Most gastro-oesophageal reflux events are triggered by transient lower oesophageal sphincter relaxations (TLOSRs). Acid-related reflux disease with typical heartburn and reflux oesophagitis generally responds well to acid suppression with proton pump inhibitors (PPI), but treating non-acid and mixed gaseous reflux has proven more challenging. Unfortunately, the majority of refractory gastrooesophageal reflux disease (GORD) and laryngopharyngeal reflux (LPR) is linked to functional gut disease or proximal weakly acid reflux, which is more associated with upper GI dysmotility. Although considered to be our gold standard, detecting proximal oesophageal and airway reflux with oesophageal pH impedance has serious limitations. Oesophageal mucosal impedance and reflux scintigraphy have the potential to assess proximal reflux more accurately with the latter able to accurately detect even minute amounts of airway contamination of the larynx, lungs, sinuses, and ears. Our current treatment algorithm completely ignores the effect of downstream colonic faecal and/or gaseous distension, which may be occult or associated with irritable bowel syndrome. Colonic distension has not only been shown to trigger TLOSR and increase reflux events, but also induce upper GI dysmotility associated with LPR and functional upper gut disease. Simple patient screening with abdominal x-rays and treatment with laxative therapy to reverse motility reflexes provides an easy way to optimise outcomes in refractory GORD or LPR. Refractory GORD and LPR do not respond well to even high dose PPI therapy because acid suppression does not address the underlying pathophysiology.
Refractory gastro-oesophageal reflux disease, Laryngopharyngeal reflux, Reflux scintigraphy, Oesophageal pH impedance monitoring, Oesophageal mucosal impedance, Colonic distension reflexes, Proton pump inhibitors, Nizatidine, Prucalopride