Emp Gastrointestinal Bleeding

EMERGENCY MEDICINE
PRACTICE
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EMPRACTICE NET
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
March 2004
Gastrointestinal Bleeding: An
Evidence-Based ED Approach
To Risk Stratification
Volume 6, Number 3
Authors
John L. Westhoff, MD
CPT, MC, USA; Emergency Medicine Residency, Madigan
Army Medical Center / University of Washington, Fort
Lewis, WA.
A foul stench arises from behind one of the patient curtains. The wafting, horrid
smell seems to permeate all corners of the ED. You are on shift. There is no escape.
A brave nurse emerges from behind that particular curtain and gestures to you. You
enter the patient area. A mildly sweaty, elderly man is there in a patient gown. His
skin color approximates that of the white bed linen. A bedpan in the nurses hands
is nearly full with foul black liquid. An older woman that you barely noticed before
speaks. Hes now telling me that his stools have been somewhat dark since his
doctor started him on that new medicine. Do you think hell be okay?
ROBLEMS associated with GI bleeding are challenging for patients and

physicians. Seemingly deadly bright red blood from the anus can arise
from simple, benign hemorrhoids. Robust patients with brown stools that
test positive for occult blood, on the other hand, may harbor a deadly
malignancy or a rapidly fatal aortoenteric fistula.
Blood in the GI tract may not present in a way that is readily apparent
to patients. When digested blood is expelled as coffee-ground vomitus or as
black diarrhea, patients may not even recognize this as bleeding. On the
other hand, there are times when there appears to be GI bleeding when
there is not. Both unsuspecting physicians and patients may be misled by
foods or medications that alter the appearance of stools in such a way as to
simulate GI bleeding when, in fact, there is none. These challenges are
perhaps greatest for chronic alcoholics, who are frequently stricken by GI
bleeding and have both social problems and physiologic abnormalities that
increase the risk of serious complications.
Bleeding in the GI tract is, to some extent, mysterious. The actual
location of the bleeding is seldom immediately apparent based solely on the
history and physical examination. Even after endoscopic evaluation, this
may remain elusive. In addition to the location being unclear, the cause of
the bleeding can also be difficult to determine. The etiologies are myriad
and include infections, malignancies, vascular disorders, medication effects,
and coagulopathies. The treatments available are similarly diverse, includGuest Editor
Editorial Board
Lance Brown, MD, MPH, FACEP,

Chief, Division of Pediatric
Emergency Medicine;
Associate Professor,
Department of Emergency
Medicine; Loma Linda
University Medical Center
and Childrens Hospital, Loma
Linda, CA.
Judith C. Brillman, MD, Associate

Professor, Department of
Emergency Medicine, The
University of New Mexico Health
Sciences Center School of
Medicine, Albuquerque, NM.
Associate Editor
Andy Jagoda, MD, FACEP,
Vice-Chair of Academic
Affairs, Department of
Emergency Medicine;
Residency Program Director;
Director, International Studies
Program, Mount Sinai School
of Medicine, New York, NY.
Francis M. Fesmire, MD, FACEP,

Director, Heart-Stroke Center,
Erlanger Medical Center;
Assistant Professor of Medicine,
UT College of Medicine,
Chattanooga, TN.
Valerio Gai, MD, Professor and
Chair, Department of Emergency
Medicine, University of Turin,
Italy.
Michael J. Gerardi, MD, FAAP, FACEP,
Clinical Assistant Professor,
Medicine, University of Medicine
and Dentistry of New Jersey;

Director, Pediatric Emergency
Medicine, Childrens Medical
Center, Atlantic Health System;
Medicine, Morristown
Memorial Hospital.
Michael A. Gibbs, MD, FACEP, Chief,
Medicine, Maine Medical Center,
Portland, ME.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor,
MI; Clinical Professor, Department
of Emergency Medicine,
University of Michigan Medical
School, Ann Arbor, MI; Past
President, ACEP.
Francis P. Kohrs, MD, MSPH, Lifelong
Medical Care, Berkeley, CA.
Kurtis R. Holt, MD
MAJ, MC, USA; Associate Program Director, Emergency
Medicine Residency, Department of Emergency
Medicine, Madigan Army Medical Center / University of
Washington, Fort Lewis, WA.
Peer Reviewers
Michelle Gill, MD
Assistant Professor, Department of Emergency
Medicine, Loma Linda University Medical Center,
Loma Linda, CA.
Carolyn J. Sachs, MD, MPH
Associate Professor, UCLA Emergency Medicine Center,
Los Angeles, CA.
CME Objectives
Upon completing this article, you should be able to:
1. describe the most common causes of and risk factors
for gastrointestinal hemorrhage;
2. describe the elements of the history, physical
examination, and laboratory studies that are
most useful in evaluating a patient with
gastrointestinal hemorrhage;
3. discuss which criteria delineate the low-risk
population, acceptable for discharge to home from
the ED;
4. discuss which patients with gastrointestinal
hemorrhage are at increased mortality risk and
require ICU admission; and
5. summarize the findings of the important literature on
gastrointestinal hemorrhage published in the past
several years.
Date of original release: March 1, 2004.

Date of most recent review: February 3, 2004.
See Physician CME Information on back page.
Michael S. Radeos, MD, MPH,

Attending Physician, Department
of Emergency Medicine, Lincoln
Medical and Mental Health
Center, Bronx, NY; Assistant
Professor in Emergency Medicine,
Weill College of Medicine, Cornell
University, New York, NY.
Steven G. Rothrock, MD, FACEP,
FAAP, Associate Professor
University of Florida; Orlando
Regional Medical Center; Medical
Director of Orange County
Emergency Medical Service,
Orlando, FL.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Professor of Emergency Medicine
and Chairman, Department of
Emergency Medicine, Vanderbilt
University Medical Center;
Medical Director, Metro Nashville
EMS, Nashville, TN.
Mark Smith, MD, Chairman,
Medicine, Washington Hospital
Center and Georgetown
University School of Medicine,
Washington, DC.
Charles Stewart, MD, FACEP,
Colorado Springs, CO.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
Emergency Medicine, University
of Alabama at Birmingham,
Birmingham, AL.
COPYRIGHTED MATERIALDO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC
When this body of literature is reviewed, even given

the inherent limitations and inconsistencies, some
features of high-risk and low-risk patients are suggested.
(See Table 1.)
In the past, GI bleeding had been an indication
for admission to the hospital in all but the most trivial
cases. Clinicians probably recognized that this approach
was in all likelihood excessively risk averse, but given
the mysterious nature of GI bleeding and medicolegal
concerns, it was difficult to safely select patients for
discharge from the ED. Over the past 20 years, a
number of studies have been published addressing this
problem. The typical approach has been to first identify
risk factors either through a review of the available
literature, a chart review, or retrospective study comparing risk factors with outcome. The specific outcomes of
interest vary from paper to paper, but the emphasis on
minimizing risk in the management of GI hemorrhage is
a common theme.
A small number of studies looked at risk stratifying
patients based solely on clinical features without including endoscopy findings. Bordley et al published one of
the earliest such studies in 1985.1 The paper identified six
early predictors defining the low-risk patient. The
authors asserted that a patient was low-risk if he or she
met the following criteria: 1) age less than 75 years; 2) no
unstable comorbid illness; 3) no evidence of ascites on
examination; 4) normal prothrombin time; 5) systolic
blood pressure of 100 mmHg or greater; and 6) a nasogas-
ing antibiotics, surgical excision, endoscopically guided

procedures, and medications.
Given all of these initial difficulties, the prognosis is
sometimes just a guess. Bleeding that initially seems
inconsequential may rapidly become deadly. Bleeding
that is initially very frightening to all involved may
spontaneously resolve without consequence. Fortunately,
evidence-based risk stratification can help the emergency
physician move past these uncertainties and offer the
patient the best information possible.
This article sheds light on some of the more mysterious aspects of GI bleeding. A practical, evidence-based
approach emphasizing a strategic plan for addressing the
needs of patients with suspected GI bleeding who
present to the ED is provided.
Critical Appraisal Of The Literature

There is an abundance of literature regarding GI bleeding. The subset of this literature that is most relevant to
emergency physicians involves the identification and
assessment of risk factors for subsequent complications,
including rebleeding, the need for surgery to control
hemorrhage, the need for transfusion, and death. Risk
stratification studies range from large, multicenter,
prospective studies with thousands of patients to very
small retrospective studies. There is no standardization of
terms in the literature, and, at times, terms are used
without specific definitions.
Table 1. Risk Stratification Of Patients With Hematemesis Or Melena.

Low-risk patient characteristics
High-risk patient characteristics
No debilitation
No severe liver disease
No serious concomitant disease
No anticoagulation
No severe anemia (severe anemia defined as a hemoglobin < 8 g/dL)
Age < 60 years
Stable vital signs
Systolic blood pressure 100 mmHg
Pulse < 100
No orthostatic vital sign changes (decrease in systolic
blood pressure > 10 mmHg and/or heart rate 20 beats
per minute)
No fresh, voluminous hematemesis or multiple episodes
of melena on the day of presentation
Low-risk esophagogastroduodenoscopy findings
No varices
No portal hypertensive gastropathy
No stigmata of recent hemorrhage
Flat ulcer bed without pigmentation
Mallory-Weiss tear
No lesion identified
Use of oral anticoagulants

Previously diagnosed peptic ulcer
Use of oral corticosteroids
Dyspepsia in the past year
Diabetes mellitus
Congestive heart failure
Current smoking
NSAID use
Long-term aspirin use
Known liver disease
Syncope or near-syncope as a presenting complaint
Elevated blood urea nitrogen on laboratory studies
Age > 60 years
Elevated prothrombin time
Erratic mental status
Low systolic blood pressure
Alcoholism
Supine tachycardia
High-risk esophagogastroduodenoscopy findings

Blood present in the stomach at endoscopy
Stigmata of hemorrhage (blood, clot, or
active bleeding)
Note: Not all terms are clearly defined in the available literature. Studies often used terms that were not directly comparable. In all cases, assessment
of risk involved patients undergoing endoscopy. Patients were assessed for the risk of complications, including rebleeding, the need for surgery to
control hemorrhage, the need for transfusion, and death.
Emergency Medicine Practice
www.empractice.net March 2004
Table 2. Glossary Of GI Bleeding Terms.

Angiodysplasia: small vascular abnormalities, especially of
the intestinal tract
Hemorrhoid: a varicose dilatation of a vein of the superior

or inferior hemorrhoidal plexus, resulting from a persistent increase in venous pressure
Anoscopy: examination of the anus and lower rectum by

means of a speculum (anoscope)
Cirrhosis of the liver: a group of chronic diseases of the
liver characterized by loss of normal lobular architecture
with fibrosis, and by destruction of parenchymal cells and
their regeneration to form nodules
Mallory-Weiss syndrome (tear): hematemesis or melena

that follows typically upon many hours or days of severe
vomiting and retching, traceable to one or several slit-like
lacerations of the gastric mucosa, longitudinally placed at
or slightly below the esophagogastric junction
Colonoscopy: examination of the entire colon with an

elongated flexible endoscope
Melena: the passage of dark and pitchy stools stained with

blood pigments or with altered blood
Dieulafoys lesion: a GI mucosa defect such that a submucosal artery is in abnormally close contact with the
mucosa and causes a pressure erosion, eventually
rupturing into the stomach
Peptic ulcer: an ulceration of the mucous membrane of the

esophagus, stomach, or duodenum, caused by action of
the acidic gastric juice
Portal hypertension: abnormally increased blood pressure
in the portal venous system, a frequent complication of
cirrhosis of the liver
Endoscope: an instrument for examination of the interior of

a cavity or hollow viscus
Sclerotherapy: the injection of a chemical irritant into a

vein to produce inflammation and eventual fibrosis and
obliteration of the lumen, done for treatment of hemorrhoids and esophageal varices
Endoscopy: visual inspection of any cavity of the body by

means of an endoscope
Esophageal varices: enlarged and tortuous branches of the
azygos vein that anastomose with tributaries of the
portal vein in the lower esophagus, occurring in patients
with portal hypertension
Stress ulcer: a peptic ulcer, usually gastric, resulting from

stress; possible predisposing factors include changes in
the microcirculation of the gastric mucosa, increased
permeability of the gastric mucosa barrier to acid, and
impaired cell proliferation
Esophagogastroduodenoscopy (EGD): endoscopic

examination of the esophagus, stomach, and duodenum
Gastric ulcer: a peptic ulcer of the stomach mucosa
Hematemesis: the vomiting of blood
Adapted from: Dorlands Illustrated Medical Dictionary. 30th ed.

Philadelphia: Saunders Publishing; 2003.
Hematochezia: the passage of bloody feces
March 2004 www.empractice.net
In 1997, Kollef et al reported on a classification tool

for risk stratifying patients hospitalized for acute upper
and lower GI bleeding.4 Although this classification tool
had a catchy name (BLEED) and used simple clinical
criteria, their logistic regression model may have been
inappropriate due to variables that were not independent, and the test characteristics reported for their model
were not very good (area under the receiver operating
characteristic curve of only 0.72).
In 2000, Blatchford et al reported a prospective
validation of a risk score based solely on clinical
criteria before endoscopy.5 This study included 197
patients. Although reasonable test characteristics were
presented for the calculated risk scores based on clinical
criteria, the dispositions of the patients and the performance of endoscopy in these subjects were not adequately described.
The small sample sizes of these studies limit the
general applicability of the results. Although it is appealing to potentially avoid the time, cost, and risk of
endoscopy in some patients, the combination of endoscopy results and clinical features to risk stratify patients
is much more common in the literature.
Prompt endoscopy is a key feature of most studies of
patients with hematemesis, melena, or hematochezia.
(See Table 2.) Several interesting risk stratification papers
were published during the mid-to-late 1990s. The size of
tric aspirate free of fresh blood. In the prospective arm of

the study, two of the 52 patients (3.8%) defined as low
risk had poor outcomes. One died and another required
urgent surgery. The study was small (111 patients in the
prospective arm), but it suggested that some patients
with acute GI hemorrhage might indeed be managed
selectively based on simple clinical features.
In 1991, Wrenn et al reported on a cohort of subjects
who presented to the ED with hematemesis, were
prospectively enrolled, had well-defined low-risk
characteristics, and were discharged home from the ED
without endoscopy.2 Although this study design should
yield results directly relevant to practicing emergency
physicians and no patients were found to have clinically
significant complications, the study included only 33
patients, and two of them were lost to follow-up. Obviously, it is difficult to draw conclusions from such a small
negative study.
In 1992, Harland et al reported on a retrospective
study of subjects with hematemesis.3 They identified two
groups and concluded that subjects who vomited only
altered blood (coffee grounds) and who did not have
melena, and patients who vomited only altered blood
and had hemoglobin concentrations greater than 12 g/
dL, had a low risk of complications. Only 145 subjects
(157 separate visits) were included in this study; 79 of
them were in the low-risk groups.
published. Derry and Loke presented a meta-analysis of

24 randomized, controlled trials and suggested that longterm aspirin use is associated with a significant increase
in the incidence of GI hemorrhage.16 Ofman et al presented a meta-analysis of 16 placebo-controlled randomized clinical trials and about 30 other studies and
reported that nonsteroidal anti-inflammatory drugs
(NSAIDs) are associated with an increased risk of GI
hemorrhage.17 Khuroo et al presented results from a
double-blind, placebo-controlled trial of omeprazole vs.
placebo for bleeding peptic ulcers and demonstrated that
omeprazole was better than nothing for preventing
recurrent bleeding.18 Several well-designed randomized,
controlled trials have demonstrated that octreotide is a
useful adjunct to endoscopic sclerotherapy for preventing
rebleeding from esophageal varices.19-22
these studies varied. Large retrospective studies examined the risk factors for complications of acute upper GI
hemorrhage. For example, Katschinski et al reported on
2217 patients,6 and Yavorski et al reported on 3294
patients.7 A different approach seemed to be taking form
when Longstreth and Feitelberg reported on their
experience using a practice guideline to select patients for
prompt discharge from the hospital following endoscopy.8,9 The patient population in their study was drawn
from a staff-model health maintenance organization
where urgent endoscopy was readily available and
patient tracking was excellent. In 1995 they reported on
the development of their practice guideline and on 141
prospectively enrolled patients with acute nonvariceal
upper GI bleeding.9 Of these patients, 34 were treated as
outpatients, and one of these patients returned with
rebleeding. Another study by Longstreth and Feitelberg
reported on a consecutive series of 176 patients who met
their practice guideline and were treated as outpatients
after endoscopy.8 In this cohort, no patients died, but two
were subsequently hospitalized and one had rebleeding.
In the historical context of all patients with GI bleeding
being hospitalized, the concept of treating some patients
as outpatients was interesting. In 1999, however, Tham et
al revealed some of the limitations to this approach for an
urban teaching hospital.10 In their study population, only
18 of 145 patients presenting to the ED with acute upper
GI hemorrhage met Longstreth and Feitelbergs criteria
for outpatient care. Rockall et al developed a similar set
of low-risk criteria and had much larger sample sizes.11,12
Unfortunately, a follow-up validation study failed to
validate the Rockall risk scoring system.13 Hay et al
produced similar results with a different practice
guideline and published the results in 1996 and 1997.14,15
The focus of Hay et als work was on decreasing the
length of hospital stay and not on discharge from the ED
following endoscopy.
Several large and interesting drug studies have been
Epidemiology, Etiology, And Pathophysiology

Epidemiology
There are probably many cases of GI bleeding that are
never represented in the medical literature. Undoubtedly,
there are times when individuals have external hemorrhoids or a single episode of scant hematemesis, for
example, and never seek medical attention. Given the
limitation that minor cases are probably under-represented in the literature, it appears that GI bleeding occurs
most commonly in the upper GI tract; that is, from the
esophagus, stomach, and proximal duodenum. The
lower GI tract is typically considered to consist of the
colon, rectum, and anus. The incidence of upper GI
bleeding in adults is quoted as ranging from 40 to 150
cases per 100,000 population per year.7,23-25 Upper GI
bleeding is more commonly reported than lower GI
hemorrhage, which has an incidence of 20-30 per 100,000
population per year.26-29 Overall, the incidence of clinically significant GI bleeding increases with age, particularly in those over 60, and is more common in men.23
Cost- And Time-Effective Strategies For Patients With GI Bleeding

hospital to await endoscopy. Some patients may be
discharged directly home after endoscopy is performed
in the ED.
1. Effective risk stratification is key.

Understanding risk stratification is critical to the costeffective ED management of GI bleeding. (See Table 1 on
page 2.) The cost of admission may be altogether avoided
in very low-risk patients. Appropriate ordering of blood
bank specimens, such as ordering a type and hold instead
of a type and cross in low-risk patients, offers some cost
savings without placing patients at increased risk.
3. Early pharmacologic therapy may result in

significant savings.
Initiation of acid-blocking therapies has been shown to
reduce the risk of rebleeding and thereby provide a
potential long-term cost savings. In the short term, IV
infusion of high-dose omeprazole in the first 72 hours
after presentation to the ED may be cost-effective. One
study found that averting a single episode of recurrent
bleeding after initial hemostasis was achieved
endoscopically is associated with over $1000 of cost
savings per patient.138
2. Early endoscopy saves time and money.

Early endoscopy is associated with an overall lower
cost of care, shortened hospital stays, and improved
outcomes.15,107,108 Although there is some inherent cost in
having endoscopy performed in the ED, this may be much
less expensive than admitting a patient directly to the
Peptic Ulcer Disease

The discovery of the role of Helicobacter pylori infection in
the development of peptic ulcer disease has revolutionized our understanding of peptic ulcer disease, the most
common cause of upper GI bleeding. H. pylori is a gramnegative, spiral, flagellated bacterium that survives in the
acidic environment of the stomach by virtue of a ureasedriven process in which it produces an alkaline local
environment. Gastritis is found in virtually all patients
infected with H. pyloriin fact, the bacterium has such a
strong causal relationship with the disease that peptic
ulcer disease is thought to be uncommon in H. pylorinegative individuals who are not taking NSAIDs.37,38
Smoking has been found to be an independent risk factor
for GI bleeding from peptic ulcers,39 and a recent study
found a synergistic relationship between smoking and
concomitant H. pylori infection.38
Etiology
There are many causes of GI bleeding.
Upper GI bleeding is most commonly due to peptic
ulcers, erosive gastritis, or esophageal varices;24,25,30-32
other causes include gastric ulcers, duodenal ulcers,
erosive esophagitis, erosive duodenitis, Mallory-Weiss
tears, aortoenteric fistula, Dieulafoys lesion, malignancy,
or angiodysplasia.30
Lower GI bleeding can be due to diverticulosis,
colitis, colonic ulcers, hemorrhoids, malignancy, or
angiodysplasia.30,33,34 One rare but rapidly deadly cause
of hematochezia is an aortoenteric fistula.35,36 An
aortoenteric fistula is a direct communication between
the aorta and the lumen of the GI tract. This rare but
deadly clinical condition can occur when an abdominal
aortic aneurysm forms an adhesion with the GI tract
and erodes through the bowel wall.35 Although this form
of primary aortoenteric fistula can occur, the fistula is
more commonly seen as a secondary process following
aortic grafting.36
In a minority of cases, no source of bleeding
is found after upper and lower endoscopy. An
esophagogastroduodenoscopy (EGD) and colonoscopy
can only go so far into the GI tract, leaving areas of the
small bowel unexplored. In these cases, small bowel
hemorrhages may be suspected, especially if intermittent
bleeding persists. This situation, however, is uncommon.
In one study of 465 patients, there were only three cases
(0.6%) of small bowel hemorrhages identified.30
Colonic Disease
There are several diseases of the colon that can cause
bleeding, and the pathophysiology of each is somewhat
unique. The common theme, however, is that there is
mucosal disruption, which allows the lumen of blood
vessels to communicate with the lumen of the gut. The
blood vessels can be very small, as might be seen in
radiation colitis, infectious colitis, or malignancy.
Alternatively, the blood vessels may be somewhat larger,
as might be seen in diverticulosis. The most dramatic
example of this process would be an aortoenteric fistula,
whereby the lumen of the aorta communicates with the
lumen of the gut.35,36
Drug-Related Causes
There is clearly an increased incidence of GI bleeding
among patients who use certain medications. NSAIDs,
including aspirin, have most commonly been implicated.16,17,37,38,40,41 However, the average patient with
NSAID-associated bleeding is older at age of onset and
has an associated decreased risk in mortality compared to
non-NSAID-related bleeding.25,42 This phenomenon is
thought to be attributable to an unmasking of subclinical
disease by widespread NSAID use. Patients at risk for GI
bleeding who require NSAID therapy are frequently put
on the new selective cyclooxygenase-2 inhibitors. As
advertised, these drugs are associated with a decreased
risk of GI bleeding compared to conventional NSAIDs.43,44
The ubiquitous use of daily aspirin among the
elderly makes this NSAID of particular interest to
epidemiologists. A recent study by the U.S. Preventive
Services Task Force on the daily use of aspirin for the
primary prevention of cardiovascular events found an
odds ratio of 1.7 for major GI bleeding in daily aspirin
users over individuals not taking aspirin.41 Even with
enteric coating or in the 81 mg daily dose, aspirin is
associated with an increased incidence of GI bleed-
Pathophysiology
Esophageal Varices
Esophageal varices are a particularly lethal source
of upper GI bleeding. They are associated with severe
liver disease, in which sclerotic tissue replaces normal
liver parenchyma; this subsequently blocks blood flow,
raises portal pressure, and thereby provides stimulus for
the formation of collateral circulation (i.e., varices).
Alcoholic liver disease and viral hepatitis (B, C, and D)
are among the most common causes of cirrhosis. Less
common precursors to the formation of varices are nonalcoholic steatohepatitis, primary biliary cirrhosis,
secondary biliary cirrhosis (e.g., a complication of
cholecystectomy), hepatotoxic medications, environmental toxins, schistosomiasis, and congestive heart failure
with liver congestion. Inheritable etiologies include
autoimmune hepatitis, alpha-1 antitrypsin deficiency,
hemochromatosis, Wilsons disease, galactosemia, and

glycogen storage diseases.
Mortality associated with GI bleeding seems to be

more directly related to advanced age and coexisting
illness than to bleeding, per se. The authors of a Dutch
study went so far as to report that only one-third of
the mortality associated with upper GI bleeding was
directly attributable to bleeding, while two-thirds of
the patients were thought to die from other causes.24
Underlying conditions including malignancy, cirrhosis,
and chronic respiratory illnesses are particularly bad
prognostic factors.25
Prehospital Care
ing16,38,41and the bleeding is not just from ulcers, as

had been previously thought. Aspirin has also been
associated with an increased incidence of variceal
bleeding in patients with cirrhosis.45 Patients intolerant of
aspirin therapy may be placed on alternative platelet
inhibitors (e.g., ticlopidine) that appear to have a lower
incidence of bleeding when compared with aspirin.46
Other medications with a definite association with GI
bleeding include chemotherapeutic agents,47-49 oral
anticoagulants,39,50 and steroids.25,39
The priorities of prehospital personnel caring for patients

with GI bleeding are essentially the same as for any
serious medical condition. Protection of the airway
against aspiration, obtaining intravenous access, and
initiation of appropriate fluid resuscitation to support
the patients circulation are the main priorities. Hypotension in the prehospital settingeven if it is resolved
by the time of the ED visitsuggests that the patient is
at a higher risk for complications than he or she would
be otherwise.
Physiologic Stress
The critical care experience with GI bleeding has led
intensivists to study the various physiologic contributors
to GI bleeding. Stressors identified as most strongly
predisposing to GI bleeding include sepsis, hypothermia,
radiation therapy, treatment for heart failure or diabetes,
renal failure, and graft-versus-host disease.39,51-58
Emergency Department Evaluation

History
For most patients with GI bleeding, the definitive cause
and location of the bleeding will come at the hands
of a gastroenterologist or general surgeon. After
considering and dismissing alternative diagnoses that
mimic GI bleeding (see Table 3), the emergency
physicians main priority is to assess cardiovascular
stability, identify historical features helpful in risk
stratifying the patient for subsequent complications, and
make a rough estimate as to whether the bleeding is from
an upper or lower source.
Risk assessment is critical in the treatment and
cost-effective disposition of a patient with GI bleeding;
therefore, focus on elements of the history that are
most closely associated with a high likelihood of
rebleeding and mortality. In a 2001 review of the available literature, the American Society for Gastrointestinal
Endoscopy identified four non-endoscopically derived
key predictors of rebleeding that should be the focus of
the initial evaluation because of their usefulness as risk
stratifiers in multiple studies: 1) older age; 2) shock
(hemodynamic instability or orthostasis); 3) comorbid
disease states; and 4) the use of anticoagulants or the
presence of coagulopathy.59
A GI bleed is characterized clinically as upper or
lower based on presentation. Questions characterizing
the manner and amount of blood will suggest a source of
bleeding, but like most things in medicine, there are no
hard-and-fast rules.
Characterization of bleeding as hematemesis,
melena, or hematocheziaterms that specify the location
as well as the physical appearance of the blood lostare
helpful. However, terms used to refer to GI bleeding are
sometimes confusing and used incorrectly in day-to-day
practice. (See Table 2 on page 3.) The term hematemesis
refers to the vomiting of blood, whether fresh or partially
digested (coffee-ground emesis). Hematemesis very
strongly suggests an upper GI source. A significant but
unusual exception is bleeding from an aortoenteric
fistula, in which such massive bleeding into the lower GI
tract occurs that retrograde filling of the tract can result
in hematemesis. In addition, lower GI bleeding from any
source can imitate an upper GI bleed when a concomitant
Differential Diagnosis
The main issue in considering GI bleeding is to decide
whether the patient is actually having GI bleeding.
Several conditions can mimic GI bleeding. (See Table 3.)
Ruling GI bleeding in or out may not be entirely straightforward. If an alternative diagnosis is not readily evident,
the conservative approach is to assume that the patient
is having GI bleeding until an EGD and colonoscopy can
be performed.
Table 3. GI Bleed Fake-Outs: Conditions

That May Mimic Gastrointestinal Bleeding.
Mimics for hematemesis
Nosebleeds
Dental bleeding
Tonsil bleeding
Red drinks (e.g., fruit punch)
Red food (e.g., cranberry jelly)
Mimics for melena

Bismuth-containing medications
(e.g., Pepto-Bismol)
Activated charcoal ingestion
Mimics for hematochezia
Partially chewed/digested red grapes

Red food (e.g., beets)
Vaginal bleeding
Gross hematuria
Weeping buttock lesions
Ingestions that may cause

false-positive occult blood testing
Red meat
Turnips
Horseradish
Vitamin C
Physical Examination
Is this patient in shock? is the first question that must
be answered on physical examination. Vital signs should
be screened for hypotension or tachycardia. Orthostatic
vital signs should be sought, as significant postural
changes in blood pressure have been independently
associated with increased mortality.8,9 Mental status
should be evaluated for signs of poor cerebral perfusion.
The color, warmth, and moisture of the skin should
be assessed.
After an assessment of shock is made, focus the
examination toward the detection of comorbid disease. A
cardiopulmonary examination should be done with
attention to the presence of congestive heart failure (e.g.,
rales on lung examination, jugular venous distention).
Examination of the abdomen should include an assessment of tenderness consistent with perforation, the
presence of a bruit or pulsatile abdominal mass, and
signs of portal hypertensionascites or caput medusae. Assess the sclera and skin for jaundice and the
stigmata of vascular disease or a hypocoagulable state
(e.g., telangectasia, purpura, petechiae, etc.).
In general, when GI bleeding is suspected, perform a
rectal examination with anoscopy or (if available)
proctosigmoidoscopy to identify a possible source of
bleeding (e.g., hemorrhoids, polyps, fissures, etc.) and to
confirm the presence of gross or occult blood in the rectal
vault if this is in doubt. When available, stool and/or
vomitus should be inspected for the presence, quantity,
and quality of blood present.
Diagnostic Studies
Nasogastric Aspiration
Although not evidence-based, it may be prudent to have
patients with melena or hematochezia without a definite
rectal source visualized on examination to have a
nasogastric tube placed and gastric aspiration performed.
The presence of blood in the aspirate is usually considered as confirmation of an upper GI bleed. However, it is
possible to have a positive aspirate in a lower GI bleed
when there is a concurrent bowel obstruction. If ongoing
bleeding (represented by persistent bright red blood in
the nasogastric aspirate) is identified, this information
can help in risk stratifying the patient and suggests that a
over-the-counter bismuth-containing dyspepsia products.

Asking directly about these substances may be quite
helpful in directing care.
Occasionally a patient will present with a previous
history of bleeding from a relatively benign source.
Although it is certainly likely that subsequent bleeding
will be from this previously known source, a more
ominous, previously undiscovered source of bleeding
may be involved. Given how difficult it is to identify the
location of GI bleeding solely using the information
provided by the history, it is prudent to assume the worst
at the outset of the ED encounter and arrange endoscopy.
obstruction forces the passage of blood back through the

pylorus. Hematochezia is sometimes used (incorrectly)
as a synonym for lower GI bleeding. The term means
literally to defecate blood and is not restricted to
bright red blood per rectum. It refers to the passage of
blood that still resembles bloodthat is, it is red or
maroon and recognizable to the patient as blood. The
passage of blood blackened by the digestive process is
referred to as melena, from a Greek verb meaning to
darken or turn black. The distinction is important
because melena suggests an upper GI source. Of course,
sometimes blood is found in stools as both red and black.
The onset, temporal pattern, and duration of
symptoms are often clinically useful. The onset of
hematemesis after vigorous non-bloody retching, for
example, would suggest an esophageal tear. Bleeding that
has been unchanged for months would merit a different
approach than bleeding that began suddenly earlier in
the day.
While it is a maxim in medicine that patient estimates of blood loss are dubious, an effort should be made
to characterize the quantity of blood lost. Patients may
identify with questions about the presence of large
clots vs. streaks of blood. A more clinically useful way
to assess for the degree of blood loss is to inquire about
signs and symptoms consistent with major intravascular
losses (i.e., a functional assessment of blood loss).
Dizziness, lightheadedness, or confusion are concerning for significant hypovolemia. Dyspnea and chest pain
in the setting of GI bleeding are ominous signs of
decreased oxygen-carrying capacity, and myocardial
ischemia must be ruled out. The presence of abdominal
pain may be a relatively benign symptom associated with
GI peristalsis during GI hemorrhage or may indicate
another serious cause of hypovolemia, such as a concurrent abdominal aortic aneurysm. A history of prior
abdominal vascular surgery increases the likelihood of an
aortoenteric fistula.35,36 A history of dyspepsia may raise
the suspicion for erosive gastroesophageal pathology, but
it is interesting to note that gastroenterologists have
failed thus far in predicting endoscopic findings based on
a history of dyspepsia, even in the presence of so-called
alarm symptoms (e.g., dysphagia, weight loss, anemia).60 Many patients with major upper GI bleeding have
no preceding symptoms.42
The past medical history should focus on clinically
important comorbid illnesses and high-risk medications.
(See Table 1 on page 2.) Important comorbid illnesses
that are predictive of increased mortality include congestive heart failure, coronary artery disease, known liver
disease, a history of alcoholism, a history of smoking,
and diabetes mellitus. A review of medications should
be made with particular attention to those agents known
to increase the risk of GI bleeding. These include warfarin, aspirin and other NSAIDs, corticosteroids, and
chemotherapeutic agents. Some medications are wellknown to cause stool color changes that mimic GI
bleeding. For example, black stools may be seen with
prompt EGD is indicated.4,30 Nasogastric aspiration may

not be necessary in patients who are undergoing very
prompt endoscopic evaluation.
passage of a nasogastric tube may lead to misleading

positive tests.
Endoscopy
Laboratory Tests
During the past 30 years, the major advances in the

diagnosis and treatment of GI bleeding have primarily
involved endoscopy. The development of endoscopy
has allowed for the ability to visualize the sites of
bleeding in the majority of GI bleeding cases. This
information can be used by the endoscopist to guide
therapy and to stratify patients according to their risk
for rebleeding. This is particularly true if bleeding
esophageal varices are identified.61
Laboratory testing should include, at minimum,

a hematocrit (or hemoglobin), blood urea nitrogen
(BUN), and coagulation studiesparticularly a prothrombin time. These lab tests have been incorporated
into clinical practice as risk stratification tools. (See
Table 1 on page 2.) Although the GI bleeding literature
has not identified thrombocytopenia as an independent
risk factor, it is intuitively appealing to check the
platelet count, as thrombocytopenia is known to be
common in alcoholics and a cause of bleeding in general.
In most instances, a blood bank specimen is indicated,
as transfusion is frequently indicated in patients with
GI bleeding.
Angiography And Scintigraphy
Because anemia can decrease the oxygen-carrying

capacity of the blood and can consequently lead to
clinically significant myocardial ischemia, an electrocardiogram is typically indicated. This is especially true
in older patients and those with known coronary
artery disease.
Scintigraphy or angiography are used to localize lower

GI bleeding, usually when colonoscopy has failed to
identify a source or is not feasible because of massive
bleeding. Scintigraphy can detect bleeding at slower rates
than can be found on angiography, but angiography has
the additional benefit of being potentially therapeutic in
centers where embolization is available.62 Localization
from either study is useful in helping a surgeon choose
the appropriate operation. Interestingly, heparin has been
used to improve the diagnostic yield of angiography in
the investigation of obscure GI bleeding.63
Occult Blood/Guaiac Testing
H. pylori Testing
Rectal guaiac testing can be used to evaluate the

contents of the rectum for occult blood when the
presence of melena or hematochezia is in doubt. The test
can be positive for up to two weeks after a bleed, and its
lack of specificity for acute bleeding means that it is
generally more useful in the diagnosis of chronic occult
bleeding than it is in the setting of acute GI bleeding. The
ingestion of some foods may lead to false-positive tests.
(See Table 3 on page 6.) Occult testing is available for
gastric aspirate, but minor trauma from vomiting or the
While testing for the presence of H. pylori plays an

important role in the outpatient management of patients
with peptic ulcer disease, this test has essentially no
practical utility in the ED. Occasionally this test may be
sent from the ED as a courtesy for the gastroenterologist
or primary physician who will be following up with the
patient as an outpatient. Serologic testing for H. pylori is
preferred in the setting of acute bleeding, as more
invasive testing has been shown to be compromised
during acute bleeding.64
Electrocardiogram
Key Points In The Management Of Patients With GI Bleeding

Involve an endoscopist early in the management of a
patient with GI bleeding.
Recommend discontinuing drugs that can increase the risk

of GI bleeding, such as NSAIDs.
If a patient is at risk for bleeding to death, promptly notify

both a gastroenterologist and a surgeon, as the patient
may need a surgical resection of the bleeding area to stop
the bleeding.
Initiate proton pump inhibitor treatment in those very lowrisk patients who are discharged from the ED without
undergoing endoscopy.
There is a high mortality associated with GI bleeding
in patients with a history of alcoholism and cirrhotic
liver disease.
Promptly consult a vascular surgeon if a patient who has

had a prior abdominal aortic aneurysm repair presents
with hematochezia. The patient may be harboring a deadly
aortoenteric fistula. Surgical repair must take place before
the bleeding becomes brisk if the patient is to have a good
chance of survival.
Promptly administer somatostatin when a patient with

suspected variceal bleeding (e.g., a history of cirrhotic liver
disease, alcoholism, or known varices) presents to the ED.
Gastric Acid Secretion Inhibition

A great deal of research into gastric acid inhibition
treatments has taken place in the intensive care unit
(ICU) setting. Whether or not data concerning stressulcer bleeding prevention in the ICU population can be
applied to controlling GI bleeding in ED patients is open
to debate, but it stands to reason that many of the same
pathophysiologic principles would apply. Data from
studies of ICU patients on the effect of ranitidine and
sucralfate in preventing GI bleeding present conflicting
results or are inconclusive.55,57,58 In contrast, proton pump
inhibitors (e.g., omeprazole) have been shown to be
superior to H2-blocking medications in preventing
recurrent bleeding in patients with upper GI bleeding in
both sub-acute and chronic settings, although the effect of
proton pump inhibitors on reducing mortality is less
clear.18,66,67,69-71 The use of proton pump inhibitors in the
setting of acute GI bleeding, especially in cases of
bleeding peptic ulcers, has been recommended.72
The first priority in the management of any patient with

GI bleeding is a rough assessment of how much blood the
patient has lost. If a patient is hemodynamically unstable,
immediate interventions are indicated. Accordingly, as
happens so often in emergency medicine, treatment must
come before a definitive diagnosis has been established.
Clinical Pathway
The Clinical Pathway on page 10 incorporates the
important evidence-based literature concerning the
evaluation and disposition of patients presenting to the
ED with GI bleeding. While it does not provide a cookbook approach to treatment and evaluation, implicit in
the decision tree are those historical, laboratory, and
clinical elements that have been validated as having
particular value in assessing risk.
Note that the clinical pathway does not include
endoscopic findings. Although much has been written
about using endoscopic findings to determine the
disposition of the patient, the ultimate interpretation of
endoscopic findings is the purview of the consultant.
H. pylori Treatment
Although it is probably reasonable that all patients with
peptic ulcer disease should be tested for H. pylori infection and treated with antibiotics,73,74 this process is not
typically undertaken in the ED.
Hemodynamic Therapy
Volume replacement with normal saline is an appropriate
initial treatment for patients presumed to be in hemorrhagic shock. As fluid resuscitation is initiated and
hemorrhagic shock is confirmed, prompt blood transfusion should be initiated with type O-negative packed red
blood cells. If fluid volume is replaced with saline, the
patient will almost certainly have a worsening of their
anemia. If this anemia reaches a critical level, the oxygencarrying capacity of the blood will be further decreased.
Patients with pre-existing coronary artery disease may
develop myocardial infarction in this setting.
For many patients with acute and ongoing GI
bleeding, particularly alcoholics, a coagulopathy should
be presumed and fresh frozen plasma administered. In
more stable patients, laboratory testing for the prothrombin time may be performed prior to the administration of
the fresh frozen plasma. Platelets may be indicated in the
thrombocytopenic patient with GI bleeding.
As with any transfusion of blood products, when
circumstances permit, the risks and benefits should be
discussed with the patient before transfusion.
Vasopressin Analogs
Vasopressin causes contraction of the smooth muscle of
the GI tract as well as all parts of the vascular bed. This
effect has been exploited successfully to stop acute
hemorrhage (albeit without U.S. Food and Drug Administration approval).75-77 Vasopressins vasoconstrictive
effects are systemic and can be associated with peripheral
necrosis, arrhythmias, myocardial ischemia, and cardiac
arrest. Because of these risks, and in the absence of any
studies that demonstrate a difference in mortality, the use
of vasopressin in GI bleeding has largely been abandoned
in favor of other drugs. Drugs unavailable in the United
States, such as glypressin, may be more effective and
have fewer side-effects associated with their use.78-82
Somatostatin Analogs
Somatostatin is a natural hormone that decreases
splanchnic blood flow and inhibits the release of various
GI messengers. Multiple studies have shown somatostatin to be more effective than vasopressin in controlling GI
bleeding, with fewer side-effects.83-86 Like vasopressin,
somatostatin is not FDA-approved for the treatment of GI
bleeding. However, the addition of somatostatin to the
endoscopic treatment of upper GI hemorrhage has been
shown to be more effective in controlling acute bleeding
than endoscopic treatment alone.68 Studies comparing
somatostatin treatment with endoscopic sclerotherapy
have found somatostatin to be similar to or even better
than sclerotherapy in the control of acute bleeding in
cirrhotic patients.87,88 Somatostatin analogs (e.g.,
Pharmacologic Therapy
Acute medical therapy in the treatment of GI bleeding is
evolving. While pharmacologic agents have in some
instances been shown to decrease the duration and
severity of bleeding or improve the efficacy of endoscopic
treatments in achieving control of hemorrhage, most
studies have found no improvement in mortality with
their use.65-69 At this time, no medical therapy has been
shown to be an effective substitute for appropriate
endoscopic intervention.
Continued on page 11
Treatment
Hematemesis
Melena
Hematochezia
Source?
Upper
Lower
Are all of the

following true?
NO
Is endoscopy
available
in the ED?
Are all of the following true?
NO
Directly visualized hemorrhoidal bleeding clinically

assessed to be self-limited
Otherwise healthy individual with normal vital signs
No comorbidities
(Class III)
YES
Are all of the

following true?
No comorbidity
that would
normally require
ICU admission
Normal mental
status
No evidence of
ongoing
bleeding
INR < 1.2
Systolic blood
pressure > 100
mmHg
(Class II)
Disposition in
consultation with
gastroenterology
(Class II)
YES
(Class II)
YES
NO
Order
endoscopy
Patient age < 60

years
No significant
comorbidities
No history of
syncope
No melena or
ascites
No fresh blood in
nasogastric
aspirate or vomit
Hemoglogin >12
g/dL, blood urea
nitrogen <18 mg/
dL, INR normal
Not hypotensive,
tachycardic, or
orthostatic
Patient is reliable
Prompt outpatient endoscopy
can be arranged
(Class II)
Discharge to home
(Consider six-hour
observation period)
(Class III)
NO
Admit to ICU
(Class II)
YES
Clinical Pathway: Management Of Gastrointestinal Bleeding
Discharge to home
(Consider six-hour
observation period)
(Class II)
Admit to floor
(Class II)
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely
recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III:
May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
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 2004 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any
format without written consent of EB Practice, LLC.
10
In practice, the more severe the presentation of GI

hemorrhage, the earlier endoscopy should be performed.
It is difficult to convince a gastroenterologist to scope a
stable patient in the middle of the night. Even so, early
endoscopy with appropriate therapeutic intervention is
associated with an overall lower cost of care, shortened
hospital stays, and similar or improved outcomes over
late endoscopy.15,107-109 Hence, the emergency physician
managing a patient with severe GI bleeding should
consult a gastroenterologist early in the ED course. If
initial pre-endoscopic assessment is that the patient is
low-risk, that patient can be admitted to the ward or held
in the ED pending endoscopy.
octreotide and vapreotide) have been shown to be more

useful as adjuncts than gastric acid secretion inhibition89
and to decrease variceal rebleeding rates with or without
associated endoscopy.90 Somatostatin has also proven
useful in the treatment of non-variceal bleeding, particularly in the setting of peptic ulcer disease.91
Other Medications
Although beta-blockers are commonly used to prevent
rebleeding in cirrhotic patients who have demonstrated
bleeding from esophageal varices, beta-blockers do
not have a role in the acute management of variceal
bleeding.90 Other medications being studied include
estrogen-progestogen, which was found not to be
useful in the prevention of rebleeding from
angiodysplasia92and factor XIII, which, contrary
to previous studies, was found to have no beneficial
effect on the treatment of bleeding associated with
steroid-refractory ulcerative colitis.93
Balloon Tamponade
In the hands of an experienced physician, esophageal
balloon tamponade will successfully, if not definitively,
control bleeding from esophageal varices in up to 90% of
cases.110 The risk of aspiration and esophageal perforation
associated with the technique is intimidating to providers
unfamiliar with the technique. Given that it appears that
somatostatin can be an effective pharmacologic therapy
in controlling GI bleeding,111,112 it is reasonable to suggest
that balloon tamponade be reserved for cases in which
upper GI bleeding is ongoing and both pharmacologic
and endoscopic treatment are unavailable or have failed.
Endoscopy
Endoscopy has become an indispensable part of the
current diagnosis and management of both upper
and lower GI bleeding. Endoscopic therapy has been
shown to be superior to all other therapies,94-97 reduce
the rate of rebleeding, and reduce short-term morbidity
and mortality.98,99
Current studies on the use of endoscopy in the
management of GI bleeding are directed at finding the
most beneficial and cost-effective strategies, particularly
for upper GI bleeding. Epinephrine injection, band
ligation, sclerotherapy, and the use of fibrin glue are
commonly employed endoscopic treatments for upper GI
bleeding. Treatments for upper GI bleeding differ based
on whether the bleeding is due to esophageal varices or
another source. The most commonly used variceal
treatments include sclerotherapy and band ligation. Band
ligation has emerged as the superior therapy, being more
effective at controlling hemorrhage with a lower complication rate.90,100,104 Therapies for non-variceal GI bleeding
include the injection of epinephrine and sclerosing agents
into ulcers and the use of fibrin glue products. Fibrin glue
is a relatively new modality, and its role and effectiveness
have not been well-defined. It has been shown to be more
effective in the treatment of ulcers than injection with
polidocanol (a sclerosing agent),105 but it has not been
shown to improve outcomes when used as an adjunct to
epinephrine injection.106
In the case of lower GI bleeding, the endoscopic
procedure is simply referred to as colonoscopy. (See Table
2 on page 3.) A bleeding vessel identified during
colonoscopy can be clipped, cauterized, or sclerosed by
injection. If hemorrhage is massive, the source of the
lesion often cannot be visualized; angiography or
scintigraphy should be pursued with radiologic and
surgical consultation.
Angiography
Angiography can be used to locate a source of bleeding
that can then be embolized. Although angiography can
be used to assess bleeding from both upper and lower
sources, endoscopic treatment has replaced angiography
as the best diagnostic and therapeutic option for upper
GI bleeding.113 Angiography may still have a role in
evaluating lower GI bleeding.
Transjugular Intrahepatic Portosystemic Shunt

Transjugular intrahepatic portosystemic shunts (TIPS)
create a low-resistance channel between the hepatic and
portal veins by the intravenous deployment of an
expandable metal stent. Placement of the shunt does not
require general anesthesia and can be done without
compromising the surgical field should the patient
subsequently undergo liver transplantation.114 When
successfully performed, it controls bleeding in almost all
patients.115-117 A meta-analysis of studies comparing
endoscopic therapy with TIPS shows that the incidence of
rebleeding was significantly more frequent with endoscopic therapy (47%) than with TIPS (19%), but there was
no difference in mortality between the two therapies. The
TIPS procedure was associated with an increased rate of
hepatic encephalopathy.118,119 Despite an associated longer
interval free from rebleeding, TIPS is probably not a costsaving strategy in comparison with endoscopic therapy.101
When available, however, TIPS can be an effective way to
stop variceal bleeding in cirrhotic patients when other
techniques have failed.
11
Continued from page 9
Surgery
comorbid illnesses (see Table 1 on page 2), the presence of

lymphoma, in particular, has been identified as an
independent risk factor for rebleeding and mortality in
patients with HIV disease.127,129
The role of surgery in the treatment of upper GI bleeding

has decreased during the past 30 years, owing to the
evolution of improved endoscopic treatments, the
development of proton pump inhibitors, and the understanding of the role of H. pylori in the pathophysiology of
peptic ulcer disease. Many patients who would have
undergone operations in the past are managed with
endoscopically guided therapy, medications, or invasive
radiologic procedures such TIPS. However, new
laparoscopic techniques for the surgical management of
GI bleeding, including devascularization and wedge and
organ resection, are being developed in some centers.120
Lower GI bleeding is managed surgically by segmental
resection of the bleeding site. Ideally, the site of bleeding
will have been identified preoperatively so as to allow
the most conservative resection possible. Surgery is the
most aggressive way to manage GI bleeding and is now
typically undertaken when the patient is hemodynamically unstable or when endoscopic therapy is not available, not feasible, has failed to identify a source of
bleeding, or is contraindicated or not tolerated. Surgery is
typically indicated for patients with diverticular bleeding
who require four or more units of transfusion with
packed red blood cells over a 24-hour period.62
Pediatric Gastrointestinal Bleeding

Pediatric GI bleeding is, in many ways, a different clinical
entity than GI bleeding in adults. A clinically useful
discussion of GI bleeding in infants and young children is
beyond the scope of this review. The differences primarily revolve around the etiology of GI bleeding in the
different age groups. Ulcers may be seen in children in
the community, but they are more commonly seen in
children already in an intensive care setting for other
major physiologic derangements (e.g., burns, trauma,
sepsis).130 Esophageal varices are seen in young children
but are typically due to biliary atresia, neonatal hepatitis,
congenital hepatic fibrosis, and cystic fibrosis, as opposed
to adult varices, which are often due to the chronic effects
of alcoholism.130 Lower GI bleeding in young children
also exists, but this is due to a different set of conditions
than in adults. In neonates who have been born outside
of the hospital (home births), vitamin K deficiency may
cause a coagulopathy that reveals itself as ecchymosis,
petechiae, and bloody stools.130 Whereas diverticular
disease and colon malignancies are relatively common in
older adults, these conditions are just not seen in children. Much more common conditions in infants and
young children include anal fissures, milk allergy,
Meckels diverticulum, intussusception, juvenile polyps,
and infectious diarrhea.130
The different etiologies seen in adults with GI
bleeding and children with GI bleeding strongly
suggests that the approach is different. It is probably
prudent for emergency physicians unfamiliar with
pediatric GI bleeding to obtain phone consultation
with a pediatric gastroenterologist or pediatric emergency physician to assist with management when
confronted with these cases.
Special Circumstances
Chronic Alcoholics And Cirrhotic Patients
Cirrhotic patients with GI bleeding represent a group at
much higher risk for mortality and, as such, warrant
special attention.90,121,122 Variceal bleeding in cirrhotic
patients can be massive and very difficult to control.
Hence, urgent endoscopy is usually indicated in any
cirrhotic patient presenting with suspected GI bleeding.
The presence of encephalopathy, the severity of the
bleeding, and the time between clinically overt bleeding
and treatment have been identified as the main predictive
factors of failure to control bleeding.123
In addition to the control of variceal bleeding,
subsequent bacterial infections are a major cause of
morbidity in these patients. Empiric antibiotic prophylaxis with ciprofloxacin has been shown to be effective in
increasing short-term survival in cirrhotic patients with
variceal bleeding.124-126
Controversies / Cutting Edge

In the future, prehospital care providers may use pharmacologic agents to manage patients with presumed
variceal bleeding. As the medical management of variceal
upper GI bleeding has developed, the use of pharmacologic agents in the prehospital environment has begun to
be considered and studied.131,132 A recent French study, for
example, found that the prehospital use of terlipressin (a
vasopressin analog) in cirrhotic patients with upper GI
bleeding reduced the mortality rate from 46.5% in the
placebo group to 27.5% in the treated group.131 Different
models for prehospital care, including the use of physicians to provide care outside the hospital, may affect the
interpretation of studies such as this.
Endoscopy and related technologies are continuing
to evolve. The development of push enteroscopes and
laparoscopically assisted enteroscopy has allowed for
HIV Disease
Although patients with HIV disease may experience GI
bleeding from the typical causes, these patients may have
conditions that are rare in patients without HIV.34 It
appears that the most common causes of upper GI
bleeding in patients with HIV disease are peptic ulcers
and Kaposis sarcoma.127 Although much less common
than upper GI bleeding, lower GI bleeding in HIV
patients is most commonly due to cytomegalovirus
colitis, idiopathic colitis, colonic ulcers, lymphoma, and
intestinal Kaposis sarcoma.128,129 Besides anemia, thrombocytopenia, endoscopic stigmata of hemorrhage, and
12
Ten Pitfalls To Avoid

1. I knew that he had a history of esophageal varices, but
he was so stable that I admitted him to the medical floor to
await endoscopy.
Esophageal varices that have recently bled have a high risk
of rebleeding; therefore, patients should be admitted to a
monitored or intensive care area until endoscopy has been
performed. Once unleashed, the bleeding from esophageal
bleeding can be brisk and can quickly result in
hemodynamic instability.
blood per rectum. I knew he had had an abdominal aortic

aneurysm repair in the past, but he was going for
colonoscopy first thing in the morning.
Some patients are at very high risk for complications
associated with GI bleeding. The most lethal is an
aortoenteric fistula. Although this can be a primary process,
it is more commonly seen in patients who have undergone
vascular grafting of their aorta in the past.
7. What do you mean, shes back in the intensive care unit?
I sent her home. Sure, she had a little bit of a fast heart rate.
I thought she was just anxious about having vomited
blood. She was the nervous type.
Supine tachycardia places a patient at high risk for
rebleeding and complications. Missing a simple warning
sign like thisespecially one thats almost always
well-documented in the medical recordis just asking
for trouble.
2. He had some abdominal pain in addition to vomiting

blood. I just figured that the pain was due to the
forceful vomiting.
Patients with peptic ulcers can have those ulcers perforate,
and the patient will then require emergent surgery. Failure
to consider perforation in the differential diagnosis of
abdominal pain in a patient with hematemesis will result in
a delay in the diagnosis of a surgical abdomen. A bad
patient outcome is likely.
8. He had a hemorrhoid. I just figured that that was where

the blood was coming from.
Assuming that a distal site is the cause of the bleeding
without placing this information in the context of the
overall clinical picture can be very dangerous. Many
patients have external hemorrhoids. This finding, by itself,
does not mean that the hemorrhoid is the cause of the
bleeding. A much more ominous site may be lurking
proximal to an external hemorrhoid.
3. Although that 10-month-old had stool that was positive

for occult blood, he looked great. What do you mean, he
ended up in the hospital?
Pediatric patients typically have different causes of
GI bleeding than adults. Infants with GI bleeding may
have conditions such as intussusception that are not
seen in adults.
4. I dont change patients medications. I leave that
up to the primary doctor. Besides, she was only
taking ibuprofen.
Young patients who appear to have minor GI bleeding
should stop taking NSAIDs. Their seemingly minor problem
may progress if modifiable risk factors for GI bleeding are
not addressed.
9. I know that he was unconscious, but since he had stool

that was positive for occult blood, I just paged the
gastroenterologist to have him scoped.
Unless the patient has hepatic encephalopathy or is in
profound hemorrhagic shock, minor GI bleeding is
probably not the cause of altered mental status. Other
etiologies must be entertained. Shock from any cause can
cause a decrease in the blood flow to the intestines and
lead to minor GI bleeding as a concomitant effect.
Assuming that the major problem is GI bleeding may
delay the identification of the true underlying
emergency condition.
5. How could he have had a heart attack? He presented

with some relatively mild GI bleeding!
Anemia may sufficiently lower the oxygen-carrying
capacity of the blood of a patient with pre-existing
coronary artery disease to the point that myocardial
ischemia or infarction develops. Since there are obvious
problems with the administration of aspirin, heparin,
thrombolytics, and other treatments for myocardial
infarction in the setting of GI bleeding, it is better to treat
mild anemias with the transfusion of packed red blood cells
before myocardial effects occur.
10. I thought that I would let the endoscopist get a good

nights rest.
In any patient with GI bleeding that is anything other than
trivialand certainly in high-risk patientscoordinated
care with a gastroenterologist experienced in endoscopy
is critical. Close consultation and prompt endoscopy can
be life-saving.
6. How could he have died? He just had a little bright red
13
sedation, and its inability to visualize the small bowel

have prompted research into wireless capsule endoscopy.135 Israeli and British researchers have developed a
self-contained endoscope small enough to be swallowed.
The device was approved by the FDA for use in humans
in August 2001 and has been used on about 4000 patients
viewing of small bowel locations that were previously

inaccessible by endoscopy.133 Injection of bleeding vessels
with cyanoacrylate is a relatively new endoscopically
based treatment for varices that has shown promise,
though the technique awaits prospective validation.134
The discomfort of traditional endoscopy, the need for
foundly changed the way physicians manage patients

with GI bleeding. Consultation with a gastroenterologist
who can perform prompt endoscopy is now a key
component in managing patients with GI bleeding.
By using the information available in the medical
history, the physical examination, and the results of
endoscopy, emergency physicians can take much of the
mystery out of managing patients with GI bleeding.
to date. The capsule is propelled by peristalsis through

the GI tract while images are transmitted using radiotelemetry to an array of receivers that record images and
triangulate the position of the capsule in the body. In its
current iteration, it is capable of about seven hours of
continuous recording, during which time the patient can
go about his or her daily routine (undergoing the GI
equivalent of a Holter monitor). The wireless capsule
endoscope has reportedly performed well when compared with push enteroscopy, imaging abnormalities
never seen before with flexible endoscopes. It is anticipated that this wireless capsule endoscopy will be
especially valuable in patients with GI bleeding when
EGD and colonoscopy both fail to identify the site of
bleeding. In development are the use of a color sensing
algorithm to improve detection of blood in the lumen
and a system of remote control via local electrical
stimulation of peristalsis.135 This wireless technology has
not been employed to evaluate acute bleeding yet, but it
is conceivable that it may be in the future.
Another new technique that may one day have a role
in the evaluation of acute GI bleeding is virtual endoscopy. The use of CT scanning in evaluating lower GI
bleeding is being studied.136 Virtual endoscopy is a
modified form of helical CT scanning that uses a technique of three-dimensional image reconstruction and
virtual reality computing.137 Unlike real endoscopy, the
scan is done without sedation, is well-tolerated, and can
be done literally in the minute it takes to acquire the
images. Bowel preparation, however, is still required.
Virtual endoscopy has not yet been studied in the setting
of acute GI bleeding.
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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
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will be included in bold type following the reference,
where available. In addition, the most informative
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authors, will be noted by an asterisk (*) next to the
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bleeding esophageal varices: a controlled, double-blind study.
Hepatology 1992 Jun;15(6):1023-1030. (Randomized, controlled trial;
33 patients)
Kravetz D, Bosch J, Teres J, et al. Comparison of intravenous
somatostatin and vasopressin infusions in treatment of acute
variceal hemorrhage. Hepatology 1984 May-Jun;4(3):442-446.
(Comparative; 61 patients)
Jenkins SA, Baxter JN, Corbett W, et al. A prospective randomised
controlled clinical trial comparing somatostatin and vasopressin in
controlling acute variceal haemorrhage. Br Med J (Clin Res Ed) 1985
Jan 26;290(6464):275-278. (Prospective, randomized, controlled
trial; 22 patients)
Bagarani M, Albertini V, Anza M, et al. Effect of somatostatin in
controlling bleeding from esophageal varices. Ital J Surg Sci
1987;17(1):21-26. (Comparative; 49 patients)
Saari A, Klvilaakso E, Inberg M, et al. Comparison of somatostatin
and vasopressin in bleeding esophageal varices. Am J Gastroenterol
1990 Jul;85(7):804-807. (Comparative; 54 patients)
Escorsell A, Bordas JM, del Arbol LR, et al. Randomized controlled
trial of sclerotherapy versus somatostatin infusion in the prevention of early rebleeding following acute variceal hemorrhage in
patients with cirrhosis. Variceal Bleeding Study Group. J Hepatol
1998 Nov;29(5):779-788. (Randomized, controlled trial; 169
patients)
Bildozola M, Kravetz D, Argonz J, et al. Efficacy of octreotide and
sclerotherapy in the treatment of acute variceal bleeding in cirrhotic
patients. A prospective, multicentric, and randomized clinical trial.
Scand J Gastroenterol 2000 Apr;35(4):419-425. (Prospective,
randomized, controlled trial; 76 patients)
Coraggio F, Rotondano G, Marmo R, et al. Somatostatin in the
prevention of recurrent bleeding after endoscopic haemostasis of
peptic ulcer haemorrhage: a preliminary report. Eur J Gastroenterol
Hepatol 1998 Aug;10(8):673-676. (Prospective, randomized,
Schoenfeld PS, Butler JA. An evidence-based approach to the
treatment of esophageal variceal bleeding. Crit Care Clin 1998
Jul;14(3):441-455. (Meta-analysis)
Imperiale TF, Birgisson S. Somatostatin or octreotide compared
with H2 antagonists and placebo in the management of acute
nonvariceal upper gastrointestinal hemorrhage: a meta-analysis.
Ann Intern Med 1997 Dec 15;127(12):1062-1071. (Meta-analysis; 1829
patients)
Junquera F, Feu F, Papo M, et al. A multicenter, randomized, clinical
trial of hormonal therapy in the prevention of rebleeding from
gastrointestinal angiodysplasia. Gastroenterology 2001
Nov;121(5):1073-1079. (Randomized, controlled trial; 72 patients)
Bregenzer N, Caesar I, Andus T, et al. Lack of clinical efficacy of
additional factor XIII treatment in patients with steroid refractory
colitis. The Factor XIII Study Group. Z Gastroenterol 1999
Oct;37(10):999-1004. (Prospective, multicenter, randomized,
Jensen DM, Kovacs TO, Jutabha R, et al. Randomized trial of
medical or endoscopic therapy to prevent recurrent ulcer
hemorrhage in patients with adherent clots. Gastroenterology 2002
Aug;123(2):407-413. (Prospective, multicenter, randomized,
Bleau BL, Gostout CJ, Sherman KE, et al. Recurrent bleeding from
peptic ulcer associated with adherent clot: a randomized study
comparing endoscopic treatment with medical therapy. Gastrointest
Endosc 2002 Jul;56(1):1-6. (Randomized, controlled trial; 56
patients)
Gralnek IM, Jensen DM, Gornbein J, et al. Clinical and economic
outcomes of individuals with severe peptic ulcer hemorrhage and
nonbleeding visible vessel: an analysis of two prospective clinical
2002 Sep;31(3):701-713. (Review, tutorial)

114. Burroughs AK, Patch D. Transjugular intrahepatic portosystemic
shunt. Semin Liver Dis 1999;19(4):457-473. (Meta-analysis)
115. Sanyal AJ, Freedman AM, Luketic VA, et al. Transjugular
intrahepatic portosystemic shunts for patients with active variceal
hemorrhage unresponsive to sclerotherapy. Gastroenterology 1996
Jul;111(1):138-146. (Prospective; 32 patients)
116. Kuradusenge P, Rousseau H, Vinel JP, et al. [Treatment of
hemorrhages by rupture of cardio-tuberous varices with
transjugular intrahepatic portosystemic shunt]. Gastroenterol Clin
Biol 1993;17(6-7):431-434. (Follow-up; 12 patients)
117. Stanley AJ, Jalan R, Ireland HM, et al. A comparison between
gastric and oesophageal variceal haemorrhage treated with
transjugular intrahepatic portosystemic stent shunt (TIPSS). Aliment
Pharmacol Ther 1997 Feb;11(1):171-176. (Comparative; 106 patients)
118. Papatheodoridis GV, Goulis J, Leandro G, et al. Transjugular
intrahepatic portosystemic shunt compared with endoscopic
treatment for prevention of variceal rebleeding: A meta-analysis.
Hepatology 1999 Sep;30(3):612-622. (Meta-analysis; 811 patients)
119. Marshall JK, Collins SM, Gafni A. Demographic predictors of
resource utilization for bleeding peptic ulcer disease: the Ontario
GI Bleed Study. J Clin Gastroenterol 1999 Sep;29(2):165-170. (Cost
analysis; 158 patients)
120. Stabile BE, Stamos MJ. Surgical management of gastrointestinal
bleeding. Gastroenterol Clin North Am 2000 Mar;29(1):189-222.
(Review, tutorial)
121. Jalan R, Hayes PC. UK guidelines on the management of variceal
haemorrhage in cirrhotic patients. British Society of Gastroenterology. Gut 2000 Jun;46 Suppl 3-4:III1-III15. (Practice guideline)
122. No authors listed. The role of endoscopic therapy in the management of variceal hemorrhage. American Society for Gastrointestinal
Endoscopy. Gastrointest Endosc 1998 Dec;48(6):697-698. (Practice
guideline)
123. Ingrand P, Rodriguez B, Silvain C, et al. Predictive factors of
variceal bleeding control by emergency sclerotherapy. Multicenter
Group. Gastroenterol Clin Biol 1998 May;22(5):519-524. (Prospective;
101 patients)
124. Soares-Weiser K, Brezis M, Tur-Kaspa R, et al. Antibiotic prophylaxis for cirrhotic patients with gastrointestinal bleeding. Cochrane
Database Syst Rev 2002;(2):CD002907. (Meta-analysis; 1367 patients)
125. Bernard B, Grange JD, Khac EN, et al. Antibiotic prophylaxis for the
prevention of bacterial infections in cirrhotic patients with
gastrointestinal bleeding: a meta-analysis. Hepatology 1999
Jun;29(6):1655-1661. (Meta-analysis; 534 patients)
126. Hsieh WJ, Lin HC, Hwang SJ, et al. The effect of ciprofloxacin in the
prevention of bacterial infection in patients with cirrhosis after
upper gastrointestinal bleeding. Am J Gastroenterol 1998
Jun;93(6):962-966. (Controlled; 120 patients)
127. Bini EJ, Micale PL, Weinshel EH. Risk factors for rebleeding and
mortality from acute upper gastrointestinal hemorrhage in human
immunodeficiency virus infection. Am J Gastroenterol 1999
Feb;94(2):358-363. (Retrospective; 297 patients)
128. Chalasani N, Wilcox CM. Etiology and outcome of lower
gastrointestinal bleeding in patients with AIDS. Am J Gastroenterol
1998 Feb;93(2):175-178. (Retrospective; 18 patients)
129. Bini EJ, Weinshel EH, Falkenstein DB. Risk factors for recurrent
bleeding and mortality in human immunodeficiency virus infected
patients with acute lower GI hemorrhage. Gastrointest Endosc 1999
Jun;49(6):748-753. (Retrospective; 312 patients)
130. Singh T, Ahrens WR. Nonsurgical gastrointestinal problems. In:
Strange GR, Ahrens WR, Lelyveld S, et al. Pediatric Emergency
Medicine: A Comprehensive Study Guide. 2nd ed. New York: McGrawHill Publishers; 2002:358-362. (Textbook chapter)
131. Combier E, Levacher S, Letoumelin P, et al. Cost-effectiveness
analysis of the terlipressin-glycerin trinitrate combination in the
pre-hospital management of acute gastro-intestinal haemorrhage in
cirrhotic patients. Intensive Care Med 1999 Apr;25(4):364-370.
(Controlled; 84 patients)
132. McCormick PA, Greenslade L, Matheson LA, et al. Vasoconstrictors
133.
134.
135.
136.
137.
138.
in the management of bleeding from oesophageal varices. A clinicoeconomic appraisal in the UK. Scand J Gastroenterol 1995
Apr;30(4):377-383. (Cost analysis)
Landi B, Tkoub M, Gaudric M, et al. Diagnostic yield of push-type
enteroscopy in relation to indication. Gut 1998 Mar;42(3):421-425.
(Observational; 152 patients)
Huang YH, Yeh HZ, Chen GH, et al. Endoscopic treatment of
bleeding gastric varices by N-butyl-2-cyanoacrylate (Histoacryl)
injection: long-term efficacy and safety. Gastrointest Endosc 2000
Aug;52(2):160-167. (Retrospective; 90 patients)
Swain P. Wireless capsule endoscopy. Gut 2003 Jun;52 Suppl 4:iv4850. (Review)
Ernst O, Bulois P, Saint-Drenant S, et al. Helical CT in acute lower
gastrointestinal bleeding. Eur Radiol 2003 Jan;13(1):114-117.
Pickhardt PJ, Choi JR, Hwang I, et al. Computed tomographic
virtual colonoscopy to screen for colorectal neoplasia in asymptomatic adults. N Engl J Med 2003 Dec 4;349(23):2191-2200. (Prospective
comparison of virtual colonoscopy to traditional colonoscopy as
the criterion standard; 1233 patients)
Lee KK, You JH, Wong IC, et al. Cost-effectiveness analysis of highdose omeprazole infusion as adjuvant therapy to endoscopic
treatment of bleeding peptic ulcer. Gastrointest Endosc 2003
Feb;57(2):160-164. (Randomized, controlled trial; 232 patients)
Physician CME Questions

33. Which of the following represents the fewest risk
factors in a patient with hematemesis or melena?
a. Age less than 60 years, stable vital signs, no
severe liver disease, no anticoagulation
b. Age greater than 60 years, erratic mental status,
use of oral anticoagulants, diabetes mellitus
c. Age less than 60 years, stable vital signs, NSAID
use, previously diagnosed peptic ulcer
d. Age less than 60 years, current smoking,
previously diagnosed peptic ulcer
34. Which of the following scenarios represents the
most risk factors in a patient with hematemesis
or melena?
a. Age less than 60 years, stable vital signs, no
severe liver disease, no anticoagulation
b. Age greater than 60 years, erratic mental status,
use of oral anticoagulants, diabetes mellitus
c. Age less than 60 years, stable vital signs, NSAID
use, previously diagnosed peptic ulcer
d. Age less than 60 years, current smoking,
previously diagnosed peptic ulcer
35. Patients with hematochezia who have had a prior
abdominal aortic aneurysm repair:
a. are at risk of harboring a deadly aortoenteric
fistula and require surgical repair before the
bleeding becomes brisk if the patient is to have a
good chance of survival.
b. require consultation with a gastroenterologist.
c. should have endoscopy if other risk factors
are present.
d. should be admitted to the floor for observation.
18
43. Multiple studies have shown vasopressin to be

more effective than somatostatin in controlling GI
bleeding, with fewer side-effects.
a. True
b. False
37. Definitive low-risk criteria to determine the need

for endoscopy in patients with GI bleeding have
been established and have been prospectively
validated in several large trials.
a. True
b. False
44. In patients with GI bleeds in whom hemorrhagic

shock is likely, fluid replacement with
normal saline reduces the risk of myocardial
ischemia/infarction.
a. True
b. False
38. Melena is defined as:

a. the vomiting of blood.
b. the passage of bloody feces.
c. the passage of dark and pitchy stools stained
with blood pigments or with altered blood.
d. an ulceration of the mucous membrane of the
esophagus, stomach, or duodenum, caused by
action of the acidic gastric juice.
45. Endoscopic therapy has been shown to be superior

to all other therapies, reduce the rate of rebleeding,
and reduce short-term morbidity and mortality.
a. True
b. False
46. Proton pump inhibitors (e.g., omeprazole):
a. have been shown to be superior to H2-blocking
medications in preventing recurrent bleeding
in patients with upper GI bleeding in both
sub-acute and chronic settings.
b. have an undemonstrated effect on
reducing mortality.
c. have demonstrated short-term cost savings
in at least one cost-benefit analysis.
d. all of the above.
39. Which of the following causes of GI bleeding,

while rare, is the most rapidly deadly?
a. Peptic ulcers
b. Mallory-Weiss tears
c. Angiodysplasia
d. Aortoenteric fistula
40. According to recent studies, early endoscopy is
associated with:
a. an overall lower cost of care.
b. shortened hospital stays.
c. improved outcomes.
d. all of the above.
e. none of the above.
47. All of the following are correct about pediatric

GI bleeding except:
a. The etiologies are generally the same as
in adults.
b. It may be wise for emergency physicians
who are unfamiliar with pediatric GI
bleeding to obtain phone consultation
with a pediatric gastroenterologist or
pediatric emergency physician.
c. Esophageal varices in young children are
typically due to biliary atresia, neonatal hepatitis, congenital hepatic fibrosis, and cystic
fibrosis, as opposed to adult varices, which are
often due to the chronic effects of alcoholism.
d. Lower GI bleeding in young children may be
due to vitamin K deficiency, anal fissures, milk
allergy, Meckels diverticulum, intussusception,
juvenile polyps, or infectious diarrhea.
41. All of the following are correct about cirrhotic

patients with GI bleeding except:
a. They do not have an increased mortality rate.
b. Variceal bleeding in these patients can be
massive and very difficult to control.
c. Urgent endoscopy is usually indicated in
these patients.
d. The presence of encephalopathy, the severity of
the bleeding, and the time between clinically
overt bleeding and treatment have been identified as the main predictive factors of failure to
control bleeding.
19
42. Which of the following medications can cause

stool color changes that mimic GI bleeding?
a. Warfarin
b. Aspirin or other NSAIDs
c. Corticosteroids
d. Chemotherapeutic agents
e. Over-the-counter bismuth-containing
dyspepsia products
36. Recent meta-analyses suggest that:

a. long-term aspirin use and other NSAID
use are associated with an increased risk
of GI hemorrhage.
b. NSAID use is associated with an increased
risk of GI hemorrhage, but long-term aspirin
therapy is not.
c. long-term aspirin use is associated with an
increased risk of GI hemorrhage, but other
NSAID use is not.
d. neither long-term aspirin use nor other
NSAID use is associated with an increased
risk of GI hemorrhage.
Physician CME Information
48. In a 2001 review of the available literature, the

American Society for Gastrointestinal Endoscopy
identified four non-endoscopically derived key
predictors of rebleeding that should be the focus
of the initial evaluation because of their usefulness
as risk stratifiers in multiple studies. Which of the
following is not one of them?
a. Older age
b. Previously diagnosed peptic ulcer
c. Shock (hemodynamic instability or orthostasis)
d. Comorbid disease states
e. The use of anticoagulants or the presence
of coagulopathy
This CME enduring material is sponsored by Mount Sinai School of Medicine and
has been planned and implemented in accordance with the Essentials and
Standards of the Accreditation Council for Continuing Medical Education. Credit
may be obtained by reading each issue and completing the printed post-tests
administered in December and June or online single-issue post-tests
administered at www.empractice.net.
Target Audience: This enduring material is designed for emergency medicine
physicians.
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.
Date of Original Release: This issue of Emergency Medicine Practice was published
March 1, 2004. This activity is eligible for CME credit through March 1, 2007.
The latest review of this material was February 3, 2004.
Discussion of Investigational Information: As part of the newsletter, faculty may
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presented as part of this activity is intended solely as continuing medical
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product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice
discusses the use of vasopressin and somatostatin to treat GI bleeding, which is
considered an off-label use. (See text.)
Coming in Future Issues:

Pulmonary Embolism Acute Coronary Syndrome
Deep Venous Thrombosis
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Guidelines, all faculty for this CME activity were asked to complete a full
disclosure statement. The information received is as follows: Dr. Holt discloses
that he is an occasional speaker on community acquired pneumonia. Dr.
Westhoff, Dr. Gill, and Dr. Sachs report no significant financial interest or other
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Proven in both efficacy and
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EMERGENCY MEDICINE

ROBLEMS associated with GI bleeding are challenging for patients and

Lance Brown, MD, MPH, FACEP,

Judith C. Brillman, MD, Associate

Francis M. Fesmire, MD, FACEP,

and Dentistry of New Jersey;

Date of original release: March 1, 2004.

Michael S. Radeos, MD, MPH,

When this body of literature is reviewed, even given

ing antibiotics, surgical excision, endoscopically guided

Critical Appraisal Of The Literature

Table 1. Risk Stratification Of Patients With Hematemesis Or Melena.

High-risk patient characteristics

Low-risk esophagogastroduodenoscopy findings

Use of oral anticoagulants

High-risk esophagogastroduodenoscopy findings

Emergency Medicine Practice

www.empractice.net March 2004

Table 2. Glossary Of GI Bleeding Terms.

Hemorrhoid: a varicose dilatation of a vein of the superior

Anoscopy: examination of the anus and lower rectum by

Mallory-Weiss syndrome (tear): hematemesis or melena

Colonoscopy: examination of the entire colon with an

Melena: the passage of dark and pitchy stools stained with

Peptic ulcer: an ulceration of the mucous membrane of the

Endoscope: an instrument for examination of the interior of

Sclerotherapy: the injection of a chemical irritant into a

Endoscopy: visual inspection of any cavity of the body by

Stress ulcer: a peptic ulcer, usually gastric, resulting from

Esophagogastroduodenoscopy (EGD): endoscopic

Adapted from: Dorlands Illustrated Medical Dictionary. 30th ed.

Hematochezia: the passage of bloody feces

March 2004 www.empractice.net

Emergency Medicine Practice

In 1997, Kollef et al reported on a classification tool

tric aspirate free of fresh blood. In the prospective arm of

published. Derry and Loke presented a meta-analysis of

Epidemiology, Etiology, And Pathophysiology

Cost- And Time-Effective Strategies For Patients With GI Bleeding

1. Effective risk stratification is key.

3. Early pharmacologic therapy may result in

2. Early endoscopy saves time and money.

Emergency Medicine Practice

www.empractice.net March 2004

Peptic Ulcer Disease

March 2004 www.empractice.net

Emergency Medicine Practice

hemochromatosis, Wilsons disease, galactosemia, and

Mortality associated with GI bleeding seems to be

ing16,38,41and the bleeding is not just from ulcers, as

The priorities of prehospital personnel caring for patients

Emergency Department Evaluation

Table 3. GI Bleed Fake-Outs: Conditions

Mimics for melena

Mimics for hematochezia

Partially chewed/digested red grapes

Ingestions that may cause

Emergency Medicine Practice

www.empractice.net March 2004

March 2004 www.empractice.net

Emergency Medicine Practice

over-the-counter bismuth-containing dyspepsia products.

obstruction forces the passage of blood back through the

prompt EGD is indicated.4,30 Nasogastric aspiration may