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See article on page 476
The report on hiatus hernia by Kahrilas et al in this issue (see page 476) represents a milestone in the investigation of the impact of hiatus hernia on the mechanics of the gastro-oesophageal junction. Casual readers will probably not appreciate this—their first reaction more likely being that there is nothing new in this report. This reaction is understandable as Kahrilaset al’s findings are what would be predicted. The study is a milestone because it has actually made real in vivo measurements in humans. These measurements give a sound foundation for studies which will undoubtedly follow in the future and which will probe how hiatus hernia influences the mechanics of individual episodes of gastro-oesophageal reflux.
The casual reader is also unlikely to appreciate fully the technical demands presented by the measurements made by Kahrilaset al which is, of course, why there has been so much theory and deduction and so little direct observation in this field. Interpretation of manometry and fluoroscopy relied on spatial referencing of major soft tissue landmarks which was provided by the novel “tags” of the radio-opaque clips. Performance of high quality pull-through manometry simultaneously with fluoroscopy, and its accurate synchronisation is also a significant task. The biggest challenge though, was to analyse and condense the imaging and pressure data in order to show accurately located axial and radial patterns of pressure across the diaphragmatic hiatus, hernial pouch and lower oesophageal sphincter.
Over this century, there have been widely differing views and major swings of mainstream opinion about whether, and if so how, hiatus hernia impairs gastro-oesophageal competence.1 ,2 There are two main reasons for this lack of agreement. Firstly, there have been very few actual data, given the measurement difficulties. Secondly, thinking about mechanisms of gastro-oesophageal reflux has been too simplistic. As Kahrilas et alindicate, various mechanisms have been championed as the cause of gastro-oesophageal reflux, such as hiatus hernia, loss of the angle of His, failure of extrinsic diaphragmatic compression of the oesophagus,2 weak basal lower oesophageal sphincter pressure,3 and transient lower oesophageal sphincter relaxations.3 Some, possibly even all, of these factors play a role, their relative contributions varying from patient to patient and within a single patient. For instance, basal lower oesophageal sphincter pressure can vary over several hours from barely recordable to a very hearty value.4 We should recognise that reflux episodes nearly always result from a combination of factors. In particular, it seems likely that hiatus hernia could increase the likelihood of occurrence of reflux during a transient lower oesophageal sphincter relaxation.
Mechanisms of gastro-oesophageal reflux have been evaluated by mechanical modelling, sampling of gastro-oesophageal junction pressures and by recording of events associated with occurrence of individual gastro-oesophageal reflux episodes. The intermittency of reflux shows that the mechanical conditions that cause reflux only occur every now and then. Mechanical modelling and sampling of gastro-oesophageal junction pressure are unlikely to be fruitful, given this complexity and the variability of mechanical events at the gastro-oesophageal junction. Events associated with occurrence of gastro-oesophageal reflux episodes can only be evaluated by monitoring of mechanical function simultaneously with monitoring for reflux episodes, usually by pH monitoring,2 but also, in the case of provocative manoeuvres, by fluoroscopy.5 This approach has given useful insights into patterns of gastro-oesophageal junction pressure and diaphragmatic hiatal activity associated with reflux episodes.
How then can the insights derived from the study of Kahrilaset al be used to advance understanding of the ways in which hiatus hernia influences gastro-oesophageal competence? This study now allows confident interpretation of two axially separated high pressure zones as being due to the hiatus hernia and the lower oesophageal sphincter. Consequently, in some studies, it is reasonable to dispense with fluoroscopic imaging, and rely on methods that give reliable monitoring of the axial patterning of pressure from below a hiatus hernia into the oesophagus. This will give continuous information about mechanical function across the gastro-oesophageal junction. These data can then be readily correlated with occurrence of reflux, recognised by simultaneous distal oesophageal pH monitoring. Such studies need a sophisticated approach to monitoring of pressures if they are to give technically adequate insights. Kahrilas et al have shown a complex pattern of change of pressures from below the diaphragm into the distal oesophagus by the use of pull-through during suspended respiration during different patterns of straining and at rest. In order to monitor pressures in this region, the recording assembly will need to be stationed, and to record pressures from as many as 21 recording sites only about 3−5 mm apart in order to resolve adequately patterns of pressure over a critical span of 6−10 cm despite movements of the gastro-oesophageal junction. Such recordings could be combined with luminal electromyographic monitoring of diaphragmatic hiatal contractions.2 Such manometric methodology now exists, and could in the near future be adapted for use in ambulatory studies which could reveal how hiatus hernia influences gastro-oesophageal competence under normal living conditions. If and when you come across such a study in the future, spare a thought for the researchers who will have evaluated up to 23 simultaneously gathered squiggly lines!
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