Influence of endoscopic variceal ligation on oesophageal motility

BACKGROUND: To determine the change of oesophageal manometry in patients with oesophageal varices before and after oesophageal variceal ligation (EVL). METHODS: Forty-five patients who had liver cirrhosis and oesophageal varices with high risk of bleeding were managed by EVL. Oesophageal manometry was performed just prior to the ligation and 4-6 weeks after obliteration of varices. Another 45 age- and sex-matched patients without hepatic, oesophageal or systemic disease served as the control group. RESULTS: At 5 cm above the lower oesophageal sphincter (LES), the amplitude of the contractive wave was significantly lower in patients before EVL (56.9 +/- 31.8 vs 80.1 +/- 30.1, P< 1.05) and returned to the level of control subjects after EVL (76.5 +/- 37.0 vs 80.1 +/- 30.1, P> 0.05). At 10 cm above LES, the amplitude of the contractive wave was significantly lower in patients before and after EVL than the control group (54.3 +/- 29.2 vs 68.1 +/- 29.5, 54.2 +/- 26.0 vs 68.1 +/- 29.5, respectively, P< 0.05). The percentage of tertiary waves was significantly higher in patients before and after EVL than in the control group (31.4 +/- 36.6 vs 5.8 +/- 15.1, 26.9 +/- 32.9 vs 5.8 +/- 15.1, respectively, P< 0.05). However, no significant swallowing disturbance was noted in patients after EVL. There was significantly greater LES length in patients before EVL (4.0 +/- 0.9 vs 3.4 +/- 0.7, P<0.05) but there was no significant difference in the LES length after EVL as compared with the control group. Eighty-six per cent (39/45) of patients developed paraoesophageal varices and 31% (14/45) developed new varices 6 months after variceal obliteration. However, there was no significant difference in manometry at the time of variceal obliteration between patients with variceal recurrence and those without. CONCLUSIONS: The presence of varices affected oesophageal motility. However, such abnormality had little clinical significance. Endoscopic variceal ligation normalized oesophageal motility and may not induce abnormal oesophageal motility. The manometric change can not be used to predict the recurrence of varices in cirrhotic patients after variceal obliteration.     

Does this patient have oesophageal motility abnormality or pathological acid reflux?

BACKGROUND AND AIMS: The diagnostic values of particular symptoms centred on oesophagus, among patients with suspected oesophageal motility abnormality or pathological acid exposure, are not yet fully understood. The aim of this study was to determine the predictive accuracy of these symptoms in diagnosis of oesophageal motility disorder or pathological acid exposure. PATIENTS AND METHODS.: A total of 462 patients who had undergone conventional oesophageal manometry and ambulatory 24-h pH monitoring to investigate a clinical suspicion of oesophageal motility disorder and pathological acid exposure were enrolled in this study. According to their principal complaints, the patients were divided into the dysphagia category, the non-cardiac chest pain category, the gastrooesophageal reflux disease-related symptom category and the extraoesophageal symptom category. RESULTS: Two hundred and two (44%) out of 462 patients yielded abnormal findings on manometry and/or pH monitoring. Dysphagia was associated with a likelihood ratio (LR) of 2.11 [95% confidence interval (CI), 1.02-4.00)] in patients exhibiting a combination of oesophageal motility abnormality and pathological acid exposure. During oesophageal manometry, the dysphagia substantially increased the likelihood of classic achalasia (LR, 6.24; 95% CI, 3.32-8.78) and diffuse oesophageal spasm (LR, 3.58; 95% CI, 1.03-7.12). When the patients with dysphagia were divided into two groups according to the severity of their symptoms, classic achalasia was significantly frequent in patients with severe dysphagia (P = 0.016). On the other hand, non-cardiac chest pain was the clinical factor that reduced the likelihood of classic achalasia (LR, 0.22; 95% CI, 0.04-0.93). The distribution of pathological acid exposure was significantly frequent between the groups of patients with and without gastrooesophageal reflux disease-related symptom (P = 0.011). CONCLUSION: A small number of oesophageal symptoms are helpful in predicting the likelihood of abnormal findings on oesophageal tests among patients with a clinical suspicion of oesophageal motility disorder and pathological acid exposure. The most useful finding is a severe dysphagia, which is likely to have classic achalasia.     

Influence of endoscopic submucosal dissection on esophageal motility

AIM: To assess esophageal motility after esophageal endoscopic submucosal dissection (ESD). METHODS: Twelve patients (6 men and 6 women) aged 53-64 years (mean age, 58 years) who underwent regular examination 3-12 mo after esophageal ESD for neoplasms of the esophageal body were included in this study. The ESD procedure was performed under deep sedation using a combination of propofol and fentanyl, and involved a submucosal injection to lift the lesion and use of a dual-knife and an insulated-tip knife to create a circumferential incision around the lesion extending into the submucosa. Esophageal motility was examined using a high-resolution manometry system. Dysphagia was graded using a five-point scale according to the Mellow and Pinkas scoring system. Patient symptoms and the results of esophageal manometry were then analyzed. RESULTS: Of the 12 patients enrolled, 1 patient hadgrade 2 dysphagia, 1 patient had grade 1 dysphagia, and 3 patients complained of sporadic dysphagia. Ineffective esophageal motility was observed in 5 of 6 patients with above semi-circumference of resection extension. Of these 5 patients, 1 patient complained of grade 2 dysphagia (with esophageal stricture), one patient complained of grade 1 dysphagia, and 3 patients complained of sporadic dysphagia. Normal esophageal body manometry was observed in all 6 patients with below semi-circumference of resection extension. The 6 patients with normal esophageal motility did not complain of dysphagia. CONCLUSION: Extensive esophageal ESD may cause esophageal dysmotility in some patients, and might also have an influence on dysphagia although without esophageal stricture.     

Oesophageal motor function in chronic intestinal idiopathic pseudo-obstruction: A study with high-resolution manometry

BackgroundChronic intestinal idiopathic pseudo-obstruction (idiopathic CIPO) is a rare heterogeneous condition for which the different phenotypes are difficult to be established. Oesophageal motility has shown to be impaired in patients with idiopathic CIPO at traditional manometry, whereas no studies have assessed it by high resolution manometry (HRM).AimsTo evaluate oesophageal motility by HRM in patients with idiopathic CIPO.Methods14 patients with idiopathic CIPO underwent oesophageal HRM. Multiple rapid swallows (MRS) were performed in order to evaluate contraction reserve. The Chicago Classification 3.0 was used to classify the oesophageal motility disorders.ResultsOne idiopathic CIPO patient had type-II achalasia, one aperistalsis and 12 had minor disorder of peristalsis (11 ineffective oesophageal motility and one fragmented peristalsis). These minor disorders were not significantly different from those of 50 other consecutive patients who underwent HRM for dysphagia or GERD and received the diagnosis of ineffective oesophageal motility. Three of the 12 idiopathic CIPO patients with minor disorder of peristalsis had no contraction reserve after MRS.ConclusionsHRM is able to identify different grades of oesophageal motor impairment in patients with idiopathic CIPO. Presence of major oesophageal dismotility or absent contraction reserve suggest a more severe and widespread motor disorder.