Upper GI Bleed transfusion threshold in patients with coronary artery disease

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

DrMetal

To shred or not shred?
Lifetime Donor
15+ Year Member
Joined
Sep 16, 2008
Messages
3,023
Reaction score
2,504
What do you guys preach for a transfusion threshold during an upper GI bleed in stable patients with a known h/o of CAD (stable CAD, not an active issue)?

I've often heard it should be HgB=8 (as opposed to the usual Hgb=7).

But that doesn't make much sense to me. Say the patient had an MI 3 years ago with one stent placed, has been asymptomatic since, is now just on ASA monotherapy (so technically he has CAD). He comes in for a slow peptic ulcer bleed, otherwise hemodynamically stable, Hgb is 7.7. You gonna transfuse him? [If he were a 6.7, I think we'd all agree he would get blood, even if stable and without symptoms.]

Members don't see this ad.
 

Seems to be the best evidence. I would use 80 in that pt you described
 
  • Like
Reactions: 1 user

Seems to be the best evidence. I would use 80 in that pt you described

I get it in the acute. Certainly someone whos' having ACS and a GI bleed at the same time warrants blood . . . but why in the case of stable CAD and stable GIB would you raise the threshold?
 
Members don't see this ad :)
8 only for active ACS. If they’re in for osteomyelitis and have a 10v cabg history, threshold still 7.
 
  • Like
Reactions: 1 users
I don't know the data for stable ACS, but if you tell me the guideline is 8, I'll say OK and I'll give you my reasoning why I think that sounds reasonable to me.

Because even in stable CAD, it's called coronary artery disease.... their arteries are diseased, man. At one point clogged enough to kill some heart. You try not to **** around with hypoxia or local or less O2 in these people basically ever after that. Even when they get angio'd and it checks out OK in places where they don't do intervention... atherosclerosis is one of those things that a huge proportion of us have setting in around teenagehood on a Western diet and just progresses through life on a spectrum, according to risk factors, some of which are modifiable and some aren't. These people have proven their arteries will clog if given half the chance. At any time thereafter, say a year, 2 years, they could have progressed somewhere with the atherosclerosis despite being optimized medically. Some people's arteries advance clogging basically no matter what you do.

You don't want the bleed and anemia to be one of those things to put them into an unstable CAD position which they're at risk of because hey, the piping to their heart isn't perfect and may be more sensitive to decreased 02 delivery. I thought I also read evidence that prior MI also seems to lower the threshold for further myocyte damage.
 
  • Like
Reactions: 2 users
I don't know the data for stable ACS, but if you tell me the guideline is 8, I'll say OK and I'll give you my reasoning why I think that sounds reasonable to me.

Because even in stable CAD, it's called coronary artery disease.... their arteries are diseased, man. At one point clogged enough to kill some heart. You try not to **** around with hypoxia or local or less O2 in these people basically ever after that. Even when they get angio'd and it checks out OK in places where they don't do intervention... atherosclerosis is one of those things that a huge proportion of us have setting in around teenagehood on a Western diet and just progresses through life on a spectrum, according to risk factors, some of which are modifiable and some aren't. These people have proven their arteries will clog if given half the chance. At any time thereafter, say a year, 2 years, they could have progressed somewhere with the atherosclerosis despite being optimized medically. Some people's arteries advance clogging basically no matter what you do.

You don't want the bleed and anemia to be one of those things to put them into an unstable CAD position which they're at risk of because hey, the piping to their heart isn't perfect and may be more sensitive to decreased 02 delivery. I thought I also read evidence that prior MI also seems to lower the threshold for further myocyte damage.

Your logic makes perfect sense . . .but then the transfusion purists who always advocate for the restrictive approach would argue that this----transfusing the stable 7.8 simply b/c he had an MI 5 years ago---would result in many excessive transfusions, adverse events, bla bla bla.
 
  • Like
Reactions: 1 users
no one has ever studied 8 but every study of transfusions has favored the restrictive level. The level of 8 comes from a study of outpatient elderly patients with a hx of CAD undergoing orthopedic surgery where they were randomized to 8 or 10.

Furthermore, even during ACS, I recommend a goal of 7 unless symptomatic. Tranfusions carry a risk of volume overload, transfusion reactions, and increase risk of thrombosis, all of which are deleterious for patients having ACS. All this for a dubious physiologic benefit and pretty poor data surrounding it's practice.

Furthermore, that systematic review is a mess and doesn't really answer the question we are asking. Someone needs to randomize patients to 7g or 10g hgb and see what happens.

The restrictive and liberal transfusion thresholds varied between trials, and the cut-off values actually overlapped (restrictive threshold 70-97 g/L; liberal threshold 90-113 g/L), which reduces the validity of pooling data across all trials.
 
  • Like
  • Love
Reactions: 2 users
What do you guys preach for a transfusion threshold during an upper GI bleed in stable patients with a known h/o of CAD (stable CAD, not an active issue)?

I've often heard it should be HgB=8 (as opposed to the usual Hgb=7).

But that doesn't make much sense to me. Say the patient had an MI 3 years ago with one stent placed, has been asymptomatic since, is now just on ASA monotherapy (so technically he has CAD). He comes in for a slow peptic ulcer bleed, otherwise hemodynamically stable, Hgb is 7.7. You gonna transfuse him? [If he were a 6.7, I think we'd all agree he would get blood, even if stable and without symptoms.]
The ABIM Choosing Wisely Pedantics vs. Team Common Sense Medicine will argue on this forever. ACP Hospitalist put out an article with the relevant papers but it doesn't do a good job of coming to any consensus. It's in a bunch of patient groups not applicable directly to this question:


There's no such evidence saying what exactly to do for 7 vs. 8. In many places in the literature, they talk about 7 for most, 8 for CAD, and 9 for select cancer/sepsis patients. I don't think you're harming anyone with going with 8 in this scenario. That said, I think the most important thing is to determine is if he's actively bleeding. From what you describe, I am imagining a guy who is not bleeding (vitals HDS, BUN/Cr, what about orthostatics, what's his baseline Hb, etc). If you have him on GIB protocols and his Hb remains stable within a 0.5 range and bounces up and down, just wait, I think if it drops, transfuse. Also, the notion that active ACS is 8 and longstanding CAD is 7 is not a thing with any robust literary support of or an official guideline, but a common path of reasoning hospitalists/cardiologists surmise... as they probably think if the ischemia is not acute, it's not bad so let's just keep them at 7 because #transfusionreactions/adverse events. I personally agree with Crayola on that point that sure active ACS is a worse state, but I think people will bad coronaries are still more susceptible to demand ischemia. At the end of the day, we don't have great evidence and you gotta rely on your own judgement.
 
Last edited:
  • Like
Reactions: 1 users
Top