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.
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 hypertensivepatients 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.
Authors: Fernando A M Herbella; Ramiro Colleoni; Luiz Bot; Fernando P P Vicentine; Marco G Patti Journal: J Neurogastroenterol Motil Date: 2016-04-30 Impact factor: 4.924