GI bleeding is bread and butter critical care. However, there are a lot of nuances – especially regarding variceal bleeding and new approaches to hematochezia.
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The IBCC chapter is located here.
- The podcast & comments are below.
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Another great review- these checklists are fantastic! Our junior residents so often reflex to PPI treatment and forget about the really important stuff like ceftriaxone and it’s easy to forget about DDAVP as an option.
so right about DDAVP
Hi Josh
Thanks for your work on this chapter. It’s an excellent read.
In terms of the vasoconstrictor, is there any difference between octreotide vs terlipressin?In the UK, we use terlipressin & I’m uncertain if it’s available in the US.
Is there much of a difference between these medications in terms of patient-orientated outcomes?
The US equivalent of terlipressin is vasopressin (vasopressin-receptor agonist drugs). Theoretically these agents (vasopressin and terlipressin) should be beneficial to support blood pressure while causing vasoconstriction to the gut – so they might be good pressors to use in hypotensive patients. The problem is that in practice they have a long half-life which makes titration difficult. Hemodynamics in GI bleeds are often very labile (e.g. as soon as volume resuscitation occurs the Bp improves), so you want a short-acting drug. Thus, my choice for vasopressor in GI bleeds is generally norepinephrine (despite the fact that vasopressin has some theoretical advantages).… Read more »
Hi Josh,
I’m an EP in the Netherlands and we use octreotide as well. But what is the evidence for it. A Cochrane review shows no benifit. This is also mentioned on thennt.com. I’d like to here your view on this.
With kind regards,
René Verbeek
very helpful, and very interesting, Josh. question: suppose one has a cirrhotic patient with severe UGI bleed. i thought that Vit K does little or nothing to correct a cirrhosis-induced coagulopathy. also, i thought that there was involved a situation of “faulty” coag’s. and thus, 1000 or 1500 units of PCC (Kcentra) might be helpful. what do you think, Josh? tom lastly, you didn’t mention Reboa, Josh. I had heard or read that there was some consideration of this in the appropriate patient, at appropriate centers, i suspect in rapidly exsanguinating patients, for certain critical bleeds below the diaphragm. thanks,… Read more »
1) agree, vitamin K does nothing to fix cirrhotic coagulopathy. Some patients may have a *combination* of cirrhosis and vitamin K deficiency however, so vitamin K is often given empirically just to make sure that there is no underlying vitamin K deficiency. 2) must admit that I don’t think PCC has a role in cirrhotic coagulopathy. There are too many factors deficient – you may need to replace more than just four. Most patients with cirrhosis aren’t truly coagulopathic (i.e. the R-time on TEG will be normal or low). If the patient does have true enzymatic coagulopathy (prolonged R-time on… Read more »
Hi Josh, Thanks for all your work. As a junior trainee I’ve found your resources incredibly value, and enjoyable. One thing I find challenging is when deciding between further crystalloid volume expansion (perhaps they’ve had 1.5-2L) or reaching for PRBC in a patient still demonstrating some haemodynamic instability (I.e shock index around 1) but Hb yet to drop much below 10. I worry about the risk of over-transfusing but also giving too much volume for someone who is possibly still bleeding internally and really just needs blood. The excellent 2013 NEJM journal you mention excluded patients with “exanguinating bleeds”, but… Read more »
I’m allowed to give water if the bleeding has stopped?
Thanks for the awesome post.
You have saved my patients from being hurt by me over and over 🙂
I have seen from time to time CRRT (high dose) being used to correct academia in MTP. I couldn’t find myself, but have you seen any evidence for high dose versus low dose CRRT use in MTP with renal failure.