About this course:
This course reviews the epidemiology, pathophysiology, and risk factors for gastroesophageal reflux disease (GERD). It also covers the clinical manifestations, diagnosis and evaluation, and the medical and surgical management strategies for GERD.
This course reviews the epidemiology, pathophysiology, and risk factors for gastroesophageal reflux disease (GERD). It also covers the clinical manifestations, diagnosis and evaluation, and the medical and surgical management strategies for GERD.
After this activity, learners will be prepared to:
review the epidemiology of and risk factors for GERD
describe the pathophysiology and clinical manifestations associated with GERD
describe the evidence-based guidelines for the diagnosis and evaluation of GERD
discuss various strategies for the medical and surgical management strategies for GERD
Gastroesophageal reflux (GER) is characterized by the regurgitation of stomach contents back into the esophagus. Most people experience infrequent episodes of GER that can be asymptomatic or mildly symptomatic (i.e., indigestion), usually after meals. GER is commonly referred to as acid indigestion, heartburn, reflux, acid reflux, and acid regurgitation. Gastroesophageal reflux disease (GERD) is a more severe, chronic condition characterized by repeated, frequent (i.e., at least 2 episodes of dyspepsia per week), and symptomatic episodes of GERD can lead to complications over time. GERD can be classified as either non-erosive reflux disease or erosive esophagitis (EE) based on the appearance of the esophageal mucosa on an upper endoscopy. Non-erosive esophagitis consists of GERD symptoms without visible esophageal mucosal injury, while EE consists of visible breaks in the distal esophageal mucosa. GERD is one of the most commonly diagnosed digestive disorders in the US, with an estimated prevalence of 20%. However, the true prevalence of GERD could be much higher since many people treat symptoms with over-the-counter (OTC) medications without seeking medical care. Studies have shown a genetic risk factor, with a 40% heritability for GERD. In addition, GERD is more prevalent in men, people over 50, smokers, non-steroidal anti-inflammatory drug (NSAID) users, pregnant women, infants, children, and obese individuals. White people have more severe manifestations and complications than other ethnicities. Females are diagnosed with non-erosive reflux disease (NERD) at a higher frequency, while males are more often diagnosed with EE (Antunes & Aleem, 2021; Eusebi et al., 2018; Kahrilas, 2022; National Institute of Diabetes and Digestive and Kidney Diseases [NIDDK], 2020a).
Anatomy and Physiology of the GI System
The digestive system comprises the GI tract, liver, pancreas, and gallbladder (i.e., solid organs). The GI tract consists of hollow organs (i.e., the mouth, esophagus, stomach, small intestine, large intestine, and anus). The hollow organs are joined in a long, twisting tube from the mouth to the anus. Abnormalities in the GI tract are numerous and represent various pathologies, including bleeding, perforation, obstruction, infection, and malignancy. Like other organ systems, the GI tract is subject to circulatory disturbances, disruptions of nervous system control, and aging. In addition, many extrinsic factors can interfere with normal GI function. For example, stress and anxiety can lead to GER, anorexia, constipation, or diarrhea. In addition, inadequate or abrupt changes in dietary intake can significantly impact the GI tract. Therefore, when people present with GI symptoms, HCPs should assess for physical and mental contributing factors (Hinkle & Cheever, 2018; NIDDK, 2017).
Anatomy of the GI System
The GI tract is up to 30 feet long in adults. The esophagus is a hollow muscular tube that is approximately 10 inches long. It is located in the mediastinum, anterior to the spine, and posterior to the trachea and heart. The esophagus passes through the diaphragmatic hiatus, an opening in the diaphragm. The remaining portion of the GI tract is located in the peritoneal cavity. The stomach is a hollow muscular organ that stores food, secretes digestive fluids, and propels partially digested food (i.e., chyme) into the small intestine. It is located in the left upper portion of the abdomen, under the left lobe of the liver and the diaphragm. The small intestine is the longest section of the GI tract, accounting for two-thirds (20-25 feet) of the total length. The small intestine has three parts that fold back and forth: the duodenum, jejunum, and ileum. The ileum terminates at the ileocecal valve, which controls the flow of digested material from the ileum into the cecal portion of the large intestine and prevents the reflux of bacteria into the small intestine (Hinkle & Cheever, 2018; NIDDK, 2017).
The large intestine consists of an ascendi
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Physiology of the GI System
The digestive system plays an important role in providing nutrients to the cells in the body for energy, growth, and repair. These nutrients are derived from the intake of foods that contain proteins, fats, carbohydrates, vitamins, and minerals. The primary functions of the GI tract include digestion, absorption, and elimination. First, digestion breaks food particles into their molecular form: proteins are broken into amino acids, fats into fatty acids and glycerol, and carbohydrates into simple sugars. Next, these small nutrient molecules are absorbed into the bloodstream. Finally, undigested, unabsorbed, and other waste products are eliminated. Various secretions within the GI tract aid in the digestion, absorption, and elimination of food and nutrients. The digestion process begins with chewing (i.e., mechanical breakdown of food into small particles) and swallowing (i.e., chemical breakdown by digestive enzymes). Swallowing is a voluntary act regulated by the medulla oblongata in the central nervous system (CNS). Next, the food is propelled into the upper esophagus, where esophageal peristalsis (i.e., rhythmic contractions of the smooth muscles of the esophagus) continues to push the food bolus toward the stomach. The lower esophageal sphincter (LES) relaxes during esophageal peristalsis, allowing the bolus to enter the stomach. The LES subsequently closes, preventing the reflux of stomach contents into the esophagus (Hinkle & Cheever, 2018; NIDDK, 2017).
After food enters the stomach, the stomach muscles mix the food. Highly acidic fluid is secreted to break food into absorbable components (chyme) and aid in destroying ingested bacteria. Hormones, neuroregulators, and local regulators found in gastric secretions control gastric motility and timing and quantity of secretion production. Peristaltic contractions in the stomach propel the chyme toward the pylorus. Food remains in the stomach for 30 minutes to several hours, depending on the volume, osmotic pressure, and chemical composition of the gastric contents. Similarly, the pyloric sphincter controls the rate at which chyme enters the small intestine to allow for efficient absorption (Hinkle & Cheever, 2018; NIDDK, 2017).
As the chyme enters the duodenum of the small intestine, enzymes (i.e., amylase, lipase, and bile) are excreted from the pancreas, liver, gallbladder, and glands in the intestinal wall. Pancreatic enzymes have an alkaline pH that neutralizes the acid from the stomach; this includes trypsin (which aids in the digestion of protein), amylase (which aids in the digestion of starch), and lipase (which aids in the digestion of fats). These secretions travel from the pancreatic duct, emptying into the common bile duct. Bile, which aids in emulsifying ingested fats, is stored in the gallbladder and secreted by the liver. The sphincter of Oddi controls the flow of bile, while hormones, neuroregulators, and local regulators in the intestinal secretions control GI motility and timing and quantity of secretion production. Two types of contractions occur regularly in the small intestine in response to chyme: segmentation contractions and intestinal peristalsis. Segmentation contractions produce a churning motion to move intestinal contents back and forth, whereas intestinal peristalsis propels the contents toward the colon. Chyme stays in the small intestine for 3 to 6 hours to allow for the continual absorption of nutrients and breakdown of proteins, fats, and carbohydrates. Small, fingerlike projections called villi line the entire intestine and allow for the absorption of nutrients. Nutrients are absorbed in specific locations along the small intestine and duodenum, and proteins, fats, carbohydrates, sodium, and chloride are absorbed in the jejunum. Finally, vitamin B12 and bile salts are absorbed in the ileum (Fish & Burns, 2021; Hinkle & Cheever, 2018).
As the residual intestinal waste reaches the terminal ileum (typically within 4 hours of eating), it slowly passes into the right colon through the ileocecal valve. The valve opens with each peristaltic wave of the small intestine, allowing some contents to move into the colon. Bacteria within the large intestine assist in the breakdown of undigested and unabsorbed proteins and bile salts. In addition, two colonic secretions (i.e., an electrolyte solution and mucus) are added to the residual material. The electrolyte solution, which is primarily bicarbonate, neutralizes the end products formed by the colonic bacterial action. The mucus provides adherence for the fecal mass and protects the colonic mucosa from the intestinal contents. Intestinal contents move slowly through the colon, aided by weak peristaltic action. This slow movement allows for the efficient reabsorption of water and electrolytes. Occasionally, stronger, Intermittent peristaltic waves propel the contents for considerable distances. This usually occurs when intestine-stimulating hormones are released or when another meal is eaten. Finally, the waste material reaches and distends the rectum. This process usually takes 12 hours, but as much as one-fourth of the waste material from a meal may be in the rectum after 3 days (Azzouz & Sharma, 2021; Hinkle & Cheever, 2018).
Pathophysiology of GERD
As described earlier, GER is the backward movement of gastric contents from the stomach to the esophagus, oral cavity, or lungs (see Figure 2). Usually, the gastric contents are neutralized by swallowed saliva and returned to the stomach by secondary peristaltic waves in the esophagus. The esophagus is a musculofibrous tube that transports food from the pharynx to the stomach via peristaltic movement and a small amount of mucous secretion. The LES regulates the flow of food from the esophagus to the stomach. There are intrinsic mechanisms (i.e., circular muscles of the distal esophagus) and extrinsic mechanisms (i.e., the portion of the diaphragm that surrounds the esophagus) to prevent reflux. Oblique muscles of the stomach are located below the LES. These muscles form a flap that contributes to the anti-reflux function of the internal sphincter. Relaxation of the LES is controlled by a brainstem reflex mediated by the vagus nerve. When relaxation of the LES occurs, gastric contents can travel back up the esophagus. Delayed gastric emptying can increase the risk of reflux due to increased gastric volume and pressure. Reflux that frequently occurs (i.e., more than twice a week) and is highly acidic (pH <4.0) makes esophageal mucosal injury likely to occur (Antunes & Aleem, 2021; Norris, 2020).
The pathophysiology of GERD is multifactorial and usually associated with transient relaxation of a weak or incompetent LES, the presence of a hiatal hernia, impaired esophageal mucosal defense against gastric refluxate, and defective esophageal peristalsis. In healthy individuals, the LES is a high-pressure zone that transiently relaxes during meals to allow food passage into the stomach. A weakened or incompetent LES allows reflux and decreases the clearance of refluxed acid. For people with GERD, transient LES relaxation occurs, not triggered by swallowing, resulting in higher intragastric pressure than LES pressure. The mechanism for increased LES transient relaxation is unknown but accounts for more than half of GERD symptoms. A hiatal hernia can increase the risk of GERD symptoms. Small hiatal hernias can be asymptomatic, while larger hernias are associated with a shorter and weaker LES, resulting in increased reflux episodes. Prolonged exposure to refluxate, consisting of acidic gastric contents (i.e., hydrochloric acid and pepsin) and alkaline duodenal contents (i.e., bile salts and pancreatic enzymes), can cause esophageal mucosal damage. Finally, impaired esophageal peristalsis can decrease gastric reflux clearance, resulting in mucosal damage (Antunes & Aleem, 2021; Norris, 2020).
Complications of GERD
Complications related to GERD can occur when symptoms are left untreated or when patients do not present with classic GERD symptoms. The most common complications are EE, esophageal strictures, and Barrett's esophagus. EE is characterized by erosions or ulcers in the esophageal mucosa, with the severity determined by the Los Angeles (LA) esophagitis classification system. Patients with EE can be asymptomatic or may present with worsening GERD symptoms. Common symptoms of EE include painful and difficult swallowing, chest pain, food impaction, and dyspepsia. If left undiagnosed or untreated, EE can lead to scarring and narrowing of the esophagus, tearing of the esophagus, or Barrett's esophagus. There are various types of esophagitis, including reflux esophagitis, eosinophilic esophagitis (EoE; allergy-causing agent or reflux), lymphocytic esophagitis (related to EoE or GERD), drug-induced esophagitis, and infectious esophagitis (i.e., bacterial, viral, or fungal infection; Antunes & Aleem, 2021).
An esophageal stricture is an abnormal narrowing or tightening of the esophagus that can limit or block the movement of food into the stomach. Esophageal strictures can be cancerous or benign. GERD is the most common cause of benign strictures, in which chronic acid irritation of the distal esophagus creates a stricture. Other causes include a hiatal hernia, dysphagia, and peptic ulcer disease (PUD). Barrett's esophagus is characterized by an alteration in the lining of the esophagus from chronic acid exposure in the distal esophagus. As a result, the distal esophageal mucosa, normally stratified squamous epithelium, is replaced by metaplastic columnar epithelium resembling the intestines. Barrett's esophagus affects approximately 5.6% of the US population and is more common in White males over 50 and those with a history of obesity and smoking. Nocturnal reflux, a hiatal hernia, and GERD presence for at least 5 to 10 years are also risk factors for Barrett's esophagus. Common symptoms can include dyspepsia, regurgitation, and difficulty swallowing. Barrett's esophagus increases the risk of esophageal cancer, making prompt diagnosis and treatment essential (Antunes & Aleem, 2021; Kahralis, 2022).
Risk Factors for GERD
Many risk factors can contribute to the development of GERD. In addition to some of the pathophysiologic risk factors described earlier, various medications, lifestyle choices, and other conditions can increase the risk of experiencing GER or GERD. For example, conditions that increase intraabdominal pressure, such as obesity or pregnancy, may lead to GERD symptoms. The rising rates of obesity in the US have contributed to the early onset of GERD, with a progressive incidence with increasing BMI. Research has shown that even a short-term weight gain leads to a 3- to 4-fold increase in the risk of developing GERD. In addition, conditions contributing to the impaired or weakened contraction of the LES include older age, certain foods, fluids, gastric distention, cigarette smoking or exposure to secondhand smoke, lying recumbent after meals, and various medications. Alcohol consumption and a gastric infection with Helicobacter pylori increase GERD risk. Finally, patients with a history of irritable bowel syndrome (IBS), Crohn's disease, obstructive airway disorders (e.g., asthma, chronic obstructive pulmonary disease [COPD], cystic fibrosis [CF]), angina, PUD, and connective tissue disorders (e.g., scleroderma) have an increased incidence of GERD (Antunes & Aleem, 2021; Argyrou et al., 2018; Hinkle & Cheever, 2018; NIDDK, 2020a, 2020c; Norris, 2020).
Certain medications and dietary supplements can irritate the lining of the esophagus or reduce the LES pressure, increasing acid reflux (Antunes & Aleem, 2021; Hinkle & Cheever, 2018; NIDDK, 2020c; Norris, 2020). Medications that can damage the esophageal or stomach mucosa by inhibiting cyclooxygenase (COX) enzymes and increasing gastric acid secretion include:
antibiotics (e.g., tetracycline, clindamycin [Cleocin])
bisphosphonates (e.g., alendronate [Fosamax], ibandronate [Boniva], risedronate [Actonel])
pain relievers (e.g., ibuprofen [Motrin], aspirin [Ecotrin]; Antunes & Aleem, 2021; Hinkle & Cheever, 2018; NIDDK, 2020c; Norris, 2020).
According to Mungan and Pinarbasi Simsek (2017), certain drugs affect esophagogastric motility, leading to increased esophageal exposure to acid reflux. Other medications can also reduce gastric emptying time and weaken LES pressure by relaxing smooth muscles. Anticholinergics alter peristaltic function, reduce LES pressure, reduce saliva, and decrease food clearance in the esophageal area so that acidic materials remain longer in the esophageal area (Mungan & Pinarbasi Simsek, 2017; NIDDK, 2020c). Medications that can alter the LES pressure and increase acid reflux include:
anticholinergics (e.g., oxybutynin [Ditropan XL])
tricyclic antidepressant (e.g., amitriptyline [Elavil], doxepin [Silenor])
calcium channel blockers (e.g., amlodipine [Norvasc], verapamil [Calan SR], diltiazem [Cardizem])
beta-blockers (e.g., atenolol [Tenormin], metoprolol [Lopressor], propranolol [Inderal])
HMG-CoA reductase inhibitors or statins (e.g., rosuvastatin [Crestor], atorvastatin [Lipitor], simvastatin [Zocor])
angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril [Zestril], enalapril [Vasotec])
narcotics (e.g., codeine [Colrex], hydrocodone [Vicodin], morphine [MS-IR])
benzodiazepines (e.g., diazepam [Valium]; Mungan & Pinarbasi Simsek, 2017; NIDDK, 2020c)
Finally, dietary choices can increase the risk of developing GER symptoms or GERD. Although the exact mechanisms for which foods cause symptoms can vary, the most common mechanism is decreased LES pressure allowing acid to regurgitate into the esophagus and delayed gastric emptying (Antunes & Aleem, 2021; Hinkle & Cheever, 2018; NIDDK, 2020c; Norris, 2020). Foods that can increase the risk of GERD include:
fatty or fried cuts of beef, pork, or lamb
full-fat dairy (e.g., butter, whole milk, sour cream, regular cheese)
cream sauces or salad dressings
desserts or snacks (e.g., ice cream or potato chips)
tomatoes, tomato sauce, salsa, and citrus fruit (e.g., oranges, grapefruit, lemons, pineapple, limes)
chocolate (i.e., contains methylxanthine that relaxes smooth muscles in the LES)
garlic, onions, and spicy foods
chili powder and pepper
mint (Antunes & Aleem, 2021; Hinkle & Cheever, 2018; NIDDK, 2020c; Norris, 2020)
GER may not always cause signs or symptoms. However, patients chiefly report dyspepsia (i.e., heartburn) and regurgitation when symptoms are present. Regurgitation describes the backward flow of stomach contents. Other common symptoms include chest pain (epigastric pain), dysphagia, nausea, a sour or bitter taste in the mouth, or a globus sensation (i.e., lump in the throat). Hoarseness, laryngitis, and respiratory symptoms such as chronic coughing or asthma symptoms, such as shortness of breath (SOB) and wheezing, may also be related to GERD. Patients with chronic GERD symptoms may have dental erosion from chronic acid exposure. With nighttime GERD, a patient may report sleep disruption or excessive salivation without the sour taste. Patients may describe nocturnal hypersalivation as being awakened due to coughing or choking from excessive salivation. Dyspepsia occurs more commonly after meals, especially if the patient eats and does not wait a few hours before retiring to bed. Patients may report a retrosternal burning sensation that radiates into the neck. In addition, patients may report taking baking soda or OTC antacids to improve the symptoms. Despite its regularity, HCPs should take GERD symptoms seriously when reported (Antunes & Aleem, 2021; Katz et al., 2022; NIDDK, 2020c).
A detailed health history and initial assessment will provide the foundation for HCPs to identify the presence of GERD. HCPs should assess medication history, including all herbals/supplements, OTC, and prescribed medications for potential causes of dyspepsia or GERD. Gastrointestinal questions prompt patients to report burning retrosternal pain after eating, excessive flatulence, bloating, eructation (belching), dysphagia, odynophagia (pain with swallowing), or other symptoms indicative of GERD. Odynophagia is less common and usually indicative of an esophageal ulcer. A respiratory assessment may indicate a chronic cough, worsening asthma symptoms, or hoarseness. The psychosocial assessment should evaluate the patient’s stress level, use of tobacco products, and alcohol intake. Family history should also be investigated during this assessment because GERD has a genetic component. GERD symptoms can be nonspecific and mimic other disorders. HCPs must consider other causes of chest pain, including cardiac and respiratory disease. The HCP should begin formulating a plan of care after completing the patient’s health history and initial assessment (Antunes & Aleem, 2021; Kahrilas, 2022; Katz et al., 2022; NIDDK, 2020c).
Typically, HCPs diagnose GERD based primarily on clinical presentation, as there is no gold standard diagnostic test for GERD. A presumptive diagnosis of GERD is made for most patients who present with dyspepsia and regurgitation. Additional diagnostic modalities, such as antisecretory therapy, endoscopy, radiographic studies, and pH monitoring, may be warranted (Antunes & Aleem, 2021; Kahrilas, 2022; Katz et al., 2022).
Proton Pump Inhibitor Trial
According to the 2022 American College of Gastroenterology (ACG) guidelines, for patients with classic GERD symptoms (dyspepsia and regurgitation), an initial 8-week trial of a prescribed proton pump inhibitor (PPI) trial once daily with meals and lifestyle modifications is recommended. A diagnosis of GERD can be made in patients with a positive response to a PPI trial. Diagnostic endoscopy is recommended for patients who do not see an improvement in symptoms in 8 weeks or whose condition worsens (Antunes & Aleem, 2021; Kahralis, 2022; Katz et al., 2022).
Diagnostic endoscopy is recommended for patients with one or more alarm symptoms or nonresponsive to a PPI trial. An endoscopy uses a thin, flexible tube equipped with a light and camera inserted into the oral airway while the patient is under procedural sedation (see Figure 3). Diagnostically, an endoscopy aids in identifying any damage to the tissues of the esophagus, stomach, and upper duodenum. An upper endoscopy is the most widely used test for evaluating the esophageal mucosa and ruling out complications of GERD (e.g., EE, Barrett's esophagus, esophageal stricture, and esophageal adenocarcinoma). During the endoscopy, a tissue sample can be obtained for biopsy to determine if adenocarcinoma, EoE, erosive or non-erosive disease, or Barrett’s esophagus is present. Esophageal biopsies have little value in diagnosing GERD but are required to establish EoE. Ideally, endoscopy with a diagnostic biopsy should be done 2 to 4 weeks after the discontinuation of a PPI (Antunes & Aleem, 2021; Kahralis, 2022; Katz et al., 2022).
Findings that indicate EE or Barrett's esophagus are specific to the diagnosis of GERD. The findings of Barrett's esophagus are diagnostic of GERD, and pH testing is not needed. For EE, the most widely used and validated scoring system is the LA criteria. The LA criteria grades EE severity based on the extent of mucosal abnormality, where a mucosal break refers to an area of slough adjacent to normal mucosa, with or without exudate (Kahralis, 2022; Katz et al., 2022).
Normal mucosa is most likely found during endoscopy for most patients with typical GERD symptoms. Since PPIs can effectively heal EE, a diagnosis of GERD should only be made if the patient has been off PPIs for 2 to 4 weeks. For patients with no GERD evidence on endoscopy, the ACG guidelines recommend that reflux monitoring be performed (Katz et al., 2022).
The Savary-Miller classification was historically the most widely used criteria for EE. However, the Savary-Miller classification has limitations due to the ambiguity of the grade IV classification. Modifications to the classification of grade IV include various subdivisions or a grade V classification for metaplasia. However, grades IV and V no longer have a consistent meaning with the various modifications (Kahralis, 2022).
Radiographic studies can help detect severe esophagitis, hiatal hernias, tumors, and esophageal strictures. However, these studies have limited value in diagnosing GERD. A barium esophagogram, or barium swallow test, is the most common radiographic study to assess for abnormalities of the pharynx and esophagus. During a barium esophagogram, the patient swallows a liquid contrast (barium), then a series of x-rays are taken of the pharynx and esophagus. The barium allows certain body parts to show more clearly on the x-ray. A barium esophagogram may be done alone or in combination with an upper gastrointestinal series, which also includes x-rays of the stomach and duodenum. The presence of reflux on a barium esophagogram or an upper GI series has poor sensitivity and specificity for diagnosing GERD compared to pH testing. In a prospective cohort study, only about 50% of patients with abnormal reflux on a barium esophagogram had abnormal pH monitoring (Kahralis, 2022; Katz et al., 2022).
Esophageal manometry, or high-resolution manometry (HRM), measures the rhythmic muscle contractions in the esophagus during swallowing. This test also measures the coordination and force exerted by the muscles in the esophagus. Although HRM can assess motility abnormalities (i.e., weakened LES), no manometric abnormality is specific to GERD. Therefore, HRM should not be used solely to diagnose GERD. According to the ACG guidelines (2022), HRM can be used to locate the LES for positioning the catheter for pH monitoring. In addition, HRM can be used to evaluate patients for achalasia who are considering surgical or endoscopic anti-reflux procedures. Achalasia can be mistaken for GERD symptoms, and if these patients are not identified before an anti-reflux procedure, devastating dysphagia can occur. HRM can also be used as part of a diagnostic workup for patients unresponsive to PPIs when pH monitoring cannot determine an etiology (Katz et al., 2022).
Ambulatory Esophageal Reflux Monitoring
Ambulatory esophageal reflux monitoring allows the assessment of esophageal acid exposure to correlate with symptomatic reflux episodes to confirm or refute a diagnosis of GERD. Ambulatory esophageal reflux monitoring is currently the only available test to detect pathological acid exposure, determine the frequency of reflux episodes, and correlate symptoms with reflux episodes. This diagnostic tool is used for patients with medically refractory GERD or extraesophageal symptoms that suggest GERD. There are two types of esophageal reflux monitoring: catheter and capsule. With catheter monitoring, the HCP passes the end of a catheter through the nose into the esophagus to measure acid and nonacid reflux (pH and impedance-pH testing). With capsule monitoring, the HCP uses an endoscope to place a wireless capsule on the esophagus lining to measure acid reflux (pH testing only). With both types of monitoring, the patient will wear a monitor that receives information from the catheter or capsule. The transnasal approach has a monitoring period of 24 hours, while the capsule approach can be monitored for 48 to 96 hours. Patients often prefer the capsule approach due to the discomfort of a transnasal catheter. Esophageal reflux monitoring does have high sensitivity and specificity for patients with GERD who have EE but is not as accurate for those with normal endoscopy findings (Antunes & Aleem, 2022; Katz et al., 2022; NIDDK, 2020b).
GERD management requires a multifaceted approach based on many factors, including symptom presentation, physiological abnormalities, and endoscopic findings. Management strategies will differ depending on the presence of a hiatal hernia, EE, Barrett's esophagus, and other physiologic abnormalities such as delayed gastric emptying. The goals for GERD management include the resolution of symptoms and the prevention of complications such as EE, Barrett's esophagus, and esophageal adenocarcinoma. Treatment options include lifestyle modifications, medication therapy, and surgical therapy. A step-up approach is recommended for patients with mild or intermittent symptoms (i.e., fewer than two episodes per week) and no evidence of EE. This approach involves incrementally increasing the potency of therapy until symptoms have resolved. Lifestyle and dietary modifications are recommended initially for patients who are naïve to treatment. Treatment should continue for at least 8 weeks after controlling symptoms (Kahrilas, 2021).
A step-down approach is recommended for patients with frequent symptoms (i.e., two or more episodes per week) or severe symptoms that impair quality of life, or EE. The step-down approach optimizes symptom relief by starting with potent antisecretory agents and incrementally decreasing the dose until breakthrough symptoms define the necessary treatment to control symptoms. Both the step-up and step-down approaches to GERD management can be used, each having its advantages. Once a treatment plan has been developed, the HCP should emphasize the importance of follow-up visits to evaluate the effectiveness of the treatment plan. The HCP should review all symptoms to monitor with the patient and if the condition worsens, whom to contact or where to go for healthcare in an emergency. Management may also focus on treating any underlying causes contributing to the GERD symptoms. H. pylori eradication therapy is often accomplished using at least two oral antibiotics and a PPI or other acid-suppressing medication for 7-14 days (Kahrilas, 2021).
Lifestyle and Dietary Modifications
Dietary and lifestyle modifications are considered the cornerstone of GERD management. Although these modifications are consistently recommended as first-line management or in combination with other medication therapy, supporting data are limited and variable. The ACG guidelines recommend dietary and lifestyle modifications based on recent evidence. Patients should be educated on certain lifestyle changes, including eating smaller meals, lowering stress levels, and decreasing or eliminating acidic or fatty foods from their diet. Patients should be encouraged to lose weight if they are obese to lower their intra-abdominal pressure. Also, patients should be counseled to avoid lying down within 3 hours of a meal and, if possible, to elevate the head of their bed on 3- to 6-inch blocks to enhance esophageal clearance. Measures should be taken to avoid increased intra-abdominal pressure from straining, lifting heavy objects, and wearing restrictive clothing. Patients should be counseled on reducing or eliminating alcohol intake and the importance of smoking cessation to reduce reflux symptoms. Dietary modifications should include avoiding trigger foods such as caffeine, chocolate, spicy foods, citrus, and carbonated beverages. A referral to a dietician would be beneficial for some patients, especially if weight reduction is needed (Antunes & Aleem, 2022; Katz et al., 2022).
OTC and prescription medications are available to treat GERD symptoms. There are three major categories of OTC medications used for this purpose: antacids, H2RAs, and PPIs. Patients self-medicating with OTC drugs for GERD for longer than 2 weeks should meet with their HCP for further evaluation (Katz et al., 2022).
Antacids neutralize gastric acid and decrease pepsin production by blocking the conversion of pepsinogen to pepsin. These medications usually contain a combination of magnesium trisilicate, aluminum hydroxide, and/or calcium carbonate. Antacids do not prevent GERD but instead provide intermittent, on-demand relief of mild GERD symptoms (i.e., occurring less often than once a week). The onset of action for antacids is usually within 5 minutes, with a duration of 30 to 60 minutes. Diarrhea is associated with magnesium hydroxide, while constipation can occur with aluminum antacids. Caution should be used when recommending magnesium antacids to patients with renal disease due to hypermagnesemia. Large amounts of aluminum-based antacids can lead to hypophosphatemia and osteomalacia. HCPs should counsel patients that these medications should not be used daily and should not be used longer than 2 weeks without HCP approval. Some of the common antacids include calcium carbonate (Tums), sodium bicarbonate (Alka Seltzer), and oral suspensions such as Mylanta, Maalox, and Gaviscon (Kahrilas, 2021; NIDDK, 2020d; Tucker, 2022).
Surface Agents and Alginates
Surface agents adhere to the mucosal surface to protect against peptic injury and promote healing. These agents have a short duration of action and have demonstrated limited efficacy compared to PPIs. Sodium alginate is a polysaccharide derived from seaweed, forming a viscous gum that neutralizes postprandial acid in the stomach. Sodium alginates are often used for patients with mild postprandial reflux or as add-on therapy for refractory GERD (Kahrilas, 2021; Katz et al., 2022; Tucker, 2022).
Histamine-2 Receptor Antagonists
H2RAs are used for heartburn symptoms, peptic ulcers, and GERD treatment. Histamine is released in the body due to straining or stress and can cause over-stimulation of hydrochloric acid production by the parietal cells in the stomach. H2RAs partially block histamine from activating the receptors, decreasing hydrochloric acid secretion. Reduced doses of H2RAs are now available OTC. However, many patients experience a decreased medication responsiveness within 2 to 6 weeks of initiation, limiting their effectiveness. H2RAs have a slower onset of action, reaching peak concentration 2.5 hours after dosing, but have a longer duration (4 to 10 hours) than antacids. However, H2RAs have limited effectiveness for patients with EE. The most common side effect of nearly all H2RAs is a headache. Other side effects can include diarrhea, constipation, vitamin B12 deficiency, and bone fractures, particularly with long-term use. Ranitidine (Zantac) is an H2RA medication removed from the US market in 2020 due to a cancer-causing impurity. Examples of H2RAs include famotidine (Pepcid), cimetidine (Tagamet), and nizatidine (Axid; Kahrilas, 2021; NIDDK, 2020d; Tucker, 2022).
Proton Pump Inhibitors
PPIs inhibit gastric acid secretion by irreversibly blocking the H+/K+ enzyme in the parietal cells of the stomach or the gastric proton pump. PPIs typically have more prolonged effectiveness than H2RAs. PPIs should be used for patients who have failed twice daily H2RA therapy, have EE, or have frequent (i.e., two or more episodes per week) or severe symptoms. These medications are most effective when taken 30 to 60 minutes before the first meal of the day because the amount of H-K-ATPase is greatest after a prolonged fast. Some PPIs are available OTC (e.g., omeprazole [Prilosec], lansoprazole [Prevacid], and esomeprazole [Nexium]), while others require a prescription (e.g., pantoprazole [Protonix], dexlansoprazole [Dexilant], and rabeprazole [Aciphex]). Side effects of PPIs include headaches, diarrhea, constipation, abdominal pain, flatulence, fevers, vomiting, and nausea. Long-term effects of chronic PPI use can include increased risk of hypocalcemia, hypomagnesemia, Clostridium difficile infections, osteoporosis-related fractures, vitamin B12 deficiency, and pneumonia. Long-term safety is unknown because most research studies have a follow-up interval of 10 years or fewer. Of the medications available, PPIs are considered the most effective (Antunes & Aleem, 2022).
Surgical and Endoscopic Management
Lifestyle modifications and medical management will successfully treat most patients with GERD. Surgical management can be considered for patients who have medically refractory GERD or experience side effects of medical therapy. This option may also be used for patients who wish to stop taking long-term GERD medications. Finally, surgery should be considered for patients with severe EE (LA grade C or D) or a large hiatal hernia (Katz et al., 2022; Schwaitzberg, 2021).
Roux-en-Y Gastric Bypass (RYGB)
The ACG guidelines recommend considering RYGB as an option for obese patients with GERD. Since GERD is strongly correlated with obesity, weight loss can significantly reduce GERD symptoms. The RYGB option is preferred for patients with obesity since there are risks to fundoplication due to elevated intra-abdominal pressure associated with obesity. The small gastric pouch created during the RYGB procedure produces far less acid than an intact stomach, and the long alimentary loop prevents bile reflux. HCPs should counsel patients choosing RYGB about the risks and lifestyle demands of bariatric surgery (Antunes & Aleem, 2022; Katz et al., 2022). For more information on this topic, see the NursingCE course Bariatric Surgery.
The most common surgery for GERD is the Nissen fundoplication (laparoscopic is more common than open). The laparoscopic Nissen fundoplication (LNF) was generally more cost-effective than long-term medication therapy for patients suffering from moderate to severe chronic GERD symptoms. The LNF showed 85% to 90% symptom improvement compared to other anti-reflux procedures. The Nissen procedure is usually performed laparoscopically to reinforce the LES by wrapping the gastric fundus around the lower portion of the esophagus. The wrapping of the top part of the stomach can be partial or complete, helping tighten the muscle and prevent reflux. Patients undergoing LNF are at risk for developing postoperative adverse effects, such as bloating (15% to 20%), belching, and dysphagia. Nursing care after surgery should focus on pain management, prevention of common surgical complications, emotional support, dietician consult for diet education, and a weight loss program (Antunes & Aleem, 2022; Katz et al., 2022).
Magnetic Sphincter Augmentation
Magnetic sphincter augmentation (MSA), with the LINX Reflux Management System, is a less invasive and more readily reversible treatment option than fundoplication. MSA is a ring of tiny beads with magnetic cores that encircle the junction of the esophagus and stomach to support the LES and prevent reflux. The magnetic attraction between the beads is strong enough to keep the junction closed. This method allows food to pass through but prevents acid from refluxing. Although no studies directly compare MSA to LNF, this method appears to be a safe and effective alternative to LNF. MSA involves minimal surgical dissection and is associated with shorter hospital stays. In addition, MSA is easier to reverse, and patients may have less bloating than LNF. One disadvantage to MSA is that patients cannot undergo magnetic resonance imaging (MRI; Katz et al., 2022).
Endoscopic Anti-Reflux Therapy
Several endoscopic devices have been introduced and subsequently taken off the market for safety and efficacy concerns. Currently, the only endoscopic GERD options are radiofrequency anti-reflux treatment (e.g., Stretta) and transoral incision-less fundoplication (TIF; e.g., EsophyX). The Stretta procedure is the most widely studied anti-reflux approach in which a specialized catheter is placed using an endoscope. However, most studies have not included patients with a large hiatal hernia, grade C or D severe EE, esophageal strictures, or Barrett's esophagus. Therefore, the use of the Stretta should be limited to patients with mild symptoms. The exact mechanism of action of the Stretta is not precise, but researchers propose the procedure might alleviate symptoms by altering sensation in the distal esophagus. Studies have found improvement in GERD symptoms and quality of life with the Stretta, but this procedure did not significantly change esophageal acid exposure. The TIF involves tightening the LES by creating a partial wrap around the lower esophagus using polypropylene fasteners. Since TIF is performed with an endoscope, no surgical incision is needed. Other advantages of the TIF procedure are quick recovery times and patient tolerance. For patients with a large hiatal hernia, TIF can be combined with a laparoscopic hiatal hernia repair. Studies have found that TIF improved the quality of life and symptoms of GERD but did not significantly impact esophageal acid exposure (Antunes & Aleem, 2022; Katz et al., 2022).
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