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EM Critical Care



Resuscitation Of The Volume 3, Number 2

Patient With Massive Upper


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

Assistant Professor of Emergency Medicine/Critical Care,

Gastrointestinal Bleeding Wright State University, Boonshoft School of Medicine,

Dayton, OH
John-Adam Bonk, MD
Department of Emergency Medicine, Wright State University,
Abstract Boonshoft School of Medicine, Dayton, OH
Meaghan P. Keville, MD
Managing an unstable patient with massive gastrointestinal bleeding Department of Emergency Medicine, Wright State University,
can be challenging, but effective management can optimize patient Boonshoft School of Medicine, Dayton, OH

outcomes. These patients require prompt recognition of severe ill- Peer Reviewers
ness, resuscitation and stabilization, and diagnostic and treatment Michelle Lin, MD
modalities directed at identification and control of the source of Associate Professor of Clinical Emergency Medicine,
University of California San Francisco; San Francisco
bleeding. Multiple consultants (including gastroenterology, general General Hospital and Trauma Center, San Francisco, CA
surgery, and interventional radiology) are often required, and early John L. Westhoff, II, MD, MPH, FACEP
consultation of these subspecialists can improve morbidity and mor- Deputy Commander for Clinical Services, U.S. Army Public
Health Command Region-Pacific; Staff Emergency Physician,
tality. Underlying comorbidities add complexity to the management U.S. Naval Hospital, Yokosuka, Japan
of the bleeding patient and are associated with increased mortality.
Guest Editor
Most cases of massive bleeding are due to an upper gastrointestinal
source, and these patients have a higher mortality rate than those Catherine A. Gogela Carlson, MD
Critical Care Medicine Fellow, Departments of Critical Care
presenting with lower gastrointestinal bleeding. Common sources of Medicine and Emergency Medicine, University of Pittsburgh
upper gastrointestinal bleeding include gastric and duodenal ulcers, Medical Center, Pittsburgh, PA
esophageal and gastric varices, and erosive esophagitis. Depending CME Objectives
on the source of the bleeding, medical and/or surgical treatment mo- Upon completion of this article, you should be able to:
dalities may be required. Utilization of emergent upper endoscopy 1. Describe the differential diagnosis of massive GI
and other medical therapies as well as transfusion of blood products bleeding.
are often necessary to ensure optimal patient outcomes. Knowledge 2. Discuss the importance of the resuscitation of patients
with massive GI bleeding.
of the emergency procedures and medications available, as well as 3. List the available medical and surgical therapeutic
familiarity with the treatment modalities used by consultants, will options for patients with massive GI bleeding.
help the emergency physician orchestrate the care necessary to en- 4. Apply a standardized approach to the management of
massive GI bleeding.
sure patient survival.
Prior to beginning this activity, see the back page for faculty
disclosures and CME accreditation information.

Editor-in-Chief Center for Resuscitation Science, Andy Jagoda, MD, FACEP Julie Mayglothling, MD Emanuel P. Rivers, MD, MPH, IOM
Robert T. Arntfield, MD, FACEP, Philadelphia, PA Professor and Chair, Department Assistant Professor, Department Vice Chairman and Director
FRCPC, FCCP of Emergency Medicine, Mount of Emergency Medicine, of Research, Department of
Assistant Professor, Division Lillian L. Emlet, MD, MS, FACEP Sinai School of Medicine; Medical Department of Surgery, Division Emergency Medicine, Senior
of Critical Care, Division of Assistant Professor, Department of Director, Mount Sinai Hospital, New of Trauma/Critical Care, Virginia Staff Attending, Departments of
Emergency Medicine, Western Critical Care Medicine, Department York, NY Commonwealth University, Emergency Medicine and Surgery
University, London, Ontario, of Emergency Medicine, University Richmond, VA (Surgical Critical Care), Henry
Canada of Pittsburgh Medical Center; William A. Knight, IV, MD, FACEP Ford Hospital, Clinical Professor,
Program Director, EM-CCM Assistant Professor of Emergency Christopher P. Nickson, MBChB, Department of Emergency
Fellowship of the Multidisciplinary Medicine, Assistant Professor of MClinEpid, FACEM Medicine and Surgery, Wayne State
Associate Editor Critical Care Training Program, Neurosurgery, Medical Director - Senior Registrar, Intensive Care University School of Medicine,
Scott Weingart, MD, FACEP Pittsburgh, PA Emergency Medicine Mid-Level Unit, Royal Darwin Hospital, Detroit, MI
Associate Professor, Department of Provider Program, Associate Darwin, Australia
Emergency Medicine, Mount Sinai Michael A. Gibbs, MD, FACEP Medical Director of Neuroscience Isaac Tawil, MD, FCCM
School of Medicine; Director of Professor and Chair, Department ICU, University of Cincinnati Jon Rittenberger, MD, MS, FACEP Assistant Professor, Department
Emergency Critical Care, Elmhurst of Emergency Medicine, Carolinas College of Medicine, Cincinnati, Assistant Professor, Department of Anesthesia and Critical Care /
Hospital Center, New York, NY Medical Center, University of North OH of Emergency Medicine, Department of Emergency Medicine,
Carolina School of Medicine, University of Pittsburgh School Director, Neurosciences ICU,
Chapel Hill, NC Haney Mallemat, MD of Medicine; Attending Physician, University of New Mexico Health
Editorial Board Assistant Professor, Department Emergency Medicine and Post Science Center, Albuquerque, NM
Benjamin S. Abella, MD, MPhil, Robert Green, MD, DABEM, of Emergency Medicine, University Cardiac Arrest Services, UPMC
FACEP FRCPC of Maryland School of Medicine, Presbyterian Hospital, Pittsburgh,
Assistant Professor, Department Baltimore, MD PA
Research Editor
Professor, Department of
of Emergency Medicine and Amy Sanghvi, MD
Anaesthesia, Division of Critical
Department of Medicine / Evie Marcolini, MD, FAAEM Department of Emergency
Care Medicine, Department of
Section of Pulmonary Allergy Assistant Professor, Department of Medicine, Mount Sinai School of
Emergency Medicine, Dalhousie
and Critical Care, University of Emergency Medicine and Critical Medicine, New York, NY
University, Halifax, Nova Scotia,
Pennsylvania School of Medicine; Canada Care, Yale School of Medicine,
Clinical Research Director, New Haven, CT
Case Presentation searched for guidelines for the acute treatment of
severe GI bleeding. Table 1 summarizes the current
You receive a medic call for a 45-year-old male who called guidelines related to GI bleeding.3-6 The literature
911 for massive hematemesis. The medics report that the review and these guidelines suggest a general con-
patient is an alcoholic who has been binge drinking since sensus about the importance of early evaluation and
losing his job 1 week ago. He has vomited a large amount resuscitation in the ED as well as early involvement
of frank blood twice. He is hypotensive, with a MAP of 50 of appropriate consultants in order to avoid negative
mm Hg and a pulse of 128 beats per minute. EMS person- outcomes in patients with massive GI bleeding.
nel have established a peripheral IV line and are infusing
normal saline as fast as possible; they are 5 minutes out. Etiology And Pathophysiology
After you page the gastroenterologist and ask the unit sec-
retary to activate your institutions massive transfusion The presence of GI bleeding with evidence of hem-
protocol, you consider the potential causes of massive GI orrhagic shock requires prompt identification of the
bleeding, the available therapeutic options, and the inter- bleeding source. The most common etiologies of
ventions you should undertake in the next few minutes to upper GI bleeding include: duodenal ulcers (28%),
improve this critically ill patients chance for survival gastric ulcers (26%), gastritis (13%), varices (12%),
and esophagitis (8%).1 GI bleeding due to esopha-
Introduction geal or gastric varices and peptic ulceration carry
the highest mortality.2 Exclusion of other bleeding
Providing optimal care in the emergency depart- sources (such as pulmonary or intranasal sources)
ment (ED) for patients with massive gastrointesti- is important. As with management of all cases of
nal (GI) bleeding requires coordination of multiple undifferentiated hypotension, initiation of resuscita-
consultants as well as knowledge of both medical tion based on hemodynamic decompensation should
and surgical therapeutic options. For the purposes not be delayed, regardless of the underlying source
of this review, massive GI bleeding is defined as of the bleeding.
bleeding in a patient that has resulted in hemody-
namic instability, with signs and symptoms consis- Treatment
tent with hemorrhagic shock and evidence of either
hematemesis or hematochezia. In order to provide Stabilization And Monitoring
initial resuscitation in the ED (either as a bridge to Initial resuscitation of patients with massive GI bleed-
continued resuscitation in the intensive care unit ing involves restoration of intravascular volume in
or to diagnostic/therapeutic interventions in the order to achieve the relative hemodynamic stability
operating room or interventional radiology), emer- required to proceed with diagnostic and therapeutic
gency physicians must be familiar with the wide interventions. An initial primary survey to evaluate
variety of both diagnostic and therapeutic options as the airway, breathing, and circulation should almost
well as the underlying pathophysiology for massive always include endotracheal intubation in order to
GI hemorrhage. The majority (> 75%) of massive protect the patients airway in the setting of active
GI bleeding cases are due to an upper GI source.1 hemorrhage and to assist in identifying the bleeding
Mortality rates for patients with massive GI bleeding source and facilitating these additional interventions.
range from 20% to 39%.2 Treatment options depend Early resuscitation may start with 2 large-bore pe-
upon the underlying cause of the bleeding, and ripheral intravenous (IV) catheters, but resuscitation
early intervention can mean the difference between of massive hemorrhage may be aided by the use of
survival and death. This issue of EMCC provides an larger, introducer-sized central venous catheters that
overview of the current evidence for the treatment of can more efficiently restore lost intravascular volume
patients with massive upper GI bleeding. during hemorrhagic shock.
The importance of early mobilization of special-
Critical Appraisal Of The Literature ists cannot be overemphasized. In patients with
massive GI bleeding, medical therapy alone is
A literature search of PubMed, Ovid MEDLINE, and unlikely to be sufficient to achieve hemostasis. Early
the Cochrane Library was performed using the fol- mobilization of the available subspecialists expe-
lowing keywords: GI bleeding, severe GI bleeding, upper dites time to definitive therapy. The lack of available
GI bleeding, and variceal bleeding treatment. The search subspecialty support should prompt consideration
focused only on literature in the English language for for transfer to a tertiary care facility that can provide
adult patients. More than 100 articles were reviewed, this care. Depending on the underlying cause of the
which provided the background information and bleeding as well as patient comorbidities, gastroen-
basis for further literature review. Additionally, both terology, general surgery, and interventional radiol-
national and international guidelines as well as the ogy may all play a role in the care of these patients.
Cochrane Database of Systematic Reviews were

EMCC 2013 2 Volume 3, Number 2

Patients with massive GI bleeding require con- In cases of nonvariceal hemorrhage, a bolus of a
tinuous cardiac and pulse oximetry monitoring, with PPI should be initiated and then followed by a
frequent blood pressure checks. Central venous access continuous infusion. This is thought to promote
may be required in the ED if the patient has poor pe- ulcer healing and decrease the rate of rebleeding.7
ripheral access or if more the rapid infusion of fluids Additionally, in cases of variceal hemorrhage with
or blood products is needed. Invasive monitoring, subsequent endoscopic intervention, patients who
including an arterial line, will enable prompt recogni- are given PPIs intravenously have demonstrated less
tion and response to the rapid changes in physiology rebleeding8 because PPIs work against stomach acid
that may occur in massive GI hemorrhage. and pepsin, which are thought to destabilize platelet
Initial laboratory values can help guide initial plugs and the hemostatic clot.9-11
therapy, but serial coagulation studies in the ED are
not likely to aid in decision making and may be dif- Procedural Therapies
ficult to interpret in patients being treated with fresh Endoscopy
frozen plasma (FFP), cryoprecipitate, or factor concen- Endoscopy is an important diagnostic and thera-
trate. Likewise, an initial D-dimer may offer prognos- peutic tool for upper GI hemorrhage and should
tic information, but it should not influence immediate be performed promptly upon patient stabilization.
management in the acute setting. Endoscopy provides definitive therapy in many
Regardless of the source of upper GI bleeding, cases. The gastroenterologist may employ various
proton-pump inhibitors (PPIs) are typically recom- endoscopic techniques, including clips, banding,
mended until the etiology of the bleeding can be thermocoagulation, or sclerosant injection with or
identified. While PPIs will not impact the immedi- without epinephrine. All patients with massive GI
ate stabilization of a hemodynamically unstable bleeding should be intubated to facilitate endos-
bleeding patient, their use may improve outcomes. copy, control the airway, reduce the risk of aspira-

Table 1. Current Guidelines For Gastrointestinal Bleeding

Organization Topic Type of Guideline Recommendations

American College of Management of patients Consensus 1. Early evaluation, resuscitation, and risk stratification is recom-
Physicians with nonvariceal upper mended.
GI bleeding3 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
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 manage- Systematic review 1. Somatostatin analogues do not reduce mortality in variceal GI
ment of patients with GI bleeding; however, they may reduce the need for blood transfusion
bleeding4,5 by 0.5 units.
2. PPI administration prior to endoscopy for upper GI bleeds sig-
nificantly 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 for initial treat- Systematic review 1. PRBC transfusion should be considered after loss of 30% of the
Guidelines Network ment of patients with circulating blood volume.
significant GI bleeding6 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 mea-
sure to gain hemostasis in uncontrolled variceal hemorrhage.

Abbreviations: GI, gastrointestinal; PPI, proton-pump inhibitor; PRBC, packed red blood cell. Volume 3, Number 2 3 EMCC 2013

tion, and improve patient safety during treatment. Additional Procedural Therapies
Airway management in severe upper GI bleeds can In severe cases of massive GI bleeding, where ur-
be technically challenging due to poor visualization. gent endoscopy is unable to provide a diagnosis or
A topic within itself that cannot be covered in this is- therapy, urgent or emergent angiography can be
sue, extra personnel and airway adjuncts (including performed to identify the location of the hemorrhage.
2 suction catheters) is advisable for airway manage- Angiography is indicated in patients with nonvariceal
ment of this population. upper GI bleeding when medical management and
endoscopic therapy have failed to control the bleed-
Balloon Tamponade ing. Angiographic intervention should be considered
Balloon tamponade may be required if endoscopy is as an alternative to surgery in patients who are high
either not available or not successful in achieving he- risk for more invasive surgical intervention.13 Angiog-
mostasis. Insertion of a balloon tamponade device is raphy can detect bleeding at rates of at least 0.5 mL/
a rare but potentially life-saving procedure. It can be min with 100% specificity and variable sensitivity
used as a temporary rescue device by providers who (based on the rate).14 During angiography, lesions
practice in a setting where specialty consultation is can be treated by use of vasopressin or transcatheter
not readily available. Use of a balloon-tamponade embolization.
device is associated with a high risk of rebleeding Another option for identifying the source of
upon balloon deflation. Its most lethal complication bleeding is radionuclide imaging, which can de-
is esophageal necrosis and rupture. tect bleeding occurring at slower rates than can be
There are several different types of commercially detected by angiography. The primary purpose of
available devices for balloon tamponade. The 3 most these studies is to localize the source of the bleed-
common include the Sengstaken-Blakemore, the ing and to facilitate surgical intervention. An emer-
Minnesota tube, and the Linton-Nachlas tube.12 (See gency surgical consult should be sought in patients
Figure 1.) Each of these tubes varies slightly based with massive hemorrhage who cannot be stabilized
on the number of lumens and balloons. Providers in the ED, who have contraindications to endos-
should be familiar with the specific device used at copy, or who have peritoneal signs on examination
their institution. The following is a general guide for (which can occur from a ruptured peptic ulcer).
their use: While surgery is typically only considered as a last
1. Prior to insertion, secure the airway. resort after medical, endoscopic, and interventional
2. After applying a lubricant to the tube, insert the radiology approaches have been exhausted or are
tube through the mouth or nostril to a depth of contraindicated, not all types of bleeding (such as
at least 50 cm, depending upon the height of the variceal bleeding) are amenable to surgical interven-
patient. tion. Nonetheless, early involvement of surgery and
3. After evaluation by air injection, confirm place- gastroenterology services can facilitate a cooperative
ment in the stomach with radiography. (The bal- treatment approach and may make surgical inter-
loon should NOT be inflated until its location is vention, if necessary, safer and less emergent.
verified radiographically so as to avoid potential
complications associated with malpositioning of Pharmacologic Therapies
the tube.) There are multiple proposed pharmacologic treat-
4. Inflate the gastric balloon (approximately 400- ments for the management of acute upper GI bleed-
500 mL of air), and clamp the inlet. ing. Understanding the mechanism of action of these
5. Retract the tube until resistance is felt (the bal-
loon at the gastroesophageal junction). Tension
must be maintained on the tube in order to Figure 1. Minnesota Tube For Balloon
produce the tamponade effect. Tamponade
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 esopha-
geal necrosis.

It is important to remember that these are tem-

porizing 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. 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 Volume 3, Number 2

medications can facilitate a deeper understanding of bleeding from esophageal varices.4 Some data sug-
the rationale for the existing guidelines for their use. gest that the combination of these medications with
upper endoscopy may be beneficial.
Proton Pump Inhibitors Given their relatively low-risk side-effect pro-
PPIs, which include omeprazole, pantoprazole, and files, the use of these medications can be considered
esomeprazole, are considered to be a mainstay of in patients with acute hemorrhage that is possibly
early therapy for acute GI bleeding in the ED. PPIs caused by variceal bleeding.16
suppress gastric acid stimulation by inhibiting the pa-
rietal cell H+/K+ ATPase (adenosine triphosphatase) Vasopressin
pump. One potential benefit of the early use of PPIs A third class of pharmacologic agents, vasopressin
may be the reduction of hemorrhage during endos- and its analogues, can reduce portal hypertension by
copy.3,5 Additionally, PPIs may create a more optimal causing systemic and splanchnic vasoconstriction.
environment for the stabilization of blood clots by Much like somatostatin, the use of vasopressin
neutralizing the intraluminal gastric acid that would in the management of upper GI bleeding is contro-
otherwise serve to promote continued bleeding.9 versial. The risks (eg, myocardial infarction, arrhyth-
There has been concern about the potential mias, mesenteric ischemia, peripheral soft tissue ne-
increased risk of thrombotic stroke or myocardial crosis, cardiac arrest) of using this medical therapy
infarction with the addition of PPIs to long-term are similar tobut usually less severe thanthose
clopidogrel therapy. Based on cohort studies, a 2009 seen with the use of other vasopressor medications.
United States Food and Drug Administration warn- In patients with variceal bleeding, adding nitro-
ing cited a 50% increased risk of these complications glycerin to vasopressin therapy appears to decrease
when PPIs and clopidogrel were taken concurrently.15 systemic complications from the use of vasopressin
However, current data are inconclusive and suggest alone while not affecting the efficacy of the vaso-
that these complications are typically associated with pressin.17,18 In patients with massive GI bleeding, the
long-term use of PPIs and clopidogrel. These risks risk of systemic vasoconstriction and the potential
have not yet been described in the acute, short-term for end-organ ischemia must be weighed against
use of these medications during the stabilization of the potential benefit of splanchnic vasoconstriction,
patients with massive GI bleeding. which can help to achieve hemostasis in the actively
At this time, guidelines continue to encourage the bleeding patient.
use of PPIs (either before or immediately following In spite of the potential deleterious effects of
upper endoscopy) in patients with undifferentiated vasopressin, use of vasopressin (or vasopressin plus
upper GI bleeding.3 However, there has not yet been nitroglycerin) in a patient in extremis due to massive
a study showing a statistical improvement in the rate GI bleeding may be justified.
of rebleeding, the need for surgical intervention, or
mortality from their use. Nonetheless, their cost effec- Blood Product Transfusion
tiveness and excellent safety profile make the benefit
The goal of blood product transfusion for acute
of giving these agents greater than the potential risks,
bleeding is to replace the blood cells and coagulation
particularly in high-risk patient populations.
factors that are being lost. Whole blood is a complex
heterogeneous solution that serves 3 basic func-
tions: (1) to maintain intravascular volume, (2) to
Somatostatin and its analogues (including octreo-
provide oxygen-carrying capacity, and (3) to provide
tide and vapreotide) represent another class of
the coagulation factors that are required to reverse
pharmacologic agents that may be used early in the
coagulopathy and to assist in achieving (and main-
management of acute GI bleeding due to a suspect-
taining) hemostasis. The ability to achieve hemostasis
ed variceal source. Somatostatin (also known as
can be complicated by the use of anticoagulation or
growth-hormone-inhibiting hormone) suppresses
antiplatelet agents. Because there are inherent risks
the release of GI hormones such as gastrin, chole-
involved with transfusing blood products, the risks
cystokinin, motilin, and secretin. The secondary
must be considered along with the potential benefits
effects of blocking the release of these hormones
for each individual patient.
include a reduction of portal venous blood flow

due to splanchnic vasoconstriction and subsequent
Goal #1: Provide Intravascular Volume Resuscitation
decreased GI bleeding.
Prompt volume resuscitation with IV crystalloid
To date, there are minimal data regarding the
fluids should be initiated in a bleeding, hypotensive
use of somatostatin or its analogues for nonvariceal
patient in order to achieve a perfusing mean arterial
upper GI bleeding. The data on their use in severe
pressure (MAP) until blood products are available.
variceal bleeding are also mixed. A Cochrane review
Given that it lacks oxygen-carrying capacity and
found no significant change in mortality, the rebleed-
does not replenish clotting factors, the role of crystal-
ing rate, or the number of units of blood transfused
loid fluid for volume resuscitation should ideally
with the use of somatostatin in patients with acute Volume 3, Number 2 5 EMCC 2013

be restricted to this early phase of resuscitation in a myocardial oxygen delivery.22 However, for patients
bleeding patient. In cirrhotic patients with suspected with suspected variceal bleeding (even with con-
variceal hemorrhage, excessive crystalloid resuscita- comitant coronary artery disease), consider keeping
tion may be particularly harmful due to their suscep- the hemoglobin goal to between 7 and 8 gm/dL until
tibility to extravascular fluid shifts in the setting of hemostasis is achieved, as the additional blood vol-
underlying low intravascular oncotic pressure. ume required to achieve this higher target may lead
In patients with massive GI bleeding (especially to increased portal pressure and worsening bleeding
those with hemoglobin < 8.0 gm/dL, coagulopathy, or rebleeding.
or persistent hypotension despite volume infusion), When there is a need for emergent transfusion
the use of blood products (such as PRBCs) is im- of PRBCs for acute blood loss anemia with signs of
portant in order to restore hemodynamic stability hypovolemic shock, O-negative PRBCs (or O-positive
and to achieve hemostasis. However, transfusion of PRBCs in women past childbearing age and in men)
PRBCs alone is not sufficient because they do not can be given until type-specific crossmatched blood is
contain the required coagulation factors. For this available. For patients requiring massive transfusion
reason, PRBCs should be accompanied by FFP and/ of blood products, it is important to remember that the
or platelets. The military literature on traumatic blood transfusion will have metabolic complications such as
loss recommends a PRBC:FFP:platelet ratio approach- depletion of intravascular cations due to chelation by
ing 1:1:1.19,20 Other sources disagree on the exact the sodium citrate used to anticoagulate blood compo-
ratio, citing a lack of a specific survival benefit to a nents during storage. Citrate is primarily metabolized
higher PRBC to FFP ratio.21 Many large centers have by the liver, so in cirrhotic patients receiving massive
massive transfusion protocols that allow the rapid transfusion, this effect may be more profound. For
release of blood products in varying ratios. While the these patients, consider giving calcium replacement
survival benefit remains unclear, most protocols have (calcium gluconate 1-2 g IV or calcium chloride 0.5-1
PRBC:FFP:platelet ratios near 1:1:1. g IV per 500 mL of transfused blood). Magnesium can
also be affected, and low levels have unwanted side
Goal #2: Optimize Oxygen-Carrying Capacity effects and should be repleted as necessary, keeping
The goal of improving oxygen-carrying capacity by in mind that overly rapid infusion of magnesium can
transfusing PRBCs is to ensure sufficient oxygen exacerbate hypotension.
delivery to the tissues in order to prevent end-
organ ischemia and secondary dysfunction. Clinical Goal #3: Reverse Coagulopathy
signs and symptoms of decreased oxygen delivery Treatment of coagulopathy can be tailored to its
can include: likely or known etiology. Coagulopathy may arise
Decreased level of consciousness due to an underlying chronic disorder, but it may
Evidence of cardiac ischemia (as shown by elec- also be caused by metabolic acidosis due to tissue
trocardiographic changes or troponin elevation) hypoxemia in the setting of acute hypotension.
Increasing serum lactate To reverse coagulopathy, consider an initial
Decreased central venous oxygen saturation transfusion of 10 mL/kg of FFP. Prothrombin
(ScvO2) time (PT)/international normalized ratio (INR),
partial thromboplastin time (PTT), platelet count,
The International Consensus guidelines recom- and fibrinogen levels can be used to guide patient
mend maintenance of hemoglobin levels between 7 management. While there are no specific guidelines,
and 8 gm/dL.3 However, there are no randomized keeping the platelet count > 50,000/mm3, PTT
controlled trials to suggest an exact hemoglobin goal < 60 seconds, and INR < 1.8 is common practice and
for transfusion. Target hemoglobin levels should be is recommended by the authors. Because D-dimer
individualized for each patient and should be based levels have been shown to be inversely related to
upon the suspected etiology of the bleed (ie, variceal prognosis in upper GI bleeding, a D-dimer may be
vs nonvariceal hemorrhage) as well as patient comor- drawn as a prognostic marker, but it has no role in
bidities. In the setting of ongoing massive bleeding, guiding intervention.23 If available, the thromboelas-
the recommended hemoglobin level of 7 to 8 gm/dL tography (TEG) test can evaluate platelet function
should not be considered to be an endpoint of resus- and coagulation and may be more efficient to direct
citation. Instead, a MAP of > 60 mm Hg and evidence the type of transfusion products necessary.
of adequate end-organ perfusion should be the target. The role of recombinant activated factor VII
Though the International Consensus guidelines (rFVIIa) is continuing to evolve. While it may be
suggest maintenance of hemoglobin between 7 and useful in certain situations (eg, when a patient is
8 gm/dL, patients with certain comorbidities may on a direct thrombin inhibitor), it is expensive, it
require greater hemoglobin goals. For instance, carries the risk of thromboembolic complications,
evidence suggests that patients with suspected active and studies of its use have had conflicting results. A
ischemic coronary artery disease may benefit from prospective randomized trial of 245 patients found
a target hemoglobin closer to 10 gm/dL to support no benefit with rFVIIa over standard therapy for

EMCC 2013 6 Volume 3, Number 2

nonvariceal upper GI bleeding.24 However, a small rate of 1 mg/min is necessary to achieve a sustained
uncontrolled study suggested that, in patients with reversal of the INR; however, it is insufficient when
liver disease and an increased INR refractory to FFP given as a single agent, as it has an onset of action of
therapy, rFVIIa was effective in stopping bleeding 2 to 6 hours and requires up to 24 hours to achieve a
and normalizing the INR.25 Similarly, a study of pa- complete response.27 For this reason, FFP must also
tients with moderate to severe cirrhosis showed that be administered.
administration of rFVIIa in addition to endoscopic Although controversial, rFVIIa can be consid-
hemostatic strategies decreased rebleeding rates.26 ered for reversal of effects of warfarin. However,
Due to the conflicting nature of the literature, use of it is expensive, it has minimal proven therapeutic
rFVIIa in patients with massive GI bleeding is not benefit for warfarin reversal, it is not FDA ap-
routinely recommended. proved for this use, and its use may cause throm-
It should be noted that, although the transfu- botic complications.24-26
sion of blood products is indicated in patients with
massive GI bleeding, it is associated with some Dabigatran: Dabigatran (Pradaxa) is a direct
risks. The lethal triad of hypothermia, coagulopa- thrombin inhibitor. To quantify the degree of
thy, and acidosis must be addressed in order to dabigatran coagulopathy, obtain a PTT and
prevent clinical deterioration. (See Figure 2.) Use thrombin time (if rapidly available).28 PT/INR is not
warmed fluids, warmed blankets, and other pas- useful in assessing dabigatran coagulopathy. The
sive external rewarming measures as needed to PTT is only useful to qualitatively assess the degree
maintain normothermia. of coagulopathy because it lacks sufficient sensitivity
with therapeutic dabigatran levels. A very high PTT
Reversal Of Medically Induced Coagulopathy value should be confirmed by another method (eg,
Warfarin: Warfarin (Coumadin, Jantoven) thrombin time),28 although this may be impractical
inhibits vitamin K-dependent coagulation factor in the emergent setting. Like other anticoagulant
synthesis. Prothrombin complex concentrates medications, even therapeutic levels may require
(PCCs) should be the first-line treatment in a reversal in the setting of active bleeding.
patient who is on warfarin. PCCs do not require At this time, an evidence-based reversal strategy
crossmatch and act more quickly than FFP alone; for dabigatran is not available. Many institutions
however, because PCCs in the United States do have a pathway for bleeding patients who are on
not contain significant amounts of factor VII, dabigatran that may inform local practice patterns.
FFP must also be administered. Dosages are Management strategies may range from expectant
individually calculated based on weight and management to aggressive use of blood products,
desired factor IX level; 1 unit/kg will increase the including FFP and even hemodialysis.
factor IX level approximately 1%.
If PCCs are not available, coagulopathy can be Rivaroxaban: Rivaroxaban (Xarelto) is a factor
reversed by discontinuing warfarin therapy and Xa inhibitor. Administer PCCs for reversal of
administering vitamin K. Vitamin K at a dose of 5 rivaroxaban; if PCCs are not available, consider
to 10 mg diluted in D5W or D5 saline infused at a administration of FFP.29

Figure 2. Coagulopathy Chart

Hemorrhage Hypothermia Tissue damage

Fluid replacement Acidosis Shock

Dilution Coagulopathy Hypoperfusion

Consumption of platelets and clotting

Inflammation Hyperfibrinolysis

Reprinted from: Cherkas D. Traumatic Hemorrhagic Shock: Advances In Fluid Management. Emerg Med Pract. 2011;13(11):1-20.
Copyright 2011 EB Medicine. Volume 3, Number 2 7 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)

Are there signs of altered mental status and/or

active hematemesis?

Intubate (Class II) Are there signs or symptoms of shock?


Transfuse PRBCs, FFP, and platelets (Class II) Is there a history of esophageal varices or signs of cirrhosis?


Octreotide 50-mcg bolus and 50-mcg/h infusion (Class II) Perform labs: CBC with differential, BMP, LFTs, PT/PTT, ECG, CXR
and Consider: D-dimer, lactate, ABG
Ciprofloxacin 400 mg bid (Class I) or ceftriaxone 1g IV qd (Class II)

Coagulopathy (INR > 1.7

with active bleeding)

Transfuse 2 units FFP (Class II)

If there is severe liver disease with coagulopathy and refractory If hemoglobin < 7.0 gm/dL: transfuse PRBCs (Class II)
bleeding, consider PCCs or rFVIIa (Class II) If hemoglobin > 8.0 gm/dL (or with bleeding varices): do not
If the patient is taking warfarin, add vitamin K 10 mg slow IV transfuse PRBCs (Class II)
push (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, elec-
trocardiogram; 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 Class II Class III Indeterminate tatives from the resuscitation
Always acceptable, safe Safe, acceptable May be acceptable Continuing area of research councils of ILCOR: How to De-
Definitely useful Probably useful Possibly useful No recommendations until velop Evidence-Based Guidelines
Proven in both efficacy and Considered optional or alterna- further research for Emergency Cardiac Care:
effectiveness Level of Evidence: tive treatments Quality of Evidence and Classes
Generally higher levels of Level of Evidence: of Recommendations; also:
Level of Evidence: evidence Level of Evidence: Evidence not available Anonymous. Guidelines for car-
One or more large prospective Non-randomized or retrospec- Generally lower or intermediate Higher studies in progress diopulmonary resuscitation and
studies are present (with rare tive studies: historic, cohort, or levels of evidence Results inconsistent, contradic- emergency cardiac care. Emer-
exceptions) case control studies Case series, animal studies, tory gency Cardiac Care Committee
High-quality meta-analyses Less robust randomized con- consensus panels Results not compelling and Subcommittees, American
Study results consistently posi- trolled trials Occasionally positive results Heart Association. Part IX. Ensur-
tive and compelling Results consistently positive Significantly modified from: The
Emergency Cardiovascular Care ing effectiveness of community-
Committees of the American wide emergency cardiac care.
Heart Association and represen- 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 Volume 3, Number 2

Unfractionated Heparin: Unfractionated heparin acts The foundation of the resuscitation includes
at multiple sites in the clotting cascade and serves as initial management of the airway, breathing, and
a catalyst for clotting factors. Administer protamine circulation. Volume resuscitation requires crystal-
sulfate to reverse heparin. loid fluids and transfusion of blood products. Early
consultation with gastroenterology, interventional
Clopidogrel: Clopidogrel (Plavix) is a nonreversible radiology, and general surgery will improve the
platelet inhibitor. Empiric transfusion of platelets patients time to definitive care. Endoscopy should be
can be considered for patients on clopidogrel or performed promptly upon stabilization. In addition
other platelet inhibitors (such as aspirin), although to volume resuscitation, medical therapies such as
no randomized controlled trials have demonstrated PPIs, somatostatin and its analogues, and vasopressin
a favorable impact with this approach. should be considered either empirically based upon
hemodynamic stability of the patient or directed at
Special Circumstances the underlying etiology of the bleeding, if known.
Surgical intervention may ultimately be necessary if
When treating a patient who refuses blood based less-invasive treatments fail or are contraindicated.
on religious beliefs (eg, Jehovahs Witnesses), it Depending on the clinical scenario, balloon tampon-
is important to ask the patient or legal guardian ade may be needed as a temporizing and life-sustain-
whether they are willing to receive blood prod- ing measure until the resources required for definitive
ucts. Even though the patient may be a Jehovahs therapy become available.
Witness, it is important to carefully establish and
document the patients current medical wishes. In a Case Conclusion
small case study, investigators found a portion of a
Jehovahs Witness congregation who would accept The critically ill 45-year-old male patient arrived to your
blood transfusions because they disagreed with the resuscitation bay with vital signs that were unchanged
official doctrine.30 Further, The Watchtower, a legal from the prehospital report. You made a decision to intubate
organization of the Jehovahs Witnesses, asserts with the patient in order to protect his airway and to facilitate
respect to blood transfusion: Ultimately, you (the anticipated upper endoscopy. Shortly after intubation,
patient or the parent) must decide. Because your (or the patient continued to have frank blood coming from his
your childs) body, life, ethics, and relationship with oropharynx. The nurses established a second large-bore
God are involved.31 Regardless of the patients or peripheral IV, and emergency release blood was given. Each
power of attorneys decision, carefully document large-bore peripheral IV had blood infusing, and the initial
conversations about risk and benefit as well as the hemoglobin came back at 5.8 gm/dL. You ordered 4 more
subsequent management based on that decision. units of type-specific blood as well as 2 units of FFP and 2
single-donor units of platelets, and you subsequently placed
Disposition an introducer catheter to expedite large volume infusion of
blood products via a level 1 infuser, which warmed the in-
Most patients who present to the ED with massive fusing fluid. The gastroenterologist came and performed an
GI bleeding will ultimately require admission to the endoscopy in the ED, during which he attempted to band
intensive care unit, although this will depend on the the large esophageal varices. He was uncertain whether or
success of early intervention and the clinical stability not he was able to obtain complete hemostasis during the
of the patient. Consideration should be made early procedure. The patient initially improved with your re-
for involvement of subspecialists. Facilities without suscitation but continued to have a MAP in the 50s and a
gastroenterology, general surgery, or interventional pulse rate in the 120s. You administered an octreotide bolus
radiology backup should have a rapid interfacility and infusion as well as a PPI infusion. In consultation with
transfer protocol in place to expedite patient transfer your intensivist team, you started a vasopressin drip with
to a facility capable of providing the definitive man- a goal MAP of > 60 mm Hg. This improved not only the
agement that will be needed after the initial resusci- variceal bleeding but also the patients hemodynamic stabil-
tation and stabilization. ity. In total, the patient required 4 more units of PRBCs
and 2 more units of FFP. He was admitted to the ICU,
Summary where the gastroenterologist repeated an endoscopy and
found less blood but 2 more bleeding varices, which were
The unstable patient with massive upper GI bleed- subsequently banded. The patient developed renal failure
ing is a high-risk case for the emergency physi- and liver failure (acute on chronic) with ischemic hepatitis
cian, requiring the coordination of resources and secondary to hemorrhagic shock. He had a prolonged course
consideration of various treatment modalities. in the ICU but eventually improved and was ultimately
Initial resuscitation efforts should occur concomi- discharged from the hospital.
tantly, with diagnostic measures aimed at finding
the etiology of the bleed. Volume 3, Number 2 9 EMCC 2013

Must-Do Markers Of Quality Care Accessed March 1, 2013. (Practice management guideline)
7. Chan WH, Khin LW, Chung YF, et al. Randomized controlled
trial of standard versus high-dose intravenous omeprazole
Control the airway by endotracheal intubation after endoscopic therapy in high-risk patients with acute
prior to endoscopy. peptic ulcer bleeding. Br J Surg. 2011;98(5):640-644. (Prospec-
tive randomized; 122 patients)
Establish central venous access after inserting
8.* Hidaka H, Nakazawa T, Wang G, et al. Long-term admin-
2 large-bore peripheral IVs and utilizing an in- istration of PPI reduces treatment failures after esophageal
troducer to facilitate high-volume infusions and variceal band ligation: a randomized, controlled trial. J
central venous pressure monitoring. Consider Gastroenterol. 2012;47(2):118-126. (Prospective randomized;
43 patients)
the internal jugular vein as the location for cen- 9. Green FW Jr, Kaplan MM, Curtis LE, et al. Effect of acid and
tral line placement in coagulopathic patients due pepsin on blood coagulation and platelet aggregation. A pos-
to vascular compressibility. Line placement with sible contributor prolonged gastroduodenal mucosal hemor-
ultrasound guidance is the standard of care. rhage. Gastroenterology. 1978;74(1):38-43. (In vitro study)
10. Berstad A. Does profound acid inhibition improve hae-
Initiate volume resuscitation with crystalloid flu- mostasis in peptic ulcer bleeding? Scand J Gastroenterol.
ids and O-negative blood (if available). Switch 1997;32(4):396398. (Review article)
to type-specific crossmatched blood as soon as it 11. Vreeburg EM, Levi M, Rauws EA, et al. Enhanced mucosal
becomes available. fibrinolytic activity in gastroduodenal ulcer haemorrhage
and the beneficial effect of acid suppression. Aliment Pharma-
Consider transfusion of other blood products or col Ther. 2001;15(5):639646. (Prospective observational; 29
infusions of medications based on the suspected patients)
etiology of the bleed and the patients comor- 12. Borquez E, Swadron S, Winter M, et al. The unstable patient
bidities. with gastrointestinal hemorrhage. In: Emergency Department
Resuscitation of the Critically Ill. American College of Emer-
Aggressively treat hypothermia and acidosis in gency Physicians (Ed), Dallas 2011. (Book chapter)
order to facilitate correction of coagulopathy. 13. Millward SF. ACR Appropriateness Criteria on treatment of
acute nonvariceal gastrointestinal tract bleeding. J Am Coll
Radiol. 2008;5(4):550-554. (Consensus statement)
References 14. Fiorito JJ, Brandt LJ, Kozicky O, et al. The diagnostic yield
of superior mesenteric angiography: correlation with the
Evidence-based medicine requires a critical ap- pattern of gastrointestinal bleeding. Am J Gastroenterol.
1989;84(8):878-881. (Retrospective; 58 patients)
praisal of the literature based upon study methodol- 15. FDA. Public health advisory: updated safety information
ogy and number of subjects. Not all references are about a drug interaction between clopidogrel bisulfate (mar-
equally robust. The findings of a large, prospective, keted as Plavix) and omeprazole (marketed as Prilosec and
randomized, and blinded trial should carry more Prilosec OTC). Available at:
weight than a case report. sandProviders/DrugSafetyInformationforHeathcareProfes-
To help the reader judge the strength of each sionals/PublicHealthAdvisories/ucm190825.htm. Accessed
reference, pertinent information about the study, March 1, 2013. (FDA public health advisory)
such as the type of study and the number of patients 16. Corley DA, Cello JP, Adkisson W, et el. Octreotide for acute
esophageal variceal bleeding: a meta-analysis. Gastroenterol-
in the study, will be included in bold type following ogy. 2001;120(4):946-954. (Meta-analysis; 475 patients)
the reference, where available. In addition, the most 17. Tsai YT, Lay CS, Lai KH, et al. Controlled trial of vasopressin
informative references cited in this paper, as deter- plus nitroglycerin vs. vasopressin alone in the treatment of
bleeding esophageal varices. Hepatology. 1986;6(3):406-409.
mined by the authors, will be noted by an asterisk (*)
(Prospective randomized controlled trial; 39 patients)
next to the number of the reference. 18. Gimson AE, Westaby D, Hegarty J, et al. A randomized trial
of vasopressin and vasopressin plus nitroglycerin in the con-
1. Peura DA, Lanza FL, Gostout CJ, et al. The American College trol of acute variceal hemorrhage. Hepatology. 1986;6(3):410-
of Gastroenterology Bleeding Registry: preliminary findings. 413. (Prospective randomized trial; 72 bleeding episodes in
Am J Gastroenterol. 1997;92(6):924-928. (Retrospective survey; 57 patients)
1235 respondents) 19. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of
2.* Afessa B. Triage of patients with acute gastrointestinal bleed- blood products transfused affects mortality in patients
ing for intensive care unit admission based on risk factors receiving massive transfusions at a combat support hospital.
for poor outcome. J Clin Gastroenterol. 2000;30(3):281-285. J Trauma. 2007;63(4):805-813. (Retrospective; 246 patients)
(Prospective; 411 patients) 20. Perkins JG, Cap AP, Andrew CP, et al. An evaluation of the
3.* Barkun AN, Bardou M, Kuipers EJ, et al. International impact of apheresis platelets used in the setting of massively
consensus recommendations on the management of patients transfused trauma patients. J Trauma. 2009;66(4 Suppl):S77-
with nonvariceal upper gastrointestinal bleeding. Ann Intern S84. (Retrospective; 694 patients)
Med. 2010;152(2):101-113. (Multidisciplinary consensus 21. Scalea TM, Bochicchio KM, Lumpkins K, et al. Early aggres-
group; 34 experts from 15 countries) sive use of fresh frozen plasma does not improve outcome in
4.* Gotzsche PC, Hrobjartsson A. Somatostatin analogues for critically injured trauma patients. Ann Surg. 2008;248(4):578-
acute bleeding esophageal varices. Cochrane Database Syst 584. (Prospective; 806 patients)
Rev. 2008;(3):CD000193. (Systematic literature review) 22. Hbert PC, Yetisir E, Transfusion Requirements in Criti-
5. Sreedharan A, Martin J, Leontiadis GI, et al. Proton pump cal Care Investigators for the Canadian Critical Care Trials
inhibitor treatment initiated prior to endoscopic diagnosis in Group, et al. Is a low transfusion threshold safe in critically
upper gastrointestinal bleeding. Cochrane Database Syst Rev. ill patients with cardiovascular diseases? Crit Care Med.
2010;(7):CD005415. (Systematic literature review) 2001;29(2):227-234. (Prospective randomized; 357 patients)
6.* Scottish Intercollegiate Guidelines Network (SIGN). Man- 23. Gutirrez A, Snchez-Pay J, Marco P, et al. Prognostic value
agement of acute upper and lower gastrointestinal bleeding. of fibrinolytic tests for hospital outcome in patients with
Available at: acute upper gastrointestinal hemorrhage. J Clin Gastroenterol.

EMCC 2013 10 Volume 3, Number 2

2001;32(4):315-318. (Prospective; 84 patients) 1. The most common cause of massive upper GI
24. Bosch J, Thabut D, European Study Group on rFVIIa in UGI
bleeding is:
Haemorrhage, et al. Recombinant factor VIIa for upper gas-
trointestinal bleeding in patients with cirrhosis: a random- a. Esophageal varices
ized, double-blind trial. Gastroenterology. 2004;127(4):1123- b. Diverticula
1130. (Prospective randomized trial; 245 patients) c. Arteriovenous malformations
25. Ejlersen E, Melsen T, Ingerslev J, et al. Recombinant activated
factor VII (rFVIIa) acutely normalizes prothrombin time in
d. Gastritis
patients with cirrhosis during bleeding from oesophageal e. Gastric and duodenal ulcers
varices. Scand J Gastroenterol. 2001;36(10):1081-1085. (Pro-
spective observational; 10 patients) 2. In regard to the stabilization and monitoring
26.* Thabut D, de Franchis R, Bendtsen F, et al. Efficacy of acti-
vated recombinant factor VII in cirrhotic patients with upper
of patients with massive upper GI bleeding,
gastrointestinal bleeding: a randomized placebo-controlled which of the following is TRUE?
double-blind multicenter trial. Gastroenterology. 2003;124(4) a. PPIs are not recommended.
(Suppl1):A697. (Prospective randomized; 245 patients) b. Initial and serial coagulation studies should
27. Ansell J, Hirsh J, Hylek E, et al. Pharmacology and manage-
ment of the vitamin K antagonists: American College of be used to guide decision making.
Chest Physicians Evidence-Based Clinical Practice Guide- c. Continuous cardiac and pulse oximetry
lines (8th Edition). Chest. Jun 2008;133(6):160S-198S. (Practice monitoring are required.
guideline) d. Consultation with subspecialists should
28. van Ryn J, Stangier J, Haertter S, et al. Dabigatran etexilate--a
novel, reversible, oral direct thrombin inhibitor: interpreta- be delayed until after stabilization and
tion of coagulation assays and reversal of anticoagulant resuscitation.
activity. Thromb Haemost. 2010;103(6):1116-1127. (Literature
3. In regard to the use of angiography in patients
29. Eerenberg ES, Kamphuisen PW, Sijpkens MK, et al. Reversal
of rivaroxaban and dabigatran by prothrombin complex with massive upper GI bleeding, which of the
concentrate. Circulation. 2011;124(14):1573-1579. (Prospective following is TRUE?
randomized; 12 patients) a. Angiography is highly specific for detection
30. Findley LJ, Redstone PM. Blood transfusion in adult
Jehovahs Witnesses. A case study of one congregation.
of bleeding at rates of at least 0.5 mL/min.
1982;142(3):606-607. (Retrospective survey; 70 respondents) b. Angiography can detect bleeding at slower
31. Watch Tower Bible and Tract Society of Pennsylvania. How rates than can be detected by radionuclide
can blood save your life? Available at: imaging.
life/. Accessed March 1, 2013. (Website)
c. Angiography has the disadvantage of being
diagnostic but not therapeutic.
d. Angiography is contraindicated in patients
CME Questions with nonvariceal upper GI bleeding.

Take This Test Online! 4. In regard to blood product transfusion for pa-
tients with massive upper GI bleeding, which
Current subscribers can receive CME credit of the following is TRUE?
absolutely free by completing the following test. a. A hemoglobin level of 7 to 8 gm/dL should
This issue includes 3 AMA PRA Category 1 CreditsTM. be considered the endpoint of resuscitation.
Online testing is now available for current and b. The recommended PRBC:FFP:platelet
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this issue, scan the QR code below or visit 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. Volume 3, Number 2 11 EMCC 2013

CME Information
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EMCC 2013 12 Volume 3, Number 2