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.
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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:
Dysfunctional lower esophageal sphincter: Mean LES pressures are lower in patients with peptic strictures compared with healthy controls or patients with milder degrees of reflux disease. A study by Ahtaridis et al showed that patients with peptic esophageal strictures had a mean LES pressure of 4.9 mm Hg versus 20 mm Hg in control patients.[1] An LES pressure of less than 8 mm Hg appeared to correlate significantly with the presence of peptic esophageal stricture without any overlap in controls.
Disordered motility resulting in poor esophageal clearance: In the same study, Ahtaridis et al demonstrated that 64% of patients with strictures had motility disorders compared with 32% of patients without strictures.[1]
Other possible associated factors include the following:
Presence of a hiatal hernia: Hiatal hernias are found in 10-15% of the general population, 42% of patients with reflux symptoms and no esophagitis, 63% of patients with esophagitis, and 85% of patients with peptic esophageal strictures. This suggests that hiatal hernias may play a significant role.
Acid and pepsin secretion: This does not appear to be a major factor. Patients with peptic esophageal strictures have been demonstrated to have the same acid and pepsin secretion rates as sex-matched and age-matched controls with esophagitis but no stricture formation. In fact, some authors believe that alkaline reflux may play an important role.
Gastric emptying: No good evidence suggests that delayed emptying plays a role in peptic esophageal strictures.
Proximal or mid esophageal strictures may be caused by the following:
Caustic ingestion (acid or alkali)
Malignancy
Radiation therapy[2, 3]
Infectious esophagitis -Candida, herpes simplex virus (HSV), cytomegalovirus (CMV), human immunodeficiency virus (HIV)
Acquired immunodeficiency syndrome (AIDS) and immunosuppression in patients who have received a transplant
Medication-induced stricture (pill esophagitis) - Alendronate, ferrous sulfate, nonsteroidal anti-inflammatory drugs (NSAIDs), phenytoin, potassium chloride, quinidine, tetracycline, ascorbic acid.[4] Drug-induced esophagitis often occurs at the anatomic site of narrowing, with the middle one third of the esophagus behind the left atrium predominating in 75.6% of cases.[5]
Diseases of the skin - Pemphigus vulgaris, benign mucous membrane (cicatricial) pemphigoid, epidermolysis bullosa dystrophica
Graft versus host disease
Idiopathic eosinophilic esophagitis
Extrinsic compression
Squamous cell carcinoma
Sequela of endoscopic submucosal dissection for superficial squamous cell neoplasms.[6]
Miscellaneous - Trauma to the esophagus from external forces, foreign body, surgical anastomosis/postoperative stricture, congenital esophageal stenosis
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.
Race-, sex-, and age-related demographics
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.
Surgical intervention
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.
Mortality/morbidity
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
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.
Reinforce the need for patients with esophageal stricture to comply with the usual antireflux precautions and lifestyle modifications.
Encourage weight loss.
Patients are told to eat smaller meals, avoid eating in a hurried fashion, and chew their food well.
Ill-fitting dentures or poor dentition should be corrected if possible.
Educate all patients with esophageal stricture about avoiding medications known to cause esophagitis, including over-the-counter medications such as aspirin and nonsteroidal anti-inflammatory drugs.
Inform all patients that the stricture recurrence rate for esophageal stricture is higher if they are noncompliant with PPI therapy.
For patient education resources, see Heartburn and GERD Center and Digestive Disorders Center, as well as Acid Reflux (GERD) and Heartburn.
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:
The obstruction is usually perceived at a point that is either above or at the level of the lesion.
Dysphagia for solids and liquids simultaneously should alert the clinician to the possibility of a motility disorder such as achalasia or collagen vascular disorders.
Dysphagia secondary to a Schatzki ring is usually intermittent and nonprogressive.
Dysphagia for solids and liquids early in the course of disease should alert the clinician to the possibility of achalasia as an etiology of a peptic esophageal stricture.
Benign esophageal strictures usually produce dysphagia with slow and insidious progression (ie, months to years) in the frequency and severity, with minimal weight loss.
Malignant esophageal strictures result in rapid progression (ie, weeks to months) of severity and frequency of dysphagia and are associated frequently with significant weight loss.
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.
Liver profile studies
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.
Complete metabolic panel
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.
Chest radiography
Posteroanterior (PA) and lateral films: Chest radiography should be used as an adjunct if extrinsic compression is considered a possible etiology of esophageal stricture.
Computed tomography (CT) scanning
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%.
Endoscopic ultrasound (EUS)
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.
Esophageal manometry
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.
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.
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
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]
General rules of esophageal dilation
Consider the following:
Many authors have questioned the need for mandatory fluoroscopy, and no published data exist to advocate safety of fluoroscopy. However, one may consider using fluoroscopy in complicated strictures, especially in guiding the blind passage of a guidewire.
Rule of 3s: The first bougie passed should be approximately equal to the estimated diameter of the stricture. Pass no more than 3 consecutive bougies of progressively increasing size after the first one that meets moderate resistance during any one dilation session. The rule of 3s has been questioned because of a lack of data verifying the increased efficacy or safety if one adheres to this rule. This rule was formulated for dilation using mercury-filled bougies resulting in dilation no greater than 1.3 mm in one session. However, polyvinyl dilators may not provide adequate tactile perception to follow this rule.
A study by Kozarek et al showed only one perforation in 400 patients dilated with polyvinyl dilators to greater than 2 mm in one session.[23]
Balloon dilators frequently dilate greater than that prescribed by the rule of 3s without any increased risk of complications.
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.
Intralesional steroid injection
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.
Endoscopic stricturoplasty
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
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.
Expandable polyester silicone-covered stent
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:
Esophageal-sparing procedures - Standard antireflux surgery (Nissen total or Belsey partial fundoplication), esophageal lengthening with antireflux surgery (Collis-Nissen or Belsey gastroplasty)
Esophageal resection and reconstruction - Gastric or colon interposition or jejunal segment
If the benign peptic stricture is dilatable, an esophageal-sparing operation is performed. Note the following:
If the length of the esophagus is normal, standard antireflux surgery and postoperative dilation as necessary is recommended.
If the esophagus is short, performing Collis gastroplasty and postoperative dilation as necessary is recommended.
If the stricture is undilatable, esophageal resection and interposition is recommended.
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:
Patients are told to avoid fatty and spicy foods, alcohol, tobacco, chocolate, and peppermint.
Patients should eat smaller meals, avoid eating in a hurried fashion, and chew their food well.
Patients should be encouraged not to eat at least 2-3 hours before bedtime.
Weight reduction should be encouraged.
Ill-fitting dentures or poor dentition should be corrected if possible.
Several studies have shown that aggressive acid suppression using PPIs is extremely beneficial in the long-term management of peptic esophageal strictures in terms of stricture recurrence (see Medical Care).
Patients must continue to follow antireflux precautions and modify their lifestyle as necessary to complement medical therapy.
Reviewing all prescription and over-the-counter medications on a regular basis is important to prevent medication-induced stricture recurrence or worsening.
Educate all patients about not taking medications known to cause esophagitis, including over-the-counter medications such as aspirin and nonsteroidal anti-inflammatory drugs.
Two studies have shown that the number of stricture dilatations has decreased dramatically in North America since the introduction of PPIs in the market.
In a study by Dunne et al, the annual number of dilatations decreased from approximately 120 in the pre-PPI era to 50 in the post-PPI era in Kingston, Ontario.[41]
In another study by Ugheoke et al in the United States, the number of dilatations performed in 4-year intervals decreased from 504 in the pre-PPI era to 144 in the post-PPI era in one institution.
Computerized databases from 1986-2001 of 2 large community hospitals were analyzed by Guda et al.[42] The need for stricture dilation peaked in 1994 but dropped significantly from 1998-2001, corresponding to an increase in the use of PPIs from 1995 onward.
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:
Suppresses gastric acid secretion by specifically inhibiting H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells.
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.
Kavitha Kumbum, MD, Associate Program Director and Attending Physician, Gastroenterology Fellowship Program, Division of Gastroenterology, Bronx Lebanon Hospital Center, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF, Associate Professor of Clinical Medicine, Albert Einstein College of Medicine of Yeshiva University; Associate Professor of Clinical Medicine, Hofstra Medical School
Disclosure: Nothing to disclose.
Acknowledgements
Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center
Rajeev Vasudeva, MD, FACG Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine
Rajeev Vasudeva, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Columbia Medical Society, South Carolina Gastroenterology Association, and South Carolina Medical Association
Disclosure: Pricara Honoraria Speaking and teaching; UCB Consulting fee Consulting
Dunne DP, Rupp T, Rex DK, Lehman GA. Five year follow-up of prospective randomized trial of Savary dilation with or without intra-lesional steroids for benign gastroesophageal reflux strictures [abstract]. Gastroenterology. 1999. 116:A152.
Raijman I, Siddique I, Rachal LT. Endoscopic stricturoplasty in the management of recurrent benign esophageal strictures. Gastrointest Endosc. 1999. 49:AB172.
Dunne D, Mercer D, Paterson WG. Decreasing frequency of esophageal dilation for peptic stricture correlates with omeprazole use. Can J Gastroenterol. 1997. 11(suppl A):43A.
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