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Gastroesophageal Reflux Disease

6 min read

References:

  1. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, 15th Edition, ISBN 978-197-51-6103-3, by Janice L. Hinkle, Kerry H. Cheever, and Kristen J. Overbaugh (Ch. 39, [ebook] pp. 3411–3416) + Barrett Esophagus

The reflux (backward flow) of stomach contents into the esophagus. This also results in inflammatory changes in the esophageal mucosa: reflux esophagitis. Its causes vary, including inappropriate relaxation or decreased tone of the lower esophageal sphincter (LES), elevated gastric volume or intra-abdominal pressure, and delayed gastric emptying.

Incidence

The incidence of GERD seems to increase with aging and is seen in patients with irritable bowel syndrome and obstructive airway disorder exacerbations (e.g., asthma, COPD, cystic fibrosis), Barrett Esophagus, peptic ulcer disease, and angina.

GERD is associated with tobacco use, coffee drinking, alcohol consumption, and gastric infection with Helicobacter pylori.

Assessment Findings

Heartburn (Pyrosis), a substernal/retrosternal burning sensation that may radiate to the neck, jaw, and back; and regurgitation, where warm fluid travels up the throat with a sour or bitter taste (which also creates a risk for aspiration), are the hallmark symptoms. Assess for crackles (sign of pulmonary edema from congestion) in the lungs as GERD may sometimes mimic the pain felt in coronary artery disease or in myocardial infarctions.

  • Dyspepsia (indigestion)
  • Dysphagia (difficulty in swallowing) and odynophagia (painful swallowing)
  • Water Brash: excessive production of saliva (hypersalivation) mixes with stomach acid, and is then refluxed. This is different with regurgitation as it does not require the presence of undigested food.
  • Other manifestations:
    • Chronic cough (especially nocturnal due to positioning) from micro-aspiration/aspiration of refluxed gastric contents.
    • Asthma either due to aspiration or from neurogenic induction of inflammation.
    • Introduction of gas (secondary manifestation to GERD): eructation (belching), flatulence (farting), and bloating.
    • Nausea and Vomiting
    • Erosion of dental enamel can occur.

Diagnostic Examination

24-hour ambulatory pH monitoring (up to 36 hours) is the gold standard for GERD diagnosis. A transnasal catheter or endoscopic wireless capsule is placed for approximately 24 hours.

  • Endoscopy or barium swallow is used to evaluate damage to the esophageal mucosa and rule out strictures and hernias.
  • Bilirubin Monitoring is used to measure to bile reflux patterns.
  • Esophageal Manometry: a form of “motility testing” where a water-filled catheter is inserted through the mouth or nose then into the distal esophagus, slowly being withdrawn as it measures the pressure created by the esophagus’ peristaltic movements. However, this is not reliable for a diagnosis of GERD.

Nursing Interventions

Management begins with educating the patient to avoid situations that decrease lower esophageal sphincter pressure or cause esophageal irritation. Lifestyle modifications include tobacco cessation, limiting alcohol, weight loss, elevating the head of the bed, avoiding eating before bed, and altering the diet.

Diet Therapy

  • Limit food that decrease LES tone e.g. fat and caffeine, peppermint, spicy, highly seasoned, irritating or acidic foods e.g. orange juice and tomatoes, alcoholic, and carbonated beverages that increase gastric pressure.
  • Cease smoking
  • Consume four to six small meals a day. Large meals may induce GERD due to a fuller stomach and increased acid production. Do not eat or snack in the evening or 2 to 3 hours before bed.
  • Eat slowly and chew thoroughly. This will reduce belching from swallowing air.
  • Remain upright for 1 to 2 hours after meals (if possible) to reduce incidence of GERD.

Lifestyle Changes

  • Sleeping with a left side-lying (decubitus) position improves acid clearance and acid exposure which improve normal and nocturnal symptoms.
  • Standing or sitting after meals help reduce episodes.
  • Always sleep with your head elevated 8 to 12 inches as an aspiration precaution and to reduce the effects of GERD.
  • Reduce weight if overweight.
  • Avoid wearing constrictive clothing, and avoid heavy lifting or exercise (that increases intra-abdominal pressure)

Management

Medical Management

  • Proton Pump Inhibitors: the main treatment for GERD. This inhibits the proton pump of the parietal cells, which subsequently inhibits acid secretion.
    • Omeprazole (Prilosec), Lansoprazole (Prevacid), Rabeprazole (AcipHex), Pantoprazole (Protonix), Esomeprazole (Nexium)
    • These products may increase intragastric bacterial growth and the risk of infection.
  • Antacids: these neutralize hydrochloric acid and deactivates pepsin.
    • Aluminum Hydroxide, Magnesium Hydroxide, Maalox, Mylanta
  • Histamine (H2) Receptor Antagonist: decreases acid production by the parietal cells.
    • Famotidine (Pepcid), Ranitidine (Zantac), Cimetidine (Tagamet), Nizatidine (Axid)
  • Prokinetic Agents are used for faster gastric emptying. This is only used for short-term management due to its potential for tardive dyskinesia (especially Metoclopramide)
    • Metoclopramide (Reglan)
  • Reflux inhibitors stimulate parasympathetic action (cholinergic) to enhance gastric emptying and improves LES tone, thereby inhibiting reflux.

Nursing Considerations

A potential risk of gastric acid suppression (Antacids, Histamine-2 receptor antagonists, proton pump inhibitors) is the loss of protective flora and an increased risk of infection, especially with Clostridium difficile.

Surgical Management

If medical management is unsuccessful, surgical intervention may be necessary. Surgical management involves an open or laparoscopic Nissen fundoplication, which involves wrapping of a portion of the gastric fundus around the sphincter area of the esophagus.

  • Stretta Procedure (Endoscopic Therapy): a non-invasive esophageal reconstruction done via an endoscope placed near the gastroesophageal junction, where therapeutic levels of energy produced via radiofrequency pulse is applied to the lower esophageal sphincter (LES), reshaping it and enhancing

Barrett Esophagus

Esophagitis and Barrett Epithelium or Barrett Esophagus is the abnormal conversion of normally squamous epithelia to columnar epithelia. This is a result of the repeated inflammatory healing process attempting to become more acid-resistant. These cells can become considered as pre-malignant for patients with prolonged GERD.

  • This occurs predominantly in White men aged 50 or older, and occurs in association with family history of BE or esophageal adenocarcinoma (EAC), GERD, smoking, and obesity. Risk factors are additive—the rates of BE increased by 1.2% for each additional risk factor.
  • BE is the only known precursor to EAC, one of the fastest rising cancers in Western populations (2019). The 5-year survival rate for EAC does not exceed 20%.

Clinical Manifestations

The patient complains of symptoms of GERD, notably frequent heartburn. The patient may also complain of symptoms related to peptic ulcers or esophageal stricture, or both.

Assessment and Diagnostic Findings

An EGD provides screening in patients with multiple risk factors. This usually reveals an esophageal lining that is pink rather than pale white.

  • Biopsies are performed, and BE is diagnosed when the squamous mucosa of the esophagus is replaced by columnar epithelium (columnar metaplasia) at least 1 cm above the gastric folds, and that area resembles that of the stomach or intestines (intestinal metaplasia) as evidenced by the presence of goblet cells.

Management

Monitoring varies depending on the extent of cell changes. When BE is caught and treated early, endoscopic ablation techniques have been shown to eliminate BE in up to 80% of patients, thereby preventing progression to dysplasia, the bizarre cell growth resulting in cells that differ in size, shape, or arrangement from other cells of the same tissue type.

Such dysplasia is indicative of early EAC. Follow-up biopsies are recommended no sooner than 3 to 5 years after a biopsy shows no evidence of dysplasia. Treatment is individualized for each patient. Recommendations include surveillance with biopsies, the use of PPIs to control reflux symptoms, followed by endoscopic resection and/or radiofrequency ablation (high-frequency heat/cold energy that kills surrounding cells and tissues) for progression of dysplasia.

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