EM Critical Care

UNDERSTANDING AND CARING FOR

CRITICAL ILLNESS IN EMERGENCY MEDICINE

Resuscitation Of The
Patient With Massive Upper
Gastrointestinal Bleeding

Authors

Ryan G. K. Mihata, MD, MPH, FACEP

Assistant Professor of Emergency Medicine/Critical Care,

Wright State University, Boonshoft School of Medicine,
Dayton, OH

John-Adam Bonk, MD

Department of Emergency Medicine, Wright State University,

Boonshoft School of Medicine, Dayton, OH

Abstract
Managing an unstable patient with massive gastrointestinal bleeding
can be challenging, but effective management can optimize patient
outcomes. These patients require prompt recognition of severe illness, resuscitation and stabilization, and diagnostic and treatment
modalities directed at identification and control of the source of
bleeding. Multiple consultants (including gastroenterology, general
surgery, and interventional radiology) are often required, and early
consultation of these subspecialists can improve morbidity and mortality. Underlying comorbidities add complexity to the management
of the bleeding patient and are associated with increased mortality.
Most cases of massive bleeding are due to an upper gastrointestinal
source, and these patients have a higher mortality rate than those
presenting with lower gastrointestinal bleeding. Common sources of
upper gastrointestinal bleeding include gastric and duodenal ulcers,
esophageal and gastric varices, and erosive esophagitis. Depending
on the source of the bleeding, medical and/or surgical treatment modalities may be required. Utilization of emergent upper endoscopy
and other medical therapies as well as transfusion of blood products
are often necessary to ensure optimal patient outcomes. Knowledge
of the emergency procedures and medications available, as well as
familiarity with the treatment modalities used by consultants, will
help the emergency physician orchestrate the care necessary to ensure patient survival.
Editor-in-Chief

Volume 3, Number 2

Meaghan P. Keville, MD

Department of Emergency Medicine, Wright State University,

Boonshoft School of Medicine, Dayton, OH
Peer Reviewers

Michelle Lin, MD

Associate Professor of Clinical Emergency Medicine,

University of California San Francisco; San Francisco
General Hospital and Trauma Center, San Francisco, CA

John L. Westhoff, II, MD, MPH, FACEP

Deputy Commander for Clinical Services, U.S. Army Public

Health Command Region-Pacific; Staff Emergency Physician,
U.S. Naval Hospital, Yokosuka, Japan
Guest Editor

Catherine A. Gogela Carlson, MD

Critical Care Medicine Fellow, Departments of Critical Care

Medicine and Emergency Medicine, University of Pittsburgh
Medical Center, Pittsburgh, PA
CME Objectives
Upon completion of this article, you should be able to:
1.
2.
3.
4.

Describe the differential diagnosis of massive GI

bleeding.

Discuss the importance of the resuscitation of patients

with massive GI bleeding.
List the available medical and surgical therapeutic
options for patients with massive GI bleeding.

Apply a standardized approach to the management of

massive GI bleeding.
Prior to beginning this activity, see the back page for faculty
disclosures and CME accreditation information.

Andy Jagoda, MD, FACEP

Julie Mayglothling, MD
Professor and Chair, Department
Assistant Professor, Department
of Emergency Medicine, Mount
of Emergency Medicine,
Sinai School of Medicine; Medical
Department of Surgery, Division
Lillian L. Emlet, MD, MS, FACEP
Director, Mount Sinai Hospital, New
of Trauma/Critical Care, Virginia
Assistant Professor, Department of
York, NY
Commonwealth University,
Critical Care Medicine, Department
Richmond, VA
of Emergency Medicine, University
of Pittsburgh Medical Center;
William A. Knight, IV, MD, FACEP
Program Director, EM-CCM
Assistant Professor of Emergency Christopher P. Nickson, MBChB,
Fellowship of the Multidisciplinary
Medicine, Assistant Professor of
MClinEpid, FACEM
Associate Editor
Critical Care Training Program,
Neurosurgery, Medical Director Senior Registrar, Intensive Care
Pittsburgh, PA
Emergency Medicine Mid-Level
Scott Weingart, MD, FACEP
Unit, Royal Darwin Hospital,
Provider Program, Associate
Associate Professor, Department of
Darwin, Australia
Medical Director of Neuroscience
Emergency Medicine, Mount Sinai Michael A. Gibbs, MD, FACEP
ICU, University of Cincinnati
School of Medicine; Director of
Professor and Chair, Department
Jon Rittenberger, MD, MS, FACEP
College of Medicine, Cincinnati,
Emergency Critical Care, Elmhurst
of Emergency Medicine, Carolinas
Assistant Professor, Department
OH
Hospital Center, New York, NY
Medical Center, University of North
of Emergency Medicine,
Carolina School of Medicine,
University of Pittsburgh School
Chapel Hill, NC
Haney Mallemat, MD
of Medicine; Attending Physician,
Editorial Board
Assistant Professor, Department
Emergency Medicine and Post
Benjamin S. Abella, MD, MPhil,
of Emergency Medicine, University
Robert Green, MD, DABEM,
Cardiac Arrest Services, UPMC
FACEP
of Maryland School of Medicine,
Presbyterian Hospital, Pittsburgh,
FRCPC
Assistant Professor, Department
Baltimore, MD
PA
Professor, Department of
of Emergency Medicine and
Anaesthesia, Division of Critical
Department of Medicine /
Evie Marcolini, MD, FAAEM
Care Medicine, Department of
Section of Pulmonary Allergy
Assistant Professor, Department of
Emergency Medicine, Dalhousie
and Critical Care, University of
Emergency Medicine and Critical
University, Halifax, Nova Scotia,
Pennsylvania School of Medicine;
Care, Yale School of Medicine,
Canada
Clinical Research Director,
New Haven, CT
Robert T. Arntfield, MD, FACEP,
FRCPC, FCCP
Assistant Professor, Division
of Critical Care, Division of
Emergency Medicine, Western
University, London, Ontario,
Canada

Center for Resuscitation Science,

Philadelphia, PA

Emanuel P. Rivers, MD, MPH, IOM

Vice Chairman and Director
of Research, Department of
Emergency Medicine, Senior
Staff Attending, Departments of
Emergency Medicine and Surgery
(Surgical Critical Care), Henry
Ford Hospital, Clinical Professor,
Department of Emergency
Medicine and Surgery, Wayne State
University School of Medicine,
Detroit, MI
Isaac Tawil, MD, FCCM
Assistant Professor, Department
of Anesthesia and Critical Care /
Department of Emergency Medicine,
Director, Neurosciences ICU,
University of New Mexico Health
Science Center, Albuquerque, NM

Research Editor
Amy Sanghvi, MD
Department of Emergency
Medicine, Mount Sinai School of
Medicine, New York, NY

Case Presentation
You receive a medic call for a 45-year-old male who called
911 for massive hematemesis. The medics report that the
patient is an alcoholic who has been binge drinking since
losing his job 1 week ago. He has vomited a large amount
of frank blood twice. He is hypotensive, with a MAP of 50
mm Hg and a pulse of 128 beats per minute. EMS personnel have established a peripheral IV line and are infusing
normal saline as fast as possible; they are 5 minutes out.
After you page the gastroenterologist and ask the unit secretary to activate your institutions massive transfusion
protocol, you consider the potential causes of massive GI
bleeding, the available therapeutic options, and the interventions you should undertake in the next few minutes to
improve this critically ill patients chance for survival

Introduction
Providing optimal care in the emergency department (ED) for patients with massive gastrointestinal (GI) bleeding requires coordination of multiple
consultants as well as knowledge of both medical
and surgical therapeutic options. For the purposes
of this review, massive GI bleeding is defined as
bleeding in a patient that has resulted in hemodynamic instability, with signs and symptoms consistent with hemorrhagic shock and evidence of either
hematemesis or hematochezia. In order to provide
initial resuscitation in the ED (either as a bridge to
continued resuscitation in the intensive care unit
or to diagnostic/therapeutic interventions in the
operating room or interventional radiology), emergency physicians must be familiar with the wide
variety of both diagnostic and therapeutic options as
well as the underlying pathophysiology for massive
GI hemorrhage. The majority (> 75%) of massive
GI bleeding cases are due to an upper GI source.1
Mortality rates for patients with massive GI bleeding
range from 20% to 39%.2 Treatment options depend
upon the underlying cause of the bleeding, and
early intervention can mean the difference between
survival and death. This issue of EMCC provides an
overview of the current evidence for the treatment of
patients with massive upper GI bleeding.

Critical Appraisal Of The Literature

A literature search of PubMed, Ovid MEDLINE, and
the Cochrane Library was performed using the following keywords: GI bleeding, severe GI bleeding, upper
GI bleeding, and variceal bleeding treatment. The search
focused only on literature in the English language for
adult patients. More than 100 articles were reviewed,
which provided the background information and
basis for further literature review. Additionally, both
national and international guidelines as well as the
Cochrane Database of Systematic Reviews were

EMCC 2013 2

searched for guidelines for the acute treatment of

severe GI bleeding. Table 1 summarizes the current
guidelines related to GI bleeding.3-6 The literature
review and these guidelines suggest a general consensus about the importance of early evaluation and
resuscitation in the ED as well as early involvement
of appropriate consultants in order to avoid negative
outcomes in patients with massive GI bleeding.

Etiology And Pathophysiology

The presence of GI bleeding with evidence of hemorrhagic shock requires prompt identification of the
bleeding source. The most common etiologies of
upper GI bleeding include: duodenal ulcers (28%),
gastric ulcers (26%), gastritis (13%), varices (12%),
and esophagitis (8%).1 GI bleeding due to esophageal or gastric varices and peptic ulceration carry
the highest mortality.2 Exclusion of other bleeding
sources (such as pulmonary or intranasal sources)
is important. As with management of all cases of
undifferentiated hypotension, initiation of resuscitation based on hemodynamic decompensation should
not be delayed, regardless of the underlying source
of the bleeding.

Treatment
Stabilization And Monitoring

Initial resuscitation of patients with massive GI bleeding involves restoration of intravascular volume in
order to achieve the relative hemodynamic stability
required to proceed with diagnostic and therapeutic
interventions. An initial primary survey to evaluate
the airway, breathing, and circulation should almost
always include endotracheal intubation in order to
protect the patients airway in the setting of active
hemorrhage and to assist in identifying the bleeding
source and facilitating these additional interventions.
Early resuscitation may start with 2 large-bore peripheral intravenous (IV) catheters, but resuscitation
of massive hemorrhage may be aided by the use of
larger, introducer-sized central venous catheters that
can more efficiently restore lost intravascular volume
during hemorrhagic shock.

The importance of early mobilization of specialists cannot be overemphasized. In patients with
massive GI bleeding, medical therapy alone is
unlikely to be sufficient to achieve hemostasis. Early
mobilization of the available subspecialists expedites time to definitive therapy. The lack of available
subspecialty support should prompt consideration
for transfer to a tertiary care facility that can provide
this care. Depending on the underlying cause of the
bleeding as well as patient comorbidities, gastroenterology, general surgery, and interventional radiology may all play a role in the care of these patients.
www.ebmedicine.net Volume 3, Number 2


Patients with massive GI bleeding require continuous cardiac and pulse oximetry monitoring, with
frequent blood pressure checks. Central venous access
may be required in the ED if the patient has poor peripheral access or if more the rapid infusion of fluids
or blood products is needed. Invasive monitoring,
including an arterial line, will enable prompt recognition and response to the rapid changes in physiology
that may occur in massive GI hemorrhage.

Initial laboratory values can help guide initial
therapy, but serial coagulation studies in the ED are
not likely to aid in decision making and may be difficult to interpret in patients being treated with fresh
frozen plasma (FFP), cryoprecipitate, or factor concentrate. Likewise, an initial D-dimer may offer prognostic information, but it should not influence immediate
management in the acute setting.

Regardless of the source of upper GI bleeding,
proton-pump inhibitors (PPIs) are typically recommended until the etiology of the bleeding can be
identified. While PPIs will not impact the immediate stabilization of a hemodynamically unstable
bleeding patient, their use may improve outcomes.

In cases of nonvariceal hemorrhage, a bolus of a

PPI should be initiated and then followed by a
continuous infusion. This is thought to promote
ulcer healing and decrease the rate of rebleeding.7
Additionally, in cases of variceal hemorrhage with
subsequent endoscopic intervention, patients who
are given PPIs intravenously have demonstrated less
rebleeding8 because PPIs work against stomach acid
and pepsin, which are thought to destabilize platelet
plugs and the hemostatic clot.9-11

Procedural Therapies

Endoscopy
Endoscopy is an important diagnostic and therapeutic tool for upper GI hemorrhage and should
be performed promptly upon patient stabilization.
Endoscopy provides definitive therapy in many
cases. The gastroenterologist may employ various
endoscopic techniques, including clips, banding,
thermocoagulation, or sclerosant injection with or
without epinephrine. All patients with massive GI
bleeding should be intubated to facilitate endoscopy, control the airway, reduce the risk of aspira-

Table 1. Current Guidelines For Gastrointestinal Bleeding

Organization

Topic

Type of Guideline

Recommendations

American College of
Physicians

Management of patients
with nonvariceal upper
GI bleeding3

Consensus

1. Early evaluation, resuscitation, and risk stratification is recommended.

2. Nasogastric tube placement may have diagnostic value.
3. Transfuse PRBCs to maintain hemoglobin > 7 gm/dL.
4. Correction of coagulopathy is recommended but should not delay
endoscopy.
5. Pre-endoscopic PPIs may be considered.
6. Early endoscopy (within 24 h) is recommended.
7. Histamine-2 receptor antagonists are not recommended for patients
with acute bleeding due to a gastric or duodenal ulcer.
8. Somatostatin and octreotide are not routinely recommended for
patients with acute ulcerative bleeding.

Cochrane Library

Pharmacologic management of patients with GI

bleeding4,5

Systematic review

1. Somatostatin analogues do not reduce mortality in variceal GI

bleeding; however, they may reduce the need for blood transfusion
by 0.5 units.
2. PPI administration prior to endoscopy for upper GI bleeds significantly reduces the number of patients with recurrent serious
bleeding and the need for endoscopic intervention, but they have no
effect on the need for surgery or risk of death.

Scottish Intercollegiate
Guidelines Network

Guidelines for initial treatment of patients with

significant GI bleeding6

Systematic review

1. PRBC transfusion should be considered after loss of 30% of the

circulating blood volume.
2. PPIs should not be used prior to endoscopic diagnosis in patients
presenting with an acute upper GI bleed.
3. Early endoscopic examination should be undertaken within 24 h of
initial presentation, if possible.
4. Prior to endoscopic diagnosis, terlipressin (vasopressin analogue)
should be given to patients suspected of variceal hemorrhage.
5. Antibiotic therapy should be initiated in patients with chronic liver
disease who present with acute upper GI bleeding.
6. Balloon tamponade should be considered as a temporizing measure to gain hemostasis in uncontrolled variceal hemorrhage.

Abbreviations: GI, gastrointestinal; PPI, proton-pump inhibitor; PRBC, packed red blood cell.

www.ebmedicine.net Volume 3, Number 2

EMCC 2013

tion, and improve patient safety during treatment.

Airway management in severe upper GI bleeds can
be technically challenging due to poor visualization.
A topic within itself that cannot be covered in this issue, extra personnel and airway adjuncts (including
2 suction catheters) is advisable for airway management of this population.
Balloon Tamponade
Balloon tamponade may be required if endoscopy is
either not available or not successful in achieving hemostasis. Insertion of a balloon tamponade device is
a rare but potentially life-saving procedure. It can be
used as a temporary rescue device by providers who
practice in a setting where specialty consultation is
not readily available. Use of a balloon-tamponade
device is associated with a high risk of rebleeding
upon balloon deflation. Its most lethal complication
is esophageal necrosis and rupture.

There are several different types of commercially
available devices for balloon tamponade. The 3 most
common include the Sengstaken-Blakemore, the
Minnesota tube, and the Linton-Nachlas tube.12 (See
Figure 1.) Each of these tubes varies slightly based
on the number of lumens and balloons. Providers
should be familiar with the specific device used at
their institution. The following is a general guide for
their use:
1. Prior to insertion, secure the airway.
2. After applying a lubricant to the tube, insert the
tube through the mouth or nostril to a depth of
at least 50 cm, depending upon the height of the
patient.
3. After evaluation by air injection, confirm placement in the stomach with radiography. (The balloon should NOT be inflated until its location is
verified radiographically so as to avoid potential
complications associated with malpositioning of
the tube.)
4. Inflate the gastric balloon (approximately 400500 mL of air), and clamp the inlet.
5. Retract the tube until resistance is felt (the balloon at the gastroesophageal junction). Tension
must be maintained on the tube in order to
produce the tamponade effect.
6. If gastric balloon tension is not sufficient to stop
the hemorrhage, inflate the esophageal balloon
(25-30 mm Hg). This pressure must be checked
frequently, as overinflation can lead to esophageal necrosis.

It is important to remember that these are temporizing devices intended for short-term use and are
not definitive therapy. In some situations, the patient
may need to be transferred to another facility for
definitive care.

Additional Procedural Therapies

In severe cases of massive GI bleeding, where urgent endoscopy is unable to provide a diagnosis or
therapy, urgent or emergent angiography can be
performed to identify the location of the hemorrhage.
Angiography is indicated in patients with nonvariceal
upper GI bleeding when medical management and
endoscopic therapy have failed to control the bleeding. Angiographic intervention should be considered
as an alternative to surgery in patients who are high
risk for more invasive surgical intervention.13 Angiography can detect bleeding at rates of at least 0.5 mL/
min with 100% specificity and variable sensitivity
(based on the rate).14 During angiography, lesions
can be treated by use of vasopressin or transcatheter
embolization.

Another option for identifying the source of
bleeding is radionuclide imaging, which can detect bleeding occurring at slower rates than can be
detected by angiography. The primary purpose of
these studies is to localize the source of the bleeding and to facilitate surgical intervention. An emergency surgical consult should be sought in patients
with massive hemorrhage who cannot be stabilized
in the ED, who have contraindications to endoscopy, or who have peritoneal signs on examination
(which can occur from a ruptured peptic ulcer).
While surgery is typically only considered as a last
resort after medical, endoscopic, and interventional
radiology approaches have been exhausted or are
contraindicated, not all types of bleeding (such as
variceal bleeding) are amenable to surgical intervention. Nonetheless, early involvement of surgery and
gastroenterology services can facilitate a cooperative
treatment approach and may make surgical intervention, if necessary, safer and less emergent.

Pharmacologic Therapies

There are multiple proposed pharmacologic treatments for the management of acute upper GI bleeding. Understanding the mechanism of action of these

Figure 1. Minnesota Tube For Balloon

Tamponade

Note both the gastric and esophageal balloons. Types of tubes vary
slightly. Be familiar with the type available in your institution.
Image courtesy of Ryan G. K. Mihata, MD

EMCC 2013 4

www.ebmedicine.net Volume 3, Number 2

bleeding from esophageal varices.4 Some data suggest that the combination of these medications with
upper endoscopy may be beneficial.

Given their relatively low-risk side-effect profiles, the use of these medications can be considered
in patients with acute hemorrhage that is possibly
caused by variceal bleeding.16

medications can facilitate a deeper understanding of

the rationale for the existing guidelines for their use.
Proton Pump Inhibitors
PPIs, which include omeprazole, pantoprazole, and
esomeprazole, are considered to be a mainstay of
early therapy for acute GI bleeding in the ED. PPIs
suppress gastric acid stimulation by inhibiting the parietal cell H+/K+ ATPase (adenosine triphosphatase)
pump. One potential benefit of the early use of PPIs
may be the reduction of hemorrhage during endoscopy.3,5 Additionally, PPIs may create a more optimal
environment for the stabilization of blood clots by
neutralizing the intraluminal gastric acid that would
otherwise serve to promote continued bleeding.9

There has been concern about the potential
increased risk of thrombotic stroke or myocardial
infarction with the addition of PPIs to long-term
clopidogrel therapy. Based on cohort studies, a 2009
United States Food and Drug Administration warning cited a 50% increased risk of these complications
when PPIs and clopidogrel were taken concurrently.15
However, current data are inconclusive and suggest
that these complications are typically associated with
long-term use of PPIs and clopidogrel. These risks
have not yet been described in the acute, short-term
use of these medications during the stabilization of
patients with massive GI bleeding.

At this time, guidelines continue to encourage the
use of PPIs (either before or immediately following
upper endoscopy) in patients with undifferentiated
upper GI bleeding.3 However, there has not yet been
a study showing a statistical improvement in the rate
of rebleeding, the need for surgical intervention, or
mortality from their use. Nonetheless, their cost effectiveness and excellent safety profile make the benefit
of giving these agents greater than the potential risks,
particularly in high-risk patient populations.

Vasopressin
A third class of pharmacologic agents, vasopressin
and its analogues, can reduce portal hypertension by
causing systemic and splanchnic vasoconstriction.

Much like somatostatin, the use of vasopressin
in the management of upper GI bleeding is controversial. The risks (eg, myocardial infarction, arrhythmias, mesenteric ischemia, peripheral soft tissue necrosis, cardiac arrest) of using this medical therapy
are similar tobut usually less severe thanthose
seen with the use of other vasopressor medications.
In patients with variceal bleeding, adding nitroglycerin to vasopressin therapy appears to decrease
systemic complications from the use of vasopressin
alone while not affecting the efficacy of the vasopressin.17,18 In patients with massive GI bleeding, the
risk of systemic vasoconstriction and the potential
for end-organ ischemia must be weighed against
the potential benefit of splanchnic vasoconstriction,
which can help to achieve hemostasis in the actively
bleeding patient.

In spite of the potential deleterious effects of
vasopressin, use of vasopressin (or vasopressin plus
nitroglycerin) in a patient in extremis due to massive
GI bleeding may be justified.

Blood Product Transfusion

The goal of blood product transfusion for acute

bleeding is to replace the blood cells and coagulation
factors that are being lost. Whole blood is a complex
heterogeneous solution that serves 3 basic functions: (1) to maintain intravascular volume, (2) to
provide oxygen-carrying capacity, and (3) to provide
the coagulation factors that are required to reverse
coagulopathy and to assist in achieving (and maintaining) hemostasis. The ability to achieve hemostasis
can be complicated by the use of anticoagulation or
antiplatelet agents. Because there are inherent risks
involved with transfusing blood products, the risks
must be considered along with the potential benefits
for each individual patient.

Goal #1: Provide Intravascular Volume Resuscitation

Prompt volume resuscitation with IV crystalloid
fluids should be initiated in a bleeding, hypotensive
patient in order to achieve a perfusing mean arterial
pressure (MAP) until blood products are available.
Given that it lacks oxygen-carrying capacity and
does not replenish clotting factors, the role of crystalloid fluid for volume resuscitation should ideally

Somatostatin
Somatostatin and its analogues (including octreotide and vapreotide) represent another class of
pharmacologic agents that may be used early in the
management of acute GI bleeding due to a suspected variceal source. Somatostatin (also known as
growth-hormone-inhibiting hormone) suppresses
the release of GI hormones such as gastrin, cholecystokinin, motilin, and secretin. The secondary
effects of blocking the release of these hormones
include a reduction of portal venous blood flow
due to splanchnic vasoconstriction and subsequent
decreased GI bleeding.

To date, there are minimal data regarding the
use of somatostatin or its analogues for nonvariceal
upper GI bleeding. The data on their use in severe
variceal bleeding are also mixed. A Cochrane review
found no significant change in mortality, the rebleeding rate, or the number of units of blood transfused
with the use of somatostatin in patients with acute
www.ebmedicine.net Volume 3, Number 2

EMCC 2013

be restricted to this early phase of resuscitation in a

bleeding patient. In cirrhotic patients with suspected
variceal hemorrhage, excessive crystalloid resuscitation may be particularly harmful due to their susceptibility to extravascular fluid shifts in the setting of
underlying low intravascular oncotic pressure.

In patients with massive GI bleeding (especially
those with hemoglobin < 8.0 gm/dL, coagulopathy,
or persistent hypotension despite volume infusion),
the use of blood products (such as PRBCs) is important in order to restore hemodynamic stability
and to achieve hemostasis. However, transfusion of
PRBCs alone is not sufficient because they do not
contain the required coagulation factors. For this
reason, PRBCs should be accompanied by FFP and/
or platelets. The military literature on traumatic blood
loss recommends a PRBC:FFP:platelet ratio approaching 1:1:1.19,20 Other sources disagree on the exact
ratio, citing a lack of a specific survival benefit to a
higher PRBC to FFP ratio.21 Many large centers have
massive transfusion protocols that allow the rapid
release of blood products in varying ratios. While the
survival benefit remains unclear, most protocols have
PRBC:FFP:platelet ratios near 1:1:1.

Goal #2: Optimize Oxygen-Carrying Capacity

The goal of improving oxygen-carrying capacity by
transfusing PRBCs is to ensure sufficient oxygen
delivery to the tissues in order to prevent endorgan ischemia and secondary dysfunction. Clinical
signs and symptoms of decreased oxygen delivery
can include:
Decreased level of consciousness
Evidence of cardiac ischemia (as shown by electrocardiographic changes or troponin elevation)
Increasing serum lactate
Decreased central venous oxygen saturation
(ScvO2)

The International Consensus guidelines recommend maintenance of hemoglobin levels between 7
and 8 gm/dL.3 However, there are no randomized
controlled trials to suggest an exact hemoglobin goal
for transfusion. Target hemoglobin levels should be
individualized for each patient and should be based
upon the suspected etiology of the bleed (ie, variceal
vs nonvariceal hemorrhage) as well as patient comorbidities. In the setting of ongoing massive bleeding,
the recommended hemoglobin level of 7 to 8 gm/dL
should not be considered to be an endpoint of resuscitation. Instead, a MAP of > 60 mm Hg and evidence
of adequate end-organ perfusion should be the target.

Though the International Consensus guidelines
suggest maintenance of hemoglobin between 7 and
8 gm/dL, patients with certain comorbidities may
require greater hemoglobin goals. For instance,
evidence suggests that patients with suspected active
ischemic coronary artery disease may benefit from
a target hemoglobin closer to 10 gm/dL to support

EMCC 2013 6

myocardial oxygen delivery.22 However, for patients

with suspected variceal bleeding (even with concomitant coronary artery disease), consider keeping
the hemoglobin goal to between 7 and 8 gm/dL until
hemostasis is achieved, as the additional blood volume required to achieve this higher target may lead
to increased portal pressure and worsening bleeding
or rebleeding.

When there is a need for emergent transfusion
of PRBCs for acute blood loss anemia with signs of
hypovolemic shock, O-negative PRBCs (or O-positive
PRBCs in women past childbearing age and in men)
can be given until type-specific crossmatched blood is
available. For patients requiring massive transfusion
of blood products, it is important to remember that the
transfusion will have metabolic complications such as
depletion of intravascular cations due to chelation by
the sodium citrate used to anticoagulate blood components during storage. Citrate is primarily metabolized
by the liver, so in cirrhotic patients receiving massive
transfusion, this effect may be more profound. For
these patients, consider giving calcium replacement
(calcium gluconate 1-2 g IV or calcium chloride 0.5-1
g IV per 500 mL of transfused blood). Magnesium can
also be affected, and low levels have unwanted side
effects and should be repleted as necessary, keeping
in mind that overly rapid infusion of magnesium can
exacerbate hypotension.

Goal #3: Reverse Coagulopathy

Treatment of coagulopathy can be tailored to its
likely or known etiology. Coagulopathy may arise
due to an underlying chronic disorder, but it may
also be caused by metabolic acidosis due to tissue
hypoxemia in the setting of acute hypotension.

To reverse coagulopathy, consider an initial
transfusion of 10 mL/kg of FFP. Prothrombin
time (PT)/international normalized ratio (INR),
partial thromboplastin time (PTT), platelet count,
and fibrinogen levels can be used to guide patient
management. While there are no specific guidelines,
keeping the platelet count > 50,000/mm3, PTT
< 60 seconds, and INR < 1.8 is common practice and
is recommended by the authors. Because D-dimer
levels have been shown to be inversely related to
prognosis in upper GI bleeding, a D-dimer may be
drawn as a prognostic marker, but it has no role in
guiding intervention.23 If available, the thromboelastography (TEG) test can evaluate platelet function
and coagulation and may be more efficient to direct
the type of transfusion products necessary.

The role of recombinant activated factor VII
(rFVIIa) is continuing to evolve. While it may be
useful in certain situations (eg, when a patient is
on a direct thrombin inhibitor), it is expensive, it
carries the risk of thromboembolic complications,
and studies of its use have had conflicting results. A
prospective randomized trial of 245 patients found
no benefit with rFVIIa over standard therapy for
www.ebmedicine.net Volume 3, Number 2

nonvariceal upper GI bleeding.24 However, a small

uncontrolled study suggested that, in patients with
liver disease and an increased INR refractory to FFP
therapy, rFVIIa was effective in stopping bleeding
and normalizing the INR.25 Similarly, a study of patients with moderate to severe cirrhosis showed that
administration of rFVIIa in addition to endoscopic
hemostatic strategies decreased rebleeding rates.26
Due to the conflicting nature of the literature, use of
rFVIIa in patients with massive GI bleeding is not
routinely recommended.

It should be noted that, although the transfusion of blood products is indicated in patients with
massive GI bleeding, it is associated with some
risks. The lethal triad of hypothermia, coagulopathy, and acidosis must be addressed in order to
prevent clinical deterioration. (See Figure 2.) Use
warmed fluids, warmed blankets, and other passive external rewarming measures as needed to
maintain normothermia.

rate of 1 mg/min is necessary to achieve a sustained

reversal of the INR; however, it is insufficient when
given as a single agent, as it has an onset of action of
2 to 6 hours and requires up to 24 hours to achieve a
complete response.27 For this reason, FFP must also
be administered.

Although controversial, rFVIIa can be considered for reversal of effects of warfarin. However,
it is expensive, it has minimal proven therapeutic
benefit for warfarin reversal, it is not FDA approved for this use, and its use may cause thrombotic complications.24-26

Dabigatran: Dabigatran (Pradaxa) is a direct
thrombin inhibitor. To quantify the degree of
dabigatran coagulopathy, obtain a PTT and
thrombin time (if rapidly available).28 PT/INR is not
useful in assessing dabigatran coagulopathy. The
PTT is only useful to qualitatively assess the degree
of coagulopathy because it lacks sufficient sensitivity
with therapeutic dabigatran levels. A very high PTT
value should be confirmed by another method (eg,
thrombin time),28 although this may be impractical
in the emergent setting. Like other anticoagulant
medications, even therapeutic levels may require
reversal in the setting of active bleeding.

At this time, an evidence-based reversal strategy
for dabigatran is not available. Many institutions
have a pathway for bleeding patients who are on
dabigatran that may inform local practice patterns.
Management strategies may range from expectant
management to aggressive use of blood products,
including FFP and even hemodialysis.

Reversal Of Medically Induced Coagulopathy

Warfarin: Warfarin (Coumadin, Jantoven)

inhibits vitamin K-dependent coagulation factor

synthesis. Prothrombin complex concentrates
(PCCs) should be the first-line treatment in a
patient who is on warfarin. PCCs do not require
crossmatch and act more quickly than FFP alone;
however, because PCCs in the United States do
not contain significant amounts of factor VII,
FFP must also be administered. Dosages are
individually calculated based on weight and
desired factor IX level; 1 unit/kg will increase the
factor IX level approximately 1%.

If PCCs are not available, coagulopathy can be
reversed by discontinuing warfarin therapy and
administering vitamin K. Vitamin K at a dose of 5
to 10 mg diluted in D5W or D5 saline infused at a

Rivaroxaban: Rivaroxaban (Xarelto) is a factor

Xa inhibitor. Administer PCCs for reversal of

rivaroxaban; if PCCs are not available, consider
administration of FFP.29

Figure 2. Coagulopathy Chart

Hemorrhage

Hypothermia

Tissue damage

Fluid replacement

Acidosis

Shock

Dilution

Coagulopathy

Hypoperfusion

Inflammation

Consumption of platelets and clotting

factors

Hyperfibrinolysis

Reprinted from: Cherkas D. Traumatic Hemorrhagic Shock: Advances In Fluid Management. Emerg Med Pract. 2011;13(11):1-20.
Copyright 2011 EB Medicine.

www.ebmedicine.net Volume 3, Number 2

EMCC 2013

Clinical Pathway For The Initial Management Of

Patients With Massive Upper Gastrointestinal Bleeding
Initial actions: insert 2 large-bore IVs (Class I); establish monitoring
(Class I); provide a PPI bolus & drip (Class I); consider insertion of
a nasogastric tube (Class II); provide a crystalloid bolus (Class II);
and keep the patient warm (Class II)

YES

Are there signs of altered mental status and/or

active hematemesis?

Intubate (Class II)

NO

Are there signs or symptoms of shock?

NO

YES
Transfuse PRBCs, FFP, and platelets (Class II)

Is there a history of esophageal varices or signs of cirrhosis?

NO

YES
Administer:
Octreotide 50-mcg bolus and 50-mcg/h infusion (Class II)
and
Ciprofloxacin 400 mg bid (Class I) or ceftriaxone 1g IV qd (Class II)

Perform labs: CBC with differential, BMP, LFTs, PT/PTT, ECG, CXR
Consider: D-dimer, lactate, ABG

Coagulopathy (INR > 1.7

with active bleeding)
Transfuse 2 units FFP (Class II)
If there is severe liver disease with coagulopathy and refractory
bleeding, consider PCCs or rFVIIa (Class II)
If the patient is taking warfarin, add vitamin K 10 mg slow IV
push (Class II)

Anemia

If hemoglobin < 7.0 gm/dL: transfuse PRBCs (Class II)

If hemoglobin > 8.0 gm/dL (or with bleeding varices): do not
transfuse PRBCs (Class II)

Abbreviations: ABG, arterial blood gas; bid, two times a day; BMP, basic metabolic panel; CBC, complete blood count; CXR, chest x-ray; ECG, electrocardiogram; FFP, fresh frozen plasma; INR, international normalized ratio; IV, intravenous; LFT, liver function test; PCCs, prothrombin complex
concentrates; PPI, proton-pump inhibitor; PRBCs, packed red blood cells; PT, prothrombin time; PTT, partial thromboplastin time; qd, 1 time a day;
rFVIIa, recombinant activated factor VII.

Class Of Evidence Definitions

Each action in the clinical pathways section of EM Critical Care receives a score based on the following definitions.
Class I
Always acceptable, safe
Definitely useful
Proven in both efficacy and
effectiveness

Level of Evidence:
One or more large prospective
studies are present (with rare
exceptions)
High-quality meta-analyses
Study results consistently positive and compelling

Class II
Safe, acceptable
Probably useful

Level of Evidence:
Generally higher levels of
evidence
Non-randomized or retrospective studies: historic, cohort, or
case control studies
Less robust randomized controlled trials
Results consistently positive

Class III
May be acceptable
Possibly useful
Considered optional or alternative treatments

Level of Evidence:
Generally lower or intermediate
levels of evidence
Case series, animal studies,
consensus panels
Occasionally positive results

Indeterminate
Continuing area of research
No recommendations until
further research

Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent, contradictory
Results not compelling
Significantly modified from: The
Emergency Cardiovascular Care
Committees of the American
Heart Association and represen-

tatives from the resuscitation

councils of ILCOR: How to Develop Evidence-Based Guidelines
for Emergency Cardiac Care:
Quality of Evidence and Classes
of Recommendations; also:
Anonymous. Guidelines for cardiopulmonary resuscitation and
emergency cardiac care. Emergency Cardiac Care Committee
and Subcommittees, American
Heart Association. Part IX. Ensuring effectiveness of communitywide emergency cardiac care.
JAMA. 1992;268(16):2289-2295.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patients individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2013 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

EMCC 2013 8

www.ebmedicine.net Volume 3, Number 2

Unfractionated Heparin: Unfractionated heparin acts

The foundation of the resuscitation includes
initial management of the airway, breathing, and
circulation. Volume resuscitation requires crystalloid fluids and transfusion of blood products. Early
consultation with gastroenterology, interventional
radiology, and general surgery will improve the
patients time to definitive care. Endoscopy should be
performed promptly upon stabilization. In addition
to volume resuscitation, medical therapies such as
PPIs, somatostatin and its analogues, and vasopressin
should be considered either empirically based upon
hemodynamic stability of the patient or directed at
the underlying etiology of the bleeding, if known.
Surgical intervention may ultimately be necessary if
less-invasive treatments fail or are contraindicated.
Depending on the clinical scenario, balloon tamponade may be needed as a temporizing and life-sustaining measure until the resources required for definitive
therapy become available.

at multiple sites in the clotting cascade and serves as

a catalyst for clotting factors. Administer protamine
sulfate to reverse heparin.

Clopidogrel: Clopidogrel (Plavix) is a nonreversible
platelet inhibitor. Empiric transfusion of platelets
can be considered for patients on clopidogrel or
other platelet inhibitors (such as aspirin), although
no randomized controlled trials have demonstrated
a favorable impact with this approach.

Special Circumstances
When treating a patient who refuses blood based
on religious beliefs (eg, Jehovahs Witnesses), it
is important to ask the patient or legal guardian
whether they are willing to receive blood products. Even though the patient may be a Jehovahs
Witness, it is important to carefully establish and
document the patients current medical wishes. In a
small case study, investigators found a portion of a
Jehovahs Witness congregation who would accept
blood transfusions because they disagreed with the
official doctrine.30 Further, The Watchtower, a legal
organization of the Jehovahs Witnesses, asserts with
respect to blood transfusion: Ultimately, you (the
patient or the parent) must decide. Because your (or
your childs) body, life, ethics, and relationship with
God are involved.31 Regardless of the patients or
power of attorneys decision, carefully document
conversations about risk and benefit as well as the
subsequent management based on that decision.

Case Conclusion
The critically ill 45-year-old male patient arrived to your
resuscitation bay with vital signs that were unchanged
from the prehospital report. You made a decision to intubate
the patient in order to protect his airway and to facilitate
anticipated upper endoscopy. Shortly after intubation,
the patient continued to have frank blood coming from his
oropharynx. The nurses established a second large-bore
peripheral IV, and emergency release blood was given. Each
large-bore peripheral IV had blood infusing, and the initial
hemoglobin came back at 5.8 gm/dL. You ordered 4 more
units of type-specific blood as well as 2 units of FFP and 2
single-donor units of platelets, and you subsequently placed
an introducer catheter to expedite large volume infusion of
blood products via a level 1 infuser, which warmed the infusing fluid. The gastroenterologist came and performed an
endoscopy in the ED, during which he attempted to band
the large esophageal varices. He was uncertain whether or
not he was able to obtain complete hemostasis during the
procedure. The patient initially improved with your resuscitation but continued to have a MAP in the 50s and a
pulse rate in the 120s. You administered an octreotide bolus
and infusion as well as a PPI infusion. In consultation with
your intensivist team, you started a vasopressin drip with
a goal MAP of > 60 mm Hg. This improved not only the
variceal bleeding but also the patients hemodynamic stability. In total, the patient required 4 more units of PRBCs
and 2 more units of FFP. He was admitted to the ICU,
where the gastroenterologist repeated an endoscopy and
found less blood but 2 more bleeding varices, which were
subsequently banded. The patient developed renal failure
and liver failure (acute on chronic) with ischemic hepatitis
secondary to hemorrhagic shock. He had a prolonged course
in the ICU but eventually improved and was ultimately
discharged from the hospital.

Disposition
Most patients who present to the ED with massive
GI bleeding will ultimately require admission to the
intensive care unit, although this will depend on the
success of early intervention and the clinical stability
of the patient. Consideration should be made early
for involvement of subspecialists. Facilities without
gastroenterology, general surgery, or interventional
radiology backup should have a rapid interfacility
transfer protocol in place to expedite patient transfer
to a facility capable of providing the definitive management that will be needed after the initial resuscitation and stabilization.

Summary
The unstable patient with massive upper GI bleeding is a high-risk case for the emergency physician, requiring the coordination of resources and
consideration of various treatment modalities.
Initial resuscitation efforts should occur concomitantly, with diagnostic measures aimed at finding
the etiology of the bleed.
www.ebmedicine.net Volume 3, Number 2

EMCC 2013

Must-Do Markers Of Quality Care

Control the airway by endotracheal intubation
prior to endoscopy.
Establish central venous access after inserting
2 large-bore peripheral IVs and utilizing an introducer to facilitate high-volume infusions and
central venous pressure monitoring. Consider
the internal jugular vein as the location for central line placement in coagulopathic patients due
to vascular compressibility. Line placement with
ultrasound guidance is the standard of care.
Initiate volume resuscitation with crystalloid fluids and O-negative blood (if available). Switch
to type-specific crossmatched blood as soon as it
becomes available.
Consider transfusion of other blood products or
infusions of medications based on the suspected
etiology of the bleed and the patients comorbidities.
Aggressively treat hypothermia and acidosis in
order to facilitate correction of coagulopathy.

References
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
randomized, and blinded trial should carry more
weight than a case report.

To help the reader judge the strength of each
reference, pertinent information about the study,
such as the type of study and the number of patients
in the study, will be included in bold type following
the reference, where available. In addition, the most
informative references cited in this paper, as determined by the authors, will be noted by an asterisk (*)
next to the number of the reference.
1.

2.*

3.*

4.*
5.

6.*

Peura DA, Lanza FL, Gostout CJ, et al. The American College
of Gastroenterology Bleeding Registry: preliminary findings.
Am J Gastroenterol. 1997;92(6):924-928. (Retrospective survey;
1235 respondents)
Afessa B. Triage of patients with acute gastrointestinal bleeding for intensive care unit admission based on risk factors
for poor outcome. J Clin Gastroenterol. 2000;30(3):281-285.
(Prospective; 411 patients)
Barkun AN, Bardou M, Kuipers EJ, et al. International
consensus recommendations on the management of patients
with nonvariceal upper gastrointestinal bleeding. Ann Intern
Med. 2010;152(2):101-113. (Multidisciplinary consensus
group; 34 experts from 15 countries)
Gotzsche PC, Hrobjartsson A. Somatostatin analogues for
acute bleeding esophageal varices. Cochrane Database Syst
Rev. 2008;(3):CD000193. (Systematic literature review)
Sreedharan A, Martin J, Leontiadis GI, et al. Proton pump
inhibitor treatment initiated prior to endoscopic diagnosis in
upper gastrointestinal bleeding. Cochrane Database Syst Rev.
2010;(7):CD005415. (Systematic literature review)
Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal bleeding.
Available at: http://guideline.gov/content.aspx?id=13167.

EMCC 2013 10

7.

8.*

9.

10.
11.

12.

13.
14.

15.

16.
17.

18.

19.

20.

21.

22.

23.

Accessed March 1, 2013. (Practice management guideline)

Chan WH, Khin LW, Chung YF, et al. Randomized controlled
trial of standard versus high-dose intravenous omeprazole
after endoscopic therapy in high-risk patients with acute
peptic ulcer bleeding. Br J Surg. 2011;98(5):640-644. (Prospective randomized; 122 patients)
Hidaka H, Nakazawa T, Wang G, et al. Long-term administration of PPI reduces treatment failures after esophageal
variceal band ligation: a randomized, controlled trial. J
Gastroenterol. 2012;47(2):118-126. (Prospective randomized;
43 patients)
Green FW Jr, Kaplan MM, Curtis LE, et al. Effect of acid and
pepsin on blood coagulation and platelet aggregation. A possible contributor prolonged gastroduodenal mucosal hemorrhage. Gastroenterology. 1978;74(1):38-43. (In vitro study)
Berstad A. Does profound acid inhibition improve haemostasis in peptic ulcer bleeding? Scand J Gastroenterol.
1997;32(4):396398. (Review article)
Vreeburg EM, Levi M, Rauws EA, et al. Enhanced mucosal
fibrinolytic activity in gastroduodenal ulcer haemorrhage
and the beneficial effect of acid suppression. Aliment Pharmacol Ther. 2001;15(5):639646. (Prospective observational; 29
patients)
Borquez E, Swadron S, Winter M, et al. The unstable patient
with gastrointestinal hemorrhage. In: Emergency Department
Resuscitation of the Critically Ill. American College of Emergency Physicians (Ed), Dallas 2011. (Book chapter)
Millward SF. ACR Appropriateness Criteria on treatment of
acute nonvariceal gastrointestinal tract bleeding. J Am Coll
Radiol. 2008;5(4):550-554. (Consensus statement)
Fiorito JJ, Brandt LJ, Kozicky O, et al. The diagnostic yield
of superior mesenteric angiography: correlation with the
pattern of gastrointestinal bleeding. Am J Gastroenterol.
1989;84(8):878-881. (Retrospective; 58 patients)
FDA. Public health advisory: updated safety information
about a drug interaction between clopidogrel bisulfate (marketed as Plavix) and omeprazole (marketed as Prilosec and
Prilosec OTC). Available at: http://www.fda.gov/Drugs/
DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/PublicHealthAdvisories/ucm190825.htm. Accessed
March 1, 2013. (FDA public health advisory)
Corley DA, Cello JP, Adkisson W, et el. Octreotide for acute
esophageal variceal bleeding: a meta-analysis. Gastroenterology. 2001;120(4):946-954. (Meta-analysis; 475 patients)
Tsai YT, Lay CS, Lai KH, et al. Controlled trial of vasopressin
plus nitroglycerin vs. vasopressin alone in the treatment of
bleeding esophageal varices. Hepatology. 1986;6(3):406-409.
(Prospective randomized controlled trial; 39 patients)
Gimson AE, Westaby D, Hegarty J, et al. A randomized trial
of vasopressin and vasopressin plus nitroglycerin in the control of acute variceal hemorrhage. Hepatology. 1986;6(3):410413. (Prospective randomized trial; 72 bleeding episodes in
57 patients)
Borgman MA, Spinella PC, Perkins JG, et al. The ratio of
blood products transfused affects mortality in patients
receiving massive transfusions at a combat support hospital.
J Trauma. 2007;63(4):805-813. (Retrospective; 246 patients)
Perkins JG, Cap AP, Andrew CP, et al. An evaluation of the
impact of apheresis platelets used in the setting of massively
transfused trauma patients. J Trauma. 2009;66(4 Suppl):S77S84. (Retrospective; 694 patients)
Scalea TM, Bochicchio KM, Lumpkins K, et al. Early aggressive use of fresh frozen plasma does not improve outcome in
critically injured trauma patients. Ann Surg. 2008;248(4):578584. (Prospective; 806 patients)
Hbert PC, Yetisir E, Transfusion Requirements in Critical Care Investigators for the Canadian Critical Care Trials
Group, et al. Is a low transfusion threshold safe in critically
ill patients with cardiovascular diseases? Crit Care Med.
2001;29(2):227-234. (Prospective randomized; 357 patients)
Gutirrez A, Snchez-Pay J, Marco P, et al. Prognostic value
of fibrinolytic tests for hospital outcome in patients with
acute upper gastrointestinal hemorrhage. J Clin Gastroenterol.

www.ebmedicine.net Volume 3, Number 2

1. The most common cause of massive upper GI

bleeding is:

a. Esophageal varices

b. Diverticula

c. Arteriovenous malformations

d. Gastritis

e. Gastric and duodenal ulcers

2001;32(4):315-318. (Prospective; 84 patients)

24. Bosch J, Thabut D, European Study Group on rFVIIa in UGI
Haemorrhage, et al. Recombinant factor VIIa for upper gastrointestinal bleeding in patients with cirrhosis: a randomized, double-blind trial. Gastroenterology. 2004;127(4):11231130. (Prospective randomized trial; 245 patients)
25. Ejlersen E, Melsen T, Ingerslev J, et al. Recombinant activated
factor VII (rFVIIa) acutely normalizes prothrombin time in
patients with cirrhosis during bleeding from oesophageal
varices. Scand J Gastroenterol. 2001;36(10):1081-1085. (Prospective observational; 10 patients)
26.* Thabut D, de Franchis R, Bendtsen F, et al. Efficacy of activated recombinant factor VII in cirrhotic patients with upper
gastrointestinal bleeding: a randomized placebo-controlled
double-blind multicenter trial. Gastroenterology. 2003;124(4)
(Suppl1):A697. (Prospective randomized; 245 patients)
27. Ansell J, Hirsh J, Hylek E, et al. Pharmacology and management of the vitamin K antagonists: American College of
Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. Jun 2008;133(6):160S-198S. (Practice
guideline)
28. van Ryn J, Stangier J, Haertter S, et al. Dabigatran etexilate--a
novel, reversible, oral direct thrombin inhibitor: interpretation of coagulation assays and reversal of anticoagulant
activity. Thromb Haemost. 2010;103(6):1116-1127. (Literature
review)
29. Eerenberg ES, Kamphuisen PW, Sijpkens MK, et al. Reversal
of rivaroxaban and dabigatran by prothrombin complex
concentrate. Circulation. 2011;124(14):1573-1579. (Prospective
randomized; 12 patients)
30. Findley LJ, Redstone PM. Blood transfusion in adult
Jehovahs Witnesses. A case study of one congregation.
1982;142(3):606-607. (Retrospective survey; 70 respondents)
31. Watch Tower Bible and Tract Society of Pennsylvania. How
can blood save your life? Available at: http://www.jw.org/
en/publications/books/blood/how-can-blood-save-yourlife/. Accessed March 1, 2013. (Website)

2. In regard to the stabilization and monitoring

of patients with massive upper GI bleeding,
which of the following is TRUE?

a. PPIs are not recommended.

b. Initial and serial coagulation studies should

be used to guide decision making.

c. Continuous cardiac and pulse oximetry

monitoring are required.

d. Consultation with subspecialists should

be delayed until after stabilization and
resuscitation.
3. In regard to the use of angiography in patients
with massive upper GI bleeding, which of the
following is TRUE?

a. Angiography is highly specific for detection

of bleeding at rates of at least 0.5 mL/min.

b. Angiography can detect bleeding at slower

rates than can be detected by radionuclide
imaging.

c. Angiography has the disadvantage of being

diagnostic but not therapeutic.

d. Angiography is contraindicated in patients

with nonvariceal upper GI bleeding.

CME Questions

4. In regard to blood product transfusion for patients with massive upper GI bleeding, which
of the following is TRUE?

a. A hemoglobin level of 7 to 8 gm/dL should

be considered the endpoint of resuscitation.

b. The recommended PRBC:FFP:platelet

ratio is 1:2:1.

c. Use of crystalloids should ideally be

restricted to the initial phase of resuscitation.

d. Calcium gluconate should be administered

to all patients receiving PRBCs.

Take This Test Online!

Current subscribers can receive CME credit
absolutely free by completing the following test.
This issue includes 3 AMA PRA Category 1 CreditsTM.
Online testing is now available for current and
Take This Test Online!
archived issues. To receive your free CME credits for
this issue, scan the QR code below or visit
www.ebmedicine.net/C0413

www.ebmedicine.net Volume 3, Number 2

11

EMCC 2013

CME Information
Date of Original Release: April 1, 2013. Date of most recent review:
March 1, 2013. Termination date: April 1, 2016.
Accreditation: EB Medicine is accredited by the Accreditation Council
for Continuing Medical Education (ACCME) to provide continuing
medical education for physicians. This activity has been planned and
implemented in accordance with the Essential Areas and Policies of the
ACCME.
Credit Designation: EB Medicine designates this enduring material for a
maximum of 3 AMA PRA Category 1 Credits. Physicians should claim only
the credit commensurate with the extent of their participation in the activity.
AOA Accreditation: EMCC is eligible for up to 18 American Osteopathic
Association Category 2A or 2B credit hours per year.
Needs Assessment: The need for this educational activity was
determined by a survey of medical staff, including the editorial board of
this publication; review of morbidity and mortality data from the CDC,
AHA, NCHS, and ACEP; and evaluation of prior activities for emergency
physicians.
Target Audience: This enduring material is designed for emergency
medicine physicians, physician assistants, nurse practitioners, and
residents as well as intensivists and hospitalists.

EMCC Has
Gone Mobile!

Goals: Upon completion of this article, you should be able to: (1)
demonstrate medical decision-making based on the strongest clinical
evidence; (2) cost-effectively diagnose and treat the most critical ED
presentations; and (3) describe the most common medicolegal pitfalls for
each topic covered.
Discussion of Investigational Information: As part of the newsletter,
faculty may be presenting investigational information about
pharmaceutical products that is outside Food and Drug Administrationapproved labeling. Information presented as part of this activity is
intended solely as continuing medical education and is not intended to
promote off-label use of any pharmaceutical product.

You can now view all EMCC content on your

iPhone or Android smartphone. Simply visit
www.ebmedicine.net from your mobile device,
and youll automatically be directed to our
mobile site.

Faculty Disclosure: It is the policy of EB Medicine to ensure objectivity,

balance, independence, transparency, and scientific rigor in all CMEsponsored educational activities. All faculty participating in the planning
or implementation of a sponsored activity are expected to disclose to the
audience any relevant financial relationships and to assist in resolving
any conflict of interest that may arise from the relationship. In compliance
with all ACCME Essentials, Standards, and Guidelines, all faculty for this
CME activity were asked to complete a full disclosure statement. The
information received is as follows: Dr. Mihata, Dr. Bonk, Dr. Keville, Dr.
Lin, Dr. Westhoff, Dr. Gogela Carlson, Dr. Arntfield, and their related
parties report no significant financial interest or other relationship
with the manufacturer(s) of any commercial product(s) discussed in
this educational presentation.

On our mobile site, you can:

View all issues of EMCC since inception, including
issues on NIV, blunt trauma, ACS, and more
Take CME tests for all issues thats over 20 AMA
Category 1 CreditsTM!
View your CME records, including scores, dates of
completion, and certificates
Comment on EMCCs Whats Your Diagnosis blog, by
visiting www.ebmedicine.net/emccblog
Renew your subscription or purchase additional
content

Commercial Support: This issue of EMCC did not receive any commercial
support.
Earning Credit: Two Convenient Methods: (1) Go online to
www.ebmedicine.net/CME and click on the title of this article.
(2) Mail or fax the CME Answer And Evaluation Form with your
December issue to EB Medicine.

Check out our mobile site, and give us your

feedback! Simply click the link at the bottom of
the mobile site to complete a short survey to tell
us what features youd like us to add or change.

Hardware/Software Requirements: You will need a Macintosh or PC to

access the online archived articles and CME testing.
Additional Policies: For additional policies, including our
statement of conflict of interest, source of funding, statement
of informed consent, and statement of human and animal rights,
visit www.ebmedicine.net/policies.

CEO & Publisher: Stephanie Williford Marketing Manager: Robin Williford

Managing Editor: Dorothy Whisenhunt Director of Member Services: Liz Alvarez

EB Medicine

Phone: 1-800-249-5770 or 1-678-366-7933

Fax: 1-770-500-1316
5550 Triangle Parkway, Suite 150, Norcross, GA 30092
E-mail: ebm@ebmedicine.net
Website: www.ebmedicine.net
To write a letter to the editor, please email:
arntfieldmd@ebmedicine.net

EMCC Subscription Information:

6 print issues per year, 18 AMA PRA Category 1 CreditsTM,
and full online access to searchable archives
and additional CME: $299
(Call 1-800-249-5770 or go to
www.ebmedicine.net/EMCCinfo to order)

EM Critical Care (EMCC) (ISSN Print: 2162-3031, ISSN Online: 2162-3074, ACID-FREE) is published 6 times per year by EB Medicine (5550 Triangle Parkway, Suite 150, Norcross, GA 30092).
Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is
intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The
materials contained herein are not intended to establish policy, procedure, or standard of care. EM Critical Care and EMCC are trademarks of EB Medicine. Copyright 2013 EB Medicine. All
rights reserved. No part of this publication may be reproduced in any format without written consent of EB Medicine. This publication is intended for the use of the individual subscriber only
and may not be copied in whole or part or redistributed in any way without the publishers prior written permission -- including reproduction for educational purposes or for internal distribution
within a hospital, library, group practice, or other entity.

EMCC 2013 12

www.ebmedicine.net Volume 3, Number 2