Gastroesophageal Reflux Disease 

  • Author: Marco G Patti, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Aug 19, 2011
 

Background

Gastroesophageal reflux is a normal physiologic phenomenon experienced intermittently by most people, particularly after a meal. Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing symptoms with or without associated esophageal mucosal injury (ie, esophagitis).

A study by Richter and a Gallup Organization National Survey estimated that 25-40% of healthy adult Americans experience symptomatic GERD, most commonly manifested clinically by pyrosis (heartburn), at least once a month. Furthermore, approximately 7-10% of the adult population in the United States experiences such symptoms on a daily basis.[1, 2] (See Epidemiology.)

In most persons with GERD, endogenous defense mechanisms either limit the amount of noxious material that is introduced into the esophagus or rapidly clear the material from the esophagus so that symptoms and esophageal mucosal irritation are minimized. Examples of the defense mechanisms include actions of the lower esophageal sphincter (LES) and normal esophageal motility. When the defense mechanisms are defective or become overwhelmed so that the esophagus is bathed in acid or bile and acid-containing fluid for prolonged periods, GERD can be said to exist. (See Pathophysiology.)

Patients with GERD can exhibit various symptoms, both typical and atypical. Typical symptoms include heartburn, regurgitation, and dysphagia. Atypical symptoms include noncardiac chest pain, asthma, pneumonia, hoarseness, and aspiration.[3, 4] Patients typically have numerous daily episodes of symptomatic reflux, including pyrosis, water brash or sour taste in the mouth, nighttime coughing or aspiration, pneumonia or pneumonitis, bronchospasm, and laryngitis and voice changes, including hoarseness. In addition, objective evidence of esophageal damage can be seen on esophagogastroduodenoscopy as manifested by the incremental grades of esophagitis discussed below. (See Clinical Presentation.)

Laboratory tests are seldom useful in establishing a diagnosis of GERD. Esophageal manometry and pH monitoring are considered essential before performing an antireflux operation. Endoscopy reveals that 50% of patients do not have esophagitis. The only way to determine if abnormal reflux is present and if symptoms are actually caused by gastroesophageal reflux is through pH monitoring. Achalasia can present with heartburn. Only esophageal manometry and pH monitoring can be used to distinguish achalasia from GERD. Therapy is completely different for the 2 conditions. (See Workup.)

GERD is treated via a stepwise approach that is based on lifestyle modification and control of gastric secretion by means of medical or surgical treatment.[5, 6, 7, 8, 9, 10] (See Treatment Strategies and Management.)

GI disorders are some of the most frequent complaints during pregnancy, and gastroesophageal reflux is among these complaints. Some women have certain GI disorders that are unique to pregnancy, and others have chronic GI disorders that require special consideration during pregnancy. Understanding the presentation and prevalence of various GI disorders is necessary in order to optimize care for these patients.

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Anatomy

The anatomy of the esophagus, stomach, and esophagogastric junction is critical in the understanding of the pathogenesis of reflux.

The esophagus is divided into 3 parts: cervical, thoracic, and abdominal. The body of the esophagus is made up of inner circular and outer longitudinal muscular layers. The proximal third of the esophagus is striated muscle, which transitions to smooth muscle in the distal two thirds. The proximal esophagus contains the upper esophageal sphincter (UES), which comprises the cricopharyngeus and thyropharyngeus muscles.

The distal thoracic esophagus is located to the left side of midline. As the thoracic esophagus enters the abdomen through the esophageal hiatus in the diaphragm, it becomes the abdominal esophagus. The hiatus is formed by the right crus of the diaphragm, which forms a sling around the esophagus with the right and left pillars, so that the esophagus narrows when the diaphragm contracts.[11, 12, 13] The actual contribution the diaphragm provides in maintaining an adequate length of intra-abdominal esophagus is not clearly understood; however, careful identification and approximation of the pillars during surgical treatment is crucial for preventing recurrence of reflux disease.

At this level, the phrenoesophageal ligament or membrane (see the image below), which is the reflection of the subdiaphragmatic fascia onto the transversalis fascia of the anterior abdominal wall, also encircles the esophagus. A prominent fat pad located on the anterior surface of the esophagus marks the lower limit of the phrenoesophageal ligament, which corresponds to the esophagogastric junction. This junction lies in the abdomen and forms the angle of His. The acute angle and the length of abdominal esophagus both contribute to the normal closure of the esophagus when intragastric and intra-abdominal pressures are high.

Relationship of the phrenoesophageal ligament to tRelationship of the phrenoesophageal ligament to the diaphragm and esophagus.

The lower esophageal sphincter—or, more accurately, the distal esophageal high-pressure zone (HPZ)—is the distal most segment of the esophagus (3-5 cm in adults) and can be anywhere from 2-5 cm in length. Maintenance of an adequate intra-abdominal HPZ is crucial in preventing GERD. This HPZ does not correspond to any visible anatomic structure. It is a zone created by a complex architecture of smooth muscle fibers, and it is typically identified during manometry.

Usually, GERD is caused by a malfunction of one or more of these anatomic features. Proper surgical treatment requires complete preoperative and intraoperative evaluation and correction of all defective features.

Blood supply of esophagus and stomach

The blood supply of the esophagus is segmental (see the image below). The inferior thyroid artery supplies the cervical esophagus. Branches of the bronchial arteries and branches directly off of the aorta supply the proximal and distal thoracic esophagus, respectively. Finally, branches of the left gastric and inferior phrenic artery supply the abdominal esophagus. A relatively constant branch connects the left gastric and inferior phrenic arteries, called the Belsey artery.

Arterial blood supply and lymphatic drainage of thArterial blood supply and lymphatic drainage of the esophagus.

The blood supply of the stomach is rich, with overlap among the vessels. The lesser curve is supplied by the left and right gastric arteries, branches of the celiac trunk and proper hepatic artery, respectively. The greater curve is supplied by the right gastroepiploic artery arising from the gastroduodenal artery and the left gastroepiploic artery and the short gastric arteries originating from the splenic artery. This excellent collateral blood supply of the stomach allows the surgeon to ligate much of the arterial supply (ie, the short gastric arteries during fundoplication) without risk of ischemia (see the image above).

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Pathophysiology

Schematically, the esophagus, lower esophageal sphincter (LES), and stomach can be envisioned as a simple plumbing circuit as described by Stein and coworkers.[14] The esophagus functions as an antegrade pump, the LES as a valve, and the stomach as a reservoir. The abnormalities that contribute to GERD can stem from any component of the system. Poor esophageal motility decreases clearance of acidic material. A dysfunctional LES allows reflux of large amounts of gastric juice. Delayed gastric emptying can increase volume and pressure in the reservoir until the valve mechanism is defeated, leading to GERD. From a medical or surgical standpoint, it is extremely important to identify which of these components is defective so that effective therapy can be applied.

Esophageal defense mechanisms

Esophageal defense mechanisms can be broken down into 2 categories (ie, esophageal clearance and mucosal resistance). Proper esophageal clearance is an extremely important factor in preventing mucosal injury. Esophageal clearance must be able to neutralize the acid refluxed through the lower esophageal sphincter. (Mechanical clearance is achieved with esophageal peristalsis; chemical clearance is achieved with saliva.) Normal clearance limits the amount of time the esophagus is exposed to refluxed acid or bile and gastric acid mixtures. Abnormal peristalsis can cause inefficient and delayed acid clearance.

Whether peristaltic dysfunction is secondary to esophageal exposure to acids or a primary defect is not understood clearly. In a review by Kahrilas et al, peristaltic dysfunction was progressively more common in patients with greater degrees of esophagitis.[15] Abnormal peristalsis was identified in 25% of patients with mild esophagitis and 48% of patients with severe esophagitis.

Buttar and associates described the importance of esophageal mucosal resistance as a protective mechanism.[16] They classified the factors into pre-epithelial, epithelial, and postepithelial defenses. When the defenses fail, esophagitis and other complications of reflux disease arise.

Dysfunction of the lower esophageal sphincter

The lower esophageal sphincter (LES) is defined by manometry as a zone of elevated intraluminal pressure at the esophagogastric junction. For proper LES function, this junction must be located in the abdomen so that the diaphragmatic crura can assist the action of the LES, thus functioning as an extrinsic sphincter. In addition, the LES must have a normal length and pressure and a normal number of episodes of transient relaxation (relaxation in the absence of swallowing).

LES dysfunction occurs via one of several mechanisms: transient relaxation of the LES (most common mechanism), permanent LES relaxation, and transient increase of intra-abdominal pressure that overcomes the LES pressure.

Delayed gastric emptying

The postulated mechanism by which delayed gastric emptying may cause GERD is an increase in gastric contents resulting in increased intragastric pressure and, ultimately, increased pressure against the lower esophageal sphincter. This pressure eventually defeats the LES and leads to reflux. However, objective studies have produced conflicting data regarding the role of delayed gastric emptying in the pathogenesis of GERD.

Hiatal hernia

When discussing mechanisms for GERD, the issue of hiatal hernia must be addressed. Hiatal hernias can be encountered frequently in patients with reflux disease; however, it has been well proven that not all patients with hiatal hernias have symptomatic reflux.

Buttar and coworkers state that a hiatal hernia may contribute to reflux via a variety of mechanisms.[16] (see image below). The lower esophageal sphincter may migrate proximally into the chest and lose its abdominal high-pressure zone (HPZ), or the length of the HPZ may decrease. The diaphragmatic hiatus may be widened by a large hernia, which impairs the ability of the crura to function as an external sphincter. Finally, gastric contents may be trapped in the hernial sac and reflux proximally into the esophagus during relaxation of the LES. Reduction of the hernias and crural closure is key to restoring an adequate intra-abdominal length of esophagus and recreating the HPZ.

Barium swallow indicating hiatal hernia. Barium swallow indicating hiatal hernia. Hiatal hernia. Hiatal hernia.

Obesity as contributing factor

Some studies have shown that GERD is highly prevalent in patients who are morbidly obese and that a high body mass index (BMI) is a risk factor for the development of this condition.[17, 18, 19, 20, 21, 22] The hypothesis that obesity increases esophageal acid exposure is supported by the documentation of a dose-response relationship between increased BMI and increased prevalence of GERD and its complications. Therefore, the pathophysiology of GERD in patients who are morbidly obese might differ from that of patients who are not obese. The therapeutic implication of such a premise is that the correction of reflux in patients who are morbidly obese might be better achieved with a procedure that first controls obesity.

The mechanism by which a high BMI increases esophageal acid exposure is not completely understood. Increased intragastric pressure and gastroesophageal pressure gradient, incompetence of the lower esophageal sphincter (LES), and increased frequency of transient LES relaxations may all play a role in the pathophysiology of GERD in patients who are morbidly obese.

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Etiology

Excessive retrograde movement of acid-containing gastric secretions or bile and acid-containing secretions from the duodenum and stomach into the esophagus is the etiologic effector of GERD. Reflux of these secretions to some degree into the esophagus is prevalent in the United States. From a therapeutic point of view, informing patients that gastric refluxate is made up not only of acid but also of duodenal contents (eg, bile, pancreatic secretions) is important.

A functional (frequent transient LES relaxation) or mechanical (hypotensive LES) problem of the LES is the most common cause of GERD. Transient relaxation of the LES can be caused by foods (coffee, alcohol, chocolate, fatty meals), medications (beta-agonists,[23] nitrates, calcium channel blockers, anticholinergics), hormones (eg, progesterone), and nicotine.

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Epidemiology

Western dietary habits have made GERD a common disease. Richter and associates reported that 25-40% of Americans experience symptomatic GERD at some point.[18] Approximately 7-10% of Americans experience symptoms of GERD on a daily basis. Because many individuals control symptoms with over-the-counter (OTC) medications and without consulting a medical professional, the actual number of individuals with GERD is probably higher.

No sexual predilection exists: GERD is as common in men as in women. However, the male-to-female incidence ratio for esophagitis is 2:1-3:1. The male-to-female incidence ratio for Barrett esophagus is 10:1. White males are at a greater risk for Barrett esophagus and adenocarcinoma than other populations.

GERD occurs in all age groups. The prevalence of GERD increases in people older than 40 years.

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Prognosis

Most patients with GERD do well with medications, although a relapse after cessation of medical therapy is common and indicates the need for long-term maintenance therapy.

Identifying the subgroup of patients who may develop the most serious complications of GERD and treating them aggressively is important. Surgery at an early stage is most likely indicated in these patients. After a laparoscopic Nissen fundoplication, symptoms resolve in approximately 92% of patients.

Most cases of gastroesophageal reflux in infants and very young children are benign and respond to conservative nonpharmacologic treatment (developmental disabilities represent an important diagnostic exception); 80% resolve by age 18 months (55% resolve by age 10 mo). Some patients require a "step-up" to acid-reducing medications, and only a very small minority require surgery. Because symptomatic gastroesophageal reflux after age 18 months likely represents a chronic condition, long-term risks are increased. For patients whose gastroesophageal reflux persists into later childhood, long-term therapy with antisecretory agents is often required.

In refractory cases or when complications related to reflux disease are identified (eg, stricture, aspiration, airway disease, Barrett esophagus), surgical treatment (fundoplication) is typically necessary. The prognosis with surgery is considered excellent. The surgical morbidity and mortality is higher in patients who have complex medical problems in addition to gastroesophageal reflux.

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Patient Education

For excellent patient education resources, visit eMedicine's Heartburn/GERD/Reflux Center. Also, see eMedicine's patient education articles Reflux Disease (GERD), Gastroesophageal Reflux Disease (GERD) FAQs, and Understanding Heartburn/GERD Medications.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

Showkat Bashir, MD  Assistant Professor, Department of Medicine, Division of Gastroenterology, George Washington University, Washington, DC

Showkat Bashir, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Medical Association

Disclosure: Nothing to disclose.

Jack Bragg, DO  Associate Professor, Department of Clinical Medicine, University of Missouri School of Medicine

Jack Bragg, DO is a member of the following medical societies: American College of Osteopathic Internists and American Osteopathic Association

Disclosure: Nothing to disclose.

Abhishek Choudhary, MD  Resident Physician, Department of Internal Medicine, University Hospital of Missouri-Columbia

Abhishek Choudhary, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Abraham H Dachman, MD, FACR  Professor, Department of Radiology, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine; Director of CT, Department of Radiology, The University of Chicago Hospitals

Abraham H Dachman, MD, FACR is a member of the following medical societies: Radiological Society of North America

Disclosure: iCAD, Inc. Consulting fee Consulting; GE Healtcare, Inc. Honoraria Speaking and teaching

Gautam Dehadrai, MD  Department Chair, Section Chief, Department of Interventional Radiology, Norman Regional Hospital

Gautam Dehadrai, MD is a member of the following medical societies: American College of Radiology, Medical Council of India, and Radiological Society of North America

Disclosure: Nothing to disclose.

Fernando AM Herbella, MD, PhD, TCBC  Affiliate Professor, Attending Surgeon in Gastrointestinal Surgery, Esophagus and Stomach Division, Department of Surgery, Federal University of Sao Paulo, Brazil; Private Practice; Medical Examiner, Sao Paulo's Medical Examiner's Office Headquarters, Brazil

Fernando AM Herbella, MD, PhD, TCBC is a member of the following medical societies: Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Eugene C Lin, MD  Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine

Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine

Disclosure: Nothing to disclose.

Mohamed Othman, MD  Resident Physician, Department of Internal Medicine, University of New Mexico School of Medicine

Disclosure: Nothing to disclose.

Praveen K Roy, MD, AGAF  Gastroenterologist, Ochsner Clinic Foundation; Adjunct Associate Research Scientist, Lovelace Respiratory Research Institute; Editor-in-Chief, The Internet Journal of Gasteroenterology; Editorial Board, Signal Transduction Insights; Editorial Board, The Internet Journal of Epidemiology; Editorial Board, Gastrointestinal Endoscopy Review Letter

Praveen K Roy, MD, AGAF is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Michael AJ Sawyer, MD  Consulting Staff, Department of Surgery, Southwestern Medical Center; Consulting Staff, Department of Surgery, Comanche County Memorial Hospital; Consulting Staff, Great Plains Surgical Clinic, Inc

Michael AJ Sawyer, MD is a member of the following medical societies: American College of Surgeons, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, and Society of Laparoendoscopic Surgeons

Disclosure: Nothing to disclose.

Homayoun Shojamanesh, MD  Former Fellow, Digestive Diseases Branch, National Institutes of Health

Homayoun Shojamanesh, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Manish K Varma, MD  Chief of Interventional Radiology, Department of Radiology, Tripler Army Medical Center

Manish K Varma, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, and Radiological Society of North America

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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

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.

David Chelmow, MD  Leo J Dunn Distinguished Professor and Chair, Department of Obstetrics and Gynecology, Virginia Commonwealth University Medical Center

David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical Decision Making

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

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 & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Piero Marco Fisichella, MD and Thomas F Murphy, MD, to the development and writing of the source articles.

References

  1. Gallup Organization. Heartburn Across America: A Gallup Organization National Survey. Princeton, NJ: Gallup Organization.; 1988.

  2. Richter JE. Surgery for reflux disease: reflections of a gastroenterologist. N Engl J Med. Mar 19 1992;326(12):825-7. [Medline].

  3. Chen CL, Robert JJ, Orr WC. Sleep symptoms and gastroesophageal reflux. J Clin Gastroenterol. Jan 2008;42(1):13-7. [Medline].

  4. Sveen S. Symptom check: is it GERD?. J Contin Educ Nurs. Mar 2009;40(3):103-4. [Medline].

  5. Giannini EG, Zentilin P, Dulbecco P, Vigneri S, Scarlata P, Savarino V. Management strategy for patients with gastroesophageal reflux disease: a comparison between empirical treatment with esomeprazole and endoscopy-oriented treatment. Am J Gastroenterol. Feb 2008;103(2):267-75. [Medline].

  6. Katz PO. Medical therapy for gastroesophageal reflux disease in 2007. Rev Gastroenterol Disord. Fall 2007;7(4):193-203. [Medline].

  7. Fass R, Sifrim D. Management of heartburn not responding to proton pump inhibitors. Gut. Feb 2009;58(2):295-309. [Medline].

  8. Fass R. Proton pump inhibitor failure--what are the therapeutic options?. Am J Gastroenterol. Mar 2009;104 Suppl 2:S33-8. [Medline].

  9. Heidelbaugh JJ, Goldberg KL, Inadomi JM. Overutilization of proton pump inhibitors: a review of cost-effectiveness and risk [corrected]. Am J Gastroenterol. Mar 2009;104 Suppl 2:S27-32. [Medline].

  10. Dial MS. Proton pump inhibitor use and enteric infections. Am J Gastroenterol. Mar 2009;104 Suppl 2:S10-6. [Medline].

  11. Mittal RK, Rochester DF, McCallum RW. Sphincteric action of the diaphragm during a relaxed lower esophageal sphincter in humans. Am J Physiol. Jan 1989;256(1 Pt 1):G139-44. [Medline].

  12. Mittal RK, McCallum RW. Characteristics of transient lower esophageal sphincter relaxation in humans. Am J Physiol. May 1987;252(5 Pt 1):G636-41. [Medline].

  13. Mittal RK, Rochester DF, McCallum RW. Effect of the diaphragmatic contraction on lower oesophageal sphincter pressure in man. Gut. Dec 1987;28(12):1564-8. [Medline]. [Full Text].

  14. Stein HJ, DeMeester TR. Outpatient physiologic testing and surgical management of foregut motility disorders. Curr Probl Surg. Jul 1992;29(7):413-555. [Medline].

  15. Kahrilas PJ, Dodds WJ, Hogan WJ, Kern M, Arndorfer RC, Reece A. Esophageal peristaltic dysfunction in peptic esophagitis. Gastroenterology. Oct 1986;91(4):897-904. [Medline].

  16. Buttar NS, Falk GW. Pathogenesis of gastroesophageal reflux and Barrett esophagus. Mayo Clin Proc. Feb 2001;76(2):226-34. [Medline].

  17. [Best Evidence] Hampel H, Abraham NS, El-Serag HB. Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med. Aug 2 2005;143(3):199-211. [Medline]. [Full Text].

  18. Herbella FA, Sweet MP, Tedesco P, Nipomnick I, Patti MG. Gastroesophageal reflux disease and obesity. Pathophysiology and implications for treatment. J Gastrointest Surg. Mar 2007;11(3):286-90. [Medline].

  19. Merrouche M, Sabaté JM, Jouet P, Harnois F, Scaringi S, Coffin B, et al. Gastro-esophageal reflux and esophageal motility disorders in morbidly obese patients before and after bariatric surgery. Obes Surg. Jul 2007;17(7):894-900. [Medline].

  20. Murray L, Johnston B, Lane A, Harvey I, Donovan J, Nair P, et al. Relationship between body mass and gastro-oesophageal reflux symptoms: The Bristol Helicobacter Project. Int J Epidemiol. Aug 2003;32(4):645-50. [Medline]. [Full Text].

  21. Pandolfino JE, El-Serag HB, Zhang Q, Shah N, Ghosh SK, Kahrilas PJ. Obesity: a challenge to esophagogastric junction integrity. Gastroenterology. Mar 2006;130(3):639-49. [Medline].

  22. El-Serag HB, Graham DY, Satia JA, Rabeneck L. Obesity is an independent risk factor for GERD symptoms and erosive esophagitis. Am J Gastroenterol. Jun 2005;100(6):1243-50. [Medline].

  23. Tutuian R,. Adverse effects of drugs on the esophagus. Best Pract Res Clin Gastroenterol. Apr 2010;24(2):91-7. [Medline].

  24. DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. Jan 2005;100(1):190-200. [Medline].

  25. Bhatia J, Parish A. GERD or not GERD: the fussy infant. J Perinatol. May 2009;29 Suppl 2:S7-11. [Medline].

  26. Levine MS, Rubesin SE. Diseases of the esophagus: diagnosis with esophagography. Radiology. Nov 2005;237(2):414-27. [Medline].

  27. Yang YX, Lewis JD, Epstein S, Metz DC. Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. Dec 27 2006;296(24):2947-53. [Medline]. [Full Text].

  28. Agency for Healthcare Research and Quality. Comparative Effectiveness of Management Strategies for Gastroesophageal Reflux Disease - Executive Summary. AHRQ pub. no. 06-EHC003-1. December 2005. Available at http://effectivehealthcare.ahrq.gov/healthInfo.cfm?infotype=rr&ProcessID=1&DocID=42. Accessed September 27, 2010.

  29. Galmiche JP, Hatlebakk J, Attwood S, et al. Laparoscopic antireflux surgery vs esomeprazole treatment for chronic GERD: the LOTUS randomized clinical trial. JAMA. May 18 2011;305(19):1969-77. [Medline].

  30. Boerema I. Hiatus hernia: repair by right-sided, subhepatic, anterior gastropexy. Surgery. Jun 1969;65(6):884-93. [Medline].

  31. Allison PR. Hiatus hernia: (a 20-year retrospective survey). Ann Surg. Sep 1973;178(3):273-6. [Medline]. [Full Text].

  32. Varshney S, Kelly JJ, Branagan G, Somers SS, Kelly JM. Angelchik prosthesis revisited. World J Surg. Jan 2002;26(1):129-33. [Medline].

  33. Nissen R, Rossetti M, Siewert R. [20 years in the management of reflux disease using fundoplication]. Chirurg. Oct 1977;48(10):634-9. [Medline].

  34. Kazerooni NL, VanCamp J, Hirschl RB, Drongowski RA, Coran AG. Fundoplication in 160 children under 2 years of age. J Pediatr Surg. May 1994;29(5):677-81. [Medline].

  35. Dallemagne B, Weerts JM, Jehaes C, Markiewicz S, Lombard R. Laparoscopic Nissen fundoplication: preliminary report. Surg Laparosc Endosc. Sep 1991;1(3):138-43. [Medline].

  36. Nilsson G, Larsson S, Johnsson F. Randomized clinical trial of laparoscopic versus open fundoplication: blind evaluation of recovery and discharge period. Br J Surg. Jul 2000;87(7):873-8. [Medline].

  37. Wenner J, Nilsson G, Oberg S, Melin T, Larsson S, Johnsson F. Short-term outcome after laparoscopic and open 360 degrees fundoplication. A prospective randomized trial. Surg Endosc. Oct 2001;15(10):1124-8. [Medline].

  38. Somme S, Rodriguez JA, Kirsch DG, Liu DC. Laparoscopic versus open fundoplication in infants. Surg Endosc. Jan 2002;16(1):54-6. [Medline].

  39. Rangel SJ, Henry MC, Brindle M, Moss RL. Small evidence for small incisions: pediatric laparoscopy and the need for more rigorous evaluation of novel surgical therapies. J Pediatr Surg. Oct 2003;38(10):1429-33. [Medline].

  40. Rothenberg SS. The first decade's experience with laparoscopic Nissen fundoplication in infants and children. J Pediatr Surg. Jan 2005;40(1):142-6; discussion 147. [Medline].

  41. Lundell L, Miettinen P, Myrvold HE, Pedersen SA, Liedman B, Hatlebakk JG, et al. Continued (5-year) followup of a randomized clinical study comparing antireflux surgery and omeprazole in gastroesophageal reflux disease. J Am Coll Surg. Feb 2001;192(2):172-9; discussion 179-81. [Medline].

  42. Spechler SJ. Epidemiology and natural history of gastro-oesophageal reflux disease. Digestion. 1992;51 Suppl 1:24-9. [Medline].

  43. Anvari M, Allen C, Marshall J, Armstrong D, Goeree R, Ungar W, et al. A randomized controlled trial of laparoscopic nissen fundoplication versus proton pump inhibitors for treatment of patients with chronic gastroesophageal reflux disease: One-year follow-up. Surg Innov. Dec 2006;13(4):238-49. [Medline].

  44. [Best Evidence] Grant AM, Wileman SM, Ramsay CR, Mowat NA, Krukowski ZH, Heading RC, et al. Minimal access surgery compared with medical management for chronic gastro-oesophageal reflux disease: UK collaborative randomised trial. BMJ. Dec 15 2008;337:a2664. [Medline]. [Full Text].

  45. El-Serag HB. Time trends of gastroesophageal reflux disease: a systematic review. Clin Gastroenterol Hepatol. Jan 2007;5(1):17-26. [Medline].

  46. Mattioli S, Lugaresi ML, Di Simone MP, D'Ovidio F, Pilotti V, Bassi F, et al. The surgical treatment of the intrathoracic migration of the gastro-oesophageal junction and of short oesophagus in gastro-oesophageal reflux disease. Eur J Cardiothorac Surg. Jun 2004;25(6):1079-88. [Medline].

  47. Scheffer RC, Samsom M, Haverkamp A, Oors J, Hebbard GS, Gooszen HG. Impaired bolus transit across the esophagogastric junction in postfundoplication dysphagia. Am J Gastroenterol. Aug 2005;100(8):1677-84. [Medline].

 
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Relationship of the phrenoesophageal ligament to the diaphragm and esophagus.
Arterial blood supply and lymphatic drainage of the esophagus.
Barium swallow indicating hiatal hernia.
Ambulatory pH monitoring indicating episodes of reflux correlating with the heartburn experienced by the patient.
Peptic esophagitis. A rapid urease test (RUT) is performed on the esophageal biopsy sample. The result is positive for esophagitis.
Reflux esophagitis is demonstrated on barium esophagram.
Esophagogastroduodenoscopy indicating Barrett esophagus.
Gastroesophageal reflux disease (GERD)/Barrett esophagus/adenocarcinoma sequence.
Endoscopy demonstrating intraluminal esophageal cancer.
The image is a representation of concomitant intraesophageal pH and esophageal electrical impedance measurements. The vertical solid arrow indicates commencement of a nonacid gastroesophageal reflux (GER) episode (diagonal arrow). The vertical dashed arrow indicates the onset of a normal swallow.
Nissen fundoplication.
Laparoscopic Nissen fundoplication.
Hiatal hernia.
 
 
 
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