Intended for medical personnel

1. Upper GI Bleeding

3. Background
• Upper gastrointestinal bleeding (UGIB) is
defined as bleeding derived from a source
proximal to the ligament of Treitz.
• Acute gastrointestinal (GI) bleeding is a
potentially life-threatening abdominal
emergency that remains a common cause of
hospitalization

4. Epidemiology
• The incidence of UGIB is approximately 100
cases per 100,000 population per year.
• Bleeding from the upper GI tract is
approximately 4 times more common than
bleeding from the lower GI tract and is a
major cause of morbidity and mortality.
• Mortality rates from UGIB are 6-10% overall.

5. • In patients with UGIB, comorbid illness, rather
than actual bleeding, is the major cause of
death.
• Comorbid illness has been noted in 50.9% of
patients, with similar occurrences in males
(48.7%) and females (55.4%).
• One or more comorbid illnesses have been noted
in 98.3% of mortalities in UGIB; in 72.3% of
patients, comorbid illnesses have been noted as
the primary cause of death.
• Rebleeding or continued bleeding is associated
with increased mortality; therefore,
differentiating the patient with a low probability
of rebleeding and little comorbidity from the
patient at high risk for rebleeding with serious
comorbidities is imperative.

6. Peptic ulcer disease and UGIB
• Peptic ulcer disease (PUD) remains the most
common cause of UGIB.
• High-risk patient populations at risk for PUD
include those with a history of alcohol abuse,
chronic renal failure, and/or nonsteroidal anti-
inflammatory drug (NSAID) use.
• Peptic ulcer disease is strongly associated
with Helicobacter pylori infection.
• In most cases, the bleeding is caused by the
erosion of an artery at the base of the ulcer. In
approximately 80% of patients, bleeding from a
peptic ulcer stops spontaneously.

7. The image below depicts an ulcer with
active bleeding.

8. Other causes of UGIB
• Mucosal tears of the esophagus or fundus
(Mallory-Weiss tear), erosive gastritis, erosive
esophagitis, Dieulafoy lesion, gastric cancer, and
ulcerated gastric leiomyoma.
• Patients with chronic liver disease and portal
hypertension are at an increased risk for variceal
hemorrhage and portal gastropathy in addition to
ulcer hemorrhage.
• Rare causes of UGIB include aortoenteric fistula,
gastric antral vascular ectasia, angiectasias, and
Osler-Weber-Rendu syndrome.

9. Large esophageal varices with red wale
signs seen on endoscopy.

10. NSAIDs in UGIB
• NSAIDs cause gastric and duodenal ulcers by
inhibiting cyclooxygenase, which causes
decreased mucosal prostaglandin synthesis and
results in impaired mucosal defenses. Daily NSAID
use causes an estimated 40-fold increase in
gastric ulcer creation and an 8-fold increase in
duodenal ulcer creation.
• Long-term NSAID use is associated with a 20%
incidence in the development of mucosal
ulceration.
• Medical therapy includes avoiding the
ulcerogenic drug and beginning a histamine-2
(H2)–receptor antagonist or a proton pump
inhibitor that provides mucosal protection.

11. Prognosis
• The following risk factors are associated with an
increased mortality, recurrent bleeding, the need for
endoscopic hemostasis, or surgery[:
1. Age older than 60 years
2. Severe comorbidity
3. Active bleeding (eg, witnessed hematemesis, red blood
per nasogastric tube, fresh blood per rectum)
4. Hypotension
5. Red blood cell transfusion greater than or equal to 6
units
6. Inpatient at time of bleed
7. Severe coagulopathy
• Patients who present in hemorrhagic shock have a
mortality rate of up to 30%.

12. History
• Important information to obtain includes potential
comorbid conditions, medication history, and potential
toxic exposures, as well as the severity, timing,
duration, and volume of the bleeding
• History findings include weakness, dizziness, syncope
associated with hematemesis (coffee ground vomitus),
and melena (black stools with a rotten odor).
• Patients may have a history of dyspepsia (especially
nocturnal symptoms), ulcer disease, early satiety, and
NSAID or aspirin use
• A history of chronic alcohol use
• Any previous history of hematuria (Schistomiasis)
• The presence of postural hypotension indicates more
rapid and severe blood loss

13. Physical Examination
• The goal of the patient's physical examination is to
evaluate for shock and blood loss.
• Assessing the patient for hemodynamic instability and
clinical signs of poor perfusion is important early in the
initial evaluation to properly triage patients with massive
hemorrhage to ICU settings.
• Worrisome clinical signs and symptoms of hemodynamic
compromise include tachycardia of more than 100 beats
per minute (bpm), systolic blood pressure of less than
90 mm Hg, cool extremities, syncope, and other obvious
signs of shock, ongoing brisk hematemesis, or the
occurrence of maroon or bright-red stools, which
requires rapid blood transfusion.
• Pulse and blood pressure should be checked with the
patient in supine and upright positions to note the effect
of blood loss. Significant changes in vital signs with
postural changes indicate an acute blood loss of
approximately 20% or more of the blood volume.

14. • Signs of chronic liver disease should be noted,
including spider angiomata, gynecomastia,
increased luneals, splenomegaly, ascites,
pedal edema, and asterixis.
• Signs of tumor are uncommon but portend a
poor prognosis. Signs include a nodular liver,
an abdominal mass, and enlarged and firm
lymph nodes.

15. Workup
• A complete blood cell (CBC) count with platelet count
and differential is necessary to assess the level of
blood loss in a patient with upper gastrointestinal
bleeding (UGIB). Where possible, having the patient's
previous results is useful to gauge this loss. CBC should
be checked frequently (q4-6h) during the first day.
• Based on the patient's initial hemoglobin level and
clinical assessment of shock, a type and screen or type
and crossmatch should be ordered. The patient should
be crossmatched for 2-6 units, based on the rate of
active bleeding. The hemoglobin level should be
monitored serially in order to follow the trend.

16. • The patient's prothrombin time (PT), activated partial
thromboplastin time (PTT), and international normalized ratio (INR)
should be checked to document the presence of coagulopathy.
• A platelet count of less than 50 with active acute hemorrhage
requires a platelet transfusion and fresh frozen plasma in an attempt
to replete lost clotting factors.
• The coagulopathy could be a marker of advanced liver disease.
• Liver disease–associated blood tests (eg, aspartate aminotransferase
[AST], alanine aminotransferase [ALT], bilirubin, alkaline phosphatase
[ALP])
• Endoscopy should be performed immediately after endotracheal
intubation (if indicated), hemodynamic stabilization, and adequate
monitoring in an intensive care unit (ICU) setting have been achieved.
• The 2010 American College of Radiology (ACR) appropriateness
criteria for UGIB recommend upper endoscopy as the initial
diagnostic examination for all patients presumed to have UGIB

17. Treatment & Management
• The goal of medical therapy in upper gastrointestinal
bleeding (UGIB) is to correct shock and coagulation
abnormalities and to stabilize the patient so that further
evaluation and treatment can proceed.
• Resuscitation of a hemodynamically unstable patient
begins with assessing and addressing the ABCs (ie,
airway, breathing, circulation) of initial management.
• Patients who cannot protect their airway, especially when
hematemesis is present, are at an increased risk for
aspiration, which is a potentially avoidable complication
that can significantly affect morbidity and mortality. This
situation must be recognized early, and patients should be
electively intubated in a controlled setting.
• Nothing by mouth (NPO)
• Intravenous access must be obtained. Bilateral, 16-gauge
(minimum), upper extremity, peripheral intravenous lines
are adequate for volume resuscitative efforts.

18. • Either colloid or crystalloid solutions may be used
to attain volume restoration prior to administering
blood products. A rough guideline for the total
amount of crystalloid fluid volume needed to
correct the hypovolemia is the 3-for-1 rule
• Foley catheter placement for continuous
evaluation of urinary output as a guide to renal
perfusion
• Urgent endoscopy is indicated when patients
present with hematemesis, melena, or postural
changes in blood pressure
• Contraindications to upper endoscopy include an
uncooperative or obtunded patient, severe cardiac
decompensation, acute myocardial infarction
(unless active, life-threatening hemorrhage is
present), and perforated viscus (eg, esophagus,
stomach, intestine).

19. • Primary surgical intervention should be considered in
patients with a perforated viscus (eg, from perforated
duodenal ulcer, perforated gastric ulcer, or Boerhaave
syndrome).
• Emergency surgery in UGIB typically entails oversewing
the bleeding vessel in the stomach or duodenum (usually
preoperatively identified by endoscopy), vagotomy with
pyloroplasty, or partial gastrectomy.
• Intravenous PPI such as IV Pantoprazole or Rabeprazole
should be continued for 48 – 72 hours, the relative
efficacy of the PPIs may be due to their superior ability to
maintain a gastric pH at a level above 6.0, thereby
protecting an ulcer clot from fibrinolysis
• If variceal bleeding is suspected, Octreotide is the
pharmacologic agent of choice. This agent is a synthetic
analogue of somatostatin (an endogenous hormone that
at pharmacologic doses decreases portal blood flow by
splanchnic vasoconstriction), that is usually administered
at a constant infusion of 50 mcg/h.

20. Therapeutic Endoscopy
• Endoscopy is now the method of choice for
controlling active ulcer hemorrhage
• Aside from ulcer hemorrhaging, other causes
of gastrointestinal bleeding, including mucosal
tears in the esophagus or upper stomach due
to vomiting (Mallory-Weiss tears), venous
blebs, and vascular ectasias, can also be
treated with endoscopic coagulation.
• Endoscopic procedures such as sclerotherapy
and variceal ligation can be used to prevent
the recurrence of variceal hemorrhage

21. • The following endoscopic techniques have been
developed for achieving hemostasis:
1. Injection of epinephrine or sclerosants
2. Bipolar electrocoagulation
3. Band ligation
4. Heater probe coagulation
5. Constant probe pressure tamponade
6. Argon plasma coagulator
7. Laser photocoagulation
8. Rubber band ligation
9. Application of hemostatic materials, including
biologic glue
10.Application of hemoclips or endoclips
11.Application of nanopowder (experimental)

22. Prevention of UGIB
• Antibiotic therapy should be given if H pylori is present in
the setting of any history of ulcer disease. Eradication of H
pylori has been demonstrated to reduce the risk of
recurrent ulcers and, therefore, recurrent ulcer
hemorrhages.
• NSAIDs should be avoided. If not possible, they should be
used at the lowest dose and duration.
• PPI cotherapy should be used along with NSAIDs.
• Noncardioselective beta-blockers are used most commonly
for primary prophylaxis of variceal bleeding e.g. propanolol;
these nonselective beta-blockers reduce portal and
collateral blood flow as well as have smaller effects on the
increase in portal resistance and decrease on portal
pressure. Reduction in cardiac output (via blockade of
beta1 adrenoreceptors) occurs, as does splanchnic
vasoconstriction (via blockade of vasodilatory
adrenoreceptors of the splanchnic circulation