This particular patient I have just treated is quite interesting and worth sharing. The patient is young man who has been suffering with acid reflux for the past 15 years. He is currently in his early thirties and his GERD related symptoms are poorly controlled with high dose Dexilant. He has heartburn and food regurgitation on a daily basis. He avoids most food items in order to prevent a heartburn attack. He reports no dysphagia or food impaction. An upper endoscopy showed distal esophagitis but no hiatal hernia. His DeMeester score on ambulatory pH testing was high and he had positive symptom correlation to heartburn and food regurgitation. In preparation for Nissen fundoplication surgery, I performed an esophageal manometry. He had elevated intra-bolus pressure and slightly elevated residual lower esophageal sphincter (LES) pressure with incomplete relaxation. These findings indicate asymptomatic esophageal outflow obstruction in the setting of severe GERD. Of note, LES length was shorter than normal.
Esophageal outflow obstruction is sometimes encountered in large hiatal hernia cases. The obstruction is attributed to distortion of the GEJ anatomy by the hernia. In our case, however, the patient did not have any hernia. Instead, I found extensive adhesions surrounding the distal esophagus and “trapping” the LES in a fixed position just at the diaphragmatic level. Indeed, the intra-abdominal esophagus prior to dissection measured less than 2 cm. In my opinion, severe gastric content reflux has led to significant scarring around the distal esophagus and possibly leading to failure of the LES to completely relax. A non-relaxing LES did not prevent, however, reflux from occurring. Contrary to what LINX™ device proponent would like you to believe, LES augmentation is not a solution for GERD. GERD is not simply the result of a weak LES. It is rather a complex pathophysiological condition that results from abnormal esophago-gastric motility. Common sense interpretation limits our understanding of GERD to LES weakness or transient LES relaxation. However, LES weakness is secondary to an underlying complex motility problem that is currently only addressed by a floppy and short Nissen fundoplication. A floppy and short Nissen fundoplication does not really reinforce the LES. Any attempt at reinforcing the LES is likely to lead to postoperative dysphagia and esophageal dysmotility in the long run. In fact, in this particular patient who already has elevated LES pressure, any LES reinforcement would most likely lead to post-operative dysphagia.
Our patient had a great outcome from his laparoscopic fundoplication. I performed a short and floppy Nissen fundoplication that resulted in no dysphagia after surgery and in complete resolution of all GERD related symptoms. Can you imagine treating this patient with a LINX™ device?
It would be interesting to repeat esophageal manometry 3 to 6 months after surgery to check for the resolution of the incomplete LES relaxation and elevated residual pressure.