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Key Clinical Updates in Gastroesophageal Reflux Disease
As an alternative to endoscopic screening, the 2022 American College of Gastroenterology guideline endorses a swallowable capsule-sponge to obtain esophageal cytology for the assessment of biomarkers that predict the presence of Barrett esophagus.
Shaheen NJ et al. Am J Gastroenterol. [PMID: 35354777]
Alginate-containing formulations may be superior to other antacids in reducing postprandial symptoms.
For patients with refractory symptoms without clear evidence of reflux disease, it is recommended to perform ambulatory esophageal pH testing after stopping PPI therapy for 96 hours to determine whether significant esophageal acid reflux is present and if the symptoms are associated with reflux episodes.
Yadlapati R et al; CGIT GERD Consensus Conference Participants. Clin Gastroenterol Hepatol. [PMID: 35123084]
Katz PO et al. Am J Gastroenterol. [PMID: 34807007]
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ESSENTIALS OF DIAGNOSIS
Heartburn; may be exacerbated by meals, bending, or recumbency.
Typical uncomplicated cases do not require diagnostic studies.
Endoscopy demonstrates abnormalities in one-third of patients.
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GENERAL CONSIDERATIONS
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GERD is a condition that develops when the reflux of stomach contents causes troublesome symptoms or complications. In a 2020 survey of US adults, 31% reported GERD symptoms within the prior week. The two most common symptoms are heartburn and regurgitation. However, other symptoms of GERD include dyspepsia, dysphagia, belching, chest pain, cough, and hoarseness. Although most patients have mild disease, esophageal mucosal damage (reflux esophagitis) develops in up to one-third and more serious complications develop in a few others. Several factors may contribute to GERD.
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A. Dysfunction of the Gastroesophageal Junction
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The antireflux barrier at the gastroesophageal junction (eFigure 17–4) depends on LES pressure, the intra-abdominal location of the sphincter (resulting in a “flap valve” caused by angulation of the esophageal-gastric junction), and the extrinsic compression of the sphincter by the crural diaphragm. In most patients with GERD, baseline LES pressures are normal (10–35 mm Hg). A subset of patients with GERD have an incompetent (less than 10 mm Hg) LES that results in increased acid reflux, especially when supine or when intra-abdominal pressures are increased by lifting or bending. A hypotensive sphincter is present in up to 50% of patients with severe erosive GERD.
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Hiatal hernias are found in one-fourth of patients with nonerosive GERD, three-fourths of patients with severe erosive esophagitis, and over 90% of patients with Barrett esophagus. They are caused by movement of the LES above the diaphragm, resulting in dysfunction of the gastroesophageal junction reflux barrier. Hiatal hernias are common and may cause no symptoms (eFigure 17–5); however, in patients with gastroesophageal reflux, they are associated with higher amounts of acid reflux and delayed esophageal acid ...