[Congenital esophageal stenosis or stenosis caused by reflux esophagitis?].
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Esophageal stenosis caused by an intrinsic congenital deformity is uncommon in infants and children. The main forms of stenosis are congenital esophageal web congenital stricture caused by tracheobronchial remnants, and congenital idiopathic muscular hypertrophy. The authors report on two patients who were successfully treated and managed after being diagnosed as having upper esophageal stenosis. One patient underwent resection of the web and primary anastomosis of the esophagus and was discharged 6 days after surgery. After 1 year, this patient has had no symptoms of dysphagia or other postoperative difficulties. The second patient underwent balloon dilatation of the esophageal stricture and was discharged on the day of surgery; however, this patient required numerous repeat dilatations.
BACKGROUND/PURPOSE: Congenital esophageal stenosis (CES) is a rare condition that is associated with various foregut symptoms. The aim of the current study was to investigate esophageal motor function in pediatric patients with isolated CES. METHODS: Four boys with CES (age, 3 weeks to 4 years old) were studied before treatment. The initial symptoms were dysphagia or stridor. The CES was caused by fibromuscular stenosis (FMS) in 2, tracheobronchial remnants (TBR) in 1, and membranous diaphragm (MD) in 1. An esophagram, endoscopy, 24-hour esophageal pH monitoring, and manometry were conducted. RESULTS: The esophagram showed the stasis of contrast medium proximally to the distal esophageal narrowing in FMS/TBR patients. Endoscopic esophagitis was not found in any patients. Three patients were documented with pathologic esophageal acid exposure by 24-hour esophageal pH monitoring. Manometry showed that esophageal contractions predominantly were synchronous in FMS/TBR patients but were peristaltic in an MD patient. Basal lower esophageal sphincter (LES) pressure was at least 20 mm Hg in all. Swallow-induced LES relaxations were incomplete in FMS/TBR patients. CONCLUSIONS: The presence of gastroesophageal reflux and impaired esophageal motility are common in patients with CES.
BACKGROUND: Although bleeding and perforation are generally recognized major complications of endoscopic mucosal resection, esophageal stricture after endoscopic mucosal resection has not been well studied. Factors associated with the occurrence and severity of esophageal stenosis after endoscopic mucosal resection were investigated. METHODS: Two hundred sixteen superficial esophageal lesions in 137 consecutive patients who underwent endoscopic mucosal resection from February 1993 through March 2001 were retrospectively studied. The circumferential extent of the mucosal defect after endoscopic mucosal resection was classified into 4 groups: under one fourth, one fourth to one half, one half to three fourths, and over three fourths. The longitudinal length of the mucosal defect was also evaluated. Stenosis was diagnosed when a standard endoscope (11-mm diameter) could not be passed through the stricture. RESULTS: Esophageal stenosis developed after endoscopic mucosal resection of 13 lesions (6.0%). In all these cases endoscopic mucosal resection resulted in a mucosal defect that involved over three fourths of the luminal circumference. In the subgroup of patients with mucosal defects involving over three fourths of the circumference, those with a mucosal defect over 30 mm long required more frequent balloon dilatation (mean 8 [4.3] times) and the stenosis was of longer duration (mean 16 [17.7] months) than those with defects 30 mm or less in length (respectively, 1 [0.6] times and 2 [1.9] months). CONCLUSIONS: A circumferential mucosal defect involving over three fourths the circumference of the esophagus after endoscopic mucosal resection was significantly associated with the subsequent development of esophageal stenosis. In addition, mucosal defects longer than 30 mm were associated with greater severity of stenosis. When endoscopic mucosal resection is performed for superficial esophageal lesions, removal of excess mucosa should be avoided.
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Acute monilial esophagitis generally responds well to oral nystatin therapy, and long-term sequelae of this condition have not been well recognized. Nor is it generally appreciated that Candida infections of the esophagus may occur in subacute or chronic form. Four men, 34, 40, 41, and 49 years old, have been treated for esophageal stenoses resulting from different types of chronic monilial esophageal involvement. All were seen with painless dysphagia and strictures of the upper half of the thoracic esophagus. In 2 patients, an associated roentgenographic pattern of "intramural esophageal pseudodiverticulosis" was present. Two patients have been treated successfully with esophageal dilation, 1 required substernal colonic bypass of the stenotic, perforated esophagus, and 1 is being evaluated for esophageal bypass. Esophageal moniliasis must be considered in the differential diagnosis of benign esophageal strictures, particularly those involving the upper half of the thoracic esophagus.
A 69-year-old man attempted suicide by abdominal penetrating injury and taking sulfonyl acid. After a laparotomic drainage operation, corrosive esophageal stenosis occurred. Esophageal bougienage was not effective. An expandable metallic stent (GIANTURCO-ROCHE Z stent, Cook Bloomington U.S.A.) was inserted aiming to achieve temporary oral diet and nutritional improvement. But diet did not improve sufficiently because of the awareness of the prosthesis, severe hiccup, uncontrolled regurgitation esophagitis and restenosis caused by intraluminal mucosal growth. After 4 months of insertion, an esophago-bronchial fistula was produced by the wire of EMS. An operation became necessary for this complication. No data exist on the long-term use of the EMS and it is not suitable for benign esophageal stenosis. Unavoidably if the palliative treatment of endoprosthesis is necessary for benign esophageal stenosis such as corrosive esophageal stenosis, a removable esophageal tube prosthesis is preferable.
The incidence of congenital esophageal stenosis (CES) is approximately 1 in 25,000 to 50,000 live births. There is associated esophageal atresia in one third of cases; the remainder are classified as isolated CES. Histologically, the anomaly may include tracheobronchial remnants, a membranous diaphragm, or diffuse fibrosis of the muscularis and submucosa. The authors report their experience with three patients who had isolated CES. The patients were free of symptoms for the first 6 months of life. All had difficulty with feeding from 6 to 12 months of age, which corresponded with the introduction of solids. Most solid feedings were regurgitated. Evaluation consisted of cine-esophagogram, pH monitoring, manometry, and endoscopy, with biopsies to exclude the diagnosis of gastroesophageal reflux. All patients underwent hydrostatic dilatation, but the benefit was only transient. The patients were referred for surgical correction when symptoms recurred. Limited resection of the esophageal stenosis with primary anastomosis was performed on all three patients via a left thoracotomy. The stenoses were located in the distal third of esophagus, near the junction with the middle third. Pathological examination showed tracheobronchial remnants in one patient and fibrotic muscle in the other two. The average age at the time of surgery was 19 months. The hospital stay averaged 8 days. The contrast study 1 week postthoracotomy showed esophageal patency in all patients, with no leakage. All were discharged from the hospital, tolerating solid food. CES should be sought for in patients who present with dysphagia to solid food that begins after the first 6 months of life.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: Congenital esophageal stenosis is thought to be a rare disease confined to infancy and childhood with only a few case reports in adults described. METHODS: We report five patients between the ages of 19 and 46 yr who presented with this disorder over a 2-yr period. RESULTS: Patients had been labeled with reflux strictures, webs, or as idiopathic in the past. All patients had chronic solid food dysphagia, some since early childhood. The location of the stricture varied, occurring in the mid or proximal esophagus in four, but throughout the esophagus in one. Radiographic and endoscopic appearance was a smooth concentric stricture or multiple rings, sometimes tracheal in appearance. Endosonography was performed in two patients, both of whom had focal circumferential hypoechoic wall thickening with disruption of the normal layer pattern corresponding to the areas of luminal narrowing. All patients dilated had good symptomatic response, with resolution of symptoms up to 6 months in follow-up. CONCLUSIONS: We suggest that congenital esophageal stenosis does occur in adults and may be underrecognized. Its endosonographic appearance is described.
Esophageal stenosis secondary to lye ingestion and surgical repair of esophageal atresia have been treated traditionally with bougienage. More recently, it has been described a new technique to treat them, based in the works of GRUNTZIG which employs balloon catheters for vascular stenosis. We present a series of 11 patients treated by these method, with a total of 17 stenosis. Ten patients had ingested lye and one had an esophageal atresia. We describe the method employed. 91% of the cases had a satisfactory evolution.
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