Upper Gastrointestinal Bleeding

(UGIB)

No.1 Hospital of Zhengzhou University

Fei-fei Li
 Definitions
 the blood is coming from above the
ligament of Treitz( esophagus, stomach,
or first part of the small intestine).
 A common medical condition
 250,000 – 500,000 admissions/year US
 UGI bleeding incidence 100/100,000 adults
 Incidence increases 20-30 fold from third to
ninth decade of life
 GI bleeding stops spontaneously in 80 %
 Morbidity Data
 Majority will receive blood transfusions
 2 – 10 % require urgent surgery to arrest
bleeding
 Mortality rates for UGI bleeding 2 – 15 %

 Mortality for patients who develop bleeding

after admission to hospital for another
reason is 20 – 30 %
 Clinical presentation :Clinical
manifestations of GI bleeding
depends upon extent & rate
 Hematemesis 25 %,250-300 cc of blood in stomach will
render “Red blood” hematemesis and“Coffee ground”
emesis
 Melena alone 25 %, 50 – 100 cc of blood /day will render
stool melenic
 Hematochezia 15 %, seen in massive UGI hemorrhage
 Occult bleeding, 5-10 cc of blood/day will render stool
occult bleeding
 Clinical presentation : other
 General abdominal discomfort
 Classic signs and symptoms of shock

 Fatigue & exertional dyspnea typical

symptoms with slow, chronic blood loss
 Causes

 Peptic Ulcer Disease

 Gastritis
 Varix Rupture
 Mallory-Weiss Tear
 Esophagitis
 Duodenitis
Causes
Peptic Ulcer
NSAID induced ulcers
 Esophageal Varices

 Causes
 Chronic alcohol
abuse and liver
cirrhosis
 Ingestion of caustic
substances
 History
 Epigastric or right upper quadrant discomfort, often
described as “gnawing” or “burning”, may be
reported in patients with peptic ulceration involving
either the stomach and distal esophagus or the
duodenum .The history may reveal that discomfort is
relieved with food or antacid intake and that it often
recurs several hours after eating.
 Recent or chronic ingestion of steroids, aspirin,or
other nonsteroidal antiinflammatory agents may
predispose to gastrointestinal bleeding.
 History
 Hematemesis beginning after an initial bout
of retching is often due to the development
of a Mallory-Weiss mucosal laceration; a
history of dietary and alcohol indiscretion is
also frequently obtained.
 Physical examination
 A.Abdominal pain elicited by palpation is
often noted in patients with esophagitis ,
peptic ulcer, diverticulitis, inflammatory
bowel disease,colorectal carcinoma, and
infectious diarrhea.
 Physical examination
B. Signs of hyperestrogenism secondary to
liver disease, including jaundice, palmar
erythema, gynaecomastia, spider angioma,
and testicular atrophy ,all support the
diagnosis of significant liver damage, which
may be associated with portal hypertension
and esophageal varices.
 Laboratorial examination

fecal occult blood test (FOBT)

Blood rule test
electrolytes/renal function
liver function tests
 Diagnosis
 History

 Signs and symptom

 Physical examination

 diagnostic tests
 Prognosis

Despite a decreased incidence of ulcer

disease and improvements in the
management of acute upper GI bleeding,
mortality remains at 6-7 % in most series
in the literature for the past 30 years.
 Scoring System for Predicting Rebleeding and
Mortality
Variable Score
Age  A simplified scoring system
<60 0
60-79 1 based on endoscopic and
>79 2 clinical variables has been
Shock
None 0
developed
Tachycardia 1  Rockhall TA et al.: Selection
Hypotension 2
Comorbidity of patients for early
None 0 discharge or outpatient care
CAD, CHF, other major comorbidity
Renal failure, liver failure, malignancy
1
2
after acute upper
Diagnosis gastrointestinal
Mallory Weiss tear or no lesion observed 0 haemorrhage. Lancet
All her
ot diagnoses 1
Malignant lesion 2 1996:347: 1138-1140
Stigmas of recent hemorrhage
None or spot in ulcer base 0
Blood in the GI tract, clot, visible vessel 2
in ulcer base
 Scoring is not Boring
Score Rebleeding Mortality %
%
1 3 0
2 5 0
3 12 2
4 13 4
5 17 8
6 30 15
7 40 20
8 48 39
Upper Gastrointestinal Bleeding

Severe UGIB is a common

and
serious medico-surgical problem
 Therapy:
 Pharmacological Therapy
 Endoscopic Therapy

 Surgical therapy

 Angiography and transcatheter embolization

 Pharmacological Therapy
♦ Vasopressin
lowers splanchnic blood pressure
induces vasoconstriction
high rate of complications
 Pharmacological Therapy
♦ Somatostatin and Octreotide
 Lower toxicity

 additional effects of decreasing

gastric acid secretion and increasing

duodenal bicarbonate secretion
 decreased risk of re-bleeding

compared to H2RAs(H2 Receptor Antagonists)

 Pharmacological Therapy

At intragastric pH < 7, coagulation is deficient due to

ineffective function of clotting factors and platelets
♦ Acid suppressing agents
 - H2 Receptor Antagonists
 - Proton Pump Inhibitors
(Omeprazole Pantoprazole)
 Endoscopic Therapy

Endoscopic hemostatic therapy

has been demonstrated to be the
mainstay of management.
 Endoscopic Therapy
Effectively reduces
 Rebleeding

 Need for Surgery

 Mortality (by meta-analysis)

 However, 10 – 20 percent of patients have

rebleeding after (initially successful) endoscopic
therapy
 Endoscopic therapy
 Endoscopic therapy:
Coagulation (injection, cautery, heater probe,
laser)
Variceal injection or band ligation
Polypectomy
 Acute U.G.I. Bleeding
**General management:
 • Drug therapy
1. Somatostatin and Octreotide
2. Proton pump inhibitors or H2 – receptor antagonists
 • Factors in reassessment
1. age: 60 +  greater mortality
2. recurrent hemorrhage: +++ mortality
3. re-bleeding: mostly within the 1st 48 hrs
4. surgical procedures in case of severe bleeding.
Thanks
 Proton Pump Inhibitors
 NEJM 1997: high dose oral omeprazole effective in
reducing rebleeding rates. No endoscopic therapy
performed in this study from India
 Two multicenter trials from Scandinavia showed benefit of
high dose I.V. omeprazole (1997)
 Taiwanese study of 100 patients randomized between IV
omeprazole and cimetidine. Intragastric pH was around 6.0
for first 24 hours in omeprazole group but only between 4.5
to 5.5 for cimetidine group. 12 pts in the cimetidine group
and 2 pts in the omeprazole group rebled. No change in
LOS, number of procedures, or mortality (1998)
PROTONIX® (Pantoprazole Sodium)
Formulations

• 40-mg Delayed-Release Tablet

• 40-mg Lyophilized Powder for Injection

PROTONIX® (Pantoprazole
Sodium)
Specific Cysteine Binding Sites
Binds two cysteine residues critical for the
inhibition of gastric acid secretion
(Cys 813 and 822)

Modlin IM, Sachs G. Acid Related Diseases, Biology and Treatment. Schnetztor-Verlag. 1998:126-145.
 PROTONIX® I.V. (Pantoprazole Sodium)
for Injection in Inhibition of Acid Output
40 mg I.V. vs. Placebo

100

80

60
% Inhibition

PROTONIX I.V. 40 mg (n=8)

40
Placebo (n=4)

20

-20

-40

Hours

8am 10am Noon 2pm 4pm 6pm 8pm 10pm 12pm 2am 4am 6am 8am

Data on file, Wyeth-Ayerst Laboratories. Study 100-US.

Pisegna JR et al. Am J Gastroenterol. 1999;94:2874-2880.
 PROTONIX® I.V. (Pantoprazole Sodium)
for Injection
Dosage and Administration

 Dosage
The recommended dose is one
vial (the equivalent of 40 mg
pantoprazole) given once daily
by intravenous infusion for 7 to
10 days.
 Administration
PROTONIX I.V. for Injection
should be administered
intravenously over a period of
approximately 15 minutes at a
rate not greater than 3 mg/min (7
mL/min). PROTONIX I.V. for
Injection should be administered
using the in-line filter provided.
The filter must be used to
remove the precipitates that may
form when the reconstituted drug
product is mixed with I.V.
solutions

PROTONIX I.V. for Injection Prescribing Information. Wyeth-Ayerst Laboratories, Philadelphia, Pa

 PROTONIX® I.V. (Pantoprazole Sodium)
for Injection
Summary

•Impressive acid suppression

•No evidence of tolerance in a clinical study (oral

10 days; I.V. 7days)
•Fast onset (within 15-30 minutes) and long acting

•Generally well tolerated

•No known clinically relevant drug interactions

Data on file, Wyeth-Ayerst Laboratories.