CBG23

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So, I was reading about ischemic colitis and was curious as to the exact mechanism by which it can cause rectal bleeding. I checked Uptodate, harrisons, a couple of path books, and a couple of Databases (MD Consult, AccessMedicine) and I haven't found the answer. Does anyone understand why this is the case and provide any type of source (textbook, journal article, etc.) with the explanation. Thanks!
 
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This is somewhat of a hand wavy explanation, because I have been taught contradicting things on this very topic.

Ischemic colitis = ischemia of the mucosa which leads to sloughing of that tissue. Leads to raw exposed submucosa which bleeds until it is re-epithelialized.

The part that is contradictory is that I was taught in class that it was due to occlusion of the IMA as a result of atherosclerosis. However, patients that have the IMA ligated in aortic bypass grafting don't have super high rates of ischemic colitis. I remember a paper from some time ago that suggested a micro vascular inflammatory response in response to infection.
 
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I haven't read any actual paper on colonic ischemia, but here is what I found on my surgical text.

"Unlike small bowel ischemia, colonic ischemia are rarely associated with major arterial or venous occlusion. instead, most colonic ischemia appears to result from low flow and or small vessel occlusion. occasionally thrombosis and embolism can caused colonic ischemia, ligation of IMA in aortic repair predisposes to colonic ischemia. "---Schwartz.

I know from reading many papers on C diff colitis-a toxin mediated mucosal disease that eventually lead to a low flow state, which in turn kills the colon.
 
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Maybe because ischemia causes decreased oxygen and nutrients to the endothelium leading to mucosal atrophy and then colonic flora can damage the lining? Just speculating.
 
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theseeker4

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From my understanding, which may be incomplete/incorrect:
Ischemia --> tissue damage --> leaky capillaries and necrotic mucsoa/submucosa, which in the presence of collateral/restored circulation and/or continued circulation through obstructed, but not totally occluded blood vessels --> bleeding into lumen.
The ischemic damage along with the other factors from other posters above all lead to the ability for blood to make it from the blood vessels into the lumen, and the blood is coming from the collateral/restored/insufficient-but-still-present circulation.
 

Instatewaiter

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This is somewhat of a hand wavy explanation, because I have been taught contradicting things on this very topic.

Ischemic colitis = ischemia of the mucosa which leads to sloughing of that tissue. Leads to raw exposed submucosa which bleeds until it is re-epithelialized.

Agree. It's usually in someone who also has a high rate of atherosclerosis so they have other flow limiting lesions which prevent robust collateralization
 
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Charles_Carmichael

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The part that is contradictory is that I was taught in class that it was due to occlusion of the IMA as a result of atherosclerosis. However, patients that have the IMA ligated in aortic bypass grafting don't have super high rates of ischemic colitis. I remember a paper from some time ago that suggested a micro vascular inflammatory response in response to infection.

Here's my rationale: if you have significant atherosclerosis of the SMA, you likely have some atherosclerosis of the IMA as well. When there's a subsequent low flow states, there's decreased blood flow through both the SMA and IMA, which results in the watershed areas becoming ischemic. If the ischemia is bad enough to cause necrosis, you have sloughing of mucosa, bleeding, etc. On the other hand, when you surgically ligate the IMA when putting in an aortic graft, there's still pretty good collateral flow coming from the SMA to supply blood for the hindgut as well (through all those interconnected arteries).

I could be wrong, but that's how I'm thinking about it.

The next question then, I guess, would be, if someone had a AAA and needed a graft placed, what's the likelihood of them having clinically significant atherosclerosis of the SMA/IMA? I don't know the answer to that.
 

Dires

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From my understanding, which may be incomplete/incorrect:
Ischemia --> tissue damage --> leaky capillaries and necrotic mucsoa/submucosa, which in the presence of collateral/restored circulation and/or continued circulation through obstructed, but not totally occluded blood vessels --> bleeding into lumen.
The ischemic damage along with the other factors from other posters above all lead to the ability for blood to make it from the blood vessels into the lumen, and the blood is coming from the collateral/restored/insufficient-but-still-present circulation.

This is also how I have wrapped my head around it :)

I think specifically the marginal links SMA and IMA circ
 
Nov 28, 2018
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This is a difficult question, one that has bothered me for years. When I ask professors to explain it, they do so with only one-sentence, circular reasoning, like, "It bleeds because its ischemic, duh."

Logically, how it is possible that LACK of blood flow (aka ischemia) can CAUSE bleeding?

I can only conjecture because I've never gotten a logical, full explanation from any source.

But I suppose it might have to do with a reperfusion injury. For example, we know that in the kidney or brain or lung or any other solid organ, a hemorrhagic lesion causes a pooling of blood that can settle in any dependent area, while in contrast, ischemia will cause a wedge. The wedge represents the area once nourished by blood flow from the now-occluded artery. This wedge shape however, does not always remain pale. Sometimes, the tissue remains anoxic and dies in place, leaving a white infarcted wedge. Other times, collateral circulation reperfuses the area, making it red and bloody.

Perhaps the GIT, being well vascularized, reperfuses the ischemic area, making it bloody? Anyway, the GIT as we know sloughs constantly, so the anoxic tissue will get sloughed, rather than remain in place. Perhaps that creates a bleeding ulcer.
 
Feb 28, 2017
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This is a difficult question, one that has bothered me for years. When I ask professors to explain it, they do so with only one-sentence, circular reasoning, like, "It bleeds because its ischemic, duh."

Logically, how it is possible that LACK of blood flow (aka ischemia) can CAUSE bleeding?

I can only conjecture because I've never gotten a logical, full explanation from any source.

But I suppose it might have to do with a reperfusion injury. For example, we know that in the kidney or brain or lung or any other solid organ, a hemorrhagic lesion causes a pooling of blood that can settle in any dependent area, while in contrast, ischemia will cause a wedge. The wedge represents the area once nourished by blood flow from the now-occluded artery. This wedge shape however, does not always remain pale. Sometimes, the tissue remains anoxic and dies in place, leaving a white infarcted wedge. Other times, collateral circulation reperfuses the area, making it red and bloody.

Perhaps the GIT, being well vascularized, reperfuses the ischemic area, making it bloody? Anyway, the GIT as we know sloughs constantly, so the anoxic tissue will get sloughed, rather than remain in place. Perhaps that creates a bleeding ulcer.
In the setting of decreased blood flow, wouldn't there be neovascularization and therefore weak, leaky capillaries? Similar to how retinal ischemia stimulates neovascularization via VEGF, which is exactly why anti VEGF like Avastin work for diabetic retinopathy?
 
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