outcome of
large resections.
The patient goes to surgery and a section of necrotic small bowel of 100cm is
removed distal jejunum and proximal ileum.
Is this the most common etiology for short bowel syndrome?
Yes, the main cause of short bowel syndrome is surgical resection for ischemia.
Crohn’s disease is the second most common cause. Recurrent chronic obstruction
from adhesive disease from prior surgeries is another etiology.
Following resection, the patient has a slow but consistent recovery.
Case 2: Mesenteric Vein Thrombosis (MVT) A 73-year-old man with a history of
metastatic renal cell carcinoma presents to the ER with a history of acute onset of
mid-abdominal pain. There is moderate abdominal tenderness and decreased bowel
sounds. Laboratories reveal leukocytosis and mild metabolic acidosis. A CT scan
reveals thrombosis of the SMV and portal vein with edema and dilation of small
bowel loops. The impression is that this patient has acute mesenteric vein thrombo-
sis. A surgical consult is called, but the decision is made to treat with
anticoagulation.
Should you do a thrombophilia work-up in all of these patients?
Statistically, the majority of patients who develop mesenteric venous thrombosis
have a primary hypercoagulable disorder as the cause. A smaller percentage have a
malignancy causing a secondary hypercoagulable state. So, in this case, although he
has a malignancy, it’s not unreasonable to do a limited hypercoagulable work-up.
The patient is found to have factor V Leyden deciency.
Is it sufcient to treat with anticoagulation? Is surgery ever indicated? If
so, when?
Anticoagulation is the primary therapy [1]. If they don’t improve or if the patient
progresses to peritonitis and presumed infarction, surgery would be necessary.
Is there usually a different clinical presentation in acute SMV thrombosis vs
acute SMA thrombosis?
SMV thrombosis is more common in males, while SMA thrombosis is more
common in females. Many patients with SMV thrombosis have a history compati-
ble with or have a diagnosis of chronic mesenteric ischemia. They often have a his-
tory of postprandial abdominal pain and weight loss.
In comparison with SMA thrombosis which presents acutely, patients with SMV
thrombosis have a more insidious course with chronic or subacute symptoms. SMA
thrombosis tends to present with more acute, severe pain, while SMV thrombosis
typically presents with a dull pain that develops over days to weeks.
Which veins tend to be involved in acute MVT? How does this lead to organ
damage, does gangrene occur?
Most of the time it’s the SMV, which leads to damage of the distal small bowel
[2]. Rarely is it the IMV.The pathophysiology is like any form of venous outow
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obstruction. The bowel wall gets edematous causing increased intramural pressure
resulting in a reduction in arterial ow through the bowel wall. If the reduction in
submucosal arterial blood ow is severe, bowel infarction can occur.
How successful is anticoagulation?
Very successful. Anticoagulation almost eliminates in-hospital mortality in these
patients. Overall mortality is less than 5% in patients who have been treated quickly
and adequately anticoagulated. Most of these patients will need to remain on long-
term anticoagulation since their thrombotic risk continues indenitely.
Case 3: Chronic Mesenteric Ischemia A 75-year-old man presents with a 1-month
history of abdominal pain and weight loss. The pain is periumbilical and tends to
occur about a half hour after meals. The patient also experiences mild nausea after
meals. To prevent nausea and abdominal pain, he has been avoiding eating and lost
15lbs. over the past month. The abdominal examination is benign without a bruit.
The CBC, chem panel, and liver enzymes are all normal. EGD is negative. US abdo-
men is normal. CT abdomen and pelvis reveal a normal-appearing pancreas, but
there is extensive atherosclerosis of the mesenteric vessels. There is no suggestion
of acute ischemia. Bowel loops appear normal. Because of these ndings in the set-
ting of abdominal pain and weight loss, the diagnosis of possible CMI is raised.
Is there any way to make a clear-cut positive diagnosis of CMI or do you
have to exclude other causes rst and then chronic ischemia becomes a diagno-
sis of exclusion if the CTA or angio are consistent?
In most cases, it’s hard to come to a denite diagnosis of CMI.Only a small
percentage of patients have the classic clinical trial of abdominal pain, weight loss,
and abdominal bruit. In general, you rst want to rule out other potential causes of
postprandial pain, like biliary tract disease, that can mimic the same clinical presen-
tation as CMI.Once other causes of postprandial abdominal pain and weight loss
have been excluded, and a CTA shows signicant stenosis in at least 2 of the 3
mesenteric arteries, then there is a high likelihood of CMI.
What percentage of patients in this age range will have vascular abnormali-
ties simulating CMI, and yet be asymptomatic?
About 60% of older patients have radiologic ndings of mesenteric vascular dis-
ease in one or two vessels but are asymptomatic. Another 15–20% will have athero-
sclerotic disease in all three vessels and are asymptomatic.
What is the role, if any, of duplex Doppler?
I think a lot of people would gravitate to this test rst to screen for CMI but a
CTA should be done to conrm the diagnosis. Duplex Doppler is more of a physi-
ologic test that is highly sensitive and specic at detecting abnormally high mesen-
teric arterial velocities suggesting CMI [1].A peak systolic velocity>275cm/sec
in the SMA suggests signicant stenosis [2].
If you’ve convinced yourself this is CMI, how do you manage it?
The rst approach usually involves radiologic revascularization, specically
angioplasty and stenting.
The patient is evaluated by IR and surgery, and the decision is made to perform
endovascular revascularization. Following this, the patient’s pain resolves and he
gains back the weight lost over the next 2months.
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Case 4: Nonocclusive Mesenteric Ischemia (NOMI) A 72-year-old man with a
history of CHF and the recent diagnosis of chronic cholecystitis is scheduled to
have an elective cholecystectomy. When presenting to the pre-op area of the hospi-
tal, he was noted to be hypotensive BP-90/50. IV uids were started, but the patient
started complaining of increased pain across his abdomen, different from his usual
gallbladder pain. An urgent CT was performed, which revealed small bowel edema
with probable pneumatosis. There were scattered plaques in the abdominal aorta
and mesenteric vasculature but no occlusive disease. There was also a spasm of the
arterial cascade emanating from the SMA.Because there was concern for bowel
ischemia, urgent laparoscopy was performed. A section of dusky appearing distal
jejunum was identied and resected. Adequate pulsations to the rest of the bowel
were ascertained. There was no evidence of thrombosis or embolism to any blood
vessels. The post-op impression was nonocclusive mesenteric ischemia.
What are the risk factors for NOMI? Which patients are most at risk?
This patient was hypotensive on presentation possibly due to evolving sepsis
from cholecystitis. Most often these are critically ill patients in ICUs who have
some form of hemodynamic instability [3], whether it’s septic shock, hemorrhagic
shock, or cardiogenic shock [2, 4]. Be alert to a critically ill ICU patient with hypo-
tension who develops abdominal pain, distension, or signs of a GI bleed as NOMI
would be a concern.
Was surgery mandatory? Can you make a case for pre-op vasodilators?
Yes, especially with the nding of possible pneumatosis on CT.Other ndings
concerning severe bowel ischemia are fever, leukocytosis, and an elevated lactate
level. If NOMI is suspected, vasodilator treatment should be promptly initiated [4].
Vasodilators, like PGE1 or papaverine, infused directly into the SMA or IV are
options. Equally important and what is still primary therapy is treating the underly-
ing cause of the hemodynamic instability.
Could the diagnosis be ascertained by CTA alone with condence?
Yes, the classic nding is the irregularity of the vascular arcade suggesting spasm
[3]. There may also be hypo-enhancement of the intestinal wall. Many of these
patients also have some degree of atherosclerotic narrowing of their SMA without
occlusion. The degree of narrowing, however, is generally not sufcient to explain
the severity of ischemia and symptoms.
Case 5: Colon Ischemia (CI) A 65-year-old man presents to the ER with a history
of rectal bleeding. He has no past history of cardiovascular disease, hypertension,
etc. He does have occasional constipation. His last screening colonoscopy 2years
earlier was negative except for mild diverticulosis.
He is on no meds. He was ne until that afternoon when he felt a sudden weak-
ness, sweating, and nausea causing him to sit down and compose himself. Shortly
after the episode, he developed abdominal cramping, following which he had two or
three bowel movements that were loose and mixed with blood. In the ER, he was
normotensive, his HR was 90 and regular, and he was afebrile. On the abdominal
examination, there was minimal abdominal tenderness and no rebound, and bowel
sounds were normal without a bruit. His laboratories showed a Hgb of 12 and a
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WBC of 13,000. There was no metabolic acidosis, but a CRP was 30. A CT scan was
obtained and showed colitis involving the splenic exure. CI is suspected. Overall,
the patient appears quite stable.
How would you manage this patient, other than starting IV uids? Would
you start antibiotics? Would you do a colonoscopy?
In general, you don’t need to start antibiotics if the patient appears stable and
doesn’t have any worrisome clinical ndings, such as a high white count, fever,
signicant abdominal tenderness, or more evidence of signicant damage on
CT. Current ACG guidelines indicate you should consider starting antibiotics in
patients with moderate or severe disease, which is based primarily on colonoscopy
ndings. Findings of severe CI include deep ulcerations and cyanosis of the mucosa.
If these abnormalities are found on colonoscopy, then antibiotics should be started.
The vast majority of these patients have mild disease and do well with supportive
care alone. As to whether you perform a colonoscopy on a patient that has sugges-
tive ndings such as segmental colitis in the watershed regions on CT depends on
whether there are concerns for other causes of segmental colitis such as Crohn’s
disease. A colonoscopy can be helpful in differentiating between CI and other
causes. A nding that is pathognomonic for CI [5] is longitudinal ulcerations, the
so- called stripe sign, which extend down the long axis of the colon. It’s generally
safe to do a colonoscopy as long as you don’t advance the scope past the area
of injury.
Colonoscopy is performed to the splenic exure where there is a region of typical
ischemic colitis noted with longitudinal ulcers, dusky mucosa, and bluish blebs.
Because these ndings are consistent with severe CI, the patient was started on IV
antibiotics.
CI seems to occur in a number of patients who have no risk factors.
Comments?
Because most cases of CI occur in the 60–80-year age group, they often have
undiagnosed atherosclerotic mesenteric vascular disease, especially if they have
other risk factors such as a history of hypercholesterolemia, hypertension, coronary
artery disease, or peripheral vascular disease.
Another risk factor is constipation which the patient reported. Yes, based on sev-
eral studies, constipation is a risk factor for ischemic colitis [5, 6]. The reason that
constipation is a risk factor, along with other causes of bowel distension such as
colonoscopy [7] or prepping for a colonoscopy, is that distension can lead to com-
pression of submucosal vessels resulting in ischemia.
There are some medicines that have been associated with precipitating ischemic
colitis [5, 2] including nasal decongestants, methamphetamines, digoxin, cocaine,
Tamiu, rizatriptan, diuretics, alosetron, estrogens, and clozapine.
Some patients have microvascular thrombotic disease or a previously undiag-
nosed hypercoagulable state, but still most patients with CI have small or large ves-
sel atherosclerotic vascular disease.
The patient’s clinical course is unremarkable and he goes home after a few days’
hospitalization.
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107
The outcome in most of these CI cases is almost uniformly excellent in my
experience. Has that been your experience as well?
Yes, usually it takes longer for patients with more severe damage to improve,
often several days, as in the example case, but the majority who have mild disease
improve in 2–3days.
Do you do any follow-up colonoscopy?
No, not routinely. If there is a concern, for instance, for a neoplasm based on a
history of constipation or IBD, then a follow-up colonoscopy would be appropriate.
It seems to me that a number of these patients present with nausea or weak-
ness prior to developing abdominal pain, diarrhea, or rectal bleeding, just like
this patient. Any comments?
It may be due to a vagal response to some degree of pain or they’re simply not
eating or drinking enough uids due to a mild ileus that potentially may develop
preceding the ischemic event.
Case 6: Median Arcuate Ligament Syndrome (MALS) A 53-year-old woman with
a history of epigastric pain and postprandial nausea and early satiety presents with
20lb. weight loss. There is no history of smoking or cardiovascular risk factors. She
is placed on a PPI without relief. She has an EGD that is normal and a gastric
emptying scan that reveals mild delay. A gastroparesis diet does not help much. A
CT scan is negative except for mild small bowel dilation that is no longer present on
CTE.She visits the ED after an episode of more severe pain where she is found to
have mild abdominal tenderness, an abdominal bruit, slightly elevated lipase and
lactate. A CT scan is ordered and suggests MALS.
Is MALS a real entity? Do some of these patients have functional symptoms,
and do they really require surgery?
The European Society of Vascular Surgery guidelines consider this to be one of
the most common causes of mesenteric ischemia that is not associated with athero-
sclerosis or thrombosis. In other words, they consider it a real entity.
One of my patients who had surgery for MALS did well for about a year, but then
started having recurrent abdominal pain likely due to untreated depression. I realize
now that part of her disease process was probably untreated depression. There are
studies showing that patients who have untreated psychiatric problems frequently
have poorer outcomes after surgical treatment of MALS [8].While this was a mixed
result for my patient, MALS surgery should still be considered after a thorough
evaluation ruling out other causes and rst treating associated conditions such as
depression.
How does duplex Doppler US help you?
A duplex Doppler US has good sensitivity (80%) and even better specicity
(95%) when used to screen for MALS.There are specic velocity patterns that are
seen in MALS including a change in pulse velocity with respiration. A dynamic
MRA or preoperative angiography is also sometimes done to see if there is com-
pression of the celiac artery during the respiratory cycle.
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Why are you interested in a dynamic MRA? Why is there a change during
the respiratory cycle?
A hallmark of MALS is expiratory compression of the celiac artery by the liga-
ment of the diaphragm crux with an increase in ow velocity that can be found on
Doppler US.Most of the time it is related to an anatomic variation in the location of
takeoff of the celiac artery that is higher than normal.
How would you manage this patient?
I would refer the patient to a vascular surgeon who has experience treating
patients with MALS.
Pre-op angiogram shows narrowing of the celiac with expiration. Surgery is per-
formed, releasing the ligament and decreasing vascular resistance. The patient
remains asymptomatic 1year after surgery.
References
1. Clair DC, Beach JM.Mesenteric Ischemia. N Engl J Med. 2016;374:959–68.
2. Ahmed M.Ischemic bowel disease in 2021. World J Gastroenterol. 2021;27(29):4746–62.
3. Gnanapandthan K, Feuerstadt P.Review article: mesenteric ischemia. Curr Gastroenterol Rep.
2020;22:17.
4. Blaser AR, et al. A clinical approach to acute mesenteric ischemia. Curr Opin Crit Care.
2021;27:183–92.
5. YuShuang X, etal. Diagnostic methods and drug therapies in patients with ischemic colitis. Int
J Color Dis. 2020;36:47–56.
6. Fitzgerald JF, Hernandez LO III.Ischemic colitis. Clin Colon Rectal Surg. 2015;28:93–8.
7. Sadalla S, et al. Colonoscopy-related colonic ischemia. World J Gastroenterol.
2021;27(42):7299–310.
8. Goodall R, etal. Median arcuate ligament syndrome. J Vasc Surg. 2020;70:2170–6.
J. Nelson
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109© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_17
Chapter 17
Polypectomy
ZacharySmith andMattMohorek
Cold vs. Hot Snare forFlat Polyps
Case 1 A 52-year-old male comes in for his rst screening colonoscopy and is
found to have a 1.2-cm at polyp in the sigmoid colon.
How do you decide whether to use cold snare polypectomy or hot snare?
I will start by saying that I frequently favor cold snare over hot snare polypec-
tomy, but anyone doing a polypectomy should evaluate three things. The rst is the
anatomic location of the polyp, the second is the polyp morphology, and the third is
whether to do en bloc vs. piecemeal resection.
In this case, most gastroenterologists would resect the polyp en bloc using hot
snare polypectomy. While hot snare polypectomy is more likely to lead to delayed
bleeding, in this case, we’re dealing with a polyp in the left colon and we know that
polyps in the left colon are less likely to have delayed bleeding compared to polyps
in the right colon [1]. The second thing is that if you take a 12-mm polyp out with a
cold snare, the chance of complete en bloc resection is far less compared to taking
that polyp out with a hot snare. So, for those reasons hot snare polypectomy may be
favorable in this situation.
Unfortunately, we don’t have good data to evaluate polyp recurrence rates in
comparing cold snare piecemeal polypectomy with hot snare en bloc polypectomy.
Now intuitively, one would think that en bloc resection is going to have less of a
Z. Smith (*)
Division of GI and Hepatology, Department of Medicine, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: zsmith@mcw.edu
M. Mohorek
Department of Gastroenterology, GI Associates, Wauwatosa, WI, USA
e-mail: matthewm@wigia.com
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chance of recurrence compared to piecemeal and hot is going to have less chance of
recurrence compared to cold. Per the guidelines, if you have a single 10mm+ade-
noma removed en bloc, that’s a 3-year interval for repeat colonoscopy, whereas if
you take it piecemeal, you might feel less comfortable waiting 3years.
So, there are a lot of things to consider in this case, but I think, putting together
all of the available data, hot snare polypectomy is still probably the preferred modal-
ity in this case.
Let’s say you are referred a patient with a large, laterally spreading granu-
lar tumor. You favor cold snare polypectomies. Do you have a size limit beyond
which you will not use cold snare?
No, I do most of my EMRs cold and I have taken out polyps that occupy >50%
of the circumference of the right colon cold. What cold snare EMR has done is that
it has changed the conversation and allowed us to have very safe options for remov-
ing large polyps in high-risk patients. We are frequently referred patients who were
scoped by community gastroenterologists after being found to be anemic, and large
polyps were discovered. Some of them are in their eighties, on Eliquis, and they’re
poor surgical candidates. The referring doctor is uncertain how to manage the situ-
ation. Whereas previously I might have been reluctant to offer one of these high-risk
patients conventional (hot snare) EMR due to the inherent risk of delayed bleeding,
etc., I am now much more willing to proceed, using cold snare EMR.It expands the
patient pool where we are able to offer therapy with polypectomy while maintaining
a risk/benet ratio that is still favorable. After all, it’s hard to assess whether a 7cm
laterally spreading granular tumor without high-grade dysplasia will turn into colon
cancer during a patient’s lifetime. It’s much more satisfying if we can safely remove
the polyp.
With hot snare EMR it is advised to ablate the margins of the resection site.
Do you ablate the margins when you do a cold snare polypectomy?
No, I don’t. The technique is still in its infancy where we don’t have a lot of data
on the optimal way to do things. Conventional, hot EMR has been around for
decades, and we just found out in 2019 that ablating the edge of the polyp is a good
way to minimize recurrence [2]. I don’t know if we are going to have cold EMR
ablation data for quite a while so my practice personally is to do more of a wide-
eld resection where you are taking several millimeters on the circumference of
normal-looking mucosa.
When you are doing this, you are thinking of a couple of things. First, the safety
prole of cold EMR is favorable, but it is also much more cost-effective. We were
able to show this in a cost-effectiveness study published in Endoscopy [3]. The
main determinant of cost-effectiveness for cold EMR is the lack of need for prophy-
lactic clipping. On the sensitivity analysis, when you are looking at various factors
determining cost-effectiveness, including the cost of clips, cost related to polyp
recurrence, and cost related to complications such as bleeding or perforation, it
turns out that the number one determinant of cost-effectiveness is the cost of clips
and the reason is that Medicare and most commercial insurances don’t reimburse
the cost of endoscopic clips. So, if you take out a 6-cm polyp and you use 8 clips
and each clip is $200, that is a signicant cost to the patient.
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Therefore, consistent with this, when I perform a large polyp EMR cold, I try to
keep my device usage as low as possible. If you are going to ablate the edges of a
polyp that would require opening up some other device, either a hot snare (using the
tip for ablation) or an APC catheter. Until we have evidence that it helps tremen-
dously, it is not my practice to ablate the edges when using cold EMR technique.
Can you discuss the different types of snares on the market and the advan-
tages and disadvantages of each type?
There are a host of snare sizes, shapes, and designs. One can get very over-
whelmed with the available options. My suggestion is to get comfortable with at
most ve and know how to use those. There are a lot of snare options, such as duck-
billed snares and rotatable snares, and in my opinion, a lot of this is overly nuanced
and not clinically useful. So, I think that if you have a cold snare that you are com-
fortable with, and a couple of hot snares of various sizes, you can do most anything.
Certainly, be willing to try new snares, but folks are going to be most successful by
knowing their own arsenal and what they are most comfortable with.
Now, for cold snares specically, there are a handful of dedicated cold snares out
on the market. Boston Scientic and STERIS are probably the two most well-
known. Boston makes the Captivator cold, which is a 10-mm oval snare. Steris
makes the Exacto, which is a 9-mm hexagonal snare. Both of these function simi-
larly. There are some other companies that have dedicated cold snares with various
shapes and sizes. Diversatek has both a 10-mm and 15-mm cold snare that is
rotatable.
What you want with a cold snare is something that is going to capture tissue and
cut reliably. Without the use of diathermy, you need to rely on the mechanical force
of the snare to get through tissue. There are some technical nuances to that as well,
but what you don’t want to do is use a snare designed for hot polypectomy for cold
snare EMR.The manufacturers of hot snares don’t put a premium on using mechan-
ical force to cut through the polyp without heat, and so it is going to be much more
challenging to do cold EMR with those devices.
Anticoagulation After Polypectomy
Case 2 A 65-year-old woman who is on apixaban for atrial brillation (held for
2days prior to colonoscopy) is found to have a 1.5-cm sessile polyp in the right colon.
Would you prefer to use cold snare or hot snare to remove this, why?
Personally, if anybody is on an antithrombotic, I am using a cold snare. Post-
polypectomy and post-EMR bleeding can be morbid, and over 50% of the time, it
will require a second colonoscopy, so there is a signicant cost associated with that
complication. Back in the days when I was doing more frequent conventional EMR,
I would instruct patients to avoid traveling for 2weeks because if they are going to
have a delayed bleed, they need to be where good health care is accessible. We’re
seeing very low bleeding rates with cold EMR, the delayed bleeding risk is
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