Description/Etiology
Barrett’s esophagus (BE) is a precancerous condition in which normal squamous cells in the lower esophagus are replaced by columnar epithelium. This change is believed to be caused by chronic esophageal reflux. BE often causes no symptoms and is discovered incidentally. Over time, cells can become dysplastic (i.e., having abnormal shape, size, and organization), and 5–8% of cases of BE progress to esophageal adenocarcinoma (EAC). The prognosis for BE is favorable, but fewer than 15% of patients who develop EAC survive beyond 5 years.
Although most persons with gastroesophageal reflux disease (GERD) do not develop BE, having GERD for > 10 years increases risk for BE. In GERD, a poorly functioning lower esophageal sphincter (LES) allows acid from the stomach to back up into the esophagus. Tobacco use, certain foods and beverages (e.g., chocolate, caffeine), certain medications (e.g., anticholinergics), and certain body positions (e.g., supine) compromise the LES and increase esophageal reflux. The resulting frequent exposure to gastric acid causes chronic inflammation, and the squamous cell lining of the lower esophagus is subsequently replaced by the more acid-tolerant columnar epithelium of the intestines, which predisposes the patient to the development of EAC.
The goal of treatment is to control GERD-related signs and symptoms and maintain healed esophageal mucosa. Patients with signs and symptoms of GERD—including those with low-grade dysplasia and those without dysplasia—are usually treated with a proton pump inhibitor (PPI; e.g., omeprazole), an antisecretory agent that results in esophageal healing in up to 90% of patients. Over-the-counter histamine H2-receptor antagonists (H2- blockers; e.g., famotidine) result in healing in approximately 50% of patients. PPIs and H2-receptor blockers do not cause regression of BE, but PPI therapy may be associated with decreased risk of progression to EAC (see Food for Thought, below). Some clinicians also recommend antisecretory agents for patients who are asymptomatic. Anti-reflux surgery (e.g., laparoscopic Nissen fundoplication)appears to eradicate dysplasia and is the preferred treatment for patients who have BE with high-grade dysplasia. In some cases, patients with high-grade dysplasia undergo esophagectomy (i.e., surgical removal of the esophagus) or newer, less invasive endoscopic techniques, including mucosal resection of the area with dysplasia, laser irradiation, photodynamic therapy, multipolar electrocoagulation, argon plasma coagulation, radiofrequency ablation, and cryotherapy.
Because of the increased risk for EAC in patients with BE, screening by performing esophagogastroduodenoscopy (EGD) with biopsies is recommended. The frequency of surveillance is controversial, and no study results have demonstrated that surveillance increases life expectancy. Recommendations for surveillance frequency vary according to presence and grade of dysplasia. If no dysplasia is present, surveillance is recommended every 2–3 years. If low-grade dysplasia has developed, surveillance is recommended every 6–12 months. If high-grade dysplasia is present, EGD may be repeated with biopsy prior to surgery and histologic examination performed by an expert pathologist. Antisecretory agents may be given prior to initiation of a program for surveillance to avoid confounding inflammation due to acid reflux. Patient education is important to improve quality of life and to reduce the potential for anxiety and depression during surveillance.
Facts and Figures
BE is present in 1.2–1.6% of the general population and 5–15% of patients undergoing endoscopy for symptoms of GERD. BE is 4 times more common in men than in women and 10–20 times more common in Whites and Hispanics than in Blacks. Mean age at BE development is 40 years, and mean age at diagnosis of BE is 55–60 years. BE increases risk for EAC by a factor of 11–20. Patients with BE develop EAC at a rate of 0.12–0.5% per year. In patients with BE and high-grade dysplasia, annual risk of progression to EAC is 6–19%. The incidence of EAC has increased more than 7-fold over the past several decades.
Risk Factors
A typical person with BE is White, middle-aged, and male with a higher than average income. Risk factors include having symptomatic GERD for > 10 years, genetic predisposition for BE (~ 7% of patients with BE have at least one blood relative with BE), smoking, obesity, and consuming a diet high in meat and fast food. Risk of developing long-segment disease (i.e., when the cell lining that is characteristic of BE spans > 7 cm from the bottom of the esophagus upward toward the mouth) is increased in patients with symptomatic GERD. Risk of developing BE decreases when one consumes a diet rich in fruits, vegetables, and nonfried fish.
Signs and Symptoms/Clinical Presentation
Symptomatic patients have manifestations of GERD that include heartburn, dysphagia with solid foods, regurgitation, and epigastric tenderness. Less frequently, patients report having chest pain, hematemesis, or melena.
Assessment
Laboratory Tests That May Be Ordered
Histopathologic analysis of biopsied tissue will show metaplastic columnar epithelium proximal to the gastroesophageal junction in BE
Other Diagnostic Tests/Studies
EGD typically shows dull-red mucosa rather than healthy pink tissue
Confocal laser endomicroscopy (CLE), which is a new imaging technique, can be performed for in vivo visualization of the esophageal mucosa during endoscopy in patients with BE
Treatment Goals
Promote Esophageal Healing and Reduce Risk for Complications
Assess for signs and symptoms of GERD, pain, and other discomfort and review laboratory/diagnostic study results. Administer medications (e.g., omeprazole), as ordered, and monitor treatment efficacy and for adverse effects
Request referral to a dietitian for evaluation of nutritional status and for patient education about nutrition and meal planning to avoid esophageal irritation and BE exacerbation
Follow facility pre- and posttreatment protocols if patient becomes a candidate for radiofrequency ablation, laparoscopic Nissen fundoplication, or another treatment procedure; reinforce pre- and posttreatment education and verify completion of facility informed consent documents
Perform the following monitoring and care, as appropriate after surgery:
Assess for surgery-related pain and administer analgesia, as ordered
Assess for aching in neck and shoulders due to abdominal gas resulting from laparoscopic surgery; encourage lying flat with pillows beneath the hips for ~ 15 minutes and repeat as needed
Assess nutritional status and ability to swallow; advance to full liquid or soft diet, as ordered and tolerated
Monitor for signs of infection at incision sites; follow facility infection control protocols to reduce risk of infection
Perform the following monitoring and care following treatment with a less invasive endoscopic technique (e.g., laser irradiation, photodynamic therapy, multipolar electrocoagulation), as appropriate:
Assess for pain and administer analgesia, as ordered
Assess nutritional status and ability to swallow; advance to full liquid or soft diet, as ordered and tolerated
Monitor for signs of bleeding, perforation, and stricture formation
Provide Emotional Support and Education
Assess anxiety level and coping ability; provide emotional support, educate, and encourage discussion about BE pathophysiology, potential complications, treatment risks and benefits, individualized prognosis, and the necessity of ongoing medical surveillance
Request referral to a mental health clinician, as appropriate, for counseling on strategies for coping with having a potentially life-threatening condition
Food for Thought
Although high-dose PPI therapy is commonly prescribed for treatment of patients with BE and GERD, there is a lack of strong evidence demonstrating that its use is associated with reduced risk of progression to EAC
Helicobacter pylori infection, which is strongly associated with peptic ulcer disease, may be protective against BE
Investigators who conducted a systematic review and meta-analysis determined that PPI use by patients with BE is associated with a 71% decreased risk of progression to EAC or high-grade dysplasia; they found no association between use of H2-receptor blockers and risk of progression to EAC or high-grade dysplasia (Singh et al., 2014)
Researchers in a case-control study of 226 patients with BE and 1,424 controls found evidence that sedentary jobs and exposure to asbestos may be risk factors for BE (Qureshi et al., 2013)
Red Flags
Red Flags Although patients being treated with PPIs may be asymptomatic, they can still have elevated levels of acid secretion
What Do I Need to Tell the Patient/Patient’s Family?
Discuss the risks and benefits of regular endoscopic surveillance for assessment of high-grade dysplasia or EAC
Emphasize the importance of making certain lifestyle modifications, including
increasing consumption of fruits, vegetables, and nonfried fish
decreasing consumption of meat and fatty foods
Educate patients with GERD regarding the importance of elevating the head of the bed during sleep; sitting upright at meals and for one hour after meals; avoiding overeating by eating small meals frequently; avoiding chocolate, tobacco, caffeine, mints, alcohol, and certain medications (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs]); and losing weight if overweight