Esophageal impedance monitoring and pathophysiology of gastroesophageal reflux disease.

Up until now, most pathophysiological concepts about gastroesophageal reflux derived from measurement of esophageal pH. However, pH monitoring does not detect all gastroesophageal reflux events, particularly when little or no acid is present in the refluxate. Esophageal impedance measurements made possible to detect and quantify all types of reflux i.e. acid, weakly acidic and non-acid reflux and to characterize the air-liquid composition of the refluxate. This new tool stimulated us to re-examine different aspects of the pathophysiology of GERD, but considering all gastroesophageal reflux events rather than only acid reflux. In this text we first analyzed gastric factors and the impact of gastric emptying on the characteristics of the refluxate. We then foccussed on the antirreflux barrier at the gastro-esophageal junction and we analysed the patterns of air and liquid reflux during transient lower esophageal sphincter relaxations (TLESRs), the most frequent mechanism for reflux in patients with GERD. With failure of the antireflux barrier, reflux occurs and we discussed in detail the air-liquid patterns, composition and proximal extent of the refluxate in normal subjects and patients with GERD both in resting and ambulatory conditions. The volume and chemical clearance mechanisms triggered after acid and non-acid reflux were characterized. The effect of esophagitis or Barrett's mucosa on electrical conductivity and impedance was analyzed as an expression of mucosal damage and increased ionic permeability. We discussed the role of non acid and gas reflux in esophageal and extraesophageal symptoms in patients with GERD. We believe that better understanding of the pathophysiology of GERD can help to characterize the relationship between gastroesophageal reflux and symptoms; the factors that determine esophageal and extraesophageal mucosal damage and/or eventual carcinogenesis related to reflux and to provide a tailored treatment to each patient targeting the individual pathophysiological defect.