AACN Advanced Critical Care

Volume 29, Number 4, pp 369-376

© 2018 AACN

Drug Earnest Alexander, PharmD, BCCCP, FCCM,

Update and John Allen, PharmD, CPh, BCPS, BCCCP
Department Editors

Acute Management of Upper Gastrointestinal

Bleeding
Whitney Gibson, PharmD
Nicholas Scaturo, PharmD
Christopher Allen, PharmD, BCPS, BCNSP

A cute upper gastrointestinal bleeding (UGIB) is a common medical emer-

gency in the United States that is associated with significant morbidity
and mortality, frequent hospital admissions, and costs of more than $2 billion
annually to the health care system.1 Upper gastrointestinal hemorrhage is
defined as bleeding from any enteric source proximal to the ligament of Treitz.
Upper gastrointestinal bleeding is approximately 5 times more likely to occur
than lower gastrointestinal bleeding.2 Male patients and elderly patients tend
to be more commonly affected.2
Initial management of clinically significant acute UGIB includes volume
resuscitation to restore hemodynamic stability, diagnostic studies to identify
the source and severity of bleeding, and pharmacological interventions to
increase gastric pH and assist with hemostasis. Data on patients with UGIB
from 1993 to 2000 showed a decreasing incidence of the condition, suggest-
ing that prevention strategies are improving. Despite advances in therapeutic
management of UGIB, however, the risk of rebleeding and mortality rates have
remained unchanged.3 In this article, we discuss risk factors, initial evaluation
and restoration of intravascular volume, and pharmacological management
of acute UGIB.

Pathophysiology
Upper gastrointestinal bleeding can be separated into 2 categories: nonvariceal
and variceal. The most common etiology (62%) of UGIB is peptic ulcers. Other
causes of nonvariceal bleeding include gastritis and duodenitis (8%), Mallory-
Weiss tear (4%) and upper gastrointestinal tract malignancy (2%), and other
diagnoses (10%); no exact cause is identified in 8% of cases. Gastroesopha-
geal varices account for a small percentage (6%) of all UGIB cases but are
present in 50% of cirrhotic patients and are the most common fatal complica-
tion in this subset of patients.4,5

Nonvariceal Bleeding
Nonvariceal bleeding most commonly arises from peptic acid–related com-
plications, either chronic peptic ulcer disease (PUD) or stress-related mucosal

Whitney Gibson is Critical Care Pharmacist, Department of Pharmacy Services, Tampa General Hospital,
1 Tampa General Circle, Tampa, FL 33606 (wgibson@tgh.org).
Nicholas Scaturo is Emergency Medicine Clinical Pharmacist, Sarasota Memorial Hospital, Sarasota, Florida.
Christopher Allen is Critical Care Clinical Pharmacist, Trauma Surgical Critical Care, Department of
Pharmacy Services, Tampa General Hospital, Tampa, Florida.
The authors declare no conflicts of interest.
DOI: https://doi.org/10.4037/aacnacc2018644

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DRUG UPDATE
disease (SRMD). Acute UGIB stemming from
chronic PUD usually develops outside of the
hospital setting, whereas SRMD is more likely
to occur in critically ill patients during hospi-
tal admissions.6 An imbalance between gas-
tric acid and pepsin secretions and mucosal
defense mechanisms is the shared pathophysi-
ology leading to UBIG in chronic PUD and
SRMD. Under normal physiological conditions,
mucosal defense and repair mechanisms such
as mucus and bicarbonate secretion, endoge-
nous prostaglandin production, and mucosal
blood flow protect gastroduodenal mucosa
from destruction by gastric acid and pepsin.5
Mucosal lesions due to chronic PUD usually
result from Helicobacter pylori infection or
nonsteroidal anti-inflammatory drugs. Whereas
H pylori degrades the gastric mucosa through
bacterial enzymes and direct gastric inflam-
mation, nonsteroidal anti-inflammatory drugs
cause direct irritation to the gastrointestinal
mucosa and inhibit prostaglandin synthesis.7
In contrast, SRMD develops in the setting of
diminished defense and repair mechanisms
stemming from an overwhelming stress response
during critical illness and mucosal ischemia.6
Variceal Bleeding
Cirrhosis stemming from poison consump-
tion, autoimmune conditions, chronic alco-
holism, nonalcoholic fatty liver disease, or
chronic hepatitis leads to a gradual buildup
of scar tissue in the liver. These fibrotic changes
alter hepatic architecture, causing an increased
resistance in portal flow and subsequent devel-
opment of varices to decompress the portal
vein. However, as portosystemic collateral
circulation develops, splanchnic vasodilation
and increased cardiac output occur, worsen-
ing portal hypertension.8 The thinnest tissue
layer of all varices is found at the gastroesoph-
ageal junction, making this area more prone
to rupture. Hemorrhage becomes more likely
as pressure, flow, and size of varices continue
to increase.
Risk Factors
Several precipitating risk factors for non-
variceal bleeding have been identified, includ-
ing use of specific pharmacological agents
and coexisting disease states that alter nor-
mal physiological conditions in the gastroin-
testinal tract (Table 1).4-7 However, in cases
of variceal bleeding the single most impor-
tant predictor of hemorrhage is the size of
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W W W . A A C N A C C O N L I N E . O RG
Table 1: Risk Factors for Acute Upper
Gastrointestinal Bleeding
Nonvariceal Bleeding
Chronic NSAID use
Helicobacter pylori infection
Mechanical ventilation > 48 h
Coagulopathies (platelet count < 50 000/mm3,
INR > 1.5, or partial thromboplastin time > 2 times
the control value)
Antiplatelet/anticoagulant therapies
Variceal Bleeding
Size of varices (> 5 mm)
Hepatic vein pressure gradient > 12 mm Hg
Varix location (esophageal)
Red wale mark on endoscopy
Advanced liver failure (Child-Pugh class B or C)
Abbreviations: INR, international normalized ratio; NSAID, non-
steroidal anti-inflammatory drug.
the varices. Patients with large varices have a
15% risk of hemorrhage during the first year,
compared with a risk of about 6% for patients
with small varices.4 Other identifiable risk
factors are listed in Table 1.4-7
Initial Resuscitation
Patients with UGIB generally present with
weakness, dizziness, or syncope associated
with hematemesis, melena, or hematochezia.
The initial evaluation should include a thor-
ough medical history, a complete physical
examination, and basic laboratory tests to
assess the severity and possible location of
the bleeding, as well as any underlying medi-
cal issues that may affect management of UGIB.
Providers also can use these initial findings to
derive risk stratification scores. The Glasgow-
Blatchford score or the Rockall score may be
used to aid in clinical decision-making, such
as timing of endoscopy or need for hospital
admission, or in assessing a patient’s mortal-
ity risk.5,9
A primary assessment should address basic
resuscitation principles: assessment of airway,
breathing, and circulation. Patients with altered
mental status or large-volume hematemesis
may need to be intubated for airway protec-
tion and to prevent aspiration. Intubation also
may facilitate early endoscopy by minimizing
concerns about administering sedative agents
in hypotensive patients without a definitive
airway. Hemodynamic assessment is central
to the initial treatment of a patient with
UGIB given the inherent risk of intravascular
VO L U M E 2 9 • N U M B E R 4 • W I N T E R 2 018
hypovolemia leading to shock and multior-
gan failure due to blood loss. If patients are
initially hemodynamically unstable, guideline
recommendations for both variceal and non-
variceal bleeding include early resuscitation
with crystalloid fluids and/or red blood cell
transfusions.4,5,9 To our knowledge, no ran-
domized controlled trials have been conducted
to assess the ideal volume of fluid to resusci-
tate an actively hemorrhaging patient; how-
ever, an isotonic crystalloid fluid, such as 0.9%
sodium chloride, generally should be used as
a temporizing measure until blood products
are available for administration. Aggressive
fluid resuscitation should be avoided in the
setting of hemorrhagic shock, as it can dis-
lodge formed clots and impede the clotting
process through dilution of clotting factors.
Using cold fluids may inhibit the clotting
cascade.10 In cases of suspected variceal bleed-
ing due to cirrhosis, aggressive crystalloid
resuscitation poses additional risks, including
an increased rate of rebleeding, worsening
ascites, or fluid accumulation at other sites.4
Restrictive red blood cell infusion strategies
are preferred in both variceal and nonvariceal
bleeding, as these strategies have been found
to significantly improve 6-week survival and
reduce rebleeding rates.11
Patients on anticoagulation or antiplatelet
therapies pose an additional concern in acute
hemorrhagic situations. Warfarin is an anti-
coagulant commonly used for prevention of
thrombus formation in atrial fibrillation,
mechanical valve replacement, or venous
thromboembolism. Warfarin inhibits synthe-
sis of clotting factors II, VII, IX, and X through
depleting hepatic phytonadione (vitamin K1)
stores. For patients on warfarin therapy who
are not experiencing shock at presentation
but have an elevation in international nor-
malized ratio (INR), oral phytonadione at a
dose of 5 mg is an appropriate intervention
to avoid rebound coagulopathies. In severe,
life-threatening cases of UGIB, phytonadione
at a dose of 10 mg intravenously (IV) is pre-
ferred because of its rapid onset (1-2 hours
for IV form vs 6-10 hours for oral formula-
tions).12-14 Intravenous administration of phy-
tonadione may cause anaphylaxis; therefore,
to minimize the risk, administration should
be performed slowly at a rate of 1 mg/min.12-14
Additionally, current practice guidelines rec-
ommend the administration of 4-factor pro-
thrombin complex concentrate (4F-PCC) in
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DRUG UPDATE
patients receiving warfarin therapy who are
experiencing serious, life-threatening bleeding
with elevations in INR.5 Four-factor PCC is
preferred over administration of fresh frozen
plasma because of its higher concentration of
clotting factors, leading to more rapid INR
correction, lower risk for allergic reactions or
infection transmission, and smaller volume
of administration.12 Disadvantages of 4F-PCC
use include cost (up to $10 000 per treatment),
unavailability at smaller institutions, and risk
of thrombosis.12 United States Food and Drug
Administration–approved dosing of prothrom-
bin complex concentrate (human) (Kcentra;
CSL Behring, King of Prussia, Pennsylvania)
is based on pretreatment INR and is weight-
based, ranging from 25 to 50 units/kg with a
maximum dose of 5000 units. Recent evidence
suggests that fixed-dose 4F-PCC at 1500 units
may be as effective as the US Food and Drug
Administration–approved dosing in reversing
the INR of acutely hemorrhaging patients.13
Some institutions have adopted this strategy
given the significant cost savings14; however,
the strategy should be used with caution in
obese patients or patients with severely elevated
INRs, populations that may require higher
doses. A follow-up INR should be obtained
30 minutes after administration to ensure
adequate reversal.14
Direct oral anticoagulants (DOACs) include
therapies that directly inhibit thrombin or
factor Xa, ultimately preventing the forma-
tion of fibrin clots. Currently no guidelines
exist that address use of DOACs in treating
patients with UGIB. Given that several DOAC
therapies exist, reversal must be tailored to
the specific DOAC being taken. In general,
all DOACs have short half-lives, ranging from
5 to 17 hours.12 Withholding the medication
during acute bleeding may be an acceptable
strategy in hemodynamically stable patients;
however, further reversal may be required in
patients with hemodynamic instability.5 If a
dose of the DOAC medication was taken
recently, activated charcoal may be given to
prevent absorption.
Idarucizumab is a reversal agent specifically
for dabigatran and has been shown to reverse
anticoagulant effects within minutes. Dabiga-
tran is also the only DOAC that is dialyzable,
which may be a necessary strategy if idaruci-
zumab is not available. Andexanet alfa is a
reversal agent that recently has been approved
by the US Food and Drug Administration
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DRUG UPDATE W W W . A A C N A C C O N L I N E . O RG

Table 2: Pharmacotherapy Management of Upper Gastrointestinal Bleeding

Medication Route Dosing Administration Adverse Effects Monitoring

Proton Pump Inhibitors
Pantoprazole Continuous 80 mg loading
IV infusion dose followed Maximum rate Injection site pain/
by 8 mg/h 2mg/min thrombophlebitis
Peripheral or Allergic/anaphy-
Pantoprazole Intermittent 40 mg every
central catheter lactic reaction
IV infusion 12 h
Headache
Pantoprazole Oral 40 mg daily (all PPIs)
Do not crush
or chew NA
Omeprazole Oral 40 mg daily enteric-coated
formulations
Antidiuretic Hormone
Vasopressin Continuous 0.2-0.8 U/min Central catheter Ischemia (cardiac, Anaphylaxis/
IV infusion preferred peripheral, hypersensitivity
and bowel), reaction
arrhythmias, Arrhythmias
hypertension, Angina
fluid retention
Nitrate
Nitroglycerin Continuous 40-400 μg/min to Peripheral or Hypotension, Hypotension
IV infusion maintain SBP > central headache Headache
90 mm Hg catheter Allergic reactions
Somatostatin Analogue
Octreotide Continuous 25-100 μg loading Peripheral or Bradycardia, Bradycardia
IV infusion dose followed central palpitations, Flushing
by 25-50 μg/ catheter peripheral edema, Injection site pain/
hour hypertension, thrombophlebitis
fatigue, head- Allergic/anaphy-
ache, dizziness, lactic reaction
hyperglycemia

Abbreviations: IV, intravenous; NA, not applicable; PPI, proton pump inhibitor; SBP, systolic blood pressure.

for the reversal of oral factor Xa inhibitors15;
however, it currently has limited availability
due to manufacturing delays. For hospitals
without access to andexanet alfa, adminis-
tration of 4F-PCC in cases of acute bleeding
while on DOAC therapy is a presumably
effective strategy based on in vitro and ani-
mal studies.12 However, this strategy should
be reserved for severe, life-threatening cases
of bleeding.
Administration of platelets can be consid-
ered for patients who are hemodynamically
unstable and on antiplatelet therapy or are
thrombocytopenic.12 For cirrhotic patients
with significant baseline coagulopathies or
thrombocytopenia, guidelines recommend
that fresh frozen plasma and platelets be
given. However, no evidence exists to suggest
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that administration of PCCs is necessary or
beneficial in this subset of patients unless
they are receiving DOAC or warfarin therapy.
Pharmacological Management
A list of common medications used for
management of UGIB is provided in Table 2,
along with dosing and administration recom-
mendations, common adverse effects, and
monitoring parameters.4,5,8,16-21
Histamine Receptor Antagonists
Histamine 2 receptor antagonists (H2RAs)
have been studied alongside proton pump
inhibitors (PPIs) for management of variceal
and nonvariceal UGIB. Studies have shown
H2RAs to be inferior to PPIs, probably because
of tachyphylaxis and loss of an antisecretory
VO L U M E 2 9 • N U M B E R 4 • W I N T E R 2 018
effect that occurs during the 72-hour infusion
period, as well as an inability to maintain a
gastric pH greater than 4 (the goal is greater
than 6).5,16,17 Therefore, H2RAs should not
be used for management of acute UGIB.
Proton Pump Inhibitors
The use of PPIs is widely accepted as the
standard of therapy for both nonvariceal and
variceal UGIB. Both gastric acid and pepsin
alter coagulation by interference with the intrin-
sic and extrinsic clotting pathways (impairing
clot formation), promotion of fibrinolysis,
and inhibition of platelet aggregation. In vitro
studies have shown lack of platelet aggregation
when plasma pH is less than 6.5,16,17 Addition-
ally, this acidic environment favors clot lysis.
Proton pump inhibitors inhibit the parietal
H+/K+ adenosine triphosphatase pump, thereby
suppressing gastric acid production, which
helps maintain a neutral pH.5,16,17 Time of ini-
tiation varies depending on the indication for
use. For use in nonvariceal bleeding, studies and
meta-analyses have shown no benefits with
regard to mortality, rebleeding rates, or need
for surgical intervention if PPIs are used before
endoscopy.17,18 In patients with active bleeding,
or if the type of UGIB is unknown (variceal
vs nonvariceal), PPI therapy can be started
before endoscopy despite the lack of eviden-
tial benefit. Therapy should be discontinued
in these patients after endoscopy has been
completed, unless there is a source (ulcers
and erosions) that would benefit from contin-
uation of therapy.5,17,18 When PPIs are used
for management of variceal bleeding, the rec-
ommendation is to begin therapy as soon as
the patient arrives at the hospital; studies
have indicated benefits such as reduction of
need for surgical intervention or transfusions
and reduced rates of rebleeding when PPI ther-
apy is initiated before endoscopy.4,19
The dosing of PPI therapy consists of admin-
istering a bolus of 80 mg IV followed by a
continuous infusion of 8 mg/h.4,5,17-20 This
dosing regimen has been studied with multi-
ple PPI formulations (pantoprazole, omepra-
zole, esomeprazole) and is appropriate for all
PPIs. The continuous infusion should be con-
tinued for 72 hours after endoscopy. Once
the initial 72 hours of therapy has been com-
pleted, twice-daily oral or IV PPI use, if
appropriate for the patient, is recommended
to continue for 11 to 14 days, at which time
a daily PPI may be instituted.16,21
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DRUG UPDATE
Alternate PPI dosing strategies have been
evaluated for the management of UGIB.20
A meta-analysis investigated whether twice-
daily IV boluses of PPIs would be just as effec-
tive as a continuous infusion.20 Results of this
analysis showed twice-daily injections to be
just as efficacious as a single bolus followed
by a continuous infusion.20 Although both of
these dosing strategies are effective, continuous
infusion dosing was associated with a reduction
of approximately 3% in recurrence of ulcer
bleeding at 7 days.20 On the basis of these
findings, the European guidelines recommend
continuous infusion over intermittent PPI use;
the American guidelines have not been updated
since the publication of these outcomes.17,19
Concerns about use of PPIs include an
increased incidence of Clostridium difficile
diarrhea and pneumonia. By inhibiting gas-
tric acid secretion (one of the body’s natural
defenses against infection), PPIs create an
environment that promotes bacterial growth
that can translocate into the lungs or allow
further growth in the gastrointestinal tract.
Several studies and meta-analyses have been
published with conflicting results, most dem-
onstrating no increased incidence of either
infectious complication.22-25 However, as criti-
cally ill patients are vulnerable and at increased
infection risk at baseline, care should be taken
to minimize and discontinue PPI therapy as
soon as possible.17 Of most concern are drug
interactions and potential reduced absorption
of other pertinent medications the patient
may be receiving. Proton pump inhibitors act
as major substrates of CYP2C19 and minor
substrates of CYP2D6 and CYP3A4. The effi-
cacy and metabolism of PPIs can be altered
if they are given concomitantly with inhibi-
tors of CYP2C19, CYP2D6, and CYP3A4,
or with inducers of CYP219 and CYP3A4.
Proton pump inhibitors will reduce absorp-
tion of some medications that require an acidic
environment for absorption, including aspirin,
ketoconazole, atazanavir, some cephalosporin
antibiotics, and fluoroquinolone antibiotics.26
Somatostatin Analogues and
Vasopressin
Several vasoactive options have been stud-
ied for gastrointestinal hemorrhage, includ-
ing vasopressin, octreotide, and terlipressin.
Terlipressin is a synthetic analogue of vaso-
pressin and has shown significant benefits with
improved control of bleeding and survival
373
DRUG UPDATE
compared with placebo. Terlipressin is the
only pharmacotherapeutic agent to have
shown mortality benefit; however, it is not
yet available in the United States.4,19 Octreotide
and vasopressin are currently the only avail-
able options in the United States.
Vasopressin is a potent splanchnic vaso-
constrictor with the ability to decrease por-
tal pressure and portal venous flow. Although
vasopressin has several beneficial mechanisms,
limiting factors including cardiac, peripheral,
and bowel ischemia, and increased incidence
of arrhythmias, hypertension, and fluid reten-
tion have made it a last-line pharmacological
option for management of UGIB. Concomi-
tant use of nitrates enhances the efficacy and
safety of vasopressin therapy, although the
combined side effect profile reported is greater
than with somatostatin analogues (eg, octreo-
tide) or with terlipressin.4,19 Vasopressin is dosed
at a rate of 0.2 to 0.4 units/min and can be
titrated up to a maximum dose of 0.8 units/
min.4 Nitroglycerin should be given in conjunc-
tion with vasopressin to counter the vasocon-
strictive effects, at a rate of 40 μg/min titrated
to a maximum of 400 μg/min to maintain sys-
tolic blood pressure greater than 90 mm Hg.4
Octreotide is a somatostatin analogue that,
when given at pharmacological doses, offers
benefit in UGIB through inhibition of secretion
of several substances, including serotonin,
gastrin, insulin, and, most importantly, gluca-
gon, which is a vasodilatory peptide, resulting
in splanchnic vasoconstriction and a reduction
in portal venous flow. The inhibition of these
secretions reduces variceal pressure, thereby
improving the ability to gain control of the
variceal hemorrhage.4,19,27 The primary indica-
tion and benefit of octreotide is in the manage-
ment of variceal bleeding. Studies examining
octreotide use in nonvariceal bleeding have
shown no benefit; however, octreotide may be
initiated if the source of bleeding is unknown
or the patient has a questionable history of
alcoholism or cirrhosis.4,18,19,27 Additionally, if
endoscopy is not readily available or the patient
has another issue prolonging time to endoscopic
intervention, octreotide may be an appropri-
ate alternative to initiate in the interim.4,18,19,27
A Cochrane review assessing octreotide therapy
in variceal bleeding found no benefit regard-
ing mortality or risk of rebleeding; how-
ever, significant benefit was shown in
reducing the amount of blood transfused
(roughly one-half unit of blood saved per
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W W W . A A C N A C C O N L I N E . O RG
patient) and the number of patients not
achieving initial hemostasis.28 The authors
concluded that a large trial with thousands
of patients enrolled would be needed to detect
an actual mortality benefit.28 Guidelines cur-
rently recommend an initial IV bolus of 25
to 100 μg followed by a continuous infusion of
25 to 50 μg/h for 2 to 5 days.4,8,19 Octreotide
has a benign adverse effect profile; however,
bradycardia, palpitations, peripheral edema,
hypertension, fatigue, headache, dizziness, and
hyperglycemia may occur with its use.
Antibiotics
Patients with cirrhosis who present with
UGIB are at elevated risk for developing
severe bacterial infections within their ascitic
fluid that may translocate into the blood
and/or other organ systems. These infections
are associated with increased incidence of
recurrent variceal hemorrhage and mortality.
For these reasons, a short course of prophy-
lactic antibiotics should be initiated immedi-
ately to help reduce the risk of death and
the incidence of bacterial infections.4,19,27
Norfloxacin, 400 mg orally twice a day
for 7 days, has been recommended on the
basis of previous studies; however, ceftriax-
one, 1 g IV daily, was compared with nor-
floxacin for this indication and was found
to be superior in preventing bacterial infec-
tions.29 For cirrhotic patients who present
with UGIB, ceftriaxone, 1 g IV, should be
initiated and continued for 7 days.
Helicobacter pylori is a prominent cause
of UGIB resulting from ulcers. Serum testing
for H pylori is recommended during the
acute phase of UGIB; however, caution should
be exercised regarding the validity of the results.
Medications used for treatment of patients
with acute UGIB (antibiotics and PPIs) may
cause false-positive results.17,18 If initial test-
ing results are negative, a second test is rec-
ommended after bleeding cessatin to rule
out a false-negative result. Repeat testing
should be performed at least 2 weeks after
cessation of PPI therapy.17,18 All patients with
a positive test result should receive a repeat
test 1 month after treatment to ensure eradi-
cation of the bacteria. A meta-analysis pub-
lished in 2004 found that H pylori eradication
significantly reduced recurrent bleeding
compared with antisecretory therapy alone.30
A patient with a positive serum result should
be treated with triple therapy: PPI, amoxicillin,
VO L U M E 2 9 • N U M B E R 4 • W I N T E R 2 018
and clarithromycin. In areas with prevalent
antibiotic resistance, quadruple therapy with
a PPI, bismuth subsalicylate, metronidazole,
and tetracycline is recommended.
Conclusion
Although mortality rates remain high for
UGIB, specifically variceal bleeding, no signifi-
cant advances or changes have occured in
the past decade regarding initial resuscitation
and pharmacological management options.
Proton pump inhibitors remain the mainstay
of treatment for patients with UGIB, with the
addition of somatostatin analogues recom-
mended due to variceal bleeding. Histamine
receptor antagonists are not recommended
given available evidence of their inferiority
to PPIs. Helicobacter pylori eradication is
effective and may help reduce the incidence
of recurrent UGIB. Prompt identification and
treatment of UGIB is essential to maximize
patient survival and minimize complications.
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DRUG UPDATE W W W . A A C N A C C O N L I N E . O RG

CE Evaluation Instructions
This article has been designated for CE contact hour(s). The evaluation demonstrates your knowledge of the
following objectives:
1. Distinguish risk factors associated with variceal and nonvariceal acute upper gastrointestinal bleeding.
2. Describe strategies for initial resuscitation of a patient experiencing acute upper gastrointestinal bleeding.
3. Explain appropriate pharmacotherapy options, including mechanisms and dosing strategies, for management of
acute upper gastrointestinal bleeding.
Contact hour: 1.0
Pharmacology contact hour: 0.5
Synergy CERP Category: A
To complete evaluation for CE contact hour(s) for this article #ACC8342, visit www.aacnacconline.org and click the
“CE Articles” button. No CE evaluation fee for AACN members. This expires on December 1, 2021.
American Association of Critical-Care Nurses is an accredited provider of continuing nursing education by the American Nurses
Credentialing Center’s Commission on Accreditation. AACN has been approved as a provider of continuing education in nursing by
the State Boards of Registered Nursing of California (#01036) and Louisiana (#LSBN12).

376
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 Acute Management of Upper Gastrointestinal Bleeding
Whitney Gibson, Nicholas Scaturo and Christopher Allen
AACN Adv Crit Care 2018;29 369-376 10.4037/aacnacc2018644
©2018 American Association of Critical-Care Nurses
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