eMedicine Specialties > Emergency Medicine > Gastrointestinal

Gastritis and Peptic Ulcer Disease: Treatment & Medication

Author: Philip Shayne, MD, Associate Professor, Residency Program Director, Vice Chair for Education, Department of Emergency Medicine, Emory University School of Medicine
Coauthor(s): Wendi S Miller, MD, Resident Physician, Department of Emergency Medicine, Emory University School of Medicine
Contributor Information and Disclosures

Updated: Nov 10, 2009

Treatment

Prehospital Care

  • Pursue aggressive fluid resuscitation in patients with evidence of massive upper GI bleeding.

Emergency Department Care

  • Most patients with gastritis or peptic ulcer disease do not require acute interventions.
  • Antacids or a GI cocktail (ie, typically an antacid with an anesthetic such as viscous lidocaine and/or an antispasmodic) may be used therapeutically for symptoms.
  • Administer supportive therapy as needed.
  • Massive gastric bleeds are the most difficult complication to treat. Mainstays of resuscitation include the following:
    • Establishment of adequate IV access and volume replacement, initially with crystalloid. In the face of continued hypotension after 2 L, consider blood transfusion.
    • Airway protection with intubation should be considered in the case of massive bleeding.
    • NG suction helps to keep the stomach empty and contracted.
    • IV PPI has been shown to reduce mortality in upper GI bleed and reduces the incidence of rebleeding and need for surgical intervention.6
    • Emergent surgical or endoscopic intervention may be required.
  • Empiric treatment of H pylori is not recommended. Therapy is only indicated after confirmation of infection.
  • Testing for H pylori is recommended only with the intention to treat positive results. These tests are not performed in the ED.
  • Empiric trial of acid suppression in patients younger than 55 years without alarm features may be initiated with PPI for 4-8 weeks. Appropriate follow-up is required to assess response in 2-4 weeks.7

Consultations

  • Consult with a general surgeon for most acute complications including suspected perforation, penetration, outlet obstruction, and bleeding.
  • Consultation with a gastroenterologist for emergent endoscopy may be required for active bleeding.

Medication

Treatment goals in the acute setting are the relief of discomfort and protection of the gastric mucosal barrier to promote healing. Eradication of H pylori infection is a prolonged and complicated process requiring confirmation of the presence of the organism and eventual evidence of eradication, both of which are beyond the scope of practice in the ED.

Cessation of the causative agent and antacids may be sufficient outpatient therapy in mild cases. Most patients require an H2-receptor antagonist (H2RA) or a proton pump inhibitor (PPI), which has been proven to provide faster and more reliable healing than antacids. Either an H2RA or a PPI can be used as a first-line agent. With continued symptoms, they may be used together. In refractory cases, sucralfate also may be indicated.

PPIs are more effective than H2RAs in reducing upper GI bleeds in patients taking NSAIDs, aspirin, or clopidogrel. None of the antisecretory agents has a significant effect in reducing bleeding risk in patients taking other anticoagulants.

Antacids

Aluminum-containing and magnesium-containing antacids can be helpful in relieving symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe.


Aluminum and magnesium hydroxide (Maalox, Mylanta)

Neutralizes gastric acidity, resulting in increase in stomach and duodenal bulb pH. Aluminum ions inhibit smooth muscle contraction, thus inhibiting gastric emptying. Magnesium and aluminum antacid mixtures are used to avoid bowel function changes.

Adult

2-4 tsp PO qid prn

Pediatric

0.5 mL/kg PO qid prn

Both drugs reduce efficacy of fluoroquinolones, corticosteroids, benzodiazepines, and phenothiazines; aluminum and magnesium potentiate effects of valproic acid, sulfonylureas, quinidine, and levodopa

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use aluminum containing antacids with caution in patients who have recently suffered a massive upper GI hemorrhage

Proton pump inhibitors

Bind to the proton pump of parietal cell, inhibiting secretion of hydrogen ions into gastric lumen. Proton pump inhibitors relieve pain and heal peptic ulcers more rapidly than H2 receptor antagonists do. Drugs in this class are equally effective. Standard doses of PPIs inhibit more than 90% of 24-hour acid secretion, compared to 50-80% with H2-blockers. They all decrease serum concentrations of drugs that require gastric acidity for absorption, such as ketoconazole or itraconazole. Five drugs are now FDA approved in this category, and omeprazole is now available in generic form. They are most effective when taken 30-60 minutes before the first meal of the day.8


Omeprazole (Prilosec)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. May be prescribed for up to 8 wk to treat all grades of erosive esophagitis.

Adult

20 mg PO qd for 4-8 wk

Pediatric

Not established

May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Bioavailability may be increased in elderly patients


Esomeprazole (Nexium)

S-isomer of omeprazole. Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. May be prescribed for up to 8 wk to treat all grades of erosive esophagitis.

Adult

20-40 mg PO qd

Pediatric

Not established

Amoxicillin or clarithromycin may increase plasma levels of esomeprazole when used concurrently; may reduce absorption of dapsone; may increase levels of diazepam and GI absorption of digoxin; may decrease absorption of iron, ketoconazole and itraconazole

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy


Lansoprazole (Prevacid)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. May be prescribed for up to 8 wk to treat all grades of erosive esophagitis.

Adult

30 mg PO qd for 4-8 wk

Pediatric

Not established

May decrease effects of ketoconazole and itraconazole; may increase theophylline clearance

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in liver impairment


Rabeprazole (Aciphex)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. For short-term (4-8 wk) treatment and symptomatic relief of gastritis.
Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. May be prescribed for up to 8 wk to treat all grades of erosive esophagitis.

Adult

20 mg tab PO qd 4-8 wk

Pediatric

Not established

May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy


Pantoprazole (Protonix)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. For short-term (4-8 wk) treatment and symptomatic relief of gastritis.
Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. May be prescribed for up to 8 wk to treat all grades of erosive esophagitis.

Adult

40 mg PO qd

Pediatric

Not established

May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy

H2-receptor antagonists

Inhibit the action of histamine on the parietal cell, which inhibits acid secretion. The 4 drugs in this class are all equally effective and are available over the counter in half prescription strength for heartburn treatment. None are as effective as PPIs.


Cimetidine (Tagamet)

Inhibits histamine at H2 receptors of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Adult

150 mg PO qid; not to exceed 600 mg/d
50 mg/dose IV/IM q6-8h; not to exceed 400 mg/d

Pediatric

Not established
Suggested dose: 20-40 mg/kg/d PO/IV/IM divided q4h

Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Elderly patients may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur


Famotidine (Pepcid)

Competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Adult

40 mg PO qhs
20 mg/dose IV q12h; not to exceed 40 mg/d

Pediatric

Not established
Suggested dose: 1-2 mg/kg/d PO/IV divided q6h; not to exceed 40 mg/dose

May decrease effects of ketoconazole and itraconazole

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

If changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment


Nizatidine (Axid)

Competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Adult

300 mg PO hs or 150 mg PO bid

Pediatric

Not established

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment


Ranitidine (Zantac)

Competitively inhibits histamine at the H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Adult

150 mg PO bid or 300 mg PO qhs; not to exceed 300 mg/d
50 mg/dose IM/IV q6-8h

Pediatric

<12 years: Not established
>12 years: 1.25-2.5 mg/kg/dose PO q12h; not to exceed 300 mg/d
0.75-1.5 mg/kg/dose IV/IM q6-8h; not to exceed 400 mg/d

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment

Gastrointestinal agents

Are effective in the treatment of peptic ulcers and in preventing relapse. Their mechanism of action is not clear. Multiple doses are required, and they are not as effective as the other options.


Sucralfate (Carafate)

Binds with positively charged proteins in exudates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts. Used for short-term management of ulcers.

Adult

1 g PO qid

Pediatric

Not established
Suggested dose: 40-80 mg/kg/d PO divided q6h

May decrease effects of ketoconazole, ciprofloxacin, tetracycline, phenytoin, warfarin, quinidine, theophylline, and norfloxacin

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure and impaired excretion of absorbed aluminum

Prostaglandins

Can prevent peptic ulcers in patients taking NSAIDs and may be used with NSAIDs in patients at a high risk of complications.


Misoprostol (Cytotec)

A prostaglandin analog that protects the lining of the GI tract by replacing depleted prostaglandin E1 in prostaglandin inhibiting therapies.

Adult

200 mcg PO qid with food; if not tolerated, decrease to 100 mcg qid or 200 mcg bid with food

Pediatric

Not established

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution with elderly patients and in renal impairment

More on Gastritis and Peptic Ulcer Disease

Overview: Gastritis and Peptic Ulcer Disease
Differential Diagnoses & Workup: Gastritis and Peptic Ulcer Disease
Treatment & Medication: Gastritis and Peptic Ulcer Disease
Follow-up: Gastritis and Peptic Ulcer Disease
Multimedia: Gastritis and Peptic Ulcer Disease
References
[ CLOSE WINDOW ]

References

  1. Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease. Lancet. Aug 13 2009;[Medline].

  2. Yuan Y, Padol IT, Hunt RH. Peptic ulcer disease today. Nat Clin Pract Gastroenterol Hepatol. Feb 2006;3(2):80-9. [Medline].

  3. Tahara T, Arisawa T, Shibata T, Nakamura M, Okubo M, Yoshioka D. Association of endoscopic appearances with dyspeptic symptoms. J Gastroenterol. 2008;43(3):208-15. [Medline].

  4. Turkkan E, Uslan I, Acarturk G, Topak N, Kahraman A, Dilek FH. Does Helicobacter pylori-induced inflammation of gastric mucosa determine the severity of symptoms in functional dyspepsia?. J Gastroenterol. 2009;44(1):66-70. [Medline].

  5. [Guideline] Chey WD, Wong BC,. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. Aug 2007;102(8):1808-25. [Medline].

  6. Tajima A, Koizumi K, Suzuki K, Higashi N, Takahashi M, Shimada T. Proton pump inhibitors and recurrent bleeding in peptic ulcer disease. J Gastroenterol Hepatol. Dec 2008;23 Suppl 2:S237-41. [Medline].

  7. [Guideline] Talley NJ, Vakil N. Guidelines for the management of dyspepsia. Am J Gastroenterol. Oct 2005;100(10):2324-37. [Medline].

  8. Treatment of peptic ulcers and GERD. Treat Guidel Med Lett. Aug 2008;6(72):55-60. [Medline].

  9. [Guideline] Lanza FL, Chan FK, Quigley EM. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. Mar 2009;104(3):728-38. [Medline].

  10. Aro P, Storskrubb T, Ronkainen J, Bolling-Sternevald E, Engstrand L, Vieth M. Peptic ulcer disease in a general adult population: the Kalixanda study: a random population-based study. Am J Epidemiol. Jun 1 2006;163(11):1025-34. [Medline].

  11. Logan RP, Walker MM. ABC of the upper gastrointestinal tract: Epidemiology and diagnosis of Helicobacter pylori infection. BMJ. Oct 20 2001;323(7318):920-2. [Medline].

  12. Lowell M. Esophagus, stomach, and duodenum. In: Marx J, Hockberger R, Walls R, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 2. 6th ed. Mosby; 2006:1390-1394.

  13. Moss SF, Sood S. Helicobacter pylori. Curr Opin Infect Dis. Oct 2003;16(5):445-51. [Medline].

  14. Pang SH, Leung WK, Graham DY. Ulcers and gastritis. Endoscopy. Feb 2008;40(2):136-9. [Medline].

  15. Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med. Oct 10 2002;347(15):1175-86. [Medline].

  16. Yeomans ND. Management of peptic ulcer disease not related to Helicobacter. J Gastroenterol Hepatol. Apr 2002;17(4):488-94. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

gastritis, peptic ulcer disease treatment, peptic ulcer disease symptoms, peptic ulcer, peptic ulcer disease, PUD, esophagitis, gastroesophageal reflux, GERD, abdominal pain, erosive gastritis, reflux gastritis, hemorrhagic gastritis, infectious gastritis, gastric mucosal atrophy, Helicobacter pylori, H pylori, NSAID-induced gastritis, peritonitis, Curling ulcers, gastrinoma, Zollinger-Ellison syndrome

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Philip Shayne, MD, Associate Professor, Residency Program Director, Vice Chair for Education, Department of Emergency Medicine, Emory University School of Medicine
Philip Shayne, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Wendi S Miller, MD, Resident Physician, Department of Emergency Medicine, Emory University School of Medicine
Wendi S Miller, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Southern Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Glenn Bowman, MD, MS, Consulting Staff, Highfield MRI, Columbus, Ohio
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eugene Hardin, MD, FAAEM, FACEP, Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.