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Gastric pH is one of the primary determinants of gastro-oesophageal reflux disease (GORD). The severity of both oesophageal mucosal damage and symptoms is directly related to the pH of the refluxate and thereby intragastric pH. The proximal stomach is particularly relevant as it is the most immediate source of the refluxate, particularly in patients with hiatus hernia. An important characteristic of gastro-oesophageal reflux is the postprandial increase in reflux episodes. Indeed, the majority of reflux episodes in most patients occur in the postprandial period. However, meals lead to transient buffering of gastric acid, particularly in the proximal stomach,1 2 yet, early in the postprandial period, acid and weakly acidic reflux episodes are often interspersed.3 Conventional intragastric pH monitoring 5 cm below the lower oesophageal sphincter (LOS) often reveals discrepancies between gastric pH and that of the refluxate in the oesophagus, with a lower pH in the oesophagus than in the stomach during reflux episodes.
Important insights into this apparent discrepancy between gastric and oesophageal pH during reflux were obtained by Fletcher and colleagues.4 Using a stepwise pull-through of a pH electrode from the proximal stomach across the gastro-oesophageal junction, they were able to demonstrate that 15 min after a meal, there was a short zone of apparently unbuffered highly acidic gastric juice extending 2 cm below the LOS that they termed the “acid pocket”. The median pH in this zone was 1.6 compared with 4.4 in the meal-buffered region below. Subsequent studies have confirmed these findings.2 5–7 Concurrent pH monitoring in the gastric cardia and distal oesophagus during reflux episodes has also shown the pH in the cardia to be consistently lower than that in the distal oesophagus.6 Thus, reflux from this acid pocket provided a plausible explanation for acid reflux in the …
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