eMedicine Specialties > Gastroenterology > Esophagus

Gastroesophageal Reflux Disease: Treatment & Medication

Author: Piero Marco Fisichella, MD, Assistant Professor of Surgery, Stritch School of Medicine, Loyola University; Director, Esophageal Motility Center, Loyola University Medical Center
Coauthor(s): Marco G Patti, MD, Professor of Surgery, Director, Center for Esophageal Diseases, University of Chicago Pritzker School of Medicine
Contributor Information and Disclosures

Updated: Apr 28, 2009

Treatment

Medical Care

Treatment of gastroesophageal reflux disease (GERD) is a stepwise approach. The goals are to control symptoms, to heal esophagitis, and to prevent recurrent esophagitis or other complications. The treatment is based on lifestyle modification and control of gastric acid secretion.

  • Lifestyle modifications include the following:  
    • Losing weight (if overweight)
    • Avoiding alcohol, chocolate, citrus juice, and tomato-based products
    • Avoiding large meals
    • Waiting 3 hours after a meal before lying down
    • Elevating the head of the bed 8 inches
  • Pharmacologic therapy  
    • Antacids were the standard treatment in the 1970s and are still effective in controlling mild symptoms of gastroesophageal reflux disease (GERD). Antacids should be taken after each meal and at bedtime.
    • Histamine H2-receptor antagonists are the first-line agents for patients with mild to moderate symptoms and grades I-II esophagitis. Histamine H2 receptor antagonists are effective for healing only mild esophagitis in 70-80% of patients with gastroesophageal reflux disease (GERD) and for providing maintenance therapy to prevent relapse. Tachyphylaxis has been observed, suggesting that pharmacologic tolerance can reduce the long-term efficacy of these drugs.
    • Additional H2 blocker therapy has been reported to be useful in patients with severe disease (particularly those with Barrett esophagus) who have nocturnal acid breakthrough.
    • PPIs are the most powerful medications available for treating this condition. These agents should be used only when gastroesophageal reflux disease (GERD) has been objectively documented. PPIs work by blocking the final step in the H+ ion secretion by the parietal cell. They have few adverse effects and are well tolerated for long-term use. However, data have shown that PPIs can interfere with calcium homeostasis and aggravate cardiac conduction defects. These agents have also been responsible for hip fracture in postmenopausal women.7
    • A research review by the Agency for Healthcare Research and Quality (AHRQ) concluded, on the basis of grade A evidence, that PPIs were superior to histamine H2-receptor antagonists for the resolution of gastroesophageal reflux disease (GERD) symptoms at 4 weeks and healing of esophagitis at 8 weeks.8 In addition, the AHRQ found no difference between individual PPIs (omeprazole, lansoprazole, pantoprazole, and rabeprazole) for relief of symptoms at 8 weeks. For symptom relief at 4 weeks, esomeprazole 20 mg was equivalent, but esomeprazole 40 mg superior, to omeprazole 20mg.8
    • Prokinetic agents improve the motility of the esophagus and stomach. These agents are somewhat effective but only in patients with mild symptoms; other patients usually require additional acid-suppressing medications, such as PPIs. Long-term use of prokinetic agents may have serious, even potentially fatal, complications and should be discouraged.

Surgical Care

Approximately 80% of patients have a recurrent but nonprogressive form of gastroesophageal reflux disease (GERD) that is controlled with medications. Identifying the 20% of patients who have a progressive form of the disease is important, because they may develop severe complications, such as strictures or Barrett esophagus. For patients who develop complications, surgical treatment should be considered at an earlier stage to avoid the sequelae of the disease that can have serious consequences.

  • Indications for fundoplication include the following:  
    • Patients with symptoms that are not completely controlled by PPI therapy can be considered for surgery. Surgery can also be considered in patients with well-controlled gastroesophageal reflux disease (GERD). who desire definitive, one-time treatment.
    • The presence of Barrett esophagus is an indication for surgery. Whether acid suppression improves the outcome or prevents the progression of Barrett esophagus remains unknown, but most authorities recommend complete acid suppression in patients with histologically proven Barrett esophagus.
    • The presence of extraesophageal manifestations of gastroesophageal reflux disease (GERD) may indicate the need for surgery. These include the following: (1) respiratory manifestations (eg, cough, wheezing, aspiration); (2) ear, nose, and throat manifestations (eg, hoarseness, sore throat, otitis media); and (3) dental manifestations (eg, enamel erosion).
    • Young patients
    • Poor patient compliance with regard to medications
    • Postmenopausal women with osteoporosis
    • Patients with cardiac conduction defects
    • Cost of medical therapy
  • Laparoscopic fundoplication  
    • Laparoscopic fundoplication is performed under general endotracheal anesthesia. Five small (5- to 10-mm) incisions are used (see Image 5 or below). The fundus of the stomach is wrapped around the esophagus to create a new valve at the level of the gastroesophageal junction.
      Laparoscopic Nissen fundoplication.

      Laparoscopic Nissen fundoplication.

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      Laparoscopic Nissen fundoplication.

      Laparoscopic Nissen fundoplication.

    • The essential elements of the operation are as follows:
      • Complete mobilization of the fundus of the stomach with division of the short gastric vessels
      • Reduction of the hiatal hernia
      • Narrowing of the esophageal hiatus
      • Creation of a 360° fundoplication over a large intraesophageal dilator (Nissen fundoplication)
    • Laparoscopic fundoplication lasts 2-2.5 hours. The hospital stay is approximately 2 days. Patients resume regular activities within 2-3 weeks.
    • Approximately 92% of patients obtain resolution of symptoms after undergoing laparoscopic fundoplication.
    • The AHRQ found, on the basis of limited evidence, that laparoscopic fundoplication was as effective as open fundoplication for relieving heartburn and regurgitation, improving quality of life, and decreasing use of antisecretory medications.8
  • Several randomized clinical trials have challenged the benefits of surgery in controlling gastroesophageal reflux disease (GERD).  
    • Lundell followed up his cohort of patients for 5 years and did not find surgery to be superior to PPI therapy.9
    • Spechler found that, at 10 years after surgery, 62% of patients were back on antireflux medications.10
    • A very rigorous, randomized study by Anvari et al reestablished surgery as the criterion standard in treating gastroesophageal reflux disease (GERD).11  The investigators showed that, at 1 year, the outcome and the symptom control in the surgical group was better than that in the medical group.11
    • A British multicenter randomized study conducted by Grant et al also compared surgical treatment versus medical therapy in patients with documented evidence of gastroesophageal reflux disease (GERD).12 The type of laparoscopic fundoplication was decided by the respective surgeons. Individuals who had received medication for their condition had taken them for a median of 32 months before participating in the study. The investigators reported that by 12 months, 38% of those who had undergone surgery were taking reflux medication compared with 90% of the individuals randomized to medical management.12  In addition, other health measure favored the randomized surgical group.
  • Long-term results of laparoscopic antireflux surgery have shown that, at 10 years, 90% of patients are symptom free, and only a minority still takes PPIs.13  

Medication

The goals of pharmacotherapy are to prevent complications and to reduce morbidity in patients with gastroesophageal reflux disease (GERD).

H2-Receptor Antagonists

H2-receptor antagonists are reversible competitive blockers of histamine at the H2 receptors, particularly those in the gastric parietal cells where they inhibit acid secretion. The H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents. Although intravenous (IV) administration of H2 blockers may be used to treat acute complications (eg, gastrointestinal bleeding), the benefits are not yet proven.


Ranitidine (Zantac)

Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen concentrations.

Adult

150 mg PO bid (300 mg PO bid or 150 mg qid)

Pediatric

<12 years: Not established

>12 years

PO: 1.25-2.5 mg/kg/dose q12h; not to exceed 300 mg/d

IV/IM: 0.75-1.5 mg/kg/dose q6-8h; not to exceed 400 mg/d

May decrease the effects of ketoconazole and itraconazole; may alter the 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 patients with renal or liver impairment; if changes in renal function occur during therapy, consider adjusting the dose or discontinuing treatment


Cimetidine (Tagamet)

Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

Adult

400 mg PO bid (800 mg bid or 400 mg PO qid)

Pediatric

Not established

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

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


Famotidine (Pepcid)

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

Adult

20 mg PO bid (40 mg bid)

Pediatric

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

May decrease the 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 the dose or discontinuing treatment.


Nizatidine (Axid)

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

Adult

150 mg PO bid (300 mg PO qhs)

Pediatric

Not established

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

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

Proton Pump Inhibitors

Proton pump inhibitors inhibit gastric acid secretion by inhibition of the H+/K+ ATPase enzyme system in the gastric parietal cells. These agents are used in cases of severe esophagitis and in patients whose conditions do not respond to H2 receptor antagonist therapy.


Omeprazole (Prilosec)

Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. May use for up to 8 wk to treat all grades of erosive esophagitis.

Adult

20 mg PO qd or bid

Pediatric

Not established

May decrease the effects of itraconazole and ketoconazole; may increase the 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 increase in the elderly.


Lansoprazole (Prevacid)

Inhibits gastric acid secretion. Used for up to 8 wk to treat all grades of erosive esophagitis.

Adult

15-60 mg PO qd or 15 mg bid

Pediatric

Not established

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

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

Consider adjusting the dose in patients with liver impairment.


Rabeprazole (Aciphex)

For short-term (4- to 8-wk) treatment and relief of symptomatic erosive or ulcerative GERD. In patients not healed after 8 wk, consider additional 8-wk course.

Adult

20 mg PO qd for 4-8 wk

Pediatric

Not established

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 response does not exclude the possibility of malignancy.


Esomeprazole (Nexium)

S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ ATPase enzyme system at secretory surface of gastric parietal cells.

Adult

20-40 mg PO qd for 4-8 wk

Pediatric

Not established

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 the symptoms of gastric malignancy.

Prokinetics

Prokinetic agents increase LES pressure to help reduce reflux of gastric contents. They also accelerate gastric emptying.


Metoclopramide (Reglan)

GI prokinetic agent that increases GI motility, increases resting esophageal sphincter tone, and relaxes pyloric sphincter.

Adult

10 mg PO qid

Pediatric

Not established

May antagonize the effects of metoclopramide; opiate analgesics may increase metoclopramide toxicity in the CNS

Documented hypersensitivity; pheochromocytoma or GI hemorrhage, obstruction, or perforation; history of seizure disorders

Pregnancy

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

Precautions

Caution in patients with a history of mental illness and Parkinson disease

More on Gastroesophageal Reflux Disease

Overview: Gastroesophageal Reflux Disease
Differential Diagnoses & Workup: Gastroesophageal Reflux Disease
Treatment & Medication: Gastroesophageal Reflux Disease
Follow-up: Gastroesophageal Reflux Disease
Multimedia: Gastroesophageal Reflux Disease
References
Further Reading
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Further Reading

Additional resources on asthma are available at Medscape’s Gastroesophageal Reflux Disease Resource Center.

Related eMedicine Topics

Clinical Trials

National Guidelines Clearinghouse

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Keywords

gastroesophageal reflux disease, GERD, reflux, heartburn, esophagitis, gastritis, peptic ulcer disease, PUD, lower esophageal sphincter, LES, hiatal hernia, obesity, regurgitation, dysphagia, Barrett esophagus, adenocarcinoma, laryngitis, proton pump inhibitor, PPI, esophagogastroduodenoscopy, EGD, laparoscopic fundoplication, Nissen fundoplication

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Contributor Information and Disclosures

Author

Piero Marco Fisichella, MD, Assistant Professor of Surgery, Stritch School of Medicine, Loyola University; Director, Esophageal Motility Center, Loyola University Medical Center
Piero Marco Fisichella, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Surgery of the Alimentary Tract, and Society of American Gastrointestinal and Endoscopic Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Marco G Patti, MD, Professor of Surgery, Director, Center for Esophageal Diseases, University of Chicago Pritzker School of Medicine
Marco G Patti, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Surgeons, American Gastroenterological Association, American Medical Association, American Surgical Association, Association for Academic Surgery, Pan-Pacific Surgical Association, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, Southwestern Surgical Congress, and Western Surgical Association
Disclosure: Nothing to disclose.

Medical Editor

John Gunn Lee, MD, Director of Pancreaticobiliary Service, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of California at Irvine School of Medicine
John Gunn Lee, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Noel Williams, MD, Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada
Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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