I am 66 years old and have been on dialysis for 10 years. Last year, I was diagnosed with GAVE(gastric antral vascular ectasia) aka watermelon stomach. I am being treated with APC(argon plasma coagulation) but it has had little effect in stopping the bleeding. The specialist told me he sees quite a few dialysis patients whose G.I. bleeding does not respond well to treatment. I have been reading that there are alternatives to heparin for patients who have some form of G.I. bleeding or are going to have surgery. Do you think a change from heparin to a less potent anticoagulant is a good idea and will make a difference?
I am 65 years old and have been on dialysis for 10 years. I was diagnosed with GAVE(gastric antral vascular ectasia) aka watermelon stomach and am experienceing bleeding in the stomach. I have been treated with APC (argon plasma coagulation) but with little effect on the bleeding. I was told by the specialist that many dialysis patients have trouble with G.I. bleeding that does not respond well to treatment. I read that there are less potent anticoagulants than Heparin and that patients who are experiencing bleeding or are going to have surgery should change What is your opinion on the relationship between Heparin and G.I. bleeding?
There are several options other than standard heparin when problems with anticoagulation arise.
If standard (unfractionated) heparin is currently being used for your anticoagulation, there is, first of all, the option of ‘low heparin’ or ‘no heparin’ regimes using conventional unfractionated heparin. This is dialysis where the amount of heparin is reduced and/or the dialyser is pre-rinsed with heparin prior to dialysis and no heparin is used as prime or as an infusate. Obviously, the risk of this is the clotting of the extra-corporeal circuit and the loss of the lines and dialyser … and the loss of a chunk of your blood volume. In addition, and especially if the access is a catheter, there is the added risk of clotting in or of the catheter. It is OK(ish) to do this now and then when the risks of heparin are high for brief periods, but it is an issue for ongoing maintenance dialysis and we prefer to keep low/no heparin runs to a minimum in my unit.
Low molecular weight heparin has largely (if not wholly) replaced standard unfractionated sodium heparin in Australia – indeed we have used enoxaparin now exclusively as our bog-standard heparin regime for some 6-8 years. Low molecular weight heparin is not only effective but there is some evidence it may be less likely to risk causing osteoporosis, while improvement in lipids, reduced itch, less hair loss and less transfusion requirement has been reported too.
Some people form antibodies against heparin (a condition called HITS - for heparin induced thrombocytopenia) and drop their platelet counts … making them more prone to belld. They need to be treated with alternative anticoagulation. There are heparin-like substances – danaparoid is one we use in one or two patients – and though it (and other similar substances) are more expensive – some much more – and are certainly more fiddly to use, they can still be good and/or useful choices.
For those at long-term risk of significant bleeding – especially if that risk can’t be avoided – the best option is probably regional citrate anticoagulation.
Todd Ing – who occasionally writes reviews for Dori at this site has much more experience with citrate than I do and may like to add a comment if Dori asks him to. With regional citrate, citrate is infused into the arterial line where it ‘chelates’ (‘binds’ is a good a synonym as I can think of) magnesium and calcium and inhibits coagulation in the out-of-body (extracorporeal) lines and dialyser. Calcium is restored in the venous line to restore a normal Ca++ level before the blood is returned.
Citrate is fiddly. As citrate is processed by the liver to form bicarbonate – an alkalosis (too much base and not enough acidity to the blood) can result … this means the dialysate bicarbonate may need to be reduced to compensate. This isn’t usually an issue for intermittent dialysis and is more a problem in the ICU when continuous methods of dialysis are being used (like SLED = slow low efficiency dialysis). It can also push up the sodium level in the blood so the dialysate sodium needs to be reduced.
If you are not already on low molecular weight heparin … this is definitely step 1. Citrate is, in my view, step 2 … if your local team can do it. It’s fiddly. It’s a nuisance. But, I think it is likely worth the effort if it can be arranged.
There are many experts in the US who know lots about citrate dialysis – far, far more than I do – and if your team hasn’t experience in this anticoagulation method, there are lots of people they can ask.
Hope that has been of some help
This question has been posted twice.
My answer is at the second post - same day, same post heading.