For the 1st of 30 days of #DistanceMedEd, I am going to touch on a question that is near and dear to my heart:

Why is upper GI bleeding so deadly and sometimes difficult to treat?
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Let's start with a poll to assess some basic understanding

Why do we start a PPI for a presumed upper GI bleed?

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Throughout history, internal bleeding has been one of the most common causes of death.

This is largely because it is a shared final end to many diseases including:
• Gastric cancer
• Ulcers
• Viral hemorrhagic fevers
• Cirrhosis

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Your kid falls off their bike and scrapes their knee. It bleeds for about 10 minutes and stops, within a few days it is completely healed.

Why is an ulcer or erosion in the stomach so different from an abrasion of the knee?

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The first key difference between external (knee) and internal (gastric) bleeding is the effect of bleeding into a hollow space.

Without the ability to apply pressure or form a natural tamponade with a hematoma, the blood can flow unimpeded.

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The second key difference is the environment in which the bleeding occurs:

The pH of blood is 7.4

The stomach goes from a resting pH of 6 down to 2 when stimulated by food

https://pubs.rsc.org/en/content/articlehtml/2015/fo/c5fo01085c

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With the initiation of a PPI, the gastric pH comes much closer to the physiologic pH of blood.

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This has three critical effects on hemostasis during an upper GI bleed.

First, this allows a fibrin plug to form

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Second, it decrease the rate of fibrinolysis.

In thrombelastography studies, a pH < 6.8 catalyzes hyperfibrinolysis

https://pubmed.ncbi.nlm.nih.gov/16966998/ 

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And third, it allows platelets to aggregate, which is a pH dependent process

https://jamanetwork.com/journals/jamasurgery/article-abstract/585285

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These three effects explain why the most reproducible effect PPIs have in multiple RCTs is need for endoscopic intervention.

If a thrombus forms and there is no longer an active bleed, intervention might actually make things worse.

https://pubmed.ncbi.nlm.nih.gov/20614440/ 

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This is all complicated further by the number of patients that are on antiplatelet agents (aspirin or plavix) or anticoagulation because of ischemic/thrombotic disease.

In some cases, fresh platelets need to be given in order to stop a bleed.

But remember HEART >>> GUT

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So this addresses the main challenges to hemostasis & why upper GI bleeds can be so deadly.

Our main tools work on:
• Improving the environment (bypH, giving fresh platelets) to allow a clot to form
• Trying to tamponade w/in a hollow space (via EGD)

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I'll end w/ basic pearls for upper GIB mgmt:
• 2 large bore IVs at all times
• IV PPI (my pref: push > bolus)
• NPO (not only to clear stomach, but alsostimulation of gastric acid secretion)
• EGD w/in 24 hrs
• Intubate if hematemesis threatens airway
• Tx for Hb <7

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Thank you all for following along!

Together we can learn from each other and become better communicators during this time.

As a reminder, I will retweet anyone teaching using #DistanceMedEd

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