Gastroesophageal Reflux Disease
Sophia Lee
Eric J. DeMaria
Andrew Grant is a 45-year-old man who has a 3-year history of heartburn that is particularly bothersome at night when he is in bed. The heartburn worsens when he bends over; antacids provide relief. Occasionally, he wakes up at night coughing and choking.
Mr. Grant’s medical history is significant for hypertension and bronchial asthma, for which he takes calcium channel blockers and albuterol by inhaler, respectively. He smokes a pack of cigarettes and drinks 10 cups of coffee daily. He also admits to significant intermittent consumption of alcohol.
The physical examination reveals no problems; Mr. Grant is well developed and well nourished, his vital signs are within normal limits, and his chest, cardiovascular system, and abdomen appear to be normal. The rectal examination is normal and the stool is guaiac negative. The physician makes a provisional diagnosis of gastroesophageal reflux disease (GERD) on the basis of the history.
What is the prevalence of GERD in the United States?
View Answer
GERD is a chronic illness that affects approximately 7% of the adult population daily in the United States. Although about 38% of the population has heartburn, only those with severe symptoms (approximately 10% of this group) seek the advice of their physician (1).
What are the clinical features of GERD?
View Answer
The typical symptoms of GERD are heartburn and regurgitation. However, the absence of these symptoms does not exclude GERD. Conversely, only about a third of patients with typical symptoms have endoscopic evidence of GERD.
Atypical symptoms of GERD include substernal chest pain (approximately 50% of patients with noncardiac chest pain have reflux disease), hoarseness caused by reflux laryngitis, hiccups, asthma (34% to 89% of asthmatics have GERD) (2,3), ear pain, loss of dental enamel, night sweats, chronic coughing, globus sensation, hypersalivation, heartburn during intercourse (reflux dyspareunia), and dysphagia secondary to stricture.
What is the pathophysiology of GERD?
View Answer
Gastroesophageal reflux to a certain extent is a normal continual phenomenon. Prolonged contact of the esophageal mucosa with gastric juice leads to pathologic conditions such as esophagitis and subsequently to stricture and metaplasia (Barrett’s esophagus). Innate mechanisms protect the esophagus from abnormal reflux (4), and when these fail, signs and symptoms of GERD appear. These protective mechanisms can be described as esophageal, gastric, and duodenal.
Esophageal Factors
Lower esophageal sphincter mechanism. Dysfunction of the lower esophageal sphincter (LES) is the most important esophageal factor in the pathophysiology of reflux. Once the high-pressure zone of the lower esophageal sphincter is lost, reflux of gastric contents occurs. Many factors affect the LES and can precipitate reflux symptoms. The anatomic factors that are believed to contribute to the LES are mentioned later in this chapter.
Peristalsis. Another important factor is esophageal peristalsis. Primary peristalsis results from a swallowing reflex that propels the bolus of food down the esophagus and lowers the LES to allow the bolus passage into the stomach. Secondary peristaltic waves are initiated in the esophagus. These so-called stripping waves clear any refluxed material from the esophagus into the stomach.
Salivary bicarbonate. Swallowed salivary bicarbonate neutralizes gastric acid in the esophagus and thus protects the esophageal lining.
Esophageal mucosa. The esophageal mucosa has inherent defense mechanisms against the noxious gastric secretions. Bicarbonate in the unstirred water layer adjacent to the mucosa protects the mucosa from H+ and pepsin. This mechanism is believed to play only a minor role in humans. Other protective mechanisms of the esophageal mucosa are intercellular tight junctions, epithelial transport (Na+-H+ exchange), epithelial buffers, and the lipid bilayer of the stratum corneum (3). Along with these factors, an adequate esophageal blood supply helps in cell replication, regeneration, and repair and in adequate nutrition of the epithelium.
Gastric Factors
Gastric distention. Gastric distention reduces the LES pressure and promotes reflux. Patients with Zollinger-Ellison syndrome are prone to reflux disease because of the increased gastric volume secondary to gastric hypersecretion.
Increased intraabdominal pressure. Obese patients and pregnant women have increased intraabdominal pressure, which raises the pressure gradient across the LES, causing reflux of gastric contents.
Duodenal Factors
Alkaline reflux. The alkaline reflux of biliary and pancreatic juices can injure the esophagus (4), a well-documented occurrence after resection of the LES following total gastrectomy.
A possible role for Helicobacter pylori in the pathogenesis of GERD has been suggested in number of studies. However, the link between GERD and H. pylori is complex and poorly defined.
What are the differential diagnoses?
View Answer
GERD needs to be distinguished from gastritis, infectious esophagitis, pill esophagitis, peptic ulcer disease, non-ulcer dyspepsia, biliary tract disease, coronary artery disease, and esophageal motor disorders.
What investigations aid in the diagnosis of GERD?
View Answer
The initial diagnosis is based largely on the history. Several tests can help in diagnosis and management of the disease.
Tests for Mucosal Injury
Esophagogastroduodenoscopy. Esophagogastroduodenoscopy (EGD) is usually the first test to be performed. It is useful for the detection of mucosal injury and for the surveillance of Barrett’s metaplasia. Endoscopic appearance can be misleading, as biopsy of a “normal” mucosa may reveal florid inflammatory changes. Histology helps make the diagnosis of esophagitis and Barrett’s metaplasia.
Barium esophagram. Reflux may be demonstrated with a barium esophagram even in normal persons. Reflux becomes pathologic when it is excessive, frequent, and associated with symptoms and signs of reflux disease. A barium esophagram reveals mucosal abnormalities, strictures, motility dysfunction, and a short esophagus. This allows surgery to be customized to the patient’s needs.
Tests for Abnormal Reflux
The 24-hour pH monitor. One of the most specific and sensitive tests for GERD, pH monitoring quantifies the actual periods when acid is in contact with the esophageal mucosa. The pH electrode is positioned 5 cm above the manometrically defined upper limit of the LES. It allows the correlation of these exposures with the subjective feeling of heartburn. A normal 24-hour pH study virtually rules out reflux disease. Some new probes (e.g., Bilitec) also monitor any biliary contents in the esophagus.
Barium study. A barium study of the upper gastrointestinal (GI) tract can demonstrate reflux and the presence of hiatal hernia. Reflux itself is not considered pathologic because some degree of reflux is normal, as mentioned earlier. A barium study may also show evidence of mucosal injury, abnormalities of esophageal motility, and gastroparesis.
Test for Gastric Emptying
Gastroesophageal scintiscan. Delayed gastric emptying can be detected with this scan, in which a technetium 99 (99Tc) sulfur colloid-labeled diet is used. About 5% of patients with reflux disease have poor gastric emptying. If these patients undergo antireflux surgery, the steep increase in intragastric pressure postoperatively can cause wrap disruption or gastric perforation. To prevent these complications, a pyloroplasty may be added to the fundoplication.
Test for Esophageal Motility
Esophageal manometry. This test is helpful in individualizing the surgery and to exclude major motor disorders. The LES pressure in patients with reflux disease is usually 6 mm Hg or less. Most patients, therefore, require a 360° wrap. A partial wrap is indicated if the LES pressure is high or if the esophageal motility is poor. Patients with a high LES pressure may still have abnormal reflux, and patients with a low LES pressure may have a normal esophagus.
Other Test
Bernstein’s test. This test is useful to determine symptom correlation with esophageal acidification in patients without endoscopic evidence of esophagitis. Saline or 0.1N HCl at a rate of 6 to 8 mL per min is infused via a nasogastric tube into midesophagus.
What are the recommended changes to Mr. Grant’s lifestyle?
View Answer
The first step in the treatment of reflux disease is a change in lifestyle.
Diet. A diet low in fat, mint, chocolates, coffee, and alcohol improves the LES pressure and reduces reflux. Also avoid foods known to cause symptoms. Many beverages have a very acidic pH and can exacerbate symptoms, including colas, red wine, and orange juice (pH 2.5 to 3.5). Obese patients who lose weight by dieting may have less heartburn as a result of both better diet and decreased intraabdominal pressure.
Sleeping position and time. Patients are advised to raise the head end of the bed and sleep on their left side. Head of bed elevation is important for individuals with nocturnal or laryngeal symptoms. Gravity helps to clear the esophagus of the gastric refluxate and to decrease the symptoms of reflux. Patients are also advised to delay going to bed until 3 to 4 hours after the last meal to allow the stomach to empty.
Smoking. Smoking worsens reflux disease by decreasing the LES pressure and increasing the time taken for esophageal clearance.
Medications. Medications that decrease the LES (e.g., calcium channel blockers in the case of Mr. Grant) should be changed. Medications that worsen reflux are listed in Table 5.1.
TABLE 5.1. Factors that Affect Les Pressure | ||
|---|---|---|
|
Other factors. Tight clothes and exercise can aggravate the symptoms of reflux. Although stress does not directly cause GERD, it makes the patient more sensitive to the symptoms of reflux and has therefore been historically associated with GERD. Promotion of salivation with either chewing gum or oral lozenges may help relieve mild heartburn because salivation neutralizes refluxed acid.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
