CHAPTER 20

Gastroesophageal Reflux Disease

Michelle Santomassino, DNP, RN, FNP-C

Gastroesophageal reflux disease (GERD) is such a common problem that it affects 10% to 20% of the Western world (Dent, El-Serag, Wallander, & Johanasson, 2005). The presence or absence of a hiatal hernia often helps to determine the severity of GERD and the ease or difficulty with which it can be treated. Several treatment options are available and typically include some combination of medication therapy and lifestyle modification.

ANATOMY, PHYSIOLOGY, AND PATHOLOGY

GERD occurs for various reasons, ranging from dietary factors to disruption of the anti-reflux barrier, allowing gastric content to reflux into the esophagus. In addition to these reasons, the lower esophageal sphincter (LES) normally relaxes several times per hour. Relaxation occurs during swallowing to allow the passage of food into the stomach and during the transient phase to allow the venting of gas from the stomach (belching) (Holloway, Boeckxtaens, Penagini, Sifrm, & Smout, 2011; van Wijk et al., 2011). These periods of LES relaxation increase the risk for reflux of gastric juices.

The anti-reflux barrier is composed of the crura diaphragm, the phrenoesophageal ligament, the acute angle of His, and the LES. These components physically block the reflux of gastric juices into the esophagus. The crura diaphragm wraps around the esophagus and helps create this barrier. The acute angle of His is the angle created where the esophagus passes through the diaphragm and empties into the stomach.

The LES is perhaps the most important component of this anti-reflux barrier. The intrinsic pressure of the LES keeps it closed until swallowing occurs. Once a bolus of food is swallowed, the LES receives a signal to relax and allows the bolus to pass into the stomach. The normal relaxation of the LES, also known as transient lower esophageal sphincter relaxation (TLESR), is believed to occur as part of digestion, perhaps to allow accumulating gases to escape. This relaxation is believed to play a major role in the etiology of reflux disease. Seasoned foods, cigarette smoking, alcohol ingestion, and caffeine are all well-known causes of LES relaxation with resultant reflux. Progesterone has also been found to decrease the LES pressure (Jain, Dharmarajan, & Pitchumoni, 2012; Malfertheiner et al., 2009).

Hiatal Hernias

A hiatal hernia occurs when parts of the abdominal cavity are displaced through the esophageal hiatus of the diaphragm, disrupting the anti-reflux barrier. Although the LES still functions normally, because the LES is displaced upward and separated from the other components of the anti-reflux barrier, the barrier is not as effective. The sliding hiatal hernia is the most common form of hiatal hernia. This type of hiatal hernia slides back and forth through the diaphragmatic hiatus. Because of this sliding back and forth, hiatal hernias, especially when small, may seem to appear and disappear on various diagnostic studies.

Paraesophageal hiatal hernias are more dangerous and far less common than sliding hiatal hernias. With paraesophageal hernias, GERD is not a complication, because the LES is not displaced. Rather, a distal portion of the stomach actually migrates upward and becomes trapped between the diaphragm and the esophagus. This can lead to ischemic changes and eventually necrosis of the stomach, with catastrophic consequences.

There is a strong correlation between reflux symptoms, Barrett’s esophagus, esophageal adenocarcinoma, reflux esophagitis, and the presence of a hiatal hernia. Furthermore, the larger the size of the hiatal hernia, the more significant the risk of developing Barrett’s esophagus, esophageal adenocarcinoma, or reflux esophagitis (Hyun & Bak, 2011).

Histological Changes

Histological changes can be found in GERD, especially in patients with chronic GERD. The repetitive insult of the gastric juices causes metaplastic changes in the esophagus. Barrett’s esophagus (intestinal metaplasia of the esophagus) represents the replacement of the squamous epithelia of the esophagus with columnar epithelia, which is normally found in the stomach or small bowel. Barrett’s esophagus is a premalignant condition that is diagnosed in 10% to 15% of patients with GERD who undergo endoscopy (Sharma, 2009). The incidence of adenocarcinoma in the presence of Barrett’s esophagus varies, but studies suggest an initial prevalence ranging from 0.2% to 3.5% per year (Sikkema, De Jonge, Steyerberg, & Kuipers, 2010).

A diagnosis of GERD is often made by history alone. Guideline groups agree that GERD may be diagnosed in patients with the classic symptoms of heartburn, epigastric pain, and regurgitation, who respond to proton pump inhibitor (PPI) therapy (Kahrilas, Shaheen, & Vaezi, 2008, www.sciencedirect.com/science/article/pii/S0016508508016065; Katz, Gerson, & Vela, 2013, gi.org/guideline/diagnosis-and-management-of-gastroesophageal-reflux-disease/; American Society of Gastrointestinal Endoscopy (ASGE), 2007, www.asge.org/assets/0/71542/71544/39A574DC-1EA9-4175-BE3D-8E21E5EA764F.pdf; University of Michigan Health System, 2012, www.med.umich.edu/1info/fhp/practiceguides/gerd/gerd.12.pdf). In patients who are refractory to therapy or who have more concerning signs and symptoms, diagnosis may be made by endoscopy or by pH probe monitoring.

HISTORY AND PHYSICAL EXAMINATION

Heartburn and reflux are the two classic symptoms of GERD (Kamal & Vaezi, 2010; Katz et al., 2013). Dysphagia is another classic complaint but one that warrants diagnostic evaluation with endoscopy to assess for complications. The patient’s description of the pain is usually burning and substernal, although often patients describe it as a dull ache. Other common features of the pain are that onset of symptoms occurs when the patient is supine or after meals, temporary relief is provided by antacids, and intermittent dysphagia occurs.

When obtaining the history, it is prudent to determine the duration of symptoms, the timing of symptoms (day or night), whether there has been a significant change in symptoms, and relieving or aggravating factors. Nocturnal symptoms are common because of the supine position at bedtime. When supine, gravity causes layering of gastric juices, which results in cephalad flow toward the distal esophagus.

Less typically presenting manifestations are cough and hoarseness. The cough is usually nocturnal and must be differentiated from other causes, such as asthma, postnasal drip, or heart failure. GERD is sometimes diagnosed by the otolaryngologist when persistent hoarseness, secondary to inflammation of the vocal cords, is caused by acid reflux.

Water brash, another manifestation of GERD, is described as excess saliva (“water”) in the mouth. Typically, it has a bitter or sour taste and is caused by the reflux of gastric juices. Water brash occurs mostly at night and represents a more severe form of GERD.

Benign peptic strictures causing dysphagia may be a presenting manifestation of GERD. However, the provider can never be certain whether the stricture is benign or malignant by history alone. Clues in the history that suggest benignity include a prolonged history of reflux with a recent decrease in reflux symptoms. This is caused by the presence of the stricture.

DIAGNOSTIC STUDIES

Currently, there is no gold standard study for the diagnosis of GERD. Commonly, the disease is diagnosed based on the successful management of symptoms with PPI therapy. In patients refractory to therapy, the next line of diagnostic testing is typically esophageal impedance and pH monitoring (Katz et al., 2013).

Esophogastroduodensocopy (EGD) is considered in patients who are refractory to therapy; in patients with negative pH reflux monitoring; in patients with positive findings on imaging; and in patients with alarm symptoms of early satiety, weight loss, gastrointestinal bleed, anemia, dysphagia, or vomiting (Kahrilas et al., 2008, American Society of Gastrointestinal Endoscopy (ASGE), 2007, University of Michigan Health System, 2012). EGD enables the provider to evaluate the esophagus for the degree of inflammation, erosive changes, Barrett’s metaplasia, stricture formation, and hiatal hernia. This is achieved through visualization and biopsy tissue sampling (Katz et al., 2013). If a perforation is suspected, a chest radiograph and computed tomography scan of the chest to find free air in the mediastinum are the first studies performed. EGD is contraindicated in patients with suspected perforation because of the likelihood of further spillage into the mediastinum, with resultant severe mediastinal infection.

Few other laboratory studies are needed when diagnosing or treating GERD. If a patient has hemorrhage, the hemoglobin/hematocrit becomes important. Another diagnosis to consider in patients with difficult-to-treat GERD is Zollinger–Ellison syndrome. A fasting serum gastrin level and, if indicated, a secretin stimulation test can be obtained (see Chapter 25, “Peptic Ulcer Disease,” for a description of the secretin stimulation test).

TREATMENT OPTIONS, EXPECTED OUTCOMES, AND COMPREHENSIVE MANAGEMENT

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