ESOPHAGEAL STRICTURE
There are two benign disease processes that may result in esophageal strictures:
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Extrinsic disease
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Intrinsic disease
The etiology of these strictures may be elucidated based on the patient’s symptoms, physical examination, contrast radiographic imaging, endoscopy, and pathology.
Strictures may be further classified as
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Simple
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Esophageal lumen permits passage of endoscope
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Straight
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Short (<2 cm)
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Complex
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Too narrow to allow for easy passage of the endoscope
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Angulated stricture
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Irregular
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BENIGN ETIOLOGIES OF ESOPHAGEAL STRICTURE
General Causes
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Peptic stricture
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Schatzki’s ring
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Motility disorder of esophagus
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Autoimmune
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Immunocompromised state
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Graft versus host disease
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Collagen vascular disease
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Crohn’s disease
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Infectious esophagitis
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Hiatal hernia
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Caustic
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Congenital, iatrogenic
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Medication related
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Prior photodynamic therapy (PDT)
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Foreign body reaction
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Radiation therapy
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Malignancy
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Idiopathic
Peptic Stricture
The most common cause of benign esophageal stricture and accounts for approximately 75% of all benign esophageal strictures.
ETIOLOGY
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The primary inciting factor is exposure of the esophagus to acid resulting in collagen deposition and eventually a fibrous esophageal stricture.
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Dysfunctional or impaired lower esophageal sphincter (LES)
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LES pressure usually less than 8 mm
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Impaired esophageal motility, with decreased clearance
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Association with hiatal hernia exists.
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Alkaline reflux may play a role.
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Approximately 70% of all esophageal strictures are peptic strictures secondary to reflux.
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Use of proton pump inhibitors (PPIs) has decreased the need for dilatation as well as the risk of recurrence.
CLINICAL FEATURES
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Progressive dysphagia to solids is very common. It is believed that dysphagia is the best predictor of esophageal stricture.
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Food impaction
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Weight loss
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Heartburn
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Chest pain
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Pulmonary symptoms
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Adult onset asthma, usually secondary to aspiration
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Chronic cough
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Stricture diameter is only partially responsible for symptoms of dysphagia. Esophagitis has an equal or greater impact on the level of dysphagia a patient feels.
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When the luminal diameter is less than 5 mm, then luminal diameter will be the determinant for the degree of dysphagia.
DIAGNOSIS
Diagnosis and cause should be established because treatment depends on etiology. Dysphagia is the most common symptom. Frequently, patients will describe a progression of dysphagia from solids to liquids. The presence of dysphagia should prompt an investigative workup to find the cause behind it.
Imaging Studies
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Esophagram
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Very sensitive test to detect luminal narrowing
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Provides information about the location, diameter, contour, length, size and complexity of the lesion.
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May help identify malignancy
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May show associated abnormalities that may impact the choice of therapeutic intervention.
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Findings on barium swallow can help guide future endoscopic evaluation ( Fig. 57-1A and B ).
Figure 57-1
A, Schatzki’s ring. B, Barium esophagram with Schatzki’s ring.
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Computed tomography scan (CT)
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CT is helpful in evaluation of strictures due to malignancy.
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Can help with determining the size of the lesion
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Helpful in the evaluation of extraluminal spread or invasion of neighboring structures by malignancy
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Useful in evaluating metastatic spread
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Esophagogastroduodenoscopy (EGD)
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EGD is useful in identifying stricture.
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Evaluating for evidence of esophagitis
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Identify possible malignant lesion
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Obtain tissue for pathologic examination
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Endoscopic ultrasound (EUS)
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EUS most useful in cases of malignancy
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Very accurate in determining depth of invasion and nodal involvement
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EUS has a sensitivity of 93% and a specificity of 100% when combined with fine-needle aspiration for regional nodal staging.
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Esophageal manometry
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Useful in evaluating patients with suspected esophageal dysmotility
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Information about the patient’s esophageal motility can help guide planning for those who will undergo possible antireflux surgery.
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24-hour pH
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Helpful in identifying patients with acid reflux who may benefit from PPIs
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Can help identify patients who may benefit from an antireflux procedure
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Treatment
The goal of treatment is to relieve the dysphagia. Initial therapy is usually esophageal dilatation, but concomitant implementation of medical therapy is essential to promote healing as well as decrease the chance of recurrence. Esophageal resection may be necessary for patients refractory to the above treatments.
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Medical therapy
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Treatment with PPIs is very beneficial.
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Studies have demonstrated that the use of PPIs has decreased the need for dilatation as well as the risk of recurrence and need for repeat dilation.
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Dilatation
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Esophageal dilation dates back to the 16th century. During that time, wax fashioned in the shape of a wand was used to dilate the esophagus. The current word bougie was derived from an Algerian city named Boujiyah, which was the main site for candle trade during medieval times.
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Both balloon and mechanical (bougie type) dilators are used.
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Balloon dilator
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Passed and used under direct visualization by the endoscope
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Not reusable
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Fluoroscopy not mandatory
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Mechanical dilators include
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Maloney
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Flexible rubber dilators weighted with mercury
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Indicated for uncomplicated strictures
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Not wire guided
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Diameter of stricture greater than 10 mm
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Savary—Gilliard dilators
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Wire guided, flexible polyvinyl chloride
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Fluoroscopy guided
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Radio-opaque at the base of the taper
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Indicated for more complex strictures: (1) irregular, (2) long, (3) tight
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American dilation system
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Wire guided, flexible poly-vinyl chloride
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Fluoroscopy guided
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Short, less tapered
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Impregnated with barium so they are radio-opaque throughout the length of the dilator.
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Indicated for more complex strictures: (1) Irregular, (2) long, (3) tight
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Risk of perforation ranges 0.1% to 0.4%
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No clear difference in perforation rates between mechanical and balloon dilators
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The choice of which type of dilator to use is dependent mostly on the characteristics of the stricture and endoscopist’s preference.
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Balloon dilators are not reusable, whereas mechanical dilators can be reused.
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A postdilation luminal diameter of at least 12 mm is required to relieve symptoms of dysphagia
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Most patients experience relief after successful dilatation up to 40 to 54 French, some will even attempt to dilate up to 60 French.
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Dilation is tailored specifically for each patient based on findings, technical difficulty during the procedure, and symptomatic response of the patient to level of dilatation.
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Thirty to forty percent of patients with benign strictures have recurrence within 1 year of dilation, even with the aid of concomitant acid suppression.
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Refractory strictures most commonly occur in patients with stricture secondary to caustic ingestion or radiation
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Steroid injection
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Steroid injection into the stricture may reduce stricture recurrence.
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May be effective for patients
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Requiring frequent dilations
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Poor symptomatic relief from dilation
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Both Long strictures and short strictures
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Stent: There exist both metal and nonmetal stents, as well as covered and noncover stents.
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Stents are commonly used in patients with dysphagia secondary to malignancy.
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Stents are both permanent and removable.
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Indications:
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Recurrent stricture after repeated dilations
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Recurrent stricture after steroid injection
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Patients with inoperable malignancy
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Recurrent stricture after nonsurgical treatment
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Esophageal fistula
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Surgery: Reserved for those patients with strictures refractory to the above-mentioned interventions
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Benign dilatable strictures
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Esophageal sparing operation
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Anti-reflux procedure
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With or without esophageal-lengthening procedure, as indicated (Collis)
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Stricture not dilatable
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Esophageal resection may be needed
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BARRETT’S ESOPHAGUS
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Replacement of the normal esophageal squamous mucosa with columnar epithelium containing goblet cells (metaplasia).
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Found in 7% to 10% of patients with chronic, severe gastroesophageal reflux disease (GERD)
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Barrett’s esophagus predisposes patients to the development of mucosal dysplasia and, ultimately, adenocarcinoma; therefore, the condition should be considered a premalignant (50- to 100-fold increased risk of cancer compared with the general population).
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The frequency of Barrett’s esophagus has quadrupled over the past few decades, most likely due to improved diagnostic capability with the expansion of flexible endoscopy.
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The risk of developing adenocarcinoma in patients with Barrett’s esophagus has been estimated to be 0.5% per year ( Fig. 57-2A and B ).
Figure 57-2
A, Normal gastroesophageal junction. B, Barrett’s esophagus.
CLINICAL FEATURES
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Risk factors for the development of Barrett’s esophagus are
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Male sex
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Smoking history
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Obesity
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White ethnicity
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Age older than 50 years
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Greater than 5-year history of reflux symptoms
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Esophageal motility in Barrett’s esophagus
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Weak lower esophageal sphincter allowing for pathologic reflux to occur.
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Esophageal peristalsis is often impaired, exacerbating the delay in acid clearance from the distal esophagus.
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Chronic inflammation and fibrosis may lead to esophageal stricture, frequently at the proximal end of the involved segment.
SIGNS AND SYMPTOMS
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Most patients with Barrett’s esophagus have a history of heartburn and acid regurgitation.
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Less frequent symptoms include
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Dysphagia
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Chest pain
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Hematemesis
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Melena
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Cough
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Wheezing
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Only 4% to 10% of patients with such clinical symptoms, however, have Barrett’s esophagus.
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No symptoms are specific for Barrett’s esophagus
PATHOPHYSIOLOGY
It is believed that Barrett’s esophagus may progress from metaplasia to dysplasia and eventually to carcinoma.
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Barrett’s esophagus usually arises in the setting of chronic gastroesophageal reflux, with the incidence increasing proportionally to the degree of acid exposure.
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Bile reflux is very closely associated with Barrett’s esophagus.
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In Barrett’s esophagus, the squamous epithelium in the distal portion of the esophagus is replaced by a columnar epithelium, which contains goblet cells.
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The cuboidal cell population located at the true gastroesophageal junction is postulated to be the cell of origin of the metaplastic epithelium with the aberrant proliferation of these cells accounting for the development of intestinal metaplasia.
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This cell exhibits markers of both squamous and columnar epithelia, and is abundant in microvilli and secretory vesicles.
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Evidence that Barrett’s metaplasia can progress from dysplasia to carcinoma is as follows :
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Metaplastic and dysplastic epithelium are often found adjacent to each other in pathologic specimens.
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The progression from metaplasia to low-grade dysplasia then high-grade dysplasia and, ultimately, to carcinoma has been described.
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Helicobacter pylori does not infect the esophagus and is not associated with an increased risk of Barrett’s esophagus or the development of esophageal adenocarcinoma.
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Postulated inverse relation between strains of H. pylori infection and the risk of esophageal/gastric cardia adenocarcinoma
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It is postulated that H. pylori may actually protect the esophagus by decreasing gastric acidity and, hence, the effects of acid reflux.
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DIAGNOSIS
The diagnosis of Barrett’s esophagus is suggested by finding abnormal columnar epithelium lining the distal esophagus on endoscopy; however, this finding must be confirmed by biopsy showing intestinal metaplasia, usually with the hallmark presence of mucin-producing goblet cells.
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One must remember that shorter segments or even just tongues of columnar epithelium may be associated with adenocarcinoma of the gastroesophageal junction.
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Traditionally, the diagnosis of Barrett’s esophagus was based on the finding of long segments (≥3 cm) of columnar epithelium, but intestinal metaplasia has been identified by short segments of columnar epithelium, even in the absence of GERD
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Barrett’s esophagus is classified as follows :
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Long-segment Barrett’s esophagus (≥3 cm of specialized intestinal metaplasia)
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Short-segment Barrett’s esophagus (≤3 cm of specialized intestinal metaplasia)
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Same management for both
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TREATMENT OF GASTROESOPHAGEAL REFLUX
The goal of therapy for GERD is to ameliorate or eliminate the signs and symptoms of GERD and to prevent the development of complications from this disease. Medical treatment has been H 2 -receptor antagonists or more recently PPIs. Surgical treatment is gastric fundoplication, which effectively reduces or eliminates reflux symptoms. Both treatments are effective in reducing acid reflux symptoms (>90% symptomatic improvement). Despite the effectiveness in the control of symptoms, neither medical nor surgical antireflux therapy has been definitively proven to decrease the risk of esophageal adenocarcinoma.
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Antisecretory therapy
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Goal is acid suppression.
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Should be based on the severity of the associated esophagitis
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Control the reflux in the hope of preventing its deleterious effects
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Allows for more reliable pathologic evaluation of epithelium in looking for dysplasia by decreasing the amount of esophagitis in the field
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Currently, PPIs are frequently prescribed as the first line of therapy.
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pH studies may demonstrate continued reflux even when symptoms resolve.
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Despite twice-a-day administration of PPIs, up to 80% of patients continue to demonstrate nocturnal gastric acid reflux.
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Aggressive use of PPIs has been shown to promote partial regression of esophageal intestinal metaplasia. In a study of patients with Barrett’s esophagus and acid reflux, the use of acid suppression with PPI (omeprazole 40 mg) twice a day was compared with H2-blockers (ranitidine 150 mg) twice daily.
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The PPI (omeprazole) treatment reduced reflux in 99% of patients.
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Although small, a statistically significant regression in the length and area of Barrett’s was achieved.
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These findings do not necessarily translate into a decreased risk of cancer.
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Therefore, the need for continued surveillance is unchanged.
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There are some data that suggest that the use of antisecretory medical therapy on a long-term chronic basis may actually increase the chance of developing cancer. Furthermore, achlorhydria is believed to be a risk factor for the development of adenocarcinoma of the stomach secondary to the propagation of bacteria that produce carcinogenic compounds which flourish with achlorhydria.
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Is Barrett’s esophagus better treated with surgery than with medical treatment?
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To date, no randomized trial has definitively answered this question.
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Some studies have shown that control of reflux by fundoplication can result in regression of Barrett’s esophagus.
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Additionally, several large nonrandomized series have seen a reduction in the overall risk of cancer progression.
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In a study of endoscopic surveillance for Barrett’s esophagus, no patients who underwent Nissen fundoplication developed dysplasia or adenocarcinoma, whereas some patients in the medically treated group developed low-grade dysplasia, high-grade dysplasia, and some even progressed to adenocarcinoma with medical treatment alone.
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Five-year follow-up after fundoplication for Barrett’s esophagus showed
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Regression from low-grade dysplasia to nondysplastic Barrett’s epithelium in 44% of patients.
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No development of high-grade dysplasia or carcinoma during 410 patient-years of follow-up.
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Failure of surgical therapy is due to
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Technical error in wrap construction, especially in re-operative cases.
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Failure to recognize and identify the presence of a shortened esophagus.
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DeMeester and colleagues showed a high rate of regression of low-grade dysplasia after an adequate fundoplication. That is not typically seen with maximal medical therapy regimens. Intestinal metaplasia of the esophagus is unlikely to regress after antireflux surgery, although intestinal metaplasia confined to the cardia may regress.
Conclusions Regarding Surgery for Barrett’s Esophagus
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Surgical correction of the lower esophageal sphincter mechanism may offer the best long-term results in the treatment of patients with Barrett’s esophagus and minimize the risk of progression to cancer.
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Fundoplication can be performed using minimally invasive techniques.
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Fundoplication is safe and effective with long-lasting results.
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This approach should be strongly considered in patients with Barrett’s esophagus.
SURVEILLANCE
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Patients with either long-segment or short-segment Barrett’s esophagus require regular endoscopic surveillance.
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The objective is to identify any dysplastic changes, progression of dysplasia, or progression to adenocarcinoma. Biopsy results may reveal
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No dysplasia
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Inclusive biopsies
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Low-grade dysplasia
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High-grade dysplasia
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Invasive adenocarcinoma.
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High-grade dysplasia is characterized pathologically by enlarged pleomorphic nuclei, loss of nuclear polarity, decreased or absent mucus production, and abnormal glandular architecture.
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When this process penetrates and extends beyond the basement membrane, it is classified as adenocarcinoma.
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Among patients with Barrett’s esophagus,
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Approximately 15% to 25% have low-grade dysplasia.
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Five to ten percent have high-grade dysplasia.
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Approximately 5% to 10% of patients will progress from metaplasia to dysplasia per year, and 1% will progress to adenocarcinoma.
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Dysplasia exhibits no gross distinctive features that can be identified visually; therefore, multiple random biopsies from the affected Barrett’s segment should be obtained.
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One third to one half of patients diagnosed with high-grade dysplasia on biopsy already have an invasive malignancy if a resection is performed.
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There should be high suspicion of an underlying cancer if a nodularity or stricture is present in patients with high-grade dysplasia
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Although the natural history of dysplasia in general is not well understood, high-grade dysplasia is known to be associated with the development of adenocarcinoma.
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Ten to twenty-eight percent of patients progress from high-grade dysplasia to adenocarcinoma within 5 years.
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Unsuspected cancer was found in 33% to 45% of patients with Barrett’s esophagus who underwent esophagectomy for high-grade dysplasia without preoperative evidence of carcinoma.
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Thus, in patients with high-grade dysplasia, endoscopic surveillance is performed every 3 to 6 months.
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Performing four-quadrant biopsies taken at 1-cm intervals to help maximize the sensitivity for the detection of early cancers.
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Surveillance is controversial because no randomized trial has proven that surveillance improves survival.
TREATMENT OPTIONS FOR DYSPLASIA
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High-grade dysplasia has three potential treatment options: (1) intensive surveillance (as described above); (2) endoscopic ablative therapy; (3) esophagectomy.
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Endoscopic ablative therapies:
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Employ thermal or photochemical energy to destroy the metaplastic esophageal epithelium.
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The esophageal columnar epithelium may be removed with the aid of
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Laser coagulation
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Electrocautery
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Heater probe
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Radiofrequency ablation
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Argon beam coagulator
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PDT
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Endoscopic mucosal resection (EMR)
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Barrett’s esophagus is generally a localized, superficial process for which ablative modalities may represent a potentially viable treatment modality.
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Because early carcinoma identified in high-grade dysplasia is typically intramucosal (>90%), so local ablative therapy may be reasonable.
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EMR is an option in patients with neoplastic lesions smaller than 2 cm in diameter and with no sign of submucosal infiltration, positive lymph nodes, or distant metastasis.
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EMR allows for ( Fig. 57-3A and B ) :
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Complete resection of affected area
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Preserves architecture of resected specimen
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Enhanced staging (EUS)
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Ninety percent local remission
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Positive deep margins and submucosal invasion require surgical resection.
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Relatively new and controversial procedure
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