A prospective study on changes in anti-reflux barrier function of the esophageal gastric junction after anti-reflux surgery

Gastric content is prevented from re-entering the esophagus by the
esophagogastric junction (EGJ) formed by the lower esophageal sphincter (LES)
and crural diaphragm 1. In patients suffering from gastroesophageal reflux
disease (GERD) this barrier function is compromised and reflux of gastric
content can occur freely causing symptoms (heartburn, regurgitation) as well as
damage to the esophagus (esophagitis)2. Most reflux episodes occur during
Transient Relaxations of the Lower Esophageal Sphincter (TLESR) 3. These are
spontaneous sphincter relaxations and are not induced by swallowing.
An anatomical abnormality which can contribute to GERD is a hiatal hernia4. A
hiatal hernia is characterized by a displaced LES which no longer coincides
with the crural diaphragm at the esophageal gastric junction. This can lead to
dysfunction of anti-reflux barrier and is therefore often associated with
GERD4. A recent study investigated the role of the hiatal hernia and the
so-called postprandial acid pocket5. The acid pocket is an unbuffered pool of
acid floating on top of the meal in the proximal stomach, where it is the most
important source of refluxate5. The most important finding of a recent study
was that in patients with a large hiatal hernia, the acid pocket may be trapped
in the hiatal sac above the diaphragm allowing acid reflux to occur during
episodes of low LES pressure5.

The exact mechanisms by which anti-reflux surgery prevents gastroesophageal
reflux are still unclear. Currently, it is believed that three mechanisms may
play a role. The first mechanism is anatomical restoration of the EGJ by
repairing a hiatal hernia if present. This could theoretically lead to
decreased entrapment of the acid pocket in the hiatal sac. Second, the rate of
TLESRs has been demonstrated to decrease in patients that underwent anti-reflux
surgery as well as there is a decrease in the association of TLESRs with acid
reflux6. The third mechanism by which antireflux surgery causes a reduction in
reflux episodes is a decreased distensibility of the EGJ. This change in
distensibility has previously been demonstrated to differ between patients
after anti-reflux surgery and normal subjects7,8. However, these three
mechanisms have not yet been investigated by measuring before and after
anti-reflux surgery except for the rate of TLESRs.

We hypothesize that in patients after anti-reflux surgery there is, beside the
proven decrease in TLESRs, also 1) a decreased distensibility and 2) decreased
acid entrapment in the hiatal sac when compared to the pre-surgery state.

The aim of the study is to investigate whether there are differences in
esophagogastric junction distensibility, acid entrapment in the hiatal sac and
rate of TLESRs in the pre and post-surgery state.

A prospective study using combined high-resolution manometry/pH/impedance
measurements and scintigraphy and an EndoFLIP measurement before and after
patients undergoing anti-reflux surgery.

Patients have to stop PPI or medication influencing GI-motility and have to
travel to the AMC. There are no known risks associated with the investigations.