The document discusses management of gastrointestinal bleeds in the emergency department, noting that identifying the bleed source is important but often challenging without endoscopy. While medications like H2 blockers, PPIs, and octreotide are commonly used, the evidence for their effectiveness is mixed and in some cases they may even increase mortality risk, so the priority should be stabilizing unstable patients and arranging prompt endoscopy.

1. ED Management of GI
Bleeds
Summary of Curbside Consult with Dr. Raddawi

2. Defining GI Bleed
Identifying the bleed source is important and does change
management
Classic characteristics:
PUD – Pain stops once bleeding starts (only 40% of all UGIBs)
Perforation – Pain concomitant with bleeding
Blood = cathartic, if no BMs, likely no active bleeding
Bright red blood…
Per mouth = UGI source (always)
Same for coffee-ground emesis
Per rectum = LGI source (most of the time)
BRBPR in a stable pt is NOT a UGIB

3. Melena
Black, foul-smelling, tarry stool caused by bacteria in
the small intestine digesting blood, signifying
bleeding proximal to the cecum
Requires 60cc of bleeding
Requires 8h of transit time

4. NG Tube Insertion
The ED literature says no need…if you get blood it’s great, if you
don’t, it means nothing
+hematemesis = NGT insertion, -hematemesis = none
Witting, Annals of EM, 2004, 43(4):525
Diagnostic NG aspiration sens 42%/spec 91%, PPV/NPV were 92%/64%,
PLR/NLR were 11/0.6
The final diagnosis was correctly predicted by the results of NG
aspiration in 66% of the patients
NG aspiration was positive in only 69% of the patients with a
definitive upper GI source of bleeding (20/29)
CONCLUSIONS: These results illustrate the limited value of NG
aspiration for the evaluation of GI bleeding in patients without
hematemesis. A positive test is a good predictor of an upper GI
source of bleeding, but a negative test provides virtually no useful
diagnostic information!

5. NGT for Cirrhotics or
Variceal Bleeds?
Go for it, perfectly safe!
Digestive Dis 1973;18(12):1032
Anesth Analg 1988;67:283
Variceal bleeds are often brisk, an NG tube is
essential to avoid aspiration

6. Guiac Positive
Only takes 2.5cc blood in the GI tract to turn the card
positive
Technically, development requires 2-3min (not secs)
Iron, pepto makes stools look black, but are –guiac
False positives…
Red meat Turnips
Vit C Horseradish

7. History
In the ED, probably our best strategy at defining the
source is to ask the patient…
UGI Source Likely If…
Alcoholic/heavy drinker
Frequent NSAID/ASA/alka-
selzer user
History of PUD/gastritis
Prior UGIBs
High stress lifestyle
Recent ICU admission,
intubation, prolonged
hospitalization

8. But Does Source Matter?
It all depends on the patient…
If they are…
Stable – Probably not
Going home – Probably not (they need to f/u anyway)
Admitted (asx’ic anemia, high risk pt, multiple co-morbidites,
etc) – Probably not
Unstable – Probably so
But the unstable hemorrhaging patient will get scoped above
and below anyway; so once they are stabilized, you are done
It depends on your belief as to whether medications help or not
The research does not always adequately identify source!

9. This Score Might
Glasgow-Blatchford Bleeding Score (GBS)
Risk stratifies those patients at risk for requiring medical
intervention (who stays and who goes)
BUN sBP
≥6.5 – 8 2 100-109 1
≥8.1 – 10 3 90-99 2
≥10.1 – 25 4 <90 3
≥25.1 6 Other Markers
Hemoglobin HR>100 1
≥12 – 13 (men) 1 +melena 1
≥10 – 12 (men) 3 +syncope 2
<10 (men) 6 +liver dz 2
≥10-12 (women) 1 +CHF 2
<10 (women) 6
Score >6 associated with 50% risk of complications
Masaoka, et al. J Gast Hep, 2006

10. Medical Management
Let’s get to the heart of the matter…ED interventions
As previously stated, most GI bleeders are stable and likely
can be managed without much more than a H2-blocker or
PPI and lifestyle modifications with outpatient follow up (if
no other risk factors) or obs admission for a scope.
If they are unstable, resuscitate them, inform GI
emergently and watch the patient closely
For everyone else…the data is suspect to say the least

11. Stomach pH
Green, et al (1978): Acid and pepcin’s effects on platelet
aggregation and prolonged bleeding (in vitro)
@pH 7.4 – 70-80% platelet aggregation
@pH 6.8 – 20%
@pH 5.9 – 0%
Similar trend with PT and PTT
Lowe, et (1980): Gastric juices promote fibrinolysis
Bottom Line: Increasing gastric pH>7.4 will facilitate
hemostasis by disinhibiting platelet aggregation and
fibrinolysis

12. What is Important?!?!
Before we continue, it is important to ask, what is important?
Morbidity, mortality, patient outcomes? To the ED doctor, this is
true
In the many research studies herein outlined, these don’t matter
as much as things like…
Quality of ulcer base on endoscopy (based on Forrest Classification
which has poor inter-relater reliability among GI specialists)
Rate of re-bleeding at 5 days
Units of blood transfused, etc…
Just keep this in mind!

13. H2-Blockers
Levine JE, et al. Meta-analysis: the efficacy of intravenous
H2-receptor antagonists in bleeding peptic ulcer. Aliment.
Pharmacol. Ther. 2002;16(6):1137-1142.
Placebo vs. H2 during UGIB, n=4000
No difference in mortality, 2.5-3% ARR in re-bleeding (p=0.053)
for H2, need for surgery 2.5% ARR (p=0.057), 7% ARR in re-
bleeding and need for surgery of specifically gastric ulcers,
including trend toward decreased mortality for H2B (sub-group
analysis)
Leontiotis has Astra-Zeneca ties (makes protonix), works for
Cochrane
Underpowered review

14. H2-Blockers
Levine recommend stopping H2B usage and use PPIs,
citing rate of H2 tolerance as cause
Netzer Am J Gastroent, 1999, compared stomach pH’s and
showed no difference in pH at 24h b/w H2B and PPI, but
lower pH in PPI group at 48-72h
But does this matter in the ER?
We need to reduce the acid to reduce bleeding rate,
and H2Bs are effective in first 24h!
Bottom Line: H2Bs do reduce stomach pH and do reduce re-
bleeding rate, need for surgery, and possible reduce patient
mortality compared to placebo

15. IV vs PO Pepcid?
IV (20mg) better than PO for gastric acid secretion
Ryan, JR et al. Comparison of effects of oral and
intravenous famotidine on inhibition of nocturnal
gastric acid secretion. Am J Med 1986;81(4), 60-64
After 1h, gastric pH ~7.2 for pepcid 20mg IV

16. PPIs (i.e. Protonix)
This is touted as the standard of care, but with little
supporting evidence
Theory: PPIs more specifically blunt gastric acid secretion,
greater onset of action, no tolerance effect by patients

17. PPIs
Sreedharan A, et al. PPI treatment initiated prior to
endoscopic diagnosis in UGIB. Cochrane Rev.
2010;(7):CD005415
Took undifferentiated ED GIB pts and compared PPIs vs
placebo before endoscopy, n=2000
No difference in mortality, no benefit for rate of re-bleeding,
no difference in need for surgery
PPIs improved characteristics of ulcer base at time of
endoscopy (9% over placebo) based on Forest Classification
Note no value in giving PPI prior to EGD
Bottom Line: Prior to EGD, PPIs have no benefit on clinically
significant outcomes

18. Are PPIs Toxic?!?!
Daneshmend TK, et al. Omeprazole versus placebo for
acute UGIB: randomised double blind controlled trial. BMJ.
1992;304(6820):143-147
n=1147, pts get EGD 24h after enrollment from ED
Rate of re-bleeding and need for transfusion no different
between PPI and placebo
Mortality (death over next 2-3wks)…
6.9% (PPIs), 5.3% (plac), p>0.05 (not sig)
Author states, “high dose PPIs might be toxic!”
Bottom Line: WTF?!?! PPIs have possibly greater (or equal)
mortality over doing nothing!

19. More on PPIs
Lau JY, et al. Omeprazole before endoscopy in patients with
GIB. N. Engl. J. Med. 2007;356(16):1631-1640
Industry-supported study through author affiliations, n=638
“No sig diff b/w omep and placebo group in transfusion
requirements, rebleeding, mortality, or pts needing emergent
surgery, however, fewer clean-based ulcers and non-bleeding
ulcers on EGD (stigmata).”
This study is listed as “pro PPIs” in most reviews, but…
The author’s initial protocol iteration defined “mortality” as
primary outcome, not “need for EGD tx”…mid-study primary
outcome change!!! (BAD!)

20. Does Anyone Benefit
From PPIs?
Leontiadis GI, et al. PPI treatment for acute peptic ulcer
bleeding. Cochrane Rev. 2006;(1):CD002094
Study doesn’t stipulate, but this implies that you know the
source of the bleed as peptic (so likely, post-endoscopy, in the
ED, we don’t know!)
n=4400, equal morality, 6.5% (p<0.05) benefit in re-bleeding vs
“control groups” (not all placebo), 3% (p=0.05) fewer going to
OR
Asians have mortality benefit to receive PPIs (no non-Asian
sub-group analysis performed)

21. PPIs for Non-Asians?
Post-hoc analysis of the following studies show…
Daneshmend study (1992), 5% increase in mortality in PPIs for
bleeding PUD pts
Hasselgren (1997)…stopped early for harm (p>0.05 in
mortality for older pts, 6% vs 1%), met only 75% of enrollment
goal before study stopped (using low-dose PPI, 20mg PO)
Schaffalitzky (1997)…no mortality difference, ~8%, only
enrolling younger patients, stopped early along with
Hasselgren because of similar design features
Bottom Line: For non-Asian UGIB pts with the source being a
peptic ulcer, a trend toward increased mortality exists
1. Daneshmend TK, et al. Omeprazole versus placebo for acute UGIB: randomised double blind controlled trial. BMJ. 1992;304(6820):143-147
2. Hasselgren G, et al. Continuous intravenous infusion of omeprazole in elderly patients with peptic ulcer bleeding. Results of a placebo-controlled
multicenter study. Scand. J. Gastroenterol. 1997;32(4):328-333
3. Schaffalitzky de Muckadell OB, et al. Effect of omeprazole on the outcome of endoscopically treated bleeding peptic ulcers. Randomized double-
blind placebo-controlled multicentre study. Scand. J. Gastroenterol. 1997;32(4):320-327.

22. PPIs & Stomach pH
Metz DC, et al. Lansoprazole regimens that sustain intragastric
pH>6.0: an evaluation of intermittent oral and continuous
intravenous infusion dosages. Aliment. Pharmacol. Ther.
2006;23(7):985-995
Their goal was to raise pH>6, achieved this ~33% of the time, mean
pH=5.45
Wang C-H, et al. High-dose vs non-high-dose PPI after endoscopic
treatment in patients with bleeding peptic ulcer: a systematic
review and meta-analysis of randomized controlled trials. Arch.
Intern. Med. 2010;170(9):751-758
Hi-dose = 80mg bolus w/ 8mg/h gtt (higher doses do achieve higher
pH), but hi vs low has no bearing on OR, need for transfusion,
mortality outcomes, etc
No difference between PO vs IV
Bottom Line: PPIs are equivalent IV or PO, higher doses achieve
higher pH, but no studies show the pH exceeding 7.4!

23. Official GI Society
Guidelines on GIBs
Barkun AN, et al. International consensus recommendations
on the management of patients with nonvariceal upper
gastrointestinal bleeding. Ann. Intern. Med. 2010;152(2):101-
113
Pre-endoscopic PPI’s may be considered to (1) downstage the
endoscopic lesion and (2) mitigate need for endoscopy, but
should not delay EGD
Bottom Line: PPIs have no clear benefit and might be
harmful! All patients with a UGIB need endoscopy, early if
sick, later if stable!!!

24. Helping the Endoscopist
So you have a patient who had hematemesis at home
(none currently), HR 120, BP 80/50, guiac+ tongue and
stool, you have fluids running…
No need to insert an NGT (not actively vomiting)
This pt needs a scope, and the best outcomes are achieved
by the cleanest views of the bleeding ulcer…so clear out
the stomach so the endoscopist can see!

25. Erythromycin
Motilin receptor agonist, promotes gastric emptying
1x dose at 3 mg/kg given 20 to 120 minutes prior to
procedure more effective than NGT and placebo!
Coffin B, Pocard M, Panis Y, at al.. Erythromycin improves the quality of EGD in
patients with acute upper GI bleeding: a randomized controlled study. Gastrointest
Endosc 2002;56:174-9.
Frossard JL, Spahr L, Queneau PE, at al.. Erythromycin intravenous bolus infusion in
acute upper gastrointestinal bleeding: a randomized, controlled, double-blind trial.
Gastroenterology 2002;123:17-23.
Bottom Line: Note the dates on these studies, this is NOT new
research; erythromycin works, give it if your patient needs an
emergent endoscopy!

26. Octreotide
The last of the commonly prescribed drugs needs its time in the
spotlight
Theory: Synthetic somatostatin with greater potency and longer
half-life than endogenous somatostatins which function to reduce
splanchnic blood flow
Cirrhotics have baseline splanchnic dilation secondary to excessive
CO levels, making them pressor-resistant as well
Note: Octreotide is NOT FDA approved for treatment of variceal
bleeding
Note: UCB (pharma company manufacturing octreotide) failed to
release data from a clinical trial comparing octreotide vs placebo
because (and this is a direct quote) “UCB is an ethical company
and that all data are proprietary solely to the UCB”!!!

27. Class IA Recommendation
ACGE 2007 recommended octreotide for all variceal bleeds
(class IA recommendation)
Only looked at a meta-analysis of 8 clinical trials, only
concerned about 5d re-bleed rate on pts treated with
octreotide (was some benefit, NNT=6), but no other factors
had clinical significance
Many of the included studies had major problems…
Clinical heterogeneity (Corley, 2001)
Inaccurate mortality data that was incalculable from the
numbers presented (Besson, 1995)
Noted failure of included studies to report calculated data
(D’Amico, 2002)
Failure to demonstrate a mortality benefit

28. Flawed Pathophysics?
Møller S, et al. Effect of octreotide on systemic, central, and
splanchnic haemodynamics in cirrhosis. J. Hepatol.
1997;26(5):1026-1033
Showed that central and mesenteric arterial blood volume
decreases with octreotide and mesenteric vasoconstriction occurs,
but hepatic venous pressure gradients and blood flow do NOT
change
Escorsell A, et al. Desensitization to the effects of intravenous
octreotide in cirrhotic patients with portal hypertension.
Gastroenterology. 2001;120(1):161-169
Portal HTN pts w/ varices are desensitized to octreotide’s effects.
Pt’s had a decrease in portal pressures and increase in arterial
pressures, but effect lasted only 5 minutes and then reversed (the
effects weren’t even sustained with a drip)

29. Failure to Launch
ACGE recommendations are based on morbidity data of a
5d re-bleeding benchmark, but octreotide failed to show in
any of the included studies any mortality benefit,
differences in blood transfusion reuirements, length of
hospital stay, etc.
Bottom Line: Octreotide has a Class IA recommendation for
use in patients with a variceal bleed, but a close look at the
literature shows a lack of support for this recommendation
for any ED-specific, clinically relevant outcomes!

30. Summary
Critical bleeding from a gastric source is exacerbated by low
stomach pH
NG tubes are not needed during the diagnostic process
H2 Blockers do have utility in the acute stages of bleeding but
tolerance develops, more studies are needed
PPIs don’t have data that shows patients benefit from receiving
it in the ER and might increase mortality, some benefit in
Southeast Asian populations
Octreotide shows decreased incidence in 5d rebleeding, not
much other benefits
It is important to constantly look at the things we do “all the
time” in medicine to make sure we are always doing what’s best
for the patients.