Welcome. In this presentation, we're going
to be covering mesenteric ischemia.
Essentially, this is intestinal hypoperfusion and if it's severe
enough and long enough, we will get frank ischemia
and then, necrosis due to infarction. You can have either
very acute, a sudden decrease in blood supply
or you can have more chronic low-grade hypoperfusion.
If it's sudden, it's usually due to a decrease
in blood flow through embolization or a volvulus
or something else that acutely compromises vascular supply.
For chronic diseases, it's usually due to atherosclerosis,
so, kind of a chronic occlusion of the vessel,
the main vessels coming off of the aorta
that are limiting flow into the GI tract.
So, on our road map for mesenteric ischemia,
let's first look at the epidemiology.
About 0.1% of all hospital admission
are due to acute mesenteric ischemia.
So, not a common cause but a very serious cause.
This is typically seen in the geriatric population,
patients who are 60 years and older.
Unfortunately, although it has a relatively lower frequency
of hospital admission, it has a relatively high mortality rate.
So, about 60% of patients who have this will end up infracting
their bowel and having severe mortal complications.
In chronic disease, it's relatively rare to be a cause for hospitalization
but can still have significant symptomatology.
In chronic disease, a majority of the cases are inpatients who are more
elderly and it does occur more commonly in women.
In terms of the pathophysiology.
Again, we're going to break this down in terms of acute and chronic.
In acute as I've already mentioned, it's going to
be due at least 50% of the time to embolization.
So, an arrhythmia or endocarditis, or myocardial infarction
leading to the formation of a thrombus
or a vegetation within the lumen of the heart
can have a subsequent effect of embolizing
into distal vessels, including into the mesenteric arteries.
That occlusion will cause an acute mesenteric ischemia.
Arterial thrombosis on the other hand will happen
in the setting of more chronic atherosclerosis.
Acute plaque rupture of significant arterial disease
can also lead to acute mesenteric ischemia.
Hypoperfusion can also be a cause
of acute mesenteric ischemia.
So, just low blood flow with or without vascular compromise,
say, due to atherosclerotic disease
can lead to areas of relative
hypoperfusion within the bowel.
What's being circled are actually the
watershed zones in the large colon.
So, the one at the top at the splenic flexure is the watershed
zone between the superior mesenteric artery
and the inferior mesenteric artery and that anastomosis collateralization
is going to be most susceptible to hypoperfusion.
The one on the bottom within the sigmoid colon
is going to be at the watershed
between inferior mesenteric artery distribution
and the right iliac internal artery.
Venous thrombosis is a relatively infrequent
cause of acute mesenteric ischemia
but tumor or hypercoagulability
can lead to occlusion of the vessel
and that will lead to relatively poor flow through
the venous circulation through the capillary bed
and compromising the arterial inflow into the tissue.
In chronic disease, the major cause overall
is atherosclerosis where we have
accumulation of a plaque.
And then, progressive, chronic
occlusion of the vasculature.
So, we have diminished flow and it gets worse,
and worse, and worse overtime.
If we have an acute change in the atherosclerotic plaque,
that can give us acute mesenteric ischemia
but this chronic progressive occlusion compromising
flow is the cause of chronic.
There are rare causes as you can see
here and read quite well.
For the mesenteric ischemia, but we're not going to
go into any particular detail on these.
So, we're looking here at the perfusion of the inferior mesenteric
artery and you can see again that predominantly,
from the splenic flexure down to the sigmoid colon is what the
inferior mesenteric artery is supposed to be perfusing.
On the other hand, we're showing the perfusion for the
superior mesenteric artery and it goes more or less,
when it goes for the entire small bowel
but also provides perfusion from the cecum all the way up
the ascending colon through the transverse
colon, to the splenic flexure.
As we cut off the blood supply to the bowel,
we're going to start seeing mucosal damage
that will occur within about three hours of ischemia.
These cells have a relatively high metabolic rate
and can die relatively quickly.
If the mucosa dies as a result of ischemia, then, we'll get gastrointestinal
bleeding and we will begin to have this real pain.
That inflammation associated with the bleeding
is going to release vasoactive mediators and bacteria
and toxic byproducts that are going to further
compromise the vascular flow into the tissue.
Within six hours, we'll have transmural necrosis
of the bowel and at that time,
now, we can have perforation and peritonitis.
The clinical presentation depends on whether it's acute or chronic.
In acute mesenteric ischemia, the classic triad
is said to be diffuse and severe abdominal pain,
out of proportion to any clinical findings and it doesn't seem
to be reproduced or worsened with palpation.
The gut is emptying, so, there is diarrhea
and vomiting due to ischemia
and then, increased bowel contractions.
And there will be classically red, so called currant jelly stools.
Now, other things can do this.
So, just because you have these findings
doesn't mean acute mesenteric ischemia but certainly,
the findings of these should send you in that general direction.
Between acute mesenteric ischemia where we haven't
had infarction to now where we do have infarction,
if there's peritonitis, so, now, if we have
guarding, rigidity, and absent bowel sounds,
if the patient has fever, tachycardia,
and hypotension, signs suggestive of sepsis.
Or if there's bright red blood per rectum,
then, we can start worrying that we have in fact gone beyond
just ischemia and have gone into frank infarction
and we're at risk of perforation.
With chronic mesenteric ischemia, we get episodic abdominal pain.
It's the equivalent of intestinal angina.
As you eat, you increase the need for blood supply into the colon
and if you're not getting adequate blood supply,
a postprandial pain will kind of signal that intestinal angina.
It tends to be dull and crampy.
It tends to be up in the areas, kind of
epigastrium and into the splenic flexure.
So, at areas where we have our normal watershed areas
between the inferior and superior mesenteric arteries.
With chronic ischemia, you may not be
getting appropriate absorption of nutrition.
So, there will be weight loss.
And in these settings, you frequently will hear, although,
not always, an abdominal bruit due to atherosclerotic
disease involving one of the major vessels,
the superior mesenteric artery or the inferior mesenteric artery.
How do we make the diagnosis?
So, the laboratories are somewhat non-specific.
If we see lactic acid that says that we have ischemia someplace.
An elevated LDH may also suggest
that we have bowel ischemia.
A metabolic acidosis going along with a lactic acidosis
is indicative potentially bowel ischemia
if we don't have an ischemic focus someplace else.
Leukocytosis with a left shift
is indicative impending perforation and transmural
infarction and you may have elevated amylases
due to a contemporaneous pancreatitis
due to poor perfusion.
Imaging studies are usually quite helpful.
You can do plain x-ray and look for distended loops of bowel.
You can do an ultrasound looking for areas of
induration and edema and CT with angiography
is the preferred method for diagnosis where you try to see that
there's normal perfusion of all portions of the colon.
So, what do we do about this?
If it is a case of acute mesenteric ischemia,
we are going to want to obviously provide
fluid resuscitation to maintain blood pressure.
We're going to give broad spectrum antibiotics in anticipation
that we're going to have a bowel perforation.
We want to decompress the upper GI tract.
So, nothing by mouth and a nasogastric tube
put down to section out anything
that may be sloshing around in the stomach.
Pain control is a must.
We will give system anticoagulation such as heparin
because if the occlusion, the mesenteric ischemia,
is due to a ruptured atherosclerotic plaque and thrombosis
that will help us in terms of maintaining perfusion.
You may also do endovascular angioplasty
in the same way that we can put in a balloon and dilate
a vessel in the setting of acute myocardial infarct.
We can do exactly the same thing in acute mesenteric ischemia.
And in the event that none of that works, you can do surgery
because now, you have loops of infarcted bowel
and the relatively blue, black loops of bowel
that you see there have infarcted and need
to be removed before you have frank perforation.
With that, mesenteric ischemia top to bottom.