This document summarizes a presentation on the epidemiology, definition, etiologies, risk stratification, and management of upper gastrointestinal bleeding (UGIB). Some key points: - UGIB accounts for 50% of GI bleeding admissions and has a mortality rate of 5-10% despite medical advances. - Peptic ulcer disease, esophageal/gastric varices, Mallory-Weiss tears, and Dieulafoy's lesions are common causes. - Risk scoring systems like Glasgow-Blatchford and Rockall are used to predict outcomes and guide management. High-risk stigmata on endoscopy indicate need for intervention. - Prevention focuses on H. pylori

1. Presenter:- Dr. Misale H. (IM.RI)
Moderator:- Dr. Aschalew T. (Internist,
Assistant prof. of I/Medicine)
September, 2023
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2.  Introduction
 Epidemiology
 Definition
 Etiologies
 Approach to UGIB
 Reference
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3.  Know epidemiology and definition of UGI bleeding
 Identify etiologies of UGIB
 Understand the approach to Upper GI bleeding
 Determine the prognosis based on risk stratification
 Determine different management options in patients
presenting with UGIB
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4.  Gastrointestinal bleeding presents as either overt or occult bleeding.
 Overt GIB:- manifested by hematemesis, melena &hematochezia.
 Occult GIB:- in the absence of overt bleeding when patients
present with:-
symptoms of blood loss or anemia
routine diagnostic evaluation reveals IDA or a positive FOBT.
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5. GIB is also categorized by the site of bleeding as:-
 Upper GI bleeding – bleeding proximal to the ligament of
Treitz (esophagus, stomach, duodenum)
 Lower GI bleeding – bleeding below the ligament of Treitz
 Obscure GI bleeding – recurrent acute or chronic bleeding
for which no known source is identified
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6. Severe GI bleeding:- documented GI bleeding (hematemesis,
melena, hematochezia, or positive NG lavage) accompanied by
 shock or orthostatic hypotension
 decrease in the hematocrit value by at least 6% (or a decrease
in the hemoglobin level of at least 2 g/dL)
 transfusion of at least 2 units of packed red blood cells
(RBCs).
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7.  Acute Upper GI bleeding is a common emergency condition.
 Approximately 50% of admissions for GI bleeding are for UGIB ,
40% are for LGIB, and 10% are for obscure bleeding
 The annual incidence of hospital admissions for UGIB in the US
and Europe is 0.1% per year.
 The mortality rate of severe UGIB is 5-10% despite advances in
medical therapy, ICU care, endoscopy, and surgery.
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8.  Endoscopic therapy has been shown to reduce the rate of
rebleeding, the need for blood transfusions, and surgery.
 Bleeding is self-limited in 80% of patients with Upper GI
hemorrhage, even without specific therapy.
 Of the remaining 20% who continue to bleed or rebleed, the
mortality rate is 30% to 40%, they benefit from acute
medical, endoscopic, angiographic or surgical therapy.
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10.  Upper GI bleeding refers to bleeding from oesophagus, stomach,
duodenum (i.e. Proximal to ligmanet of treitz).
Presentation
 Hematemesis:- vomiting of fresh blood or coffee ground vomit
 Melena:- black tarry, foul-smelling stool, may persist for 5-7 days
 Hematochezia:- fresh blood, clot, or currant jelly stool, most often
with lower GI bleed, and can be massive UGIB.
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11. 1. Esophageal causes
▪ Esophageal varices
▪ mallory-Weiss tear
▪ Esophagitis
▪ cancer
2. Gastric causes
▪ Gastric ulcer
▪ Gastritis
▪ cancer
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3. Duodenal causes
▪ Duodenal ulcer
▪ Aortoenteric fistula
4. Vascular
▪ Gastric antral vascular ectasia
▪ Dieulafoy’s lesion,
▪ aortoenteric fistula
5. Bleeding disorders

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15.  A defect in the gastric or duodenal mucosa (>5 mm ), extends
through the muscularis mucosa into the deeper layers of the wall.
 PUD is the most common cause of UGIB, ~50% of cases.
 Prevalence of H.pylori infection is >80% (developing) 20-50%
(developed)
 Lifetime risk of PUD from Hp infection is 3% in US, 25% in Japan
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16.  Peptic ulcers may present with dyspeptic or other gastrointestinal
symptoms, or may be initially asymptomatic and then present with
complications such as hemorrhage or perforation.
 Greater than 50% of patients with ulcer-related hemorrhage bleed
without any preceding warning signs or symptoms.
 Peptic ulcers are most commonly caused by a decrease in mucosal
defense mechanisms attributable to aspirin or other NSAIDs,
H. pylori infection, or both.
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18.  Prevention of recurrent bleeding focuses on the 3 main factors
 Helicobacter pylori, NSAIDs and acid.
 Eradication of H. pylori decreases rates of rebleeding to <5%.
 Majority of patients with bleeding PUD will stop bleeding
spontaneously & one third of patients will rebleed within the
next 1–2 years if no preventive strategies are employed
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 Endoscopic, clinical, and laboratory features may be useful for
risk stratification of patients who present with acute UGIB
 Stratified for risk of mortality , rebleeding and to triage patients
for best care and urgent endoscopy
 Pre-endoscopy scoring systems for non-variceal bleeding
 Blatchford Score ▪ Clinical Rockall Score
 AIMS65 score ▪ Artificial neural network score

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23.  Simple risk score that predicts in-hospital mortality, LOS, cost
in patients with acute UGIB
Score >2 are
considered high risk
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Variables Score
lbumin <3.0 g/dl 1
NR > 1.5 1
ental status altered 1
ystolic BP <90 1
+ years old 1
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24.  Overall, the predictive value of the GBS was superior as
compared to pre-endoscopy Rockall score and AIMS65.
 Prior to endoscopy we will discharge patients with a GBS of 0-1
 Most patients who have received endoscopic treatment for high-
risk stigmata should be hospitalized for 72 hours to monitor for
rebleeding
 In validation goup, scores of 6 or more were associated with a
greater than 50% risk of needing an intervention.
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25.  IA : Active or Spurting hemorrhage
 IB : Oozing hemorrhage
 IIA: Non-bleeding visible vessel
IIB: Adherent clot
 IIC: A flat pigmented spot
 III: A clear ulcer base
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Forrest's Classification
It describes the ulcer, predicts rebleeding risk and provides
clue for subsequent management.

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28.  Passed through the working channel of an endoscope & applied to an
ulcer to determine if blood flow is present beneath the ulcer base.
 DEP has been utilized to risk stratify patients with SRH into:
 High risk: active arterial bleeding [FIA], NBVV [FIIA] &
adherent clot [FIIB]
 Intermediate risk: oozing bleeding [FIB], & flat spots [FIIC]
 Low risk: clean ulcer base [FIII])
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30.  UGIB hospitalizations due to varices ranges from 2–40%, and is
the 2nd most common cause of severe UGI bleeding.
 The mortality rate with each bleeding is ~30%
 Rate of new varices development in cirrhotic patients is 5% per year and
rate of growth from small to large varices is 10% per year
 Variceal hemorrhage occurs in 25 – 40% of patients with cirrhosis
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31.  GEV present in 50% cirrhotic patients:
30-40% compensated, 85% decompensated
 In Compensated cirrhosis, varices develop at a rate of 7-8% per year.
 Two years risk of bleeding in in patients with varices
<5 mm in diameter is 7%, >5 mm in diameter is 30%.
 Up to 25% of patients with newly diagnosed varices will experience
variceal bleeding within 2 years.
 The best clinical predictor of bleeding appears to be variceal size.
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32. Screening endoscopy is recommended as cirrhosis is
diagnosed:
 Compensated + no varices Q2-3yr
 compensated + small varices Q1-2yr
 At time of decompensation
LS <20 kPa and Platelet count >150,000/mm3 a very low
probability (<5%) of having high-risk varices.

33.  Factors predict the risk of bleeding;
the size and location of the varix
 Severity of cirrhosis (Child's class)
 Patients with tense ascites.
the height of wedged-hepatic vein pressure
certain endoscopic stigmata, including red wale signs, hematocystic
spots, diffuse erythema, cherry-red spots, or white-nipple spots.
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34.  Of patients who have stopped bleeding, approximately one third will
rebleed within the next 6 weeks. (40% within 5 days)
 Predictors of rebleeding include;
 active bleeding at emergency endoscopy
 bleeding from gastric varices
 hypoalbuminemia
 renal insufficiency
 HVPG greater than 20 mm Hg.
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35. The highest risk of death:
 Patients who rebleed early
 MELD score over 18
 Require more than 4 units of packed RBC transfusions
 Renal failure
 Alcoholic liver cirrhosis
 Higher serum bilirubin level
 Lower serum albumin level
 Hepatic encephalopathy
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36.  The best known criteria are those compiled by the Japanese Research
Society for Portal Hypertension.
 The descriptors include;
 red color signs,
 color of the varix,
 form (size) of the varix
 location of the varix
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38.  Isolated gastric varices (IGV)
◦ IGV 1 (7%)
 Isolated in the fundus
◦ IGV 2 (2%)
 Found in the antrum,
corpus and around
 Gastro-esophageal varices (GOV)
◦ GOV 1 (70%)
 continuous with esophageal
varices and extend along the
lesser curve
◦ GOV 2 (21%)
 extend from the esophagus
below the GE junction toward
the fundus
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39.  Account for 2–10% of UGIB hospitalizations.
 It is characterized by longitudinal mucosal lacerations (intramural
dissection) in the distal esophagus and proximal stomach.
 Mucosal lacerations develops secondary to a sudden increase in
intraabdominal pressure.
 Bleeding occurs when the tear involves the underlying esophageal
venous or arterial plexus.
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40.  Bleeding from gastric side of the gastroesophageal junction, stops
spontaneously in 80–90% of patients and recurs in only 0–10%.
 The classic history is vomiting, retching, or coughing preceding
hematemesis, especially in an alcoholic patient.
 Precipitating factors include vomiting, straining or lifting,
coughing, seizures, blunt abdominal injury, nasogastric tube
placement, and gastroscopy.
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41.  Is a large (1- 3 mm) submucosal artery that protrudes through
the mucosa in the absence of a primary ulcer.
 It is located in the proximal stomach (fundus) along the lesser
curvature, near the esophagogastric junction (typically within
5cm), although they have been found in all areas of the GI tract,
including the esophagus, duodenum, and colon.
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42.  Patients who bleed from Dieulafoy's lesions are typically
men with cardiovascular disease, hypertension, chronic
kidney disease, diabetes, or alcohol abuse.
 The use of NSAIDS is also common among patients with
Dieulafoy's lesions; one theory is that NSAIDS incite bleeding
by causing mucosal atrophy and ischemic injury.
 Bleeding episodes are often self-limited, although bleeding
can be recurrent and profuse.
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43.  Linear erosions or ulcerations in the proximal stomach at the end of a
large hiatal hernia
 Caused by mechanical trauma and local ischemia as the hernia moves
against the diaphragm and only secondarily by acid and pepsin
 present as chronic GI bleeding and IDA(can be source of acute UGIB)
 a common cause of obscure GI bleeding
 Long-term medical management is usually with iron supplements
and an oral PPI
 Surgical repair of the hiatal hernia(recurrent bleeding)
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44.  Endoscopically visualized subepithelial hemorrhages and erosions.
 These are mucosal lesions and do not cause major bleeding due to the
absence of arteries and veins in the mucosa.
 Erosions develop in various clinical settings, the most important of
which are NSAID use, alcohol intake, and stress.
 Stress-related gastric mucosal injury occurs only in extremely sick pts.
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45.  Malignancy accounts for 1% of severe UGI bleeds.
 The tumors are usually large, ulcerated masses in the esophagus,
stomach, or duodenum.
 Endoscopic hemostasis can temporarily control acute bleeding in
most patients and allow time to determine the appropriate long-
term management.
 Angiography with embolization should be considered for patients
with severe UGI bleeding who do not respond to endoscopic
therapy.
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46. GAVE
 Located at Gastric Antrum
 Watermelon stomach
 Patients usually present with slow
UGIB and iron deficiency anemia.
 Mucosal vascular ectasia, fibrin
thrombi, fibrohyalinosis & spindle
cell proliferation (Biopsy)
 Endoscopic hemostasis with
thermal heat modalities have been
reported successful.
PHG
 Located mostly @ gastric fundus &
upper body of stomach
 DX: diffuse oozing from lesions
 Subclinical bleeding, IDA
 Mild(snake skin mosaic pattern)
 Severe( Mild+ flat or bulging red
marks /black brown spots)
 Beta blockers are recommended
 Iron supplements
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47. Initial assessment
The initial evaluation of a patient with acute UGIB includes;
 the airway, breathing, circulation
History, physical examination, and laboratory tests.
Identify potential sources and severity of the bleed
 Determine if there are conditions present that may affect subsequent
management.
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48.  If the patient is hemodynamically stable & no evidence of active
bleeding (out /and in patient management)
 Manage at ICU If the patient:
◦ Is hemodynamically unstable
◦ Is continuously bleeding
◦ Hct drops by 6%
◦ Significant comorbidities: Ischemic liver, CAD
◦ Advanced elderly
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49.  Localizing symptoms: Hematemesis, Melena, Hematochezia
 History of prior GIB: 60% bleed at the same site
 Odynophagia, Dysphagia: esophageal ulcer
 Dizziness, SOB, syncope: severity of bleeding
 Recent Abdominal surgery: ulcer at site of anastomosis
 History of bleeding problems: coagulopathy
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50. 50
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51.  Signs of hypovolemia
Resting tachycardia
Orthostatic & Supine hypotension
 Rebound tenderness or involuntary guarding, perforation
 Stigmata of liver disease
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52. 52
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53. Nasogastric lavage
 The use of nasogastric tube (NGT) placement in patients with
suspected acute upper GI bleeding is not recommended, as studies
have failed to demonstrate a benefit with regard to clinical outcomes
(mortality, length of hospital stay, surgery, or transfusion requirement)
 Patients only undergo NGT lavage if particulate matter, fresh blood,
or clots need to be removed from the stomach to facilitate endoscopy.
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54. Upper GI endoscopy-
 Diagnostic, Therapeutic, Prognostic for acute upper GI bleeding.
 Early endoscopy (within 24 hrs) is recommended for acute UGIB
Prokinetics(erythromycin, metoclopramide) 30 to 90 minutes before
EGD to aid gastric motility and emptying
When severe hemorrhage requires rapid interventions, endoscopy
may be performed with simultaneous blood product administration.
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55. Goals of Therapy
 Hemodynamic resuscitation
 Cessation of bleeding source
 Prevention of future recurrence
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58. 58
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59. PUD
Low risk
Flat pigmented spot or clean base (Forrest grade IIC or III)
Do not perform endoscopic hemostasis.
Consider early hospital discharge after endoscopy if the
patient has low clinical risk and safe home environment.
Treat with an oral proton-pump inhibitor
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60. 60
 High Risk Stigmata
Perform endoscopic hemostasis using
 contact thermal therapy alone
 mechanical therapy using clips
 epinephrine injection, followed by contact thermal therapy
 Endoscopic removal of adherent clot if underlying active
bleeding or nonbleeding visible vessel is present
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62.  Primary prophylaxis is indicated in any patient with
◦ Large varices, small varices (red wale marks, Child class C)
 Most trials addressed the use of NSBB for primary
prophylaxis demonstrated a decrease in the risk of
bleeding(25% vs 15%)
 In patients with cirrhosis who have large varices, it is
recommended that 10 prophylaxis either NSBB or EVL
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63.  Thermal contact probes
Multipolar electrocoagulation (MPEC)
bipolar electrocoagulation probe
 Injection therapy
 Endoscopic hemoclips (clips)
 Band ligation
 Hemostatic spray
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64. 64
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66.  Only be used in uncontrolled bleeding as a temporary ‘bridge’
until definitive treatment can be instituted for max 24hrs
 Varices are easily compressed b/c (superficial and thin-walled)
Achieves hemostasis in the majority of cases (70-90%).
 Recurrent bleeding after decompression of the balloon 30-50%
 Self-expanding covered esophageal metal stents , efficacious ,
safer option than balloon tamponade
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67.  Rebleeding risk (60% in the first year),
with a mortality of up to 33%
 Combined therapy with EVL and NSBB
(long-acting propranolol or nadolol)
 TIPS:- bleeding recures despite
combined pharmacological and
endoscopic therapy
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68. Angiography
 Diagnostic , setting of non-localized lesions
 Therapeutic through the arterial instillation of vasoactive drugs,
arterial embolization, or a combination of the two.
 This therapy is low risk and may lead to greater than 65 %
success
 It treats severe bleeding (Rate bleeding (>0.5 ml/min)
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69.  Ongoing bleeding despite endoscopic & percutaneous interventions
 Bleeding related to a prior surgical procedure,
 Development of an acute abdomen (Perforation)
 Massive hemorrhage with failed resuscitation
 Need more than 6 Unit of blood in the 1st 24hr
 Slow continuous bleeding >24hrs
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Upper Gastrointestinal and Ulcer Bleeding 2021

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72.  Harrison principle of internal medicine 21st edition
 Sleisenger & Fordtran’s Gastrointestinal and Liver Disease11th edition
 Uptodate 2023
 ACG Clinical Guideline 2021: Upper Gastrointestinal and Ulcer Bleeding
 ESGE Guideline 2021: Endoscopic diagnosis and management of
nonvariceal upper gastrointestinal hemorrhage (NVUGIH)
 AASLD Practice Guideline 2016
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