With the development of improved fiberoptic technology and with the ability to monitor both acid and nonacid reflux from the stomach into the more proximal gastrointestinal tract, the question of reflux injury or symptoms relating to the larynx has been a focus of considerable research and discussion. One of the important consequences of a growing awareness of the potential for laryngopharyngeal reflux (LPR) has been the dichotomy between gastroenterologists (GIs) and otorhinolaryngologists (ORLs) regarding the importance of this phenomenon—how to be certain of the diagnosis, how to manage it, or simply whether it truly exists. In this issue of the journal, Doctors Yuksel and Vaezi have provided a comprehensive and thoughtful review of the therapeutic approaches available to the patient with possible LPR.1 In this commentary, they provide a discussion of the evidence, or lack thereof, for effective therapies for this potential condition. Throughout the discussion, there are many indications of a lack of reliable evidence in favor of one therapy over another. To me, this reflects the overall confusion regarding the clinical relevance of LPR reported by investigators from a laboratory in which careful study of LPR has been the rule for several years.
The potential for refluxed gastric contents to move proximally into the larynx and airway is generally accepted. However, the details of frequency, type of refluxate, diagnostic testing, and therapy lag far behind. We should make no mistake—the clinical condition of acid reflux–related symptoms and injury to the larynx is well established. This is supported by the paper from Swoger et al2 in which 65% of a group of patients selected because of abnormal symptoms and laryngeal findings plus a positive ambulatory pH test for distal esophageal acid reflux responded to treatment with a proton pump inhibitor (PPI). The unfortunate argument between the GIs and the ORLs regarding this phenomenon relates to that simple fact. That is to say that only patients initially treated with PPIs who fail to respond are subsequently referred to GIs for evaluation and consultative opinion, after the true LPR patients have been “cherry-picked.” Hence, the perspective of the GI community is that perhaps acid reflux as a cause of ongoing ear extra-esophageal (EE) symptoms may not exist.
The discussion is further confused by observations regarding the frequency or number of reflux events required to travel into the proximal esophagus or pharynx to establish this diagnosis. It has been suggested that even one reflux episode within a 24-hour period is abnormal.3 However, other evidence from studies in normal volunteers indicates that 10% of subjects may have >1 pharyngeal reflux episodes in a 24-hour period.4 In addition, recent data from our laboratory of reflux episodes that are associated with symptoms show that proximal reflux (acid or nonacid) is not more likely to be seen with EE symptoms (throat clearing or cough) than they are with more typical gastroesophageal reflux disease symptoms (heartburn or regurgitation).5 The proximal extent of these reflux episodes as monitored by combined impedance-pH testing was no different with any of these 4 symptoms. Additional data from our laboratory indicate that, when monitoring with impedance-pH in large numbers of patients with EE symptoms, there is roughly an 80% chance that a reflux symptom relationship will not be identified in the patient who has already failed to respond to long-term, high-dose PPI therapy. Having said that, however, it is important to recognize that there is also a 20% chance that such a relationship may be found.6 From our own experience, we believe strongly that symptomatic LPR in the patient failing adequate PPI therapy is not common; however, it does occur and does respond to appropriate therapy such as a fundoplication when the diagnosis is correctly established.7
I believe that the following conclusions are appropriate for LPR.
* ENT symptoms secondary to LPR, either acid or nonacid, do occur.
* Proximal esophageal reflux (acid or nonacid) is not more common with EE symptoms.
* Most of these patients (80%) will have a negative symptom association for reflux.
But 20% to 25% will be positive (ie, appropriate testing for reflux is needed).
* A different etiology should be considered for this large group of patients with negative testing.
1. Yuksel ES, Vaezi MF. Therapeutic strategies for laryngeal manifestations of gastroesophageal reflux disease. J Clin Gastroenterol. 2013;47:195–204
2. Swoger J, Ponsky J, Hicks D, et al. Surgical fundoplication in laryngopharngeal reflux unresponsive to aggressive acid suppression. Clin Gataroentrol Hepatol. 2006;4:433–441
3. Hoppo T, Sanz A, Nason K, et al. How much pharyngeal exposure is “normal”? J Gastrointest Surg. 2012. (In press)
4. Maldonado A, Diederich L, Castell D, et al. Laryngoparyngeal reflux identified using a new catheter design. Laryngoscope. 2003;113:349–355
5. Roberts J, Aravapalli A, Pohl D, et al. Extraesophageal gastroesophageal reflux disease (GERD) symptoms are not more frequently associated with proximal esophageal reflux than typical GERD symptoms. Dis Esophagus. 2012. (In press)
6. Mainie I, Tutuian R, Shay S, et al. Acid and non-acid reflux in patients with persistent symptoms despite acid suppressive therapy. Gut. 2006;55:1398–1402
7. Mainie I, Tutuian R, Agrawal A, et al. Combined multichannel intraluminal impedance-pH monitoring to select patients with persistent gastro-esophageal reflux for laparoscopic Nissen fundoplication. Br J Surg. 2006;93:1483–1487