Upper Gastrointestinal Bleeding Medication

  • Author: Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF; Chief Editor: John Geibel, MD, DSc, MA   more...
 
Updated: Nov 23, 2011
 

Medication Summary

Rebleeding is associated with increased morbidity and mortality; therefore, this is the major goal of therapy.

As advised in the 2008 SIGN guidelines, patients with chronic liver disease who present with acute UGIB should be started on antibiotic therapy.[27]

The use of H2-receptor antagonists has not been shown to be effective in altering the course of UGIB. A meta-analysis concluded that there was a possible minor benefit with intravenous H2 antagonists in bleeding gastric ulcers but no benefit in duodenal ulcers.[68]

The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer hemorrhage, although only when not combined with aspirin therapy. Concerns have been raised about an increase in myocardial infarction and stroke in patients taking selective cyclooxygenase-2 inhibitors.

As demonstrated in the study by al-Assi et al, the combination of H pylori infection and NSAID use may increase the risk of ulcer hemorrhage; however, the treatment of H pylori in patients who are taking NSAIDs remains controversial.[23]

The 2008 SIGN guidelines clearly advocate the discontinuation of aspirin and NSAIDs in patients who present with peptic ulcer bleeding. When ulcer healing and eradication of H pylori are confirmed, aspirin and NSAIDs should only be resumed if there is a clear indication for their use.[27]

Eradication of H pylori can reduce the risk of rebleeding. Current anti-H pylori regimens include a variety of drug combinations. Typically, an antimicrobial agent is combined with an H2-receptor antagonist or a PPI.

The treatment regimens approved by FDA have eradication rates for H pylori of 70-90%.[11]

Drugs used to treat H pylori infection include the following:

  • Omeprazole
  • Ranitidine bismuth citrate
  • Bismuth subsalicylate
  • Lansoprazole
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Proton Pump Inhibitors

Class Summary

PPIs inhibit gastric acid secretion by inhibition of the H+/K+/ATPase enzyme system in the gastric parietal cells. IV therapy may be a useful adjunct via stabilization of the clot by increasing intragastric pH. High-dose intravenous dosing is the norm; however, high-dose oral therapy may be able to maintain the intragastric pH about 6 as well.[36]

View full drug information

Pantoprazole (Protonix intravenous formulation)

 

This agent suppresses gastric acid secretion by specifically inhibiting the H+/K+/ATPase enzyme system at the secretory surface of gastric parietal cells. Use of the IV preparation has been studied only for short-term use (ie, 7-10 d).

IV dosing has been approved by FDA for the treatment of gastroesophageal reflux disease (GERD) that cannot be managed by oral medication.

The dosing has not been approved by FDA for the treatment of UGIB at present but has been suggested in literature.

IV use should be limited to 2 settings: (1) when the patient is NPO and (2) after endoscopic therapy, to maintain the gastric pH above 6 for clot stability.

Esomeprazole magnesium (Nexium intravenous formulation)

 

This agent suppresses gastric acid secretion by specifically inhibiting the H+/K+/ATPase enzyme system at the secretory surface of gastric parietal cells. Use of the IV preparation has been studied only for short-term use (ie, 7-10 d).

IV dosing has been approved by FDA for the treatment of gastroesophageal reflux disease (GERD) that cannot be managed by oral medication.

The dosing has not been approved by FDA for the treatment of UGIB at present but has been suggested in literature.

IV use should be limited to 2 settings: (1) when the patient is NPO, and (2) after endoscopic therapy, to maintain the gastric pH above 6 for clot stability.

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Contributor Information and Disclosures
Author

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF  Associate Professor of Clinical Medicine, Albert Einstein College of Medicine of Yeshiva University; Associate Professor of Clinical Medicine, Hofstra Medical School

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, and New York Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Shahzad Iqbal, MD  Advanced Endoscopy Fellow, Department of Gastroenterology, Columbia University Medical Center

Shahzad Iqbal, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA  Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Consulting; ARdelyx Ownership interest Board membership

Additional Contributors

James de Caestecker, DO Instructor, Department of Surgery, MCP Hahnemann University

James de Caestecker, DO is a member of the following medical societies: American College of Surgeons

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Alex Jacocks, MD Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine

Disclosure: Nothing to disclose.

Jason Straus, MD Staff Physician, Department of Surgery, Wright State University School of Medicine

Jason Straus, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Ulcer with active bleeding.
Ulcer with a clean base.
Diagram of an ulcer with a clean base.
Ulcer with a flat spot.
Ulcer with an overlying clot.
Ulcer with a visible vessel.
Diagram of an ulcer with a visible vessel.
Table 1. Probable Source of GI Bleeding Within the Gut
Clinical IndicatorProbability of Upper GI SourceProbability of Lower GI Source
HematemesisAlmost certainRare
MelenaProbablePossible
HematocheziaPossibleProbable
Blood-streaked stoolRareAlmost certain
Occult blood in stoolPossiblePossible
Table 2. Estimated Fluid and Blood Losses in Shock
Class 1Class 2Class 3Class 4
Blood Loss, mLUp to 750750-15001500-2000>2000
Blood Loss,% blood volumeUp to 15%15-30%30-40%>40%
Pulse Rate, bpm< 100>100>120>140
Blood PressureNormalNormalDecreasedDecreased
Respiratory RateNormal or IncreasedDecreasedDecreasedDecreased
Urine Output, mL/h>3530-4020-3014-20
CNS/Mental StatusSlightly



anxious



Mildly



anxious



Anxious,



confused



Confused,



lethargic



Fluid Replacement, 3-for-1 ruleCrystalloidCrystalloidCrystalloid and bloodCrystalloid and blood
Table 3. Effect of Number of Packed Erythrocyte Transfusions on Need for Surgery and Mortality from UGIB
Number of Units TransfusedNeed for Surgery, %Mortality Rate, %
044
1-3614
4-51728
>55743
Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIB Mortality Rate
Nasogastric Aspirate ColorStool ColorMortality Rate, %
ClearBrown or red6
Coffee-groundBrown or black8.2
Red19.1
Red bloodBlack12.3
Brown19.4
Red28.7
Table 5. Ulcer Characteristics and Correlations
Ulcer CharacteristicsPrevalence Rate, %Rebleeding Rate, %Surgery Rate, %Mortality Rate, %
Clean base4250.52
Flat spot201063
Adherent clot1722107
Visible vessel17433411
Active bleeding18553511
Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations for Duodenal Ulcer
Original OperationRecurrence Rate, %Postgastrectomy Syndrome Rate, %Mortality Rate, %
Proximal gastric vagotomy1050.1
Truncal vagotomy and drainage720-30< 1
Truncal vagotomy and antrectomy



Billroth I or Billroth II



130-500-5
Truncal vagotomy and antrectomy



Roux-en-Y



5-1050-600-5
Table 7. Effects of Operations for PUD on Gastric Emptying and Motility
OperationAntral InnervationLiquid EmptyingSolid Emptying
Proximal gastric vagotomyPreservedFastNormal
Truncal vagotomyDividedFastSlow
Truncal vagotomy and drainageDividedFastFast
Truncal vagotomy and antrectomyDividedFastFast
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