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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Herpetic esophagitis is an infrequent ulcerative infection of the esophagus caused by Herpes Virus type I. It is usually seen in immunocompromised patients though it may present in immunocompetent ones. Odynophagia and/or dysphagia associated with chest pain are the most frequent clinical symptoms. Radiology, endoscopy, biopsy and serological markers are the basis for diagnosis. We report 3 patients with herpetic esophagitis diagnosed between 1984-1989 and evaluated the clinical, endoscopic and biopsy characteristics. Certain clinical and endoscopic findings common to our patients tend to identify the disease, with biopsy and or serological markers the diagnosis may be established.
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PMID:[Herpetic esophagitis]. 196 85

Nonpropulsive esophageal contractions radiologically described as tertiary contractions or "corkscrew" esophagus suggest the presence of an underlying motility disorder and may lead to impaired acid clearance. The goals of this study were to determine the prevalence and role of gastroesophageal reflux (GER) in patients with tertiary contractions. Thirty-five consecutive patients with spontaneous, repetitive, nonpropulsive esophageal contractions noted on esophagography were studied with endoscopy, infusion esophageal manometry, and 24-h ambulatory pH monitoring. All patients had esophageal symptoms, mainly dysphagia, heartburn, and chest pain, but only three were found to have esophagitis by endoscopy and biopsy. Nineteen patients had repetitive, nonlumen-obliterating, nonperistaltic (tertiary) contractions, six had corkscrew esophagus, and 10 had forceful, lumen-obliterating simultaneous contractions (rosary bead esophagus). Twenty patients (58%) had GER by pH criteria with mean values: % time pH less than 4, 40.9; %upright pH less than 4, 41; %supine pH less than 4, 44.3%; number of episodes with greater than 5 min of pH less than 4, 12. Esophageal motility revealed "nutcracker" esophagus in eight, low LESP in two, and nonspecific esophageal motility disorder in 10. Symptoms or severity of nonperistaltic contractions did not correlate with GER. Radiologically demonstrable free reflux or the presence of heartburn did not predict GER. We conclude that 1) GER occurs in up to 58% of patients with nonpropulsive (tertiary) esophageal contractions on esophagography, and may play a role in the induction of abnormal peristaltic activity of the esophageal body; 2) GER is usually not associated with endoscopic evidence of esophagitis or characteristic symptoms, and is recognized by 24-h pH monitoring. We speculate that detection and treatment of GER may improve the symptomatic management of patients with nonpropulsive esophageal contractions.
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PMID:Nonpropulsive esophageal contractions and gastroesophageal reflux. 199 26

Abnormalities in esophageal peristaltic function and acid clearance appear to be responsible for prolonged esophageal acid exposure, a major determinant of the reflux esophagitis and esophageal stricture. We evaluated esophageal motility by manometry in 50 healthy controls and in 35 symptomatic reflux patients before, within 6 months, and 1 year after Nissen fundoplication. Preoperative motility was analyzed in relation to the presence or absence of both nonobstructive dysphagia and erosive esophagitis. We found that (a) preoperative dysphagia was related more to peristaltic dysfunction than to esophagitis; (b) peristaltic wave amplitude and duration were significantly lower than control values in patients with reflux, without correlation to degree of esophagitis or lower esophageal sphincter hypotension; (c) dysphagia ceased in most patients after antireflux surgery at the same time that normal motility was restored independently of lower esophageal sphincter pressure increments. These results suggest that motility disturbances are an important cause of dysphagia in reflux disease, and that reflux is the cause of, rather than the consequence of, peristaltic dysfunction.
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PMID:Dysphagia and esophageal motor dysfunction in gastroesophageal reflux are corrected by fundoplication. 200 30

Eleven patients with dysphagia caused by severe esophageal stricture (length 2 to 10 cm) resulting from reflux esophagitis were treated with fibroendoscopic dilation (Eder-Puestow) and Roux-en-Y partial gastrectomy with vagotomy during 10 years (1979 to 1988). There was no operative mortality, but complications developed in three patients: One patient had a mediastinal abscess demanding thoracotomy as a result of esophageal perforation after dilatation; one had postoperative pneumonia; and one patient had ileus. After a mean follow-up of 4 years (range 1 to 10 years) esophagitis healed in all cases, as judged by endoscopy. Eight patients were asymptomatic, but three had slight transient dysphagia. Postoperatively one to eight dilations (average three to four) were needed to relieve dysphagia in the first postoperative year, but later the stricture healed in every case. Postoperative pH measurement was performed in six latest patients and showed complete absence of reflux in all cases. It is concluded that Roux-en-Y partial gastrectomy with vagotomy and endoscopic dilation is an effective, simple, and safe procedure in the management of severe peptic esophageal (acid or alkaline esophagitis) stricture. However, occasional postoperative dilations at the outpatient clinic are often needed in severe cases in the first postoperative year.
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PMID:Treatment of severe peptic esophageal stricture with Roux-en-Y partial gastrectomy, vagotomy, and endoscopic dilation. A follow-up study. 200 14

The causes of dysphagia in childhood are variable. The swallowing mechanism may be influenced by a cleft palate, choanal atresia or tumors of the tongue. The causes related to the esophagus are especially based on malformations and complications following their treatment. In infancy, blockage of the esophagus with foreign bodies or scar tissue secondary to lye--or acid ingestion are most significant. Gastro-esophageal reflux is the leading cause for regurgitation and esophagitis in the lower esophagus. Occasionally, increased intracranial pressure causes dysphagia. Finally, a normal swallowing mechanism can be lost if it is not continuously practiced (parenteral nutrition, esophageal diversion). The variable spectrum of cause for dysphagia makes precise investigation and specific treatment mandatory.
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PMID:[Dysphagia in childhood]. 204 20

Esophageal pH monitoring is recognized as the best diagnostic procedure for gastroesophageal reflux (GER) and operation is seldom recommended in the absence of abnormal pH data. To emphasize that operation should not be ruled out for children who may have false-negative pH studies, we report 14 patients operated on for GER in spite of normal pH-monitoring. The mean age was 54 months (range, 18 to 90). Clinical features included vomiting, dysphagia, respiratory disease, anemia, and torticollis. All had radiologic evidence of GER, and 10 had endoscopic and histological esophagitis. Conventional pH-monitoring values were normal but lower esophageal sphincter pressure and propulsive peristalsis were significantly decreased whereas nonpropulsive contractions were predominant. Operation was recommended after an average of 24 months of unsuccessful medical treatment. Independent postoperative assessment showed that 13 of the 14 patients were relieved of their symptoms and dysphagia persists in one. We suggest that the diagnosis of GER should be accepted on the basis of sound clinical judgement plus more than one abnormal test even when pH results are normal. Operation should not be withheld when clinically indicated. There are several explanations for false-negative pH studies, of which alkaline reflux is probably the most important and warrants further investigation in children.
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PMID:Surgery for gastroesophageal reflux in children with normal pH studies. 206 6

Barrett's esophagus, a condition in which the distal esophagus is lined by columnar epithelium, is almost always caused by gastroesophageal reflux and often occurs in conjunction with a sliding hiatal hernia. Patients are typically white men in their 50s who smoke and drink, and they present with complaints of regurgitation, heartburn, and/or dysphagia. Endoscopic biopsies are required to confirm the diagnosis. Complications, such as stricture, ulcer, dysplasia, and malignant degeneration, occur in many cases. Adenocarcinoma is the most serious complication. Medical treatment, including life-style changes as well as pharmacologic therapy, usually relieves symptoms and heals esophagitis, but when it fails, antireflux surgery is indicated. Patients without evidence of dysplasia should undergo endoscopy yearly; those with mild dysplasia require more frequent surveillance. If biopsies disclose severe dysplasia, esophagogastrectomy should be performed.
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PMID:Barrett's esophagus. A continuing conundrum. 206 52

Extended esophageal pH-metering is the best method for GER diagnosis, but it has a certain number of false negatives. In a attempt to judge in which extent we can indicate surgery with a "normal" pH-metering study, we have reviewed our 110 operated children since 1982, and selected 12 in whom pH studies were normal. There where five females and seven males with ages ranging between 18 and 90 months. The clinical course until the diagnosis was accepted was long. Nine patients had vomiting, five respiratory disease, six dysphagia, four anemia and three torticollis. Only two were malnourished. There was radiologic GER in all children (with only one hiatal hernia). In spite of "normal" pH-metering, eight had decreased lower esophageal sphincter, and 11 disturbed motility. Nine had endoscopic esophagitis and eight histologic esophagitis. After operation, indicated only after long periods of medical treatment, vomiting disappeared in all, and so did respiratory disease and torticollis. Five families were very satisfied, six rather satisfied (gas bloat syndrome) and one frankly dissatisfied (dysphagia with severe immotility). Based on this evidence, we believe that some limited indications for surgery in GER are acceptable even in the presence of "normal" pH-studies.
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PMID:[False negatives in pH measurement. A retrospective study of 12 surgical cases]. 207 69

Esophageal candidosis was found endoscopically in 135 of 496 AIDS patients with upper gastrointestinal symptoms. Vomiting, dysphagia and retrosternal pain were the leading symptoms. Endoscopy showed different stages of esophagitis with Candida patches as early changes up to severe esophagitis with hemorrhage. 36 patients were treated with fluconazole orally or intravenously administered (100 mg per day). In 33 of 36 patients clinical, endoscopic and microbiological results were good with complete cure of the lesions after 7, 14 or 21 days of treatment. In 3 patients with wasting syndrome and severe opportunistic infections a resistance to the drug was discussed because of lack of sufficient therapy results. Maintenance therapy seems to be necessary to prevent relapses.
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PMID:[The therapy of Candida esophagitis in AIDS patients with fluconazole]. 210 62

Dysphagia in patients with pulmonary tuberculosis may be due to tuberculous esophagitis or compression of the esophagus by enlarged mediastinal lymph nodes or mediastinal fibrosis. We studied the clinical and radiologic findings in nine patients with advanced pulmonary tuberculosis who presented with dysphagia. In each patient, dysphagia first occurred while the patient was on antituberculous therapy. Chest radiographs in each case showed extensive tuberculous disease of the lung, affecting especially the left upper lobe. In addition, dense mediastinal pleural fibrosis was seen along the medial aspects of the upper thorax. Tomograms did not show mediastinal lymph node enlargement. Barium esophagograms showed extrinsic compression and various degrees of narrowing of the supracarinal part of the esophagus. No mucosal abnormality was seen on esophagoscopy. On the basis of these findings, the compression of the esophagus in these patients was attributed solely to tuberculous mediastinal fibrosis. The dysphagia remained constant in all patients except one, in whom worsening dysphagia improved after balloon dilatation. We conclude that mediastinal fibrosis is a significant cause of dysphagia in patients with advanced pulmonary tuberculosis.
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PMID:Dysphagia due to mediastinal fibrosis in advanced pulmonary tuberculosis. 210 27


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