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Query: UMLS:C0014848 (achalasia)
 2,804 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results of an ongoing clinical study treating achalasia patients with a transabdominal laparoscopic Heller myotomy and Toupet partial fundoplication are presented. Twelve patients underwent surgery between January 1992 and October 1993. All patients had barium esophagograms, preoperative endoscopy, esophageal manometry, 24-h pH studies, and extensive GI history preoperatively. Surgical complications included two perforations of the mucosa at the gastroesophageal junction repaired laparoscopically. There were no surgical mortalities and the average hospital stay was 39 h. Postoperatively all patients at follow-up had a repeat GI history, esophagogastroscopy, 24-h pH testing, and esophageal manometry. This follow-up showed good-to-excellent relief of dysphagia in all 12 patients with one patient complaining of heartburn documented to be from reflux postoperatively. Manometry showed a mean decrease in the lower esophageal sphincter pressure from 33.4 mmHg preoperatively to 19.3 mmHg postoperatively; 24-hour pH testing showed no significant reflux in the nine patients who had Heller myotomy plus a Toupet fundoplication. However, two of three patients who had Heller myotomy alone demonstrated abnormal 24-h pH testing. One of these patients was symptomatic and was found to have mild esophagitis by biopsy on postoperative endoscopy. These good results have persisted for mean follow-up of 16 months.
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PMID:Laparoscopic esophagomyotomy for achalasia. 759

A 69-year-old man with achalasia who had received cytoxan and prednisone over a 6-week period for presumed Wegener's granulomatosis presented with massive esophageal bleeding. He did not respond to aggressive medical management, and an emergent esophagectomy was performed. Histologic examination revealed extensive cytomegalovirus esophagitis. He had a long but progressive hospital course and was discharged 1 month after admission. This case illustrates that cytomegalovirus esophagitis may cause massive hemorrhage that necessitates surgical intervention.
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PMID:Massive esophageal bleeding in achalasia complicated by cytomegalovirus esophagitis. 769 81

The role of pneumatic dilatation and oesophagomyotomy in the management of achalasia cardia was evaluated. Twenty patients with achalasia cardia managed either by pneumatic dilatation (n = 10) and oesophagomyotomy (n = 10) were studied. Patients undergoing dilatation were followed up for a mean of 20 months (12-30 months) and those undergoing myotomy for 17 months (6-48 months). The patients were evaluated clinically, radiologically and endoscopically. Relief of dysphagia was excellent in 20%, good in 50% and fair in 30% of those who underwent dilatation. In the myotomy group, 60% had an excellent result, 30% had a good result and fair results was observed in 10%. Oesophagitis on endoscopic evaluation, was found in two patients in myotomy group. The diameter of the gastro-oesophageal junction increased from a mean of 2 mm (range 1 to 4 mm) to a mean of 11 mm (range 4 to 15 mm) in dilatation group while in myotomy group it changed from a mean of 2 mm (range 0.5 to 8 mm) to a mean of 9 mm (range 5 to 15 mm). Symptomatic improvement was better after myotomy than after pneumatic dilatation and correlated poorly with radiological features.
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PMID:An audit of pneumatic dilatation and oesophagomyotomy in patients with achalasia cardia. 786 51

The optimal management of reflux-induced esophageal strictures that occur after esophagomytomy for achalasia is uncertain. This paper presents our experience with the nonsurgical treatment of postesophagomyotomy strictures in achalasia patients using endoscopic dilation and gastric acid suppression. Six patients with achalasia who had undergone prior esophagomyotomy subsequently developed recurrent dysphagia and were found to have an esophageal stricture. Esophagrams typically showed a markedly dilated esophagus with a narrowed, sharply angulated gastroesophageal junction. Esophageal manometry confirmed esophageal aperistalsis and, when measured, the LES pressure was < 5 mm Hg. Endoscopy showed esophageal inflammation and a fixed stricture at the gastroesophageal junction. Strictures were dilated under direct visualization using through-the-scope balloon dilators. Patients began gastric acid suppressive treatment at the same time. Five patients who remained symptomatic underwent repeat endoscopy, which demonstrated improvement in esophagitis. Dilation was then repeated with a larger balloon dilator. Over a mean follow-up period of 3.8 years, the average number of repeat dilations per patient was 3.6 (range: 0-12). All patients had symptomatic improvement and weight gain. No patient required surgery. We conclude that esophageal strictures after esophagomyotomy for achalasia can be safely treated using endoscopic dilation and gastric acid suppression, thus avoiding the need for reoperation.
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PMID:Nonoperative management of esophageal strictures following esophagomyotomy for achalasia. 792 28

Achalasia is characterized by failure of relaxation of the lower esophageal sphincter and absence of progressive peristalsis in the esophageal body. Few data are available regarding the morphologic features of achalasia, in particular its histologic progression. The esophagi of 42 patients with achalasia treated with total thoracic esophagectomy were examined histologically in order to systematically identify morphologic features of clinically unresponsive achalasia and to determine what could be learned about the disease's evolution. In all cases, myenteric ganglion cells within the esophageal body were markedly diminished, with 20 specimens having none. Twenty specimens had residual ganglion cells in the proximal esophagus, and 15 specimens had a few randomly distributed ganglion cells in the mid- and distal portions of the esophagus. Inflammation within myenteric nerves, present in all cases, generally consisted of a mixture of lymphocytes and eosinophils, occasionally with plasma and mast cells. Focal replacement of myenteric nerves by collagen occurred in all cases, and there was almost complete replacement in several cases. Actual destruction of the residual ganglion cells was not seen. The resected esophagi also shared extramyenteric morphologic features. Some features probably stemmed from physiologic obstruction, such as muscular hypertrophy, mainly of the muscularis propria (all cases), with secondary degeneration and fibrosis (29 cases), and eosinophilia of the muscularis propria (22 cases). Other changes, probably resulting from chronic stasis of ingested materials in the lumen, included diffuse squamous hyperplasia (all cases), lymphocytic mucosal esophagitis (28 cases), lymphocytic inflammation of the lamina propria and submucosa with prominent germinal centers (all cases), and submucosal periductal or glandular inflammation with complete loss of submucosal glands in half of the cases. One patient had high-grade squamous dysplasia, and another had superficially invasive squamous cell carcinoma. A third group of changes was probably due to previous esophagomyotomy, including abnormal gastroesophageal reflux, as shown by pH reflux testing (13 cases) and Barrett's mucosa (four cases). In one case of Barrett's there was low-grade dysplasia. Clinically unresponsive, surgically resected achalasia has almost total loss of ganglion cells, and widespread destruction of myenteric nerves has already occurred. The only active component is myenteric inflammation. However, it cannot be determined whether this inflammation is a manifestation of ongoing nerve destruction or whether it is a secondary phenomenon.
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PMID:Achalasia. A morphologic study of 42 resected specimens. 814 27

During the past decade technologic progress has led to the increase use of oesophageal function testing, which is now available in clinical current practice. Ambulatory oesophageal pH monitoring is advocated as one of the best means for assessing the reflux of acid into the oesophagus. This technique can document abnormal gastro-oesophageal reflux (GOR) in patients with atypical symptoms or no endoscopic oesophagitis. The event marker allows to establish the correlation between occurrence of reflux and symptoms. This relationship can be quantified in the form of a symptom index; 24-hours pH monitoring can indicate objective criteria to define success of medical or surgical treatment. Oesophageal manometry analyses the lower oesophageal sphincter pressure and the oesophageal peristaltic function. This technique has a high prognostic value. The lower oesophageal sphincter pressure is not significantly different in patient with GOR but a severe hypotensive value is correlated with the severity of peptic oesophagitis. Peristaltic dysfunction is not specific but also increases with the severity of reflux disease. Pre-operative oesophageal manometry is recommended for identifying patients with oesophageal motility disorders and achalasia in whom anti-reflux surgery may precipitate postoperative dysphagia. The control of postoperative manometric data may be useful in the evaluation of surgery failure or recurrence of reflux symptoms.
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PMID:[Functional esophageal exploration in the assessment of gastroesophageal reflux]. 819 Nov 66

This paper is a review of esophageal anatomy, physiology and pathophysiology. The diagnosis and therapy of benign and malignant esophageal strictures are discussed including the specifics of esophageal dilation and tumor ablation procedures. The diagnosis and therapy of esophagitis in the immunocompromised (HIV, chemotherapy, transplant recipient) host is discussed. The pathophysiology and treatment of achalasia and esophageal spasm are reviewed. Finally, current concepts of the pathophysiology and therapy of gastroesophageal reflux disease. Emphasis is placed on the dual sphincter theory of gastroesophageal junction competence and the need for maintenance anti-secretory therapy.
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PMID:Esophageal dysphagia. 820 80

Esophageal diseases frequently cause symptoms such as heartburn, epigastric pain and dysphagia. This article discusses the indications, techniques and limitations of currently available diagnostic procedures. Investigation of symptoms should proceed in a logical stepwise manner, beginning with endoscopy to exclude esophagitis or neoplasia. Symptoms due to acid reflux can be identified by 24h esophageal pH-metry to document a temporal association between symptoms and episodes of esophageal acidification. Stationary or ambulatory manometric recording of esophageal pressures can be used to diagnose esophageal motor disorders such as achalasia, nutcracker esophagus, diffuse esophageal spasm, or dysfunction of the upper or lower esophageal sphincter. Combined 24 h pH-manometry should be used to test the temporal association between pain, reflux, or abnormal motility in patients with non-cardiac chest pain. Video-fluoroscopy is the most appropriate technique to diagnose swallowing disorders. Pulmonary aspiration of gastro-esophageal reflux can be documented with scintigraphy.
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PMID:[Motility disorders and assessment methods of the esophagus]. 821 Oct 52

Esophageal replacement remains a challenge. Colon and jejunum provide alternative conduits to replace the lower esophagus when stomach is not suitable. Between 1971 and 1991, 41 patients underwent short-segment interposition of the esophagus with jejunum or colon. Indications were failed antireflux procedures (n = 21), nondilatable stricture (n = 9), achalasia (n = 2), moniliasis (n = 2), Barrett's esophagus with carcinoma in situ (n = 2), hemorrhagic esophagitis after esophagogastrectomy (n = 1), motility disorder (n = 1), instrumental perforation (n = 1), carcinoma (n = 1), and leiomyosarcoma (n = 1). Thirty-one patients (75.6%) had prior surgical procedures. Interposition with colon was performed in 22 patients and with jejunum in 19. Major complications occurred in 45% after colon interposition (10/22) and hospital mortality was 4.5% (1/22). Major complications after jejunal interposition occurred in 31% (6/19) and hospital mortality was 10.5% (2/19). A contained anastomotic leak occurred in 1 patient, perforation of a colon segment in 1, and jejunal graft necrosis in a third. Late functional results in 34 patients with a mean follow-up of 87 months were excellent or good in 26, fair in 5, and poor in 1. Colon interposition failed to improve symptoms in 2 patients with gastrointestinal motility disorders. Six patients underwent manometry and barium food provocation study. Two colon segments and 3 jejunal interpositions were hypoperistaltic or aperistaltic according to manometry. There was 1 case of aperistaltic jejunum with a distended afferent loop. When stomach is not available, successful palliation of swallowing can be accomplished with either jejunum or colon. Surgeons involved in the management of esophageal disease should be familiar with the technical details of both procedures.
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PMID:Short-segment intestinal interposition of the distal esophagus. 823 Dec 8

History taking is the first step in the evaluation of a patient. An analysis of the information obtained provides the basis for the choice and order of diagnostic tests. In addition, it provides the clinician with the necessary information to determine the relevance of "abnormal tests" to the patient's problem. Dysphagia is a reliable symptom that indicates an abnormality in the swallowing mechanism. The history should contain a detailed description of the symptoms associated with dysphagia from the onset. Especially relevant are questions to determine if dysphagia is experienced every day or intermittently, with solid food or liquids or both, as well as presence and timing of associated symptoms such as, choking, coughing and regurgitation, changes in speech, heartburn and chest pain. It is clinically useful to divide swallowing into three phases: oral, pharyngeal and esophageal. Oral dysphagia is usually due to a neurologic disorder, decreased salivary flow or painful oropharyngeal lesions. Pharyngeal dysphagia is most frequently caused by neuromuscular disorders and less frequently by a Zenker's diverticulum, neoplasm or a mucosal web. Esophageal dysphagia is caused by a structural narrowing, such as produced by a peptic stricture, neoplasm or a Schatzki's ring or by a primary motility abnormality, such as achalasia or diffuse esophageal spasm or by motility abnormalities produced by inflammation caused by gastroesophageal reflux, medication-induced esophageal ulceration or infectious esophagitis.
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PMID:Art and science of history taking in the patient with difficulty swallowing. 846 26


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