- Author: Kavitha Kumbum, MD; Chief Editor: BS Anand, MD more...
Disease processes that can produce esophageal strictures can be grouped into 3 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.
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.  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.
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)
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.  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. 
Diseases of the skin - Pemphigus vulgaris, benign mucous membrane (cicatricial) pemphigoid, epidermolysis bullosa dystrophica
Idiopathic eosinophilic esophagitis
Squamous cell carcinoma
Sequela of endoscopic submucosal dissection for superficial squamous cell neoplasms. 
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
Peptic stricture - Gastroesophageal reflux disease, Zollinger-Ellison syndrome
Collagen vascular disease - Scleroderma, systemic lupus erythematosus (SLE), rheumatoid arthritis
Alkaline reflux following gastric resection
Sclerotherapy and prolonged nasogastric intubation
United States data
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 2 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. 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.
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.
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.
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:
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.
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