The post-surgical gastroesophageal junction
What are the consequences of the structural changes of the anatomic cardia in controlling reflux after fundoplication?
J. Bancewicz (Salford)
The precise means by which fundoplication controls gastroesophageal reflux (GER) is still a matter of debate. The principal anatomical alteration that takes place is a changed spatial relationship between the gastric fundus and the esophagus. Depending on the precise operative technique that is used there may be:
1) a change in the length of the intra-abdominal esophagus,
2) a change in the pressure exerted by the fundus on the esophagus,
3) a change in the tightness of the esophageal hiatus in the diaphragm.
It is often assumed that these three changes always occur and that reflux is controlled by increased resting lower esophageal sphincter (LES) pressure and intra-abdominal length. However, there is no consistent evidence that this is the case.
All studies of the LES changes in groups of patients following fundoplication have shown an increased resting pressure in the LES for the group as a whole. However, there are several studies that show that the resting pressure does not always increase and that in the majority of such cases reflux is perfectly controlled. Resting LES pressure may even decrease [1, 2] and our own studies have shown that the same is true for the intra-abdominal length of the esophagus . The critical thing is that the fundoplication remains intact . Thus some of the measured changes that take place are probably artefacts of the operation rather than the means by which it controls reflux.
In recent years the concept of inappropriate transient lower esophageal sphincter relaxation (TLESR) has been a dominant theme in the pathogenesis of GER. Ireland et al.  have found that following fundoplication there was a reduced number of TLESRs, a fall in the proportion of transient relaxations accompanied by reflux and an increase in the mean residual pressure at the gastroesophageal junction during swallows. They suggested that fundoplication controls reflux by reducing the triggering of TLESR and by altering the mechanical behaviour of the lower esophagus to prevent full relaxation during swallows.
Despite the elegance of the studies from Dent's group, it is questionable whether the major anatomical change of fundoplication produces all of its effects by producing a relatively subtle neurophysiological change. Nissen fundoplication is widely acknowledged to produce an overcompetent cardia. This can be demonstrated by measuring the yield pressure i.e. the pressure at which the cardia opens during progressive distention of the stomach with air . Following fundoplication yield pressure increases to supranormal values. Conversely, yield pressure is reduced in those with reflux and the reduction is proportional to the severity of reflux. There is also a close relationship between the yield pressure and the presence and size of a hiatal hernia.
We have recently performed vector volume analysis of the LES during progressive gastric distention. Not surprisingly the vector volume decreased, but the reduction was due entirely to a reduction of the LES length rather than a reduced pressure. Following Nissen fundoplication vector volume did not decrease and the LES did not shorten during gastric distention. We believe that this abnormal behaviour of the LES accounts for most of the clinical effects of fundoplication.