JNM : Original Article ; An Evidence of Esophageal Decompensation in Patients With Achalasia in the View of Its Subtype: A Retrospective Study

Background/Aims Achalasia is a primary motility disorder of esophagus. Many parameters represent esophageal function and morphologic changes, but their interrelationship is not yet established. We hypothesized that esophageal body would need to generate unusual pressure to empty the food bolus through the non-relaxing lower esophageal sphincter in patients with achalasia; therefore, higher is the residual lower esophageal sphincter pressure, greater would be the contraction pressure in the esophageal body in these patients. To verify the hypothesis, correlations among parameters from esophageal manometry, esophagography and esophageal transit study had been investigated. Methods A retrospective review of 34 patients was conducted. Resting lower esophageal sphincter pressure and contraction pressure of esophageal body were obtained from conventional esophageal manometry. Diameter of esophageal body was measured from barium column under esophagography. Radionuclide imaging was performed to assess the esophageal transit, designated as R30, which was the residual radioactivity at 30 seconds after ingesting radioactive isotope. Results In vigorous achalasia group, contraction pressure of esophageal body was negatively correlated to dilated diameter of esophageal body (P = 0.025, correlation coefficient = -0.596). Esophageal transit was more delayed as dimensions of esophageal body increased in classic achalasia group (P = 0.039, correlation coefficient = 0.627). Conclusions Diameter of esophageal body in classic achalasia was relatively wider than that of vigorous achalasia group and the degree of delayed esophageal transit was proportionate to the luminal widening. Patients with vigorous achalasia had narrower esophageal lumen and relatively shorter transit time than that of classic achalasia group. Proper peristalsis is not present in achalasia patients but remaining neuromuscular activity in vigorous achalasia patients might have caused the luminal narrow - ing and shorter transit time. (J Neurogastroenterol Motil 2013; 19:319-323)