Laryngopharyngeal Reflux and Voice Disorders

It has been estimated that half of otolaryngology (ORL) patients with laryngeal and voice disorders have laryngopharyngeal reflux (LPR) as the primary cause or as a significant etiologic cofactor. This appears to be true for patients with diverse clinical manifestations.  Many voice clinicians (including the authors) recommend that LPR be routinely assessed in patients with laryngeal and voice disorders; however, even among otolaryngologists who have a relatively high index of suspicion for LPR, it appears that this disorder is still often underdiagnosed and undertreated.  There appears to be a four-part explanation:

1. The symptoms, manifestations, patterns, and mechanisms of LPR and gastroesophageal reflux disease (GERD) are different. Consequently, patients with LPR usually deny symptoms of  heartburn and/or regurgitation. Fewer than half of ORL patients with LPR documented by pH monitoring complain of heartburn or regurgitation, symptoms that clinicians have traditionally felt must be present to diagnose reflux disease.

2. The findings of LPR on laryngeal examination vary considerably, and laryngeal edema, a hallmark of LPR, is often unappreciated as a positive finding. Most otolaryngologists rely solely on the findings of erythema or of posterior laryngitis (red arytenoids and piled-up, hypertrophic, posterior commissure mucosa) as the diagnostic sine qua non of LPR. Unfortunately, those findings are not present in many LPR patients. In the authors’ experience, edema (and not erythema) is the principal, and most common, finding of LPR. The edema may be diffuse, or it may create the illusion of sulcus vocalis, an appearance that is the result of subglottic edema in Reinke’s space. When the edema involves both the true and false vocal folds, it may cause the laryngeal ventricles to swell shut. This relatively common finding is termed ventricular obliteration.

3. Traditional diagnostic tests for gastroesophageal reflux disease (GERD) lack both sensitivity and specificity for LPR. Barium esophagography, radionuclide scanning, the Bernstein acid-perfusion test, and esophagoscopy with biopsy are all often negative in LPR patients.

3 This is probably because most LPR patients do not develop esophagitis, which is typically observed in gastroenterology patients with GERD. In addition, LPR is frequently intermittent, and exacerbations depend to some extent on ever-changing dietary and lifestyle factors.

4. Therapeutic trials using traditional antireflux therapy often fail in LPR patients, so that clinicians may falsely conclude that LPR is not present. The traditional treatment for GERD, particularly in a patient with esophagitis, includes dietary and lifestyle modifications and use of antacids, H2-blockers,
and/or single-daily-dose proton pump inhibitors (PPIs). Such treatment fails to control LPR in up to 50% of patients. In many cases, the treatment dose is inadequate (as most LPR patients require b.i.d. PPI treatment; also, the duration of the therapeutic trial is often too “short.”  Many clinicians believe that a therapeutic trial of antireflux therapy of few weeks duration is adequate, but that is not the case. Patients with longstanding LPR often require 6 months or more of optimal treatment (acid suppression) with PPIs to resolve their symptoms and findings. Also, PPI resistance in LPR patients is not uncommon, being about 10%.

Within the last two decades, with the availability of new diagnostic methods and treatments, researchers have begun to elucidate the clinical patterns and mechanisms of LPR. It now appears that patients with LPR are quite different from typical gastroenterology (GI) patients with heartburn and esophagitis
(ie, GERD). How are LPR patients different than those with GERD? Why do ORL patients usually deny heartburn? What are the differences in the mechanisms of LPR and GERD?

Previously, the diagnosis of LPR was erroneously based on the gastroenterologist’s esophagitis model of GERD. Improved diagnostic technology and effective treatments are beginning to yield important information about LPR and how it differs from GERD.

In a relative sense, ambulatory 24-hour doubleprobe (simultaneous esophageal and pharyngeal) pH monitoring (pH-metry) has become the diagnostic gold standard for LPR; however, as a diagnostic, it is expensive and it is not widely available. Nevertheless, pH-metry effectively documents LPR with a high degree of specificity and sensitivity. The next tier of reflux-testing, impedance,43 may prove to be even better for diagnosis in certain LPR subgroups, such as those with a chief complaint of chronic cough.

Transnasal esophagoscopy (TNE) is performed in the clinic setting without anesthesia or sedation (other than topic numbing of the nose).26-28 TNE has allowed the otolaryngologist to screen the esophagus. In a large series, Postma et al28 reported that 50% of the patients had positive findings on TNE, including, esophagitis 17%, hiatal hernia 8%, Barrett’s metaplasia 5%, candida esophagitis 5%, and stricture 4%.

The treatment of LPR took a giant leap forward with the introduction of proton pump inhibitors (PPIs) into the United States in 1989. Compared to previous treatments, PPIs more effectively reduce gastric acid production.  In addition, antireflux surgery has been shown to be very effective for patients with recalcitrant or life-threatening LPR.

Read: Laryngopharyngeal Reflux and Voice Disorders
Jamie A. Koufman, MD, FACS, S. Carter Wright, Jr., MD

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