Until now, the prevalence of acid reflux was unknown. In addition, it is clear that not all refluxers have classic gastroesophageal reflux disease (GERD). Many people have symptoms and manifestations of reflux without having heartburn or indigestion, including hoarseness, post-nasal drip, sinus, chronic cough, difficulty swallowing, a sensation of a lump in the throat, and sore throat. This latter group has laryngopharyngeal reflux (LPR), sometimes called silent reflux.

We interviewed 1,010 people (U.S. citizens) in Times Square in New York City, who were in line waiting to buy discount theater tickets (at TKTS). Thus, we obtained a random sample of respondents from all over the nation. The data showed that 40% of the American population had reflux. Twenty-two percent (22%) had known (diagnosed by a doctor) GERD; another 18% had reflux symptoms (including LPR and GERD) but weren’t under a doctors care. One of the biggest surprises in this study was that young people in the 20-30 year-old age group had almost as much reflux (37%) as older people.

Click here to see the entire study abstract (printable PDF version)

Transnasal esophagoscopy (TNE) is particularly useful in patients with reflux, swallowing disorders, strictures, and other esophageal and aerodigestive tract pathology.   The purpose of this article is to report the authors’ present experience and to compare it with previously reported past experience (indications, techniques, complications, and results).

Read more: Transnasal Esophagoscopy: Revisited (over 700 Consecutive Cases)
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Gregory N. Postma, MD; Jacob T. Cohen, MD, Peter C. Belafsky, MD, PhD; Stacey L. Halum, MD;  Sumeer K. Gupta, MD; Kevin K. Bach, MD; Jamie A. Koufman, MD

Most esophagoscopy is now performed flexibly with endoscopes that use a charge-coupled device (CCD) to capture the images and display them on a video screen. Recent technological advances have led to further miniaturization of the CCD, allowing the production of thinner endoscopes. These newer “ultrathin” endoscopes have reached a size at which they can be passed comfortably through the nose and directed into the esophagus. In doing so, the gag reflex can be largely avoided, allowing patients to avoid sedation.

The introduction of transnasal esophagoscopy (TNE) has provided an important advance in the care of patients with reflux, dysphagia, and esophageal pathology. The TNE endoscope offers brilliant illumination and excellent image quality with air-insufflation and irrigation capability through a 2-mm working channel, which can also be used to obtain biopsies and/or to perform procedures. Since 2000, otolaryngologists have popularized TNE and expanded its diagnostic applications for globus, dysphagia, laryngopharyngeal reflux (LPR), and gastroesophageal reflux disease (GERD).

In this paper, we will discuss the role of TNE in clinical practice and review the literature with regard to the utility of the TNE in diagnosing pathology in the esophagus.

Read more: Transnasal esophagoscopy: A position statement from the American Bronchoesophagological Association (ABEA)
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Milan R. Amin, MD, Gregory N. Postma, MD, Michael Setzen, MD, and Jamie A. Koufman, MD, New York City, Manhasset, and Valhalla, NY; and Augusta, GA

Ambulatory 24-hour double-probe (simultaneous esophageal and pharyngeal) pH monitoring (pH-metry) is the current gold standard for diagnosis of LPR, but it is far from being an ideal test. First, the reported sensitivity of pH-metry is only 50% to 80%.  Second, approximately 12% of otolaryngologic patients cannot tolerate the procedure.  Third, dietary modifications (to standardize the test) may lead to false-negative pH studies. And finally, pH-metry is expensive and has limited availability. Thus,
there appears to be a need for a sensitive, noninvasive, and inexpensive diagnostic test for LPR.

Pepsinogens belong to a family of aspartic proteinases and are produced primarily by chief cells within the gastric fundus. In the acidic environment of the stomach, pepsinogen is activated by HCL (acid). Pepsin plays a major role in the development of many reflux-related disorders.

Gastroesophageal reflux always contains pepsin, but not all reflux occurs below pH 4.0. Thus, with use of traditional gastroenterology standards for pH-metry, significant LPR may be under diagnosed. Indeed, pepsin exhibits enzymatic activity at pH levels well above, and it is only irreversibly inactivated at a pH greater than 6.5. Thus, a patient could conceivably have a negative pH study (no reflux events pH ≤ 4) but might still have significant LPR-related disease. We have previously reported that the laryngeal epithelium is far more sensitive to damage by pepsin in the presence of acid than is esophageal epithelium, and that may help explain why the patterns of reflux, reflux mechanisms, and clinical manifestations of LPR and GERD are so different.

We postulated that measurement of pepsin in airway secretions might provide a sensitive diagnostic marker for LPR, and furthermore, because pepsin is a large molecule, that it might be detected in airway secretions long after gastric reflux had occurred, making it a good diagnostic marker (U.S. Patent No. 5,879,897). Our strategy was to develop an enzyme-linked immunosorbent assay (ELISA) to detect pepsin and then to test its diagnostic sensitivity and specificity in a clinical setting.

Read more: Sensitive Pepsin Immunoassay for Detection of Laryngopharyngeal Reflux

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John Knight, PhD; Mark O. Lively, PhD; Nikki Johnston, PhD; Peter W. Dettmar, PhD; Jamie A. Koufman, MD

Some patients who present with dyspnea, stridor, and airway obstruction have paradoxical vocal fold movement (PVFM). PVFM is characterized by inappropriate adduction of the vocal folds during inspiration (Appleblatt & Baker, 1981; Maschka et al., 1997; Mathers-Schmidt, 2001; Murry, Tabaee, & Aviv, 2004). The persistence and the degree of inappropriate glottal closure with PVFM determines the degree of obstruction. In some patients, the problem is constant and severe, requiring airway intervention; in others, the problem is intermittent and relatively mild.

In addition to the term PVFM, there have been a number of other terms used in the literature to identify this complex and often confusing disorder in adults and children, including Munchausen’s stridor (Patterson, Schatz, & Horton, 1974), vocal cord dysfunction (Christopher et al., 1983), paradoxical vocal cord motion (Martin, Blager, Gay, & Wood, 1987; Sandage & Zelazny, 2004), and irritable larynx syndrome  (Andrianopoulos, Gallivan, & Gallivan, 2000; Morrison, Rammage, & Emami, 1999). Maschka et al. (1997) and Mathers-Schmidt (2001) provided classifications and discussions of some of the causes of this condition.

In this article, we provide a concise differential diagnosis for PVFM in adults (see Appendix A). We reserve the term PVFM to refer to inappropriate vocal fold adduction during inspiration, and we present differentiating features of specific etiologies. We offer a new classification of PVFM because accurate diagnosis is a prerequisite for effective treatment.

Read more: Differential Diagnosis of Paradoxical Vocal Fold Movement
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Jamie A. Koufman, Voice Institute of New York and New York Medical College; Christie Block, Private Practice, New York, and New York University

The treatment for LPR currently consists of dietary and lifestyle modification along with proton pump inhibitor (PPI) therapy. Results from treatment with PPIs have generally been excellent; improvement has been measured both in eradication of symptoms and improvement in laryngeal findings. Unfortunately, not all patients respond as expected to PPIs. Some patients require higher doses of medication, a change in their PPI, or antireflux surgery to control LPR. This report reviews our experience with the treatment of LPR with PPIs, and defines the relative failure rate of this class of
medication in treating this problem.

Read more: Proton pump inhibitor resistance in the treatment of laryngopharyngeal reflux
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MILAN R. AMIN, MD, GREGORY N. POSTMA, MD, PAUL JOHNSON, MD, NICHOLAS DIGGES, MD, and JAMIE A. KOUFMAN, MD, Philadelphia, Pennsylvania, Winston-Salem, North Carolina, and Omaha, Nebraska

The most common symptoms associated with LPR are hoarseness, dysphagia, globus pharyngeus, chronic throat clearing and cough, and excessive throat mucus. Common laryngeal findings of LPR are localized or diffuse laryngeal edema, opalescence and/or hypertrophy of the posterior commissure, erythema, granulation, and, sometimes, granuloma formation. Classic posterior laryngitis (red arytenoids and piled-up interarytenoid mucosa) is not seen in most patients with LPR. Instead, laryngeal edema, not erythema, is by far the most common laryngeal finding.

The first reports of the use of ambulatory 24-hour pH monitoring in otolaryngologic patients with hoarseness and other throat symptoms appeared in the 1980s.  Wiener et al reported the use of simultaneous monitoring of the pH in the distal esophagus and in the pharynx by placement of a second pH probe in the hypopharynx behind the laryngeal inlet. This diagnostic technique was used to document the presence of extraesophageal reflux (ie, true LPR). This test is the current gold standard for diagnosis of LPR.

Although LPR is now a widely recognized clinical entity, the incidence of this disease process remains unknown. The purpose of this study was to investigate the prevalence of reflux disease in a consecutive series of patients with laryngeal and voice disorders with ambulatory 24-hour double-probe pH testing.

Read more: Prevalence of reflux in 113 consecutive patients with laryngeal and voice disorders
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JAMIE A. KOUFMAN, MD, FACS, MILAN R. AMIN, MD, and MARGUERITE PANETTI, MA,Winston-Salem, North Carolina, and Philadelphia, Pennsylvania

Diagnostic assessment of patients with laryngopharyngeal symptoms using pH monitoring of the esophagus was first reported in the 1980s, but Wiener et al. were the first to use simultaneous esophageal and pharyngeal pH monitoring in this group. This technique accurately determines acid reflux events above the upper esophageal sphincter, at the laryngeal inlet, and within the esophagus. When guided by manometry, double-probe pH monitoring remains the gold standard for the diagnosis of LPR.

Screening of the esophagus in patients with GERD for associated disease (e.g., esophagitis, Barrett’s metaplasia, stricture, neoplasm) has long been the standard of medical  practice. Before the availability of transnasal esophagoscopy (TNE), most otolaryngologists relied on barium esophagography to screen the esophagus for related disease because it was a relatively noninvasive method.  However, barium studies have a relatively low sensitivity for esophagitis and Barrett’s metaplasia; reflux is radiographically apparent in only 33% of patients with pH-documented GERD and in only 25% of patients with endoscopically proven esophagitis.

Esophagoscopy is a far more sensitive and specific test for esophagitis and associated pathological conditions, particularly when coupled with biopsy of the esophageal mucosa. Transnasal esophagoscopy is a relatively new technology that has the additional advantages of allowing esophagoscopy to be performed in the office with the patient seated and not sedated, requiring only topical anesthesia.  Currently at our center, we routinely employ TNE as a screening and as a diagnostic tool. We have virtually abandoned barium esophagography as a part of our reflux testing battery. The purpose of the present investigation was to determine the prevalence of endoscopically and histologically demonstrated esophagitis in otolaryngologic patients with pH-documented LPR.

Read more: Prevalence of Esophagitis in Patients With pH-Documented Laryngopharyngeal Reflux
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James A. Koufman, MD; Peter C. Belafsky, MD, PhD; Kevin K. Bach, MD; Elena Daniel, MD; Gregory N. Postma, MD

Some people who deserve credit for seminal thinking in LPR and who most influenced me were Nels Olson, Paul Ward, Paul Chodosh, and Bob Toohill. I remember Dr. Olson warning me that LPR was contentious. He told me that some of his academic contemporaries had tried to discredit him because of his beliefs that LPR was ubiquitous and caused a myriad of airway diseases. Of course when Dr. Olson talked about reflux, it was GERD. It wasn’t until 1991 that I coined the term laryngopharyngeal reflux, the same year as the publication of my thesis.1 I felt that we needed a new term to for the type of “silent” reflux disease that our patients demonstrated. I chose the term laryngopharyngeal reflux to call attention to the fact that the symptoms and manifestations were laryngeal and pharyngeal, that is, not esophageal. I also believed that the diagnosis and treatment of LPR were different than those for GERD.

The idea was to intentionally create a nosological schism between the specialties so that otolaryngologists would consider new ideas that were not yet acknowledged by gastrointestinal (GI) colleagues. Incidentally, the term silent reflux was coined by Dr. Walter Bo, chair of the anatomy department at Wake Forest University. Walter was my patient in 1988, and he had LPR.  After I had explained how one could have reflux without heartburn, Dr. Bo rolled his eyes and then announced, “I see; I have the silent kind of reflux.”

Early on I recognized that LPR was controversial, because for almost five years I couldn’t get anything published on the subject. Papers on the laryngeal findings, prevalence of LPR, as well as papers about the possible relationship between LPR and laryngeal cancer were rejected outright.  Perhaps intended as a warning, the comments of one anonymous reviewer for a prestigious journal were forwarded to me, “Something has to be done about Koufman’s preoccupation with GERD”;  and the reviewer went on to actually suggest that I was on the payroll of one of the big pharmaceutical companies. This was certainly untrue! I was surprised and disappointed by that communication and its implications; it wasn’t exactly a positive testimonial for peer review.

Even before publication of my thesis, it was apparent that resolution of the controversies about the diagnosis and treatment of LPR, as well as its causal relationship to airway disease, would require credible bench research, that is, more than pH-monitoring data. Table 1 summarizes many of the types of research that have helped establish LPR entity.  Twenty years later, the cell biology of LPR is beginning to yield some answers about epithelial defenses of the larynx, the mechanisms of reflux-related inflammation and tissue injury, and the causal relationship between LPR and many laryngeal diseases.

Read more:  FROM SILENCE TO OMNIPRESENCE: PERSPECTIVE ON THE EVOLUTION OF LARYNGOPHARYNGEAL REFLUX
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Jamie A. Koufman, M.D., F.A.C.S.
Jamie A. Koufman, M.D., F.A.C.S., Director, Voice Institute of New York