ugi bleeding

8/9/2019 UGI Bleeding

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Upper Gastrointestinal Bleeding

(UGIB)

No.1 Hospital of Zhengzhou University

Fei-fei Li


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Definitions

the blood is coming from above the

ligament of Treitz( esophagus, stomach,

or first part of the small intestine).


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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 %


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Morbidity DataMajority 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 %


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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

andCoffee ground

emesis

Melena alone 25 %, 50 100 cc of blood /day willrender stool melenic

Hematochezia 15 %, seen in massive UGI

hemorrhage Occult bleeding, 5-10 cc of blood/day will render

stool occult bleeding


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Clinical presentation : other General abdominal discomfort

Classic signs and symptoms of shock

Fatigue & exertional dyspnea typical

symptoms with slow, chronic blood loss


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Causes

Peptic UlcerDisease

Gastritis

Varix Rupture

Mallory-Weiss Tear

Esophagitis

Duodenitis


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Causes


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Peptic Ulcer


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Esophageal Varices

CausesChronic alcohol

abuse and livercirrhosis

Ingestion of caustic

substances


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History Epigastric or right upper quadrant discomfort,

often described as gnawing orburning, may

be reported in patients with peptic ulcerationinvolving either the stomach and distal esophagusor the duodenum .The history may reveal thatdiscomfort is relieved with food or antacid intakeand that it often recurs several hours after eating.

Recent or chronic ingestion of steroids, aspirin,orother nonsteroidal antiinflammatory agents maypredispose to gastrointestinal bleeding.


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History Hematemesis beginning after an initial bout

of retching is often due to the development

of a Mallory-Weiss mucosal laceration; ahistory of dietary and alcohol indiscretion is

also frequently obtained.


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Physical examination A. Abdominal pain elicited by palpation is

often noted in patients with esophagitis ,

peptic ulcer, diverticulitis, inflammatorybowel disease,colorectal carcinoma, and

infectious diarrhea.


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Physical examinationB. 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 hypertensionand esophageal varices.


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Laboratorial examination

fecal occult blood test (FOBT)

Blood rule test

electrolytes/renal function

liver function tests


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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 seriesin the literature for the past 30 years.


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Scoring System for Predicting Rebleeding and

Mortality

A simplified scoringsystem based onendoscopic and clinical

variables has beendeveloped

Rockhall TA et al.:Selection of patients forearly discharge or

outpatient care after acuteupper gastrointestinalhaemorrhage. Lancet1996:347: 1138-1140

Variable Score

Age

79 2

ShockNone 0

Tachycardia 1

Hypotension 2

Comorbidity

None 0

CAD, CHF, other major comorbidity 1

Renal failure, liver failure, malignancy 2

DiagnosisMallory Weiss tear or no lesion observed 0

All other diagnoses 1

Malignant lesion 2

Stigmas of recent hemorrhage

None or spot in ulcer base 0

Blood in the GI tract, clot, visible vessel

in ulcer base

2


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Scoring is not Boring

Score Rebleeding

%

Mortality %

1 3 0

2 5 0

3 12 2

4 13 4

5 17 86 30 15

7 40 20

8 48 39


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Upper Gastrointestinal Bleeding

Severe UGIB is a commonand

serious medico-surgical problem


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Therapy:

Pharmacological Therapy

Endoscopic Therapy

Surgical therapy

Angiography and transcatheter embolization


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Pharmacological Therapyj Vasopressin

lowers splanchnic blood pressure

induces vasoconstriction

high rate of complications


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Pharmacological Therapyj 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 ReceptorAntagonists)


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Pharmacological Therapy

At intragastric pH < 7, coagulation is deficient

due to ineffective function of clotting factors

and platelets

j Acid suppressing agents - H2 ReceptorAntagonists

- Proton Pump Inhibitors

(Omeprazole PantoprazolePantoprazole))


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Endoscopic Therapy

Endoscopic hemostatic therapy

has been demonstrated to be the

mainstay of management.


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Acute U.G.I. BleedingAcute U.G.I. Bleeding**General management:

y Drug therapy

1. Somatostatin and Octreotide2. Proton pump inhibitors or H 2 receptor

antagonists

y Factors in reassessment

1. age: 60 + greater mortality

2. recurrent hemorrhage: +++ mortality

3. re-bleeding: mostly within the 1st48 hrs

4. surgical procedures in case of severe


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Thanks


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Proton Pump Inhibitors NEJM 1997: high dose oral omeprazole effective in

reducing rebleeding rates. No endoscopic therapyperformed in this study from India

Two multicenter trials from Scandinavia showed benefit ofhigh dose I.V. omeprazole (1997)

Taiwanese study of 100 patients randomized between IVomeprazole and cimetidine. Intragastric pH was around 6.0for first 24 hours in omeprazole group but only between 4.5to 5.5 for cimetidine group. 12 pts in the cimetidine groupand 2 pts in the omeprazole group rebled. No change inLOS, number of procedures, or mortality (1998)


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PROTONIXPROTONIX(Pantoprazole Sodium)(Pantoprazole Sodium)

Formulations

Formulations

40-mg Delayed

-Release Tablet

40-mg Lyophilized Powder for Injection


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PROTONIXPROTONIX(Pantoprazole(Pantoprazole

Sodium)Sodium)

Specific Cysteine Binding SitesSpecific Cysteine Binding Sites

Modlin IM, Sachs G. Acid RelatedDiseases, Biology and Treatment. Schnetztor-Verlag. 1998:126-145.

Binds two cysteine residues critical for theinhibition of gastric acid secretion

(Cys 813 and 822)


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PROTONIXPROTONIXI.V. (Pantoprazole Sodium)I.V. (Pantoprazole Sodium)

for Injectionfor Injection in Inhibition of Acid Output

40 mg I.V. vs. Placebo40 mg I.V. vs. Placebo

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

Pisegna JR et al.Am J Gastroenterol. 1999;94:2874-2880.

-40

-20

0

20

40

60

80

100

Hours

%I

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

Placebo (n=4)

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


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for Injectionfor Injection

Dosage and AdministrationDosage and Administration

DosageThe recommended dose is one

vial (the equivalent of 40 mg

pantoprazole) given once daily

by intravenous infusion for 7 to

10 days.

AdministrationPROTONIX 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


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for Injectionfor Injection

SummarySummary

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.

ugi bleeding

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