Complete i.e Nissen or Partial such as Toupet fundoplication certainly effects oesophageal transit time and lower oesophageal sphincter pressure based on manometry studies. To the best of my knowledge, non of these procedures have any effect on gastric emptying if there were no issues preoperatively  (i.e. normal gastric physiology) . I am happy to be corrected!!

I had a Nissen complete fundoplication in 2005 and  no issues were raised at the time regarding gastric transit times and none have been experienced.  I had a cholecystectomy at the same time.

Fundoplication has no effect on Gastric emptying if preoperatively normal.Post operatively unless accidental division of vagii,there will not be any change.Having said the above some patients complain of early dumping, Increased Gastro colic reflex.

I agree with my colleagues.  Nissen funduplication does not significantly affect  gastric emptyng.  Nissen may induce recrudescence of mild gastroparesia which can be seen in about 5% of patients with GERD. This recrudescence may be falsely interpreted as cause –effect association. That is the reason why some recommend searching clinically manifested gastoparesia before performing Nissen operation. In the other side, vagus nerve injury during hiatus dissection has been suggested as a cause of gastric emptying delay. In my opinion this is a very infrequent event.

Regarding effects of funduplication on increased gastric emptying by reducing gastric accommodation may be possible. Nevertheless gastric fundic capacitance is big and if manifestations of increase gastric emptying take place, surly they are not clinically significant. Patients with diarrhea post funduplication are infrequent.

This is a very interesting area and one in which we have spent a lot of time researching. The likely underlying mechanism for gastroparesis in the refluxing patient is due to gastric Venting caused by increased transient lower esophageal sphincter relaxations. We know from x-ray studies performed in the 1950s and 60s that patients with significant reflux carry their bolus in the fundus in the upper body of the stomach, in an area unfortunately proximal to where the gastric pacemaker begins contracting. Patients without reflux to any significant degree have been demonstrated to carry the food bolus in the mid to distal body closer to the actual portion of the stomach where the food can be proposed into the duodenum. Since approximately upwards of 35 to 40% of patients with refractory reflux have accompanying gastroparesis, we found that the majority of these patients would experience complete correction of the gastroparesis following Nissen fundoplication. What we have demonstrated is that following Nissen fundoplication because there is no further Venting of the gastric yield pressure into the esophagus, distal transport of gastric contents is facilitated. The same occurs with other anti-reflux procedures such as the Stretta procedure, which I published on in 2007. So while the reflux corrective procedure itself does not directly affect gastric motility and therefore gastroparesis, the correction of the reflux does improve emptying due to an increase in gastric yield pressure. The only caveat to this is in those patients who have functional pyloric outlet obstruction diagnosed on electrogastrogram, in which case the gastroparesis is caused by dyskinesia at the level of the pylorus. This is in fact easily addressed with pyloric dilation.

Thank you Mark. Could you please explain hoe we can detect the functional pyloric outlet with EGG? Which parameters we can rely on? Thank you

Is a great pleasure to respond to your request Serhat. Of course, the electrogastrogram measures gastric slow waves over a period of time. This is most efficiently done following a nonnutritive challenge such as a water load during which the patient drinks water until completely full over a five-minute period of time. There is a 15 minute baseline that is obtained prior to the water loading process following which 30 minutes of continued recordings are obtained. The electrodes are placed across the upper abdomen and roughly correspond to the location of the antroduodenal angle, mid body and proximal left lateral margin of stomach. The recording of the patient is compared to population-based values for normal patients. In particular with regard to functional pyloric outlet obstruction, we look at the percent frequency of normal three cycle permitted or 3CPM activity. If this begins high even in the baseline period, and then gets even higher as the result of water loading this is considered superhigh normal and consistent with functional outlet obstruction. We have the paper that were in the process of preparing for publication that not only confirms these findings but also demonstrates that it can be used to selectively identify patients whose gastroparesis will respond to pyloric balloon dilation or other methods such as botulinum toxin injection or pyloroplasty. 

Interesting work  Mark. In the study where you assessed electrogastrography for diagnosis of functional pyloric outlet obstruction, can you tell me what was your gold standard of diagnosis and the sensitivity, specificity, negative and positive predictive value of electrogastropraphy?

Best Regards

The gold standard of diagnosis is the electrogastrogram, in particular the percentage of three cycle per minute activity in response to a water load. These patients had all previously been diagnosed with abnormal standard nuclear solid phase gastric emptying scans. The Electrogastrography permits us to directly measure the percentage of various levels of normal, tachygastria, bradygastria, and then miscellaneous higher frequencies. The interpretation software in the 3CPM electrogastrogram is based off of 60 population-based normal patients against which the subject patient is compared. I cannot share with you at this time the sensitivity, specificity, as well as predictive values as this will be in the paper and is best not revealed until the paper is published. I can tell you that the results are quite significant.

If you assess EGG for diagnosis of functional pyloric outlet obstruction you should have a different and well recognized gold standard of diagnosis. In this way you can obtain sensitivity, specificity and predictive values. In evaluation of diagnostic test if you do not obtain these values or you do not have gold standard the results are not valid.

In practice, the use of EGG is not extended. Many patients with  diagnosis of tachygastria and bradygastria by EGG have not clinical correlation and  studies have not strong gold standard of diagnosis. This is expected since evaluation of gastric emptying is quite difficult since results of this procedure can be affected by several factors (type of test meals, chemical composition and osmolarity of the test meals, quantity of liquid, etc.). For this reason these procedures must be carefully standardized in every laboratory. In regards to the above mentioned, presently highly sensitive and specific procedures for measuring gastric emptying are not available.

Diego

I could not agree with your comments more!

This is why the EGG equipment we use  is the 3CPM equipment which is the only one  with an NIST certified signal detection process .  This s also the reason why we use a water load  as  a nonnutritive  stimulant to the stomach that avoids the  activation of enzymes that affect motility when giving a nutritive meal.  In addition the standard clinical water load protocol  with this EGG device has population-based norms , based upon 60 normal patients who underwent Electrogastrography on four separate occasions. Therefore the patient's results are compared to these norms.  This provides the data for the gold standard that you are referring to.  There is no other manner to diagnose functional outlet obstruction other than the detection of  excessively high  normal range three cycle per minute activity that increases to even higher levels and percentages  following the administration of the water load stimulus.

The functional pyloric outlet obstruction diagnosis, was actually quite a different mechanism  of action compared to that of bradygastria or tachygastria.  Bradygastria is actually a lack of conduction issue  which can be affected by many metabolic conditions, thus the variability.  Tachygastria is equally difficult because that is usually mostly reentrant rhythms  or disordered rhythms that spiral out of control  which is more often associated with poor ICCs.

The ICC concept is actually one of the more exciting ones that has good  histological evidence that clearly demonstrates that poor three cycle  per minute activity in association with elevated tachygastria  positively correlates with degradation of the ICCs.

Thank you, Mark for answering my doubts. In fact design of your research seems to me adequate. It illustrates the difficulties of evaluating a diagnostic test for functional GI disorders. It may be the same if you try to diagnose IBS with a new radiologic or neuro endocrinological   marker.