Effect of tense ascites on esophageal body motility and lower esophageal sphincter pressure.

BACKGROUND: Esophageal motility and lower esophageal sphincter (LES) pressure change with rapid changes in intraabdominal pressure (IAP); the response of these to slow change in IAP is not known. AIMS: To study esophageal body motility and LES pressures in patients with cirrhosis with tense ascites in the basal state and after paracentesis. METHODS: Twenty four patients with cirrhosis of liver and tense ascites and 13 with cirrhosis without ascites (controls) were studied. Basal intragastric (IGP) and LES pressures, and esophageal body response to water swallows, were recorded using a water perfusion system; IAP was measured in patients with ascites. In patients with ascites, the study was repeated twice: after paracentesis of two liters of fluid and after adequate control of ascites. RESULTS: Basal IGP (p = 0.002) and duration of esophageal contraction (p = 0.01) were lower in controls, but basal LES pressures were similar in the two groups. After control of ascites, IAP (p = 0.02) and IGP (p = 0.005) decreased; amplitude and duration of distal esophageal contraction decreased (p < 0.05). The frequency of high-amplitude waves also decreased (p = 0.04). LES pressure remained unaltered. CONCLUSIONS: Esophageal contraction duration is increased in the presence of ascites, and decreases after control of ascites; LES pressure is not affected by ascites.

Early changes in esophageal motility after endoscopic variceal sclerotherapy or ligation.

INTRODUCTION: Endoscopic variceal sclerotherapy (EVS) and ligation (EVL) are reported to be associated with altered esophageal motility. Most studies have been in patients with alcoholic cirrhosis and ascites. AIMS: To study the early effect of EVS and EVL in patients with portal hypertension without ascites. METHODS: Forty six portal hypertensive patients without ascites underwent esophageal manometry 24 h prior to EVS or EVL and within 24 h of two subsequent sessions. Nineteen such patients but without prior gastrointestinal bleed were studied once as controls. RESULTS: The protocol was completed in 35 patients (cirrhosis--16, noncirrhotic portal hypertension--19; 27 men; mean age 36 years). Basal midexpiratory lower esophageal sphincter pressure was similar in the study group (mean [SD] 20.1 [9.1] mmHg) and controls (17.6 [6.0] mmHg); the pressure did not change following EVS or EVL. Amplitude of contractions in the lower 5 cm of the esophageal body was similar in the two groups (84.8 [43.1] mmHg and 95.9 [59.6] mmHg), and decreased (63.6 [34.0] mmHg; p = 0.03) after two sessions of variceal therapy. The duration of contraction did not change following intervention. Nonperistaltic waves > 2 of 10 swallows were present during the baseline study in 9 patients in each group; 13 and 21 patients (p < 0.02 compared to baseline) developed them after the first and second sessions of therapy, respectively. Percentage of abnormal waves also increased following therapy. Thirteen patients developed esophageal ulcers; there was no correlation between the presence of ulcers and dysmotility. There was no difference in the changes between the EVS and EVL groups, and between patients with cirrhosis and noncirrhotic portal hypertension. CONCLUSION: Both EVS and EVL affect esophageal motility; these changes do not cause significant esophageal symptoms.