Approximately 10% of patients seeking treatment for GERD suffer from peptic stricture. Like other patients suffering from complicated GERD, these patients tend to have a lower resting LES pressure. One study noted that 64% of patients with stricture suffered from motility disorders versus 32% of patients without stricture, suggesting that impaired clearance of acid may be a causative factor in GERD.11
Strictures usually form in the lower esophagus as a result of severe esophagitis. When esophagitis extends to the full thickness of the esophageal wall, healing may result in stricture. Schatzki rings are short, web-like stenoses associated with GERD. They may be the result of mucosal and submucosal inflammation and subsequent fibrosis. The ring does not involve the muscular portion of the esophagus. Peptic strictures typically present at the squamocolumnar junction. (In patients with Barrett esophagitis, the squamocolumnar junction lies above the GEJ.) These strictures usually measure 1 cm in length or less and are rarely longer than 3 cm. Other factors predisposing to stricture formation include Zollinger—Ellison syndrome, prolonged nasogastric tube placement, and scleroderma.
Dysphagia is the most common presenting symptom of peptic stricture. Many strictures form gradually. Patients tend to adapt their diet to prevent the physical discomfort, and therefore, complaints regarding the severity of dysphagia correlate very loosely with severity of the stricture. Because the stricture is a mechanical obstruction, the dysphagia typically is more pronounced with solid foods than with liquids. Most patients have a prior history of GERD, along with an associated hiatal hernia. Weight loss is uncommon with peptic stricture in contrast to malignant strictures, which typically occur in patients over 50 years of age, develop more suddenly, may not be accompanied by a hiatal hernia, and are almost always associated with weight loss.
Strictures typically are diagnosed by barium swallow. As noted earlier, benign strictures are located at the squamocolumnar junction; associated with a hiatal hernia; and typically have smooth, tapered proximal and distal segments. Associated esophagitis may be present. In contrast, malignant strictures may not be associated with a hiatal hernia and have irregular narrowing with abrupt or “shouldered” proximal or distal edges. EGD should be performed. Associated esophagitis is seen often. Biopsy should be performed proximally throughout the stricture and beyond, if possible. Use of a thinner pediatric endoscope may facilitate passage. Coexisting Barrett metaplasia may be found. Dilation of the stricture with serial Maloney dilators may permit passage of the endoscope and yield a more detailed examination.
Initial management of peptic stricture involves dilation (see Chapter 44) and PPI therapy. Use of PPIs rather than H2-receptor antagonists results in a lower incidence of stricture recurrence. Three different types of esophageal dilators may be used. The soft, flexible, mercury-filled Maloney dilator is used more commonly for benign strictures. These tapered dilators come in various sizes up to 60F (20 mm). They are designed with flexible tips to follow the course of the esophageal lumen. These dilators are preferred for their ease of use, provided that the stricture is not extremely tight or tortuous. Savary dilators are similar in shape to the Maloney dilators, but they are stiffer, have a central channel, and are designed to be passed over a flexible guidewire. These dilators are used for more tortuous or tight strictures, where there is a greater concern for perforation, or if there may be difficulty engaging the stricture. The wire is passed through the stricture under direct vision and is verified with fluoroscopy to end in the stomach. A series of dilators then may be passed using Seldinger technique. These dilators range in size from 15 to 60 F (5–20 mm). Through-the-scope balloon dilators are also available, although they are disposable and more expensive.
The typical peptic stricture may be dilated safely with Maloney dilators without the use of fluoroscopy. The risk of perforation should be <1%. One-third to one-half of patients require long-term repeat dilations. After two or more dilations, additional dilations are required in nearly all patients. Surgery is indicated in patients who cannot be dilated, as well as in patients who have recurrent strictures while on PPI therapy. The preferred treatment in patients who can be dilated is a laparoscopic fundoplication. Any patient who has concomitant esophageal shortening also should undergo an esophageal lengthening procedure. If the patient cannot be dilated, then esophagectomy is usually needed; however, this is extremely rare, and a thorough effort should be made to exclude unusual malignancies. In a patient with an otherwise healthy esophagus, distal esophagectomy is an acceptable procedure. Colon or jejunum interposition typically is used because a high incidence of recurrent reflux and stricture has been described with the gastric pull-up procedure after distal esophagectomy. Distal esophagectomy is also reasonable in patients suffering from perforation after dilation, especially if they have required several dilations. In these patients, repair of the perforation is associated with a very high incidence of recurrent, difficult-to-dilate strictures. Repair of the stricture and perforation using a Thal patch of stomach to widen the esophagus has been described. This technique is prone to leakage and often leaves the patient with wide-open reflux. For this reason, distal esophagectomy usually is preferred.
Barrett metaplasia is defined as the presence of a “specialized” columnar epithelium in the distal esophagus. The term specialized is used because the epithelium is different from that found in the gastric cardia, with features of gastric, small intestinal, and colonic mucosa, including goblet cells. It is most similar to intestinal epithelial cells. Before Barrett metaplasia can be diagnosed, first it must be identified by the endoscopist. The GEJ is defined endoscopically as the point where the gastric folds are first apparent in the minimally distended esophagus. The squamocolumnar junction, or Z-line, typically coincides with the GEJ. Barrett metaplasia exists when the usual pale pink stratified squamous epithelium of the distal esophagus is replaced by a beefy red columnar intestinal mucosa. The exact location of the GEJ may be difficult to discern, especially in patients with a hiatal hernia. Varying distances have been proposed for the length of columnar mucosa that must be identified before the diagnosis of Barrett esophagus can be made. Patients with less than 3 cm of Barrett metaplasia have short-segment Barrett. Those with more than 3 cm of metaplasia have long-segment Barrett. This distinction is important because patients with short-segment Barrett may not have the same risk of dysplasia.
Barrett metaplasia is caused by frequent, repeated, and prolonged exposure of the esophagus to the gastroduodenal contents. Patients with Barrett metaplasia have been shown to have more severe reflux than patients with esophagitis. Average LES pressure in Barrett patients is about half that of patients with uncomplicated reflux esophagitis (5 vs. 9 mm).12 Most Barrett patients have a hiatal hernia of significant size (76% vs. 50% with uncomplicated esophagitis).13 Exposure to acid and bile is higher in Barrett patients than in patients with non-Barrett esophagitis. The origin of the specialized metaplastic cells is unclear. A number of hypotheses have been proposed. For example, these specialized cells may result from migration of gastric cardia cells to the distal esophagus, they may represent metaplasia of esophageal squamous cells, or they may develop from esophageal glandular cells. Experimental and clinical evidence exists for each of these hypotheses without clear consensus.
Approximately 10% of patients with esophagitis eventually will develop Barrett metaplasia. The disease is twice as prevalent in men as in women. Barrett patients have a 30- to 125-fold chance of developing esophageal adenocarcinoma compared with the general population. The rate of cancer development is 1 in 200 patient-years for those with metaplasia. Not all Barrett patients are at equal risk of developing adenocarcinoma. Risk factors for the development of adenocarcinoma in these patients include male gender, smoking, greater length of Barrett esophagus, Barrett ulcer, peptic stricture, white race, and older age. Most Barrett patients have symptoms that are indistinguishable from those of uncomplicated esophagitis. Barrett patients tend to have more complications from esophagitis (e.g., bleeding and stricture). The development of a stricture at the squamocolumnar junction well above the GEJ in a patient with a hiatal hernia is nearly pathognomonic for Barrett esophagus.
Barrett carcinoma is believed to progress in the following sequence: metaplasia < low-grade dysplasia < high-grade dysplasia < adenocarcinoma. Progression from low-to-high—grade dysplasia may take many years, whereas progression from high-grade dysplasia to adenocarcinoma occurs on average in 14 months.14 The annual incidence of the development of cancer in a patient with Barrett esophagus has been estimated to be from 0.2% to 1.9%.15 Dysplasia indicates the development of neoplastic changes that consist of alterations in the cellular and glandular architecture. Cell nuclei may be hyperchromatic and enlarged, with increased mitotic figures. The nuclei may show loss of polarity and, instead of appearing uniformly at the base of cells, may migrate toward the luminal surface. In high-grade dysplasia, nuclei extend toward the luminal one-third of the cell. The differentiation between low- and high-grade dysplasia is often difficult.
The treatment of Barrett esophagus with low-grade and high-grade dysplasia is controversial and continues to evolve. The natural history and progression of low-grade dysplasia to high-grade dysplasia to intramucosal carcinoma and eventually to cancer with metastatic potential has yet to be well defined. The surveillance and treatment of Barrett Esophagus is discussed in detail in Chapter 41.