How can I be sure that the patient has an esophageal stricture?
An esophageal stricture is a narrowing of the esophagus that impedes the progress of a bolus as it transits to the stomach. There are multiple causes of esophageal strictures (Table I).
Table I.
| Gastroesophageal reflux disease (peptic stricture) |
| Radiation therapy |
| Caustic injury (lye ingestion; button batteries) |
| Ischemic injury (cocaine; vascular insult) |
| Congenital stricture |
| Postablation therapy for Barrett’s esophagus (photodynamic therapy or radiofrequency ablation) |
| Pill esophagitis |
| Eosinophilic esophagitis |
| Schatzki’s ring |
| Webs (i.e., Plummer-Vinson syndrome) |
| Postsurgical – Antireflux surgery – Myotomy – Anastomotic – Esophageal atresia repair – Tracheo-esophageal fistula repair |
| Postvariceal therapy (banding or sclerotherapy) |
| Crohn’s disease |
| Graft-vs-host disease |
| Benign mucous membrane pemphigoid |
| Epidermolysis bullosa dystrophica |
| Adenocarcinoma of the esophagus |
| Squamous cell carcinoma of the esophagus |
| Extrinsic compression |
The prototypical symptom of an esophageal stricture is dysphagia. Because dysphagia is nonspecific and has a broad differential diagnosis (see Table II), a careful history and physical exam are required.
Table II.
| STRUCTURAL CAUSES |
| Benign |
| Stricture – Peptic – Radiation – Caustic – Ischemic – Congenital – Postablation (endoscopic mucosal resection, photodynamic therapy, or radiofrequency ablation) |
| Esophagitis – Reflux – Pill – Infections (candidal; HSV; CMV; HIV) – Eosinophilic – Graft-vs-host disease |
| Schatzki’s ring |
| Webs (i.e., Plummer-Vinson syndrome) |
| Diverticula – Pharyngeal (Zenker’s) – Mid-esophageal (parabronchial) – Distal esophageal (epiphrenic) |
| Esophageal duplication cysts |
| Crohn’s disease |
| Benign mucous membrane pemphigoid |
Dysphagia is defined as the sensation of food being hindered in its passage from the mouth to the stomach. The first distinction to make with regard to history is whether there is oropharyngeal (transfer) dysphagia or esophageal (transport dysphagia). The former is characterized by inability to move the food bolus from the mouth to the pharynx and into the esophagus (i.e., difficulty initiating a swallow, with symptoms of choking, aspiration, or nasal regurgitation) and is not a symptom of an esophageal stricture. The latter is characterized by a sensation of food sticking or “hanging up” in the esophagus after a swallow is initiated and is the typical symptom of an esophageal stricture.
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After the symptom of esophageal dysphagia is confirmed, it should be further characterized. What is the time course? The frequency? Is the dysphagia progressive? Where does the food stick? A location below the sternal notch, while not specific, is suggestive of an esophageal location. Has the patient compensated by altering their diet, chewing food very slowly until it is mushy, or eating extremely slowly? Are there associated symptoms of chest pain, odynophagia, heartburn/pyrosis, or weight loss? Has there been an acute food impaction or esophageal obstruction? Each of these can help narrow the differential diagnosis. It is critical to determine whether the picture is predominantly of solid food dysphagia, often indicating a structural etiology, or a combination of dysphagia to both liquids and solids, which can suggest esophageal dysmotility as the cause.
Overall, the symptom of solid food dysphagia (which, if progressive over time, could involve liquid dysphagia as well) is suggestive of an esophageal stricture. The presence of heartburn can suggest a peptic stricture. Antecedent radiation treatment or a caustic ingestion points to a radiation stricture or a caustic stricture. A strong history of concomitant atopic disease and food impaction in a younger individual brings to mind eosinophilic esophagitis. If there is associated weight loss, anemia, or overt GI bleeding, an esophageal malignancy should be considered. Because this symptom complex is not specific (see Table II), further evaluation is necessary to confirm the diagnosis and determine the treatment plan.
A tabular or chart listing of features and signs and symptoms
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How can I confirm the diagnosis?
Because the symptom of solid food dysphagia is nonspecific, further testing is required to confirm the diagnosis. The two main diagnostic modalities are upper endoscopy (esophagogastroduodenoscopy, EGD) and barium swallow (contrast esophagogram).
In almost every case, EGD is now considered the diagnostic test of choice. It allows careful inspection of the esophagus mucosa, visualization and identification of structural lesions such as strictures, and procurement of esophageal biopsies. In many cases, EGD is also a therapeutic modality (see below).
Because EGD is invasive, somewhat costly, and not immediately available in all health-care settings, barium esophagram is also useful. It can be considered a first-line test if there is suspicion for a very proximal esophageal lesion (cricopharyngeal bar, Zenker’s diverticulum), suspicion for achalasia, or when there is history of a complex esophageal stricture or prior esophageal surgery, where a “roadmap” of the esophagus is desired before passing an endoscope. Barium swallow should not be performed in the setting of acute esophageal bolus impaction or when there is inability to tolerate oral secretions because of the risk of aspiration.
Endoscopic characteristics of selected causes of esophageal strictures are the following:
– A normal esophagus is a conduit lined with nonkeratinized, stratified squamous epithelium that is widely patent. The normal mucosa has a fine vascular pattern that is readily visible (Figure 1).
Figure 1.
– A peptic stricture due to gastroesophageal reflux disease is typically located in the distal esophagus, at the gastroesophageal junction (GEJ). There is often concomitant erosive esophagitis present, so the narrowing in the esophagus is often irregular. There can be scar tissue present as well, a result of the cycle of inflammation, erosion, and healing (Figure 2).
Figure 2.
– A Schatzki’s ring is a thin mucosal band at the squamocolumnar junction, typically associated with a hiatal hernia. It is a commonly encountered cause of solid food dysphagia. While the etiology of these rings is unknown, they are thought to be associated with gastroesophageal reflux disease (GERD) and have a high rate of recurrence (Figure 3).
Figure 3.
– Radiation therapy for head and neck or chest malignancies is a common cause of esophageal strictures that is readily identified by a patient’s past medical history. The therapeutic window for XRT of the esophagus is narrow, and usual treatment doses cause esophageal toxicity (radiation esophagitis causing odynophagia) in 10% to 30% of patients, with approximately 5% to 10% developing radiation strictures. In a smaller proportion of patients, these strictures completely obstruct the esophagus (Figure 4). It is important to differentiate a radiation stricture from a recurrence of the original cancer.
Figure 4.
– Either inadvertent or intentional ingestion of caustic agents, such as bleach or lye, various concentrated acids, or chemicals that leach from batteries, can lead to acute esophageal injury with severe inflammation or even necrosis. The healing process can result in long, complicated strictures with diffuse esophageal narrowing that can be difficult to treat (Figure 5). This cause is also elicited on history, but some patients may be reluctant to report or share details about such an event.
Figure 5.
– Eosinophilic esophagitis (EoE) is an increasingly recognized cause of dysphagia, and has been rapidly increasing in incidence and prevalence over the past decade. It is felt to be an allergy-medicated disease, wherein high levels of eosinophils infiltrate the esophageal epithelium. The cardinal endoscopic features are esophageal rings (previously termed corrugations, felinization, or trachealization), longitudinal linear furrows, and white plaques or exudates (representing eosinophilic microabscesses histologically) (Figure 6). The esophagus can also be diffusely narrowed, which can be hard to appreciate, congested or edematous, and have a decreased vascular pattern. The mucosa can also be delicate and tear with the passage of an endoscope or a dilator; this is termed “crêpe-paper” mucosa.
Figure 6.
– Malignancy of the esophagus presents with progressive solid food dysphagia, and is often associated with weight loss or anemia. The two major pathologic subtypes are squamous cell carcinoma and adenocarcinoma, and, over the last several decades, the incidence of the later has been increasing rapidly and is now more common than the former. On endoscopy, a mass can be seen growing into or even obstructing the esophageal lumen (Figure 7), and biopsies are needed to confirm the diagnosis.
Figure 7.
What other diseases, conditions, or complications should I look for in patients with esophageal strictures?
The full differential diagnosis for esophageal strictures is presented in Table II. For full details about each condition, please see the associated chapter in Clinical Decision Support System on Gastroenterology and Hepatology.
One major complication of an esophageal stricture is acute food bolus impaction. This is when an ingested food bolus becomes lodged in the esophagus, does not pass distally into the stomach, and the patient is unable to clear it proximally by inducing vomiting. This is a GI emergency requiring urgent evaluation and prompt endoscopy to clear the bolus. There can be local injury to the esophageal wall from the impacted bolus and, in some instances, acute food bolus impaction can result in esophageal perforation or Boerhaave’s syndrome. Perforation needs to be excluded in a patient presenting with food impaction and chest pain prior to passing an endoscope.
Another complication of esophageal malignancies and radiation strictures is complete esophageal obstruction. This is when the malignancy or stricture completely occludes the esophagus and prevents even liquids or oral secretions from passing. This is a difficult clinical situation, but a possible solution for managing these cases is presented below (combined antegrade-retrograde dilation).
What is the right therapy for the patient with esophageal stricture?
There are several therapeutic options for patients with esophageal strictures (see Table III), but the specific treatment and most effective initial therapy needs to be aligned with the underlying etiology. However, in many cases, esophageal dilation is the treatment of choice. The patient with a stricture may have clinical benefit with only one dilation, but serial dilations over time are frequently needed to slowly and safely increase the esophageal diameter and lead to symptom resolution. Other options, discussed later, include intrastricture steroid injection, esophageal stenting, needle-knife sphincteroplasty, and, in the most refractory cases, esophagectomy.
Table III.
| Dilation |
| Mechanical – Blindly passed bougie – Wire-guided bougie |
| Balloon – Through-the-scope – Over-the-wire |
| Combined antegrade-retrograde technique (for complete esophageal obstruction) |
| Second-line options for refractory strictures |
| Intralesional steroid injection |
| Esophageal stenting – Fully covered self-expanding metal stents – Self-expanding plastic stents |
| Incisional stricturoplasty |
| Antiproliferative drug application |
| Surgery |
What is the most effective initial therapy?
N/A
Listing of usual initial therapeutic options, including guidelines for use, along with expected result of therapy.
Dilation overview
For the majority of stricture types where the esophagus is patent (i.e., peptic, radiation, caustic, ischemic, congenital, postablation, and reflux strictures; Schatzki’s rings; webs; and eosinophilic esophagitis and malignancy) esophageal dilation is the treatment of choice.
There are two major approaches to esophageal dilation: bougie (mechanical) dilation and balloon dilation.
Bougie dilation. For mechanical dilation, there are two general types of bougies: those that are blindly passed and those that are wire-guided. An example of a blindly passed bougie is the Maloney dilator. This is a plastic dilator with a tapered tip, which historically was weighted with mercury (but now contains tungsten). This dilator is primarily restricted to use in simple strictures (see discussion below), and is less commonly used in current practice. An example of a wire-guided bougie is the Savary-Gilliard dilator. This is also a plastic dilator with a tapered tip, as well as a central channel through which a guidewire can pass. This dilator is commonly used in a wide variety of strictures. Both types of dilator are available in a variety of sizes, from as small as 5 mm (15 F) to as large as 20 mm (60 F), and are reusable.
Balloon dilation. For balloon dilation, there are also two general types of dilators: a through-the-scope (TTS) balloon and an over-the-wire (OTW) balloon. As indicated by the name, the TTS balloon passes through the instrument channel of an upper endoscope, and dilation proceeds by direct visualization. The OTW balloon can be positioned over a guidewire that is placed endoscopically or fluoroscopically. Both types of balloon dilator are available in multisize increments, ranging from as small as 6 mm to as large as 20 mm. Typically, each balloon size has a range of approximately 2 to 3 mm (e.g., 6-7-8 mm or 12-13.5-15 mm), and the desired diameter size is achieved by inflating the balloon with water to a corresponding pressure. These balloon dilators are single-use only.
There have been multiple randomized trials comparing different bougie and balloon dilation techniques and, overall, the safety and efficacy appears comparable, particularly in the largest of the trials. The choice of which technique to use is often determined by local expertise and the individual gastroenterologist’s preference or comfort with one technique over the other. Anatomic considerations can play a role in dilator choice, however. Lesions that are in the very proximal esophagus are typically difficult to dilate with a TTS balloon. Because these balloons are usually 5 to 8 cm in length, when deployed in the proximal esophagus, they can extend across the upper esophageal sphincter and into the hypopharynx, an area that can be uncomfortable or not tolerated by a patient under conscious sedation.
Dilation considerations
When performing esophageal dilation, there are several general considerations and well as specific nuances for each technique. First, most guidelines suggest distinguishing between simple and complex strictures. A simple stricture has a diameter greater than 1 cm, allows passage of a standard adult upper endoscopy, is short in length, is not tortuous, is symmetrical, and does not have evidence of ulceration, erosions, or inflammation. This is the only stricture type that is generally amenable to blind dilation by nonwire-guided bougies. An example of this stricture could be a web, a Schatzki’s ring, or a mild peptic stricture.
In contrast, a complex stricture is narrower than 1 cm, can be long or tortuous, can have abnormal mucosa or associated diverticula (or pseudodiverticula), and might require use of a thinner scope, such as a neonatal upper endoscope. These types of strictures are characteristic of caustic, ischemic, or radiation injury, or eosinophilic esophagitis. For complex strictures, wire-guided bougies or TTS balloon dilators are commonly used.
A second consideration is how much to dilate at each session. There is a balance between trying to achieve a large diameter to improve symptoms rapidly and causing a complication such as an esophageal perforation (see discussion below). Based on experience, most gastroenterologists follow the so-called “rule of threes.” This rule, first applied to bougie dilators but extended to balloon dilators, holds that no more than three progressively larger dilator sizes should be passed against resistance. For example, an endoscopist would start with a bougie that is thought to match the internal diameter of the stricture. If this passes without resistance, the next larger size is used. This process is repeated until there is resistance for three sizes. The same principle can be applied to balloon dilation.
A final consideration is whether the patient may have an esophageal stricture due to eosinophilic esophagitis. In initial reports of esophageal dilation in this condition, there were very high rates of mucosal laceration and esophageal perforation with dilation. However, as a larger experience with esophageal dilation has accumulated in this patient population, esophageal dilation, if approached cautiously, appears to be safe and effective. Nevertheless, there are likely increased complication rates in patients with eosinophilic esophagitis (see below).
Dilation technique
Esophageal dilation is typically an outpatient procedure performed under a standard sedation protocol for upper endoscopy. After performing the initial endoscopic evaluation, the dilation technique depends on the dilator type used.
For a blindly passed bougie, after the endoscope is removed, the tapered end of the dilator is guided through the patient’s oropharynx into the esophagus with gentle forward pressure. The endoscopist assesses any sensation of resistance with the passage of the dilator to determine if additional dilation with larger sized bougies will be performed.
For a wire-guided bougie, with the endoscope in the stomach, a spring-tipped guidewire is placed under direct visualization. The endoscope is then removed, leaving the wire in place. The bougie is then passed over the wire and advanced into the esophagus with gentle forward pressure. The endoscopist again will assess for any sensation of resistance with the passage of the dilator.
For a TTS balloon, the balloon catheter is advanced through the instrument channel with the endoscope positioned in the stomach. Under direct visualization, the scope and deflated balloon are withdrawn into the esophagus and the balloon is centered over the stricture zone. (For this step, it is important to have a measurement of the stricture location from the incisors and be knowledgeable about the length of the balloon.) The balloon is inflated to the target size and dilation is performed. The inflated balloon is typically left in place for 30 to 60 seconds, with the catheter securely held (often by the fifth finger of the left hand) to prevent balloon migration during the dilation. The balloon can be deflated and the stricture zone assessed for mucosal rents, and then inflated to the next larger size.
Finally, for an OTW balloon, a compatible guidewire is placed across the stricture zone, either by direct visualization with the scope or with fluoroscopic guidance. The balloon is advanced over the wire and positioned in the stricture zone. This can be achieved by direct visualization (the endoscope can be reinserted next to the guidewire and balloon catheter) or by fluoroscopic visualization (the balloon can be filled with a mixture of water and contrast). The balloon is then inflated as noted above.
A listing of a subset of second-line therapies, including guidelines for choosing and using these salvage therapies
There are a number of second-line and salvage therapies for refractory or special cases of strictures.
The combined antegrade-retrograde approach to dilation can be considered when there is a complete esophageal stricture, most typically due to prior radiation therapy. When the patient has an existing gastrostomy tube in place, it is possible to approach the stricture in retrograde fashion by advancing a neonatal scope through the gastrostomy and into the esophagus. At the same time, an otolaryngologist can use a rigid scope or a gastroenterologist can use a flexible scope (depending on local collaborations or specific patient characteristics) to approach the stricture in antegrade fashion. Then, using a variety of techniques, the stricture zone can be bridged by a guidewire and dilation performed.
For refractory strictures that are not completely obstructing the esophagus, there are multiple options. The first option that is typically pursued is injection of steroids into the stricture zone. Several studies, including one randomized controlled trial, have shown that intralesional steroid injection appears to reduce the frequency of repeat dilations and increase the symptom-free period between dilations in patients with refractory strictures. Typically, a steroid such as triamcinolone (40 mg/mL) is injected in four quadrants in the stricture zone in 0.5 to 1.0 mL aliquots. While the data to date are suggestive, they are not definitive, the response in patients with refractory strictures from different etiologies is not known, and the optimal steroid type, dose, injection pattern, and frequency of injection have yet to be fully determined.
Second, the use of esophageal stents has been studied both for malignant and benign strictures. In malignant strictures, a stent is typically a palliative option, whereas in benign strictures, removable stents can be used with the goal of maintaining esophageal patency for the esophagus to remodel. There are a number of different stent types, including uncovered and covered self-expanding metal stents (SEMS), and self-expanding plastic stents (SEPS). Both fully covered metal stents and plastic stents are theoretically removable. Recent guidelines and meta-analyses inform current recommendations.
For malignant strictures, partially covered SEMS are felt to be superior to uncovered SEMS due to less tumor ingrowth and recurrent dysphagia (and, therefore, increased need for re-intervention), although there is a higher chance of migration. In addition, SEMS are preferred to SEPS due to lower complication rates for hemorrhage, tumor overgrowth, and migration.
For benign strictures, uncovered and partially covered SEMS are not recommended because they are difficult to remove. Fully covered SEMS have recently been developed and join SEPS as options for stenting benign strictures. While these stents are effective for relieving dysphagia, the major complication is migration, which is typically seen in 30% to 50% of cases. Biodegradable stents are being developed, but additional data are required before they can be used clinically.
Finally, there are several salvage techniques. When a refractory stricture is short (<1 cm), the technique of incisional stricturoplasty has been reported; however, the data are limited and the safety is not well established. In this technique, a needle knife is used to make a series of incisions parallel to the longitudinal axis of the esophagus, thus opening up the stricture zone. Next, there have been case reports where mitomycin C, an antiproliferative agent, is applied to the stricture zone with good effect. Last, for strictures that do not respond to any medical or endoscopic therapy, surgical referral for consideration of esophagectomy is an option.
Listing of side effects, including any guidelines for monitoring side effects.
Esophageal perforation is the most serious, and potentially life-threatening, complication of esophageal dilation. American Society for Gastrointestinal Endoscopy (ASGE) guidelines quote the risk of perforation as 0.1% to 0.4%, with a higher rate in complex strictures and a lower rate in simple strictures. In addition, the rate might be slightly elevated from this baseline in patients with eosinophilic esophagitis, but the risk is probably not as high as originally reported.
Perforation may not be recognized immediately during the dilation and should be suspected post dilation if the patient has severe chest pain, dyspnea, fever, tachycardia, crepitus in the neck or chest, or other signs of acute illness. A chest X-ray cannot definitively exclude perforation, so the test of choice is a water-soluble contrast esophagram (which, if negative, is typically followed by a barium swallow); in some cases a chest CT scan is required.
The key to managing this condition effectively is a high degree of suspicion in order to make a rapid diagnosis, consultation with thoracic surgery, and institution of appropriate therapy in short order. In some cases, esophageal perforations due to dilation, which are detected during the procedure, can be managed nonoperatively with endoscopic clips or esophageal stenting, antibiotics, and supportive care.
Chest pain post dilation in the absence of esophageal perforation is less common in most patient populations. However, in patients with eosinophilic esophagitis, a prospective assessment of post-dilation symptoms revealed that chest pain after dilation is the rule, and this should be discussed with this patient subgroup prior to endoscopy.
Bleeding and aspiration are also possible complications of esophageal dilation.
If both esophageal dilation and esophageal biopsies are required during the same endoscopy session, which is a common, it is typical practice to perform dilation first and then obtain biopsies after dilation is complete. There is a theoretical chance of increasing the risk for perforation if biopsies are taken prior to dilation, as they might compromise mucosal integrity.
Although there were past recommendations to provide predilation antibiotic prophylaxis to patients at elevated risk for infective endocarditis, predilation antibiotic prophylaxis is no longer recommend in the most recent GI and cardiology society guidelines.
How should I monitor the patient with an esophageal stricture?
Clinical symptoms of dysphagia correlate well with improvement or resolution of the esophageal stricture. If symptoms of dysphagia return, they are often indications that repeat dilation is needed. However, as with the dilation strategy itself, monitoring and ongoing treatment is determined by the underlying cause of the stricture. For a peptic stricture, for example, treatment of GERD with acid suppression is required to prevent recurrence. Similarly, if eosinophilic esophagitis is the underlying cause, then ongoing medical or dietary therapy is usually required in addition to dilation. Patients with complex strictures or a narrow esophagus – for example, from a caustic ingestion or radiation therapy – will require serial dilations. The frequency of the dilations is individualized for each patient, depending on the initial response to dilation and to the size achieved, but some patients initially require dilation as frequently as once per week if the stricture is severe.
What’s the evidence?
Spechler, SJ.. “American gastroenterological association medical position statement on treatment of patients with dysphagia caused by benign disorders of the distal esophagus”. Gastroenterology. vol. 117. 1999. pp. 229-33. (Note that this has not been updated since eosinophilic esophagitis has been widely recognized, so it does not include the current recommendation to perform esophageal biopsies in patients with dysphagia.)
Wilcox, CM, Alexander, LN, Clark, WS.. “Localization of an obstructing esophageal lesion: is the patient accurate?”. Dig Dis Sci. vol. 40. 1995. pp. 2192-6.
Egan, JV, Baron, TH, Adler, DG. “Esophageal dilation”. Gastrointest Endosc. vol. 63. 2006. pp. 755-60.
“Tools for endoscopic stricture dilation”. Gastrointest Endosc. vol. 59. 2004. pp. 753-60.
Siersema, PD, de Wijkerslooth, LR.. “Dilation of refractory benign esophageal strictures”. Gastrointest Endosc. vol. 70. 2009. pp. 1000-12.
Saeed, ZA, Winchester, CB, Ferro, PS. “Prospective randomized comparison of polyvinyl bougies and through-the-scope balloons for dilation of peptic strictures of the esophagus”. Gastrointest Endosc. vol. 41. 1995. pp. 189-95.
Scolapio, JS, Pasha, TM, Gostout, CJ. “A randomized prospective study comparing rigid to balloon dilators for benign esophageal strictures and rings”. Gastrointest Endosc. vol. 50. 1999. pp. 13-7. (The largest of the clinical trials comparing different dilation techniques.)
Hernandez, LV, Jacobson, JW, Harris, MS.. “Comparison among the perforation rates of Maloney, balloon, and savary dilation of esophageal strictures”. Gastrointest Endosc. vol. 51. 2000. pp. 460-2.
Furuta, GT, Liacouras, CA, Collins, MH. “Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment”. Gastroenterology. vol. 133. 2007. pp. 1342-63.
Dellon, ES, Gibbs, WB, Rubinas, TC. “Esophageal dilation in eosinophilic esophagitis: safety and predictors of clinical response and complications”. Gastrointest Endosc. vol. 71. 2010. pp. 706-12.
Madanick, RD, Shaheen, NJ, Dellon, ES.. “A novel balloon pull-through technique for esophageal dilation in eosinophilic esophagitis (with video)”. Gastrointest Endosc. vol. 73. 2011. pp. 138-42.
Jacobs, JW, Spechler, SJ.. “A systematic review of the risk of perforation during esophageal dilation for patients with eosinophilic esophagitis”. Dig Dis Sci. vol. 55. 2010. pp. 1512-5.
Tierney, W, Chuttani, R, Croffie, J. “Enteral stents”. Gastrointest Endosc. vol. 63. 2006. pp. 920-6.
Sharma, P, Korazek, R. “Role of esophageal stents in benign and malignant diseases”. Am J Gastroenterol. vol. 105. 2010. pp. 258-73.
Repici, A, Hassan, C, Sharma, P. “Systematic review: the role of self-expanding plastic stents for benign oesophageal strictures”. Aliment Pharmacol Ther. vol. 31. 2010. pp. 1268-75.
Thomas, T, Abrams, KR, Subramanian. “Esophageal stents for benign refractory strictures: a meta-analysis”. Endoscopy. vol. 43. 2011. pp. 386-93.
Repici, A, Vleggaar, FP, Hassan, C. “Efficacy and safety of biodegradable stents for refractory benign esophageal strictures: the BEST (Biodegradable Esophageal Stent) study”. Gastrointest Endosc. vol. 72. 2010. pp. 927-34.
Dellon, ES, Cullen, NR, Madanick, RD. “Outcomes of a combined antegrade and retrograde approach for dilatation of radiation-induced esophageal strictures (with video)”. Gastrointest Endosc. vol. 71. 2010. pp. 1122-9.
Bueno, R, Swanson, SJ, Jaklitsch, MT. “Combined antegrade and retrograde dilation: a new endoscopic technique in the management of complex esophageal obstruction”. Gastrointest Endosc. vol. 54. 2001. pp. 368-72.
Maple, JT, Petersen, BT, Baron, TH. “Endoscopic management of radiation-induced complete upper esophageal obstruction with an antegrade-retrograde rendezvous technique”. Gastrointest Endosc. vol. 64. 2006. pp. 822-8.
Ramage, JI, Rumalla, A, Baron, TH. “A prospective, randomized, double-blind, placebo-controlled trial of endoscopic steroid injection therapy for recalcitrant esophageal peptic strictures”. Am J Gastroenterol. vol. 100. 2005. pp. 2419-25.
Wills, JC, Hilden, K, Disario, JA. “A randomized, prospective trial of electrosurgical incision followed by rabeprazole versus bougie dilation followed by rabeprazole of symptomatic esophageal (Schatzki’s) rings”. Gastrointest Endosc. vol. 67. 2008. pp. 808-13.
Lee, TH, Lee, SH, Park, JY. “Primary incisional therapy with a modified method for patients with benign anastomotic esophageal stricture”. Gastrointest Endosc. vol. 69. 2009. pp. 1029-33.
Uhlen, S, Fayoux, P, Vachin, F. “Mitomycin C: an alternative conservative treatment for refractory esophageal stricture in children?”. Endoscopy. vol. 38. 2006. pp. 404-7.
Wills, JC, Hilden, K, Disario, JA. “A randomized, prospective trial of electrosurgical incision followed by rabeprazole versus bougie dilation followed by rabeprazole of symptomatic esophageal (Schatzki’s) rings”. Gastrointest Endosc. vol. 67. 2008. pp. 808-13.
“Antibiotic prophylaxis for GI endoscopy”. Gastrointest Endosc. vol. 67. 2008. pp. 791-8.
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