Disease processes that can produce esophageal strictures can be grouped into three general categories: (1) intrinsic diseases that narrow the esophageal lumen through inflammation, fibrosis, or neoplasia; (2) extrinsic diseases that compromise the esophageal lumen by direct invasion or lymph node enlargement; and (3) diseases that disrupt esophageal peristalsis and/or lower esophageal sphincter (LES) function by their effects on esophageal smooth muscle and its innervation.
Many diseases can cause esophageal stricture formation. These include acid peptic, autoimmune, infectious, caustic, congenital, iatrogenic, medication-induced, radiation-induced, malignant, and idiopathic disease processes.
The etiology of esophageal stricture can usually be identified using radiologic and endoscopic modalities and can be confirmed by endoscopic visualization and tissue biopsy. Use of manometry can be diagnostic when dysmotility is suspected as the primary process. Computed tomography (CT) scanning and endoscopic ultrasonography are valuable aids in staging of malignant stricture. Fortunately, most benign esophageal strictures are amenable to pharmacologic, endoscopic, and/or surgical interventions.
Because peptic strictures account for 70-80% of all cases of esophageal stricture, peptic stricture is the focus of this article. A detailed discussion of possible benign and malignant processes associated with esophageal stricture and its management is beyond the scope of this article.
See the image below.
View Image | Esophageal stricture. Endoscopic appearance of the distal esophagus showing a smooth stricture with a benign appearance. |
Peptic esophageal strictures are sequelae of gastroesophageal reflux -induced esophagitis, and they usually originate at the squamocolumnar junction and average 1-4 cm in length.
Two major factors involved in the development of a peptic esophageal stricture are as follows:
Other possible associated factors include the following:
Proximal or mid esophageal strictures may be caused by the following:
Distal esophageal strictures may be caused by the following
Gastroesophageal reflux affects approximately 40% of adults. Esophageal strictures are estimated to occur in 7-23% of untreated patients with reflux disease.
Gastroesophageal reflux disease accounts for approximately 70-80% of all cases of esophageal stricture. Postoperative strictures account for about 10%, and corrosive strictures account for less than 5%.
The overall frequency of initial and subsequent dilations for peptic stricture appears to have decreased gradually since the introduction of proton pump inhibitors (PPIs) in 1989. This has been borne out by data at the author's institution and in two large community hospitals in Wisconsin. It is also in keeping with the general experience of gastroenterologists in the United States.
Peptic strictures are 10-fold more common in whites than blacks or Asians. However, this is controversial as a recent retrospective study reported comparable frequencies between blacks and non-Hispanic whites.[7] The authors reported that distribution of reflux esophagitis and the grade and frequency of reflux-related esophageal ulcer and hiatal hernia were also similar in non-Hispanic whites and blacks. However, heartburn was more frequent and nausea/vomiting less frequent in non-Hispanic whites compared with blacks with erosive esophagitis or its complications.[7]
Peptic strictures are 2- to 3-fold more common in men than in women.
Patients with peptic stricture tend to be older, with a longer duration of reflux symptoms.
Several studies have shown that progressive dilation of peptic strictures to 40-60F resulted in effective relief of dysphagia in approximately 85% of cases, with a low rate of complications. However, 30% of patients require repeat dilation in 1 year despite optimal acid suppression therapy. This is in comparison to a 60% recurrence rate without adequate acid suppression therapy.
Poor prognostic factors include a lack of heartburn and significant weight loss at initial presentation.
The severity of the initial stenosis and the type and size of dilator used have no effect on esophageal stricture recurrence.
The outcome of surgery is highly dependent on the surgeon's experience and whether or not it is performed in high-volume centers. Most surgical series report a good-to-excellent outcome in 77% of cases, with the range being 43-90%.
The repeat dilation rate is reported to be 1-43% after surgery, requiring 1-2 sessions at most.
Mortality and morbidity rates are reported to be less than 0.5% and 20%, respectively.
Currently, no good controlled trials exist comparing the efficacy, outcome, and safety of surgery with aggressive medical management that includes PPIs and dilation as necessary.
The mortality rate of peptic strictures is not increased unless a procedure-related perforation occurs or the stricture is malignant. However, the morbidity for peptic strictures is significant.
Most patients undergo a chronic relapsing course with an increased risk of food impaction and pulmonary aspiration.
Frequently, coexistent Barrett esophagus and its attendant complications occur.
The need for repeated dilatations potentially increases the risk of perforation.
Complications include perforation, bleeding, and bacteremia.
Bleeding
A 1974 American Society of Gastrointestinal Endoscopy (ASGE) survey estimated rates of perforation to be 0.1% and bleeding to be 0.3%. A 1984 ASGE survey estimated the overall complication rate to be 2.5%. In general, both of these complications seem to occur with equal frequency, but significant variation in published reports exists. Providing precise estimates is difficult because of flawed methodologies in the published literature. However, based on this review, one would estimate that the risk of serious complications is approximately 0.5%.
A multivariate analysis found that predictors of massive bleeding following stent placement for malignant esophageal stricture/fistulae included the presence of esophageal fistulae, previous radiotherapy, and concomitant tracheal stent.[8]
Bacteremia
Bacteremia appears to occur in approximately 20-45% of all dilations based on some reports in the literature; however, it usually is clinically insignificant, and reports of endocarditis and brain abscesses are rare. Antibiotic prophylaxis is recommended in all high-risk cases as defined by the American Heart Association guidelines.
Consider the following:
Patients with peptic strictures may present with heartburn, dysphagia, odynophagia, food impaction, weight loss, and chest pain. Progressive dysphagia for solids is the most common presenting symptom. This may progress to include liquids.
Atypical presentations include chronic cough and asthma secondary to aspiration of food or acid.
The clinician cannot rely on the presence or absence of heartburn to definitely determine whether dysphagia is secondary to a peptic esophageal stricture. Of patients with peptic esophageal strictures, 25% have no previous history of heartburn. Heartburn may resolve with worsening of a peptic stricture.
Approximately two thirds of patients with adenocarcinoma in Barrett esophagus have a history of long-standing heartburn.
The abnormal esophageal motor activity in achalasia can produce a heartburn sensation.
Important points regarding dysphagia include the following:
Determining whether the patient takes any medications known to cause pill esophagitis is important.
Determining whether a history of collagen vascular disease or immunosuppression exists may provide clues to the underlying etiology.
Physical examination frequently does not provide clues to the cause of dysphagia. Assessing the patient's nutritional status is important.
Patients with collagen vascular diseases may exhibit joint abnormalities, calcinosis, telangiectasias, sclerodactyly, or rashes.
The presence of atypical gastroesophageal reflux disease may be suggested by hoarse voice, posterior oropharyngeal erythema, diffuse dental erosions, wheezing, or epigastric tenderness.
Patients with adenocarcinoma of the gastroesophageal junction may have left supraclavicular lymphadenopathy (Virchow node).
Usually, the results of a CBC are within the reference range; however, anemia may develop due to chronic bleeding from severe esophagitis or carcinoma.
Usually, the findings are within the reference range; however, the liver profile may be abnormal if metastatic disease is present in patients with an underlying malignancy.
This study may allow assessment of the patient's nutritional status, especially in conjunction with weight loss.
A barium esophagram provides an objective baseline record of the esophagus before medical therapy or endoscopic intervention.[9] This study also provides information about the location, length, and diameter of the stricture and the smoothness or irregularity of the esophageal wall (road map). The information obtained can complement endoscopic findings.
Lesions, such as diverticula and paraesophageal hernias, that potentially may lead to increased risk of complications during endoscopy can be identified.
This study may be more sensitive than endoscopy for detection of subtle narrowings of the esophagus such as those caused by rings and peptic strictures that are greater than 10 mm in diameter.
This study has 100% sensitivity with luminal diameter less than 9 mm, and 90% sensitivity with luminal diameter greater than 10 mm.
Posteroanterior (PA) and lateral films: Chest radiography should be used as an adjunct if extrinsic compression is considered a possible etiology of esophageal stricture.
CT scans can be used to stage malignancies that produce esophageal strictures. Accuracy in estimating the depth of tumor invasion is 60-69%. Accuracy in determining spread to other organs is 82%.
EUS is the most accurate means of identifying the extent of local invasion of an esophageal malignancy. Accuracy in estimating the depth of tumor invasion in the esophagus is 92%.
This study may be helpful in evaluating and documenting the adequacy of therapy in patients who remain symptomatic despite treatment with PPIs or fundoplication.
This test is used to evaluate any patient suspected of having esophageal dysmotility. It may be used as a preoperative tool before antireflux surgery to evaluate the presence of severe esophageal dysmotility.
Esophagogastroduodenoscopy (EGD)
This procedure can be used to establish or confirm the diagnosis of esophageal stricture, to seek evidence of esophagitis, to exclude malignancy, to obtain biopsy and brush cytology specimens, and to implement therapy.
EGD is more sensitive than barium esophagram in the identification of subtle mucosal lesions.
Subtle strictures may be missed when smaller and thinner endoscopes are employed, especially in the setting of minimal sedation.
Initial histologic changes in the peptic stricture process include edema, cellular infiltration, basal cell hyperplasia, and vascular changes with a slight increase in type III collagen deposition on healing.
If untreated, the process can lead to progressive inflammation and ulceration involving the submucosa and muscularis mucosa. This can lead to damage of the muscular layer and the intrinsic nervous system of the esophagus, resulting in deposition of type I collagen with subsequent formation of scar tissue and stricture formation.
CT scanning and EUS are used mainly to stage malignancies that produce esophageal strictures.
CT scanning: Sixty to 69% accurate in estimating the depth of tumor invasion and 82% accurate in determining spread to other organs
EUS: Most accurate means of identifying the extent of local invasion; it is 92% accurate in estimating the depth of tumor invasion in the esophagus
Traditionally, more emphasis has been placed on mechanical dilatation, and coexistent esophagitis has been relatively ignored. However, several studies have demonstrated that aggressive acid suppression using PPIs is extremely beneficial in the initial treatment of esophageal stricture, as well as long-term management.
A dysphagia score developed by Dakkak et al in a study of 64 patients revealed that the stricture diameter only contributed to 30% of the dysphagia score and that esophagitis and other factors accounted for 70% of the score.[10] A linear association existed between the dysphagia score only when the luminal diameter was less than 5 mm. Overall, the degree of dysphagia was worse with increasing esophagitis independent of the degree of stenosis.[10]
Smith et al showed in a randomized study of 366 patients that omeprazole 20 mg/d was superior to ranitidine 300 mg twice a day in preventing stricture recurrence with redilation rates of 30% and 46%, respectively, at 12 months (P< 0.01).[11]
Marks et al showed that the redilation rate in patients treated with omeprazole 20-40 mg/d was 41% versus 73% in patients treated with ranitidine 150-300 mg twice per day and almost reached significance (P< 0.07).[12] Moreover, the omeprazole group showed higher rates of dysphagia relief and healing of esophagitis when compared with histamine 2 (H2) blockers.
In contrast, two other studies by Swarbrick et al[13] and Silvis et al[14] did not show any significant differences in the redilation rates at 12 and 10 months, respectively.
PPI treatment of patients with esophageal stricture is more cost effective than H2 blocker therapy. Marks et al found that over a 6-month period, the cost of omeprazole therapy was $1744 compared with $2957 with H2 blockers.[12]
H2 blockers have not been shown to be any better than placebo in various trials, and no reliable data on prokinetic agents exist.
The following discussion concerns the endoscopic and surgical modalities employed for the management of peptic esophageal stricture. The choice of dilator and technique is dependent on many factors, the most important being stricture characteristics. It is also based on other factors, including patient tolerance, operator preference, and experience. No clear consensus on the optimal end point exists. In summary, dilation therapy should be tailored individually.
Endoscopic dilation dates to the 16th century, when physicians used wax wands for esophageal dilation.[15, 16] The word bougie is derived from Boujiyah, an Algerian city that was the center of the medieval candle trade. Three types of dilators are used, as discussed below.
Mercury-filled bougies, such as Maloney or Hurst dilators, are indicated in uncomplicated strictures with diameters greater than 10-12 mm. They are inexpensive and simple to perform without fluoroscopic guidance. In addition, minimal or no sedation is necessary. Self-bougienage may be performed at home.
Wire-guided polyvinyl bougies, such as Savary-Gilliard and American dilators, are relatively stiff and better suited for longer, tighter, and irregular strictures. The need for fluoroscopy is variable. The range is 5-20 mm, and these dilators are reusable. However, drawbacks include trauma to the laryngeal wall and patient discomfort. American dilators are shorter, less tapered, and impregnated with barium for better fluoroscopic visualization.
Savary dilators appear to be safe and effective in the treatment of esophageal narrowing related to pediatric eosinophilic esophagitis (EoE).[17] In a retrospective study (2004-2015) of 50 pediatric cases of EoE in which 11 cases had esophageal narrowing (22%), 19 dilation sessions in 10 cases resulted in good response in all cases. The esophageal size improved from a median of 7 mm to 13.4 mm. Although longitudinal esophageal tear occurred in all cases, no esophageal perforation or chest pain was reported.[17] The investigator noted that a combination of dilation with dietary or medical intervention is required in managing these patients.
Through-the-scope (TTS) balloon dilators are used through the endoscope, and they allow for direct visualization. These are relatively expensive and not reusable. Fluoroscopy is not mandatory, but it is useful in difficult cases. However, studies conflict about the benefits of balloon dilators compared with Savary dilators.[18]
Two separate retrospective institutional studies indicate that fluoroscopic balloon dilatation (FBD) is safe and effective for treating, respectively, esophageal anastomic stricture after surgical repair and caustic esophageal stricture.
In Thyoka et al's review of 12-years of data (1999-2011) from 103 consecutive patients with esophageal anastomotic stricture following surgical repair who underwent 378 FBD sessions, 93 patients (90%) achieved symptomatic relief after a single session (n=44; 47%) or after multiple sessions (n=49; 53%).[19] Of 10 patients who underwent more procedures, 3 had stent placement, 3 had stricture resection, and 4 had esophageal reconstruction. No deaths were reported, but there were 4 esophageal perforations following FBD.[19]
In Uygun et al's review of 8 years of data (2004-2012) from 38 children who underwent FBD for caustic esophageal stricture, 369 FBD sessions were successful overall.[20] Patients who underwent FBD earlier following caustic ingestion had significantly faster and shorter treatment than those who underwent the procedure later after caustic ingestion. In addition, children with shorter esophageal strictures also had significantly shorter FBD treatment than those who had longer esophageal strictures. No deaths were reported, but 5 patients suffered 6 esophageal perforations, which were managed with conservative therapy.[20]
In a prospective, randomized study with 17 patients in each arm comparing balloon dilators with Savary dilators performed over a 2-year period, with the end point being 45F, stricture recurrence was similar in the first year but lower in the second year for balloons, fewer sessions were needed for balloons (1.1 sessions +/- 0.1 versus 1.7 sessions +/- 0.2), and less procedural discomfort occurred (P< 0.05).[21] Both devices were effective in relieving dysphagia.
Another prospective, randomized study by Scolapio et al that included 251 patients with peptic strictures found that Schatzki rings did not show any differences in complications, the degree of immediate relief, or the time to recurrent dysphagia.[22]
Consider the following:
No consensus exists regarding the end point of esophageal dilation for peptic strictures. Most patients experience complete relief when dilated to 40-54F. Therefore, using this end point as a benchmark is recommended. Thus, in summary, the extent of the dilatation should be individualized based on symptomatic response and technical difficulty encountered during therapy.
Limited anecdotal data exist showing that intralesional steroid injection of peptic strictures may be beneficial. The mechanism is unclear; it may inhibit collagen formation and enhance collagen degradation, thus increasing stricture compliance.[24]
Triamcinolone 10 mg/mL in 0.5 mL aliquots was injected in 4 quadrants in 2 patients with a successful outcome as reported by Kirsch et al.[25]
Lee at al showed a higher rate of achieving greater luminal diameters and duration between dilations in a nonrandomized cohort of patients with strictures of varying etiologies.[26] Similar results were obtained by Kochhar et al in 71 patients, although 8 injections of 20 mg of triamcinolone in 0.5-mL aliquots were given at the proximal margin and into the stricture itself.[27]
A randomized prospective trial of Savary dilation with or without intralesional steroids was conducted in 42 patients by Dunne et al[28] ; it demonstrated a decreased need for second dilations in the steroid group (1.95 vs 5.5) at 1 year. Similar results were seen in a study by Ramage et al in 30 patients, but the latter study was also double blinded with a sham group.[29] Two patients (13%) in the steroid group and 9 patients (60%) in the sham group needed repeat dilation over a 12-month period.
Therefore, a trial of steroid injection may be reasonable in patients with benign strictures who experience no significant relief of dysphagia despite repeated dilations and aggressive antireflux therapy. Hishiki et al reported the use of repeated endoscopic dilatation with systemic steroids in a child with severe esophageal anastomotic stricture that did not respond to endoscopic dilatation and local steroid injection of the stricture.[30] At 18 months follow-up, the child remained asymptomatic without any further endoscopic dilations.
Two case series described a technique using a needle knife to make four quadrant incisions followed by Savary dilation. This was successful in 8 of 8 patients as reported by Raijman et al[31] and 5 of 6 patients as reported by Hagiwara et al.[32]
Pharyngoesophageal puncture is a term recently coined by Tang et al to describe the technique of endoscopic dilation of radiation-induced severe or complete pharyngoesophageal strictures.[33] A combination of guide wires, endoscopic balloons, puncture and techniques learned from ERCP were successfully applied in 3 patients with severe/complete stenosis.
Repici et al presented a case series of 15 patients whose condition had failed endoscopic therapy.[34] A temporary placement of a stent for 6 weeks was successful in 12 patients over a long-term period (mean follow-up, 22.7 [2.6] mo). However, the exact duration of stent placement remains unclear, as strictures can recur following stent removal.[35] Furthermore, a variety of complications have been described following stent deployment.[36, 37] More recently, biodegradable stents have shown some promise in animal studies and were used to treat severe corrosive esophageal stenosis in a child.[38]
In a retrospective multicenter study of 70 patients who underwent fully or partially covered self-expandable stent placement (114 procedures) for benign esophageal diseases (benign refractory esophageal strictures, surgical anastomotic strictures, esophageal perforations, esophageal fistulae, surgical anastomotic leaks), investigators found an overall treatment success rate of 55.7%.[39] They reported 100% success rates for esophageal perforations, followed by 80% for anastomotic leaks, 71.4% for fistulae, 33.3% for refractory benign strictures, and 23.1% for anastomotic strictures. The investigators suggested that esophageal stenting be considered as a first-line therapy for benign esophageal perforations, fistulae, and leaks.[39, 40]
The role of surgical treatment in peptic stricture remains in dispute. Indications include failed aggressive medical therapy or an unsuitable candidate for aggressive medical therapy. This is usually a rare occurrence in the era of PPI therapy. Various procedures advocated include the following:
If the benign peptic stricture is dilatable, an esophageal-sparing operation is performed. Note the following:
In the literature, some anecdotal reports exist of minimally invasive surgery, including laparoscopic transhiatal esophagectomy and laparoscopic Collis gastroplasty with Nissen fundoplication. With continuing advances in technology, whether or not minimally invasive surgery would play a major role in the surgical management of peptic stricture remains to be determined.
Surgical consultation is indicated for esophageal stricture if aggressive medical therapy fails or the patient is an unsuitable candidate for aggressive medical therapy.
Surgical consultation is also indicated if the stricture is malignant and amenable to curative or palliative resection.
The usual antireflux precautions and lifestyle modifications should be reinforced, although no published data exist showing that these measures are efficacious in peptic strictures. Note the following:
Consider the following:
Closely follow patients' cases to determine the adequacy of esophageal dilation or surgery in relieving dysphagia and the adequacy of pharmacologic antireflux therapy.
Individualize the interval of follow-up visits.
Recurrent dysphagia or inadequate reflux symptom relief should prompt repeat dilation and more aggressive antireflux therapy as necessary.
Counsel patients with esophageal stricture on an ongoing basis regarding the benefits of antireflux dietary precautions and lifestyle modifications.
Antisecretory medications are generally used for the treatment of acid-peptic stricture of the esophagus. PPIs are the most efficacious drugs, and this class is usually used routinely.
Long-term PPI therapy (almost indefinitely) is extremely important in patients with esophageal stricture. The dosage of PPIs may be guided by the patient's response and is based on endoscopic findings on repeat endoscopies and dilation. Not unusually, these patients require high-dose PPI therapy to achieve the most satisfactory response.
Clinical Context: Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.
Clinical Context: Suppresses gastric acid secretion by specifically inhibiting H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells.
Clinical Context: Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Clinical Context: Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.
Clinical Context: S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase enzyme system at secretory surface of gastric parietal cells.
PPIs specifically inhibit the H+/K+ -ATPase enzyme system at the secretory surface of the gastric parietal cell, resulting in a potent antisecretory effect.