Supraesophageal Reflux: Approach to Diagnosis and Management?

M. Brian Fennerty, MD


March 25, 2004


What are the strategies for diagnosing supraesophageal reflux, and what is the recommended approach to treatment?

Response from M. Brian Fennerty, MD

There are many manifestations of reflux outside the well-recognized symptoms of heartburn and regurgitation. The terms supraesophageal, atypical, and extraesophageal have all been used to describe additional gastroesophageal reflux disease (GERD)-related symptoms, such as cough, hoarseness, voice change, asthma, sinusitis, otitis media, and dental enamel loss, that have either been proven or thought to be associated with gastroesophageal reflux. In fact, many of the patients referred to me for evaluation of reflux are done so after the finding of erythema or edema on a pharyngeal/laryngeal exam by an otolaryngologist evaluating the aforementioned symptoms. It should be emphasized that these pharyngeal/laryngeal findings are not specific for GERD as a causative factor, nor have their sensitivity been appropriately documented. The precise pathophysiologic mechanism(s) responsible for the production of supraesophageal GERD symptoms remains contentious, but likely represents either an esophageal-bronchial reflex response to refluxate or the result of upper airway-reflux contact and/or aspiration of refluxate.[1] Somewhat surprisingly, patients presenting with supraesophageal reflux symptoms often do not concomitantly manifest the usual symptoms of GERD -- ie, heartburn and/or regurgitation. These above factors often lead to a clinical dilemma regarding how to effectively diagnose supraesophageal GERD as well as to issues regarding the optimal management of these "GERD" patients.

The options available for diagnosing GERD include the following: the presence of classical heartburn and regurgitation; the response of symptoms thought to be GERD-related to an empirical trial of antireflux therapy; ambulatory, esophageal pH monitoring demonstrating pathologic intraesophageal acid exposure; and/or upper gastrointestinal endoscopy demonstrating esophagitis, strictures, Barrett's esophagus, or other objective signs of GERD. The first and last of these "diagnostic" tests are not very useful in the case of suspected supraesophageal GERD because many of these patients fail to demonstrate the typical symptoms of heartburn and regurgitation, and most do not have esophagitis when looked at endoscopically. Thus, a diagnosis of GERD-related cough, asthma, hoarseness, etc, requires either a response to empirical antireflux therapy or documentation of reflux by esophageal pH monitoring.

Empirical, potent antisecretory therapy has been shown to be effective as a diagnostic tool for GERD-related chest pain, cough, and perhaps, even hoarseness.[2,3] This approach has also been used in patients with asthma and other such symptoms, but there are little or no data regarding its effectiveness in these other clinical situations. Furthermore, the optimal dose, frequency, duration, and end point to be measured are unclear in all of the various manifestations of supraesophageal GERD. Nonetheless, this initial diagnostic approach appears to be the most widely practiced method to determine whether a patient suspected of having supraesophageal GERD actually has the disease. Most authorities do recommend a trial of at least twice-daily, proton-pump inhibitor therapy, for 2-4 weeks for chest pain and cough and 2-3 months for asthma, with this approach.[1] This is based on the fact that one would like to ensure normalization of intraesophageal acid exposure in any diagnostic trial. The latter will frequently require twice-daily dosing to achieve, and in the case of asthma, the inflammatory response may take weeks or months to resolve, thus limiting diagnostic trials of therapy to longer duration in "inflammatory" diseases vs those not related to inflammation (ie, cough and chest pain).

The other approach to diagnosing supraesophageal reflux involves performing esophageal pH testing. It is important to remember that the presence of pathologic intraesophageal acid exposure defines GERD; however, it does not establish causation of symptoms. Whether a dual-pH probe with 1 site placed proximally in the esophagus, cricopharyngeus, or pharynx increases the diagnostic yield or accuracy of this test has never been firmly established, but this technique is commonly performed (and is the approach I use in practice). My own bias is that demonstration of pathologic intraesophageal acid exposure at either the distal or proximal site is sufficient to warrant a probable diagnosis of supraesophageal GERD.

What then is the optimal management for patients with confirmed or strongly suspected supraesophageal GERD? Like any manifestation of GERD, one should use the lowest but effective dose to manage the patient's GERD symptoms.[4] This strategy may involve a single, daily dose of a proton-pump inhibitor, but not uncommonly, will require more frequent dosing as well as very high doses of these agents to achieve and maintain clinical remission. Surgical antireflux therapy is also an option for these patients, but despite some proponents' comments, no strong data exist suggesting surgical therapy is more effective than pharmacologic therapy for this patient population.


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