0814-H GI Bleeding Sample Issue2

Hospital Medicine
Practice
Empowering Hospitalists
With Evidence-Based Reviews
Evidence-Based
Hospital Management Of
Gastrointestinal Bleeding
August 2014
Volume 2, Number 8
Authors
Abstract
Gastrointestinal bleeding is one of the most common causes of
hospitalization. Effective initial patient evaluation determines the
potential source of gastrointestinal bleeding (upper vs lower),
provides risk stratification, and guides further management. The
gastroenterologist, interventional radiologist, and surgeon can
offer different invasive therapeutic interventions, and the hospitalist is often involved in the crucial management before and after
these procedures. Hemodynamic resuscitation, pharmacological
interventions, and triage to the appropriate setting of care are
initial supportive measures. Timely consultation and knowledge
of therapeutic measures provides appropriate and cost-effective
care, including individualized transfusion strategies and correction of coagulopathy. This issue provides an evidence-based
review of management strategies for gastrointestinal bleeding in
the hospitalized patient to optimize the quality of care, facilitate
cost-effective treatment, and improve clinical outcomes.
Editor-in-Chief
Editorial Board
Alpesh N. Amin, MD, MBA, MACP, SFHM

Thomas & Mary Cesario Endowed Chair
of Medicine
Professor of Medicine, Business, Public
Health, Nursing Science & Biomedical
Engineering
Executive Director, Hospitalist Program
University of California Irvine, Irvine,
CA
Amish A. Dangodara, MD, FACP

Professor of Medicine, Director of
Preoperative Clinic and General Internal
Medicine Consultation, Hospitalist
Program, University of California Irvine,
Irvine, CA
Clinical Pearls Contributor

David J. Rosenberg, MD, MPH, FACP,
SFHM
Chief, Division of Hospital Medicine,
North Shore LIJ Department of Medicine,
Associate Professor of Medicine, Hofstra
North Shore LIJ School of Medicine,
Hempstead, NY
Nancy Dawson, MD, FACP

Assistant Professor, Hospital Practice
Chair, Division of Hospital Medicine, Mayo
Clinic, Jacksonville, FL
Steven Deitelzweig, MD
System Chairman, Hospital Medicine,
Regional Vice President of Medical Affairs,
Ochsner Health System, New Orleans, LA
Daniel Dressler, MD, MSc, SFHM

Professor of Medicine, Director of Internal
Medicine Teaching Services, Emory
University Hospital; Associate Director
Charting Contributor
for Education, Emory Division of Hospital
James B. Haering, DO, SFHM
Medicine, Associate Program Director, J.
Associate Professor of Medicine, Michigan
Willis Hurst Internal Medicine Residency
State University College of Osteopathic
Program, Emory University School of
Medicine and Michigan State University
Medicine, Atlanta, GA
College of Human Medicine, East
Amir Jaffer, MD
Lansing, MI
Professor of Medicine, Vice Chair, Patient
Safety, Quality, and Compliance, Division
Chief, Hospital Medicine, Department of
Medicine, University of Miami Miller School
of Medicine, Miami, FL
Sunil Dacha, MD
Gastroenterology Fellow, Emory University School of Medicine,
Atlanta, GA
Stephen H. Berger, MD
Atlanta, GA
Mehul Parikh, MD
Atlanta, GA
Mohammad Wehbi, MD
Associate Professor of Medicine, Emory University School of
Peer Reviewers
Abebe Abebe, MD, FACP
Assistant Professor, Department of Internal Medicine/Hospital
Medicine, Division of General and Geriatric Medicine, University
of Kansas Medical Center, Kansas City, KS
Ivan Pavlov, MD
Hospitalist and Emergency Physician, Departments of General
and Emergency Medicine, Hpital de Verdun, Montral, Qubec,
Canada
Prior to beginning this activity, see Physician CME Information
on the back page.
Solomon Liao, MD
Director of Palliative Care Services,
Associate Clinical Professor, Hospitalist
Program, University of California Irvine,
Irvine, CA
Daniel Robitshek, MD, SFHM

Assistant Professor of Medicine, Medical
College of Georgia; Program Director,
Internal Medicine Residency, Associate
Director, Hospitalist Program, Redmond
Regional Medical Center, Rome, GA
David Likosky, MD, SFHM

Medical Director, Evergreen Neuroscience Tomas Villaneuva, DO, MBA, FACPE, SFHM
Institute, Kirkland, WA; Clinical Faculty,
Assistant Vice President, Medical Director
of Primary Care and Hospital Medicine,
University of Washington, Seattle, WA
Baptist Health Medical Group, Baptist
Sylvia C. McKean, MD, FACP, SFHM
Health South Florida, Coral Gables, FL
Associate Professor of Medicine, Harvard
Mike Wang, MD
Medical School; Associate Physician,
Brigham and Womens Hospital, Boston, MA Director of Hospital Medicine, Associate
Professor of Clinical Medicine, Keck
Geno J. Merli, MD
Medical Center of USC, Los Angeles, CA
Professor of Medicine and Surgery,
Thomas Jefferson University; Co-Director, David Wooldridge, MD, FACP
Program Director, Internal Medicine
Jefferson Vascular Center; Senior Vice
Residency Program, Associate Professor
President and CMO, Thomas Jefferson
of Internal Medicine, University of
University Hospital, Philadelphia, PA
Missouri-Kansas City School of Medicine,
Franklin A. Michota, MD, FACP, FHM
Kansas City, MO
Associate Professor of Medicine, Director
Nejat Zeyneloglu, MD
of Academic Affairs, Department of
Medical Director, Hospital Medicine
Hospital Medicine, Cleveland Clinic,
Program, New York Hospital Queens, WeillCleveland, OH
Cornell Medical College, New York, NY
Ivan Pavlov, MD
Hospitalist and Emergency Physician,
Pharmacology Contributor
Departments of General and Emergency
James Damilini, PharmD, MS, BCPS
Medicine, Hpital de Verdun, Montral
Clinical Pharmacy Specialist, Emergency
(Qubec) Canada
Medicine, St. Joseph's Hospital and
Medical Center, Phoenix, AZ
www.hmpractice.com
Clinical Pearls
Coagulopathy
Treat high INR with fresh-frozen plasma or
4-factor prothrombin complex concentrate; use
vitamin K when bleeding is due to warfarin.
Transfuse platelets when platelets < 50,000/mm3.
Withold antiplatelet agents until hemostasis is
established.

Therapeutic Measures
Discharge from the emergency department
without endoscopy is appropriate for patients
with BUN < 18.2; Hb > 13 for men, 12 g/dL for
women; systolic blood pressure > 110 mm Hg;
pulse rate < 100; and absence of melena, syncope,
cardiac failure, and liver disease (2012 American
College of Gastroenterology practice guidelines).
Arrange endoscopy within 12 hours of admission
for high-risk patients (tachycardia, hypotension,
bloody emesis, or bloody nasogastric aspirate)
Arrange endoscopy within 24 hours for low-risk
patients (this reduces transfusion requirements,
ICU stay, and hospital stay).
Upper endoscopy (esophagogastroduodenoscopy) is the diagnostic modality of choice for UGIB;
lower endoscopy (colonoscopy) is the diagnostic
modality of choice for LGIB.
Etiology And Prevalence (Pages 4-5)
UGIB: 50% of cases are due to peptic ulcers.

LGIB: Diverticular disease is the major etiology
(up to 55%).
OGIB: 75% of cases are from the small bowel.
History (Page 6)
Presentation:
UGIB: hematochezia, hematemesis, melena.
LGIB: hematochezia, occult bleeding, and
systemic symptoms of blood loss or anemia.
Current medications should be reviewed for
etiology.

Physical Examination (Page 7)
Look for orthostatic hypotension.

Supine hypotension represents 40% blood
volume loss.
Look for signs of chronic liver disease to suggest
a portal hypertensive bleed.
Diagnostic Testing (Pages 7-9)
Initial workup includes complete blood count,

complete metabolic profile, coagulation profile,
and blood type with crossmatching.
Monitor Hb every 2 to 8 hours, depending on the
severity of the GIB.
Obtain serial ECGs and cardiac enzymes in patients at risk for myocardial ischemia or presenting with active chest pain or dyspnea.
Nasogastric lavage is commonly used, but it is
inaccurate, has no effect on overall clinical outcomes, and is not required by guidelines.
Appropriate Setting Of Care And Discharge

(Pages 13, 16)
UGIB
Whenever feasible, arrange early endoscopic
evaluation of UGIB to identify high-risk lesions.
Discharge from the emergency department or
hospital day 1: patients with low-risk endoscopic
features, low-risk clinical features (stable vital
signs, stable Hb, no serious comorbidities), and
good social support. Provide oral PPI therapy
and appropriate follow-up.
Admit to the ICU: patients with high-risk endoscopic features and/or ongoing bleeding, unstable vital signs, or unstable comorbidities.
Treat high-risk stigmata for at least 3 days
to receive IV PPI therapy and to monitor for
rebleeding.
Do not obtain second-look endoscopy; this is
usually performed 24 hours after the initial
therapeutic endoscopy.
LGIB
Endoscopic risk stratification does not exist for
LGIB.
Patients can be discharged with resolution of
bleeding, stable vital signs, and stable Hb.

Treatment (Pages 9-11)
Initial Supportive Measures

Hemodynamic resuscitation precedes endoscopic intervention. Insert 2 large-bore IV lines ( 18
gauge); resuscitate with isotonic crystalloid fluid.
Transfuse PRBCs for Hb < 7 g/dL (< 9 in CAD),
or any value if the Hb is anticipated to fall significantly with fluid resuscitation.
Intubate for altered mental status, ongoing
significant hematemesis, or severe cardiopulmonary disease.
Consider admission to ICU.
Pharmacologic Interventions
Acute Peptic UGIB
Initiate IV PPI infusion before endoscopy.
Treat high-risk lesions (active bleeding, visible
vessels, or adherent clots) with continuous infusion of PPI for 72 hours.
Switch low-risk patients to oral once-daily PPI
therapy.
Suspected Variceal Bleed
Treat with octreotide; continue for 3 to 5 days
after the diagnosis is confirmed.
Copyright 2014 EB Medicine. All rights reserved.
Abbreviations: BUN, blood urea nitrogen; CAD, coronary

artery disease; ECG, electrocardiogram; GIB, gastrointestinal bleeding; Hb, hemoglobin; ICU, intensive care
unit; INR, international normalized ratio; IV, intravenous;
LGIB, lower gastrointestinal bleeding; OGIB, obscure
gastrointestinal bleeding; PPI, proton pump inhibitor;
PRBCs, packed red blood cells; UGIB, upper gastrointestinal bleeding.
www.hmpractice.com August 2014
per gastrointestinal bleeding (UGIB) accounts for

300,000 to 400,000 hospital admissions annually.1,2
The incidence of UGIB in the general population
is 1 per 1000 persons per year, with the risk higher
among males and increasing with age.3 Despite
the use of new treatment modalities, the mortality
rates are as high as 10% in patients without variceal hemorrhage and nearly 14.5% in patients with
variceal hemorrhage.4 The hospitalization rates for
lower gastrointestinal bleeding (LGIB) have been
estimated to be 20% higher than hospitalization
rates for UGIB. Independent predictors of rebleeding and death in these patients include increasing
age, comorbidities, and hemodynamic compromise.
Clinical outcomes are better for patients with LGIB.
International consensus guidelines recommend early
stratification for the assessment of goal-oriented
therapy.5 Appropriate workup and management in
this patient population impacts the clinical outcome.
Case Presentations
You are called to the ED for admission of a 45-year-old
man with no known past medical history other than
significant alcohol use after he presented to the ED with
complaints of episodes of bloody vomitus and dizziness
and weakness. The initial assessment reveals a blood pressure of 100/50 mm Hg, a pulse rate of 120 beats/min, and
an oxygen saturation of 99% on room air. His physical
examination is remarkable for mild icterus, spider angiomas on the chest, and dullness to percussion in the flank
areas. His labs are significant for a hemoglobin of 9 g/dL,
a platelet count of 45,000/mm3, an INR of 1.8, a total bilirubin of 2 mg/dL, a BUN of 68 mg/dL, and a creatinine of
1.2 mg/dL. What is the most likely cause of this patient's
bloody vomitus, and how should he be managed?

A 47-year-old woman, apparently healthy, presents to the ED with the chief complaint of dizziness and
generalized weakness of 1 days duration. On further
questioning, she mentions that she has passed black stools
on multiple occasions for the last 2 days. She reports
taking headache powders and ibuprofen tablets daily for
headaches. On physical examination, there is evidence of
conjunctival pallor and epigastric tenderness. Her vital
signs are within normal limits. Her hemoglobin is 6.5 g/
dL, BUN is 36 mg/dL, and creatinine is 1.2 mg/dL. Her
platelet count and INR are within the normal range.
When you review her chart for admission, you observe
that she is anemic, but what should the transfusion strategy be and how can you manage her bleeding?

A 76-year-old man with a history of coronary artery
disease and atrial fibrillation on warfarin presents to ED
with a chief complaint of bright red blood per rectum
for 3 days. He is currently on 325 mg aspirin daily. His
vital signs are within normal limits and he is, otherwise,
asymptomatic. He had a colonoscopy 2 years ago, which
showed extensive diverticulosis. His INR is 4, his hemoglobin is 12.3 g/dL, and his laboratory workup is otherwise unrevealing. As you prepare him for admission, you
consider what the guidelines say about managing bleeding
in an anticoagulated patient...

The paramedics bring in a 39-year-old man in an
unconscious state, and you are called in to manage his admission. He has a history of alcoholic cirrhosis, and there
is a report of him vomiting blood prior to passing out. On
initial assessment, he is responding to commands. On
presentation, his vital signs include a blood pressure of
80/50 mm Hg, a pulse rate of 140 beats/ min, and an oxygen saturation of 99% on room air. His physical exam is
significant for spider angiomas and ascites. His labs show
hemoglobin of 9 g/dL, a platelet count of 60,000/mm3 and
INR of 1.4. What would be the appropriate transfusion
strategy for this patient and timing for endoscopy?
Critical Appraisal Of The Literature

The etiology of GIB and its management have been
widely studied. Major societies have published
consensus statements and clinical guidelines for
the effective management of GIB based on these
studies, and they are a valuable reference for
physicians. The strength of the evidence is noted
in most of these guidelines. While some guidelines
for LGIB (such as the American College of Gastroenterology [ACG] guidelines) appear somewhat
outdated, with the last update released in 1998,
many guidelines have been updated within the last
few years.6-15 The ACG guideline for management
of patients with ulcer bleeding was updated in
2012 and the American Society of Gastrointestinal
Endoscopy (ASGE) similarly updated their practice
recommendations in 2010 for the role of endoscopy
in obscure GI bleeding (OBIG) and peptic ulcer
disease. The American Gastroenterological Association (AGA) also issued a medical position statement in 2007 on management and prevention of
varices and variceal hemorrhage.6-10

An extensive PubMed search was performed
using the search terms gastrointestinal bleeding, upper
gastrointestinal bleeding, lower gastrointestinal bleeding, and obscure gastrointestinal bleeding. Focus was
placed on randomized clinical control trials, metaanalyses, and review articles. In addition, guidelines of the major gastrointestinal societies were
reviewed. Overall, a majority of the major societies'
recommendations were guided by high-quality clinical trials. Some current guidelines (such as early risk
assessment strategies and use of prokinetic agents)
lack clinical trials with prospective reproducibility.
Other guidelines (such as gastric lavage) remain
controversial, with a history of nonrandomized,
low-quality studies with conflicting results.
Introduction
Gastrointestinal bleeding (GIB) is the most common
cause of gastrointestinal (GI) emergencies. UpAugust 2014 www.hmpractice.com
Reprints: www.hmpractice.com/hmpissues
The studies evaluating use of gastric lavage and

prokinetic agents (such as erythromycin prior to
esophagogastroduodenoscopy [EGD] to clear blood
and blood clots in the stomach) have provided
variable results. A recent meta-analysis suggested
a decreased need for a repeat EGD due to better
visualization of the upper GI tract after prokinetic
agent use.16 These findings were not reproduced in
another study, which showed that erythromycin,
gastric lavage, or both together did not improve visualization of the upper GI tract during EGD.17 The
potential benefit of these agents in the management
of UGIB merits further prospective trials.
Nonportal Hypertensive Upper Gastrointestinal

Bleeding
Among hospitalized patients, peptic ulcers are the
most common cause of UGIB, followed by erosive
esophagitis, Mallory-Weiss tears, and vascular lesions.
The pathophysiology of these underlying conditions
is highly dependent on the etiology. Peptic ulcers are
defined by location as gastric or duodenal. Duodenal
ulcers are most commonly associated with Helicobacter
pylori infections. Gastric ulcers, on the other hand, are
mainly caused by nonsteroidal anti-inflammatory drug
(NSAID) use, which inhibits cyclooxygenase, leading
to decreased production of prostaglandin that acts to
protect the stomach mucosa.

Erosive esophagitis occurs secondary to gastroesophageal reflux disease (GERD), alcohol abuse,
NSAID use, infection, and radiation therapy. Mallory-Weiss tears are associated with the vomiting,
retching, and coughing that precede hematemesis.
Alcoholics are the population in which these lesions
tend to be identified. Vascular etiologies such as
Dieulafoy lesions (superficial submucosal arteriole),
arteriovenous malformations, telangiectasia, and
gastric antral vascular ectasia can cause clinically
significant UGIB. A rare, but severe cause of UGIB is
aortoenteric fistula.18

Portal Hypertensive Upper Gastrointestinal Bleeding
Portal hypertension is defined as a pathological
increase in the pressure of the portal venous system,
most commonly associated with cirrhosis. Other
Etiology And Pathophysiology

Upper Gastrointestinal Bleeding
UGIB is defined as hemorrhage in the GI tract

proximal to the ligament of Treitz. Table 1 lists the
common causes of UGIB. According to data compiled from hospitalized patients from 2000 to 2009,
peptic ulcers comprise nearly 50% of the lesions,
and varices comprise 6% to 39% of the lesions,
depending on the patient population.6 Given the
variability in the prevalence and the differences in
overall treatment and management, it is important
to distinguish variceal from nonvariceal causes of
suspected UGIB. In order to do so, it is of utmost
importance to be aware of whether portal hypertension is present, as this will broaden the differential for development of varices.
Table 1. Causes Of Upper Gastrointestinal Bleeding18

Etiology
Incidence
Risk Factors
Comments
Peptic ulcer disease
40%-50%
NSAID use, H pylori, stress-induced (ICU) ulcers
Most common cause of UGIB
Esophageal/gastric varices
20%-30%
Cirrhosis, splenic vein thrombosis
History or suspected history of liver disease
Mallory-Weiss tear
5%-15%
Alcohol use, severe retching, coughing
Cough and retching precede hematemesis
Erosive esophagitis
10%
Alcohol use, GERD, NSAID use, infection, radiation
History of GERD and hiatal hernia
Vascular malformations
(angiodysplasia, Dieulafoy
lesion, GAVE, portal gastropathy, telangiectasia)
< 5%
Angiodysplasia, chronic kidney disease, cirrhosis
Can range from minimal to very significant UGIB;

can be missed endoscopically
Neoplasm
1%
H pylori, smoking, family history
Anemia, weight loss
Others causes (aortoenteric fistula, hemosuccus pancreaticus, and

hemobilia)
Rare
Hemobilia, liver biopsy, hepatobiliary manipulation

Hemosuccus pancreaticus, acute or chronic
pancreatitis, pancreatic duct manipulation,
pancreatic cancer
Aortoenteric fistula, aortic aneurysm or repair
Rare, but can be clinically catastrophic if misdiagnosed

Presence of aortic graft should lead to suspicion
for aortoenteric fistula
Abbreviations: GAVE, gastric antral vascular ectasia; GERD, gastroesophageal reflux disease; H pylori, Helicobacter pylori; ICU, intensive care unit;
NSAID, nonsteroidal anti-inflammatory drug; UGIB, upper gastrointestinal bleed.
as dilated, tortuous submucosal vessels that appear

endoscopically as expanded dilated capillaries with
a central origin. Bleeding from these vessels is venous in origin and is rarely life-threatening.15 Other
vascular etiologies include ischemia and radiation.
Radiation exposure can predispose a patient to the
development of rectal telangiectasia or proctitis
(which occur in the setting of treatment for pelvic
cancer) typically within 6 weeks of the initial radiation therapy, though chronic radiation-induced
LGIB has been noted to occur many years after
radiation. Colitis is the major inflammatory etiology
of LGIB. This includes infectious colitis and inflammatory bowel disease (such as Crohn disease and
ulcerative colitis). Colitis accounts for 10% to 21% of
LGIB cases.15,18

Miscellaneous etiologies include anorectal disorder such as malignancy, hemorrhoids, rectal ulcers,
anal fissures, rectal varices, and Dieulafoy lesions.
noncirrhotic etiologies are classified anatomically

as prehepatic (portal vein thrombosis), intrahepatic
(primary biliary cirrhosis, schistosomiasis, sarcoidosis), and posthepatic (inferior vena cava obstruction
or cardiac disease).

The pathophysiology of portal hypertension in
the setting of cirrhosis involves architectural distortion of the liver induced by fibrosis and vasoconstriction of the intrahepatic vessels caused by
decreased endogenous nitric oxide production.19,20
Concomitant splanchnic arteriolar vasodilation occurs to increase venous inflow into the portal venous
system. As a direct consequence of these physiologic
disturbances, portosystemic collaterals develop. As
a result of their lower resistance compared to that
of the portal system, the formation of pathologic
esophageal and gastric varices ensues.21,22

Gastroesophageal varices are present in approximately 50% of patients with cirrhosis. Their prevalence increases as the portal hypertension worsens.
The size of varices is the most important predictor
for the risk of bleeding.23 While almost all gastric
varices tend to be associated with cirrhosis, the presence of isolated gastric varices in the fundus requires
the exclusion of splenic vein thrombosis.10
Obscure Gastrointestinal Bleeding
OGIB is defined as bleeding from the GI tract that

occurs without etiology identified on upper endoscopy, colonoscopy, and radiologic evaluation of the
small bowel. OGIB can be further categorized as overt,
if frank GIB is observed or occult, if no overt GIB is
seen.7 Table 3 (page 6) notes the causes of OGIB.

OGIB accounts for nearly 5% of GIB and most
likely originates from the small bowel.28,29 The remainder of cases are due to missed lesions in either
the upper or lower GI tract. Causes can range from
upper, lower, and midgastrointestinal bleeding.9
Lower Gastrointestinal Bleeding
LGIB is defined as hemorrhage in the GI tract distal

to the ligament of Treitz. Table 2 lists the common
causes of LGIB. Diverticular disease is the major etiology, accounting for 15% to 55% of LGIB cases.24,25
The prevalence of diverticulosis is 40% to 60%, and it
increases with age.26,27 Given that diverticular bleeding is arterial, it can be potentially life-threatening.

Causes of LGIB can be further classified as vascular or inflammatory. The most common vascular
cause in LGIB is angiodysplasia, and it accounts for
up to 37% of cases.15,18 Angiodysplasia is defined
Differential Diagnosis
For information on the diagnosis of GIB, including
incidence and risk factors, see Tables 1, 2, and 3.
Differential diagnosis varies, based on the clinical
Table 2. Causes Of Lower Gastrointestinal Bleeding15,18,24,25

Etiology
Incidence
Risk Factors
Comments
Diverticular
disease
15%-55%
Old age, constipation, low-fiber diet
Arterial, and can be life-threatening; most common cause

of LGIB
Angiodysplasia
3%-37%
Chronic kidney disease, aortic stenosis (Heyde syndrome), anticoagulation
Venous in origin; rarely life-threatening
Neoplasms
15%
HNPCC, old age, family history, IBD, polyposis syndromes
Anemia and weight loss
UGIB
13%
N/A
Hemodynamic instability present
Colitis
10%
Ischemia, IBD, radiation, infections (bacterial: Salmonella, Shigella, E coli O157: H7; viral: CMV, etc)
Can be caused by acute or chronic radiation (6 weeks to 1

year out, respectively)
Hemorrhoids
10%
Constipation
Only external hemorrhoids visible by physical examination
Abbreviations: CMV, cytomegalovirus; Escherichia coli, E coli; HNPCC, hereditary nonpolyposis colorectal cancer; IBD, inflammatory bowel disease;
LGIB, lower gastrointestinal bleeding; N/A, not applicable; UGIB, upper gastrointestinal bleeding.
August 2014 www.hmpractice.com
scenario. It is important to be thinking of all potential causes, especially in the setting where a patient's
past medical history is unobtainable.
acute UGIB. The severity of the GIB correlates with

red blood in the gastric lavage, tachycardia, and
hemoglobin < 8 g/dL.30

History
Initial Evaluation
There are 5 types of GIB presentations: (1) hematemesis, (2) melena, (3) hematochezia, (4) obscure
bleeding, and (5) systemic symptoms of blood loss
or anemia. (See Table 4, page 7.)

The clinical presentation can help in the appropriate localization of the bleeding as upper or
lower. Hematemesis and melena are usually associated with UGIB, while hematochezia is usually
associated with LGIB. Melena can be a presenting manifestation of small intestinal bleeding and
right-sided colonic lesions. Up to 13% of patients
presenting with hematochezia have a primary upper
GI source.31 Bleeding from the left colon presents as
bright red blood, whereas bleeding from the right
colon presents as maroon-colored blood that is
intermixed with stool. The combination of accurate
history taking and the presenting symptomatology
can aid physicians in significantly narrowing down
the differential diagnosis.

Past medical history plays a major role in determining the triage and management strategies. Prior
GIB is an essential risk factor for GIB, with up to
60% of patients having a history of UGIB from the
same lesion.32 History of liver disease should raise
the suspicion for a portal hypertensive etiology.
History of NSAID use or potential H pylori infection
should raise the suspicion for peptic ulcer disease.
Retching and vomiting should raise the suspicion
for a Mallory-Weiss tear. History of weight loss
should raise the suspicion for a malignancy. History
of aortic stenosis, renal disease, or hereditary hemorrhagic telangiectasia should raise the suspicion of
angiodysplasia.

Comorbidities such as coronary artery disease,
heart failure, pulmonary disease, coagulopathies,
and end-stage renal disease significantly affect
morbidity and mortality in patients with GIB. Patients with a history of coronary artery disease have
a higher threshold for target hemoglobin with or
without evidence of ongoing ischemia. Patients with
heart failure and end-stage renal disease require
closer monitoring in an intensive care setting, as the
potential for volume overload and subsequent respiratory failure is high. Patients with coagulopathies
need closer hematologic monitoring and administration of blood products. Poor mental status may
necessitate intubation.6,14,33

Current medication history should be obtained.
Antiplatelet and anticoagulation therapy result in
bleeding that is difficult to control. The intake of bismuth or iron may alter the clinical presentation, as it
is associated with darkening in the color of stools.

Initial evaluation determines management in patients who present to the hospital with suspected
GIB. A 2012 study described a retrospective data
analysis of 1776 patients admitted for a suspected
Table 3. Causes Of Obscure Gastrointestinal

Bleeding
Upper GI Bleeding
Sources
Risk Factors
Cameron erosions in hiatal

hernia
Hiatal hernia, reflux esophagitis,

mechanical trauma
Peptic ulcers
NSAID use, alcohol use, Helicobacter pylori infection
Angioectasias
Chronic kidney disease, aortic

stenosis (Heyde syndrome),
anticoagulation, cirrhosis
Dieulafoy lesions
Men with comorbidities and

NSAID use
Hemosuccus pancreaticus
Chronic pancreatitis, pancreatic pseudocysts, pancreatic

tumors, recent endoscopic
therapy
Hemobilia
Recent biliary tract instrumentation/injury, liver biopsy, or

gallstones, tumors, infection
Aortoenteric fistula
Atherosclerotic aortic aneurysm,

syphilis, tuberculosis
Lower GI Bleeding
Sources
Risk Factors
Angioectasias of small bowel
Chronic kidney disease, aortic

stenosis (Heyde syndrome),
anticoagulation
NSAID-induced ulcers or erosions
NSAID use
IBD-induced ulcers or erosions
IBD
Tumors (eg, leiomyomas, carcinoid tumors, lymphomas, and

adenocarcinomas) in patients
aged > 50 years
Multifactorial
Meckel diverticulum in young

patients
Congenital
Dieulafoy lesions
Men with comorbidities and

NSAID use
Less common: celiac disease,

radiation enteritis, and smallbowel varices
Disease-specific history
Abbreviations: GI, gastrointestinal; IBD, inflammatory bowel disease;

NSAID, nonsteroidal anti-inflammatory drug.
(ICU) admission.

Given the limitations and the lack of routine
clinical use of the Glasgow-Blatchford and Rockall
scoring systems, The AIMS65 score was introduced
in 2013 as a pre-endoscopic risk stratification tool
to assess mortality. The 5 factors that are scored
in the AIMS65 score include: Albumin level < 3;
International normalized ratio (INR) > 1.5; altered
Mental status; Systolic blood pressure 90 mm
Hg; and age > 65 years.37 The AIMS65 score is better
at predicting inpatient mortality, length of hospital
stay (from 3.4 days for 0 risk factors to 8.1 days for 5
risk factors), and hospitalization cost (average cost
of $5647 USD with 0 risk factors to $15,776 USD with
5 risk factors). However, it could not predict risk of
the rebleeding after endoscopy.37
Physical Examination
The physical examination should focus on the key

signs of acute blood loss, such as hypotension, resting tachycardia, poor skin turgor, and dry mucous
membranes. Orthostatic hypotension (defined as
a decrease in systolic blood pressure of 20 mm Hg
and/or an increase in the heart rate of 20 beats/
min) is generally associated with a blood loss of at
least 15%. Supine hypotension represents a blood
loss of > 40%.34 Cardiopulmonary assessment and
digital rectal examination should be part of the
initial examination.18 Signs of chronic liver disease
(such as spider angiomas, ascites, palmar erythema,
caput medusa, and splenomegaly) should alert the
physician to the possibility of a portal hypertensive
bleed. Abdominal pain with tenderness, guarding,
and rigidity can suggest a perforation in the context
of peptic ulcer disease or inflammatory bowel disease. A crepitus in the neck or upper chest suggests
esophageal perforation in Boerhaave syndrome.
Diagnostic Studies
A summary of the various types of diagnostic studies for GI bleeding can be seen in Table 6 (page 9).
Scoring Systems
The most widely studied scoring systems for risk

stratification in patients with GIB include the
Glasgow-Blatchford Bleeding Score and the Rockall score. The Glasgow-Blatchford score includes
laboratory tests, vital signs, history of syncope, and
comorbidities. (See Table 5, page 8.) It stratifies
patients toward the need for urgent endoscopic
intervention, ranging from 0 to 23.35 It is also used
to predict inpatient mortality, inhospital rebleeding,
and blood transfusion requirements.

The Rockall score takes into account age, hemodynamic status, comorbid illnesses, diagnosis,
and endoscopic stigmata of recent hemorrhage.
(See Figure 1, page 8.) It requires early endoscopy
and provides a likelihood of further bleeding and
death.36 A score of < 2 is associated with a lower risk
of GIB. A score 2 warrants an intensive care unit
Laboratory Testing
Initial diagnostic workup includes laboratory data

in the form of a complete blood count, a complete
metabolic panel, and a coagulation profile with
prothrombin time (PT), partial thromboplastin time
(PTT), INR, and a blood type analysis with crossmatching. Hemoglobin may be falsely elevated
in patients who are dehydrated or falsely low in
patients after volume resuscitation. The hemoglobin level should be monitored every 2 to 8 hours,
depending on the severity of the GIB. Microcytosis
in the absence of hemoglobinopathies suggests chronicity of blood loss. An elevated BUN-to-creatinine
ratio can give clues to the etiology of GIB. A ratio
> 36 suggests an upper GI source.38 The ACG also
recommends obtaining serial electrocardiograms
(ECGs) and cardiac enzymes if a patient is at risk
Table 4. Presentation Of Gastrointestinal Bleeding

Presentation
Description
Comments
Hematemesis
Vomitus of red blood or coffee grounds-appearing

material
History or potential history of liver disease is more urgent

and concerning, given potential portal hypertensive
etiology.
Melena
Black, tarry stool that is foul-smelling
History of NSAID use and Helicobacter pylori infection is

most common; 60% of patients have UGIB from same
lesion.
Hematochezia
Rectal passage of red or maroon-colored blood
Up to 13% of patients have a primary upper GI source.
Obscure bleeding
May present by presence of iron deficiency or fecal occult blood test previously worked up without a known
source
Refer to Table 3 (page 6) regarding etiology and specific

risk factors.
Systemic symptoms of blood

loss or severe anemia
Syncope, chest pain, shortness of breath, or lightheadedness
Supine hypotension represents blood loss > 40%.
Abbreviations: GI, gastrointestinal; NSAID, nonsteroidal anti-inflammatory drug; UGIB, upper gastrointestinal bleeding.
for myocardial ischemia or is presenting with active

chest pain or dyspnea.
GIB.6 In 2011, Huang et al reviewed retrospective

treatment data for 630 patients and compared 30day mortality, length of hospital stay, transfusion
requirements, need for surgery, and time to endoscopy.42 The use of nasogastric lavage did not affect
mortality (odds ratio [OR], 0.84; 95% confidence
interval [CI], 0.37-1.92), or length of hospital stay (P
= .57), or transfusion requirements (P = .94). It has
been shown that, even when nasogastric lavage is
correctly performed, up to 15% of patients without
evidence of bleeding on nasogastric lavage still had
endoscopic findings of UGIB.43 Clinical suspicion for
variceal bleed is not a contraindication for inserting
a nasogastric tube.33,38
Nasogastric Lavage
Nasogastric lavage is routinely used to distinguish

UGIB from LGIB and to assess the severity of bleeding.39-41 Instilling 500 mL of saline followed by
aspirating the fluid into a syringe can help evaluate
for bleeding proximal to the ligament of Treitz. A
positive aspirate is defined as that which contains
coffee grounds-appearing material or red blood. The
benefits of using nasogastric lavage include prevention of pulmonary aspiration, clearing of the stomach contents with a consequent improvement in visualization during endoscopy, and delivering bowel
preparation if colonoscopy is needed. However,
because it is inaccurate in identifying a UGIB, and
because it has no effect on overall clinical outcomes,
its use remains controversial.41-43 Major medical
societies state that nasogastric lavage is not required
for the evaluation and management of patients with
Imaging Studies
Radiographic imaging offers noninvasive diagnostic

strategies. Barium studies are not suggested in the
setting of GIB, as they can interfere with angiography, surgery, and endoscopy. Wireless capsule
endoscopy has no role in cases of acute UGIB.

Other imaging modalities such as radionuclide
scans, computed tomography (CT) angiography,
and angiography play large roles in the diagnostic
workup of patients with GIB. These studies require
active bleeding in order to identify lesions.7,9
The radionuclide scan is the most sensitive test
for detecting GIB at rates as low as 0.1 to 0.5
mL/min.42 It requires the use of either technetium sulfur colloid or technetium pertechnetatelabeled autologous red blood cells. The sulfur
colloid is rapidly cleared and is useful shortly
after injection. The pertechnetate is not rapidly
cleared, and scans can be repeated for evidence
of rebleeding.
CT angiography is a fast and widely available
imaging modality. It can detect bleeding at a
rate of 0.3 to 0.5 mL/min.43
Angiography is the least sensitive test. It requires blood loss at a rate of 1 to 1.5 mL/min.44
However, it can allow for therapeutic intervention (such as embolization).45 Intestinal infarction is a serious risk with this procedure and can
be as high as 20%. Infarction of other organs and
renal failure are other complications.46-48

Table 5. The Glasgow-Blatchford Bleeding

Score
Admission Risk Marker
Score
Blood Urea
6.5 to < 8
8 to < 10
10 to < 25
25
6
Hemoglobin (g/L) for men
12 to < 13
10 to < 12
< 10
6
Hemoglobin (g/L) for women
10 to < 12
< 10
6
Systolic Blood Pressure (mm Hg)
100-109
90-99
< 90
3
Other Markers
Pulse 100 beats/min
Presentation with melena
Presentation with syncope
Hepatic disease
Cardiac failure
Figure 1. The Rockall Score
A total score > 8 carries high risk, justifying intensive care unit admission.
Reprinted from The Lancet, Volume 356, Issue 9238. Oliver Blatchford,
William R. Murray, Mary Blatchford. "A Risk Score to Predict Need for
Treatment for Uppergastrointestinal Haemorrhage." Pages 13181321, Copyright 2000, with permission from Elsevier.
To view the Rockall numerical risk scoring system, scan the QR code
with a smartphone or go to http://www.ncbi.nlm.nih.gov/pmc/articles/
PMC1383057/?page=3
Patients with significant GIB must be monitored in

an ICU setting. Appropriate scoring systems may be
used for risk stratification (see page 7).

Electrocardiogram And Cardiac Enzyme

Studies
The ACG recommends obtaining serial ECGs and

cardiac enzymes if a patient is at risk for myocardial
ischemia or is presenting with active chest pain or
dyspnea.15
Pharmacologic Interventions
In patients presenting with acute UGIB following

hemodynamic resuscitation, an intravenous infusion
of proton pump inhibitor (PPI) should be considered
before endoscopy. An initial 80 mg bolus is followed
by 8 mg/h infusion. If high-risk lesions are diagnosed
on upper endoscopy, patients should be maintained
on a continuous infusion of intravenous PPI therapy
for 72 hours. High-risk lesions include ulcers with
active bleeding, visible vessels, or adherent clots.6
For low-risk lesions (including ulcers that have
flat pigmented spots or a clean base), allow for the
immediate transition to standard PPI therapy with
once-daily oral dosing. A meta-analysis of 21 randomized trials compared PPI with placebo or H2RA
for bleeding ulcers, and it showed decreased need
for surgery and risk of recurrent bleeding when PPI
was used; however, there was no effect on mortality.51 A meta-analysis of 6 randomized trials with
615 patients found that, in the setting of peptic ulcer
bleeding, there was no difference in blood transfused,
need for surgery, or all-cause mortality between oral
and intravenous PPI therapy.52 Overall, the use of a
PPI drip shortens the hospital stay, reduces the risk of
rebleeding, and downgrades high-risk lesions.6 There
is little evidence to support any benefits with PPI drip
therapy if there are no lesions detected on endoscopy.
Multiple studies have shown no benefit of H2 blockers in the context of UGIB. Discontinuation of NSAID
therapy and H pylori eradication (if present) are the
standards of care.53-55

In patients with a suspected variceal bleed, the
somatostatin analogue, octreotide, should be initiated as an intravenous bolus of 50 mcg, followed by a
continuous infusion at a rate of 50 mcg/h. It should
be continued for 3 to 5 days after the diagnosis is
confirmed (Class I, Level A, per ACG guidelines).56

In patients with cirrhosis, a 7-day course of
antibiotics (either norfloxacin or ceftriaxone) is
Diagnostic Studies For Obscure

Diagnostic studies for OGIB include wireless capsule endoscopy, push enteroscopy, and deep smallbowel enteroscopy with either a single or double
balloon. In the setting of an overt OGIB, testing with
bleeding scans and angiography is recommended.9
If examinations are negative, pursuing a capsule
endoscopy is the next best step. If occult obscure GI
blood loss and iron deficiency anemia are present,
the AGA recommends capsule endoscopy.9 This
is important (especially in younger patients), as
small-bowel tumors are the most common cause of
obscure bleeding in patients aged < 50 years. ASGE
has moderate evidence to recommend iron therapy
for occult OGIB with negative capsule studies.7

Treatment
Initial Supportive Measures
Hemodynamic resuscitation is the initial approach

prior to endoscopic intervention. Resuscitation starts
with the insertion of 2 large-bore intravenous lines
(18 gauge or higher) followed by volume repletion
utilizing isotonic crystalloid fluid. The use of blood
transfusion should be individualized, and multiple
strategies have been published on its use.6,49,50 (For
more information on transfusion strategies, see the
May 2014 issue of Hospital Medicine Practice, "Anemia
In The Hospitalized Patient: Current Evidence-Based
Strategies For Evaluation And Treatment.") Oxygen
supplementation should be provided. Elective intubation of the airway should be performed if the patient
has an altered mental status, ongoing significant
hematemesis, or severe cardiopulmonary disease.
Table 6. Diagnostic Studies For Gastrointestinal Bleeding

Tests to Consider Ordering in Initial Acute GIB
Clinical Indication
Comments
Complete blood counts, PT/INR, blood type and

crossmatch, complete metabolic panel
Any suspicion of GIB
Perform serial hemoglobin checks to assess

for appropriate transfusion requirements
Nasogastric lavage
Uncertain upper versus lower GIB
Controversial, given no change in clinical outcomes; variceal suspicion is not an absolute

contraindication
Radiographic imaging
Active large-volume blood loss and unstable

or failed endoscopy (technetium vs angiography)
Barium contraindicated in GIB; perform abdominal x-ray if concern for perforation
ECG, cardiac enzymes
High-risk patients for myocardial ischemia
Consider in setting of active chest pain or

even dyspnea
Abbreviations: ECG, electrocardiogram; GIB, gastrointestinal bleeding; INR, international normalized ratio; PT, prothrombin time.
indicated to decrease overall short-term mortality

and spontaneous bacterial peritonitis with any GIB
(Class I, Level B).57-60

Metoclopramide and erythromycin have
been studied in patients with UGIB as prokinetic
agents.16,61 The ASGE recommends erythromycin
use in patients with a high probability of having
fresh blood or blood clots to aid in visualization during endoscopy.11 Doses of 250 mg administered intravenously over 20 minutes, 30 to 90 minutes prior
to the procedure, have been recommended.28 Based
on expert opinion, lactulose should not be administered in patients with an active variceal bleed who
are experiencing hepatic encephalopathy.33

peptic ulcer bleeding include epinephrine injection,

hemostatic clips, and cautery. Band ligation can be
performed for bleeding esophageal varices. Cyanoacrylate injection can be considered for bleeding
fundic gastric varices.8 Epinephrine should only be
used when combined with an additional modality.
Endoscopic Banding
In patients with actively bleeding esophageal varices, endoscopic banding is the therapeutic modality
of choice. Sclerotherapy is rarely performed if banding fails, and it is not the preferred modality. In patients with gastric varices, transjugular intrahepatic
portosystemic shunt (TIPS) is the preferred modality.
Attempts at banding can lead to ulcerations and
significant hemorrhage.10,11 Given that complications from banding are substantially fewer than with
sclerotherapy, it is used more frequently. Cumulative
complication rates are estimated at approximately
11% and generally occur locally (overtube trauma to
mucosa or ulcers from banding), but there can also
be a risk for aspiration.65 Sclerotherapy has higher
rates of cumulative complications (near 25%) that
can range from local (ulceration, bleeding, strictures)
to regional (perforation and mediastinitis) to systemic (aspiration and sepsis).66

Lower Endoscopy
Lower endoscopy is the diagnostic modality of
choice for LGIB. The therapeutic measures for LGIB
are similar to those in UGIB. The risks of endoscopy
include complications from the administration of
conscious sedation, aspiration, perforation, and
worsening of GIB.

Angiography
Angiography is a useful tool in the setting of persistent GIB and hemodynamic instability in the
context of a failed endoscopic intervention, and
this is especially true for LGIB cases. Hemostasis
can be achieved in 95% of cases.67 If bleeding is not
controlled, surgery is the next option. Per ASGE
guidelines, surgery should be considered in patients
with ongoing hematochezia who require transfusion
therapy of > 6 units of packed red blood cells in a
24-hour period or if the bleeding recurs.12 Specific
segmental resection can occur in the setting of adenocarcinoma of the colon or diverticular disease of
the colon. In patients who rebleed after initial hemostasis endoscopically, repeat endoscopy is recommended over surgery or radiologic intervention (per
ASGE, with moderate quality evidence).
Correction Of Coagulopathy Or Bleeding

Diathesis
Correction of coagulopathy in the setting of GIB

has been long debated. Wolf et al reviewed data
from 233 admitted patients from 1999 until 2004 and
assessed the primary outcome of rebleeding. Their
study showed that mild to moderate anticoagulation does not increase the risk of rebleeding following therapy for UGIB.64 They concluded that if the
INR is > 3, then it is reasonable to give fresh-frozen
plasma (FFP) before proceeding with endoscopy. In
general, if the INR is > 1.5 in patients with GIB, FFP
transfusion is recommended. In patients with active
GIB, platelets should be transfused if the platelet
count is < 50,000/mm3.

Therapeutic Measures
Upper Endoscopy
In addition to its use as the diagnostic modality of
choice for UGIB, upper endoscopy has the added
benefit of use as a therapeutic intervention. The
Forrest Classifications (see Table 7) describe endoscopic findings in patients with peptic ulcer disease,
guide management decisions, and predict the risk
of further bleeding.6,63,64 Treatment modalities for
Table 7. Forrest Classifications With

Prevalence And Risk Of Rebleeding On
Medical Management65
Endoscopic Stigmata of
Recent Hemorrhage
Prevalence
(%)
Risk of Rebleed on
Medical Management (%)
Active arterial bleeding (Forrest Ia)
10
90
Oozing without visible vessel

(Forrest Ib)
10
10-20
Nonbleeding visible vessel

(Forrest IIa)
25
50
Adherent clot (Forrest IIb)
10
25-30
Flat spot (Forrest IIc)
10
7-10
Clean ulcer base (Forrest (III)
35
3-5
Additional Options In The Management Of

Transjugular intrahepatic portosystemic shunt
(TIPS), balloon-occluded retrograde transvenous
obliteration (BRTO), balloon-occluded antegrade
10
transvenous obliteration (BATO), and cyanoacrylate

injection are other modalities in the treatment of
variceal bleeding from portal hypertension. Video
capsule endoscopy (VCE) and single- and doubleballoon endoscopy are additional options in management of occult GI bleeding.
Video Capsule Endoscopy

VCE is an excellent noninvasive imaging modality of
the small intestine. In patients with OGIB, the yield
of VCE is much higher than small-bowel enteroscopy, ranging between 30% and 70% among various
studies. VCE is the standard of care in patients with
OGIB; however, it does not offer any therapeutic options. There is reported variability in the adequacy
of small-bowel examination among inpatients and
outpatients. This may be due to various issues with
hospitalized patients. Further studies are needed to
confirm these findings.7,9,77
Transjugular Intrahepatic Portosystemic Shunt

TIPS involves creation of a channel via a stent between the hepatic vein and the intrahepatic portion
of the portal vein.68 The American Association for
the Study of Liver Disease guidelines recommend
that patients with variceal hemorrhage who rebleed
or continue to bleed despite aggressive pharmacologic and endoscopic management are candidates
for TIPS.13 A Sengstaken-Blakemore tube is used
as tamponade therapy for hemostasis while awaiting TIPS. While it is successful in up to 93% of
cases when treating variceal hemorrhage, it is also
an independent predictor of early mortality.69,70
Mortality from esophageal bleeding is significantly
less in the TIPS group.71 Right heart failure, a high
MELD score (Model for End-Stage Liver Disease),
and severe hepatic encephalopathy are contraindications for TIPS; therefore, it is beneficial to obtain
a 2-dimensional echocardiogram early in patients
with anticipation for TIPS.13
Special Circumstances
Gastrointestinal Bleeding In The Setting Of
Mandatory Antiplatelet And Anticoagulant
Therapy
Antiplatelet and anticoagulation therapy can contribute to clinically significant GIB. In a prospective
study involving 18,820 hospital admissions, 376
were related to aspirin, clopidogrel (Plavix), or
warfarin.78 The majority of those admissions were
related to GIB. A meta-analysis that included 14 randomized controlled trials (including 57,000 patients)
showed a relative risk of 2.07 (95% CI, 1.61-2.66)
for aspirin versus placebo. There was no difference
whether the aspirin dose was 76 to 162.5 mg/day or
162.5 to 325 mg/day. The absolute annual increases
attributable to aspirin risk for major GIB was 0.12%
(95% CI, 0.07-0.19).79 Factors that increased the risk
of GIB in aspirin users included a history of GI
bleeding (OR, 6.5; 95% CI, 2.0-21.2),80 prior history
of peptic ulcer disease (OR 2.1; 95% CI, 91.0-4.10),80
concomitant corticosteroid or anticoagulant use, and
the concomitant use of nonaspirin NSAIDs.81 In a
multivariate analysis from case-controlled studies,
older age did not show an increased relative risk for
GIB.80,81 However, the absolute risk of GIB, regardless of aspirin use, remains higher in older age.81,82

The data for clopidogrel in GIB are limited.
Combination therapy increases the risk of GIB. This
was evident in the Clopidogrel in Unstable Angina
to Prevent Recurrent Events (CURE) study.81 The
risk of bleeding with dual antiplatelet therapy is
1.3% in the first 30 days; however, it increases to 12%
with a history of GIB.82

The management of antiplatelet agents in
patients with acute coronary syndromes or recent
coronary stents in the setting of GIB is difficult.
The ASGE guidelines recommend withholding
antiplatelet agents until hemostasis is achieved.
Platelet transfusions may be needed in life-threatening GIB due to dysfunctional platelets, and
urgent cardiology consults should be obtained to
aid in the management.83-87

Anticoagulants increase the risk of major GIB. In
randomized controlled trials, the frequency of major
Balloon-Occluded Retrograde Obliteration

And Balloon-Occluded Antegrade Transvenous
Obliteration
BRTO is a technique that is used in the setting of
gastric and ectopic varices, and it is a technique
commonly performed in Japan. Given the difficulty of gastric variceal treatment (due to its higher
blood flow volume)72 and complications with TIPS,
BRTO has gained popularity. It involves occluding
flow using a balloon catheter followed by instillation of a sclerosant agent proximal to the site of
balloon occlusion. Long-term outcomes have been
promising; however, a 10% failure rate and complications (such as increased portal pressure) have
limited its use in the United States.72,73 BATO has
shown additional success in obliteration of gastric
and duodenal varices either alone or in unison with
the BRTO approach.74,75
Cyanoacrylate Injection
Cyanoacrylate injection has been used in the treatment of large gastric varices, but it is not approved
by the United States Food and Drug Administration
(FDA). It is approved in Europe as a potential firstline therapy and as a secondary prophylactic therapy for gastric varices.76 Given its association with
complications such as septic and embolic events, its
role remains controversial.
11
bleeding in patients on warfarin therapy with an

INR of 2 to 3 has been less than half the frequency
of that in patients with an INR > 3.83 Concomitant
aspirin therapy predisposes to mucosal breakdowns
and increases the risk of bleeding (relative risk [RR]
> 5). A history of prior GIB is associated with an
increased risk of another major GIB (30% at 3 years
vs 5% with no bleeding history).84,85 Nonbleeding
peptic ulcer disease, however, has not been associated as an independent risk factor.83

Management Of Gastrointestinal Bleeding In The
Anticoagulated Patient
The management of GIB is complicated in the setting
of clinically indicated anticoagulation therapy. The
ASGE has issued guidelines to aid management.
The degree of reversal of anticoagulation (partial vs
complete) and the associated risk of thromboembolic
events must be weighed against the risk of continued bleeding.

FFP can be used to correct a supratherapeutic
INR. One series showed that anticoagulation reversal facilitated endoscopic diagnosis and therapy in
91% of 52 patients with acute GIB. This success rate
was comparable to a control group of patients who
had no anticoagulation therapy.88 Vitamin K has
limited use in the acute setting, as it has a delayed
onset of action (12-24 h) and prolongs the time required to re-establish therapeutic anticoagulation.83
Factor VII and prothrombin complex concentrate
(PCC) can be used for immediate reversal of anticoagulation in life-threatening hemorrhage. Thrombotic complications have been reported with PCC.
The data on factor VII and PCC are limited to case
reports and a small number of patients with GIB.82

The high cost of these agents may deter physicians from their use in management; however, Guest
et al showed that the use of PCC was a more costeffective strategy for the reversal of warfarin in lifethreatening hemorrhage (intracranial, retroperitoneal, and gastrointestinal) in a decision model, with
a reduction of < 15% of the total care of costs.89 The
higher cost of factor VIIa for the same patient ($9500
USD for 6 mg of factor VIIa vs $2700 USD for 3000
units of PCC), its short half-life (from 2.5 to 3 hours),
and required repeat dosing render it much more expensive.90 More data are needed to address this area
of clinical significance. Institutions should develop
protocols to guide the clinician in using PCC appropriately. Observational studies show successful
endoscopic therapy with partial reversal of anticoagulation (INR 1.3-2.7).88,91,92 Mortality, hospital stay,
and number of transfused units using warfarin were
not significantly different from controls.

The decision to reinstitute anticoagulation after
endoscopic therapy should be individualized. A
retrospective study reviewed 442 patients who had
GIB while on warfarin and assessed the safety of
resuming anticoagulation. After a median time of 4

days, 260 patients resumed warfarin, and 26 of the
260 patients (10%) developed recurrent bleeding,
compared to 10 patients who did not resume warfarin (6%). Warfarin therapy resumption after the
index GIB was associated with a lower adjusted risk
of thrombosis (hazard ratio [HR], 0.05; 95% CI, 0.010.58) and death (HR, 0.31; 95% CI, 0.15-0.62) without
a significant increase in the risk for recurrent GIB
(HR, 1.32; 95% CI, 0.50-3.57).93 The study did not address restarting concurrent antiplatelet therapy.

Intravenous heparin can be used when rapid
resumption of anticoagulation is desired. Newgeneration anticoagulants (thrombin and factor
Xa inhibitors) are now being more widely used. A
recent systematic review showed an increased risk
of GIB (OR 1.45; 95% CI, 1.07-1.97), but there was
substantial heterogeneity among studies.86
Unidentifiable Source Of Clinically

Significant Gastrointestinal Bleeding
Seventy-five percent of cases of overt OGIB are

from the small bowel, and the remainder are from
missed lesions in the upper and lower GI tract. The
diagnostic workup should include second-look
endoscopy followed by small-bowel evaluation. A
study of 95 patients showed that push enteroscopy
identified a bleeding source in 41% of patients with
OGIB. However, 64% were within reach of a standard endoscope.94

A number of prospective studies have shown
VCE to be superior to other diagnostic modalities.
A meta-analysis including 14 studies showed that
capsule was superior to both push enteroscopy and
small-bowel radiology in diagnosing small-bowel
pathology.95 If a bleeding source is identified, deep
small-bowel enteroscopy is a potential diagnostic
and therapeutic option.

Mesenteric angiography is a diagnostic and
therapeutic option. A positive tagged red blood cell
scan and a surgical clearance may be required because of the risk of intestinal necrosis. Provocative
angiography utilizing a combination of systemic
heparin and intra-arterial vasodilator therapy may
be considered in extreme cases. The success rates
of provocative angiography vary widely between
studies (20%-100%).96
Quality Improvement
Transfusion Strategies
Blood transfusions are given to 43% of patients

hospitalized with UGIB and to 21% of patients
hospitalized with LGIB.97-99 It is estimated that 25%
of transfusions in the United States are inappropriate.100 Physician anxiety with low hemoglobin values leads to overtransfusion and adverse outcomes.
The 2010 recommendations in the management of
12
additional death) at 45 days.101 The average hospital

treats approximately 200 GIB patients annually, so
evidence-based protocol could save the lives of 8 patients per year. Quality improvement in transfusion
strategies, applied nationally, could significantly
lower healthcare costs as well as morbidity and mortality rates associated with GIB.
nonvariceal UGIB endorsed a transfusion threshold

of 7 g/dL based largely on data from the TRICC
(Transfusion Requirements in Critical Care) trial.5
However, this study excluded GIB patients. In 2013,
Villanueva et al published a randomized controlled
trial of 921 patients that supported the 2010 recommendations of a lower hemoglobin threshold.101
Patients with variceal and nonvariceal UGIB were
assigned to either a restrictive transfusion strategy
(transfusion only when hemoglobin was < 7 g/dL)
or a liberal transfusion strategy (transfusion when
hemoglobin was < 9 g/dL). Patients managed with
a restrictive approach had a lower 45-day mortality
(5% vs 9%), lower rebleeding rates (10% vs 16%),
and a lower rate of serious adverse events (40% vs
48%). The largest benefit was seen in patients with
advanced cirrhosis. A restrictive transfusion strategy
avoids rebound portal hypertension and the risk
of rebleeding.102 The trial excluded patients with
massive exsanguination, patients with a low risk
of rebleeding, patients with LGIB, and patients with
acute coronary syndromes. In addition, all patients
in the study underwent emergent endoscopy within
6 hours, and current guidelines recommend urgent
endoscopy within 24 hours. It is not clear whether
a restrictive transfusion strategy might have worse
outcomes in the setting of delayed endoscopy and
ongoing bleeding.

Cardiac disease changes the transfusion threshold in anemic patients. The myocardium is more
sensitive to anemia because it has a higher oxygen extraction ratio. Clinical studies are limited in
establishing a transfusion strategy.100 A transfusion
goal of hemoglobin > 9 g/dL can be considered in
patients with unstable coronary artery disease.

Transfusion may also be administered with
normal hemoglobin, as the laboratory value may
not reflect the patients true anemia in the setting
of hypovolemia and active bleeding. The patients
symptoms, vital signs, and physical examination
should guide transfusion requirement.

Complications of overtransfusion include acute
respiratory distress syndrome, dilutional coagulopathy, thrombocytopenia, hypothermia, and metabolic
complications in the form of hyperkalemia and
hypocalcemia. These parameters should be closely
monitored and appropriately addressed.103,104

Massive blood transfusion may also induce
coagulopathy. A useful guideline is to transfuse 1
unit of FFP for every 4 units of packed red blood
cells transfused in order to replace coagulation
factors. Platelets > 50,000/mm3 allow for endoscopic therapy.5,33

Accurate implementation of evidence-based protocols could significantly reduce blood use, shrink
healthcare costs, and decrease mortality. The number needed to treat in the Villaneuva et al study was
25 patients (ie, 25 patients would have to be treated
using a restrictive transfusion strategy to prevent 1
Appropriate Setting Of Care
Hospitalization for GIB should be dependent on

the severity of GIB. The patients history, physical
examination, laboratory results, location of bleeding,
and suspected bleeding lesion can predict severity105
and disposition to discharge, hospital bed, or ICU.
Hemodynamically stable patients with self-limited
hematochezia or infrequent melena and normal
laboratory values can be discharged with outpatient
follow-up.105 Stanley et al prospectively evaluated 123 patients with UGIB who had GlasgowBlatchford scores of 0 and who were not admitted
to the hospital; 23 patients underwent outpatient
endoscopy. No ulcers, varices, or malignancies were
found. No interventions were needed. The remaining patients were not readmitted with UGIB and did
not die during the 6-month follow-up period.106 The
2012 ACG practice guidelines recommend discharge
from the ED without endoscopy in patients with
blood urea nitrogen levels < 18.2 mg/dL, hemoglobin > 13 g/dL for men (12 g/dL for women), systolic blood pressure > 110 mm Hg, pulse rate < 100
beats/min, and absence of melena, syncope, cardiac
failure, and liver disease.6

Acute GIB can be life-threatening in 19% to 28%
of the cases requiring ICU admissions.107 Inappropriate ICU admission contributes significantly to
hospital costs. Small studies suggest that endoscopic
evaluation to identify high-risk lesions in the ED is
the best predictor of optimal hospital placement;
however, endoscopic evaluation in the ED is often
not practical.103 Kollef et al developed the BLEED
classification (ongoing Bleeding, Low systolic blood
pressure, Elevated prothrombin time, Erratic mental
status, unstable comorbid Disease) in a cohort study
of 465 patients to predict hospital outcomes for
patients with acute UGIB or LGIB. Patients meeting
any BLEED criteria were classified as high risk.
The primary outcome was occurrence of recurrent
GIB after 24 hours of stabilization; however, the
study did not predict early risk (within 24 hours),
which may be more pertinent to predict ICU admission.108 Das et al conducted a cohort study of 132 patients to develop a triage protocol. The combination
of red blood transfusions or unstable comorbidities
had a positive predictive value of 0.24 and a negative predictive value of 0.91 for GIB-related complications within 24 hours.107 The current consensus is
that patients with ongoing bleeding, unstable vital
signs, or unstable comorbidities require ICU admis13
Clinical Pathway For Diagnostic Workup In

Overt Obscure Gastrointestinal Bleeding
Patient presents with
overt obscure GI bleeding
Active bleeding
Inactive bleeding
Video
capsule
enteroscopy,
deep endoscopy, push
enteroscopy,
and/or
colonoscopy
Suspected
upper GI
bleeding
Repeat EGD
or PE
Consider
deep enteroscopy*
NEGATIVE
Consider CT
enterography or CT
angiography
Other GI
bleeding
Video capsule endoscopy and/or

scintigraphy
Consider CT
enterography or CT
angiography
NEGATIVE
Angiography
and/or
colonoscopy
Recurrent
bleeding
Consider
provocative
testing
NEGATIVE
No recurrent
bleeding
Consider interoperative
endoscopy
See Clinical
Pathway
for Occult
Obscure GI
Bleeding,
page 15
*Consider especially in patients with altered anatomy or increased suspicion of angioectasia.
Consider especially in patients who present with massive bleeding.

Dashed arrows indicate less-preferred options. Positive test results should direct specific therapy. Because diagnostic tests can be complementary, more
than 1 test may be needed, and the first-line test may be based upon institutional expertise and availability.
Abbreviations: CT, computed tomography; EGD, esophagogastroduodenoscopy; GI, gastrointestinal.
Reprinted from Gastrointestinal Endoscopy, Volume 72, Issue 3. Laurel Fisher, Mary Lee Krinsky, Michelle A. Anderson, et al. The Role of Endoscopy in
the Management of Obscure GI Bleeding. Pages 471-479. Copyright 2010, with permission from Elsevier.
14
Clinical Pathway For Diagnostic Workup In

Occult Obscure Gastrointestinal Bleeding
Patient presents with occult obscure GI bleeding
Consider trial of
empiric iron therapy
NO RESPONSE
Consider multiphase CT
enterography or
CT angiography
Small-bowel evaluation
Video capsule endoscopy
NEGATIVE
Consider repeat EGD or

colonoscopy
Consider deep
enteroscopy*
NEGATIVE
Stable
Observe; trial of iron,

if appropriate
Continued bleeding
Repeat video capsule endoscopy, especially if GI bleeding

is now overt or if hemoglobin
decrease is 4 g/dL
Repeat EGD or push enteroscopy and colonoscopy, especially

if not previously repeated
Deep enteroscopy
*Consider especially in patients with altered anatomy or increased suspicion of angioectasia.

Dashed arrows indicate less-preferred options. Positive test results should direct specific therapy. Because diagnostic tests can be complementary, more
than 1 test may be needed, and the first-line test may be based upon institutional expertise and availability.
Abbreviations: CT, computed tomography; EGD, esophagogastroduodenoscopy; GI, gastrointestinal.
Reprinted from Gastrointestinal Endoscopy, Volume 72, Issue 3. Laurel Fisher, Mary Lee Krinsky, Michelle A. Anderson, et al. The Role of Endoscopy in
the Management of Obscure GI Bleeding. Pages 471-479. Copyright 2010, with permission from Elsevier.
15
sion. Hemodynamically stable patients who have

had an acute GIB can be admitted to a step-down or
standard hospital bed.103 More prospective studies
are needed to assess the optimal utilization of inpatient and critical care resources.
severe colonic bleeding, a rapid purge prior to urgent colonoscopy can be considered. Four to 8 liters
of polyethylene glycol orally or via nasogastric tube
over 2 to 3 hours is given until the rectal effluent is
clear. Rapid purge is not always well tolerated, however. Metoclopramide (10 mg) or erythromycin (250
mg) may be given intravenously before the purge
to facilitate gastric emptying. Risks of rapid purge
include aspiration and fluid overload.113

It is unclear whether or not urgent colonoscopy
with rapid purge changes outcomes. Jensen et al
reported that urgent colonoscopy may provide high
rates of endoscopic hemostasis and may reduce the
need for future surgery.114 A randomized trial of
72 patients did not show that urgent colonoscopy
improved clinical outcomes or lowered hospital
charges compared to elective colonoscopy. A major
limitation was that the study was terminated early,
so the small sample size may not have allowed for
statistical significance.31
Early Appropriate Consultation Or Referral

To A Tertiary Center Care
The hospitalist must recognize GIB, initiate medical

resuscitation, and notify a GI consultant. The GI consultant can assist in risk stratification and the plan
for an early endoscopy. In UGIB, endoscopy within
24 hours or earlier should be performed. Colonoscopy with rapid purge can be performed urgently
if severe LGIB is suspected. Observational studies
document that early endoscopy is associated with
a reduction in the length of hospital stay, recurrent
bleeding, need for surgery, and short-term morbidity and mortality. The timing of the endoscopy
is dependent on the admission time and the local
resources. Middle-of-the-night endoscopy is usually avoided, except for life-threatening bleeding or
high-risk patients, due to the fact that well-trained
endoscopy nurses, endoscopic equipment, and surgical backup may not be available. However, a multicenter observational study showed that evening or
nighttime admissions were not associated with adverse outcomes, even though the time to endoscopy
was significantly longer.102,108,109 An observational
study examining the Nationwide Inpatient Sample
from 2002-2007 showed that, for patients with
nonvariceal UGIB, the inpatient mortality was 2.5%
for those who underwent upper endoscopy within
1 day of admission and 6.6% for those who did not
(adjusted OR, 1.32; 95% CI, 1.26-1.38).110

A few studies have shown a weekend effect. A
United States cross-sectional study by Ananthakrishnan et al showed that patients with acute nonvariceal UGIB had higher mortality (OR, 1.21; 95% CI,
1.09-1.35) and lower rates of endoscopy (OR, 0.64;
95% CI, 0.61-0.68) in both teaching and nonteaching hospitals. Early endoscopy rates in nonteaching
hospitals were lower in acute variceal hemorrhage
(OR, 0.65; 95% CI, 0.51-0.82).111 Limitations in the access to emergency endoscopy during the weekends
should lead to corrective hospital initiatives.112 In
settings where urgent interventions are not feasible
or where required technical expertise is not available, early referral and transfer to a tertiary care
setting is suggested.
Appropriate Time For Discharge
Hospital discharge after GIB should be considered

when careful monitoring, diagnostic evaluation, and
therapeutic procedures are complete. Endoscopic
risk stratification dictates the hospital course in acute
nonvariceal UGIB. Patients with low-risk endoscopic
features (clean-based ulcer, erosive disease, MalloryWeiss tear), low-risk clinical features (stable vital
signs, stable hemoglobin, no serious comorbidities),
and good social support may be discharged on the
first day of hospitalization. Cipolletta et al showed
low risk of recurrent bleeding and significant savings in hospital costs with early discharges ($340
USD for the outpatient group and $3940 USD for the
inpatient group; P = .001).115 Patients with high-risk
stigmata (active bleeding, visible vessel, and clot)
should be hospitalized longer to receive intravenous
PPI therapy and to monitor for rebleeding. Studies showed > 95% risk of rebleeding within 3 days.
Newer randomized trials showed that a minority of
patients bled beyond 3 days. The ACG guidelines
for the management of acute nonvariceal UGIB do
not recommend hospital stays beyond 3 days in the
absence of further bleeding.6

Patients who survive an acute variceal GI bleed
carry a high risk of rebleeding and mortality: 60%
and 33%, respectively, within 1 to 2 years. Therefore, secondary prophylaxis (to prevent recurrent
variceal bleeding) should be initiated, as tolerated,
prior to hospital discharge, and the patient should
be hemorrhage free for more than 24 hours.10
Secondary prophylaxis includes nonselective beta
blockers in addition to variceal banding performed
during endoscopy.

Endoscopic risk stratification does not exist for
LGIB. The patient can be discharged with resolution
of bleeding, stable vital signs, and stable hemoglo-
Additional Considerations
Bowel Preparation Strategies
Bowel preparation should be administered prior to

colonoscopy in the evaluation of LGIB. Bowel preparation increases cecal intubation rates and clears the
colon lumen of clots, stool, and blood. In suspected
16
bin. In LGIB patients with recurrent diverticular

bleeding, surgical intervention should be considered
if they are good candidates for it.

associated with more oxygen desaturation as compared to endoscopy within 12 to 24 hours.123 Another study, by Yavorski et al, showed that mortality
rates were higher for high-risk patients who did not
undergo an early endoscopic intervention than for
patients who did undergo the intervention early
(within 13 hours of clinical presentation) (11.1% vs
5.2%, respectively).124

Routine second-look endoscopy (usually performed 24 hours after the initial therapeutic endoscopy) is not recommended by any major society.
However, in patients with clinical evidence of recurrent bleeding, a repeat endoscopy with the intention to treat is warranted. This is especially true in
patients with high-risk stigmata for hemorrhage on
index endoscopy. Recurrent bleeding after a second
therapeutic endoscopic session should prompt a
surgical consultation or an interventional radiology
consultation, with consideration for transcatheter
artery embolization.67,122
Critical Care Aspects
Stress ulcerations are the major cause of GIB in critically ill patients in the ICU. A prospective multicenter cohort study identified 2 main risk factors for
bleeding: coagulopathy (OR, 4.3) and mechanical
ventilation longer than 48 hours (OR, 15.6). The frequency of clinically significant GIB to either or both
of these risk factors was 3.7%, compared with 0.1%
when neither risk factor was present. The mortality
rate was 48.5% in the group with bleeding and 9.1%
in the group without bleeding (P < .001).116 Other
proposed risk factors include history of GIB, sepsis,
ICU admission > 1 week, occult GIB lasting > 6
days, and glucocorticoid therapy.117

Prophylaxis of stress ulcerations is indicated in
high-risk groups. Pharmacological options include
H2 blocker, PPI, and sucralfate (Carafate). A metaanalysis of 13 randomized trials compared stress
ulcer prophylaxis with a PPI to prophylaxis with an
H2 blocker. Less GIB was seen among those who
received PPI (1.3 vs 6.6 %; OR, 0.30; CI, 0.17-0.54).
There was no difference in mortality or the incidence
of nosocomial pneumonia.118

Potential harms of prophylaxis include increasing gastric pH and increasing incidence of nosocomial pneumonia. However, only a trend (and not
statistical significance) has been reached in studies.
Stress ulcer prophylaxis should be discontinued
when the patient is no longer at risk.118
Use Of Proton Pump Inhibitors With

Clopidogrel
In recent years, concern has been raised about the

potential for PPIs (especially omeprazole [Prilosec,
Zegerid]) to decrease the efficacy ofclopidogrel.
This prompted both the FDA and the European
Medicines Agency (EMA) to issue warnings regarding the concomitant use of these medications.
Although pharmacodynamic studies support an
interaction between PPIs and clopidogrel, clinical
evidence from a meta-analysis suggests that concomitant use ofclopidogreland PPIs was not associated with major cardiovascular risk. In the CREDO
trial (Clopidogrel for the Reduction of Events
During Observation), the efficacy ofclopidogrelwas
not significantly affected by PPI use; however, in
the CAPRIEstudy (Clopidogrel Versus Aspirin In
Patients at Risk of Ischemic Events), clopidogrelwas
beneficial to non-PPI users while apparently harmful to PPI users. Until further conclusive evidence is
available, pantoprazole (Protonix) has been suggested to be safer compared to other PPIs in patients
at high risk for GIB who are taking clopidogrel.125-127
Controversies And Cutting Edge
Timing Of Endoscopy And Need For SecondLook Endoscopy

In patients presenting with GIB, the optimal timing
of endoscopy is guided both by the clinical condition
of the patient and the pre-endoscopy risk of significant UGIB.6 In some healthcare settings, nonavailability of resources during off hours can delay timing of endoscopy; these cases should be referred to
a center where these resources are available around
the clock.

Based on the ACG and ASGE guidelines, endoscopy in low-risk patients with no significant medical
issues should be performed after optimal hemodynamic resuscitation within 24 hours of admission.6-8
However, in high-risk patients with tachycardia,
hypotension, bloody emesis, or bloody nasogastric
aspirate, endoscopy is recommended within 12
hours, as this can potentially improve clinical outcomes.119-122 Earlier interventions might be limited
by the need for hemodynamic resuscitation. A study
by Yen et al suggested that emergent endoscopy
within 2 hours in patients with active UGIB was
Time- And Cost-Effective Strategies

Early Endoscopy
In patients with UGIB, endoscopy performed within

24 hours of admission has been shown to reduce the
blood transfusion requirements, the length of ICU
stay, and the total hospital stay. Numerous studies have confirmed that hemodynamically stable
patients with suspected UGIB should be evaluated
with an upper endoscopy. If there are low-risk stigmata for recurrent bleeding, patients can be safely
discharged with appropriate follow-up.6,14

A randomized controlled trial of 100 patients
17
compared urgent colonoscopy toexpectant or electivecolonoscopy alone or with radiographic interventions. It showed improved detection of the bleeding etiology; however, it did not significantly reduce
mortality, hospital stay, transfusion requirements,
or the need for surgery.128 On the other hand, other
studies have suggested that a therapeutic urgent
colonoscopy (< 12 hours from admission) can reduce
the risk of rebleeding and surgery in patients with
severe diverticular hemorrhage when compared to
patients treated conservatively.5,31,114,128-135
cally suspicious for a malignancy, even if biopsy

samples from the initial endoscopy are benign.
A repeat biopsy should be performed on gastric
ulcers that do not exhibit healing at follow-up
examination after 8 to 12 weeks of medical therapy. Surveillance endoscopy is also suggested
for patients who remain symptomatic despite an
appropriate course of antisecretory therapy and
previous benign biopsy specimens to rule out
refractory peptic ulceration, nonpeptic benign
etiologies, and occult malignancy.8,136-140
4. Nonselective beta blocker therapy: In patients
with variceal UGIB, propranolol or nadolol
should be initiated on discharge unless contraindicated or not tolerated.11,137
5. Instructions for patients: Written instructions
that include particular signs and symptoms to
watch for after EGD or colonoscopy should be
provided to the patient on discharge.
Use Of Intravenous Proton Pump Inhibitors

(Drip)
A Cochrane Review meta-analysis comprising 6

randomized controlled trials assessed the impact of
PPI therapy for UGIB before endoscopy. It showed
that PPI therapy decreases the proportion of patients
with high-risk lesions on endoscopy. This reduced
the need for endoscopic therapy at index endoscopy,
but it did not improve clinical outcomes (such as recurrent bleeding, surgery, or death). If no high-risk
stigmata for bleeding are identified on upper endoscopy, intravenous PPI drip should be discontinued.
Standard therapy in the form of once-daily dosing
should be initiated, as this decreases the overall
healthcare cost. Additionally, there is a rare reported
risk of anterior ischemic optic neuropathy caused by
high-dose PPI drip.14,125
Dispositions And Transition Of Care

Inpatients with a documented, actively bleeding
ulcer or other high-risk endoscopic stigmata must be
observed for at least 72 hours. Treatment should be
in the form of intravenous PPI. A patient can be discharged on oral PPI therapy once there is no clinical
or laboratory evidence of active GIB. Patients with
clean-based ulcers may be started on a regular diet
and discharged. Appropriate follow-up care should
be provided.
Prevention Of Ulcer Rebleeding
Prevention of recurrent GIB remains a cornerstone

of cost-effective care. H pylori eradication should be
confirmed. NSAIDs and COX-2 inhibitors should
be avoided. In GIB patients with non-H pylori and
non-NSAID ulcers, long-term PPI therapy should be
prescribed.6,126,131
Summary
For patients with any GI bleeding, hemodynamic resuscitation is the initial management,
and appropriate transfusion strategies should be
followed. These include packed red blood cell
transfusions, correction of coagulopathy with
FFP if the INR is > 1.5; monitoring for hypothermia and electrolyte abnormalities; and correction of thrombocytopenia if the platelet count is
< 50,000/mm3. Thrombotic thrombocytopenic
purpura should be ruled out by checking a
peripheral smear (although this is not always
possible).
LGIB is more common than UGIB, but UGIB
events are more clinically significant.
In patients with suspected nonvariceal UGIB,
the pre-endoscopic institution of intravenous
PPI may alter the endoscopic detection of
high-risk lesions; however, it does not affect
outcomes. H pylori and NSAIDs should be considered as possible etiologies of peptic ulcers.
All gastric ulcers need a follow-up endoscopy to
ensure healing and to rule out malignancy.
Patients with nonvariceal UGIB and high-risk
lesions on endoscopy must be treated with intra-
Must-Do Markers Of Quality Care

1. PPI therapy: Long-term PPI therapy should be
prescribed for patients who have NSAID-associated ulcers, who need COX-2 inhibitor therapy,
who are on aspirin for secondary cardiovascular
prevention and have a history of peptic ulcer,
and who have non-H pylori, non-NSAID-associated ulcers. PPI therapy should be discontinued after H pylori eradication is confirmed. If
aspirin is given for primary prevention (ie, no
established cardiovascular disease), antiplatelet
therapy likely should not be resumed in most
patients.6,126-132
2. Follow-up for treatment for H pylori: H pylori
should be eradicated, if present; after this is
documented, no further therapy is needed.8
3. Follow-up on resolution of suspicious gastric
ulcer: Surveillance endoscopy is recommended
in patients whose gastric ulcer is endoscopiCopyright 2014 EB Medicine. All rights reserved.
18
venous PPI therapy and monitored for 72 hours.

Patients with low-risk lesions can be discharged
on daily oral PPI.
Patients with variceal UGI bleed should be
treated with intravenous PPI therapy, octreotide
drip, and early endoscopic intervention. Prophylactic antibiotics are recommended to prevent
spontaneous bacterial peritonitis in those with
cirrhosis. A repeat EGD is warranted to confirm
the eradication of varices and the need for nonselective beta blocker therapy upon discharge.
Patients with gastric varices or esophageal varices for whom endoscopic therapy failed should
be referred for a TIPS procedure. A SengstakenBlakemore tube is a temporary intervention
allowing stabilization as the patient is prepared
for definitive therapy. Gastric varices can be
treated with TIPS, cyanoacrylate injection,
BATO, or BRTO. Interventional radiology consultation should be obtained early in these cases.
Patients with right-sided heart failure and severe hepatic encephalopathy are not candidates
for TIPS. Early 2-dimensional echocardiogram is
suggested if TIPS is anticipated.
Overtransfusion should be avoided in the setting of variceal bleeding. It increases the portal
pressure and worsens the wall tension on varices, which can worsen bleeding.
Patients with LGIB should undergo a diagnostic
colonoscopy. In patients with clinical evidence
of overt bleeding and hemodynamic instability,
initial endoscopic workup should include an
EGD. This is due to the fact that a massive UGIB
source has to be ruled out. Early surgical consultation is recommended.
Patients with repeated diverticular bleeding
need surgical referral.
In patients with brisk overt LGIB, CT angiography or tagged red cell scan is appropriate. This
is followed by angioembolization if a culprit
vessel is identified. Colonoscopy might be limited and not clinically feasible in these settings.
Patients with a history of abdominal aortic aneurysm or repair can present with a sentinel bleed.
Clinical suspicion of this scenario should warrant workup in the form of a CT angiography
of the abdomen. If the diagnosis is confirmed,
surgical therapy is recommended.
Patients with occult OGIB may need a capsule
endoscopy for diagnosis and a small-bowel
endoscopy for therapeutic intervention.
Although there have been reports of an interaction between PPI therapy and clopidogrel, with
the FDA issuing warning for omeprazole and
other PPIs, definitive data are lacking. Among
PPI drugs, pantoprazole has the least interaction
with clopidogrel.
GIB in the setting of mandatory antiplatelet or
anticoagulation therapy is a challenging situation. The risk of myocardial infarction should

be weighed against the risk of significant
life-threatening GIB. A multidisciplinary team
approach should be adopted.
The ASGE guidelines recommend holding
antiplatelet therapy until hemostasis is achieved.
Platelet transfusions may be needed in lifethreatening GIB.
PPI therapy should always be considered with
dual antiplatelet therapy.
Newer anticoagulants (such as anti Xa inhibitors) exhibit no increased bleeding risk when
compared to warfarin; however, they do not
have reversal agents. Lack of data prevents the
establishment of well-defined recommendations.
Case Conclusions
Your 45-year-old patients clinical presentation of bloody
vomiting was suggestive of variceal bleeding. The initial
acute management included hemodynamic resuscitation
along with PPI drip, octreotide drip, IV ceftriaxone to
prevent spontaneous bacterial peritonitis, and appropriate PRBC transfusion for a target hemoglobin of 7 g/dL,
avoiding overtransfusion. He was managed in an ICU
setting and was intubated electively. An emergent EGD
revealed bleeding esophageal varices. Band ligation of
varices was performed, with control of bleeding, and the
octreotide drip was continued. Nadolol and PPI were
prescribed on discharge.

Your anemic female patient's clinical history was
suspicious for peptic ulcer related to significant NSAID
use. The degree of anemia suggested significant blood loss.
Initial management included appropriate hemodynamic
resuscitation with IV fluids, PRBC transfusion, and PPI
drip, along with close monitoring. Upper endoscopy revealed numerous large gastric ulcers with visible vessels.
Endoscopic treatment with epinephrine and cautery was
performed. IV PPI was continued for 72 hours. She was
discharged on PPI with a plan for repeat EGD in 8 weeks
to assess for healing of her gastric ulcers. H pylori testing
was negative.

For the elderly patient with coronary artery disease,
you noted that his clinical history was suspicious for
diverticular LGIB in the setting of supratherapeutic INR.
His acute management included appropriate hemodynamic resuscitation with IV fluids, PRBC transfusion as
needed, and close monitoring in the hospital setting. FFP
was administered to correct his INR. A colonoscopy was
performed after appropriate bowel preparation. Old blood
clots were seen on the left side of the colon, along with diverticula; the rest of the colon along with terminal ileum
was normal, suggestive of left-sided diverticular bleeding.
Aspirin was restarted immediately after the procedure
and warfarin was restarted in 2 days, as he was felt to be
at high risk for thromboembolic events.
19
Risk Management Pitfalls For Gastrointestinal Bleeding

1. The gastric ulcer appeared suspicious on
endoscopy, but the biopsies were benign, so a
surveillance EGD was not suggested.
A gastric ulcer suspicious for a malignancy
should always be evaluated by a surveillance
EGD to assess for healing. Studies have reported
false-negative biopsy result in 2% to 5% of
malignant ulcers. Any ulcers unhealed at followup examination after 8 to 12 weeks of medical
therapy should undergo a repeat endoscopy
with a biopsy.
6. He was having massive hematemesis but I

did not intubate, as his mental status and respiratory status were normal.
Patients with massive hematemesis are at a
very high risk for aspiration of blood and can
develop chemical pneumonitis, which leads to
acute respiratory failure. Prophylactic intubation
should be considered even though mental status
and respiratory status are normal.
7. She had hypothermia and acidosis after
receiving the blood transfusion, but we continued transfusion to get her hemoglobin to
target.
Hypothermia, acidosis, and coagulopathy form
a lethal triad that can develop with massive
blood transfusion. Early identification of blood
transfusion as the etiology and correction of
these complications be life saving.
2. A patient presented with variceal UGIB and

underwent band ligation, so I did not have a
follow-up EGD scheduled and did not prescribe propranolol or nadolol due to reported
intolerance from a prior admission.
According to current ASGE guidelines, patients
with variceal UGIB should always have followup EGD every 2 to 4 weeks until the varices
are obliterated. The risk of recurrent variceal
bleeding is high and can be life-threatening.
8. He was having severe abdominal pain due to

an ulcerative colitis flare with hematochezia, so
I prescribed morphine.
Opioids are best avoided in these circumstances
as they can paralyze intestines and lead to
toxic megacolon, which can be life-threatening
without emergent surgery.
3. I did not check for H pylori, as the patient had

a negative endoscopy.
The World Health Organization has labeled
H pylori as a class 1 carcinogen. In patients
presenting with suspected UGIB and where
biopsies are not performed because of bleeding
concern, stool H pylori antigen testing should
be performed. Eradication should be confirmed
after appropriate therapy.
9. He had hemoglobin of 5 g/dL on admission

and was having hematochezia, so we transfused 5 units of packed red cells. We did not
check hemoglobin between those transfusions.
His hemoglobin was 13 g/dL when we checked
later.
It is always important to check hemoglobin/
hematocrit routinely during transfusions, as
arbitrary transfusion can lead to iatrogenic
volume overload and cardiac failure, which can
lead to the death of the patient. Special attention
is especially needed in elderly patients and in
patients with cardiac diseases.
4. I did not suggest further work-up for iron

deficiency anemia, as the patient had a normal
EGD and colonoscopy.
Occult blood loss from the GI tract remains
a diagnostic and therapeutic challenge. The
availability of capsule endoscopy for diagnosis
and enteroscopy for therapeutic management
has simplified the approach to patients with
OGIB. Appropriate management is essential to
prevent episodes of recurrent severe anemia and
the consequent need for transfusion therapy.
10. We transfused 8 units of packed red cells, as

she was having massive hematemesis, but we
did not administer FFP because her INR was
normal.
During massive blood transfusion, FFP should
always be administered, as patients can develop
coagulopathy. Evidence for this is derived from
trauma literature where a high FFP-to-PRBC
ratio suggests better outcomes. In addition,
hypothermia leads to a decrease of clotting
factors, and acidosis decreases fibrinogen,
platelets, and thrombin generation.
5. The patient had a recurrent episode of hematemesis requiring transfusion therapy, but I
discharged him, as his endoscopy was normal.
It is always possible for lesions to be missed
on endoscopy, so it is not appropriate to
discharge patients in these circumstances. This
is particularly true of Dieulafoy lesions and
arteriovenous malformations.
20
Charting & Reimbursement: What You Need To Know

As hospitalists, we are frequently called to
admit a patient with GIB. The workup may
leave an unclear cause and, therefore, a discharge diagnosis of GI bleed. Unfortunately, coding rules penalize generic statements like this with
underreported SI, mortality risk, length of stay, and
reimbursement. GIB is also frequently targeted by
auditors. Here, we will look at tips to correctly report
the SI and minimize the audit risk.

In coding, saying GI bleed, NOS [not otherwise
stated] gives the same weight to an esophageal
hemorrhage and an incidental finding of hemoccult
positive stool. Its low SI (0.69) makes inpatient status
hard to justify. Capturing comorbid conditions and
patient-specific risks can improve the reported severity of illness. (See Table.)

When possible, clarify the GIB cause. For example: A 23-year-old student is out drinking, vomits
several times, then develops hematemesis. He is
given omeprazole and observed overnight. Serial
hemoglobins remain stable. Discharge diagnosis is
Mallory-Weiss tear. No endoscopy was performed, so
how do we know its a Mallory-Weiss tear? Answer:
We dont. However, while theres a wide differential,
the clinical picture is highly suggestive of MalloryWeiss tear. Remember, uncertainty is allowed.
Key Concepts In Documenting

1. When possible, link GIB to:

Medication/substance-induced causes.
Examples: NSAID-induced ulcer, warfarinassociated hypocoagulation, alcohol-induced
gastritis.
Diseases causing/contributing to the bleed.
Examples: alcoholic liver disease, thrombocytopenia [due to], adenocarcinoma of the
colon, etc.
Procedures contributing to the bleed or performed to evaluate and/or treat it. Example:
colon polypectomy with associated LGIB.
2. Note associated abnormalities or complicating

features. Examples:
Thrombocytopenia (with cause, if known)
Cirrhosis (note cause, eg, alcohol-related,
nonalcoholic steatohepatitis)
Hepatic encephalopathy
Acute blood loss anemia
3. Patients admitted for other reasons may develop
GIB. Many causes of GIB qualify as major comorbid conditions, but only if they are documented.
Examples: gastritis with hemorrhage (state the
cause, eg, alcoholic, atrophic); diverticulosis with
hemorrhage (state whether small bowel or colon);
intestinal angiodysplasia with hemorrhage.
4. When documenting an ulcer, always note the
location, cause, and complicating features (hemorrhage, perforation, and/or obstruction). The
wording used will place the case into 1 of 3 coding categories:
Complicated ulcer (DRG 380-382). Examples:
Location: esophagus, gastrojejunal
Type or cause: Barrett esophagus, Meckel
diverticulum
Complication: any ulcer with obstruction
or perforation
Uncomplicated peptic ulcer (DRG 383, 384).
Examples: documenting gastric, duodenal, or
peptic ulcer (acute or chronic) with no mention
of hemorrhage, obstruction, or perforation.
GI hemorrhage (DRG 377-379). Documentation of any type of ulcer and hemorrhage
(only) codes to GI hemorrhage, with few
exceptions.
Gastrointestinal Bleeding: The Impact Of Documentation

MS-DRG
Diagnosis
Severity Index
G-LOS (days)
Reimbursement Amount (USD)
379
GI hemorrhage without CC/MCC
0.69
2.41
$4100
378
GI hemorrhage with CC
3.3
$6000
377
GI hemorrhage with MCC
1.76
4.8
$10,600
384
Uncomplicated peptic ulcer without CC/MCC
0.85
$5100
380
Complicated peptic ulcer with MCC
1.92
5.5
$11,500
Abbreviations: CC, comorbid condition; GI, gastrointestinal; GIB, gastrointestinal bleeding; G-LOS, geometric mean length of stay; MCC, major
comorbid condition; MS-DRG, Medicare severity diagnosis-related group; NSAID, nonsteroidal anti-inflammatory drug; SI, severity index.
21

The alcoholic cirrhotic patient's clinical history was
suspicious for variceal UGIB, and he was hemodynamically unstable. The acute GI bleeding and hemoconcentration made his initial hemoglobin unreliable. Due to
the clinical scenario, he was emergently intubated in the
ED, and the initial acute management included hemodynamic resuscitation along with PPI drip, octreotide drip,
prophylactic antibiotics in the form of IV ceftriaxone to
prevent spontaneous bacterial peritonitis, and appropriate PRBC transfusion, avoiding overtransfusion. Emergent EGD was performed after initial resuscitation, but
bleeding could not be controlled due to bleeding gastric
fundic varices. A Sengstaken-Blakemore tube was placed
for tamponade therapy. He subsequently underwent TIPS
procedure with control of his bleeding.
cal Association (AGA) Institute medical position statement

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108. Kollef MH, OBrien JD, Zuckerman GR, et al. BLEED: a

classification tool to predict outcomes in patients with acute
upper and lower gastrointestinal hemorrhage. Crit Care Med.
1997;25(7):1125-1132. (Cohort study; 465 patients)
125. Dunn SP, Steinhubl SR, Bauer D, et al. Impact of proton

pump inhibitor therapy on the efficacy of clopidogrel
in the CAPRIE and CREDO trials. J Am Heart Assoc.
2013;2(1):e004564. (Review)
109. de Groot NL, Bosman JH, Siersema PD, et al. Admission

time is associated with outcome of upper gastrointestinal
bleeding: results of a multicentre prospective cohort study.
Aliment Pharmacol Ther. 2012;36(5):477-484. (Prospective
126. Mahabaleshwarkar RK, Yang Y, Datar MV, et al. Risk of

adverse cardiovascular outcomes and all-cause mortality associated with concomitant use of clopidogrel and proton pump
inhibitors in elderly patients. Curr Med Res Opin. 2013;29(4):315-
25
323. (Nested case control study; 43,159 patients)
CME Questions
127. Waksman R, Gaglia MA Jr. Lack of association between

proton pump inhibitors and adverse events in patients taking clopidogrel and aspirin. Evid Based Med. 2013;18(3):e30.
(United Kingdom data registry analysis; 24,471 patients)
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Category 1 CreditsTM or 4 AOA Category 2A or 2B
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issue, scan the QR code below with your smartphone or visit www.hmpractice.com/H0814.
128. Green BT, Rockey DC, Portwood G, et al. Urgent colonoscopy for evaluation and management of acute lower gastrointestinal hemorrhage: a randomized controlled trial. Am J
Gastroenterol. 2005;100(11):2395-2402. (Randomized trial; 100
patients)
129. Sreedharan A, Martin J, Leontiadis GI, et al. Proton pump
inhibitor treatment initiated prior to endoscopic diagnosis
in upper gastrointestinal bleeding. Cochrane Database Syst
Rev. 2010(7):CD005415. (Meta-analysis of 6 randomized
controlled trials; 2223 patients)
130. Gisbert JP, Khorrami S, Carballo F, et al. Meta-analysis:

Helicobacter pylori eradication therapy vs. antisecretory noneradication therapy for the prevention of recurrent bleeding
from peptic ulcer. Aliment Pharmacol Ther. 2004;19(6):617-629.
(Meta-analysis of 6 studies; 335 patients)
131. Chey WD, Wong BC, Practice Parameters Committee of the
American College of Gastroenterology. American College of
Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102(8):18081825. (Guidelines)
1. What is the most common cause of LGIB?

a. Diverticulosis
b. Hemorrhoids
c. Colon cancer
d. Arteriovenous malformations
132. Cutler AF, Havstad S, Ma CK, et al. Accuracy of invasive

and noninvasive tests to diagnose Helicobacter pylori infection. Gastroenterology. 1995;109(1):136-141. (Review)
2. The initial diagnostic test of choice in a patient

with occult OGIB and a normal EGD and colonoscopy is:
a. Capsule endoscopy
b. Small-bowel enteroscopy
c. Tagged red cell scanning
d. Angiography
133. Chan FK, Chung SC, Suen BY, et al. Preventing recurrent
upper gastrointestinal bleeding in patients with Helicobacter
pylori infection who are taking low-dose aspirin or naproxen.
N Engl J Med. 2001;344(13):967-973. (Prospective study; 400
patients)
134. Lee KK, You JH, Ho JT, et al. Economic analysis of celecoxib
versus diclofenac plus omeprazole for the treatment of
arthritis in patients at risk of ulcer disease. Aliment Pharmacol Ther. 2003;18(2):217-222. (Retrospective review; 287
patients)
3. A PPI drip should be used for patients with

high-risk lesions on EGD for:
a. 24 hours
b. 48 hours
c. 72 hours
d. Once daily is sufficient
135. Chan FK, Wong VW, Suen BY, et al. Combination of a

cyclo-oxygenase-2 inhibitor and a proton-pump inhibitor for prevention of recurrent ulcer bleeding in patients
at very high risk: a double-blind, randomised trial. Lancet.
2007;369(9573):1621-1626. (Single-center prospective randomized double-blind trial; 441 patients)
136. Pruitt RE, Truss CD. Endoscopy, gastric ulcer, and gastric
cancer. Follow-up endoscopy for all gastric ulcers? Dig Dis
Sci. 1993;38(2):284-288. (Review)
4. Antibiotics administered in the setting of GI

bleeding in cirrhotic patients decreases the
incidence of:
a. Recurrent bleed
b. Spontaneous bacterial peritonitis
c. Hepatorenal syndrome
d. B and C
e. A, B, and C
137. Tatsuta M, Iishi H, Okuda S, et al. Prospective evaluation of

diagnostic accuracy of gastrofiberscopic biopsy in diagnosis
of gastric cancer. Cancer. 1989;63(7):1415-1420. (Retrospective review; 1331 patients)
138. Llanos O, Guzman S, Duarte I. Accuracy of the first endoscopic procedure in the differential diagnosis of gastric lesions. Ann Surg. 1982;195(2):224-226. (Retrospective review;
333 patients)
139. Stolte M, Seitter V, Muller H. Improvement in the quality of
the endoscopic/bioptic diagnosis of gastric ulcers between
1990 and 1997--an analysis of 1,658 patients. Z Gastroenterol.
2001;39(5):349-355. (Retrospective review; 1658 patients)
5. Which of the following is a contraindication

for TIPS?
a. Severe hepatic encephalopathy
b. Variceal bleeding
c. Right heart failure
d. A and C
e. A and B
140. de la Pena J, Brullet E, Sanchez-Hernandez E, et al. Variceal

ligation plus nadolol compared with ligation for prophylaxis of variceal rebleeding: a multicenter trial. Hepatology.
2005;41(3):572-578. (Randomized trial; 80 patients)
26
6. Secondary prophylaxis for variceal GIB includes:

a. Repeat banding and nonselective beta
blockers
b. Repeat banding only
c. Beta blockers only
d. No prophylaxis is needed.
Coming Soon In
Hospital Medicine
Practice
7. When is transarterial embolization indicated in

UGIB?
a. As the treatment of choice
b. After 2 failed endoscopic treatments
c. Never
Sickle Cell Disease: A

Comprehensive Review Of
Inpatient Management
8. Regarding the concomitant use of PPIs and

clopidogrel, which of the following is true?
a. They should never be used together.
b. Avoid clopidogrel; use aspirin instead.
c. They can be used together.
d. Use H2 blockers only.
AUTHORS:
TRUSHAR M. DUNGARANI, DO
Clinical Assistant Professor, Assistant Director of
Hospitalist Medicine, Department of Medicine,
North Shore LIJ Lenox Hill Hospital, New York, NY
9. Which anatomical location in patients with

peptic ulcers warrants a repeat endoscopy to
confirm resolution?
a. Suspicious gastric ulcers
b. Duodenal ulcers
c. Both
d. Neither
RAJI SHAMEEM, MD
Department of Internal Medicine, Lenox Hill
Hospital, New York, NY
Since the first formal report of sickle

cell disease in 1910, sickle cell disease
management and treatment in the United
States has advanced greatly. Nonetheless,
hospitalists are still faced with a persistent
challenge in managing the complications
and pain in adult sickle cell disease patients.
The large number of emergency department
visits and hospitalizations for adults with
this chronic condition leads to substantial
healthcare costs despite recognized strategies
to prevent readmissions and avoid prolonged
hospitalizations. This issue reviews relevant
topics in the hospital management of sickle
cell disease to assist hospitalists in providing
comprehensive, cost-effective care for these
patients. The initial presentation, differential
diagnosis, and treatment of common lifethreatening complications in sickle cell
disease such as acute pain crisis and acute
chest syndrome will be addressed, and special
circumstances such as the role of hydroxyurea,
appropriate transfusion practices, cost-effective
strategies, and quality improvement measures
will be examined.
10. Patients with high-risk lesions on EGD and no

other medical issues can be discharged:
a. Immediately after a therapeutic EGD
b. After 72 hours of monitoring in the hospital
c. After 24 hours of monitoring in the hospital
d. After 5 days post admission if there is no

repeat bleeding
27
Physician CME Information
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Acute Co
Current ronary Syndrom
es:
ment In Evidence For
Ma
The Ho
spital Se nagetting
Acute Coronary Syndromes:

Current Evidence For Management In The Hospital Setting
Volume
y 2014
2, Numb
er 1
Editorial Board
Alpesh N. Amin, MD, MBA, MACP, SFHM Amish A. Dangodara, MD, FACP
Thomas & Mary Cesario Endowed
Professor of Medicine, Director of
Chair of Medicine
Preoperative Clinic and General
Professor of Medicine, Business,
Internal Medicine Consultation,
Public Health, Nursing Science &
Hospitalist Program, University of
Biomedical Engineering
California Irvine, Irvine, CA
Executive Director, Hospitalist
Nancy Dawson, MD, FACP
Program
Assistant Professor, Hospital Practice
University of California Irvine,
Chair, Division of Hospital Medicine,
Irvine, CA
Mayo Clinic, Jacksonville, FL
Clinical Pearls Contributor
David J. Rosenberg, MD, MPH, SFHM

Associate Chairman, Department
of Medicine, Section Head, Hospital
Medicine, North Shore University
Hospital, Manhasset, NY; Assistant
Professor of Medicine, Hofstra
North Shore LIJ School of Medicine,
Hempstead, NY
Steven Deitelzweig, MD
System Chairman, Hospital Medicine,
Regional Vice President of Medical
Affairs, Ochsner Health System, New
Orleans, LA
Daniel Dressler, MD, MSc, SFHM

Associate Professor of Medicine,
Director of Internal Medicine Teaching
Services, Emory University Hospital;
Associate Director for Education,
Emory Division of Hospital Medicine,
James B. Haering, DO, SFHM
Associate Program Director, J. Willis
Associate Medical Director, Allegiance
Hurst Internal Medicine Residency
Hospitalists, Jackson, MI; Associate
Program, Emory University School of
Professor of Medicine, Michigan State
University College of Osteopathic
Medicine and Michigan State University Amir Jaffer, MD
Professor of Medicine, Vice
College of Human Medicine, East
Chair, Patient Safety, Quality, and
Lansing, MI
Compliance, Division Chief, Hospital
Medicine, Department of Medicine,
Charting Contributor
January 2014
www.hmp
ractic
States, and up to 30% of patients who suffer a cardiac event will

die within a year of diagnosis. "Acute coronary syndromes"
(ACS) is a general term that describes a spectrum of conditions
related to the acute manifestations of coronary disease, and it includes 3 conditions: (1) unstable angina, (2) ST-segment elevation
myocardial infarction (STEMI), and (3) non-ST-segment elevation
myocardial infarction (NSTEMI). Incorporating evidence-based
strategies in evaluation and risk stratification and determining
treatment strategies that are appropriate to the diagnosis are
vital to successful management of patients with acute coronary
syndromes. This issue reviews the evidence for the numerous
therapies for acute coronary syndromes, including drug therapies
and revascularization strategies. Inhospital complications, quality improvement, and risk management considerations for acute
coronary syndromes are also reviewed.
Editor-in-Chief
Author
s
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tion of
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Editor
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MACP,
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Mike Wang,
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Cardiovascular Medicine, University of Southern California,

Los Angeles, CA
Peer Reviewers
Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC

Professor of Medicine, Harvard Medical School; Chief of
Cardiology, VA Boston Healthcare System; Director, Integrated
Interventional Cardiovascular Program, Brigham and Women's
Hospital & VA Boston Healthcare System, Boston, MA; Senior
Investigator, TIMI Study Group
Tomas Villaneuva, DO, MBA, FACPE, SFHM
Assistant Vice President, Medical Director of Primary Care
and Hospital Medicine, Baptist Health Medical Group, Baptist
Health South Florida, Coral Gables, FL
CME Objectives
Upon completion of this article, you should be able to:

1.
Distinguish between the different types of ACS.
2.
Risk stratify a patient presenting with UA/NSTEMI, and
determine an appropriate management strategy.
University of Miami Miller School of

Medicine, Miami, FL
Solomon Liao, MD
Director of Palliative Care Services,
Associate Clinical Professor, Hospitalist
Program, University of California
Irvine, Irvine, CA
David Likosky, MD, SFHM
Medical Director, Evergreen
Neuroscience Institute, Kirkland,
WA; Clinical Faculty, University of
Washington, Seattle, WA
Sylvia McKean, MD
Harvard Medical School; Associate
Physician, Brigham and Womens
Hospital, Boston, MA
Geno J. Merli, MD
Clinical Professor, Jefferson Hospital;
Co-Director, Jefferson Vascular Center,
Philadelphia, PA
Franklin A. Michota, MD, FACP, FHM
Director of Academic Affairs,
Department of Hospital Medicine,
Cleveland Clinic, Cleveland, OH
Daniel Robitshek, MD
Medical Director, Hospitalist Program,
Floyd Medical Center, Rome, GA
Tomas Villaneuva, DO, MBA, FACPE,

SFHM
Assistant Vice President, Medical
Director of Primary Care and Hospital
Medicine, Baptist Health Medical
Group, Baptist Health South Florida,
Coral Gables, FL
Mike Wang, MD
Director of Hospital Medicine,
Associate Professor of Clinical
Medicine, Keck Medical Center of USC,
Los Angeles, CA
David Wooldridge, MD, FACP
Program Director, Internal Medicine
Residency Program, Associate
Professor of Internal Medicine,
University of Missouri-Kansas City
School of Medicine, Kansas City, MO
Nejat Zeyneloglu, MD
Medical Director, Hospital Medicine
Program, New York Hospital Queens,
Weill-Cornell Medical College, New
York, NY
Pharmacology Contributor
James Damilini, PharmD, MS, BCPS

Clinical Pharmacy Specialist,
Emergency Medicine, St. Joseph's
Hospital and Medical Center, Phoenix,
AZ
www.hmpractice.com
There is simply no other publication like this for

hospitalists. Pay it forward and help us spread the
word. Your colleagues will thank you for it.
Discussion of Investigational Information: As part of this journal, faculty

may be presenting investigational information about pharmaceutical products
that is outside Food and Drug Administration approved labeling. Information
presented as part of this activity is intended solely as continuing medical
education and is not intended to promote off-label use of any pharmaceutical
product.
Faculty Disclosure: It is the policy of EB Medicine to ensure objectivity,
balance, independence, transparency, and scientific rigor in all CMEsponsored educational activities. All faculty participating in the planning
or implementation of a sponsored activity are expected to disclose to the
audience any relevant financial relationships and to assist in resolving any
conflict of interest that may arise from the relationship. Presenters must
also make a meaningful disclosure to the audience of their discussions of
unlabeled or unapproved drugs or devices. In compliance with all ACCME
Essentials, Standards, and Guidelines, all faculty for this CME activity
were asked to complete a full disclosure statement. The information
received is as follows: Dr. Dacha, Dr. Berger, Dr. Parikh, Dr. Wehbi, Dr.
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0814-H GI Bleeding Sample Issue2

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Hospital Medicine

Alpesh N. Amin, MD, MBA, MACP, SFHM

Amish A. Dangodara, MD, FACP

Clinical Pearls Contributor

Nancy Dawson, MD, FACP

Daniel Dressler, MD, MSc, SFHM

Daniel Robitshek, MD, SFHM

David Likosky, MD, SFHM

Etiology And Prevalence (Pages 4-5)

UGIB: 50% of cases are due to peptic ulcers.

Physical Examination (Page 7)

Look for orthostatic hypotension.

Diagnostic Testing (Pages 7-9)

Initial workup includes complete blood count,

Appropriate Setting Of Care And Discharge

Treatment (Pages 9-11)

Initial Supportive Measures

Abbreviations: BUN, blood urea nitrogen; CAD, coronary

www.hmpractice.com August 2014

per gastrointestinal bleeding (UGIB) accounts for

Critical Appraisal Of The Literature

The studies evaluating use of gastric lavage and

Nonportal Hypertensive Upper Gastrointestinal

Etiology And Pathophysiology

UGIB is defined as hemorrhage in the GI tract

Table 1. Causes Of Upper Gastrointestinal Bleeding18

Peptic ulcer disease

NSAID use, H pylori, stress-induced (ICU) ulcers

Most common cause of UGIB

Cirrhosis, splenic vein thrombosis

History or suspected history of liver disease

Alcohol use, severe retching, coughing

Cough and retching precede hematemesis

Alcohol use, GERD, NSAID use, infection, radiation

History of GERD and hiatal hernia

Angiodysplasia, chronic kidney disease, cirrhosis

Can range from minimal to very significant UGIB;

H pylori, smoking, family history

Anemia, weight loss

Others causes (aortoenteric fistula, hemosuccus pancreaticus, and

Hemobilia, liver biopsy, hepatobiliary manipulation

Rare, but can be clinically catastrophic if misdiagnosed

Copyright 2014 EB Medicine. All rights reserved.

www.hmpractice.com August 2014

as dilated, tortuous submucosal vessels that appear

noncirrhotic etiologies are classified anatomically

Obscure Gastrointestinal Bleeding

OGIB is defined as bleeding from the GI tract that

Lower Gastrointestinal Bleeding

LGIB is defined as hemorrhage in the GI tract distal

Table 2. Causes Of Lower Gastrointestinal Bleeding15,18,24,25

Old age, constipation, low-fiber diet

Arterial, and can be life-threatening; most common cause

Chronic kidney disease, aortic stenosis (Heyde syndrome), anticoagulation

Venous in origin; rarely life-threatening

HNPCC, old age, family history, IBD, polyposis syndromes

Anemia and weight loss

Hemodynamic instability present

Can be caused by acute or chronic radiation (6 weeks to 1

Only external hemorrhoids visible by physical examination

August 2014 www.hmpractice.com

acute UGIB. The severity of the GIB correlates with

Table 3. Causes Of Obscure Gastrointestinal