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

Endoscopic sclerotherapy of esophageal varices is a widely used procedure. It reduces the frequency of rebleeding and improves the survival of cirrhotics with portal hypertension. The intravariceal or paravariceal injection of sclerosing agents causes structural changes of the esophageal wall recognisable radiologically. Stricture is a late complication which occurs in about 10 percent. In residual dysphagia balloon dilatation is recommended.
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PMID:[Changes in the esophageal wall following sclerotherapy of varices--roentgen morphology and therapy]. 408 67

Following the endoscopic injection sclerosis (EIS) of esophageal varices, radiographic procedures heretofore have played a minimal role in the dynamic assessment of structural and physiological alterations of the esophagus. This study includes a control esophagogram of each patient before any treatment. Esophageal studies were performed both before and after barium ingestion within a few hours of the treatment session, and findings were contrasted with those of the control esophagography and correlated with those of endoscopy. In all patients, immediately after EIS there was marked narrowing along the distal esophagus with both an upwardly convex border or shoulder effect at the sites of injection and variceal thrombosis. Functional changes of weakened peristalsis or achalasia evolved after early treatment sessions. Delayed emptying of the contrast-medium bolus was observed above the stricture and occasionally in the more proximal esophagus. The radiographic findings demonstrate the immediate sequela of transient dysphagia and the more long term complications of fibrosis and stricture.
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PMID:The esophagus after injection sclerotherapy of varices: immediate postoperative changes. 633 39

A patient is described who developed severe retrosternal pain and dysphagia immediately after sclerotherapy of esophageal varices. Extensive submucosal bleeding of the esophageal wall was demonstrated radiologically and endoscopically. This lesion resolved within 2 weeks of conservative treatment.
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PMID:Intramural hematoma of the esophagus: unusual complication of variceal sclerotherapy. 633 5

The purpose of this project was to evaluate the acute and chronic effects of sclerotherapy on esophageal motility and function. We studied motility in eight patients before and after injection sclerotherapy of esophageal varices. We injected the varices with 5% sodium morrhuate twice during the first week and then at 1, 2, 3, and 6 months. Lower esophageal sphincter pressure, contraction wave amplitude, and duration were not altered by sclerotherapy. However, the length of the high-pressure zone increased significantly from 3.6 +/- 0.3 cm to 4.2 +/- 0.2 cm during the first 3 days after initial treatment, and sclerotherapy caused considerable distortion of peristaltic wave form. Also, esophageal peristaltic velocity decreased in three patients who complained of dysphagia and subsequently developed esophageal stricture. The strictures have responded well to dilatation, and in two patients velocity has even returned toward the baseline value. Reflux esophagitis has not been a problem. Esophageal motility is altered by sclerotherapy of esophageal varices. Stricture formation seems to be reversible after sclerotherapy is stopped or discontinued.
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PMID:Esophageal motility: effects of injection sclerotherapy. 648 10

Eighty-eight patients with bleeding esophageal varices due to portal hypertension underwent splenectomy and devascularization of the upper half of the stomach and the abdominal esophagus. A Hegar dilator no. 17 was introduced into the esophagus through a gastrotomy. A ring of separated stitches was applied at cardia level, the needle being inserted as far as the metallic surface so as to include the entire wall of the esophagus. Complete interruption of all gastroesophageal vascular communication was thus obtained. After suture of the gastrotomy, a Nissen or Lind's fundoplication was performed. In 62 (70.45%) patients, the immediate postoperative course was uneventful, 21 had non-lethal complications, 13 had abdominal evisceration, six pulmonary complications, four subphrenic abscesses, five patients died, two in hepatic coma, two after reoperation for subphrenic abscess and one after massive hemorrhage due to an acute gastric ulcer. Forty-three patients (48.8%) developed transient ascites which disappeared before they were discharged from the hospital. In thirteen patients (15.6%), the hemorrhage recurred. Of the 32 patients operated one to two years ago, only one rebled. Of the 35 patients operated three to five years ago, nine rebled and three, of the 16 patients operated from five to seven years ago, rebled. With radiological and endoscopic investigations, reduced varices were seen above the suture line, in many cases, passively filled up with blood returning from the azygos vein. Reflux esophagitis was observed in 17 patients who had had a Lortat-Jacob procedure to reduce the His angle; of these, eight rebled later. No gastroesophageal reflux was seen after Nissen or Lind's fundoplication. No fistulae, dysphagia or stenosis was observed.
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PMID:A new procedure for the treatment of bleeding esophageal varices by transgastric azygo-portal disconnection. 660 5

Oesophageal stricture and dysphagia after endoscopic sclerotherapy of oesophageal varices were assessed with regard to occurrence and severity and the relation to the treatment. We followed 34 patients for three to 47 months who had two to 25 treatments with submucosal, paravenous injections of polidocanol (3%). Twenty patients (59%) developed stricture or dysphagia; 14 both dysphagia and endoscopically verified stricture, two dysphagia without stricture, and four stricture without dysphagia. Both phenomena occurred intermittently and often independent of each other, but occupied median 38% of the observation time in these 20 patients. The patients developing strictures had received significantly more treatments and greater amount of sclerosant, and they had significantly more preceding mucosal necroses. The varices were eradicated to about the same degree and the incidence of recurrent haemorrhage was the same as in the patients who had not developed stricture.
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PMID:Oesophageal stricture and dysphagia after endoscopic sclerotherapy for bleeding varices. 660 2

To study the effect of sclerotherapy of varices on esophageal function, the motility of the tubular esophagus and of the lower esophageal sphincter (LES) were recorded in 19 patients after 7 to 13 sclerotherapy sessions and in 15 healthy volunteers. In addition, esophageal functional scintigraphy (EFS) was performed in the patient group. Compared with the volunteers the patients had lower contraction amplitudes in the distal esophagus (30.5 +/- 17.5 mm Hg versus 43.6 +/- 9.1 mm Hg, p less than 0.01) and a higher percentage of non-propulsive simultaneous contractions (NPC) in the distal (33.4 +/- 23.2% versus 9.0 +/- 8.6%, p less than 0.005) and mid-esophagus (15.0 +/- 8.2% versus 8.3 +/- 8.1%, p less than 0.05). There was a negative correlation between the percentage of NPC in the distal and mid-esophagus and radionuclide transit (rs - 0.53, p less than 0.02). Three of 19 patients had a positive reflux index by EFS. The LES tone was only slightly lower in the patients than in the controls (10.7 +/- 3.2 mm Hg versus 13.4 +/- 3.6 mm Hg, p less than 0.05). Our findings indicate that sclerotherapy of esophageal varices may lead to a reduced peristaltic esophageal motility with an impaired transport function. This could contribute to the development of dysphagia or esophagitis.
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PMID:Esophageal function after sclerotherapy of bleeding varices. 698 19

A patient with varicoid carcinoma of the esophagus is reported. These tumors differ from classical esophageal carcinoma and have some resemblance to esophageal varices in their radiological and endoscopic appearances. Dysphagia is generally not the presenting symptom. The histological picture in our patient was that of a poorly differentiated adenocarcinoma with areas of signet-cell carcinoma. This is an exceptional finding since all previously reported cases of varicoid carcinoma of the esophagus have been squamous cell carcinomas.
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PMID:Varicoid carcinoma of the esophagus. Report of a patient with adenocarcinoma and review of the literature. 705 96

Seven consecutive patients presenting acutely with suspected variceal hemorrhage underwent endoscopic variceal ligation (EVL) of esophageal varices. Active bleeding had ceased by the time of the initial EVL session in all patients, although active variceal hemorrhage was controlled by EVL in one patient during a subsequent episode of bleeding. Treatment sessions were repeated at approximately monthly intervals until varices were reduced in size to grade 1 (< 4 mm diameter) or eradicated. All patients had portal hypertension secondary to intrahepatic disease. Patient age ranged from 2.4 to 14.5 years (mean, 8.5 years). One patient underwent successful liver transplantation 1 week after the initial treatment session. The remaining six patients required a mean (+/- SD) of 4.0 +/- 1.3 treatment sessions for elimination of varices. One episode of recurrent variceal hemorrhage and one episode of treatment-related hemorrhage occurred in two separate patients. Transient, mild dysphagia or odynophagia occurred in all patients. No other complications were reported during a mean (+/- SD) follow-up period of 13.8 +/- 4.6 months (range, 8-20 months). Recurrent varices were seen in three of four (75%) patients returning for follow-up endoscopy between 5 and 8 months from initial eradication. All underwent repeat EVL without complication. Endoscopic variceal ligation may be a suitable substitute for sclerotherapy in children with bleeding esophageal varices.
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PMID:Endoscopic ligation of esophageal varices in children. 771 77

Fifty consecutive patients presenting with upper gastrointestinal haemorrhage caused by oesophageal varices were subjected to endoscopic sclerotherapy during the period April 1989 to December 1991. Portal hypertension was caused by alcoholic liver cirrhosis in 22 (44pc), Hepatitis B induced liver cirrhosis in seven (14pc), cryptogenic liver cirrhosis in three (six pc), bilharzial portal fibrosis in 17 (34pc) and extrahepatic portal obstruction in one (two pc). Acute bleeding was controlled in 12 out of 13 patients, five of whom with a fresh bleed and eight who rebled while on the endoscopic sclerotherapy regimen. All patients were treated on a weekly sclerotherapy regimen. Reduction in variceal size of two or more grades was achieved in all 30 patients who had completed at least four or more endoscopic sclerotherapy courses with total eradication of varices in 27 (90pc). Three patients died. All deaths were caused by progressive hepatic encephalopathy. Complications usually seen were retrosternal pain, fever, dysphagia and oesophageal ulceration. There were no fatal complications. The study shows that endoscopic sclerotherapy is effective not only in controlling acute bleeding but also in preventing rebleeding. We recommend a weekly schedule for the early eradication of varices.
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PMID:Endoscopic sclerotherapy in Zimbabwe. 802 85


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